Introduction \par This is an up-date of the last listing published in Mouse Genome 94(3) (September 1996). A total of 478 strains are listed, though many of these must be extinct



Download 0.63 Mb.
Date conversion19.05.2016
Size0.63 Mb.
INTRODUCTION \par This is an up-date of the last listing published in Mouse Genome 94(3) (September 1996). A total of 478 strains are listed, though many of these must be extinct. If anyone knows of such extinct strains, please let me know. In a few cases data on extinct strains is given but the fact that it is extinct is noted. About 150 new references have been quoted. \par Note that the strains are listed in order according to the ASCII code, with strains having a numerical designation such as 129 listed before strains with an alphabetic designation such as A. Special characters such as a slash (/) also come before alphabetic ones. \par Some of the more widely used strains have become divided into substrains among which there are detectable genetic differences. This is likely to accelerate as we learn more about such differences using the very wide range of genetic markers which are now available. Two extensive studies on the 129 strain have recently been published, and the nomenclature of this family will be revised in due course. A similar study on the SL family has also clarified the relationships between existing substrains. \par \par Many of the strains are related, having come from the same outbred colony, or having some other form of common ancestry. Other strains are derived directly from wild mice. There is increasing evidence that laboratory mice have been developed with contributions from more than one species/subspecies of wild mouse. For example, some strains carry the \i Mus musculus domesticus \i0 Y-chromosome, while others have the \i M.m. musculus \i0 type. Thus, Nishioka (1987) found the following: \par \par \i M.m. musculus \i0 type \par A/J, AEJ/Gn, AU/SsJ, BALB/cJ, BDP/J, BXSB/MpJ, CBA/J, CE/J, C3H/HeJ, C57BL/6J, DA/HuSn, DBA/2J, HRS/J, HTG/Go,, I/Ln, LP/J, NZB/BlN, NZW/Lac, P/J, RIIIS/J, SB/Le, SEA/Gn, SEC/1ReJ, SF/Cam, SK/Cam, SM/J, WB/ReJ, WC/ReJ, YBR/Ei, 129/J. \par \par \i M.m. domesticus \i0 type \par AKR/J, BUB/J, MA/MyJ, PL/J, RF/J, SJL/J, ST/bJ, SWR/J, SWV. \par \par NOTES ON THE LISTINGS \par The number of generations of full-sib mating is given for each strain, but this should be regarded as an approximate figure, as it varies considerably between colonies, and it is very difficult to keep it updated. In any case it is doubtful whether the exact figure has much significance once 30-40 generations have been completed, except possibly in studies of substrain differentiation. \par In the case of quantitative characteristics strains have been ranked, and approximately the top and bottom quarter of the strains have been ranked as `high' and `low' ,respectively. Thus, `low intra strain aggression (13/14)' indicates that in a study of intra-strain aggression the strain in question ranked thirteenth out of fourteen strains being tested. These strain rankings should be treated with some caution, as they depend on exactly which strains happened to be chosen for the study, and the rankings could be altered by environmental influences. In some cases it will be noted that studies by different workers are contradictory. In the case of qualitative characteristics a `cf'. (compare) precedes the number responding out of the number tested. Thus good immune response to X antigen (cf. 4/8) means that the strain was one of four responders out of eight tested. Several papers describe pairs of strains which are known from previous work to differ. In this case the paper is quoted and the contrasting strain is noted in parenthases. \par Where a substantial amount of information is available for a given strain this has been classified into `\i Behaviour\i0 ', `\i Life-span and spontaneous disease\i0 ', etc. The heading `\i Drugs\i0 ' refers to response to any xenobiotic such as chemicals and drugs, and also includes response to irradiation. \par \par In compilations of this sort, substrain differences present a problem. Where there are major substrains of an inbred strain, an attempt has been made to show which one was involved in each study. However, references have been given, and where necessary the original article should be consulted. \par \par I would appreciate it if people could send me reprints and other information which describe strain characteristics which are not listed here, and bring any inaccuracies or omissions to my attention. The previous listing is already available on-line in a searchable database which can be accessed via the Jackson Laboratory (see contribution by Dr. Janan Eppig in this issue). This updated version will be put on line as soon as possible. I would like to take this opportunity of thanking the Jackson Laboratory for providing this service. \par \par INBRED STRAINS AND THEIR CHARACTERISTICS \par 101 \par Inbr: 66. Genet: \i A\i0 \i \up8 w\up0 \i0 \up8 \up0 . Origin: Dunn, 1936. \par Characteristics \par Low mammary tumour incidence; slow to breed, fertility moderate; high susceptibility to skin and lung tumour induction. Low metabolic rate (6/6) (Pennycuik, 1967). Resistant to \i Mycobacterium marinum \i0 (1/9) (Shepard and Habas, 1967). Unusual backward locomotion observed in 101/HY, somewhat similar to the hot-foot neurological mutation (Poletaeva et al 1992). Maint. by H. \par 102 \par Inbr (El) 93. Agouti: +. Origin: From 101/Rl to El, then presumed genetic contamination. Differs from 101 at the \i a,\i0 \i Car2, Gpi1\i0 \i \up8 s\up0 \i0 \i ,\i0 \i Hba\i0 and \i lop2\i0 loci. Maint. by H, El. \par 129 \par Inbr and colour depends on substrain (see below). Origin: Dunn 1928 from crosses of coat colour stocks from English fanciers and a chinchilla stock from Castle. This strain has a common origin with strain 101. Most substrains carry the white-bellied agouti gene A\up8 W \up0 though only a subset have the agouti pattern as many carry albino or chinchilla and/or the pink-eyed dilution gene, \i p\i0 , which is derived from Asian mice of the \i Mus musculus\i0 type (see also strains SJL, P/J and FS/Ei) (Brilliant et al, 1994). \par It is known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains, but more recently it has been the most widely used strain in the production of targeted mutations due to the availability of several lines of embryonic stem cells. Two recent studies show that there is major genetic variation within the 129 "family", at least some of which must be attributed to genetic contamination (Threadgill et al, 1997,Simpson et al, 1997). Strain 129/SvJ was genetically contaminated in about 1978 by an unknown strain, and differs from other 129 substrains at about 25% of SSLP genetic markers. Threadgill et al suggest that it is equivalent to a recombinant congenic strain and suggest that it is designated 129cX/Sv. Simpson et al recognised three major groups of substrains: parental substrains, steel substrains and "ter" substrains. Threadgill et al identified substrains 129/Ola, 129/J, 129/Sv, 129/ReJ and 129/RrRk, and the associated embryonic stem cells. \par Studies of 129 genealogy and genetics have resulted in major nomenclature changes for 129 substrains. See Mouse Strain 129 Substrain Nomenclature. \par "Parental" substrains \par 129/J \par 129/ReJ \par 129/ReJ-Lama2\up8 dy\up0 \par 129/OlaHsd \par 129/Sv \par 129/SvJ \par \par \par 129/Re \par Inbr (J) 89. Pale yellow: \i A\i0 \i \up8 w\up0 \i0 \i ,c\i0 \i \up8 ch\up0 \i0 \i ,p.\i0 Non-dystrophic substrain of 129/Re-\i dy.\i0 Maint. by Ola. \par \par 129/RrJ . \par Inbr (J) 97. Pale yellow, or albino. \i A\i0 \i \up8 w\up0 \i0 \i , c\i0 \i \up8 ch\up0 \i0 \i \i0 (or \i c\i0 ),\i p\i0 . Origin: Jackson Laboratory 1948. Maint. by J. \par \par 129/Sv-\i ter/+\i0 \par Inbr (Sv) N8 F49. Agouti with light belly: \i A\i0 \i \up8 w\up0 \i0 \i ,\i0 \i c\i0 \i \up8 ch\up0 \i0 \i , p\i0 \i \up8 +\up0 \i0 \i .\i0 Also carries a gene \i ter\i0 causing a high incidence of testicular teratomas. Origin: A substrain to determine the effect of the \i W \i0 gene on incidence of testicular teratomas. The\i W\i0 gene was backcrossed repeatedly to 129, and at generation N8 a female produced 38 male offspring of which 8 had testicular teratomas. All subsequent members derived from that mating. The\i W\i0 gene has been eliminated. Incidence of testicular teratomas now 30% (Stevens, 1973). Maint. by J. \par \i Behaviour\i0 \par Low avoidance conditionability (8/9) (Royce, 1972). Low shock-avoidance learning (6/6 in males, 5/6 in females) (Royce \i et al\i0 ., 1971). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged, Sv substrain) (25/26) (Lush 1988). Prefers moderate concentrations of saline (contrast C57BL/6) (Beauchamp and Fisher, 1993, Gannon and Contreras, 1995). \par \i Life-span and spontaneous disease\i0 \par Long life-span in conventional conditions (18/22 = 679 days in males, 15/22 = 648 days in females) (Storer, 1966). Long life-span in SPF fostered conditions (16/17 = 699 days in males, 11/1 7 = 666 days in females) (Festing and Blackmore, 1971). Low overall tumour incidence (7% in males, 21% in females), including lymphoma 2% in males and 7% in females, soft tissue sarcomas 2% in males and 1% in females and benign tumours 2% in males and 3% in females (Smith \i et al\i0 ., 1973). Lung tumours 4-46% (Festing and Blackmore, 1971). Testicular teratomas about 1% in most substrains, but 30% in the terSv substrain (Stevens, 1973). Incidence of teratomas increased in p53-deficient mice (Harvey et al, 1993). The Ter gene has been mapped to chromosome 18 (Asada et al, 1994). Congenital malformations about 4% in RrSvKt-\i jt\i0 substrain (Kalter, 1968). High incidence of urinary calculi (Russell and Meier, 1966). \par \i Normal physiology and biochemistry\i0 \par High plasma cholesterol at 12 and 24 weeks (2/8) (Weibust, 1973). Low plasma triglyceride levels (2/11) (Jiao et al 1990). High Na/K ratio in erythrocytes (1/9) and plasma (4/9) (Waymouth, 1973). High serum ceruloplasmin levels in males (3/26) but low levels in females (24/27) (Meier and MacPike, 1968). High plasma cholinesterase activity (3/22 in males, 8/22 in females) (Angel \i et al\i0 ., 1967). Low mean heart rate (7/7) but high mean heart adaptation rate (2/7) (Blizard and Welty, 1971). High cell turnover in J substrain as estimated by rapid clearance of DNA-bound radioactivity (3/17) (Heiniger \i et al\i0 ., 1972). Venous blood has a high pH (1/10) (Bernstein, 1966). High hepatic microsomal coumarin hydroxylase activity in females (2/8) (Van Iersel et al, 1994). High levels of apoA-IV messenger RNA in liver compared with C57BL/6 (Reue et al, 1993). \par Has defective secretory group II phospholipase A2 gene (cf strains C57BL/6 and B10.RIII) (Kennedy et al, 1995). \par \i Anatomy\i0 \par Large brain/body weight ratio (3/20) (Roderick \i et al\i0 ., 1973). Small spinal cord (21/25) (Roderick \i et al\i0 ., 1973). Small forebrain volume (8/9) and neocortex (8/9) (Wimer \i et al\i0 ., 1969). A large proportion of 129/Ola mice have major shunts between the hepatic portal system and the vena cava, allowing the passage of microspheres up to 50m in diameter.. These shunts are associated with resistance to \i Shistosoma japonicum\i0 cercariae (Coulson and Wilson 1989). High retinal ganglion cell number (19/24) in /J substrain (Williams et al, 1996). Absence of corpus callosum in about 70% of mice of the 129/J substrain. This may be related to retarded formation of the hippocampal commissure in this strain and in BALB/c mice (Livy and Wahlsten, 1997). High bone density of femur in J substrain (3/11) (Beamer et al, 1996). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to induction of subcutaneous tumours by 3-methylcholanthrene (10/14) (Kouri \i et al\i0 ., 1973). Resistant to X-irradiation (1/27) (Roderick, 1963), (1/10) (Storer, 1966). Females have long sleeping time under hexobarbital anaesthetic (14/15) (Lovell, 1976). Resistant to toxic effects of isoniazid (3/10) (Taylor, 1976b). Insensitive (eosinophil response) to cortisone acetate (cf. 3/6) (Wragg and Speirs, 1952). Sensitive uterine response to oestrogens (1/5) (Chai and Dickie, 1966; Drasher, 1955). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). \par \i Immunology\i0 \par High lymphocyte phytohaemagglutinin response (12/43) (Heiniger \i et al\i0 ., 1975). Responder to synthetic polypeptide (Glu\up8 57\up0 , Lys\up8 38\up0 , Ala\up8 5\up0 ) (cf. 3/7) (Pinchuck and Maurer, 1965). Erythrocytes have a high agglutin ability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). High responder to Dextran (cf. 4/10) (Blomberg \i et al\i0 ., 1972). Experimental systemic lupus erythematosus including severe ocular changes and blepharitis can be induced by injection of human monoclonal anti-DNA antibodies (Chan et al, 1995). \par \i Infection\i0 \par Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). \par \i Reproduction\i0 \par Poor breeding performance (19/22), colony output 0.8 young/female/wk, litter size at weaning 4.5 (19/22) (Festing, 1976a). \par \i Miscellaneous\i0 \par Recommended host for transplantable tumour haemangioendothelioma BW6473 (Kaliss, 1972). \par 201 \par Inbr (Rl) 75+. Colour: various depending on genotype. Genet. \i A\i0 \i \up8 y\up0 \i0 \i /a,\i0 \i pe\i0 . Origin: Russell, from PE/Rl and a non-inbred \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 stock. Maintained by matings of \i A\i0 \i \up8 y\up0 \i0 \i /a,pe/pe x a/a pe/pe.\i0 Occasional somatic reverse mutations. Abnormal kidney enzyme levels. Maint. by Rl. \par 615 \par Inbr 64. Chocolate: \i a,b. \i0 Origin ?: Tianjin, China. Well characterised at polymorphic loci. \par A \par Inbr: More than F150. Albino. Genet: \i a, b, c. \i0 Origin: Dr L. C. Strong, 1921, from a cross between the Cold Spring Harbor and Bagg albino random-bred stocks (and therefore relavted to BALB/c). Internationally distributed, Strain A was the third most widely used strain in cancer and immunology research (Festing, 1969), though its popularity has probably declined recently. Although it may be classified as a general-purpose strain, it is well known for a high susceptibility to induction of congenital cleft palate by cortisone and a high spontaneous incidence of lung adenomas, as well as developing a high incidence of lung tumours in response to carcinogens. Shimkin and Stoner (1975) suggest that this response may be used as a rapid in \i vivo \i0 assay for carcinogenesis. The strain also suffers from a defect in macrophage function somewhat resembling the mutant \i lps\i0 found in C3H/HeJ (Vogel et al 1981). \par The following main substrains are recognised, though they have not been defined by genetic markers: \par A/St \par Maintained by Strong. \par A/He \par Strong to Heston, 1938. \par A/GrFa \par Main British substrain, Strong to Gruneberg 1932, and mainly distributed by Falconer. \par A/WySn \par Strong to Bittner 1927, to Wooley, to Snell, 1951. \par A/J \par Strong to Cloudman 1928, to Jackson Laboratory 1947, now widely distributed. \par \i Behaviour\i0 \par Low intra-strain aggression (13/14) (Southwick and Clark, 1966), low food drive (15/15) and exploratory activity (15/15) (Thompson, 1953). Low spontaneous bar pressing activity (12/14), low open-field activity (13/14 and 14/14 in J and He substrains), low social grooming during aggressive encounters (12/14 in He substrain) and high tail rattling score (3/14 and 5/14 in J and He substrains) during aggressive encounters (Southwick and Clark, 1968). Low spontaneous locomotor activity (2/9) (Nikulina et al 1991). High shock avoidance learning (3/9) (Bovet \i et al\i0 ., 1966), high avoidance conditioning (2/9) (Royce, 1972), and (2/6 males, 1/6 females) (Royce \i et al\i0 ., 1971), but poor shock avoidance learning (8/8) (Wahlsten, 1973), poor T-maze learning (6/6) (Stasik, 1970). Long latency to attack crickets (7/7) (Butler, 1973). Long latency to emerge from home cage (7/7), low exploration in Y-maze (6/7), low rearing (6/7), long latency to climb barrier (7/7), low hole-in-the-wall entry (7/7), low stair climbing (6/7) (McClearn \i et al\i0 ., 1970). Poor shock avoidance conditioning (6/7 and 7/7 in He and J substrains) and rapid extinction (1/7 and 2/7 in J and He substrains) (Schlesinger and Wimer, 1967). Poor performance in a food-seeking task (6/6) (Henderson, 1970). High social dominance of males in competition for females (1/6) (De Fries and McClearn, 1970). High open-field defaecation (1/5) in both sexes (Bruell, 1969). Low open- field activity (12/13) (Bruell, 1964). Low proportion of paradoxical sleep (6/7) (Pagel \i et al\i0 ., 1973), low incidence of tail rattling (5/5) (St. John, 1973). High shuttle box avoidance (1/5) (Messeri \i et al\i0 ., 1972). Low wheel activity (5/5) (Messeri \i et al\i0 ., 1972), low alcohol preference (15/18) (Rodgers, 1966). \par \i Life-span and spontaneous disease\i0 \par Primary lung tumours 6% in male, 32% in female and 26% in virgin females in J substrain; 44% in males, 23% in females and 30% in virgin females in He substrains (Hoag, 1963). Zero incidence of lymphatic leukaemia in He substrain, 1% in J substrain. Mammary adenocarcinomata zero in males, 1% in virgin females, 28% in breeding females of J substrain and 54% in breeding females of He substrain (Hoag, 1963). Pulmonary tumours 90% in mice at 18 months (Heston, 1963). Leukaemia 3% in HeJ substrain (Myers \i et al\i0 ., 1970). A high proportion of the mammary tumours are of the acinar type (3/7) (Tengbergen, 1970). Lung adenomas 53-64% in BrA and A substrains, but mammary tumours zero (Muhlbock and Tengbergen, 1971). Lung tumours 4-31% and lymphatic leukaemia 10-43% (Festing and Blackmore, 1971). Spontaneous lung tumours occur at rate of 0.21 tumours/mouse at 24 weeks (Poirier \i et al\i0 ., 1975). Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in the J and HeJ substrains (Sundberg et al 1991) \par \par Life-span in conventional conditions intermediate in both sexes (9/22 = 490 days in males, 13/22 = 590 days in females (Storer, 1966). Life-span in SPF fostered conditions intermediate (8/17 = 512 days) in males and short (3/17 = 558 days) in females (Festing and Blackmore, 1971). Life-span 662 days in males and 688 days in females (Goodrick, 1975). Median life-span 400 days in HeJ substrain (Curtis, 1971). \par Spontaneous congenital cleft palate 4% and high susceptibility to teratogenic effects of cortisone, which may be associated with the \i H2\i0 \i \up8 a\up0 \i0 \i \i0 allele, (Bonner and Slavkin, 1975). Congenital malformations in new-born mice 10% (1/9), including cleft lip and palate and polydactyly (Kalter, 1968). WySn substrain has 20% cranofacial defects due to the action of two genetic loci with unequal duplicate epistasis (Juriloff, 1995). Cleft palate is a function of foetal genotype rather than maternal factors (Yoshida et al, 1996). An exclusion map for the major gene causing nonsyndromic cleft lip with or without cleft palate has swept 40% of the mouse genome, with candidate regions on chromosomes 12, 18 and 19 with a few candidate loci (Juriloff, 1993). \par Low incidence of virus-like particles in chemically induced sarcomas (6/6) (Liebelt \i et al\i0 ., 1970). Can be made obese by a suitable diet (Fenton and Dowling, 1953). Does not develop non-insulin-dependent diabetes mellitus and hypertension when fed a high fat-high simple carbohydrate diet, whereas C57BL/6 mice do (Mills et al 1993). Blood glucose levels and insulin insensitivity in crosses between diet-induced type II diabetes sensitive C57BL/6 and resistant A/J are genetically independent (Surwit et al 1991) \par High incidence of amyloidosis (Russell and Meier, 1966). No amyloidosis found by Powers \i et al\i0 . (1976) in He and HeJ substrains, in contrast to previous reports. About 4% incidence of congenital open eyelids (Dagg, 1966). High incidence of cannibalism of young restricted to anatomically defined mutilation and amputation, particularly of neck, lower jaw and digits in Ha substrain (Hauschka, 1952). \par Relatively resistant to secondary amyloidosis which does not appear to be associated with variation in the serum amyloid A gene cluster (Butler and Whitehead, 1994). \par \i Normal physiology and biochemistry\i0 \par Low metabolic rate (16/18) (Storer, 1967). High plasma testosterone level and binding capacity (1/5) (Hampl \i et al\i0 ., 1971). Low Na/K ratio in erythrocytes (7/9) and plasma (8/9) (Waymouth, 1973). Low serum ceruloplasmin in males (23/26) but intermediate in females (Meier and MacPike, 1968). \par Low systolic blood pressure (17/19) (Schlager and Weibust, 1967). Low peripheral nerve conduction velocity (5/6) (Hegmann, 1972). High concentration of prostaglandin F in epididymis (1/6) (Badr, 1975). High glucose-6-phosphate dehydrogenase and nicotinamide-adenine dinucleotide phosphate levels in erythrocytes (1/8) (Erickson, 1974). High sensitivity to thyrotrophin (2/21) (Levy \i et al\i0 ., 1965). Mammary gland insensitive to oestradiol and progesterone (1/7) (Singh \i et al\i0 ., 1970). High glucose-6-phosphate dehydrogenase activity (1/16) (Hutton, 1971). High brain acetylcholinesterase activity (1/5) (Pryor \i et al\i0 ., 1966). \par High rectal (1/9) but low tail temperature (9/9) (Shepard and Habas, 1967). Low serum calcium level at 4 months of age (6/6) (Barrett \i et al\i0 ., 1975). Responds by higher growth rate on high fat diets (1/4) (Fenton and Carr, 1951). Low cell turnover as estimated by slow clearance of DNA-bound radioactivity (16/17 and 15/17 in J and He substrains, respectively) (Heiniger \i et al\i0 ., 1972). High erythrocyte catalase level (4/18) (Hoffman and Rechcigl, 1971). Low kidney (11/12) and liver (10/12) arylsulphatase activity (Daniel, 1976). High hepatic delta-aminolaevulinic acid synthetase activity after DISC treatment (4/15 in He substrain, 5/15 in J substrain) (Gross and Hutton, 1971). High basal serum prolactin level in females of St substrain (2/6) (Sinha \i et al\i0 ., 1975). Urine has high osmolality (2/7) (Silverstein, 1961). Blood catalase has high specific activity (1/7) (Magdon, 1962). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). \par \i Anatomy\i0 \par High percent carcass lipid on a high-fat diet (7/9) (West et al 1992). Small spinal cord (25/25), small brain/body weight ratio (16/20) (Roderick \i et al\i0 ., 1973). Small relative kidney size (20/21) (Schlager, 1968). Low total leukocyte count (16/18), low erythrocyte count (18/18 J substrain, 17/18 He substrain), low haematocrit (17/18), low haemoglobin per 100 cm\up8 3\up0 blood (16/18 He substrain, 14/18 J substrain) (Russell \i et al\i0 ., 1951). Small thymus/body weight ratio (6/6) (Belyaev \i et al\i0 ., 1970). Low proportion acidophilic (5/5) and high proportion chromophobe cells in adenohypophysis (Keramidas and Symeonidis, 1973). High frequency of mast cells in spleen also found in A.CA and A.SW (1/14) (Vicklicky, 1967). Low yield of peritoneal exudate cells (5/5) with low percentage of macrophages (5/5) and granulocytes (5/5) but high percentage of lymphocytes (1/5) (Schwartz \i et al\i0 ., 1975). Adrenal gland has a high incidence of vacuolisation of the X-zone (1/6) (Delost and Chirvan-Nia, 1958). Small pituitary (6/6) (Sinha \i et al\i0 ., 1975). Number of nipples commonly less than five pairs. Small number of Peyer's patches (6/7) (Hummel \i et al\i0 ., 1966). Lower bone mass than C57BL/6 (Kaye and Kusy, 1995). Low retinal ganglion cell number (4/24) (Williams et al, 1996). \par \i Drugs\i0 \par Susceptible to urethane-induced lung tumours (1/6) (Falconer and Bloom, 1962). Sensitive to induction of pulmonary tumours (1/6) but resistant to leukaemia and liver tumour induction by DMBA given neonatally (6/6 and 5/6, respectively) (Flaks, 1968). Susceptible to the induction of lung tumours by cyclopenta(cd)pyrene (Nesnow et al, 1994). Most benzo(a)pyrine-induced lung tumours had K-ras oncogenes inherited from the A/J parent with mRNA transcribed from the allele inherited from strain A/J being 5-20 times more abundant than that from C3H in crosses involving strain C3H (Chen et al, 1994) The A/J mouse lung can be used as a model to study the effectiveness of new chemical intervention therapies for controlling malignant tumor growth (Belinsky et al, 1993), and in the study of chemopreventive agents such as dietary and green tea polyphenols (Castonguay and Packer, 1993, Katiyar et al, 1993), isothiocyanates (AdamRodwell et al, 1993, Hecht, 1995), vitamin E (Yano et al, 1994) and other substances (Yun et al, 1995). No glycerol-associated effect on active oxygen formation and thiobarbituric acid reactive substances was observed in the lungs of A/J mice treated with 4-nitroquinoline 1-oxide, in contrast with outbred ddY strain mice (Yano et al, 1993, 1994). \par Nicotine decreases shock avoidance learning in J substrain (7/9), but increases it in He substrain (2/9) (Bovet \i et al\i0 ., 1966). Low ED50 to behavioural effects of nicotine (2/19). Resistant to seizures induced by nicotine (2/19) (Marks et al 1989) Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Not sensitive to histamine (8/9) (Brown, 1965). Susceptible to the teratogenic effect (cleft palate) of cortisone acetate (1/4) (Dost\'87 l and Jel\'92 nek, 1973; Kalter, 1965, Kalter 1981). There appears to be a threshold dose of cortisone needed to induce cleft palate (Fawcett et al, 1996). \par Sensitive to teratogenic effect (malformed ribs and vertebrae) of hypoxia on ninth day of gestation (1/5) (Dagg, 1966). Sensitive to X-irradiation (22/27 in He substrain, 20/27 in J substrain) (Roderick, 1963), 9/10 in males, 8/10 in females of J substrain (Storer, 1966). Highly susceptible to endotoxin lipopolysaccharide (1/5) (Heppner and Weiss, 1965). Resistant to hyperbaric oxygen (15/18 in J substrain, 12/18 in He substrain) (Hill \i et al\i0 ., 1968). Susceptible to pulmonary hyaline-membrane formation in 90% oxygen (3/10) (Lieberman and Kellog, 1967). Low LD\dn8 50\dn0 to X-irradiation (7/9) (Yuhas and Storer, 1969). Interstitial tumours of testis readily induced with oestrogens (Heston, 1963). Sensitive to chloroform toxicity (cf. 4/9) (Deringer \i et al\i0 ., 1953). Thalidomide increases congenital malformations such as cleft lip and palate (Szabo and Steelman, 1967)..High bronchial reactivity (1/6) to methacholine and serotonin (Konno et al 1993). Susceptible (1/8) to daunomycin-induced nephorsis (Kimura et al 1993). Resistant to hepatotoxic effects of cadmium (Shaikh et al, 1993). Airways hyperreactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). Clonidene failed to produce an aggressive behavioural response (cf 3/9) (Nikulina and Klimek, 1993). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid caused a high incidence of cholesterol gallstones (like SWR, C57L, contrast SM, AKR, DBA/2) (Faulkner et al, 1995). \par \i Immunology\i0 \par Develops autoimmune phenomena, immunological deficits with ageing and autoimmunity following neonatal thymectomy (Yunis \i et al\i0 ., 1972). Low lymphocyte phytohaemagglutinin response (32/43) (Heiniger \i et al\i0 ., 1975). Serum antinuclear factor 11% (7/18) (Barnes and Tuffrey, 1967). 11% incidence of antinuclear antibody by 16 months (1/17 in J substrain) (Teague \i et al\i0 ., 1972). Good immune response to small doses of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to Cholera A and B antigens (7/9A, 6/8B) (Cerny \i et al\i0 ., 1971). Good immune response to ovomucoid but poor response to bovine serum albumin (1/6) (James and Milne, 1972). Good immune response to DNP-keyhole limpet haemocyanin (1/33 in J substrain, 3/11 in He substrain) (Borel and Kilham, 1974). Good immune response to GAT (random terpolymer of Glu\up8 60\up0 , Ala\up8 30\up0 , Tyr\up8 10\up0 ) (1/10 in He substrain, 3/10 in J substrain) (Dorf \i et al\i0 ., 1974). Poor primary haemagglutinin immune response to sheep erythrocytes at 3 x 10\up8 7\up0 and 3 x 10\up8 8\up0 dose rates (6/6 and 5/6, respectively), also poor haemolysin response at both doses (6/6) (Ghaffar and James, 1973). High IgM antibody response to sheep red blood cells compared with C57BL/10ScSn (Vetvicka et al, 1993). Non-responder to synthetic polypeptide Glu\up8 57\up0 , Lys\up8 38\up0 , m-Ala\up8 5\up0 (cf. 4/7) (Pinchuck and Maurer, 1965). High antibody affinity to HSA (1/9) (Petty \i et al\i0 , 1972). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Low immune response to ferritin in A-\i Thy1.1 \i0 (16/16) (Young \i et al\i0 ., 1976). Low responder to dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972). Non-discrimination between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). Susceptible (1/12) to experimental autoimmune orchitis induced by two or three sc injections with viable syngeneic testicular germ cells without any adjuvants (Tokunaga et al 1993). Resistant to ineduction of experimental allergic encephalomyelitis (10/10) (Lindsey, 1996). High immune response to ganglio-series gangliosides (c.f. 2/10) Kawashima et al (1992). \par Interleukin-3 alone does not support hematopoetic colony formation of bone marrow cells from these mice. Interleukin-3R alpha is not detectible on the cell surface by antibody staining, though it is present inside the cells (Ichihara et al, 1995, Leslie et al, 1996)). High immunological response to \i Salmonella typhi\i0 porins (2/4) (Gonzales et al, 1995) \par \i Infection\i0 \par Resistant to infection by \i Salmonella typhimurium \i0 strain C5 (6/7) (Plant and Glynn, 1974), (5/5) Robson and Vas (1972). This may be associated with activation of complement (Nakano et al, 1995). 100-fold more susceptible to \i Listeria monocytogenes \i0 than C57BL/6 when measured by median lethal does (Sadarangani et al 1980). This seems to be associated with reduced levels of gamma interferon and granulocyte-macrophage colony stimulating factor compared with resistant C57BL/6 mice (Iizawa et al, 1993). Susceptible to \i Plasmodium berghei \i0 (3/8) (Most \i et al\i0 ., 1966). Highly susceptible to mammary tumour virus, which is carried in an acute form in unfostered substrains (Murray and Little, 1967). High susceptibility to BALB/Tennant leukaemia virus (2/12) (Tennant, 1965). Susceptible to \i Herpes simplex \i0 virus (9/11) (Lopez, 1975). Resistant to oncogenic effects of polyoma virus given at birth (Law, 1966a). Susceptible to \i Mycobacterium marinum \i0 (1/9) but poor plateau harvest of M. \i leprae \i0 8 months after infection (7/9) (Shepard and Habas, 1967). Susceptible to infection by \i Mycobacterium marinum\i0 (2/6) (Yamamoto et al 1991). Resistant to mouse hepatitis virus type 3 infection (1/12 in J substrain and 2/12 in Orl substrain) though Ps substrain susceptible (Le Prevost \i et al\i0 ., 1975). High mortality in a natural epizootic of ectromelia (1/8) (Briody, 1966). Resistant to mouse hepatitis virus (Bang and Warwick, 1960). Susceptible (1/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994). Resistant, with low amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). \par \par Encephalomyocarditis virus causes diabetes mellitus (cp. 7/14) (Boucher \i et al\i0 ., 1975). Highly susceptible to infection by measles virus (cf. 3/6) (Rager-Zisman \i et al\i0 ., 1976). \i Legionella pneumophila\i0 replicates within and kills thioglycolate-elicited macrophages, in contrast with strain BALB/c. This is associated with differences in availability of intracellular iron (Gebran et al, 1994). Develop acute pneumonia that resembles human Legionnaire's disease 24 to 48 hours after intratracheal inoculation of \i Legionella pneumophila\i0 (Brieland et al, 1994). Susceptibility to most strains of \i Legionella\i0 depends on the Lgn1 locus (Miyamoto et al, 1996). Resistant to the lethal effects of murine hepatitis virus strain 3 (contrast BALB/c), but resistance destroyed by methylprednisolone (Fingerote et al, 1995). Highly susceptible to infection with \i Candida albicans \i0 (1/6) (Ashman et al,1996) \par \i Reproduction\i0 \par Intermediate breeding performance (16/26), colony output 0.9 young per female per week, litter size at weaning low at 4.4(21/25) (Festing, 1976a). Intermediate breeding performance (6/8), litter size 4.9, sterility 11.5%(Nagasawa \i et al\i0 ., 1973). Low litter size (5/6) and large proportion of infertile matings (5/6) (Fernandes \i et al\i0 ., 1973). Low litter size (5/6 and 4/6 in He substrain, J substrain) (Verley \i et al\i0 ., 1967). Intermediate breeding performance (10/24) (Hansen \i et al\i0 ., 1973). High ratio of females at birth (1/11) (Cook and Vlcek, 1961). dba/2 \par \i Miscellaneous\i0 \par Recommended host for the following transplantable tumours: anaplastic carcinoma 15091 AK, hepatoma H6, round cell tumour C 1300 and spindle cell sarcoma Sal (Kaliss, 1972). Injection of murine C-1300 neuroblastoma cells derived from strain A/J into the tail vein provides a reproducible model for bone marrow metastasis (Iwakawa et al, 1994) \par A2G \par Inbr: F 101. Albino. Genet: \i b, \i0 c. Originated as an illegitimate mating of strain A at Glaxo Laboratories, UK, in 1942-50, followed by b x s mating. Should not be considered as a substrain of A. Distributed mainly in European laboratories, and best known for its unique resistance to myxovirus (influenza) infections. \par \i Behaviour\i0 \par Whisker chewing 75% in cages of 2-3 mice by 60 days of age. Whisker trimming seems to be associated with social dominance (Strozik and Festing 1981). Low balsa-wood gnawing activity (3/16) in A2G-\i hrhr\i0 , but high activity in A2G (1/16) (Fawdington and Festing 1980). It is not prevented by offering the mice means of withdrawal from it (Van den Broek et al, 1993). \par \i Life-span and spontaneous disease\i0 \par Long life-span in males (13/17 = 640 days) but intermediate in females (8/17 = 644 days), and lung tumours 17-65% in SPF fostered conditions (Festing and Blackmore, 1971). \par \i Normal physiology and biochemistry\i0 \par High incidence of audiogenic seizures (Pasquini \i et al\i0 ., 1968, quoted by Al-Ani \i et al\i0 ., 1970). \par \i Anatomy\i0 \par Absence of third molar in 7% of cases (1/20) (Festing, 1975b). High incidence of absence of the 3rd. molar, which has been used as a threshold character to study the effects of weak teratogens (Berry and Nickols 1979) \par \i Drugs\i0 \par Sensitive to insulin (2/9) but insensitive to histamine (7/9) (Brown, 1965). Long survival on Warfarin (9/12) (Lush and Arnold, 1975). Long sleeping time under hexobarbital anaesthetic (13/15) (Lovell, 1976), long sleeping time under pentobarbitone anaesthetic (18/23), Lovell (1986). Highly susceptible to lung tumour induction by urethane (cf. strain A) (Festing 1980). \par \i Immunology\i0 \par Incidence of serum antinuclear factor high (2/17) at 28% (Barnes and Tuffrey, 1967). Low antibody affinity to HSA (7/9) (Petty \i et al\i0 ., 1972). \par \i Infection\i0 \par Uniquely resistant among twenty strains tested to infection with diverse strains of pneumotropic and neurotropic influenza viruses. Resistance is due to a dominant autosomal gene, (now designated Mx1) and does not depend on the immune system (Fiske and Klein, 1975; Lindenman \i et al\i0 ., 1963). The Mx1 protein exhibits GTPase activity (Nakayama et al, 1993). The Mx1 protein is inducible with interferon and has been used as a cellular marker in studying the movement of glial cells toward a spinal cord demyelinating lesion (Gout and Dubois-Dalcq, 1993). Mx1 exerts its antiviral activity by interfering with the function of the influenza virus polymerase subunit PB2 (Stranden et al, 1993). The Mx1 gene also confers resistance to the tick-born Thogoto virus (Haller et al, 1995) and the tick-born Dhori virus (Thimme et al, 1995). \par Develops a chronic non-healing lesion on infection with \i Leishmania tropica, \i0 the parasite causing cutaneous leishmaniasis (Howard et al 1980) \par \i Reproduction\i0 \par Good breeding performance (7/25), colony output 1.2 young per female per week, litter size at weaning 5.7 (12/25) (Festing, 1976a). \par AA \par Inbr. 85 (Jah). Albino \i a,B,c. \i0 Origin: Japanese laboratory mice from dealer stock (Kasukabe group), inbred by S. Nishida in 1963. Good reproductive performance, high immunity to tetanus toxin. Maintained by Jah. \par AB \par Inbr: 40 +. Genet: \i c\i0 . Origin: Agnes Bluhm to Hertwig in 1934, to Fortner in 1945, to R\'9a hrer in 1949, to Jena in 1952. b x s inbreeding started 1959. \par Characteristics \par 35-54% leukaemia and reticulosarcomatosis in virgin females; 15-30% flbro-sarcoma in virgins; moderate incidence of primary lung tumours in both sexes; sensitive to casein-induced amyloidosis (Staats, 1976); good vitality and fertility (Hg). High incidence of spontaneous amyloidosis (Zschiesche, 1972). \par ABH (formerly AB/H) \par Inbr. F46 (Dr. David Baker, Jan. 1995). Albino. Genet. \i Thy1\i0 \i \up8 a\up0 \i0 \i , Ly1\i0 \i \up8 b\up0 \i0 \i , Ly2\i0 \i \up8 b\up0 \i0 \i , Ly5\i0 \i \up8 b\up0 \i0 \up8 \up0 ,\i H2\i0 \i \up8 dq1\up0 \i0 \i \i0 (Fairchild et al 1993). Origin: Inbred (Baker et al 1990) from outbred mice selected by Biozzi for high antibody response to sheep red blood cells (Feingold et al 1976). Note that other strains originating from the same outbred selected stock may differ from ABH. Susceptible to the development of experimental allergic encephalomyelitis (EAE) following injection of spinal cord homogenate in adjuvant. The mice develop a chronic relapsing pattern of disease characterised by mononuclear infiltration of the central nervous system, with demyelination being particularly evident in relapse. Treatment with sciatic nerve homogenate results in experimental allergic neuritis (O'Neill et al 1992). These mice appear to be a good model of multiple sclerosis (Baker et al 1990). The T-cell receptor has a deletion ligand encoded by MTV7 (Fairchild et al 1993). A major encephalitogenic epitope of a protolipid protein has been identified (Amor et al 1993, 1994). Immune response genes characterised by Liu et al (1993). The MHC antibody OX6 is able to prevent and treat EAE in these mice (Smith et al 1994), and CD4-depleating or CD4 blocking monoclonal antibody significantly inhibited disease progression (O'Neill et al 1993). The experimental encephalomyelitis modulates inositol and taurine in the spinal cord (Preece et al, 1994). The protease inhibitor D-penicillamine attenuated the exacerbations even when treatment was started after the primary full-blown disease had developed (Norga et al, 1995). \par In crosses with NOD there was evidence of genetic linkage between the experimental allergic encephalomyelitis and genes on ten chromosomes, with particularly strong linkage to chromosomes 7, 11 and 18 (Baker et al, 1995). \par ABL (formerly AB/L) \par Inbr.F51 (Dr. D. Baker, Jan 1995). Albino. Origin: As for ABH but developed from outbred mice selected by Biozzi for \i low\i0 antibody response to sheep red blood cells. Markedly less susceptible to the induction of experimental allergic encephalomyelitis (EAE) than ABH (Baker et al 1990). \par ABJ \par Inbr (Le) 60. Cinnamon: \i A,b.\i0 Also carries \i ab\i0 \i \up8 J\up0 \i0 \up8 \up0 (asebia-J). Origin: \i ab\i0 \i \up8 J\up0 \i0 \up8 \up0 arose spontaneously in BALB/cJ in 1968. Allelism tested with \i ab\i0 by S.J.Mann. One outcross to C3H/HeDi, bxs, to M.C.Green 1971, to Lane 1975. Maint. by Le \par ABP/Le \par Inbr: 28. Pink-eyed fawn. Genet: \i a, b, bt, p, se, wa1 \i0 (waved-1). Origin: A. B. Griffin to Lane 1968; sib-mated since then. \par Characteristics \par Useful for linkage testing. More reactive in an open-field than C57BL/6 (Clement et al, 1995). Used in studies of anxiety-related behaviour and its association with serotonergic receptors (Clement et al, 1996, 1997). \par ACR \par Inbr ?. Albino. Origin. AKR substrain to CIBA 1949. Known as AKR/FuA. Genetic contamination in 1953 (see AKR), renamed ACR. Leukaemia only 10-36% and lung adenomas 54-67% in AKR/FuA substrain (Muhlbock and Tengbergen, 1971). Maint. by A. \par AE \par Inbr (Nctr) 80. Pink-eyed fawn: \i a\i0 \i \up8 e\up0 \i0 \i ,b,d,p,se\i0 . Origin: Two litters of stock 3H-220 from Hollander, Iowa to Inst. Cancer Research, PA in 1962 at about F3. To Nctr in 1972. Caesarian-derived and fostered to C3Hf in 1980. Markedly lower electroconvulsive thresholds without increased susceptibility to seizures induced by pentylenetetrazol. Low responsiveness to phenobarbital and valproic acid. Possibly useful for epilepsy research (Loscher et al 1986) Maint. by Nctr \par AEJ \par Inbr (Rk) 70.Black. \i a\i0 \i \up8 e\up0 \i0 \up8 \up0 Origin: Hollander, Iowa. Ames waltzer stock with miscellanenous markers to M.C.Green 1963. Crossed once to C57BL/10 followed by cross to C57BL/6-\i A\i0 \i \up8 wJ\up0 \i0 \up8 \up0 , then b x s. To Roderick 1972. Maintained by Rk. \par AG \par Inbr (Cam) c155. Colour depends on genotype: \i A\i0 \i \up8 y/\up0 \i0 \i a\i0 \i \up8 e\up0 \i0 \up8 \up0 x \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 e\up0 \i0 \i \i0 with \i A\i0 \i \up8 w,\up0 \i0 \i A,A\i0 \i \up8 s,\up0 \i0 \i a\i0 \i \up8 t,\up0 \i0 \i a\i0 and \i p\i0 continuously backcrossed to the\up8 \up0 \i \up8 \up0 \i0 \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 e\up0 \i0 \i \i0 line. Origin: R.A.Fisher, 'A' from Gruneberg in 1945 at F34 (a CBA substrain, J.R. Morton, unpublished communication). Various alleles introduced by M.E.Wallace by backcrossing and maintained mainly by sib-mated substrain until 1959, then backcrossing to a single \i A\i0 \i \up8 y\up0 \i0 \i /a \i0 substrain, then \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 e\up0 \i0 \i \i0 substrain. Non-sibmating in a very small stock for 23 generations. Stock now frozen except for close inbreeding of\up8 \up0 \i \up8 \up0 \i0 \i A\i0 \i \up8 w\up0 \i0 \i ,\i0 \i a\i0 \i \up8 t\up0 \i0 \i \i0 and\up8 \up0 \i \up8 \up0 \i0 \i a\i0 \i \up8 e\up0 \i0 \i \i0 . Maint. by Cam. \par AKR \par Albino: \i a,B,c\i0 . Origin: a dealer named Detwiler in Norristown PA. Carried by Furth as a high-leukaemia strain from 1928 to 1936, then random bred at the Rockefeller Inst. for several generations. b x s by Mrs. Rhoades to F9 then C.Lynch to F21. This strain is best known for it's high incidence of lymphatic leukaemia, and for the \i Thy1\i0 \i \up8 a\up0 \i0 \up8 \up0 T-cell antigen, which is only present in this and a few other strains. Early history is obscure, but Acton \i et al\i0 (1973) found substantial substrain differences, which can best be accounted for by genetic contamination. This could have occurred at the time the strain was maintained by random mating. The strain has an international distribution, ranks about eighth in frequency of use and is widely used in cancer research for its high leukaemia incidence (Lilly and Pincus, 1973) and in immunology as a source of the Thy1.1 (theta AKR) antigen, although this varies between substrains. Mice of this strain are viraemic from birth and express in all tissues the ecotropic retrovirus AKV, copies of which are intrgrated into the genome and which is associated with the development of the leukaemia. In some substrains additional copies of the viral genomes may be integrated (Herr and Gilbert 1982). \par \par Major substrains include: \par \par AKR/J \par Inbr ?. To Jackson Laboratory 1940. Maintained by J. \par \par AKR/LwN \par Inbr ?. To Law 1940, to N 1956 at F53. Maint. by N. \par \par AKR/FuA \par Genetically contaminated and renamed ACR/A. Maint. by A. \par \par AKR/Cum \par Inbr ?. Origin ?. Differs from other substrains in being \i Mod1\i0 \i \up8 a\up0 \i0 \up8 \up0 . \par \par AKR/FuRdA \par Oak Ridge, to ?, to Rudale, to Netherlands Cancer Institute 1953. Carries \i Thy1.1\i0 and appears similar to AKR/J. \par \par AKR/TlAld \par Carries an autosomal translocation and has a low fertility (Leonard and DeKnudt, 1967) \par \i Behaviour\i0 \par High intrastrain aggression (2/14) (Southwick and Clark, 1966). High food drive (2/15), low emotionality (13/15) (Thompson, 1953). Long time of immobility in a forced swimming test (2/9) (Nikulina et al 1991) Susceptible to audiogenic seizures (3/11) (Fuller and Sjursen, 1967). High open-field activity (2/13) (Bruell, 1964). Low shock avoidance learning in females (5/6) (Royce \i et al\i0 ., 1971). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (24/26) (Lush 1988). \par \i Life-span and spontaneous disease\i0 \par Life-span short (1/22 = 326 days in males, 276 days in females) in conventional conditions (Storer, 1966). Life-span short (1/17 = 350 days in males, 312 days in females) in fostered SPF conditions (Festing and Blackmore, 1971). \par \par Lymphatic leukaemia 57% in males, 65% in females and 4% in virgin females. Mammary adenocarcinomas and primary lung tumours less than 1% (Hoag, 1963). Lymphatic leukaemia 66-87% (Festing and Blackmore, 1971). High gross tumour incidence (1/22) (Storer, 1966). Leukaemia 80-90% in females and 70-80% in males by 18 months (Nemirovsky and Trainin, 1973). Leukaemia 88% (Myers \i et al\i0 ., 1970). Incidence of leukaemia not altered by treatment with recombinant human growth hormone (Bechensteen et al, 1993). Low incidence of leukemia (about 7% T-cell and 28% B-cell) in the AKR\i -Fv1\i0 \up8 b \up0 congenic strain with limited replication and spread of the N-tropic murine leukemia virus (Rosner et al, 1993, Haran-Ghera et al, 1993). \par \i Normal physiology and biochemistry\i0 \par Low metabolic rate (18/18) (Storer, 1967). High concentration of prostaglandin F in epididymis (2/6) (Badr, 1975). Low plasma cholinesterase activity (22/22) (Angel \i et al\i0 ., 1967). Low plasma cholesterol levels (1/11) (Jiao et al 1990). High \i N'\i0 -methylnicotinamide oxidase activity in both sexes (2/7) (Huff and Chaykin, 1967). Low serum haptoglobin levels (11/11) (Peacock \i et al\i0 ., 1967). High hepatic delta-aminolaevulinate dehydratase activity (1/8) (Doyle and Schimke, 1969). Low serum calcium at 7 months (6/6) (Barrett \i et al\i0 ., 1975). High porphyrin content in Harderian gland (1/16) (Margolis, 1971). Venous blood has a high pH (1/10) (Bernstein, 1966). Blood catalase has a high specific activity (2/7) (Magdon, 1962). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). Sensitive to the development of obesity associated with adipocyte sensitivity to insulin (contrast SWR/J) (Eberhart et al, 1994, West et al, 1995). Hyporesponsive to diets containing high levels of fat and cholesterol (8/9) (Kirk et al, 1995). Eat 30% more calories than SWR (resistant to high-fat dietary obesity) with a higher fat and lower carbohydrate intake (Smith et al, 1997). \par \i Anatomy\i0 \par Low testes weight (8/8) (Shire and Bartke, 1972). Large brain weight in females (13/18) (Storer, 1967). High percent carcass lipid on a high-fat diet (9/9) (West et al 1992). Large brain weight (3/25) (Roderick \i et al\i0 ., 1973). Low total leukocyte count (14/18), high mean corpuscular volume (2/18) (Russell \i et al\i0 ., 1951). Large relative thymus weight at 14 days (3/8), 49 days (1/8) and 90 days (1/8) (Albert \i et al\i0 ., 1966). Large relative thymus weight (1/6) (Belyaev \i et al\i0 ., 1970). Low relative spleen weight (9/9 to 7/9, depending on age) (Albert \i et al\i0 ., 1966). A significant number of acinar cells of pancreas contain up to twelve nuclei (contrast seven other strains, but cf. C58) (Pollard, 1973). Carries adrenocortical lipid depletion gene which is characterised by loss of lipid vacuoles and occurrence of many closely packed mitochondria in cytoplasm of cortical cells (Arnesen, 1963). Low bone density of femur (8/11) (Beamer et al, 1996). \par \i Drugs\i0 \par High susceptibility to transplacental tumour induction by 1-ethyl-1-nitrosourea (IfS) (Diwan \i et al\i0 ., 1973). Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to toxic effects of DMBA (1/6) (Schmid \i et al\i0 ., 1966). Resistant to teratogenic effects of 1-ethyl-1-nitrosourea (5/5) (Diwan \i et al\i0 ., 1974). Resistant to induction of tumours by 3-methylcholanthrene (10/12) (Whitmire \i et al\i0 ., 1971). Highly susceptible to the induction of tumours by N-Methyl-N-Nitrosourea (MNU) due to a gene on chromosome 7 (Angel et al, 1993). Sensitive to lethal effects of ozone (4/21) (Goldstein \i et al\i0 ., 1973), but resistant (cf 3/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). Sensitive to X-irradiation (19/27) (Roderick, 1963). Resistant to pulmonary hyaline membrane formation in 90% oxygen (2/10) (Lieberman and Kellog, 1967). High incidence of virus-like particles in chemically induced sarcomas (2/6) but low susceptibility to tumour induction by 3,4-benzpyrene (6/6) (Liebelt \i et al\i0 ., 1970). Short sleeping time under hexobarbital anaesthetic (4/15) (Lovell, 1976), short sleeping time under pentobarbitone anaesthetic (4/23), Lovell (1986). Resistant to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 4/7) (Evans \i et al\i0 ., 1977). Sensitive to seizures induced by nicotine (17/19) (Marks et al 1989). Carries gene (\i Tpmt\i0 ) for low levels of thiopurine methyltransferase activity, catalyzing the \i S\i0 -methylation of 6-mercaptopurine and other heterocyclic and aromaticthiol compounds (like C57BL/6, unlike DBA/2) (Otterness and Weinshilboum 1987a,b). Airways hyperreactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid did not cause a high incidence of cholesterol gallstones (like SM, DBA/2 contrast C57L, SWR, A) (Faulkner et al, 1995) \par \i Immunology\i0 \par Sensitive to amyloid induction (3/10) but low level of spontaneous amyloid formation (Ram \i et al\i0 ., 1969). High susceptibility to amyloid using \i Escherichia coli \i0 endotoxin (1/6) (Willerson \i et al\i0 ., 1969). High lymphocyte phytohaemagglutinin response (11/43) (Heiniger \i et al\i0 ., 1975). Good immune response to small doses of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor primary immune response to bacteriophage fd (6/7) (K\'9a lsch \i et al\i0 ., 1971). Poor splenic PFC immune response to pneumococcal polysaccharide (8/9) (Amsbaugh \i et al\i0 . 1972). Good immune response to ovomucoid, but poor response to ovalbumin (cf. 5/12) (Vaz \i et al\i0 ., 1971). Good immune response to DNP-keyhole limpet haemocyanin (2/11) (Borel and Kilham, 1974). Discriminator between `H' and `L' sheep RBC (cf. 12/18) (McCarthy and Dutton, 1975). High susceptibility to IgE-mediated passive cutaneous anaphylaxis (1/12) (De Souza \i et al\i0 ., 1974). Susceptible to the anaphylactic death following an intravenous injection of bovine serum albumin into primed mice (Lei et al, 1996). \par Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). High incidence of expression of RNA tumour virus group specific antigen (1/5) (Diwan \i et al\i0 ., 1973). Low immune response to ferritin (14/16) (Young \i et al\i0 ., 1976). Low immune response to dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972). Low immune response to ganglio-series gangliosides (c.f. 4/10) Kawashima et al (1992). Resistant to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 4/18) (Noonan and Hoffman, 1994). High expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (Muthing, 1997). \par \i Infection\i0 \par Resistant to infection by the obligate intracelluar parasite \i Besnotia jettisoni\i0 (1/8) (Lunde and Gelderman, 1971). Susceptible to a natural intestinal helminth infection (10/10) (Eaton, 1972). Susceptible to \i Herpes simplex \i0 infection (11/11) (Lopez, 1975). Low mortality in a natural epizootic of ectromelia (8/8) (Briody, 1966). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Resistant (1/7) to the induction of dental caries due to infection with \i Streptococcus mutans\i0 (Kurihara et al 1991). Susceptible to infection with murine herpes virus (1/4) (Kapoor et al 1992). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). Develop severe lesions (1/8) following infection with \i Candida albicans\i0 (Ashman et al, 1993). Resistant (4/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994). Resistant, with low amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in well developed protoscoleces (cf 4/9) (Nakaya et al, 1997). Develop paralysis (age-dependent polyomyelitis) following infection with the lactate dehydrogenase-elevating virus in common with other mouse strains (e.g. C58) which possess N-tropic ecotropic murine leukemia proviruses and are homozygous Fv-1n (Anderson et al, 1995). \par \par \par \i Reproduction\i0 \par Poor reproductive performance (22/25), output 0.74 young/female/week, litter size low (22/25) at 4.1 weaned (Festing, 1976a). Intermediate breeding performance (14/24) (Hansen \i et al\i0 ., 1973). Low post-implantation loss of embryos (1/8), but high pre-implantation losses (8/8) (Leonard \i et al\i0 ., 1971). \par \i Miscellaneous\i0 \par Recommended host for transplantable lymphatic leukaemia BW5147 (Kaliss, 1972). High spontaneous mutation rate (4/21) (Schlager and Dickie, 1967). \par AKXD- \par Set of 25 recombinant inbred strains. Origin: B.A. Taylor from a cross between AKR/J and DBA/2J. \par High incidence of lymphoma in most strains (Gilbert et al, 1993). \par AKXL- \par Set of 18 recombinant inbred strains. Inbr 15-40+. Origin: B.A.Taylor from a cross between AKR/J and C57L/J. Strain AKXL-7 has a recombinant alpha-globin gene (Lewis et al, 1993). \par Maint. by Ty. \par AL \par Inbr: F166. Albino. Genet: \i a, b, c. \i0 Believed to have originated from an illegitimate mating of strain A followed by b x s mating, but should not be considered as a substrain of strain A. Very low mammary tumour incidence (Staats, 1976). \par \i Normal physiology\i0 \par High erythrocyte catalase level (3/18) (Hoffman and Rechcigle, 1971). \par \i Drugs \i0 \par Phenobarbital i.p. does not induce hepatic epoxide hydrase (cf. 3/7) (Oesch \i et al\i0 ., 1973). Long hexobarbital sleeping time (9/9) and low liver hexobarbital oxidase level (1/9) (Vesell, 1968). \par \i Immunology\i0 \par Resistant to the induction of liver amyloid, but a high level of spontaneous amyloidosis (10/10) (Ram \i et al\i0 ., 1969). Low susceptibility to induction of amyloid (6/6) (Willerson \i et al\i0 ., 1969). Good immune response to synthetic double-stranded RNA (1/7) (strain quoted as ALN, but presumed to be AL/N) (Steinberg \i et al\i0 ., 1971). Poor immune response to Vi antigen (cf. 3/5) (Gaines \i et al\i0 ., 1965). High anti-DNP antibody concentration (1/7) (Paul \i et al\i0 ., 1970). \par \i Reproduction\i0 \par Good breeding performance with 2.3 young per female per month (5/24) (Hansen \i et al\i0 ., 1973). \par \i Miscellaneous\i0 \par AL/N has only 38 chromosomes, including two translocation submetacentrics involving Robertsonian translocations of chromosomes 5 and 19 (White and Tjio, 1975). \par AM \par Inbr (Nctr) 63. Mottled yellow, mottled agouti: \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 \i \up8 m\up0 \i0 \up8 \up0 , \i a\i0 \i \up8 m\up0 \i0 \i /a\i0 \i \up8 m\up0 \i0 \up8 \up0 . Origin: \i a\i0 \i \up8 m\up0 \i0 \i /a\i0 \i \up8 m\up0 \i0 \up8 \up0 males from L.B.Russell, Oak Ridge Nat.Lab. in 1965 at F5 to the Inst. of Cancer Research, PA. Mated by \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 females (F12) of strain VY/Wf. To Nctr in 1972. Maintained by \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 \i \up8 m\up0 \i0 \up8 \up0 x \i a\i0 \i \up8 m\up0 \i0 \i /a\i0 \i \up8 m\up0 \i0 \i \i0 sib matings. Caesarian derived and fostered on C3Hf in 1980 at F42. Highly variable coat colour patterns. Maint. by Nctr. \par AMMS/1 \par Inbr. F51 (1993). Albino \i a,b,c,D.\i0 Origin: Outbred KM mice from Shanghai Institute of Biological Products in 1972 and inbred since 1974 by Lou Zhenmei, Laboratory Animals Centre, Beijing. Uniform body weight with low sexual dimorphism. Sensitive to attenuated \i Bacillus anthracis, \i0 developing acute liver damage (Zhenmei, personal communication). \par APN \par Inbr. (1998) F26. Albino, \i c\i0 . Origin: Outbred Swiss Webster mice from Connaught Laboratories, Toronto, Canada, selected by Casley and Whitehouse, Banting Research Centre, Ottawa, Canada, for nonresponsive serum alanine aminotransferase (ALT) following administration of 150mg/kg acetaminophen per os, with brother x sister mating started in 1993 (see also APS). \par Characteristics \par Low caffeine 3-demethylation activity (8/8). Hepatic CYP1A2 mRNA, protein and enzyme activity (MROD, acetanilide 4-hydroxylation) was significantly lower than for strain C3H (Casley et al 1997a, b). \par APS \par Inbr. (1998) F26. Albino, \i c\i0 . Origin: Outbred Swiss Webster mice from Connaught Laboratories, Toronto, Canada, selected by Casley and Whitehouse, Banting Research Centre, Ottawa, Canada, for elevated serum alanine aminotransferase (ALT) following administration of 150mg/kg acetaminophen per os, with brother x sister mating started in 1993 (see also APS). \par Characteristics \par Males and females show approx. 2-fold increase in caffein 3-demethylation relative to strain APN. CYP1A2 mRNA and enzyme activity are also elevated approx 2-fold relative to the APN strain (Casley et al, 1997a,b) \par AS/Wf (now extinct) \par Inbr: F26. Genet: \i A\i0 \i \up8 Y\up0 \i0 \i /A\i0 \i \up8 s\up0 \i0 \i A\i0 \i \up8 w\up0 \i0 \i . \i0 Origin: \i A\i0 \i \up8 s\up0 \i0 \i A\i0 \i \up8 w\up0 \i0 \i /A\i0 \i \up8 s\up0 \i0 \i A\i0 \i \up8 w\up0 \i0 \i \i0 female from R. J. S. Phillips in 1965, mated to a YS/ChWf-\i A\i0 \i \up8 y\up0 \i0 \i /a\i0 male. \par AT/Wf (now extinct) \par Inbr: F27. Genet: \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 \i \up8 t\up0 \i0 \up8 \up0 . Origin: VY/Wf-\i A\i0 \i \up8 vy\up0 \i0 \i /a \i0 male x YS-\i a\i0 \i \up8 t\up0 \i0 \i a\i0 \i \up8 t\up0 \i0 \up8 \up0 female in 1966. Sib-matings \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 \i \up8 t\up0 \i0 \i x a\i0 \i \up8 t\up0 \i0 \i /a\i0 \i \up8 t\up0 \i0 \i .\i0 \par ATEB \par Inbr (Le) 42. Grey: \i a,d.\i0 Also carries \i at/+\i0 (atrichosis), \i eb/+\i0 (eye-blebs). Origin:\i at\i0 arose in DBA/1 at F15 in 1964, \i eb\i0 arose in a non-inbred hairless stock maintained by Hummel in 1960. Balanced stock bxs to M.C.Green 1972, to Lane 1975. \i at/at \i0 mice are sterile. \i eb/eb\i0 mice have defects of eyes, kidneys and feet. Maint. by Le \par AU \par Inbr: F? + 35. Genet: \i a, U, rd\i0 \i \up8 +\up0 \i0 \i . \i0 Origin: R. A. Fisher, about 1937. 50% Gruneberg's CBA, 28.5% Fisher's colour stocks and 21.5% Gruneberg's wavy stock, the latter two being unrelated stocks of American origin. To Medawar 1947, to Silvers at F23 in 1957, to Jackson Laboratory 1967. \par Characteristics \par : Females do not reject male isografts. Unusual induction of kidney beta-glucuronidase by testosterone (Staats, 1976). High plasma cholinesterase activity (1/22) (Angel \i et al\i0 ., 1967). Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). High degree of genetic distinctiveness (2/27) (Taylor, 1972). Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). F1 hybrid crosses with CBA have been suggested as a good model for auditory research (Henry and McGinn 1992). Resistant to the induction of arthritis by type II collagen (Ortman et al, 1994). \par AX \par Inbr (Pa) 27. Black. \i a\i0 \i \up8 x\up0 \i0 \up8 \up0 . Origin: L.B.Russell's balanced lethal stock \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 +\up0 \i0 \up8 \up0 6PB, to M.H.L.Snow in 1969 who separated the alleles by backcrossing \i a\i0 \i \up8 x\up0 \i0 \up8 \up0 mice to C57BL/6 for five generations. Snow to Papaioannou in 1973. Sib-mated with forced heterozygosity for the embryonic lethal \i a\i0 \i \up8 x\up0 \i0 \up8 \up0 . Maint. by Pa. \par AXB- \par Inbr circa F29-59 (1992). Set of 48 recombinant inbred strains developed by Nesbitt from A/J x C57BL/6 and C57BL/6 x A/J. (Nesbitt and Skamene 1984), now reduced to 31 living and 8 extinct strains (Marshall et al 1992). Strain distribution pattern of some markers given by Mu et al (1992). Maint. by J. \par AY \par Inbr: F41. Genet: \i A/A\i0 \i \up8 y\up0 \i0 \i , b, C, D, S. \i0 Origin: Yellow lethal mice from Misima in 1961. Frequent diabetes mellitus. \par B6NXC3N-. \par Set of 7 recombinant inbred strains developed from a cross involving C57BL/6N and C3H/HeN. Maintained by Lm. \par BA \par Inbr (Crusio) 81. Sandy: \i b\i0 . Origin: At Nmg from a non-inbred obese stock maintained by Falconer. To Crusio 1984. Maint. by Nmg. \par BAB-14. \par No details available. \par BALB/c \par Albino: \i A,b,c\i0 . Origin: Stock acquired by H.Bagg in 1913, to MacDowell, to Snell in 1932 (who added the /c). Now widely distributed and among the top 2-3 most widely used inbred strains. The strain is particularly well known for the production of plasmacytomas on injection with mineral oil. These tumours form the basis for the production of monoclonal antibodies. Used as a general-purpose strain in many different disciplines. Good breeding performance and long reproductive life-span. Normally has low mammary tumour incidence but can be infected with the mammary tumour virus by fostering to C3H (which carries the virus), and it then gets a high incidence of mammary tumours. \par \par The history and characteristics of the strain have been reviewed by Potter (1985). Three major substrains trace back to before 1940, and are listed separately below. Data on genetic markers suggest that these substrains have diverged largely through mutation or residual heterozygosity rather than genetic contamination. Hilgers et al (1985) have shown that the substrains differ as a result of mutations at the \i Raf1\i0 locus (controlling the expression of alpha-fetoprotein), the \i Qa2\i0 locus (governing cell surface antigens), the \i Gdc1 \i0 locus (governing L-glycerol 3-phosphate dehydrogenas activity in the liver) and the PR1 repetative sequence. There is no evidence for genetic contamination during the early history of the strain. A fourth substrain, BALB/cWt is also listed as it has a high incidence of hermaphroditism. \par \par BALB/cHeAn \par Inbr ?.To Snell circa 1932, to He circa 1935. Now widely distributed (including the By, AnN, HeA and AnPt substrains). This substrain is much less aggressive than the J substrain. Maint. by A, N. \par \par BALB/cJ \par Inbr 150 +?.Snell to Jackson Laboratory after 1940. Males of this substrain are extremely aggressive and will fight if housed together once mature. The Lac substrain separated in 1952 is non-aggressive. Maintained by J, Ola (JLac substrain). \par \par BALB/cRl \par Inbr ?. Snell to Green circa 1937, to W.L. and L.B.Russell c1948. \par \par BALB/cWt \par Inbr. ?. Has about a 3% incidence of true hermaphroditism, which significantly distorts the sex ratio (Eicher et al 1980) \par \i Behaviour\i0 \par High intrastrain aggression (4/14), low open-field activity (12/14), high tail rattling but low social grooming (14/14) during aggressive encounters (Southwick and Clark, 1966,1968). Low open-field activity (13/15) (Thompson, 1953). High spontaneous locomotor activity (7/9) (Nikulina et al 1991). Long time of immobility in a forced swimming test (1/9) (Nikulina et al 1991). Short latency to cross barrier in maze (2/7), high urination (2/7) and defaecation (1/7) in test apparatus (McClearn \i et al\i0 ., 1970). Low wheel activity (Messeri \i et al\i0 ., 1972). Low avoidance conditionability (9/9) (Royce, 1972) and low shock avoidance learning in males (6/6) (Royce \i et al\i0 ., 1971). Poor shock avoidance learning (7/8) (Wahlsten, 1973). Low alcohol preference ratio (4/5) (McClearn, 1965), (13/18) (Rodgers, 1966). High social dominance of males in competition for females (2/6) (DeFries and McClearn, 1970). High balsa-wood gnawing activity (14/16) (Fawdington and Festing 1980). Exhibit hypersecretion of corticosterone and marked brain catecholamine alterations and disruption of Morris water maze performance following stressors such as foot-shock. However, performance deficits were prevented by cross fostering to C57BL/6 foster mothers (Zaharia et al, 1996). \par \i Life-span and spontaneous disease\i0 \par Life-span intermediate in both sexes in conventional conditions (12/22 = 539 days in males, 11/22 = 575 days in females) (Storer, 1966). Life-span intermediate in males (7/17 = 509 days) and short in females (4/17 = 561 days) in SPF fostered conditions (Festing and Blackmore, 1971). Life-span 648 _ 20.6 days in females and 816 32.4 days in males (Goodrick, 1975). Life-span 20 months in females and 13 months in males. Amyloidosis 40% in males. Reticular neoplasms 23% females and 3% males (Ebbesen, 1971). Primary lung tumours 32% in males, 30% in breeding females and 14% in virgin females in Scott substrain. Leukaemia 5% (Myers \i et al\i0 ., 1970). Zero incidence of lymphatic leukaemia. Mammary adenocarcinomas zero in males, 5% in breeding females and 1% in virgin females (Hoag, 1963). Mammary tumours 30% at 2 years (3/7) (Bentvelzen \i et al\i0 ., 1970). Mammary tumours 20% in females at 16.7 months, but 100% at 7.1 months in BALB/cfC3H (Heston and Vlahakis, 1971). Mammary tumours 10% at 14 months (Schlom \i et al\i0 ., 1973). Low gross tumour incidence in males (20/22) (Storer, 1966). Renal tumours 25-48%, mammary tumours 3-13%, reticuloendothelial tumours 11-20%, lung tumours 10-16%, synoviomas 2-8%, depending on substrain (Sass \i et al\i0 ., 1976). Low incidence of virus-like particles in chemically induced sarcomas (5/6) (Liebelt \i et al\i0 ., 1970). Frequency of rhabdomyosarcomas was calculated to be 2.4/100,000 mice retained as breeders, and 10/14 mice found with these tumours were of the BALB/cJ substrain (Sundberg et al 1991). Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in the J and ByJ substrains (Sundberg et al 1991) \par \par Gross tumour incidence in germ-free mice 43%, with lung tumours 21%, angiomas 6%, lymphosarcomas 5% and other tumour types less than 3% each (Smith and Pilgrim, 1971). Pulmonary tumours 26-29% (Heston, 1968). \par \par Left auricular thrombosis occurs in 66% of older breeding females. This is associated with reduced levels of the prothrombin complex factors such as factor IX (40% of normal), factor XIII (60% of normal), factor X (50% of normal) and prothrombin (about 33% of normal). These deficiencies occur slightly before parturition (Meier and Hoag, 1966). High incidence of epicardial mineralisation (11% in males, 4% in females), which increases slightly with age (Frith \i et al\i0 ., 1975). Heart defects, including cardiac calcinosis 17-62% (Festing and Blackmore, 1971). Spontaneous myocardial lesions of right ventricle found in 60% of females and 30% of males. These macroscopically visible degenerative fibrosclerotic lesions may represent a last phase of myocarditis of the inflammatory type found in apparently normal mice (Bellini \i et al\i0 ., 1976). \par Carry a single recessive gene different from that found in C57BL/6J and WB/ReJ, causing age-related hearing loss (Willott et al, 1995). \par Zero incidence of spontaneous congenital malformations (cf. 2/9) in GrKt-\i tk\i0 substrain (Kalter, 1968). \par \i Normal physiology and biochemistry\i0 \par High Na/K ratio in erythrocytes (2/9) (Waymouth, 1973). Low levels of serum ceruloplasmin in males (26/26) (Meier and MacPike, 1968). Low serum haptoglobin level (9/11) (Peacock \i et al\i0 ., 1967). High systolic blood pressure (2/19) (Schlager and Weibust, 1967). Low mean heart rate (6/7) but high heart rate adaptation (3/7) (Blizard and Welty, 1971). Low plasma cholinesterase activity in females (19/22) (Angel \i et al\i0 ., 1967). High plasma cholesterol levels (9/11) (Jiao et al 1990). High erythrocyte catalase level (1/18) (Hoffman and Rechcigl, 1971). Low intra-ocular pressure (4/4) (John et al, 1997). \par High peripheral nerve conduction velocity (1/6) (Hegmann, 1972). High brain L-glutamic acid decarboxylase (GAD) and choline acetyltransferase and catechol-O-methyltransferase (1/7 in all cases); low brain acetylcholinesterase (5/7) and monoamine oxidase activity (7/7)(Tunnicliff \i et al\i0 ., 1973). High brain tyrosine hydroxylase activity (1/5) (Ciranello \i et al\i0 ., 1972). High brain plasmalogen (1/5) (Sampugna \i et al\i0 ., 1975). High proportion of time spent sleeping (1/6) with a high percentage of slow-wave sleep (2/6) and low proportion of paradoxical sleep (6/6) (Valatx and Bugat, 1974). Short tau DD, the endogenous (free-running) period of the circadian pacemaker measured in constant environmental darkness (1/12) (Schwartz and Zimmerman 1990). \par High hypoxanthene-guanine phosphoribosyl transferase in the thalamus (1/7) (Suran 1973). Low N-methylnicotinamide oxidase activity (5/7 males, 6/7 females) (Huff and Chaykin, 1967). Low rectal (9/9) and tail (8/9) temperature (Shepard and Habas, 1967). High kidney arylsulphatase activity (2/12) (Daniel, 1976). Low basal level of serum prolactin (5/6) (Sinha \i et al\i0 ., 1975). Low spermatazoal beta-glucuronidase activity (8/9) (Erickson, 1976). Urine has high osmolality (1/7) (Silverstein, 1961). High basal levels of kidney catalase (1/4), and superoxide dismutase (1/4) but low basal level of kidney glutathione peroxidase (4/4) and kidney glutathione (4/4) (Misra et al 1991). High level of alpha-fetoprotein in amniotic fluid and neonatal plasma (1/6) (Adinolfi et al 1990). Low hepatic microsomal coumarin hydroxylase activity in males (8/8) (Van Iersel et al, 1994). \par Secretory group II phospholipase A2 gene has very high expression in small intestine (contrast 129/Sv and C57BL/6) (Kennedy et al, 1995). \par \i Anatomy\i0 \par Large brain weight (1/18 in both sexes) (Storer, 1967), (2/25) (Roderick \i et al\i0 , 1973), (1/6) (Wahlsten \i et al\i0 ., 1975). Large brain to body weight ratio (2/20). Large spinal cord (5/25) (Roderick \i et al\i0 ., 1973). Large relative kidney weight (2/21) (Schlager, 1968). Large forebrain (1/9) and hippocampus (1/9) volume (Wimer \i et al\i0 ., 1969). Large number of A10 dopaminergic neurons in midbrain region (1/4) (Bernardini et al 1991). Corpus callosum absent in 39% of animals (1/6) (Wahlsten, 1974). This is associated with slow growth of the medial septum subadjacent to the cavum septi. See also strains I/LnJ and CXBG (Wahlsten and Bulman-Fleming, 1994). Absence of corpus callosum related to retarded formation of the hippocampal commissure in this strain and in 129/J mice (Livy and Wahlsten, 1997). Low bone density of femur (9/11) (Beamer et al, 1996). \par Anatomy of Ammon's horn (hippocampus and dentate gyrus) different from that of seven other strains (Barber \i et al\i0 ., 1974). High erythrocyte count (2/18 J substrain, 5/18 An substrain), high haematocrit (3/18 J substrain, 5/18 An substrain), high haemoglobin (1/18 J substrain, 4/18 An substrain) (Russell \i et al\i0 ., 1951). Large spleen at all ages (3/9 to 1/9) (Albert \i et al\i0 ., 1966). Accessory spleens in about 21% of animals, and number of nipples commonly exceeds five pairs (Hummel \i et al\i0 ., 1966). Occasional (less than 2%) cases of visceral inversion (Hummel and Chapman, 1959). Small pituitary (5/6) (Sinha \i et al\i0 ., 1975). Large proportion of sperm-head abnormalities (1/5, 44%) (Styrna et al 1991). Low level of spontaneous sister chromatid exchange (1/4) (Nishi et al, 1993). Provides a sensitive and reproducible model of focal and global brain ischemia (Barone et al, 1993). \par \i Drugs\i0 \par Susceptible to skin ulceration by 7,12-dimethylbenz(a)anthracene (DMBA) (cf. 13/23) (Thomas \i et al\i0 ., 1973). Sensitive to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Sensitive to the induction of skin tumours by methylnitrosourea in methanol (1/4) (Lijinsky et al 1991). Susceptible to tumour induction by 3-methylcholanthrene (3/12) (Whitmire \i et al\i0 ., 1971). Susceptible to induction of leukaemia (1/6) but resistant (6/6) to induction of liver tumours by neonatally administered DMBA (Flaks, 1968). High incidence of interstitial tumours of testis induced by stilboestrol, high incidence of haemangioendotheliomas, particularly in interscapular fat pad and lung in mice treated with O-aminoazotoluene (Heston, 1963). High incidence of lung tumours after administration of methycholanthrene by gavage (1/5) (Akamatsu and Barton, 1974). Injection of mineral oil i.p. induces a high incidence of transplantable plasmacytomas (myelomas). Bence Jones proteins include kappa and lamda light chains and the two-chain IgA protein. 60% of tumours are of the IgA type (Potter, 1972). Susceptibility appears to be mediated by two genes on chromosome 4 (Potter et al, 1994). Susceptible (2/8) to daunomycin-induced nephorsis (Kimura et al 1993). \par Sensitive to X-irradiation (26/27) (Roderick, 1963), (10/10) (Storer, 1966); low LD\dn8 50\dn0 to X-irradiation (9/9) (Yuhas and Storer, 1969). \par Nicotine increases shock avoidance learning (3/9) (Bovet \i et al\i0 ., 1966). Sensitive to insulin (3/9) (Brown, 1965). Poor ovulatory response to PMS at both 3 IU (6/6) and 7 IU (5/6), but response increased by exposure to males (Zarrow \i et al\i0 ., 1971). Low locomotor excitation after treatment with D-amphetamine (6/6) (Babbini \i et al\i0 ., 1974). Resistant to hyperbaric oxygen (16/18) (Hill \i et al\i0 ., 1968). Insensitive (eosinophil response) to cortisone acetate (cf. 3/6) (Wragg and Speirs, 1952). Low sensitivity to induction of malformed ribs and vertebrae by hypoxia on ninth day of gestation (5/5) (Dagg, 1966). Sensitive to chloroform toxicity (cf. 5/10) (Christensen \i et al\i0 ., 1963). Resistant to toxic effects of isoniazid (1/10) (Taylor, 1976b). Resistant (3/3) to neurotoxic effects of monocrotophos (Rao et al 1991). High transient increase in renal lipid peroxidation following treatment with nickel (1/4) (Misra et al 1991). Resistant to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (3/4), but the injury is much more persistent than in SJL and was accompanied by periductal fibrosis and occasionally by obliteration of ducts typical of sclerosing cholangitis (Bhathal et al 1990). High LD50 following injection of butylated hydroxytoluene (BHT) (1/4) (Kehrer and DiGiovanni 1990). High histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser (1/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Cultured mast cells grow more slowly and release less histamine and TNF-alpha following anti-DBN IgE antibody treatment than those of strain SJL (Bebo et al, 1996). Highly sensitive to the induction of catalepsy by haloperidol (1/8) associated with midbrain dopamine D2 receptor density levels (Kanes et al, 1993). Resistant to both acute and chronic cadmium toxicity (contrast NFS) (Abshire and Waalkes, 1994). However, cadmium can induce hematopoetic and suppress pulmonary tumours in these mice (Waalkes and Rehm, 1994). Resistant to weight loss induced by cocaine (1/7) (Shimosato et al, 1994). Clonidene induces a strong aggressive behavioural response (1/9) (Nikulina and Klimek, 1993). More resistant to acute toxic effects of aflatoxin B-1 than C57BL/6 (Almeida et al, 1996). \par The IgE response following topical application has been used to predict which chemicals may have the potential to cause sensitization of the respiratory tract (Hilton et al, 1996). More susceptible to the development of micronuclei than C57BL/6 or DBA/2 following treatment with clastogenic base analogues and nucleosides (Sato et al, 1993). Estrogen does not induce an increase in VLDL and LDL-cholesterol (like C3H contrast C57BL/6 and C57L)) (Srivastava, 1995). \par \i Immunology\i0 \par Resistant to experimental allergic encephalomyelitis (EAE) (cf. 7/18) (Levine and Sowinski, 1973). Resistant to EAE (9/10) with short duration (10/10) but moderate mortality (Lindsey, 1996). High lymphocyte phytohaemagglutinin response (14/43) (Heiniger \i et al\i0 ., 1975). Good immune response to type III pneumococcal polysaccharide (1/5) (Braley and Freeman, 1971). Good splenic PFC immune response to pneumococcal polysaccharide (1/9) (Amsbaugh \i et al\i0 ., 1972). Poor primary immune response to bacteriophage fd (7/7 in Str substrain, 5/7 in Ho substrain) (Kolsch \i et al\i0 ., 1971). Poor immune response to synthetic double-stranded RNA (7/7) (Steinberg \i et al\i0 ., 1971). Responder to synthetic polypeptide (cf. 3/7) (Pinchuck and Maurer, 1965) and Glu\up8 60\up0 , Ala\up8 30\up0 , Tyr\up8 10\up0 (2/10) (Dorf \i et al\i0 ., 1974). Very good immune response to cholera A and B antigens (1/9) (Cerny \i et al\i0 ., 1971). Good immune response to dextran -1,3-glucosyl linkages (cf. 4/10) (Blomberg \i et al\i0 ., 1972). Good primary immune haemolysin and haemagglutinin response (1/6 at various dose levels) (Ghaffar and James, 1973). Poor immune response to \i Salmonella anatum \i0 and \i S. senftenberg \i0 lipopolysaccharide (5/5) (Di Pauli, 1972). Good immune response to Vi antigen (1/5) (Gaines \i et al\i0 ., 1965). Precipitating and skin-sensitising antibodies have fast electrophoretic mobility (1/6) (Fahey, 1965). Non-discriminator between `H' and `L' sheep RBC (cf. 6/18) (McCarthy and Dutton, 1975). Low anti-DNP antibody concentration (6/7) (Paul \i et al\i0 ., 1970). Poor immune response to \i Salmonella strasbourg\i0 lipopolysac-charide (6/7) (Di Pauli, 1972). High PHA-stimulated lymphocyte blastogenic response (1/6) (Hellman and Fowler, 1972). Poor primary immune response to bacteriophage fd (5/7 and 7/7, depending on substrain) (K\'9a lsch \i et al\i0 ., 1971). Erythrocytes have a low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). High responder to dextran (cf. 4/10) (Blomberg \i et al\i0 ., 1972). \par Resistant to induction of experimental autoimmune thyroiditis (cf. 2/5) (Vladutiu and Rose, 1971a). Resistant (5/5) to induction of autoimmune prostatisis (contrast C57BL/6) (Keetch et al, 1994). \par Immunization by intraperitoneal injection of fetal human (but not calf) proteoglycan depleted of chondroitin sulphate together with complete or incomplete Freund's adjuvent produces progressive polyarthritis and ankylosing spondylitis. Clinical assessment suggests that affected mice have many similarities to human rheumatoid arthritis and ankylosing spondylitis. Eventually, the joints become stiff and deformed. Antibodies against collagen type II were detected in approximately 25% of arthritic mice, but only following cartilage degradation. Sublines differed in their response, but 9 other mouse strains and 5 F1 hybrids were resistant. See Glant et al (1993) for a review. \par Resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). Anti-BPO IgE monoclonal antibody failed to produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). Low immunological response to \i Salmonella typhi \i0 porins (4/4) (Gonzales et al, 1995). Resistant to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 4/18) (Noonan and Hoffman, 1994). Low neutrophil response to thioglycolate broth and killed bacteria (contrast C57BL/10) (Marley et al, 1994). Pristance induces immune complex glomerulonephritis in association with autoantibodies typical of lupus erythematosus, though the strain is not normally considered to be susceptible to the disease (Satoh et al, 1995). \par The IgE response following topical application has been used to predict which chemicals may have the potential to cause sensitization of the respiratory tract (Hilton et al, 1996). Diminished expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (Muthing, 1997). \par \i Infection\i0 \par Highly susceptible to infection by \i Salmonella typhimurium \i0 strain C5 (1/7) (Plant and Glynn, 1974), (2/5) (Robson and Vas, 1972). Relatively resistant to a natural intestinal helminth infection (1/10), (Eaton, 1972). High susceptibility to BALB/Tennant leukaemia virus (1/12) (Tennant, 1965). Transmission of murine leukaemia virus (Scripps) through three successive generations 100% (cf. 2/5) (Jenson \i et al\i0 ., 1976). Highly susceptible to development of leukaemia on infection with Friend virus (cf. 5/11) (Dietz and Rich, 1972). Susceptible to \i Mycobacterium marinum\i0 (3/9) and good plateau harvest of M. \i leprae \i0 8 months after infection (2/9) (Shepard and Habas, 1967). Susceptible to infection with \i Mycobacterium paratuberculosis\i0 , and develops a chronic infection (Chiodini and Buergelt, 1993). Susceptible to infection with \i Mycobacterium avium\i0 , but resistance is enhanced by Freund's incomplete adjuvent (Castro et al, 1993). Susceptible to infection with \i Yersinia enterocolitica\i0 associate with a poor interferon gamma response (contrast C57BL/6) (Autenrieth et al, 1994). Susceptible to the induction of chronic pyelonephritis with \i Escherichia coli\i0 after introduction of the bacteria by the ascending route (Gupta et al, 1995). Relatively resistant to infection with \i Helicobacter felis \i0 (contrast C57BL/6) (Mohammadi et al, 1996). Resistant to infection by \i Helicobacter felis\i0 with only mild gastritis in the antrum and no atrophy seen over time (cf CBA, contrast 4 other strains) (Sakagami et al, 1996). \par Susceptible to mouse hepatitis virus type 3 (cf. 5/14) (Le Prevost \i et al\i0 ., 1975). Resistant to mouse adenovirus type 1 (contrast C57BL/6) (Guida et al, 1995). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975. See also Hirasawa et al, 1995). Resistant to measles virus induced encephalitis, which correlates with a low cytotoxic T-lymphocyte response (contrast C3H, C57BL/6) (Niewiesk et al, 1993). \par Highly susceptible to the \i Leishmania tropica \i0 parasite, with the local disease being uncontrolled and with the development of metastases and fatal visceralization (Howard \i et al \i0 1980). Supported sustained growth of six strains of \i Leishmania mexicana mexicana\i0 (contrast C57BL/6) (Monroy-Ostria et al, 1994). Highly susceptible to \i Leishmania major\i0 , with the parasites disseminated within 10-24 hrs. from the site of subcutaneous footpad injection into the popliteal lymph node, spleen, lung, liver and bone marrow in contrast to resistant C57BL/6, CBA/J and C3H/HeJ (Laskay et al, 1995, Scott et al, 1996). \par Susceptible (1/4) to infection with the helminth worm \i Angiostrongylus costaricennsis\i0 (Ishii and Sano 1989). Susceptible (6/7) to the induction of dental caries due to infection with \i Streptococcus mutans\i0 (Kurihara et al 1991). Resistant to infection with \i Pseudomonas aeruginosa\i0 in contrast with susceptible DBA/2 mice (Morissette et al, 1995). Resistance is associated with a quicker inflamatory response and earlier initiation of bacterial clearance (Morisette et al, 1996). Develop mycotic mastitis following inoculation of the mammary gland with \i Candida krusei \i0 isolated from bovine mastitis (Guhad et al, 1995). \par Susceptible (1/7) to the development of chronic Chagas' cardiomyopathy in postacute \i Trypanosoma cruzi\i0 infection (Rowland et al 1992). Susceptible to infection with \i Trypanosoma congolense\i0 with unrestrained parasite growth to the time of death about 12 days later (contrast C57BL/6) (Ogunremi and Tabel, 1995). Resistant to lethal and body weight effects of \i Toxacaria canis\i0 , but high larval brain levels (1/5) (Epe et al, 1994). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in a multivesiculation form of hyatid development (cf 4/9) (Nakaya et al, 1997). \par \par Susceptible to \i Streptococcus suis\i0 type 2 including the type strain, two isolates from meningitis in pigs and two isolates from tonsils of clinically healthy pigs (c.f. 2/5) (Kataoka et al 1991). Resistant to street rabies virus (SRV) injected via the intraperitoneal route (Perry and Lodmell 1991). Following administration of murine cytomegalovirus, BALB/c, BALB.B, and BALB.K mice develop persistent myocarditis regardless of age at infection, and age-related cardiopathy is frequent and severe in infected and uninfected mice (contrast C57BL/10 and C3H) (Price et al 1991). Susceptible to the lethal effects of murine hepatitis virus strain 3 (contrast A/J) (Fingerote et al, 1995). The mouse hepatitis virus JHM strain induces a biphasic retinal disease (Wang et al, 1996). Susceptible to infection with the tick-born Thogoto virus, with severe symptoms and death after a few days. The congenic strain carrying the Mx1 gene from strain A2G is resistant (Haller et al, 1995). Susceptible to herpes simplex virus-1 (contrast C67BL/6) (Brenner et al, 1994). \par Develop carditis on infection with Lyme borreliosis (\i Borrelia burgdorferi)\i0 (Barthold et al 1990), but develop only mild arthritis (contrast C3H/HeJ) (Matyniak and Reiner, 1995). Hepatic amoebiasis can be induced by introducing \i Entamoeba histolytica\i0 -infected hamster liver tissue in between the adjacent liver lobes of these mice. (Bhol et al 1990). Resistant to intra-vaginally innoculated \i Neisseria gonorrhoeae\i0 (c.f. 5/5) (Johnson et al 1989). Susceptible (2/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994) \par Widely used in study of \i Plasmodium berghei\i0 infections, though much less sensitive than C57BL/6 (Scheller et al, 1994). Infection with \i P. berghei \i0 results in high peripheral blood parasitemia and death within 22-24 days, but without neuological complication, in contrast with the more susceptible C57BL/6 (Moumaris et al (1995). \par Susceptible (1/4) to\i \i0 disseminated \i Cryptococcus neoformans\i0 (Irokanulo et al, 1995).\i Nippostrongylus brasiliensis\i0 normally rejected by 14 days postinfection. However, this pattern of self-cure was not observed in a "putative" BALB/c substrain from the University of Texas (Mayberry et al, 1993). Susceptible, with high amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). Susceptible to the protozoan parasite\i Neospora canium\i0 following subcutaneous inoculation with tachyzoites of the NC-1 strain (Lindsey et al, 1995). May develop mite-associated ulcerative dermatitis with an allergic reaction to parasite-derived substances following infection with \i Mycoptes musculinus\i0 (Jungmann et al, 1996) \par \par \i Reproduction\i0 \par Good breeding performance (8/25). Colony output 1.18 young/female/wk, litter size at weaning 5.2 (15/25) (Festing, 1976a). Good breeding performance, mean 3.24 young/female/month (1/24) (Hansen \i et al\i0 ., 1973). Intermediate breeding performance (5/8), litter size 5.1 _ 0.3, sterility 32% (Nagasawa \i et al\i0 ., 1973). Low litter size (6/6) (Verley \i et al\i0 ., 1967). Low pre-implantation loss of embryos (1/8), but high post-implantation losses (8/8) (Leonard \i et al\i0 ., 1971). Embryos subject to the 2-cell block and only grow successfully in culture from the late 2-cell stage (Sekirina and Neganova, 1995). \par \i Miscellaneous\i0 \par Recommended host for transplantable tumours: melanoma HP and pleomorphic sarcoma 5180 (although the latter is not host-specific) (Kaliss, 1972). Low mortality after neonatal thymectomy (2/6) (Law, 1966a). Embryonic stem cell lines have been established (Kawase et al, 1994) \par BBT \par Inbr (Cv) 65.Black belted: \i a,bt\i0 . Origin: cross of outbred \i hr/hr, bt/bt\i0 x C57BL/Ha. To Chapman 1974. Maint. by Cv. \par BDP \par Inbr: F94. Pink-eyed fawn. Genet: \i a\i0 , \i b, d, p, rd, se. \i0 Developed by W. H. Gates 1926 from a dilute brown female from Little and a pink-eyed female from Strong (Staats, 1976). Inbred since 1926. Maint. by J. \par \i Behaviour\i0 \par Low food drive (14/15) and high emotionality (2/15) (Thompson, 1953). Nervous (Staats, 1976). \par \i Life-span and spontaneous disease\i0 \par Short life-span in conventional conditions (4/22 = 421 days in males, 6/22 = 468 days in females) (Storer, 1966). Frequent mammary tumours, polycystic or granular kidneys (Staats, 1976). \par \i Normal physiology and biochemistry\i0 \par High plasma cholesterol at 12 and 24 weeks (3/8) (Weibust, 1973). Low porphyrin content of Harderian gland (2/16) (Margolis, 1971). High susceptibility to audiogenic and electroconvulsive seizures (2/6) (Deckard \i et al\i0 ., 1976). High serum complement activity (c.f. 8/26) (Ong et al 1989) \par \i Anatomy\i0 \par Large kidney/body weight ratio (3/21) (Schlager, 1968). \par \i Drugs\i0 \par Resistant to X-irradiation (8/27) (Roderick, 1963). \par \i Immunology\i0 \par Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). \par Infection \par Murine acquired immune deficiency (MAIDS) is an immunosuppressive disease of mice induced by infection with the LP-BM5 murine leukemia retrovirus. Strain BDP has a novel disease phenotype with recovery of immune function after a period of profound immune suppression. This is inherited as a dominant character in crosses with both susceptible and resistant strains (Gilmore, 1997). \par BFM/1 \par Inbr 30 (Mpl). Light agouti colour with a light belly \i A*,B,C,\i0 where * indicates a variant allele. Origin: Wild mice trapped at Univ. of Montpellier. It has never been crossed with laboratory mice \par BFM/2 \par Inbr 15+24 (Ms). Light agouti colour with a light belly \i A*,B,C,\i0 where * indicates a variant allele. Origin: Wild mice trapped at Univ. of Montpellier. It has never been crossed with laboratory mice. BFM/2Ms was branched from the original BFM/2Mpl at F12-15 (Bonhomme et al 1982). Inbred a further 24 generations by Ms. Maint. by A. \par BIMA \par Inbr. G10F58. Colour ?. Origin: Muhlbock 1959. A partly congenic strain of C57BL/LiA following an outcross to C3H/HeA with cross-intercross matings with selection for large mammary glands to G10 then further selection with bxs mating to F11. Maint. by A. \par BIR \par Inbr. G12F61. Colour ?. Origin: Muhlbock 1958. A partly congenic strain of C57BL/LiA following an outcross to DBA/LiA with cross-intercross matings with selection for resistance to the growth of C57BL/LiA mammary tumour cell line transplanted in vivo. Maint. by A. \par BL \par Inbr: F108. Albino. Genet: \i a, b, c\i0 strain developed by Lynch from Bagg albino stock via Strong, and maintained at Rockefeller Institute since 1921. \par Characteristics \par Low mammary tumours, some lung tumours in older mice (Staats, 1976). Ovaries often appear pale and enlarged and have an infiltration of amyloid. Thought to be due to necrotising arteritis in which there is a thickening of the walls of the vessels to duodenum and ovaries due to a deposition of eosinophilic material within the intima and media (Deringer, 1959b). Aseptic necrosis of bone in 22% of females often resulting in fracture of femoral neck and other complications, so that the animals are severely crippled (Sokoloff and Haberman, 1958). \par BLN \par Inbr (Nmg) 58. Black: \i a\i0 . Origin: Cpb non-inbred yellow stock. Inbred from 1965. Very good reproductive performance. Maint. by Nmg. \par BLRB \par Inbr F20. Black. Origin: EV Moiseeva, 1981. Spontaneous translocation Rb(8.17)Iem was found originally by VS Baranov in C3HA/Iem mice and the carriers were crossed to black mice of an unknown C57BL substrain, followed by b x s mating. \i Hbb\i0 \i \up8 d\up0 \i0 \up8 \up0 . Mammary tumours in 95% of breeding females at an average age of 11.2 months. Maintained by Moiseeva, Institute of Immunology, Kashirskoe sh., 24-2 Moscow 115478, USSR. \par BN/a \par Inbr: 55. Genet: \i A, B, c, D, H2\i0 \i \up8 bp\up0 \i0 \up8 \up0 . Origin: Anna Dux, Gliwice, September 1950 from unknown parents. F13 taken to Warsaw June 1956, where it was split into two substrains, inbreeding continued. \par Characteristics \par 35% lung tumours at 662 days; 7.1% leukaemia at 647 days; 23% chronic nephritis at 562 days. Used for carrying transplantable vaginal epithelioma G93 (Czarnomska and Wezykowa, 1971). \par BN/b \par Inbr: 60. Genet and Origin: see BN/a. \par Characteristics \par Lung tumours 25% at 629 days; l.8% leukaemia at 512 days in females, 13% chronic nephritis at 493 days; used for carrying transplantable vaginal epithelioma G94. \par BNT \par Inbr (Le) 73. Black \i a\i0 . Origin: mutation to \i Bn\i0 (bent-tail) discovered by E.D.Garber. From A.B.Griffen to Lane 1960. Inbred to F27, then one outcross to C57BL/6J x CBA/Ca F1, followed by b x s. (now only maintained as frozen embryos). Maint. by Le \par BOB \par Inbr: F92. Albino. Genet: \i a, c, rd. \i0 Strain developed after 1945 from random-bred mice of unknown origin at Brown University. \par Characteristics \par Small spinal cord (22/25) (Roderick \i et al\i0 ., 1973). High lymphocyte phytohaemagglutinin response (6/43) (Heiniger \i et al\i0 ., 1975). Develops leukaemia on infection by Friend virus (cf. 5/11) (Dietz and Rich, 1972). \par BOMG \par Inbr (Kfl) 30 (1994). Albino \i a,c. \i0 Origin: Outbred Bom:NMRI mice from Bomhlotgaard, Denmark, inbred by Kfl. Mitochondrial genome like NZB/BlNJ. Used in studies of mitochondrially encoded maternally transmitted antigen, \i Mta.\i0 These mice are large and carry the Mtf(beta) allele. \i H2\i0 \i \up8 q\up0 \i0 \i , Tla\i0 \i \up8 a\up0 \i0 \i \i0 and \i Qa1\i0 \i \up8 a\up0 \i0 \up8 \up0 \par BPH /2 \par Inbr (J, 1998) F55. Albino. Gunther Schlager, U. of Kansas. Genetic selection for high blood pressure initiated in 1966 from a base population derived from an 8-way cross among LP/J, SJL/J, BALB/cJ, C57BL/J, 129/J, CBA/J, RF/J and BDP/J. Inbreeding avoided until F23 when several inbred substrains were initiated. Strain has a high systolic blood pressure, shortened life span, low norephinephrine content in whole brain, larger relative heart and kidney weight, fewer glomeruli in the kidney and larger 24-hr. urinary volume Schlager (1974, 1981,1994) (see also BPL). Maintained by J. \par BPL /1 \par Inbr (J, 1998) F55. White bellied agouti. Origin: Gunther Schlager, U. of Kansas. Genetic selection for low blood pressure initiated in 1966 from a base population derived from an 8-way cross among LP/J, SJL/J, BALB/cJ, C57BL/J, 129/J, CBA/J, RF/J and BDP/J. Inbreeding avoided until F23 when several inbred substrains were initiated. Strain has low systolic blood pressure, long life span (approx. 50% longer than BPH/2) and high norephinephrine content in whole brain (Schlager 1994) (see also BPH). Maintained by J. \par BPN/3 \par Inbr. F44 (J). Origin: see BHP/2. Developed from the unselected control strain used in the development of BPH and BPL/1. Maintained by J. \par BRSUNT \par Inbr: 130. Genet: \i a\i0 , \i b, C. \i0 Origin: Strong, a branch of BRS (from strain NH) continued without further methylcholanthrene treatment. \par Characteristics \par Gastric lesions, adiposity; 100% incidence of periodontal disease. \par BRVR \par Inbr: F83+. Albino. Genet: c. Origin: Webster (1933a,b) developed two lines resistant and susceptible to infection by \i Bacillus enteritidis \i0 (\i Salmonella \i0 sp.) by selection on the basis of a progeny test, followed by full-sib mating. Mortality under specified test conditions was 15% and 85%, respectively, and was about 39% in the unselected controls. Later tests (Webster, 1937) with louping ill and St Louis encephalitis viruses led to the development of three lines designated BSVS (bacteria-susceptible, virus-susceptible), BSVR (bacteria-susceptible, virus-resistant) and BRVS (bacteria-resistant, virus-susceptible). Later BRVR (bacteria-resistant, virus-resistant) mice were developed from a cross between BSVR and BRVS, with subsequent selection for resistance to the two agents, and full-sib mating. There may have been some confusion between the lines in the past, and authenticity should not always be assumed. \par Characteristics \par Hydronephrosis in 11% of females and 18% of males (1/13) (Taylor and Fraser, 1973), 34-42% in males and 30-34% in females (Collins \i et al\i0 ., 1971). Resistant to \i Salmonella, \i0 some encephalitic viruses and experimental allergic encephalomyelitis (Staats, 1976). Resistant to experimental allergic encephalomyelitis (cf. 6/14) (Levine and Sowinski, 1973). Resistant to induction of experimental autoimmune thyroiditis (cf. 2/5) (Vladutiu and Rose, 1971a). Carries gene for resistance to group B arbovirus infection (cf. strain PRI) (Darnell \i et al\i0 ., 1974). Differences between the responses of BRVR and BSVS to infections and various antigens are listed by Boehme(1970). \par BRX58N- \par Inbr 20+. Set of 11 recombinant inbred strains developed by B.A.Taylor from C57BR/cdJ x B10.D2(58N)/Sn. Maint. by Ty. \par BSC \par Inbr 57 (Dk). Albino; \i c\i0 . Origin: A stock incorporating BSVS mice was used to found an outbred colony at the ARC Labs. Compton, England. Inbred in 1972 by Dickinson. Sincp7. Maintained by Dk. \par BSVR \par Inbr ?. Albino.See BRVR. Maint. by Db. \par BSVS \par Inbr: F 99 +?. Albino. Genet: \i c\i0 . Origin: see BRVR. \par Characteristics \par Susceptible to \i Salmonella,\i0 some encephalitic viruses and experimental allergic encephalomyelitis (Staats, 1976). Susceptible to St Louis encephalitis and yellow fever virus (Boheme 1970). According to Levine and Sowinski (1973), resistant to experimental allergic encephalomyelitis (cf. 6/14), but 100% susceptible according to Schneider \i et al\i0 . (1957). Sensitive to anaphylaxis after sensitisation with BSA and increased sensitivity to serotonin following pertussis vaccine (Rose et \i al\i0 ., 1973). Susceptible to induction of experimental autoimmune thyroiditis (cf. 3/5) (Vladutiu and Rose, 1971a). Spontaneous congenital hydronephrosis 5% in males, zero in females (Collins \i et al\i0 ., 1971). Extremely sensitive to traumatic shock (Halevy and Altura, 1974). Has a defective immune response to DNP-haemocyanin and streptococcal group A carbohydrate, which are T-cell-dependent (Briles \i et al\i0 ., 1976). \par BT/Kt \par Inbr. F??. Resistant to teratogenic effects (cleft palate) of cortisone acetate (1/6) (Kalter 1981). Not related to BT/Os. Possibly extinct. \par BT/Os \par Inbr: F35 +. Black and tan. Genet: \i a\i0 \i \up8 t\up0 \i0 \up8 \up0 . Origin: One pair of albino mice from dealer in Gifu Prefecture. Inbreeding started in 1951. Cross made with C57BL/6 in 1954, with subsequent selection for the black colour (Tajima, 1968). \par Characteristics \par High incidence of spontaneous mammary tumours (70%), high incidence of gastric tumours following methylcholanthrene by gavage (1/5), and highly sensitive to skin carcinogenesis (Akamatsu and Barton, 1974). (NOTE: Strain BT/Kt is unrelated to this strain.). \par BTBRTF and BTNTTF \par Inbr. F100+?. Black-and-tan, brachyury tufted. Genet: \i a\i0 \i \up8 t\up0 \i0 \i , B, tf, T/+\i0 or \i +/+, H2\i0 \i \up8 b\up0 \i0 \up8 \up0 . Origin: Dobrovolskaia-Zavadskaia to Dunn who sib-mated at the Nevis Biological Station, Columbia University. Tufted from Dr. Mary Lyon was backcrossed onto the strain, followed by further sib mating. To Dorothea Bennett from 1962, then to Karen Artzt. Supports maintenance as a balanced lethal stock with matings of \i T/t x T/t.\i0 Has been selected for 50% tail length of \i T/+\i0 heterozygotes. The normal tailed segregant is sometimes known as BTNTTF. Good breeding performance (Artz personal communication, July 1997 and Artz et al, 1977). \par BUA \par Inbr: 68. Genet: a, c. Origin: From albinos of unknown origin at Brown University; maintained by random breeding until 1945. \par Characteristics \par Selected for good growth and reproductive performance; no known tumours. \par BUB \par Inbr (J) 122. Albino \i a,c\i0 . Origin: from albinos of unknown ancestry at Brown University, maintained by random mating until 1945. Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). High serum complement activity (c.f. 8/26) (Ong et al 1989, 1992). High ED50 to behavioural effects of nicotine (19/19). Sensitive to seizures induced by nicotine (17/19) (Marks et al 1989). Carries a T-cell receptor mutation which, in association with other unknown genes, makes the strain highly susceptible to the induction of inflammatory autoimmune arthritis by type II collagen (Ortman et al, 1994, Haqqi et al, 1995). \par Maintained by J. \par BXD- \par Inbr 30+. Set of 24 recombinant inbred strains developed by B.A.Taylor from C57BL/6J x DBA/2J. BXD-31 has low osmotic fragility of erythrocytes due to variation at a single genetic locus causing up-regulation of K-Cl cotransport which induces cell dehydration, a K+ deficit and resistance to osmotic lysis (Armsby et al, 1996). Maint. by Ty. \par BXH- \par Inbr 30+. Set of 13 recombinant inbred strains developed by B.A.Taylor from C57BL/6J x C3H/HeJ. Maint. by Ty. Strain BXH2 develop myeloid leukemia as a result of the expression of an ecotropic murine leukaemia virus that acts as an insertional mutagen altering the expression of cellular proto-oncogenes. This is not passed through the germ line, but is passed from one generation to the next by horizontal transmission (Bedigian et al, 1993). A homeobox locus \i Meis1\i0 is the site of viral integration in 15% of tumours (Moskow et al, 1995). \par BXSB \par Inbr (Mp) 49. Agouti; \i +\i0 . Origin: E.D.Murphy from a cross of C57BL/6J x SB, followed by selection of the satin, non-beige phenotype, followed by b x s mating. \par Characteristics \par Develops spontaneous lupus-like autoimmune syndrome which is strikingly accelerated in the males. This also occurs in F1 hybrids provided BXSB is the male parent, and appears to be due to a Y-linked gene (Murphy and Roths 1979). Cell-mediated immune function compares favourably with other strains, though there may be reduced reticuloendothelial function (Creighton et al 1979). Theofilopoulos et al (1980) have compared immune function in this and other autoimmune strains. Ultrastructural pathology of the thymic reticulum revealed several features in common with NZB and MRL-\i lpr\i0 in varying degrees according to sex and age of the mice. Main anomalies included vacuolized aspect of the thymic epithelium, an increased number of macrophages, interdigitating cells and cystic cavities, the presence of a great number of plasmocytes and mastocytes and extensive interstitial fibrosis and arteriosclerosis. The most intriguing finding was the presence of crystal-like inclusions in epithelial cells (Nabarra et al 1990). An unusual expansion of CFU-M appears in spleen and liver of male mice two weeks after birth (Vieten et al,1996). These mice develop antibodies that bind cardiolipin phosphatidylserine and phosphatidylinositol (Ahmed et al, 1993). Treatment with bacterial lipopolysaccharide enhances polyclonal B-cell activation, impairs carrier function of blood cells for immune complexes, increases deposition of immune complexes in the microcirculation and promotes glomerular inflammation and sclerosis (Granholm and Cavallo, 1995). An unusual expansion of macrophage precursor cells (CFU-M) appears in the spleen and liver of male mice two weeks after birth (Vieten et al, 1996). \par About 40-60% of mice of both sexes have ectopic cell clusters in layer I of the neocortex. Affected mice had better Morris maze learning and better long-term retention than the non-ectopic counterparts (Boehm et al, 1996a). They also had better reference memory, but less effective working memory than their non-ectopic counterparts in a Lashley III maze (Boehm et al, 1996b). Ectopic mice also took longer to learn a "working memory" water maze (Waters et al, 1997). \par Embryonic stem cell lines have been established (Kawase et al, 1994). Like other \i H2\i0 \i \up8 b\up0 \i0 \up8 \up0 mice this strain does not express the class II H2 antigen, I-E. Mice bearing this antigen as a transgene do not develop the autoimmune syndrome (Merino et al, 1993). \par Maint. by J, Ola. \par BXVII \par Inbr ?. No details. Maint. by Cri. \par C \par Inbr: 124. Genet: \i b. \i0 Origin: Strong 1920, from a cross of Bagg albino female x DBA male. Strains C3H, CBA, CHI and C121 originated from the same cross. \par Characteristics \par Moderate mammary tumour incidence. \par C.B17 \par Inbr. F55 (1993). Genet. A,b,c. Origin: Developed from the 13th. backcross of BALB/cxC57BL/Ka-Igh\up8 a\up0 /Igh\up8 b \up0 to BALB/c by Michael Potter, NIH, to E. Weiler, ICR in 1964. At ICR the mice were backcrossed to the BALB/cAnNIcr strain for four more generations by Melvin Bosma. C.B-Igh\up8 a\up0 /Igh\up8 b\up0 N17 progeny were then intercrossed to obtain mice homozygous for Igh\up8 b\up0 . In 1970 Bosma gave the C.B17-Igh\up8 b\up0 mice to the Laboratory Animal Facility at the Institute for Cancer Research at Fox Chase Cancer Center. The strain is now maintained in an SPF barrier facility. Its characteristics are essentially those of BALB/c, and its primary use is as a coisogenic control strain for C.B17/Icr-\i scid.\i0 \par C1 \par Inbr. F30 (1993). Black agouti. Origin: DeFries from a randombred stock used as a control for open-field activity selection lines (see also H1 and H2) \par C17/Icrc \par Inbr: F25 +. Light brown strain developed in 1956 from a cross of male C57BL/6 and female XVII. Life-span 26 months. Litter size 7.2-7.5 at birth and 4.4-6.2 at weaning. Low incidence of tumours of all types. Sensitive to weak skin carcinogens. (Ranadive \i et al\i0 ., 1969). \par C2 \par Inbr. F30 (1993). Albino. Replkicate of strain C1. \par C3H \par Inbr: F130 to F170 depending on substrain. Agouti. Genet: +, \i rd\i0 . Developed by Strong 1920 from a cross of Bagg albino with DBA male (see CBA) with selection for a high incidence of mammary tumours. Now among the most widely used of all mouse strains. Most substrains have a good reproductive performance. Unfostered substrains (which are now relatively rare since 'SPF' animals have become popular) have a high incidence of mammary tumours (usually > 90% at one year) caused by a virus which is passed from mother to offspring through the milk. Fostering of the young or transfer of fertilised ova to a mammary tumour virus-free strain eliminates the virus, and substantially reduces the incidence of mammary tumours. Note that all `SPF' stock will be free of this virus. \par \par The unfostered substrains are widely used in cancer research for the sake of their mammary tumours. Fostered stock are widely used as a general-purpose strain which is readily available and well known. The strain should be used with care in behavioural studies, since it carries the \i rd \i0 (retinal degeneration) gene and is blind after about 6 weeks. \par \par Some substrain differences are large, and can not be accounted for solely on the basis of mutation, and must be ascribed either to substantial residual heterozygosity or genetic contamination (McLaren and Tait, 1969), though C3H/HeJ is known to differ from C3H/He as a result of a mutation at the \i lps\i0 (lipopolysaccharide) locus. \par \par The following major substrains are recognised: \par \par C3H/Bi \par Strong to Bittner 1931, to Kirschbaum 1952. Has 83% mammary tumours in unfostered breeders. Low leukaemia. \par \par C3H/Fg \par Origin not known, but has a very high incidence of lymphatic leukaemia (over 90%) (Fuchs, 1962). \par \par C3H/He \par This substrain was passed to Heston in 1941,and is now the most widely distributed of all. Non-fostered substrains have more than 90% mammary tumours by about 11 months. Fostered substrains have a high incidence of hepatomas (Festing and Blackmore, 1971). \par \par C3H/HeJ \par Heston, to Jackson Laboratory in 1947, and now widely distributed. Has poor immune response to endotoxic lipopolysaccharide due to a B-cell deficit (Rosenstreich and Glode, 1975; Coutinho, 1976). \par \par C3HeB/De \par A substrain developed by transfer of fertilised ova to strain C57BL by Deringer. This substrain lacks the mammary tumour virus and therefore has a lower incidence of mammary tumours (4% in virgin females and 55% in breeding females and 74% in force-bred females) (Deringer, 1959a). \par \par C3HeB/FeJLe-\i a/a\i0 \par Inbr. N10F12 (1993). The a allele transferred from C57BL/6J. Now used to create a B6C3Fe-a/a non-agouti hybrid as a coat colour marker for stocks maintained by ovarian transfer. \par C3HeB/Fe (syn: TC3H) \par Developed by Fekete in 1948 by transfer of fertilized ova of C3H/HeJ to C57BL/6. Lacks mammary tumour virus. \par \par C3H/He-mg \par `Mahogany' coat colour mutation occurred spontaneously in C3H/He stock held at Laboratory Animals Centre, Carshalton, in 1967. The strain has been propagated because authenticity can be guaranteed by the colour of the coat. \par \par C3H/He-\i A\i0 \i \up8 vy\up0 \i0 \up8 \up0 \par Congenic line developed by backcrossing the \i A\i0 \i \up8 vy\up0 \i0 \i \i0 to the C3H background. Has an exceptionally high mammary tumour incidence, virtually 100% at 7-8 months. The fostered substrain C3H-\i A\i0 \i \up8 vy\up0 \i0 \up8 \up0 f\i B\i0 has a 90% incidence of mammary tumours transmitted by either parent (Vlahakis \i et al\i0 ., 1970). \par \par C3H.PRI-\i Flv\i0 \i \up8 r\up0 \i0 \i \i0 (formerly C3H.RV ) and C3H.M.Dom-\i Flv\i0 \i \up8 r\up0 \i0 \up8 \up0 \par Congenic line resistant to flavivirus (arbovirus) infection, developed by Groschel and Koprowski (1965) by backcrossing the resistance gene from PRI to C3H, and by Shallam by backcrossing the resistance gene from wild \i M.m. domesticus\i0 to C3H\i .\i0 \par \i Behaviour\i0 \par Low intrastrain aggression (10/14) (Southwick and Clark, 1966). Long latency to emerge from home-cage (6/7), low rearing (7/7), long latency to cross barrier in open-field (6/7), low hole-in-the-wall entries (6/7) and low Y-maze exploration (7/7) (McClearn \i et al\i0 ., 1970). Low open-field activity (13/13) (Bruell, 1964). Low open-field defaecation (5/5) (Bruell, 1969). High food drive (3/15) (Thompson, 1953), but poor performance in food-seeking task (5/6) (Henderson, 1970). Short time of immobility in a forced swimming test (9/9) (Nikulina et al 1991). \par Low shock-avoidance learning (8/9) (Bovet \i et al\i0 ., 1966, 1969). Good short- term but poor long-term memory in contrast with DBA/2 (Bovet \i et al\i0 ., 1969). Good T-maze learning (1/6) (Stasik, 1970). Poor water-escape learning (6/6) (Festing, 1973b). Low radial-arm maze learning (3/3) (Ammassari-Teule et al, 1993). High social grooming score during aggressive encounters (3/14) (Southwick and Clark, 1968). \par \par Carries the retinal degeneration gene and is capable of pattern discrimination up to 40 days, and brightness discrimination to at least 100 days (Nagy and Misanin, 1970). \par \i Life-span and spontaneous disease\i0 \par Almost 100% of mammary tumours in females of unfostered substrains (Heston, 1963). Mammary adenocarcinomas in unfostered substrains less than 1% in males, 95% in breeding and 88% in virgin females. Lymphatic leukaemia zero incidence (Hoag, 1963). Mammary tumours 100% at 6.8 months in C3H-\i A\i0 \i \up8 vy\up0 \i0 \up8 \up0 , 90% in C3H- \i A\i0 \i \up8 vy\up0 \i0 \up8 \up0 fC57BL at 15.3 months. Mammary tumours 40% at 18.8 months in C3HfC57BL, but 99% at 7.2 months in unfostered C3H (Heston and Vlahakis, 1971). Mammary tumours 37% at 2 years in fostered substrain (Bentvelzen \i et al\i0 ., 1970). Median latent period to develop mammary tumours in unfostered substrains ranged from 276 to 566 days, depending on breeding status and environmental stress (Riley, 1975). A high proportion of the mammary tumours are of the acinar type (2/7) (Tengbergen, 1970). Incidence of mammary tumours reduced by bromocriptine and interferon Stravoravdi et al, 1993). \par Hepatomas 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females (Heston, 1963). Hepatomas have eosinophilic cytoplasmic inclusion bodies (Liebelt \i et al\i0 ., 1971). Good model of genetic predisposition to hepatocellular tumours, susceptibility being associated with six chromosomal regions (Dragani et al, 1995). Point mutations in H-ras do not generally play a major or initiating role in spontaneous hepatocarcinogenesis in this strain (Enomoto et al, 1993). \par Lung adenomas 2-10% in fostered A substrain, leukaemia 6-30% (Muhlbock and Tengbergen, 1971). Occasional Harderian gland tumours (Heston, 1963). Rare "lipomatous" hamartomas or choristomas have been noted (Adkison et al 1991). \par Life-span in SPF fostered conditions intermediate in both sexes (11/17 = 590 days in males, 12/17 = 676 days in females). Liver tumours 9-23%, lung tumours 2-10% and mammary tumours 21-36%. Heart defects 13-26% and cystic ovaries 13-26% (Festing and Blackmore, 1971). Tail lesions similar in appearance to bit wounds were found in grouped C3H/HeJ by Les (1972). Develop dystrophic cardiac calcification which may be related to disturbed myocyte calcium metabolism (Brunnert, 1997). \par Can be made obese by a suitable diet (Fenton and Dowling, 1953). Resistant to the development of aortic cartilaginous metaplasia (contrast C57BL/6) (Qiao et al, 1995). Resistant to diet-induced aortic fatty streak lesions which correlates with a high level of paroxinase mRNA (contrast C57BL/6) (Shih et al, 1996). \par C3HeB/FeJ \par Primary lung tumours 8% in males, 4% in breeding females and 10% in Virgin females. Lymphatic leukaemia zero. Mammary adenocarcinomas zero in males, 12% in breeding females, 2% in virgin females (Hoag, 1963). Ovarian tumours 47% in Virgin and 37% in breeding females, 29% in force-bred females (Heston, 1963). Hepatomas 91% in breeding males, 58% in Virgin and 30% in breeding females (Murphy, 1966). Life-span above average in both sexes (16/22 = 652 days in males, 17/22 = 657 days in females). High gross tumour incidence in males (5/22) (Storer, 1966). \par \i Normal physiology and biochemistry\i0 \par Low blood pressure (15/17) (Mullink \i et al\i0 ., 1975). Low serum calcium in Fg substrain (5/6) but He substrain has high level at 4 months (1/6) (Barrett \i et al\i0 ., 1975). High serum cholesterol (1/5) (Bruell \i et al\i0 ., 1962). High plasma cholesterol (11/11) and triglycerides (10/11). High erythrocyte catalase (5/18) (Hoffman and Rechcigl, 1971). Low serum haptoglobin level (10/11) (Peacock \i et al\i0 , 1967). Low peripheral nerve conduction velocity (6/6) (Hegmann, 1972). Low percentage of time spent sleeping (5/6) with low percentage of slow-wave sleep (5/6) and small diurnal variation (5/6) (Valatx and Bugat, 1974). High brain glutamic acid decarboxylase (GABA) in He-\i mg\i0 substrain (2/10) (Gaitonde and Festing, 1976). High brain aromatic L-amino acid decarboxylase (1/5) in C3H/2 substrain (Pryor \i et al\i0 ., 1966). Low metabolic rate (5/6) (Pennycuik, 1967). High liver tyrosine aminotransferase level in fasted mice (1/10) (Blake, 1970). Low adrenal corticosteroid production (4/4) (Nandi \i et al\i0 ., 1967). High peptidyl proline hydroxylase activity in tumour tissue and mammary gland fat pad (1/5) (Cutroneo \i et al\i0 ., 1973). Slow cell turnover as judged by rate of clearance of DNA- bound radioactivity (14/17) (Heiniger \i et al\i0 ., 1972). Harderian gland has a high porphyrin content (2/16) (Margolis, 1971). Low hepatic ammonia-lyase activity (5/6 and 6/6 in two substrains) (Hanford \i et al\i0 ., 1974). Low spermatozoal beta-glucuronidase activity (9/9) (Erickson, 1976). Low basal level of renal glutathione S-transferase (4/4) but high basal level of renal glutathione reductase (1/4) (Misra et al 1991). Low hepatic nicotinamide N-methyltransferase levels (10/10) (Scheller et al, 1996). Maintain normal auditory sensitivity beyond one year of age in both HeJ and HeSnJ substrains, but by 30 months there was little hearing function due to sensorineural degeneration (Trune et al, 1996). \par High level of alpha-fetoprotein in plasma at 7 days (2/6) (Adinolfi et al 1990). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). Loci on chromosomes 1, 3, 5 and 11 are associated with variation in high density lipoprotein levels with coordinate expression of cholesterol-7-alpha hydroxylase in a cross involving atherosclerosis susceptible C57BL/6 mice (Machleder et al, 1997). \par Hepatic iodothyonine deiodinase activity was only 18% of that found in C57BL/6 mice (Schoenmakers et al, 1993). Decreased levels of deiodinase mRNA and hyperthyroxinemia associated with a 21-base pair insert in the promoter region of the type 1 deiodinase gene (Maia et al, 1995). Resistant to severe hypercapnia with hypoxia assessed by elevated minute ventilation rate (8/8) (Tankersley et al, 1994). Has a slow and deep breathing pattern phenotype (contrast C57BL/6) (Tankersley et al, 1997). High intra-ocular pressure (1/4) (John et al, 1997). \par C3HeB/FeJ \par Low systolic blood pressure (19/19) (Schlager and Weibust, 1967). Low plasma cholinesterase activity in females (18/22) (Angel et al, 1967). High \i N'\i0 - methylnicotinamide oxidase activity (1/7) (Huff and Chaykin, 1967). \par \i Anatomy\i0 \par Low total leukocyte count (18/18), low erythrocyte count (16/18), low haematocrit (18/18), low haemoglobin (17/18) (Russell \i et al\i0 ., 1951). Small thymus/body weight ratio (5/6) (Belyaev \i et al\i0 ., 1970), small thymus/body weight ratio (6/8 to 8/8, depending on age) (Albert \i et al\i0 ., 1965). Large pituitary (1/6) (Sinha \i et al\i0 ., 1975). Adrenal gland X zone large (1/8), with high incidence of vacuolisation (2/6) (Delost and Chirvan-Nia, 1958). Low percentage of mice have accessory spleens (9/9) (Hummel \i et al\i0 ., 1966). Many Peyer's patches (2/7) (Hummel \i et al\i0 ., 1966). Plasma volume low (4/4) at 5.97 ml/100 g and red cell volume low (4/4) at 4.64ml/100g body weight in He substrain (Kano and Mizuma, 197.4). Intermediate proportion of sperm-head abnormalities (2/5, 13%) in C3H/HeJ (Styrna et al 1991). High retinal ganglion cell number (24/24) in HeJ (Williams et al, 1996). High bone density of femur (1/11) (Beamer et al, 1996). \par Megakaryocytes have a higher average ploidy than all other mouse strains tested. This is due to multiple additive alleles (McDonald and Jackson, 1994). \par C3HeB/FeJ \par Large brain weight (15/18 male, 17/18 female) (Storer, 1967). Small brain/body weight ratio (19/20) (Roderick \i et al\i0 ., 1973). \par \i Drugs\i0 \par Susceptible to skin ulceration to DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Sensitive to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (1/14 to 4/14, depending on substrain) (Kouri \i et al\i0 ., 1973). Susceptible to tumour induction by 3-methylcholanthrene in fostered and unfostered substrains (1/8 to 2/8) (Whitmire and Salerno, 1972), (2/12) (Whitmire \i et al\i0 ., 1971). Susceptible to induction of liver (1/6) but resistant to pulmonary (5/6) tumours by neonatally administered DMBA (Flaks, 1968). High susceptibility to tumour induction by 3,4-benzpyrene (1/6) (Liebelt \i et al\i0 ., 1970). High susceptibility to induction of mammary tumours by urethane (2/7) (Bentvelzen \i et al\i0 ., 1970). High incidence of gastric tumours after administration of methylcholanthrene by gavage (2/5) (Akamatsu and Barton, 1974). Susceptible to fibrosarcoma induction by methylcholanthrene (2/15 male, 1/15 female) (Strong, 1952). Highly susceptible to the induction of hepatocellular tumours by various carcinogens, with the volume of hepatic lesions being >100-fold greater than in more resistant strains. Susceptibility is linked to at least six chromosomal regions (Dragani et al, 1995). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-\i ras\i0 and p53, respectively (Masui et al, 1997). \par Phenobarbitone in the diet to give an intake of 85mg/kg per day resulted in 70% of animals developing basophilic nodules by 91 weeks of age (contrast 4% in C57BL/6), but no increase in liver carcinomas (Evans et al, 1992). However, there was a two-fold greater level of DNA synthesis in C3H mice relative to C57BL/6 mice after partial hepatactomy, though partial hepatectomy is a tumour promoter in C57BL/6 but not in C3H mice (Bennett et al, 1995). \par Insensitive to histamine (9/9) (Brown, 1965). Airways of C3H/HeJ hyporeactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Resistant to teratogenic effect of acetazolamide (5/6) (Green \i et al\i0 ., 1973). Pentobarbital i.p. induces hepatic epoxide hydrase (cf. 4/7) (Oesch \i et al\i0 ., 1973). Sensitive to X-irradiation (25/27) (Roderick, 1963). Long survival on Warfarin (12/12) (Lush and Arnold, 1975). Sensitive to hyperbaric oxygen (2/18) (Hill \i et al\i0 ., 1968). Sensitive uterine response to oestrogens (5/5) (Chai and Dickie, 1966). Short hexobarbital sleeping time (3/9) (Vesell, 1968). Long survival in 90% oxygen (1/10) and highly susceptible to pulmonary hyaline-membrane formation (1/10) (Lieberman and Kellog, 1967). Resistant to the induction of pulmonary fibrosis by bleomycin (contrast C57BL/6) (Haston et al, 1996), and irradiation though the sensitivity of lung fibroblasts to irradiation \i in-vitro\i0 does not correlate with \i in-vivo\i0 sensitivity (Dileto and Travis, 1996). Sensitive to chloroform toxicity (cf. 4/9) (Deringer \i et al\i0 ., 1953). Susceptible to toxic effects of isoniazid (10/10) (Taylor, 1976b). High ED50 to behavioural effects of nicotine (17/19) (Marks et al 1989). Low self-selection of nicotine (5/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996). \par Low bronchial reactivity (5/6) to methacholine and serotonin (Konno et al 1993). No increase in renal lipid peroxidation following treatment with nickel (4/4) (Misra et al 1991). Susceptible to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (2/4) (Bhathal et al 1990). Low histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser ( c.f. 5/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Cadmium highly hepatotoxic (1/5) (Shaikh et al, 1993). Resistant (cf 3/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995, Kleeberger et al, 1993). Susceptible to weight loss induced by cocaine, but this is attenuated by anisomycin (cf SJL, CBA) (Shimosato et al, 1994). Estrogen does not induce an increase in VLDL and LDL-cholesterol (like BALB/c, contrast C57BL/6 and C57L)) (Srivastava, 1995). \par C3HeB/FeJ \par Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Sensitive to X-irradiation (23/27) (Roderick, 1963). Good ovulatory response (94%) to 3 I.U. PMS (1/6), but poor response (33%) to 7 I.U. PMS. Response facilitated by exposure to males (Zarrow \i et al\i0 ., 1971). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). \par \i Immunology\i0 \par Sensitive to amyloid induction (2/10) but low level of spontaneous amyloid formation (Ram \i et al\i0 ., 1969). Low lymphocyte phytohaemagglutinin response (38/43) (Heiniger \i et al\i0 ., 1975). Good immune response to small doses of bovine gamma globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to Cholera A and B antigens (8/8) (Cerny \i et al\i0 ., 1971). Good splenic PFC immune response to pneumococcal polysaccharide (2/9) (Amsbaugh \i et al\i0 ., 1972). Females fail to reject male skin grafts after 100 days (contrast nine strains) (Gasser and Silvers, 1971). Poor immune response to ovomucoid and ovalbumin (cf. 2/12) (Vaz \i et al\i0 ., 1971). Poor primary immune response to bovine serum albumin (5/6) (James and Milne, 1972). Good immune response to \i Salmonella anatum \i0 (1/5) and \i S. senftenberg \i0 (2/5) lipopolysaccharide (Di Pauli, 1972). Responder to synthetic polypeptide Glu\up8 57\up0 , Lys\up8 38\up0 , Ala\up8 5\up0 (cf. 3/7) (Pinchuk and Maurer, 1965). Good immune response to Vi antigen (2/5) (Gaines \i et al\i0 ., 1965). Precipitating and skin-sensitising antibodies have slow electrophoretic mobility (2/6) (Fahey, 1965). High antibody affinity to HSA (3/9) (Petty \i et al\i0 ., 1972). Erythrocytes have high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Low immune response to ferritin in He substrain (15/16) (Young \i et al\i0 ., 1976). Non- discriminator between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). High anti-DNP antibody concentration (2/7) (Paul \i et al\i0 ., 1970). Antibodies to lipoid A antigen do not cross-react with sheep red blood cells (contrast eight strains). Strain also resistant to toxic effect of \i Salmonella \i0 lipopolysaccharide (1/8) (Rank \i et al\i0 ., 1969). Refractory to sensitising effects of HSF from \i Bordetella pertussis \i0 to histamine (contrast sixteen strains) (Bergman and Munoz, 1968). \par Low level of "leakiness" when the \i scid\i0 mutation is maintained on this genetic background (contrast CB17) (Nonoyama et al, 1993). \par Good immune response to Pro-Gly-Pro-ovalbumin (1/7) and (Pro-Gly- Pro)\dn8 n\dn0 (2/7) (Fuchs \i et al\i0 ., 1974). High susceptibility (3/12) to IgE-mediated passive cutaneous anaphylaxis (De Souza \i et al\i0 ., 1974). Good immune response to \i Salmonella strasbourg \i0 lipopolysaccharide (1/7) (Di Pauli, 1972). Low PHA- stimulated lymphocyte blastogenic response in Ent substrain (6/6) (Hellman and Fowler, 1972). Erythrocytes of C3HeB/FeJ have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). He substrain resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). He and HeN substrains are susceptible (2/12) to experimental autoimmune orchitis induced by two or three sc injections with viable syngeneic testicular germ cells without any adjuvants, but C3H/BiKi is resistant (12/12) (Tokunaga et al 1993). High immune response to ganglio-series gangliosides in C3H/HeN (c.f. 2/10), but low response in C3H/HeJ (c.f. 4/10) (Kawashima et al 1992). Anti-BPO IgE monoclonal antibody did not produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). Carries a strain-specific allele at the alpha globin locus (Sato et al, 1996). \par High natural killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (1/6) (Pope et al, 1994). \par \i Infection\i0 \par Resistant to infection by \i Salmonella typhimurium \i0 strain C5 (5/7) (Plant and Glynn, 1974), Susceptible to \i Mycoplasma fermentens \i0 (1/6) (Gabridge \i et al\i0 ., 1972). Experimental \i Mycoplasma pulmonis\i0 infection results in acute pneumonia with severe hemorrhage, edema and often death (Faulkner et al, 1995). Susceptible to mammary tumour virus, which is carried in an active form in unfostered substrains (Murray and Little, 1967). Susceptible to oncogenic effect of polyoma virus given at birth (Law, 1966a). Susceptible to measles virus induced encephalitis, which correlates with a high cytotoxic T-lymphocyte response (like C57BL/6, contrast BALB/c) (Niewiesk et al, 1993). \par Susceptible to \i Mycobacterium marinum\i0 (2/9)(Shepard and Habas, 1967). Susceptible to infection by \i Mycobacterium marinum\i0 (1/6) (Yamamoto et al 1991). Susceptible to infection by \i Entamoeba histolytica \i0 (1/4) (Neal and Harris, 1975). Resistant to mouse hepatitis virus (Bang and Warwick, 1960). 100% transmission of murine leukaemia virus (Scripps) through three successive generations (cf. 2/5) (Jenson \i et al\i0 ., 1976). Highly susceptible to measles virus (cf. 3/6) (Rager-Zisman \i et al\i0 ., 1976). The BiDa substrain is susceptible (9/9) to tumorigenesis following infection with polyoma virus in contrast with C57BL/6 (Freund et al 1992) and C57BR/cd due to a single dominant gene \i Pyv\i0 \i \up8 s\up0 \i0 \up8 \up0 for susceptibility, which may be identical to\i Mtv-7\i0 (Lukacher et al, 1995). Highly susceptible to tumour induction by polyoma virus (1/9) (Freund et al, 1992). Following administration of murine cytomegalovirus, C3H mice exhibited minimal carditis after neonatal or adult infection. However neonatal infection appears to accelerate age-related cardiopathy, which is severe in retired breeders of this strain. (contrast BALB/c and C57BL/10) (Price et al 1991). Highly susceptible to Lyme borreliosis (\i Borrelia burgdorferi) \i0 when inoculated at 3 weeks of age (1/5) and as adults. Mice inoculated at age 3 weeks also developed polyarthritis, but severity was reduced when inoculated as adults. Carditis was also common (Barthold et al 1990), and mice were susceptible to the development of arthritis (contrast BALB/c) (Matyniak and Reiner, 1995). Resistant to intra-vaginally innoculated \i Neisseria gonorrhoeae\i0 (c.f. 5/5) (Johnson et al 1989). Resistant (3/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994). Susceptibile to infection by \i Helicobacter felis\i0 with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). \par \par C3H/HeJ \par Substrain (which carries the \i lps\i0 mutation) resistant to LCM virus (76% survival) prior to 1970, but has now become susceptible (3% survival) (Oldstone and Dixon, 1973). Resistant to LCM virus infection (1/5) (Oldstone and Dixon, 1968). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Susceptible to lethal infection with \i Rickettsia akari \i0 strain Kaplan, in contrast with seven other substrains of C3H and 24 other strains (Anderson and Osterman 1980a,b). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). High immunological response to \i Salmonella typhi\i0 porins (1/4) (Gonzales et al, 1995). Resistant to infection with \i Mycobacterium paratuberculosis\i0 (contrast BALB/c) (Tanaka et al, 1994). \par Susceptible, with high amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). Resistant to \i Leishmania major \i0 (contrast BALB/c) (Laskay et al, 1995, Scott et al, 1996). Lipopolysaccharide mutant (lps) and non-mutant mice are equally susceptible to \i Escherichia coli\i0 (Hopkins et al, 1996). \par \par C3HeB/FeJ \par Highly susceptible to mammary tumour virus, but believed to be free of the virus (Murray and Little, 1967). Low susceptibility to BALB/Tennant leukaemia virus (11/12) (Tennant, 1965). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). \par \i Reproduction\i0 \par Breeding performance intermediate/good (5/25 He substrain, 10/25 He-\i mg\i0 sub-line). Colony output 1.1 to 1.4 young/female/week. Litter size at weaning 5.9 (8/25) (Festing, 1976a). Good reproductive performance (2/8), litter size 6.4, sterility 10% (Nagasawa \i et al\i0 ., 1973). Large litter size (1/6 to 3/6), high proportion of females produce four or more litters (1/6) and high proportion of fertile matings (1/6) (Fernandes \i et al\i0 ., 1973). Good breeding performance, 2.0 to 2.2 young per female per month (9/24 to 7/24) in fostered and unfostered substrains, respectively (Hansen \i et al\i0 ., 1973). C3H/HeJ has shorter and less regular oestrus cycles than C57BL/6J (Nelson et al 1992). Early opening of vagina and first cornification (1/3 compared with C57BL/6 and DBA/2), but late onset of cyclicity (3/3) (Nelson et al 1990) \par \par \par C3HeB/FeJ \par High reproductive performance (1/8). Litter size 6.4 + 0.2, sterility 4% (Nagasawa \i et al\i0 ., 1973). \par \i Miscellaneous\i0 \par Recommended host for the following transplantable tumours: lymphosarcoma 6C3HED and mammary adenocarcinomas C3HBA and H2712 (Kaliss, 1972). Recommended host for sarcoma BP8 used as a model for screening potential anticancer drugs (E.O.R.T.C. Screening Group, 1972). High mortality after neonatal thymectomy (6/6) (Law, 1966a). \par \par High rate of spontaneous mutations (1/21) and total deviants (4/21) (Schlager and Dickie, 1967). \par \par C3HeB/FeJ \par Recommended host for transplantable hepatoma H4 (Kaliss, 1972). High incidence of spontaneous `deviants' (5/21) (Schlager and Dickie, 1967). \par C3HA \par Inbr (Y) 102. Agouti:\i + \i0 Origin\i :\i0 Pogosianz, C3H female x A male, followed by sib mating. \par Characteristics \par Originally 30% mammary tumours, but has declined. Susceptible to hepatic carcinogens. Treatment with 1,2-dimethylhydrazine resulted in 59% of mice developing hemorrhagic ovatian lesions but no unterine sarcome. The latter could be induced by DMH and estradiol dipropionate (Tutusov et al, 1994). \par Clonidene failed to produce an aggressive behavioural response (cf 3/9) (Nikulina and Klimek, 1993). \par Maint. by Y. \par C57BL \par Black, a. Origin: Little 1921 from the mating of female 57 with male 52 from Miss Abbie Lathrop's stock. The same cross gave rise to strains C57L and C57BR. Female 58 mated with the same male gave rise to strain C58. C57BL is probably the most widely used of all inbred strains, (substrain C57BL/6 alone accounts for over 14% of occasions on which an inbred strain is used) though in many ways it seems to be atypical of inbred strains of laboratory mice. In contrast to 36 other standard inbred strains, it carries a Y chromosome of Asian \i Mus musculus\i0 origin (c.f. AKR and SWR) (Tucker et al 1992), and a LINE-1 element derived from \i Mus spretus\i0 the frequency of which suggests that up to 6.5% of the genome may be of \i M. spretus\i0 origin (Rikke et al, 1995). A probe designated B6-38 to the pseudoautosomal region of the X and Y chromosome has a characteristic Pst I pattern of fragment sizes which is present only in the C57BL family of strains (Kalcheva et al, 1995). \par It usually has a good breeding performance, depending on substrain, and has been used as the genetic background for a large number of congenic strains covering both polymorphic and mutant loci. Four major substrains A, GrFa, 6 and 10 appear to be quite similar, and any differences are consistent with what might be expected from the accumulation of new mutations and a small ammount of residual heterozygosity, though McClive et al (1994) have found that B6 and B10 differ at multiple loci on chrosome 4 including the microsatellite markers D4Mit69, D4Mit71 and D4Mit72. Additional microsatellites which distinguish between B6, B10 and C57BLKS are given by Slingsby et al (1996). The former Ks substrain differs at several loci probably as a result of genetic contamination with a DBA substrain. This has been re-named C57BLKS, and is listed separately. The seven major substrains existing in 1935 are listed below. \par \par C57BL/A \par Inbr(A) ?+142. Origin. Little to A c1932. Maint. by A. \par \par C57BL/An \par Little to Andervont 1932. Differs from B6 and B10 at the \i Ce1\i0 locus. \par \par C57BL/GrFa. \par Origin: Little to Gruneberg 1932, to Falconer 1947. Most British substrains derived from this stock, though 6 and 10 substrains have been imported more recently. This substrain seems to resemble the 6 rather than the 10 substrain. Maint. by Ola \par \par C57BL/KaLwN. \par To N 1965 from Lw at F35. Maint. by N. \par \par C57BL/Ks see C57BLKS \par \par C57BL/6 \par Inbr (J) 150. Origin: substrains 6 and 10 were separated prior to 1937. This substrain is now probably the most widely used of all inbred strains. Substrain 6 and 10 differ at the \i H9, Igh2\i0 and\i Lv\i0 loci. Maint. by J,N, Ola. \par \par C57BL/10 \par Inbr (J) 158. Origin: see C57BL/6. Maint. by J. \par \par C57BL/10ScSn. \par Inbr (J) ? +136. Little to W.L.Russell to J.P.Scott at F26 as a separate substrain. To Snell at F35-36. Behaviour differs from C57BL/10J. Maint. by J,N, Ola. \par \par C57BL/10Cr \par Carries spontaneous lipopolysaccharide mutation \i lps\i0 which appears to resemble that found in C3H/HeJ (Vogel et al 1981). \par C57BL/Ola \par Carries a spontaneous mutation, \i Wld\i0 \i \up8 s\up0 \i0 \up8 \up0 , causing a marked slowing of axonal degeneration during Wallerian degeneration (Tsao et al, 1994). \par \i Behaviour\i0 \par Substrain unspecified: \par High incidence of tail rattling (1/5) (St. John, 1973). Short latency to attack and eat crickets (2/7) (Butler, 1973). High alcohol (ethanol) preference ratio (1/5) (McClearn, 1965). Short latency to emerge from home cage (1/7), short latency to cross barrier in open-field (1/7), low number of stairs climbed (7/7), low urination (6/7) and defaecation (7/7) (McClearn \i et al\i0 ., 1970). \par \par C57BL/6 \par High alcohol (ethanol) preference (1/4) (Fuller, 1964b), (2/18) (Rodgers, 1966). Achieve blood alcohol levels of 60 mg% when access to alcohol is restricted to 60 mins. per day (Le et al, 1994). Alcohol preference may be associated with strain differences in mesolimbic enkephalin gene expression (Ng et al, 1996). A quasi-congenic QTL introgression strain carrying a low alcohol consumption gene from BALB/c has lower voluntary alcohol consumption than C57BL/6, with 96% of loci in common (Vadasz et al, 1996). Low severity of ethanol withdrawal symptoms compared with DBA/2, possibly associated with differences in neuroactive steriod sensitivity (Finn et al, 1997). Alcohol preference is due to at least two recessive quantitative trait loci that are sex-restricted in expression (Melo et al, 1996). \par Low `emotionality' (12/15), high open-field exploration (2/15) (Thompson, 1953). High spontaneous locomotor activity (8/9) (Nikulina et al 1991). Short time of immobility in a forced swimming test (8/9) (Nikulina et al 1991). Low shock-avoidance learning (7/9) (Bovet \i et al\i0 ., 1966, 1969). Low shuttle-box avoidance (5/5), high wheel activity (1/5) (Messeri \i et al\i0 ., 1972). Rapid shock-avoidance learning (2/7) and slow extinction (6/7) (Schlesinger and Wimer, 1967). High shock-avoidance learning (1/8) (Wahlsten, 1973). High radial-arm maze learning (1/3) (Ammassari-Teule et al, 1993). \par High locomotor activity (1/5) (Davis and King, 1967). High locomotor activity when grouped (2/6) and single (1/6) (Davis \i et al\i0 ., 1967). Resistant to audiogenic seizures (11/11) (Fuller and Sjursen, 1967). Relatively insensitive to the primary odorant isovaleric acid (contrast seven other strains) and may provide an animal model of specific anosmia (Wysocki \i et al\i0 ., 1977). Low balsa-wood gnawing activity (2/16) Fawdington and Festing (1980). High preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (1/26) (Lush 1988). Rejects saline at moderate concentrations (contrast 129) (Beauchamp and Fisher, 1993, Gannon and Contreras, 1995). Feed restriction for nine days failed to cause stereotypic cage cover climbing (contrast DBA/2) (Cabib and Bonaventira, 1997). \par \par C57BL/10 \par High open-field activity (3/15) (Thompson, 1953). High alcohol preference (6/18) (Rodgers, 1966). Good water escape learning (1/6) (Festing 1973b). Good performance in food-seeking task (1/6) (Henderson, 1970). Insensitive to the odour of isovaleric acid (see C57BL/6). High preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (4/26) (Lush 1988). \par \i Life-span and spontaneous disease\i0 \par \i Substrain unspecified:\i0 \par Mammary tumours less than 1% (Heston and Vlahakis, 1971). Lung adenomas 0-9% in LiA substrain (M\'9f hlbock and Tengbergen, 1971). Zero incidence of mammary tumours at 2 years (cf. 3/7) (Bentvelzen \i et al\i0 ., 1970). \par \par Mean life-span 800 days in males and 750 days in females according to Rowlatt \i et al\i0 . (1976), who also give details of pathology in a large aging colony of C57BL/Icrf-\i a\i0 \up8 t\up0 mice. Hyperphalangy and polydactyly occur with a low incidence in all C57BL strains and substrains (Dagg, 1966). Hydrocephalus 4.1% (Mori, 1968). Type B reticulum cell neoplasms 75% at about 20 weeks in HeDe substrain (Dunn and Deringer, 1968). \par \par C57BL/Ka \par Median life-span 23 months in males. Main autopsy findings include reticulum cell sarcoma type B (29%), testes interstitial tumour (13%), thyroid follicular adenoma (9%), unclassified lymphoreticular tumours (9%). Nine other tumour types found. Non-neoplastic lesions include amyloid (83%), Sendai virus pneumonia (20%), periarteritis nodosa (16%), mesenteric disease (10%). Several other lesions noted. (Zurcher \i et al\i0 ., 1975). About 50% of mice develop homogeneous immunoglobulins resembling idiopathic paraproteinaemia in man by 24 months (Radl and Hollander, 1974). \par \par C57BL/Fa \par Long life-span in males (14/17 = 645 days), but intermediate in females (5/17 = 580 days) in SPF fostered conditions (Festing and Blackmore, 1971). Hydronephrosis 0.5% in females, 1.5% in males (Taylor and Fraser, 1973). \par \par C57BL/6 \par Primary lung tumours 1% in males, 3% in breeding females and zero in virgin females. Lymphatic leukaemia less than 2%, mammary adenocarcinomas less than 1% (Hoag, 1963). Leukaemia 7% (Myers \i et al\i0 ., 1970). Rare "lipomatous" hamartomas or choristomas have been noted (Adkison et al 1991). \par Susceptible to the development of atheromatous lesions on wall of aorta after 20 weeks on a high-fat diet (Thompson, 1968; Roberts and Thompson, 1976). Develop fatty streak-like lesions in the valve sinus region of the ascending aorta after 10-20 weeks on a diet enriched in saturated fat and cholesterol. After a further 15 weeks fibro-fatty lesions with many of the characteristics of human atheromatous plaques are found (Stewart-Phillips and Lough 1991). Exhibit aortic cartilaginous metaplasia (contrast C3H) (Qiao et al, 1995). Susceptible to diet-induced aortic fatty streak lesions which correlates with a low level of paroxinase mRNA (contrast C3H) (Shih et al, 1996). \par Develops non-insulin-dependent diabetes mellitus and hypertension when fed a high fat-high simple carbohydrate diet, whereas A/J mice do not (Mills et al 1993). Susceptible to the development of atherosclerosis on a semi-synthetic high fat diet (1/9) (Nishina et al, 1993). Blood glucose levels and insulin insensitivity in crosses between diet-induced type II diabetes sensitive C57BL/6 and resistant A/J are genetically independent (Surwit et al 1991). High simple carbohydrate diet for five months induced hyperglycemia, hyperinsulinemia and hypercholesterolemia and non-insulin-dependent diabetes mellitus which appeared to be associated with the metabolic characteristics of visceral fat (Rebuffe-Scrive et al, 1993). Gain more weight on high fat diets without consuming more calories than A/J mice and develop adipocyte hyperplasia. However, animals fed a low fat, high sucrose diet were leaner than those fed a high-complex-carbohydrate diet. These results suggest that genetic differences in metabolic response to fat is more important in the development of obesity and diabetes than caloric intake (Surwit et al, 1995). Loci on chromosomes 1, 3, 5 and 11 are associated with variation in high density lipoprotein levels with coordinate expression of cholesterol-7-alpha hydroxylase in a cross involving atherosclerosis resistant C3H/HeJ mice (Machleder et al, 1997). Hepatic stearoyl CoA desaturase mRNA levels significantly elevated compared with atherosclerosis-resistant BALB/c mice, and was reduced in mice fed a high fat diet (Park et al, 1997). \par Congenital abnormalities 10%, including eye defects, polydactyly and otocephaly (Kalter, 1968). Microphthalmia and anophthalmia 8-20% and hydrocephalus 1-3% (Dagg, 1966). Occular defects appear to be due to defects in development of the lens (Robinson et al, 1993). \par Develop spontaneous auditory degeneration with onset during young adulthood, with enhanced susceptibility to acoustic injury and delayed effects of toluene (contrast CBA/Ca) (Li, 1992, Willott et al, 1993, Li et al, 1993, Li and Borg, 1993). This is associated with early hair cell changes including bent and fused stereocillia, bulging of the cuticle plates, hair cell loss and swelling of affected dendrites (Hultcrantz and Li, 1993). Carry a single recessive gene different from that found in BALB/cBy and WB/ReJ, causing age-related hearing loss (Willott et al, 1995). Hearing loss is caused by degeneration of the organ of Corti, originating in the basal, high frequency region and then proceeding apically over time. This results in a severe sensorineural hearing loss by 14 months of age (Walton et al, 1995). More susceptible to noise-induced hearing loss than CBA/J (Erway et al, 1996). \par Life-span above average in both sexes in conventional conditions (17/22 = 676 days in males, 18/22 = 692 days in females) (Storer, 1966). Life-span 827 _ 34 days in males, 818 _ 21 days in females (Goodrick, 1975). Life-span 878 _ 10 days in males and 794 _ 6 days in females (Kunstyr and Leuenberger, 1975). Median life-span 600 days (Curtis, 1971). Gross tumour incidence 70%, maximum life-span about 1200 days in SPF conditions (Mewissen, 1971). \par \par Dermatitis with intense pruritis leading to self-mutilation and death, and sometimes associated with the mite \i Myobia musculi \i0 appears to be more severe in this strain than others (Csiza and McMartin, 1976). Impaired axonal regeneration involving multiple genetic loci (Lu et al, 1994) \par \par C57BL/10 \par Long life-span (826_29 days in males, 693_31 days in females). Overall tumour incidence 33% in males and 31% in females, most of which is due to lymphoma (31% in males, 29% in females) (Smith \i et al\i0 ., 1973). Microphthalmia and anophthalmia 8-20% and hydrocephalus 1-3% (Dagg, 1966). Dermatitis leading to self-mutilation as described in C57BL/6 is also common in this substrain. Incidence may reach 4% (Sparrow, personal communication). \par \i Normal physiology and biochemistry\i0 \par \i Substrain other than /6 or /10\i0 \par High thyroid activity (1/5) (Van Heyningen, 1961). Mammary gland insensitive to oestradiol and progesterone (6/7) (Singh \i et al\i0 ., 1970). Low brain aromatic L- amino acid decarboxylase (5/5) and low acetylcholinesterase activity (5/5) (Pryor \i et al\i0 ., 1966). Blood catalase has a low specific activity (6/7) (Magdon, 1962). \par \par Low hind foot pad (9/9) but high (1/9) tail temperature (Shepard and Habas, 1967). High serum calcium (2/6) (Barrett \i et al\i0 ., 1975). Low erythrocyte catalase (12/18 to 17/18, depending on substrain) (Hoffman and Rechcigl, 1971). High basal level of serum prolactin (1/6) (Sinha \i et al\i0 ., 1975). Resistant to dietary induction of obesity (Fenton and Dowling, 1953). High level of alpha-fetoprotein in plasma at 7 days (1/6) (Adinolfi et al 1990). \par \par C57BL/6 \par Low plasma cholesterol at 12 and 24 weeks (8/8) (Weibust, 1973). Low plasma triglyceride levels (1/11 in By and 3/11 in J substrains) and low plasma cholesterol (2/11 in By and 4/11 in J substrains) (Jiao et al 1990). Low serum ceruloplasmin levels in males (24/26) but intermediate in females (Meier and MacPike, 1968). High blood sugar (3/12) (Nishimura, 1969). Low serum cholesterol (5/5) in C57BL/6-\i a\i0 \i \up8 t\up0 \i0 \i a \i0 (Bruell \i et al\i0 ., 1962). Arterial blood has a low pH (10/10) (Bernstein, 1966). Low concentration of prostaglandin F in epididymis (6/6) (Badr, 1975). High liver tyrosine aminotransferase in fasted mice (3/10) but low in C57BL/6-\i ob \i0 (10/10) (Blake, 1970). Low brain \dn8 L\dn0 -glutamic acid decarboxylase (GAD) (7/7) and acetylcholinesterase activity (7/7) but high catechol-\i O\i0 -methyltransferase activity (2/7) (Tunnicliff \i et al\i0 ., 1973). Low calcium uptake by the heart (4/5) (Mokler and Iturrian, 1973). Low sensitivity to thyrotropin (20/21) (Levy \i et al\i0 ., 1965). High brain sulphatide (1/5) (Sampugna \i et al\i0 ., 1975). High hepatic benz (alpha) pyrene hydroxylase activity (1/6) (Kodama and Bock, 1970). Low hepatic delta-aminolaevulinate dehydratase activity (8/8) (Doyle and Schimke, 1969). High aldehyde dehydrogenase and alcohol dehydrogenase activity compared with DBA/2 (Sheppard \i et al\i0 ., 1968). High metabolism of \up8 131\up0 I with low 48 h retention (1/6) (Chai \i et al\i0 ., 1957). High liver arylsulphatase activity (1/12) (Daniel, 1976). Low porphyrin content of Harderian gland (16/16) (Margolis, 1971). Low hepatic urokinase activity (4/6 to 6/6) but high hepatic histidine ammonia-lyase activity (1/6 to 2/6 in two substrains) (Hanford \i et al\i0 ., 1974). Low basal levels of kidney catalase (4/4), superoxide dismutase (4/4) and renal glutathione reductase (4/4) (Misra et al 1991). Iron overload causes inhibition of hepatic uroporphyrinogen decarboxylase and uroporphyria in C57BL/10ScSn but not DBA/2 mice. This was not correlated with the Ah locus in a study involving 12 mouse strains (Smith and Francis, 1993). Low levels of apoA-IV messenger RNA in liver compared with 129/J (Reue et al, 1993) \par Low susceptibility to audiogenic seizures (6/6) (Deckard \i et al\i0 ., 1976). Long tau DD, the endogenous (free-running) period of the circadian pacemaker measured in constant environmental darkness (12/12) (Schwartz and Zimmerman 1990) \par Has defective secretory group II phospholipase A2 gene (cf strains 129/Sv and B10.RIII) (Kennedy et al, 1995). \par Susceptible to severe hypercapnia with hypoxia assessed by elevated minute ventilation rate (1/8) (Tankersley et al, 1994). Has a rapid and shallow breathing pattern phenotype (contrast C3H) (Tankersley et al, 1997). Susceptible (1/7) to cerebral ischemia following bilateral carotid occlusion with 90% of mice showing typical neuological signs such as torsion of the neck and rolling fits with selective neuronal death in the hippocampus and caudoputamen after 20 minutes of ischemia (Yang et al, 1997). \par C57BL/10 \par Low plasma testosterone level (4/5) (Hampl \i et al\i0 ., 1971). High Na/K ratio in erythrocytes (3/9) and plasma (2/9) (Waymouth, 1973). Low serum ceruloplasmin levels in males (25/26) but intermediate in females (Meier and MacPike, 1968). Low systolic blood pressure (18/19) (Schlager and Weibust, 1967). Low brain glutamic acid decarboxylase in B10.BR (10/10) and ScSn substrains (9/10) (Gaitonde and Festing, 1976). Resistant to electroconvulsive seizures (6/6) (Deckard \i et al\i0 ., 1976). Iron overload causes inhibition of hepatic uroporphyrinogen decarboxylase and uroporphyria in C57BL/10ScSn but not DBA/2 mice. This was not correlated with the \i Ah\i0 locus in a study involving 12 mouse strains (Smith and Francis, 1993). \par \i Anatomy\i0 \par Substrain unspecified \par Low proportion of basophilic cells in adenohypophysis (5/5) (Keramidas and Symeonidis, 1973). \par \par C57BL/6 \par Small kidney/body weight ratio (19/21) (Schlager, 1968). Large thyroid (1/5) (Mendoza \i et al\i0 ., 1967). High total leukocyte count (2/18), low erythrocyte count (14/18) (Russell \i et al\i0 ., 1951). Small hippocampus (9/9) (Wimer \i et al\i0 ., 1969). Accessory spleens in about 32% of mice (2/9) and low number of Peyer's patches (7/7) (Hummel \i et al\i0 ., 1966). Higher bone mass than A/J (Kaye and Kusy, 1995). Low number of haematopoetic stem cells in bone marrow (contrast DBA/2) (Muller-Sieburg and Riblet, 1996). \par Less susceptible to the development of micronuclei than BALB/c following treatment with clastogenic base analogues and nucleosides (Sato et al, 1993). High level of spontaneous sister chromatid exchange (4/4) (Nishi et al, 1993). A detailed staging of these mice between gestation days 11 and 13 (Theiler's stages 18 and 21) has been published by Miyake et al, (1996). Hematopoetic stem-cell pool 11-fold lower than in DBA/2. This is largely due to loci on chromosome 1 (Mullersieburg and Riblet, 1996). Low bone density of femur (11/11) (Beamer et al, 1996). The timing of onset and duration of condensation and onset of matrix formation of first arch cartilages has been described by Miyake et al (1996a). A detailed staging table to facilitate study of cranial skeletal development every 2hrs. between days 11 and 13 of gestation has also been described (Miyake et al, 1996b) \par C57BL/10 \par Small kidney/body weight ratio (21/21) (Schlager, 1968). High number of bristles on foot pad (1/8 to 3/8 in three congenic lines) (Festing, 1976a). High yield of peritoneal exudate cells (1/5) with a high percentage of macrophages (1/5), low percentage of lymphocytes (5/5) and high granulocytes (1/5) (Schwartz \i et al\i0 ., 1975). \par \i Drugs\i0 \par \i Substrain unspecified\i0 \par Resistant to induction of adenocarcinomas of the colon by 1, 2-dimethylhydrazine (cf. 2/4) (Evans \i et al\i0 ., 1974). Resistant to induction of pulmonary tumours (6/6) and leukaemia (5/6) by neonatal administration of DMBA (Flaks, 1968). Susceptible to the induction of pulmonary fibrosis by bleomycin (contrast C3Hf/Kam) (Haston et al, 1996) and irradiation, though the sensitivity of lung fibroblasts to irradiation \i in-vitro\i0 does not correlate with \i in-vivo\i0 sensitivity (Dileto and Travis, 1996). \par Sensitive to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Resistant to induction of mammary tumours by urethane (7/7) (Bentvelzen \i et al\i0 ., 1970). Pituitary adenoma induced in most mice by oestrogens (Heston, 1963). Resistant to skin tumour induction by methylcholanthrene (5/5) (Andervont and Edgcomb, 1956). Susceptible to fibrosarcoma induction by methylcholanthrene (4/15 males, 3/15 females) (Strong, 1952). \par Resistant to chloroform toxicity (cf. 5/9) (Deringer \i et al\i0 ., 1953). Resistant to induction of cleft palate by cortisone (4/5) (Kalter, 1965). \par \par Resistant to lethal effects of ozone (22/22) (Goldstein \i et al\i0 ., 1973). Resistant to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 4/7) (Evans \i et al\i0 ., 1977). \par \par C57BL/Fa \par Resistant to induction of lung tumours by urethane (6/6) (Falconer and Bloom, 1962). Insensitive to insulin (8/9), sensitive to histamine (2/9) (Brown, 1965). \par \par C57BL/6 \par Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (3/14) (Kouri \i et al\i0 ., 1973), (1/12) (Whitmire \i et al\i0 ., 1971). High incidence of lymphomas after methylcholanthrene administration by gavage (2/5) (Akamatsu and Barton, 1974). Susceptible to toxic effects of DMBA (6/6) (Schmid \i et al\i0 ., 1966). Pre-treatment with beta-naphthoflavone 48 hr. before administration of N-nitrosoethylurea (ENU), once weekly for 4 weeks caused a significant doubling in the number of lung tumor bearers (contrast 4 strains) (Anderson et al 1990). Phenobarbitone in the diet to give an intake of 85mg/kg per day resulted in 4% of animals developing basophilic nodules by 91 weeks of age (contrast 70% in C3H/He), but no increase in liver carcinomas (Evans et al, 1992). However, there was a two-fold lower level of DNA synthesis in C57BL/6 mice relative to C3H mice after partial hepatactomy, though partial hepatectomy is a tumour promoter in C57BL/6 but not in C3H mice (Bennett et al, 1995). \par Sensitive to teratogenic effects of acetazolamide (2/6) (Green \i et al\i0 ., 1973). Resistant to teratogenic effect (cleft palate) by cortisone acetate (2/6) (Kalter 1981). Hepatic epoxide hydrase activity induced by pentobarbital i.p. (cf. 4/7) (Oesch \i et al\i0 ., 1973). Resistant to teratogenic effects of cortisone acetate (4/4) (Dostal and Jelinek, 1973). Resistant to lethal effects of ozone (16/21) (Goldstein \i et al\i0 ., 1973), but susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995) and to airway inflammation (contrast C3H/He) (Kleeberger et al, 1993). Susceptible to ozone-induced lung inflammation, which is exacerbated by vitamin A deficiency (Paquette et al, 1996). High incidence of convulsions induced by flurothyl (1/5) (Davis and King, 1967). Susceptible to hyperbaric oxygen (4/18) (Hill \i et al\i0 ., 1968). Resistant to chloroform toxicity (cf. 5/9) (Hill \i et al\i0 ., 1975; Deringer \i et al\i0 ., 1953). Resistant to toxic effects of isoniazid (2/10) (Taylor 1976b). Sensitive, as judged by eosinophil response, to cortisone acetate (cf. 3/6) (Wragg and Speirs, 1952). High (89%) ovulatory response to 3 I.U. of PMS in immature mice (2/6), but only a 56% response to 7 I.U. No facilitation by exposure to males at these doses (Zarrow \i et al\i0 ., 1971). High locomotor activity after treatment with \dn8 D\dn0 -amphetamine (1/6) (Babbini \i et al\i0 ., 1974). Nicotine increases learning ability (1/9) (Bovet \i et al\i0 ., 1966). Resistant to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 4/7) (Evans \i et al\i0 ., 1977). Low ED50 to behavioural effects of nicotine (3/19) (Marks et al 1989). High self-selection of nicotine (1/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996). \par Low bronchial reactivity (6/6) to methacholine and serotonin (Konno et al 1993). Resistant (6/8) to daunomycin-induced nephorsis (Kimura et al 1993). Low (10/10) neural sensitivity to pentylenetetrazol convulsions (Kosobud et al 1992). Susceptible to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (1/4) (Bhathal et al 1990). Low histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser ( c.f. 5/8) (Toda et al 1989). Low histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 1/8, contrast BALB/c, C3H/He, DBA/2 etc.) (Toda et al 1989). Carries gene (\i Tpmt\i0 ) for low levels of thiopurine methyltransferase activity, catalyzing the \i S\i0 -methylation of 6-mercaptopurine and other heterocyclic and aromaticthiol compounds (like AKR, unlike DBA/2) (Otterness and Weinshilboum 1987a,b). More sensitive to acute toxic effects of aflatoxin B-1 than strains CBA/J or BALB/c (Almeida et al, 1996). \par Airways hyporeactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). High voluntary comsumption of morphine in two-bottle choice situation (1/15) (Belknap et al, 1993). Estrogen induces an increase in VLDL and LDL-cholesterol (like C57L, contrast BALB/c and C3H) (Srivastava, 1995). Nine-fold higher ED50 for haloperidol-induced catalepsy than DBA/2, but this is not associated with numbers of cholinergic neurons (Dains et al, 1996). Accumulates three to five-fold lower levels of mercury in liver and blood than DBA/2 or A.SW after 4 weeks exposure to mercuric chloride, but higher levels in spleen following 8-12 weeks of exposure (Griem et al, 1997). \par C57BL/10 \par Nicotine decreases shock-avoidance learning (8/9) (Bovet \i et al\i0 ., 1966). Low ED50 to behavioural effects of nicotine (1/19) (Marks et al 1989). Congenic line B10.BR susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (Kouri \i et al\i0 ., 1973). \par \i Immunology\i0 \par Substrain unspecified \par Poor immune response to low levels of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor primary immune response to bovine serum albumin (6/6) (James and Milne, 1972). Poor primary immune response to sheep erythrocytes (3/6 to 6/6, depending on test and dose) (Ghaffar and James, 1973). Poor immune response to Vi antigen (cf. 3/5) (Gaines \i et al\i0 ., 1965). Low antibody affinity (7/7) and small quantity of antibody production (6/7) (Alpers \i et al\i0 ., 1972). Low antibody affinity to HSA (9/9) (Petty \i et al\i0 ., 1972). \par \par C57BL/Fa \par Serum anti-nuclear factor in 12% of animals tested (5/17) (Barnes and Tuffrey, 1967). Good primary immune response to bacteriophage fd (2/7) (Kolsch \i et al\i0 ., 1971). \par \par C57BL/6 \par High susceptibility to induction of amyloid by casein (1/6) (Willerson \i et al\i0 ., 1969). Poor immune response to type III pneumococcal polysaccharide (4/5) (Braley and Freeman, 1971). Poor immune response to synthetic double- stranded RNA (6/7) (Steinberg \i et al\i0 ., 1971). Good immune response to cholera A and B antigens (2/8) (Cerny \i et al\i0 ., 1971). Resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). Rapid rejection of about 76% of male skin isografts by females by 25 days (1/10) (Gasser and Silvers, 1971). Poor immune response to GAT (random terpolymer of Glu\up8 60\up0 , Ala\up8 30\up0 , Tyr\up8 10\up0 ) (9/10) (Dorf \i et al\i0 ., 1974). Good immune response to \i Salmonella senftenberg \i0 (1/5) and \i S. anatum \i0 (2/5) lipopolysaccharide (Di Pauli, 1972). Non-responder to synthetic polypeptide Glu\up8 57\up0 , Lys\up8 38\up0 , Ala\up8 5\up0 (cf. 4/7) (Pinchuck and Maurer, 1965). High sporadic occurrence of natural haemagglutinins to sheep red blood cells (Brooke, 1965). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). Poor immune response to Pro-Gly-Pro-ovalbumin (7/7) and (Pro\up8 66\up0 , Gly\up8 34\up0 )\dn8 n\dn0 (6/7) but good immune response to (Pro-Gly-Pro)\dn8 n\dn0 (1/17) (Fuchs \i et al\i0 ., 1974). High (2/6) PHA- stimulated lymphocyte blastogenic response (Hellman and Fowler, 1972). Erythrocytes have low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). High immune response to ferritin in B6-\i Tla\i0 (2/16) (Young \i et al\i0 ., 1976). Low responder to dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972). Low responder to \i E. coli\i0 \'a7 -D-galactosidase, with "memory" developing in absence of antibody formation (de Macario and Macario 1980). Precipitating and skin sensitising antibodies have slow electrophoretic mobility (6/6) (Fahey, 1965). Resistant to anaphylactic shock (Treadwell, 1969). Susceptible (1/5) to induction of autoimmune prostatisis (contrast BALB/c) (Keetch et al, 1994). High expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (Muthing, 1997). \par Anti-BPO IgE monoclonal antibody produced potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 3/8) (Harada et al 1991). Susceptible to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 3/18) (Noonan and Hoffman, 1994). \par \par C57BL/10 \par High lymphocyte phytohaemagglutinin response (10/43) (Heiniger \i et al\i0 ., 1975). Rejection of 70% of male skin isografts by females by 25 days (2/10) (Gasser and Silvers, 1971). Poor immune response to ovomucoid, but good immune response to ovalbumin (cf. 6/12) (Vaz \i et al\i0 ., 1971). Poor immune response to DNP-keyhole limpet haemocyanin (10/11) (Borel and Kilham, 1974). Non-responder to synthetic polypeptide Glu\up8 57\up0 , Lys\up8 58\up0 , Ala\up8 5\up0 (cf. 4/7) (Pinchuck and Maurer, 1965). Low antibody affinity (6/7) and small quantity of antibody produced (7/7) in B10.D2-\i n\i0 (Alpers \i et al\i0 ., 1972). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18). Also in B10.BR and B10.D2-\i n\i0 (McCarthy and Dutton, 1975). Low IgM antibody response to sheep red blood cells compared with A/J (Vetvicka et al, 1993). Resistant to induction of passive cutaneous anaphylaxis (IgG\dn8 1\dn0 - and IgE- mediated) (12/12) (De Souza \i et al\i0 ., 1974). Erythrocytes have low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). High immune response to ferritin in B10 (4/16) and congenic lines B10.M (1/16), B10.D2 (3/I6), B10.BR (5/16) and B10.A (6/16) (Young \i et al\i0 ., 1976). Susceptible to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 3/18) (Noonan and Hoffman, 1994). High neutrophil response to thioglycolate broth and killed bacteria (contrast BALB/c) (Marley et al, 1994). Moderate susceptibility to experimental allergic encephalomyelitis with long (1/10) duration (Lindsey, 1996). \par \i Infection\i0 \par Substrain unspecified \par Resistant to oncogenic effects of polyoma virus given at birth (Law, 1966a). Resistant to \i Mycobacterium marinum \i0 (2/9) and poor plateau harvest of \i M. leprae \i0 8 months after infection (9/9) (Shepard and Habas, 1967). \par \par C57BL/Fa \par Highly susceptible to infection by \i Salmonella typhimurium \i0 strain C5 (2/7) (Plant and Glynn, 1974). \par \par C57BL/6 \par Develops a slowly progressing parasitosis ("low responder") after infection with the Cornell strain of \i Toxoplasma gondii\i0 (Macario et al 1980). Did not support sustained growth of six strains of \i Leishmania mexicana mexicana\i0 (contrast BALB/c) (Monroy-Ostria et al, 1994). Resistant to \i Leishmania major \i0 (contrast BALB/c) (Laskay et al, 1995, Scott et al, 1996). Susceptible to \i L. major mexicana\i0 , and vaccination against the parasite using liposomes with parasite membrane antigens was effective (cf CBA/Ca but contrast C57BL/10) (Lazama-Davila, 1997). \par Susceptible to \i Salmonella typhimurium \i0 strain C5 (1/5) (Robson and Vas, 1972). 100-fold more resistant to \i Listeria monocytogenes \i0 than A/J when measured by median lethal dose (Sadarangani et al 1980). This seems to be associated with increased levels of gamma interferon and granulocyte-macrophage colony stimulating factor compared with susceptible A/J mice (Iizawa et al, 1993). Resistant to \i Mycoplasma fermentens \i0 (6/6) (Gabridge \i et al\i0 ., 1972). Resistant to \i Mycoplasma pulmonis\i0 infection (cf 4/16) (Cartner et al, 1996).Resistant to infection by \i Mycobacterium marinum\i0 (6/6) (Yamamoto et al 1991). Resistant to infection by liver fluke \i Opisthorchis felineus \i0 (6/6) (Zelentsov, 1974). Resistant (1/4) to infection with the helminth worm \i Angiostrongylus costaricennsis\i0 (Ishii and Sano 1989). Relatively susceptible to infection with \i Helicobacter felis\i0 (contrast C57BL/6) (Mohammadi et al, 1996). Susceptibile to infection by \i Helicobacter felis\i0 with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). \i H. felis\i0 induces hypertropic gastropathy (Fox et al, 1996). \par Highly resistant to the mammary tumour virus which is thought not to be carried by the strain (Murray and Little, 1967). Resistant to \i Herpes simplex\i0 virus (2/11) (Lopez, 1975). Resistant to herpes simplex virus-1 (contrast BALB/c) (Brenner et al, 1994).. Susceptible to mouse hepatitis virus type 3 infection (cf. 5/14) (Le Prevost \i et al\i0 ., 1975). Develops antibodies to mouse hepatitis virus which can be reliably detected by the complement fixation test, in contrast to five other strains (Kagiyama et al 1991). Low mortality in a natural epizootic of ectromelia (7/8) (Briody, 1966). High expression of RNA tumour virus group-specific antigen in some substrains (1/8) but low in others (7/8) (Whitmire and Salerno, 1972). Resistant to development of leukaemia on infection by Friend virus (cf. 2/11) (Dietz and Rich, 1972). Resistant to diabetogenic effects of encephalomyocarditis virus, but treatment with carrageenan to compromise macrophage function makes the mice susceptible (Hirasawa et al, 1995). Susceptible to measles virus induced encephalitis, which correlates with a high cytotoxic T-lymphocyte response (like C3H, contrast BALB/c) (Niewiesk et al, 1993). Resistant to the development of tumours following inoculation with polyoma virus (Freund et al, 1992). \par Resistant (6/7) to the development of chronic Chagas' cardiomyopathy in postacute \i Trypanosoma cruzi\i0 infection (Rowland et al 1992). Resistant to infection with \i Trypanosoma congolense\i0 with an initial peak of parasitemia on day 6, followed by rapid apparent clearance in an average of 3 days (contrast BLAB/c) (Ogunremi and Tabel, 1995). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in a multivesiculation form of hyatid development (cf 4/9) (Nakaya et al, 1997). \par \par Resistant to tumorigenesis induced by polymoa virus (1/9), in contrast with C3H/Bi (Freund et al 1992). Susceptible to mouse adenovirus type 1 which causes a fatal hemorrhagic encephalomyelitis (contrast BALB/c) (Guida et al, 1995). \par Less susceptible to \i Streptococcus suis \i0 type 2 including the type strain, two isolates from meningitis in pigs and two isolates from tonsils of clinically healthy pigs (c.f. 3/5) (Kataoka et al 1991). Resistant to carditis on infection with Lyme borreliosis (\i Borrelia burgdorferi) (contrast C3H, SWR, BALB/c)\i0 (Barthold et al 1990). Thymectomized C57BL/6 mice that were intravenously infused with monoclonal antibody to selectively deplete CD4+ T cells are susceptible to disseminated \i Mycobacterium avium\i0 infection. The increased susceptibility is comparable to that of C57BL/6-\i bg\i0 . The course of such infections can be markedly restrained and in some cases the infections can be sterilized by treatment over a 120-day period with the antimycobacterial agent rifabutin (Furney et al 1990). Susceptible to infection with \i M. avium\i0 strains 101 and 2-151, and can be used to test anti-mycobacterial agents (Furney et al, 1995). Susceptible to infection with \i M. paratuberculosis\i0 (contrast C3H/HeJ) (Tanaka et al, 1994). Resistant to infection with \i Yersinia enterocolitica\i0 associate with a good interferon gamma response (contrast BALB/c) (Autenrieth et al, 1994). \par Susceptible, with high amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994) \par Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). Resistant (1/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994). Highly susceptible to \i Plasmodium berghei\i0 with all mice developing erythrocytic infection following intravenous injection of 50 sporozoites. The same level of infection could only be established in BALB/c with 10,000 sporozoites (Scheller et al, 1994). Infection with \i P. berghei \i0 results in low blood parasitemia and death with neuological symptoms within 8-10 days, in contrast with the more resistant BALB/c (Moumaris et al (1995). Resistant to chronic weakness and inflammation following infection with Tucon strain of coxsackie virus B1, in contrast with C57BL/10 and B10 congenic strains (Tam and Messner, 1996). \par C57BL/10 \par Congenic line B10.D2-n is highly susceptible to infection by \i Salmonella typhimurium \i0 strain C5 (3/7) (Plant and Glynn, 1974). Resistant to \i Herpes simplex \i0 virus (2/Il) (Lopez, 1975). B10.D2-\i o\i0 is susceptible to mouse hepatitis virus type 3 infection (cf. 5/14) (Le Prevost \i et al\i0 ., 1975). Slow immunological expulsion of \i Trichinella spiralis \i0 worms (Wakelin and Donachie 1980). Following administration of murine cytomegalovirus, C57BL/10 and B10.BR mice developed myocarditis after neonatal infection, but inflammation resolved rapidly after adult infection and age-related cardiopathy was correspondingly mild. (contrast BALB/c, C3H) (Price et al 1991). Resistant to infection with the helminth \i Mesocestoides corti \i0 (contrast SJL, NIH) (Lammas et al 1990). Resistant (2/10) to infection with \i Ehrlichia risticii\i0 (Williams and Timoney, 1994). Susceptible to chronic weakness and inflammation following infection with Tucon strain of coxsackie virus B1, in contrast with C57BL/6 (Tam and Messner, 1996). Resistant to \i Mycoplasma pulmonis\i0 infection (cf 4/16) (Cartner et al, 1996). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in a multivesiculation form of hyatid development (cf 4/9) (Nakaya et al, 1997). Susceptible to \i L. major mexicana\i0 , but vaccination against the parasite using liposomes with parasite membrane antigens was not effective (contrast CBA/Ca and C57BL/6) (Lazama-Davila, 1997). \par \par \i Reproduction\i0 \par C57BL/Fa \par Poor reproductive performance (25/25) with only 3 young weaned per litter and 0.4 young per female/week (Festing, 1976a). \par \par C57BL/Ka \par Good breeding performance, 2.2 young/female/month (6/24) (Hansen \i et al\i0 ., 1973). \par \par C57BL/6 \par Good reproductive performance (3/8). Litter size 6.2 _ 0.2, sterility 8% (Nagasawa \i et al\i0 ., 1973). Large litter size (1/6), mean 6.2 (Verley \i et al\i0 ., 1967). Good breeding performance, 2.5 young/female/month (2/24) (Hansen \i et al\i0 ., 1973). Has longer and more regular oestrus cycles than DBA/2 and C3H/HeJ (Nelson et al 1992). Late opening of vagina and first cornification (3/3), but early onset of cyclicity compared with C3H (Nelson et al 1990). \par Mice carrying the Y-chromosome from \i Mus musculus domesticus\i0 from Tirano (Italy) or \i M.m. poschiavinus\i0 from Poschiavo (Switzerland) fail to develop normal testes but instead develop ovaries and ovotestes. Some hermaphroditic males become fertile, but the XY females lack normal gonadal steroids and can not carry pregnancy to term. There is delayed expression of IGF-I which may be responsible for the low setroid expression (Villapandofierro et al, 1996). \par C57BL/10 \par Good reproductive performance (3/25) with colony output 1.4 young/female/week, litter size 6.9 (2/25) at weaning (Festing, 1976a). Intermediate breeding performance (12/24) (Hansen \i et al\i0 ., 1973). \par \i Miscellaneous\i0 \par C57BL/Ka \par High degree of genetic distinctiveness (3/27) (Taylor, 1972). \par \par C57BL/6 \par High degree of genetic distinctiveness (4/27) (Taylor, 1972). Recommended host for the following transplantable tumours: mammary adenocarcinoma BW 10232 melanoma B16, myeloid leukaemia C 1498 and preputial gland carcinoma ESR586 (Kaliss, 1972). \par Embryonic stem cell lines have been established (Kawase et al, 1994). \par High rate of spontaneous mutations at the agouti and \i W\i0 loci (1/21) (Schlager and Dickie, 1967). \par \par C57BL/10 \par High incidence of spontaneous `deviants' (possible mutants) (2/21) (Schlager and Dickie, 1967). \par C57BLKS. \par Origin: C57BL/6J to Biesele in 1947, then pen bred, to Kaliss in 1948. Ks resumed inbreeding. To J 1948. Differs from C57BL/6 and C57BL/10 at the \i Bgls, Bglt, cdm \i0 and \i H2\i0 loci as a result of a genetic contamination, probably with a DBA substrain at the time the colony was pen-bred. Resembles B6 at the \i Lv\i0 locus (at which B6 and B10 differ). Formerly known as C57BL/Ks but renamed in Dec. 1994. Maint. by J. \par Characteristics: \par Low hepatic delta-aminolaevulinate dehydratase activity in Ks substrain (7/8) (Doyle and Schimke, 1969). High susceptibility to BALB/Tennant leukaemia virus in Ks substrain (3/12) (Tennant, 1965). Resistant to \i Herpes simplex \i0 virus (2/11) in Ks substrain (Lopez, 1975). High retinal ganglion cell number (22/24) (Williams et al, 1996). \par C57BR/cd \par Inbr (J) 178. Brown: \i a,b.\i0 Origin: Little in 1921 from the same cross that gave rise to C57BL, C57BR/a and C57L. Black and brown substrains were separated in the first generation. Substrain cd was established at F13 from a cross between two brown substrains, one of which had previously given rise to C57BR/a. To Heston 1938, to J 1947 at F66. Maint. by J. \par \i Behaviour\i0 \par High intrastrain aggression (1/14), high open-field activity (1/14), high spontaneous bar-pressing (2/14) and low social grooming during aggressive encounters (11/14) (Southwick and Clark, 1966, 1968). High open-field activity (1/15) (Thompson, 1953). High shock-avoidance learning (1/9) (Bovet \i et al\i0 ., 1966), (2/9) (Bovet \i et al\i0 ., 1969). High alcohol preference (3/18) (Rodgers, 1966). \par \i Life-span and spontaneous disease\i0 \par Primary lung tumours 3% in males, 1%,, in breeding females and zero in virgin females, lymphatic leukaemia less than 1% (Hoag, 1963). Pituitary tumours 33% in old breeding females (Murphy, 1966). \par \par Long life-span in conventional conditions (20/22 = 703 days in males and 19/22 = 694 days in females), hepatomas 25% in males (Storer, 1966). Life-span intermediate in both sexes in SPF fostered conditions (10/17 = 577 days in males, 9/17 = 660 days in females) (Festing and Blackmore, 1971). \par \i Normal physiology and biochemistry\i0 \par Low systolic blood pressure (16/19) (Schlager and Weibust, 1967). High mean heart rate (2/7) but low mean heart rate adaptation (6/7) (Blizard and Welty, 1971). High metabolic rate (5/18) (Storer, 1967). High cell turnover as estimated by clearance of DNA-bound radioactivity (1/17) (Heiniger \i et al\i0 ., 1972). Low plasma cholinesterase activity (20/22 in males, 16/22 in females) (Angel \i et al\i0 ., 1967). High hypoxanthene-guanine phosphoribosyl transferase in thalamus (2/7) (Suran 1973). Low brain \dn8 L\dn0 -glutamic acid decarboxylase (GAD) (6/7) and acetylcholinesterase activity (6/7), but high monoamine oxidase activity (2/7) (Tunnicliff \i et al\i0 ., 1973). \par Low percentage of the time spent sleeping (6/6), with low percentage of slow-wave sleep (6/6) and high percentage of paradoxical sleep (1/6) (Valatx and Bugat, 1974). High proportion of paradoxical (REM) sleep (1/7) (Pagel \i et al\i0 ., 1973). \par Low sensitivity to thyrotropin (21/21) (Levy \i et al\i0 ., 1965). Low glucose-6-phosphate dehydrogenase activity (15/16) (Hutton, 1971). Low hepatic delta-aminolaevulinic acid synthetase activity after DDC treatment (15/15) (Gross and Hutton, 1971). High hepatic nicotinamide N-methyltransferase levels (1/10) (Scheller et al, 1996) Susceptible to the induction of atherosclerosis and develop large lesions with many foam cells on a high-fat, high-cholesterol diet (13/13) (Roberts and Thompson, 1976). \par \i Anatomy\i0 \par Low brain weight (24/25) (Roderick \i et al\i0 ., 1973). High total leukocyte count (5/18), high haematocrit (2/18), high mean corpuscular volume (3/18) and high haemoglobin (3/18) (Russell \i et al\i0 ., 1951). \par \i Drugs\i0 \par Nicotine decreases shock-avoidance learning (9/9) (Bovet \i et al\i0 ., 1966). Susceptible to tumour induction by 3-methylcholanthrene (4/12) (Whitmire \i et al\i0 ., 1971). Sensitive to insulin (1/9) and histamine (1/9) (Brown, 1965). Resistant to hyperbaric oxygen (18/18) with few central nervous system manifestations (Hill \i et al., \i0 1968). Resistant to X-irradiation as judged by the LD\dn8 50\dn0 (2/9) (Yuhas and Storer, 1969), (2/9) (Storer, 1966). Resistant to chloroform toxicity (cf. 5/9) (Deringer \i et al\i0 ., 1953). Sensitive (eosinophil response) to cortisone acetate (cf. 3/6) (Wragg and Speirs, 1952). Highly susceptible to the induction of liver tumours by N,N-diethylnitrosamine. At 50 weeks of age mean tumour multiplicity following a single dose of DEN given at 12 days of age was 28_13 tumours compared with only 1.4 and 0.5 in C3H and C57BL/6, respectively. Ovariectomy increased tumour multiplicity (Poole and Drinkwater, 1996). \par \i Immunology\i0 \par High lymphocyte phytohaemagglutinin response (7/43) (Heiniger \i et al\i0 ., 1975). Serum antinuclear factor in 51% of animals (1/17) (Barnes and Tuffrey, 1967). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). Erythrocytes have a low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). \par Infection \par Resistant to polyoma virus-induced tumours due to a resistance gene \i Pyv\i0 \i \up8 r \up0 \i0 \i ,\i0 which did not recombine with\i Mtv-7. \i0 Resistance can be overcome by irradiation, indicating an immunological basis (Lukacher et al, 1995). Resistant to \i Mycoplasma pulmonis\i0 infection (cf 4/16) (Cartner et al, 1996). \par \i Reproduction\i0 \par Intermediate breeding performance (12/25), colony output 0.98 young/female/week, litter size at weaning high at 6.5 (5/25) (Festing 1976a). Poor breeding performance (24/24) (Hansen \i et al\i0 ., 1973). High ratio of females at birth (2/11) (Cook and Vlcek, 1961). \par \i Miscellaneous\i0 \par High degree of genetic distinctiveness (6/27) (Taylor, 1972). Recommended host for transplantable pituitary tumour BW8685 (Kaliss, 1972). High incidence of spontaneous `deviants' (possible mutations) (1/21) (Schlager and Dickie, 1967). \par C57L \par Inbr: F 130 +. Grey (colour very similar to DBA). Genet: \i a, b, ln\i0 . Origin: Murray 1933 from a mutation in F22 of a C57BR substrain which is now extinct. Maintained by Cloudman, to Heston 1938, then to Jackson Laboratory 1947 at F45. Differs from C57BR/cd at the \i H2, Igh1, Pgk2, Qa2\i0 and\i Qa3\i0 loci. Maint. by J, N. \par \i Behaviour\i0 \par High alcohol preference (4/18) (Rodgers, 1966). High open-field activity (3/14), high spontaneous bar-pressing activity (3/14) and low tail-rattling during aggressive encounters (12/14) (Southwick and Clark, 1968). Rapid shock-avoidance learning (1/7) (Schlesinger and Wimer, 1967). High open-field activity (3/13) (Bruell, 1964). \par \i Life-span and spontaneous disease\i0 \par Low incidence of RNA tumour virus group-specific antigen expression (5/5) (Diwan \i et al\i0 ., 1973). Primary lung tumours less than 1%; lymphatic leukaemia less than 1% in males and breeding females, but about 4% in virgin females; mammary adenocarcinomas 3% in breeding females, zero in males and virgin females (Hoag, 1963). 25% incidence of Hodgkin's-like lesions, reticulum cell neoplasm type B at 18 months (Heston, 1963) (55% according to Dunn and Deringer, 1968). Pituitary tumours 33% in old breeding females (Murphy, 1966). \par \par Life-span short in males (3/17 = 473 days), intermediate in females (6/17 = 604 days) in SPF fostered conditions (Festing and Blackmore, 1971). Congenital cystic ovaries frequent (Staats, 1976). \par \i Normal physiology and biochemistry\i0 \par High systolic blood pressure (3/19) (Schlager and Weibust, 1967). Low serum ceruloplasmin levels in males (21/26) but high in females (6/27) (Meier and MacPike, 1968). Low rectal and hind foot pad temperature (8/9) but high tail temperature (2/9) (Shepard and Habas, 1967). \par \par Low glucose-6-phosphate dehydrogenase and nicotinamide-adenine dinucleotide phosphate levels in erythrocytes (8/8) (Erickson, 1974). Low sensitivity to thyrotropin (19/21) (Levy \i et al\i0 ., 1965). Low brain glutamic acid decarboxylase (7/10) (Gaitonde and Festing, 1976). High coumarin hydroxylating ability (cf. 4/13) (Lush and Arnold, 1975). Low glucose-6-phosphate dehydrogenase activity (16/16) (Hutton, 1971). Low kidney arylsulphatase activity (10/12) (Daniel, 1976). Low hepatic delta-aminolaevulinic acid synthetase activity after DDC treatment (14/15) (Gross and Hutton, 1971). Resistant to induction of high hepatic porphyrin levels, in contrast with five other strains (Hutton and Gross, 1970). Low porphyrin content of Harderian gland (15/16) (Margolis, 1971). Susceptible to the development of atherosclerosis on a semi-synthetic high fat diet (2/9) (Nishina et al, 1993). \par \i Anatomy\i0 \par High percent carcass lipid on a high-fat diet (8/9) (West et al 1992).Low brain weight (23/25) (Roderick \i et al\i0 ., 1973). High total leukocyte count (3/18), high haematocrit (1/18), high mean corpuscular volume (1/18), high haemoglobin (2/18) (Russell \i et al\i0 ., 1951). Adrenal gland has a small X zone (7/8) with a low incidence of vacuolisation (5/6) (Delost and Chirvan-Nia, 1958). About 38% of mice have accessory spleens (1/9) (Hummel \i et al\i0 ., 1966). Low bone density of femur (10/11) (Beamer et al, 1996). \par \i Drugs\i0 \par Low susceptibility to transplacental induction of tumours by 1-ethyl-1-nitrosourea (5/5) (Diwan \i et al\i0 ., 1973). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Low susceptibility to tumour induction by 3-methylcholanthrene (8/8) (Whitmire and Salerno, 1972). Resistant to the induction of tumours by N-Methyl-N-Nitrosourea (MNU) due to a gene on chromosome 7 (Angel et al, 1993). \par Susceptible to teratogenic effects of 1-ethyl-1-nitrosourea (1/5) (Diwan, 1974). Sensitive to Warfarin (4/12) (Lush and Arnold, 1975). Long sleeping time under hexobarbital anaesthetic (14/15) (Lovell, 1976), long sleeping time under pentobarbitone anaesthetic (21/23), Lovell (1986). Resistant to chloroform toxicity (cf. 5/9) (Deringer \i et al\i0 ., 1953). Susceptible to the development of lung fibrosis following a single dose of thoracic irradiation (Franko and Sharplin, 1994). Estrogen induces an increase in VLDL and LDL-cholesterol (like C57BL/6, contrast BALB/c and C3H) (Srivastava, 1995). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid caused a high incidence of cholesterol gallstones (like SWR, A, contrast SM, AKR, DBA/2) (Faulkner et al, 1995). \par \i Immunology\i0 \par Susceptible to experimental allergic encephalomyelitis (EAE) (3/18) (Levine and Sowinski, 1973). High susceptibility to EAE (3/10) with high incidence (1/10) of spontaneous relapse (Lindsey,1996). High lymphocyte phytohaemagglutinin response (2/43) (Heiniger \i et al\i0 ., 1975). No immune response to low levels of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to GAT (random terpolymer of Glu\up8 60\up0 , Ala\up8 30\up0 , Tyr\up8 10\up0 ) (8/10) (Dorf \i et al\i0 ., 1974). HSF from \i Bordetella pertussis\i0 sensitises to histamine (Bergman and Munoz, 1968). Erythrocytes have low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). Susceptible to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 3/18) (Noonan and Hoffman, 1994) \par \i Infection\i0 \par Susceptible to \i Plasmodium berghei \i0 infection (1/8) (Most \i et al\i0 ., 1966). Low susceptibility to BALB/Tennant leukaemia virus (12/12) (Tennant, 1965). Resistant to \i Mycobacterium marinum (3/9) \i0 and poor plateau harvest of \i M. leprae\i0 8 months after infection (8/9) (Shepard and Habas, 1967). Low expression of RNA tumour virus group-specific antigen (8/8) (Whitmire and Salerno, 1972). Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). Encephalomyocarditis virus causes diabetes mellitus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Resistant to development of leukaemia on infection with Friend virus (cf. 2/11) (Dietz and Rick, 1972). \par \i Reproduction\i0 \par Intermediate breeding performance (15/25), colony output 0.9 young/female/wk, litter size at weaning high at 6.0 (7/25) (Festing, 1976a). Good litter size, mean 5.6 (2/6) (Verley \i et al\i0 ., 1967). Intermediate breeding performance (16/24) (Hansen \i et al\i0 ., 1973). \par \i Miscellaneous\i0 \par High degree of genetic distinctiveness (5/27) (Taylor, 1972). Recommended host for transplantable hepatoma BW7756 and pituitary tumour BW8883 (Kaliss, 1972). \par C57P/A \par Inbr (A): 115. Origin: R.Korteweg, 1934. Cross of DBA x C57BL then N20 backcrossing to C57BL, followed by b x s mating. (formerly listed as P/A). Maint. by A. \par C58 \par Inbr: F166 +. Black. Genet: \i a\i0 . Strain developed by MacDowell in 1921 from litter mates 58 and 52 of Miss Lathrop's stock (see also C57BL). A mating of the same male but a different female gave rise to the C57 group of strains. Used largely as a high-leukaemia strain, the genetics of which has been reviewed by Lilly and Pincus (1973). \par \i Behaviour\i0 \par High avoidance conditionability (3/9) (Royce, 1972). Good T-maze learning (2/6) (Stasik, 1970). High alcohol preference (5/18) (Rodgers, 1966). \par \i Life-span and spontaneous disease\i0 \par Life-span short (2/22), 373 days in males and 351 days in females in conventional conditions (Storer, 1966). High incidence of leukaemia (Heston, 1963). High gross tumour incidence (2/22) (Storer, 1966). Leukaemia 97% (Myers \i et al\i0 ., 1970). \par \i Normal physiology and biochemistry\i0 \par Low serum ceruloplasmin levels in females (25/27), but intermediate in males (Meier and MacPike, 1968). Low systolic blood pressure (14/19) (Schlager and Weibust, 1967). Low sensitivity to thyrotropin (17/21) (Levy \i et al\i0 ., 1965). High serum haptoglobin level (3/11) (Peacock \i et al\i0 ., 1967). Harderian gland has a low porphyrin content (13/16) (Margolis, 1971). \par \i Anatomy\i0 \par Small brain/body weight (18/20). Small brain weight (Roderick \i et al\i0 ., 1973). Low number of granule cells in right area dentata of brain (5/5) (Wimer and Wimer 1982). A significant number of acinar cells of the pancreas are multinucleated (cf. AKR), in contrast to seven other strains (Pollard, 1973). Accessory spleens in about 21% of mice. One or both kidneys reduced or missing in 10-12% of individuals. Polyovular follicles common (Hummel \i et al\i0 ., 1966). \par \i Drugs\i0 \par Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (5/14) (Kouri \i et al\i0 ., 1973). Resistant to X-irradiation (6/27) (Roderick, 1963). Resistant to hyperbaric oxygen (17/18) (Hill \i et al\i0 ., 1968). High incidence of virus-like particles in chemically induced sarcomas (1/6) but low susceptibility to 3,4-benzpyrene (5/6) (Liebelt \i et al\i0 ., 1970). Susceptible to toxic effects of isoniazid (8/10) (Taylor, 1976b). High ED50 to behavioural effects of nicotine (18/19). Sensitive to seizures induced by nicotine (17/19) (Marks et al 1989) \par \i Immunology\i0 \par Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). Develop immune polioencephalomyelitis, a paralytic central nervous system syndrome characterised by mononuclear cellular infiltration of the spinal cord and brain stem when aged mice are immunised with formalin-inactivated line I\dn8 b\dn0 malignant lymphocytes (Sager \i et al\i0 ., 1973). Erythrocytes have low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). High responder to dextran (cf. 4/10) (Blomberg \i et al\i0 ., 1972). \par \i Infection\i0 \par Resistant to \i Mycoplasma fermentens \i0 (5/6) (Gabridge \i et al\i0 ., 1972). Resistant to \i Plasmodium berghei\i0 infection (7/8) (Most \i et al\i0 ., 1966). Encephalomyocarditis virus causes diabetes mellitus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Develop paralysis (age-dependent polyomyelitis) following infection with the lactate dehydrogenase-elevating virus in common with other mouse strains (e.g. AKR) which possess N-tropic ecotropic murine leukemia proviruses and are homozygous \i Fv1\i0 \i \up8 n\up0 \i0 \i \i0 (Anderson et al, 1995). \par \i Reproduction\i0 \par Poor breeding performance (22/24) (Hansen \i et al\i0 ., 1973). \par CASA \par Inbr. F?+33 (1989). Mus musculus castaneous wild mice trapped in Thailand by J.T. Marshall, to Chapman, then Roderick and Eicher in 1971.Resistant to flavivirus, unlike most laboratory mice except C3H.RV (Sangster et al 1993). Low retinal ganglion cell number (3/24) (Williams et al, 1996) \par CAST \par Inbr ?+34 (1989). Origin: same as CASA. Resistant to flavivirus, unlike most laboratory mice except C3H.RV (Sangster et al 1993). Low retinal ganglion cell number (2/24) (Williams et al, 1996). Used as a tester strain in a novel strategy for mapping new mutations in laboratory mice using simple sequence repeats (SSR) with DNA pools from mutant and wild-type F2 progeny. A set of 39 SSRs is expected to screen 94% of the autosomal genome in crosses with laboratory strains (Taylor et al, 1994). \par CAT \par Inbr. ?+26 (Lac). Albino \i c,Cat\i0 \i \up8 Fr\up0 \i0 \up8 \up0 . Origin: \i Cat\i0 \i \up8 Fr\up0 \i0 \up8 \up0 arose in strain A. Apparently outcrossed to unknown stock, then inbred by Muggleton-Harris. (Muggleton-Harris et al 1987). All mice have bilateral cateracts. The lens abnormality begins to form before 14 days of interuterine life. Selective loss of a family of gene transcripts for specific crystallin synthesis has been reported (Garber et al 1985). Maint. by Muggleton-Harris. \par CBA \par Inbr: F90-170 depending on substrain. Agouti. Genet. + . Developed by Strong in 1920 from a cross of a Bagg albino female and a DBA male. Strain CBA was selected for a low mammary tumour incidence and C3H for a high incidence. Now widely distributed, and used as a general-purpose strain. Differences between substrains are probably too large to be accounted for by mutation, and some degree of genetic contamination in the past is probable. The following major substrains are recognised: \par \par CBA/Ca or CBA/H \par Strong, to Jackson Laboratory, to Haldane and Gruneberg in 1932. To Carter 1947 and Harwell 1954. This substrain used in most British research. \par \par CBA/Br \par Jackson Laboratory, to Haldane 1932, to Bonser (Leeds) approx. 1933. \par \par CBA/CaN \par Harwell, to National Institutes of Health in 1966. Carries sex-linked immunological deficit which prevents it from responding to type III pneumococcal polysaccharide. Deficit is expressed on B cells (Gershon and Kondo, 1976; Scher \i et al\i0 ., 1976). Do not carry naturally occurring tumour-reactive antibodies commonly found in other strains (Martin and Martin, 1975). \par \par CBA/J \par Strong, to Andervont 1947, to Jackson Laboratory 1948. Carries gene for retinal degeneration \i (rd). \i0 Skin grafts between CBA/J and CBA/Ca are rejected (Green and Kaufer, 1965). \par \par CBA/St \par Original strain maintained by Strong. \par \par CBA/H-T6 \par T6 translocation backcrossed to CBA/H by Dr M. F. Lyon. Now homozygous for the marker translocation T(14;15) 6Ca, but otherwise congenic with CBA/H. \par \i Behaviour\i0 \par Low spontaneous bar-pressing activity (13/14), low tail rattling during aggressive encounters (13/14), high social grooming during aggressive encounters (2/14), low intrastrain aggression (13/14) (Southwick and Clark, 1966, 1968). Low locomotor activity (5/5) (Davis and King, 1967). Low locomotor activity when single (6/6), but intermediate when grouped (4/6) (Davis \i et al\i0 ., 1967). Low spontaneous locomotor activity (2/9) (Nikulina et al 1991). Low shock avoidance learning (9/9) (Bovet \i et al\i0 ., 1966, 1969). High shock avoidance learning in Ca substrain (2/8) but not in J substrain (5/8) (Wahlsten, 1973). High water-escape learning in CBA-T6 (2/6) (Festing, 1973b). Highly susceptible (1/9) to "pinch-induced" catalepsy (excessive freezing), possibly due to a sinlge recessive autosomal gene (Kulikov et al, 1993). \par \i Life-span and spontaneous disease\i0 \par Life-span intermediate both sexes (J substrain) in conventional conditions (11/22 = 527 days males, 10/22 = 527 days females) (Storer, 1966). Life-span (Ca substrain) short in males (4/17 = 486 days) and long in females (17/17 = 825 days) in SPF fostered conditions. Short life-span of males associated with a high incidence of haemothorax, suggesting a high sensitivity to vitamin K deficiency in SPF conditions (Festing and Blackmore, 1971). \par \par High gross tumour incidence (J) (3/22) (Storer, 1966). Overall tumour incidence 29% in males, 55% in females, including lymphoma 6% in males, 15% in females, hepatoma 24% in males, zero in females and mammary tumours 33% in females and zero in males (Smith \i et al\i0 ., 1973). Lung adenomas 2-11% in BrA substrain, leukaemia 4-10% (Muhlbock and Tengbergen, 1971). Resistant to the induction of atherosclerosis by a high-fat and high-cholesterol diet (1/13) (Roberts and Thompson, 1976). \par Develop a mild hearing loss with onset late in life (contrast C57BL/6J) (Li, 1992, Willott et al, 1993, Li et al, 1993, Li and Borg, 1993). Do not carry any of the single recessive genes found in BALB/cBy, C57BL/6 and WB/ReJ, causing age-related hearing loss. All three genes are present in DBA/2 (Willott et al, 1995). \par \i Normal physiology and biochemistry\i0 \par High systolic blood pressure (4/19) (Schlager and Weibust, 1967). Low Na/K ratio in erythrocytes (8/9) and in plasma (9/9) (Waymouth, 1973). High serum ceruloplasmin levels in males of Ca and J substrains (5/26 and 6/26), high level in females of Ca substrain (3/27) but intermediate in J substrain (Meier and MacPike, 1968). Low calcium uptake by the heart (5/5) (Mokler and Iturrian, 1973). \par High proportion of the time spent sleeping (2/6), with large percentage of slow-wave sleep (1/6) and low percentage of paradoxical sleep (5/6) (Valatx and Bugat, 1974). Low percentage of paradoxical sleep (7/7) (Pagel \i et al\i0 ., 1973). Low metabolic rate (14/18) according to Storer (1967), but high metabolic rate (2/6) according to Pennycuik (1967). High cell turnover in J substrain as estimated by rapid clearance of DNA-bound radioactivity (2/17) (Heiniger \i et al\i0 ., 1972). \par High peripheral nerve conduction velocity (2/6) (Hegmann, 1972). High brain glutamic acid decarboxylase (3/10) (Gaitonde and Festing, 1976). Low hypoxanthine-guanine phosphoribosyl transferase in thalamus (6/7), but high level in hypothalamus (2/7) (Suran, 1973). High brain monoamine oxidase (1/7) and low level of catechol-\i O\i0 -methyltransferase (6/7) activity (Tunnicliff \i et al\i0 ., 1973). Low brain tyrosine hydroxylase activity (5/5) (Ciranello \i et al\i0 ., 1972). Low peptidyl proline hydroxylase activity in mammary gland, foot pad and tumours (5/5) (Cutroneo \i et al\i0 ., 1973). High sensitivity to thyrotropin in J substrain (1/21) (Levy \i et al\i0 ., 1965). High coumarin hydroxylating ability (cf. 4/13) (Lush and Arnold, 1975). High hepatic 3 aminolaevulinic acid synthetase activity after DDC treatment (1/15) (Gross and Hutton, 1971). High porphyrin content in Harderian gland (3/16) (Margolis, 1971). High hind foot pad temperature (1/9) (Shepard and Habas, 1967). Have only about 20% of the maltase (gamma-glucoamylase) activity found in other strains, though there is no evidence for any gross metabolic abnormality resulting from this defect (Quezada-Calvillo et al, 1993). \par \i Anatomy\i0 \par Large brain weight (17/18 male, 16/18 female) (Storer, 1967). Large forebrain volume (2/9) and neocortex (2/9) (Wimer \i et al\i0 ., 1969). Small brain/body weight ratio (17/20) (Roderick \i et al\i0 ., 1973). Low testes weight (7/8) (Shire and Bartke, 1972). Large kidney/body weight ratio (5/21) (Schlager, 1968). Low thyroid weight (4/5) (Mendoza \i et al\i0 ., 1967). Small heart/body weight ratio (5/5) (Mokler and Iturrian, 1973). Large pituitary (2/6) (Sinha \i et al\i0 ., 1975). Low total leukocyte count (15/18), high erythrocyte count (6/18) (Russell \i et al\i0 ., 1951). Few bristles on foot pads (8/8) (Festing, 1974a). Third molars small and one or more absent in about 18% of individuals (Hummel \i et al\i0 ., 1966). \par \i Drugs\i0 \par Resistant to urethane-induced lung tumours (Falconer and Bloom, 1962). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Susceptible to induction of leukaemia (2/6) and liver tumours (2/6) by neonatally administered DMBA (Flaks, 1968). Susceptible to X-irradiation (27/27) (Roderick, 1963), but resistant to `CNS syndrome' with high doses of X-irradiation (1/5) (Yuhas, 1968). Susceptible to hyperbaric oxygen, showing central nervous system manifestations (11/18) (Hill \i et al\i0 ., 1968). Sensitive to lethal effect of ozone (2/21) (Goldstein \i et al\i0 ., 1973), but resistant (cf 3/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). Sensitive to teratogenic effect of acetazolamide (1/6) (Green \i et al\i0 ., 1973, Hackman and Hurley 1983), but resistant to induction of cleft palate in embryos by cortisone (5/5) (Kalter, 1965). Insensitive to insulin (7/9) (Brown, 1965). Long survival on Warfarin (11/12) (Lush and Arnold, 1975). High ED50 to behavioural effects of nicotine (16/19) (Marks et al 1989). Susceptible to weight loss induced by cocaine, but this is attenuated by anisomycin (cf C3H, SJL) (Shimosato et al, 1994). More resistant to acute toxic effects of aflatoxin B-1 than strain C57BL/6 (Almeida et al, 1996). \par \i Immunology\i0 \par Low lymphocyte phytohaemagglutinin response (35/43) (Heiniger \i et al\i0 ., 1975). Good immune response to low doses of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Good splenic PFC immune response to pneumococcal polysaccharide in CBA/H-T6 (3/9), but poor in CBA/J (9/9) and CBA/H (7/9) (Amsbaugh \i et al\i0 ., 1972). Good immune response to ovomucoid, but poor response to ovalbumin (cf. 5/12) (Vaz \i et al\i0 ., 1971). Resistant to induction of antigen-induced arthritis (contrast `most other strains') (Brackertz \i et al\i0 ., 1977). Non-responder to synthetic polypeptide Glu\up8 57\up0 , Lys\up8 38\up0 , Ala\up8 5\up0 (cf. 4/7) (Pinchuck and Maurer, 1965). Discriminator between `H' and `L' sheep red blood cells (cf. 12/18) (McCarthy and Dutton, 1975). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Low responder to dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972). Low immune response to ganglio-series gangliosides (c.f. 4/10) Kawashima et al (1992). High natural killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (2/6) (Pope et al, 1994). Diminished expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts in J substrain (cf 3/6) (Muthing, 1997). \par \i Infection\i0 \par Resistant to infection by \i Salmonella typhimurium \i0 strain C5 (7/7) (Plant and Glynn, 1974). Susceptible to infection by liver fluke \i Opisthorchis felineus \i0 (2/6) (Zelentsov, 1974). Good plateau harvest of \i Mycobacterium leprae \i0 8 months after infection (1/9) (Shepard and Habas, 1967). Low immune response to \i Mycobacterium lepraemurium\i0 is associated with an impared macrophage function (Saito and Natori 1985). Resistant to infection by \i Helicobacter felis\i0 with only mild gastritis in the antrum and no atrophy seen over time (cf BALB/c, contrast 4 other strains) (Sakagami et al, 1996). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Highly susceptible to measles virus (cf. 3/6) (Rager-Zisman \i et al\i0 ., 1976). Ca, H-T6 and N substrains carry no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). Administration of cadmium results in a high incidence of activation of latent herpes simplex virus infections. This is not seen in other strains, and does not correlate with cadmium toxicity (Fawl et al, 1996). \par J substrain resistant (2/7) to the induction of dental caries due to infection with \i Streptococcus mutans\i0 (Kurihara et al 1991). Resistant (4/4) to murine herpes virus (Kapoor et al 1992). Resistant to intra-vaginally innoculated \i Neisseria gonorrhoeae\i0 (c.f. 5/5) (Johnson et al 1989). Develop severe lesions (2/8) following infection with \i Candida albicans\i0 (Ashman et al, 1993). This correlates with low induction of \i Candida-\i0 specific gamma interferon (Ashman and Bolitho, 1993). CBA/J resistant, with low amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). \par J substrain is susceptible to several clinical isolates of penicillin-susceptible and resistant strains of \i Streptococcus pneumoniae\i0 , and may be a useful model for evaluating antibiotic efficiencies against this bacterium (Tateda et al, 1996). Resistant to \i Leishmania major \i0 (contrast BALB/c) (Laskay et al, 1995). Ca substrain susceptible to \i L. major mexicana\i0 , and vaccination against the parasite using liposomes with parasite membrane antigens was effective (cf C57BL/6 but contrast C57BL/10) (Lazama-Davila, 1997). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in well developed protoscoleces (cf 4/9) (Nakaya et al, 1997). \par \i Reproduction\i0 \par Good breeding performance (9/25), colony output 1.15 young/female/week, litter size at weaning 5.8(11/25), T6 substrain about equal (Festing 1976a, original data). Intermediate breeding performance (4/8), litter size 5.4, sterility 5.2% (Nagasawa \i et al\i0 ., 1973). Good litter size (1/6 to 3/6, depending on parity), but low proportion of females produce four or more litters (2/6) (Fernandes \i et al\i0 ., 1973). Poor breeding performance in N substrain (21/24) (Hansen \i et al\i0 ., 1973). Low percentage pre-implantation loss of embryos (2/8) (Leonard \i et al\i0 ., 1971). Females have a high rate of fetal resorption when mated with DBA/2 males, but this can be dramatically reduced by immunization with BALB/c, but not DBA/2J spleen cells. This may provide an animal model for the prevention of fetal death by vaccination (Chaouat et al 1985). Maturity of the cytoplasm in oocytes is acquired earlier than in those of the KE or other strains of mice so far studied. (Polanski 1990) \par \par \i Miscellaneous\i0 \par Recommended host for transplantable rhabdomyosarcoma BW 10139 (Kaliss, 1972). High rate of spontaneous mutations (2/21) (Schlager and Dickie, 1967). \par CBRB \par Inbr N?+F25. Agouti. Origin: EV Moiseeva. Spontaneous translocation Rb(8.17)Iem was found originally by VS Baranov in C3HA/Iem mice and carriers were crossed to CBA/CaLac. After an unknown number of backcrosses, mice were maintained by b x s matings and were sent to the Institute of Immunology, Kashirskoe Sh., 24-2, Moscow 115478, USSR, in 1984 at F11. Carries Rb(8.17)Iem translocation. More than 50% mammary tumours in breeding females by 9.3 months of age. \i Hbb\i0 \i \up8 d\up0 \i0 \up8 \up0 Maintained by Moiseeva at above address. \par CBXC- \par Inbr circa F25. Set of 9 recombinant inbred strains developed by Ola from a cross between CBA/Ca and BALB/c (Fernandez et al 1989). Now extinct. \par CBXNO-6 (reserved symbol). \par Inbr. F18 (1992). Single recombinant inbred strain developed by Herberg in 1992 from a cross between CBA/LsLt and NOD/Shi. CBXNO-7 was derived from the same cross, but separated from this strain at F12. \par CBXNO-7 (reserved symbol). \par Inbr. F18. See CBXNO-6. \par CC57BR \par Inbr: F83. Chocolate. Genet: \i a\i0 , \i b. \i0 Origin: Medvedev, 1943 from BALB/cN female x C57BL/N male. \par Characteristics \par No spontaneous mammary tumours, but about 60% when the milk agent is introduced. Primary lung tumours 22%. Incidence of all other tumours less than 1% (Heston, 1963). Life-span about 18 months (Medvedev, 1969). High spontaneous locomotor activity (9/9). Short time of immobility in a forced swimming test (7/9) (Nikulina et al 1991). Clonidene induces a strong aggressive behavioural response (3/9) (Nikulina and Klimek, 1993). \par CC57W \par Inbr: F79. Albino. Genet: \i a, b, c\i0 . Origin: Same as CC57BR. \par Characteristics \par No spontaneous mammary tumours, but 55% after introduction of mammary tumour virus (Heston, 1963). Life-span average about 15.5 months (Medvedev, 1969). \par CE \par Inbr: F? + 68. Black-eyed grey. Genet: \i A\i0 \i \up8 w\up0 \i0 \i , c\i0 \i \up8 e\up0 \i0 \up8 \up0 . Originating in 1920 from wild mice trapped by J. E. Knight. The coat colour genetics later studied by Detlefsen. However, as the strain closely resembles `laboratory mice' (Taylor, 1972) and is not wild in behaviour, it seems possible that the original mutant mice were crossed with unidentified laboratory mice before being inbred. The strain is not widely used, and has a poor reproductive performance. However, its unique coat colour ensures authenticity, and it has an interesting range of tumour types, including a high incidence of ovarian tumours. F\dn8 1\dn0 hybrids with DBA/ 1, DBA/2 and C3H have a high incidence of hepatomas (Hancock and Dickie, 1969). \par Characteristics \par Sporadic high incidence of ear chewing of young by mother in Lac substrain (Festing 1976, original observation). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (22/26) (Lush 1988). \par \par Life-span intermediate in males (6/17 = 498 days) and long in females (14/17 = 703 days) in SPF fostered stock (Festing and Blackmore, 1971). High incidence of adrenal cortical tumours following castration (Heston, 1963). Progressively severe endocrine imbalance involving the ovaries, adrenal cortex and pituitary in CE x DBA F1 hybrids (Dickie and Atkinson, 1957; Dickie \i et al\i0 ., 1957). Liver tumours 11-57% (Festing and Blackmore, 1971). Develops granulosa cell tumours of ovaries (Chai and Dickie, 1966). Ovarian tumours 34% in virgin females (Murphy, 1966). \par \par Low serum ceruloplasmin levels in females (26/27) but intermediate in males (Meier and MacPike, 1968). Low systolic blood pressure (15/19) (Schlager and Weibust, 1967). Low brain choline acetyltransferase activity (7/7) (Tunnicliff \i et al\i0 ., 1973). \par \par Accessory spleens uncommon (8/9) (Hummel \i et al\i0 ., 1966). Sensitive to Warfarin (1/12) (Lush and Arnold, 1975). Short sleeping time under hexobarbital anaesthetic (1/15 males, 2/15 females) (Lovell, 1976). High lymphocyte phytohaemagglutinin response (3/43) (Heiniger \i et al\i0 ., 1975). Non-discriminator between `H' and `L' sheep RBC (cf. 6/18) (McCarthy and Dutton, 1975). \par \par Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). Low voluntary comsumption of morphine in two-bottle choice situation (14/15) (Belknap et al, 1993). \par \par Short sleeping time under pentobarbitone anaesthetic (1/23), Lovell (1986). Highly resistant to azocasein-induced amyloidosis (contrast 5 strains). This is associated with a single novel isoform of the serum amyloid A gene (Sipe et al, 1993, De Beer et al, 1993). This is inherited as an autosomal dominant gene (Gonnerman et al, 1995). Mice produce amyloid enhancing factor (Gonnerman et al, 1996). \par \par Poor reproductive performance (23/25), colony output 0.53 young/female/wk, although litter size is large (6/22) at 6.1 (Festing, 1976a). High ratio of males at birth (1/11) (Cook and Vlcek, 1961). \par Recommended host for transplantable rhabdomyosarcoma BW10139 (Kaliss, 1972). \par CF1 \par Inbr. 30. Albino \i c. \i0 Origin: Non-inbred CF-1 mice from Carworth Farms inbred by N.Goto in 1978. High incidence of cleft palate following cortisone, and high incidence of diabetes after alloxan. Maintained by Jah. \par CFCW \par Inbr (Rl) 100+. Albino: \i c,Ca (caracul). \i0 Origin:Outbred mice from Carworth Farms to Rl, Oak Ridge in 1948. Maint. by Rl. \par CFO \par Inbr. 32. Albino: \i a,b,c,S. \i0 Origin: Outbred CF-1 mice. Carries unnamed gene causing anaemia and lipidosis. Maintained by Idr. \par CFW \par Inbr (Jic) 58. Albino: \i c. \i0 Origin: Outbred mice from Carworth Farms. Inbreeding started in 1964. Note that there are several other inbred CFW lines. They should not be assumed to be identical due to the heterozygosity of the original stock. Maint. by Jic. \par CHI \par Inbr (Man) 160. Agouti. \i +. \i0 Origin: Strong 1920 from a cross of the Bagg albino X DBA. strains C,CBA,C3H and C121 originated from the same cross. Susceptible to flbrosarcoma induction by methylcholanthrene (1/15 males, 5/15 females) (Strong, 1952). Maint. by Man. \par CHMU \par Inbr. 33 (Le). Agouti (breeders); \i A/A,ch,+/+,mu. ch,+/ch,+ \i0 identifiable and dead at birth. \i +,mu/+,mu \i0 identifiable at birth by light eyes and develop dilute hair. Origin: \i ch (\i0 congenital hydrocephalus) on B6CBA background from Gruneberg to M.C. Green 1961.\i ch/+ \i0 crossed to \i cr,+/+,f \i0 stock and maintained by \i ch,+/+,cr \i0 to F9. \i ch/+ \i0 crossed to \i sa/sa, \i0 maintained\i ch,+/+,sa \i0 to F20. \i ch/+ \i0 crossed to \i mu/mu, \i0 maintained by\i ch,+/+,mu \i0 bxs to present. \i mu \i0 from M. Lyon to Jax 1976. Crossed to C57BL/6J and bxs to F3. \i ch \i0 homozygotes die at birth and are recognised by bulging haemorrhagic cerebral hemispheres. Maintained by Le. \par CKB \par Inbr. 50. Agouti. +. Origin: C3H.SW (\i Ig1\i0 \i \up8 b,\up0 \i0 \i H2\i0 \i \up8 b\up0 \i0 \i ) \i0 x C3H (\i Ig1\i0 \i \up8 a\up0 \i0 \i ,H2\i0 \i \up8 k\up0 \i0 \i ), \i0 F1 inbred to give CKB. \par CL \par Inbr: F20 +. Strain developed by Fraser from a heterogeneous stock carrying the \i msl \i0 gene (migratory spot lesion a variable white spot on the retina), crossed to A/J and subsequently inbred with selection for high frequency of spontaneous cleft lip. Frequency of the latter now 26% in viable 17-day embryos (Bornstein \i et al\i0 ., 1970). \par CLA \par Inbr 22. Agouti. Origin: Wild mice trapped on a farm near Centreville, Maryland. Strains WSA and WSB were separated from the same stock at F3. \par CN \par Inbr(Nmg) 27. Cinnamon \i b. \i0 Origin: Fa non-inbred obese stock. Inbred from 1976. Maint. by Nmg. \par CPB-H \par Inbr: 42. Genet: \i b\i0 , \i d. \i0 Origin: At Centraal Proefdierenbedrijf TNO, Holland (Cpb), about 1950. \par Characteristics \par Females often have a pair of non-lactating supernumerary nipples (Staats, 1976). \par CPB-K \par Inbr: 54. Genet: \i a, B, c, d, P. \i0 Origin: As CPB-H. Former designation KC discontinued. \par Characteristics \par Excitable; small litters; amylase type B (other CPB strains are type A). \par CPB-MO \par Inbr: 37. Genet: \i c\i0 . Origin: Institute of Tropical Hygiene, Amsterdam, to Cpb 1957. \par Characteristics \par 100% brachypodism due to a recessive gene. \par CPB-N \par Inbr: 47. Genet: \i a\i0 , \i b, p. \i0 Origin: As CPB-H. \par Characteristics \par Normal sex difference in major urinary protein content of serum and in reaction to hexobarbital. \par CPB-P \par Inbr: 39. Genet: \i a, b, d, p. \i0 \par Characteristics \par Reacts to LSD with head twitching. Very light red-eyed grey. \par CPB-Q \par Inbr (Cpb): ? + 61. Genet: \i a, B, c\i0 \i \up8 e\up0 \i0 \i , D, P. \i0 Origin: Hagedoorn, Holland, to Hirschfeld 1937, to Cpb 1949. \par Characteristics \par More susceptible to tuberculosis than most strains; reacts to LSD with head twitching. \par CPB-R \par Inbr: ?+50. Genet: \i a, b, c, D, P. \i0 Origin: `Rhodesfarm', South Africa, to Compton, England, to Hagedoorn, Holland, to Cpb 1949. \par CPB-S \par Inbr: ? + 59. Genet: \i A, B, c, D, P.\i0 Origin: Rockefeller Institute, probably same origin as BSVS, BRVR, etc., to Laidlaw (Hampstead), to Hagedoorn, to Cpb 1949. \par Characteristics \par Rather aggressive, especially males (Cpb), territorial, with a sensitive aggression-flight balance; adapted to surface-living rather than hole-living. \par CPB-TK \par Inbr: 37. Genet: \i a, b, d, s, W. \i0 Origin: Cross between CPB-T and CPB-K in 1953. \par Characteristics \par Macrocytic anaemia. \par CPB-V \par Inbr: 54. Genet: \i c\i0 \i \up8 ch\up0 \i0 \up8 \up0 . Origin: Hagedoorn, to Cpb 1949. \par Characteristics \par Males have low major urinary protein in serum; no sex difference in response to hexobarbital. \par CPB-WG \par Inbr: 33. Genet: \i a\i0 . Origin: Waltzing mice from Hagedoorn in 1949. Crossed with strain G, now extinct, in 1953. \par Characteristics \par Carries a waltzer-shaker-like mutant; expression varies from fairly normal walking to circling; very excitable; not deaf. \par CPB-WV \par Inbr: 39. Genet: \i W\i0 \i \up8 v\up0 \i0 \i /w, A. \i0 Origin: Gruneberg, to Cpb in 1956. \par Characteristics \par Macrocytic anaemia. \par CRM \par Inbr (Pas) 24 (1994). Cream, \i c, crm.\i0 Origin: Cream mutant from Harwell in about 1987, inbred by Guenet, Pasteur Inst. \par CS \par Inbr: 61. Genet: \i a, b, c, D, s. \i0 Origin: Established in 1956 from hybrids between NBC and SII, both now extinct. Unrelated to IVCS. \par Characteristics \par Carries new endogenous mammary tumour viruses Mtv-42-45 (Wajjwalku et al 1991). Good reproductive performance; quick moving; Japanese crooked tail 16%. \par CT \par Inbr (Lac) ?+8 . Agouti: +. Origin: \i ct \i0 (curly-tail) mutation arose spontaneously in GFF inbred mice. Backcrossed to CBA an unknown number of times, then bxs of presumed \i ct/ct \i0 homozygotes. Differs from CBA at many marker loci. Expression of the \i ct \i0 gene ranges from spina-bifida causing pre-natal death to various degrees of kinky tail, to complete normality. The neural tube defects can be modified by environmental factors. Excess vitamin A increases the incidence, but low doses given at a particular stage of gestation can prevent the abnormalities (Seller and Adinolfi 1981). The exencephaly and spina bifida are manifested independently of the maternal environment (Seller et al 1981) Maint. by Lac. \par CTA \par Inbr. 65. Albino: \i a,b,c,Cts. \i0 Origin: Cateract mutation (Ohtori et al 1968) in a stock of unstated origin. Maintained by Idr. \par CWD \par Inbr (Le) 53. Non-agouti dilute: \i a,d,cw \i0 (curly-whiskers). Origin:\i cw\i0 arose in CBA/Cbi at Chester Beatty Res. Inst. To Harwell. Stock T11H from A.G.Searle to J in 1971. Crossed to B6C3Fe-\i a/a\i0 F1 then to DBA/2, then inbred. \par Characteristics \par Like AKR, HRS and C58, each of three CWD lymphomas produced infectious xenotropic murine leukemia virus related to endogenous xenotropic provirus \i Bxv1\i0 (Massey et al 1990). However, in a later study the majority of CWD tumours contained recombinant viruses which lacked \i Bxv1\i0 specific sequences (Massey et al, 1994). \par Maint. by Le. \par CXA-1 (reserved symbol) \par CXB- \par Inbr (By) 91. Set of seven Recombinant Inbred Strains (CXBD,E,G,H,I,J,K) developed by Bailey from a cross of BALB/c x C57BL/6J. CXBH and CXBK have high and low levels of opiate receptors, respectively (Marek et al 1990, Elmer et al, 1995). Absence of corpus callosum similar to the BALB/c parent in CXBG. This is associated with slow growth of the medial septum subadjacent to the cavum septi. See also strains I/LnJ and BALB/c) (Wahlsten and Bulman-Fleming, 1994). Maint. by By. \par CXS- \par Set of 14 recombinant inbred strains developed by A from a cross of BALB/cA x STS/A (Hilgers and Arends (1985). Maint. by A. \par D103/Ms \par Inbr: 57. Genet: \i A, B, \i0 c. Origin: Derivative of DM 1956. \par Characteristics \par High transplantability of MY-mouse tumour (Tajima, 1968). \par DA/Hu \par Inbr: 91. Albino. Genet: \i c\i0 \i rd. \i0 Origin: Hummel 1948 from `Swiss' mouse with mammary tumour. \par Characteristics \par Low mammary tumour incidence. Partitioned vaginas common. High serum complement activity (c.f. 8/26) (Ong et al 1989) \par \par DBA \par rey: \i a,b,d.\i0 Origin: Little 1909 from stock segregating for coat colour. Oldest of all inbred strains of mice. In 1929-30 crosses were made between substrains, and several new substrains established, including the widely used substrains /1 and /2. Differences between the substrains are probably too large to be accounted for by mutation, and are probably due to substantial residual heterozygosity following the crosses between substrains. Thus DBA/1 and DBA/2 differ at least at the following loci: \i Car2, Ce2, Hc, H2, If1, Lsh, Tla,\i0 and \i Qa3.\i0 With such large differences, they should probably be regarded as different strains rather than substrains of the same strain. In this listing the two are listed separately. DBA/LiA differs from /1 and /2 at the \i Gpd1\i0 locus, and is similar to DBA/2 at the \i Tla\i0 locus. Note that unfostered substrains carry the mammary tumour virus and have a high indicence of mammary tumours. \par \par Main substrains are: \par \par DBA/LiA \par Inbr(A) ?+126. Origin: Little to Amsterdam circa 1932. Maint. by A. \par \par DBA/1 \par Inbr (J) ?+117. Origin: Substrain maintained by Little at the Jackson Laboratory. Maint. by J,N,Ola. \par \par DBA/2 \par Inbr (J) 150. Origin: Substrain maintained at the Jackson Laboratory. Maint. by J,N, Ola. \par \i Characteristics of substrains other than DBA/1 and DBA/2:\i0 \par Ehling (1964) reported sensitivity to X-irradiation (1/5). Lung adenomas 1-11% in DBAf/A, and leukaemia 0-% in DBA/LiA and 5-8% in DBAf/A (Muhlbock and Tengbergen, 1971). DBA/Li is resistant to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 4/7) (Evans \i et al\i0 ., 1977). \par DBA/1 \par For origins see DBA \par \i Behaviour\i0 \par High food drive (4/15) and high open-field activity (4/15) (Thompson, 1953). Low open-field activity (11/13) (Bruell, 1964). Good performance in food-seeking task (2/6) (Henderson, 1970). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (23/26) (Lush 1988). \par \i Life-span and spontaneous disease\i0 \par Primary lung tumours 3% in males, 1% in breeding females and zero in virgin females; lymphatic leukaemia less than 1%. Mammary adenocarcinomas zero in males, 90% in breeding females and 61% in virgin females in unfostered substrain (Hoag, 1963). A high proportion of the mammary tumours are of the acinar type (1/7) (Tengbergen, 1970). Lung tumours 2-27% (Festing and Blackmore, 1971). Low gross tumour incidence in males (19/22) (Storer, 1966). \par \par Life-span of males short in conventional conditions (6/22 = 433 days) but long in females (21/22 = 750 days) (Storer, 1966). Life-span in SPF fostered conditions also short in males (5/17 = 487 days) and long in females (13/17 = 686 days) (Festing and Blackmore, 1971). \par \i Normal physiology and biochemistry\i0 \par High serum ceruloplasmin levels (1/26 males, 2/27 females) (Meier and MacPike, 1968). High plasma cholinesterase activity in females (2/22) (males not measured) (Angel \i et al\i0 ., 1967). Low liver tyrosine aminotransferase in fasted mice (8/10) (Blake,1970). Low cell turnover as estimated by slow clearance of DNA-bound radioactivity (17/17) (Heiniger \i et al\i0 ., 1972). Low venous (10/10) and arterial (8/10) blood pH (Bernstein, 1966). \par \i Anatomy\i0 \par Low brain weight (15/18 males, 18/18 females) (Storer, 1967). High erythrocyte count (1/18), low mean corpuscular volume (17/18) (Russell \i et al\i0 ., 1951). Large number of Peyer's patches (1/7) (Hummel \i et al\i0 ., 1966). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to induction of subcutaneous tumours by 3-methylcholanthrene (14/14) (Kouri \i et al\i0 ., 1973), (12/12) (Whitmire \i et al\i0 ., 1971). \par Sensitive to X-irradiation (21/27) (Roderick, 1963). Males have a long sleeping time under hexobarbital (15/15) (Lovell, 1976), long sleeping time under pentobarbitone anaesthetic (23/23), Lovell (1986). Insensitive (eosinophil response) to cortisone acetate (cf. 3/6) (Wragg and Speirs, 1952). Sensitive to teratogenic effect (cleft palate) by cortisone acetate (2/6) (Kalter 1981). Sensitive to seizures induced by nicotine (19/19) (Marks et al 1989). Clonidene induces a strong aggressive behavioural response (2/9) (Nikulina and Klimek, 1993). \par \i Immunology\i0 \par Low lymphocyte phytohaemagglutinin response (42/43) (Heiniger \i et al\i0 ., 1975). Poor immune response to ovomucoid, but good response to ovalbumin (cf. 6/12) (Vaz \i et al\i0 ., 197 l). Good primary immune response to bovine serum albumin (2/6) (James and Milne, 1972). Good primary immune response to sheep erythrocytes (2/6 for haemagglutinin response at 3 x 10\up8 7\up0 , 3 x 10\up8 8\up0 and 3 x 10\up8 9\up0 dose levels, 1/6 for haemagglutinin response at 3 x 10\up8 8\up0 dose only) (Ghaffar and James, 1973). Non-discriminator between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). Poor immune response to (Pro-Gly-Pro)\dn8 n\dn0 (cf. 6/7) (Fuchs \i et al\i0 ., 1974). High susceptibility to IgG\dn8 1\dn0 -mediated (2/12) but low susceptibility to IgE-mediated (10/12) passive cutaneous anaphylaxis (De Souza \i et al\i0 ., 1974). Good immune response to \i Salmonella strasbourg\i0 lipopolysaccharide (2/7) (Di Pauli, 1972). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Injection of heterologous type II collagen induces arthritis (Courtenay et al, 1980). \par \i Infection\i0 \par Susceptible to \i Mycoplasma fermentens \i0 (2/6) (Gabridge \i et al\i0 ., 1972). Resistant to \i Plasmodium berghei \i0 infection (8/8) (Most \i et al\i0 ., 1966). High mortality in a natural epizootic of ectromelia (2/8) (Briody, 1966). Rapid immunological expulsion of \i Trichinella spiralis \i0 worms (Wakelin and Donachie 1980). Susceptible (2/7) to the development of chronic Chagas' cardiomyopathy in postacute \i Trypanosoma cruzi\i0 infection (Rowland et al 1992). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in a multivesiculation form of hyatid development (cf 4/9). Protoscoleces are well developed (Nakaya et al, 1997). \par \par \i Reproduction\i0 \par Poor breeding performance (20/22), colony output 0.77 young/female/week, litter size 4.4 weaned (19/25) (Festing, 1976a). \par \i Miscellaneous\i0 \par Recommended host for the following transplantable tumours: anaplastic carcinoma dbrB, mammary adenocarcinomas CaDl and T1703, melanoma S91 and pleomorphic sarcoma S37 (which is not host-specific) (Kaliss, 1972). \par An embryonic stem cell line has been developed by Roach et al (1995). \par High incidence of spontaneous `deviants' (possible mutations) (4/21) (Schlager and Dickie, 1967). \par \par DBA/2 \par For origins see DBA \par \i Behaviour\i0 \par Low alcohol preference (4/4) (Fuller, 1964b), (18/18) (Rodgers, 1966), (5/5) (McClearn, 1965). High severity of ethanol withdrawal symptoms compared with C57BL/6, possibly associated with differences in neuroactive steriod sensitivity (Finn et al, 1997). High shock-avoidance learning (2/9) (Bovet \i et al\i0 ., 1966), (1/9) (Bovet \i et al\i0 ., 1969). Low avoidance conditionability (7/9) (Royce, 1972). Long time of immobility in a forced swimming test (3/9) (Nikulina et al 1991) Low shuttle-box avoidance (4/5), high wheel activity (Messeri \i et al\i0 ., 1972). Good long-term memory compared with C3H/He (Bovet \i et al\i0 ., 1969). Slow extinction of learned conditioned avoidance response (7/7) (Schlesinger and Wimer, 1967). Susceptible to audiogenic seizures (2/11) (Fuller and Sjursen, 1967). Long latency to attack crickets (6/7) (Butler, 1973). High rearing (1/7), low defaecation (6/7) in Y-maze (McClearn \i et al\i0 ., 1970). Low locomotor activity when grouped (6/6) but not when single (3/6) (Davis \i et al\i0 ., 1967). Low social dominance of males in competition for females (6/6) (DeFries and McClearn, 1970). Low balsa-wood gnawing activity (4/16) Fawdington and Festing (1980). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (20/26) (Lush 1988). \par DBA/2 mice failed to react to a spatial change of objects in an open field, and therefore resemble rats with dorsal lesions of the hippocampus. They may represent a model of hippocampal dysfunction (Ammassari_Teule et al, 1995). Feed restriction for nine days causes a high incidence of stereotypic cage cover climbing (contrast C57BL/6) (Cabib and Bonaventira, 1997). \par \i Life-span and spontaneous disease\i0 \par Primary lung tumours l% in males, 2% in females. Lymphatic leukaemia zero in males, 2% in females and 3% in virgin females. Mammary adenocarcinomas in unfostered substrains l% in males, 72% in breeding females and 48% in virgin females (Hoag, 1963). A high proportion of mammary tumours are of the acinar type (1/7) (Tengbergen, 1970). Overall tumour incidence 15% in males, 49% in females, including lymphomas 10% in males and 12% in females; mammary tumours zero in males and 31% in virgin females (Smith \i et al\i0 ., 1973). Leukaemia 3% (Myers \i et al\i0 ., 1970). \par \par Long life-span in SPF fostered conditions (12/17 = 629 days in males, 15/17 = 719 days in females) with 6-35% liver and 1-23% lung tumours (Festing and Blackmore, 1971). Long life-span in conventional conditions (21/22 = 707 days in males, 20/22 = 714 days in females) (Storer, 1966). Life-span 722_30 days in males and 683_26 days in females (Goodrick, 1975). \par \par High incidence of expression of RNA tumour virus group-specific antigen (2/5) (Diwan \i et al\i0 ., 1973). Type B reticulum cell neoplasms 18% at about 20 weeks (Dunn and Deringer, 1968). \par \par Spontaneous calcified heart lesions progress with age. 90% of individuals affected by 1 year (Rings and Wagner, 1971). Incidence of calcareous heart lesions high (1/5) among some related strains (Di Paola \i et al\i0 ., 1964). Dystrophic cardiac calcification may be related to disturbed myocyte calcium metabolism (Brunnert, 1997). Chronic hypertropic gastritis, duodenal polyps and calcareous pericarditis frequently observed. Other lesions include malignant lymphoma and degenerative processes in the myocardium, skeletal muscle, subcutaneous adipose tissue, cornea and blood vessels. Lesions partly depend on diet (Hare and Stewart, 1956). \par Carry three separate recessive genes similar to those found separately in C57BL/6J, BALB/cBy and WB/ReJ, causing age-related hearing loss (Willott et al, 1995). \par \i Normal physiology and biochemistry\i0 \par High metabolic rate (1/18) (Storer, 1967). High metabolic rate at 26C (1/6) (Pennycuik, 1967). High cell turnover as estimated by rapid clearance of DNA-bound radioactivity (4/17) (Heiniger \i et al\i0 ., 1972). High proportion of paradoxical (REM) sleep (2/9) (Pagel \i et al\i0 ., 1973). \par \par High concentration of epinephrine and norepinephrine in adrenals (1/5) (Ciranello \i et al\i0 ., 1972). Low Na/K ratio in erythrocytes (9/9) but high ratio in plasma (1/9) (Waymouth, 1973). Arterial blood has a high pH (2/10) (Bernstein, 1966). Low concentration of prostaglandin F in epididymis (5/6) (Badr, 1975). High plasma cholinesterase (5/22 in females, 8/22 in males) (Angel \i et al\i0 ., 1967). Low liver tyrosine aminotransferase activity in fasted mice (9/10) (Blake, 1970). High calcium uptake by the heart (1/5) (Mokler and Iturrian, 1973). High sensitivity to thyrotropin (3/21) (Levy \i et al\i0 ., 1965). High coumarin hydroxylating ability (cf. 4/13) (Lush and Arnold, 1975). High coumarin hydroxylase activity (1/8) in both sexes (Van Iersel et al, 1994). Low N'-methylnicotinamide oxidase activity in both sexes (7/7) (Huff and Chaykin, 1967). High serum haptoglobin level (1/11) (Peacock \i et al\i0 ., 1967). Low hepatic benz (alpha) pyrene hydroxylase activity (6/6) (Kodama and Bock, 1970). High hepatic delta-aminolaevulinate dehydratase activity (2/8) (Doyle and Schimke, 1969). Low aldehyde and alcohol dehydrogenase activity compared with C57BL/6 (Sheppard \i et al\i0 ., 1968). High hepatic delta-aminolaevulinic acid synthetase activity after DISC treatment (2/15) (Gross and Hutton, 1971). High hepatic urokinase activity (1/6) (Hanford \i et al\i0 ., 1974). High basal level of growth hormone at 78 days (1/6) and low basal level of serum prolactin (6/6) (Sinha \i et al\i0 ., 1975). High brain \dn8 L\dn0 -glutamic acid decarboxylase (2/7), choline acetyltransferase (2/7) and acetylcholinesterase (1/7) activity (Tunnicliff \i et al\i0 ., 1973). Low brain sulphatide (5/5) and plasmalogen (5/5) and high brain sterol (1/5) (Sampugna \i et al\i0 ., 1975). Low brain cholinesterase (5/5) (Pryor \i et al\i0 ., 1966). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). Hyporesponsive to diets containing high levels of fat and cholesterol (9/9) (Kirk et al, 1995). Mild hypercapnia with hypoxia significantly elevated minute ventilation rate (1/8) (Tankersley et al, 1994). \par \i Anatomy\i0 \par Large testes weight (2/8) (Shire and Bartke, 1972). Low brain weight (18/18 in males, 15/18 in females) (Storer, 1967). Low brain weight (25/25) (Roderick \i et al\i0 ., 1973). Low brain weight (6/6) (Wahlsten \i et al\i0 ., 1975). High total leukocyte count (6/18), high erythrocyte count (3/18), low haematocrit (15/18), low mean corpuscular volume (18/18) and low haemoglobin (16/18 or 15/18, depending on substrain) (Russell \i et al\i0 ., 1951). \par Small forebrain (9/9), neocortex (9/9) and hippocampus volume (8/9) (Wimer \i et al\i0 ., 1969). Cerebellum has an intraculminate fissure between vermian lobule IV and vermian lobule V (the ventral and dorsal lobules of the culmen) (contrast SJL, C57BL/10 and BALB/c) (Cooper et al 1991). Large heart/body weight (1/5) (Mokler and Iturrian, 1973). High proportion of acidophilic (1/5) and low proportion of chromophobe (5/5) cells in adenohypophysis of DBA/Sy substrain (Keramidas and Symeonidis, 1973). High number of haematopoetic stem cells in bone marrow (contrast C57BL/6) (Muller-Sieburg and Riblet, 1996). High level of spontaneous sister chromatid exchange (3/4) (Nishi et al, 1993). \par Hematopoetic stem-cell pool 11-fold higher than in C57BL/6. This is largely due to loci on chromosome 1 (Mullersieburg and Riblet, 1996). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to induction of subcutaneous tumours by 3-methylcholanthrene (12/14) (Kouri \i et al\i0 ., 1973), (11/12) (Whitmire \i et al\i0 ., 1971). Resistant to induction of adenocarcinomas of the colon by 1,2-dimethylhydrazine (cf. 2/4) (Evans \i et al\i0 ., 1974). \par Resistant to teratogenic effect of 1-ethyl-1-nitrosourea (4/5) (Diwan, 1974). Phenobarbital i.p. does not induce hepatic epoxide hydrase (cf. 3/7) (Oesch \i et al\i0 ., 1973). Resistant to lethal effects of ozone (21/22) (Goldstein \i et al\i0 ., 1973). Susceptible to induction of cleft palate by cortisone (2/5) (Kalter, 1965). Good ovulatory response to 3 I.U. of PMS but zero response to 7 I.v. (Zarrow \i et al\i0 ., 1971). Low incidence of convulsions induced by flurothyl (5/5) (Davis and King, 1967). Long hexobarbital sleeping time (8/9) and low liver hexobarbital oxidase level (2/9) (Vesell, 1968). Sensitive to chloroform toxicity (cf. 4/9) (Hill \i et al\i0 ., 1975; Deringer \i et al\i0 ., 1953). Sensitive to seizures induced by nicotine (1/19) (Marks et al 1989). Sensitivity may be related to brain alpha-bungarotoxin binding, which is significantly higher in ST/b than in sensitive DBA/2 mice (Marks et al, 1996). High self-selection of nicotine (2/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996). \par High bronchial reactivity (2/6) to methacholine and serotonin (Konno et al 1993). Resistant (7/8) to daunomycin-induced nephorsis (Kimura et al 1993). High (1/10) neural sensitivity to pentylenetetrazol convulsions (Kosobud et al 1992). Sensitive (1/3) to neurotoxic effects of monocrotophos (Rao et al 1991). Low histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser ( c.f. 5/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Carries gene (\i Tpmt\i0 ) for high levels of thiopurine methyltransferase activity, catalyzing the \i S\i0 -methylation of 6-mercaptopurine and other heterocyclic and aromaticthiol compounds (unlike C57BL/6 and AKR) (Otterness and Weinshilboum 1987a,b). Resistant (contrast 5 strains) to the induction of micronuclei by polycyclic aromatic hydrocarbons, presumably due to uninducible Ah locus (Sato et al, 1987). Iron overload does not cause inhibition of hepatic uroporphyrinogen decarboxylase and uroporphyria in contrast with C57BL/10ScSn . This was not correlated with the \i Ah\i0 locus in a study involving 12 mouse strains (Smith and Francis, 1993). Resistant to hepatotoxic effects of cadmium (Shaikh et al, 1993). Low voluntary comsumption of morphine in two-bottle choice situation (13/15) (Belknap et al, 1993). Less susceptible to the development of micronuclei than BALB/c following treatment with clastogenic base analogues and nucleosides (Sato et al, 1993). Unique poor responsiveness to the antinociceptive effects of nitrous oxide, a polygenic trait (Quock et al, 1996). Nine-fold lower ED50 for haloperidol-induced catalepsy than C57BL/6, but this is not associated with numbers of cholinergic neurons (Dains et al, 1996). \par Airways hyperreactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Resistant (1/4) to rate-depressant effects of ethanol on schedule-controlled behaviour (Elmer and George, 1995). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid did not cause a high incidence of cholesterol gallstones (like AKR, SM contrast C57L, SWR, A) (Faulkner et al, 1995) \par \i Immunology\i0 \par Resistant to experimental allergic encephalomyelitis (cf. 7/18) (Levine and Sowinski, 1973). Low lymphocyte phytohaemagglutinin response (43/43) (Heiniger \i et al\i0 ., 1975). Serum antinuclear factor 26% incidence (3/17) (Barnes and Tuffrey, 1967). Poor immune response to type III pneumococcal polysaccharide (5/5) (Braley and Freeman, 1971). Good immune response to synthetic double-stranded RNA (2/7) (Steinberg \i et al\i0 ., 1971). Poor immune response to cholera A and B antigens (8/9 B, 6/8A) (Cerny \i et al\i0 ., 197 l). Poor immune response to both ovomucoid and ovalbumin (cf. 2/12) (Vaz \i et al\i0 ., 1971). Precipitating and skin-sensitising antibodies have fast electrophoretic mobility (2/6) (Fahey, 1965). Non-discriminator between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). Low anti-DNP antibody concentration (7/7) (Paul \i et al\i0 ., 1970). Poor immune response to Pro-Gly-Pro-ovalbumin (6/7) and (Pro-Gly-Pro)\dn8 n\dn0 (6/7), but good immune response to (Pro\up8 66\up0 , Gly\up8 34\up0 )\dn8 n\dn0 (1/7) (Fuchs et \i of., \i0 1974). High susceptibility to IgG\dn8 1\dn0 -mediated (1/12) but low susceptibility to IgE-mediated (11/12) passive cutaneous anaphylaxis (De Souza \i et al\i0 ., 1974). Develops a lethal form of syngeneic graft-vs-host disease when treated with cyclosporine (unlike 5 other strains) (Prud'homme et al 1991). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Poor immune response to \i Salmonella strasbourg \i0 lipopolysaccharide (5/7 to 7/7, depending on substrain) (Di Pauli, 1972). Low PHA-stimulated lymphocyte blastogenic response (5/6) (Hellman and Fowler, 1972). Low immune response to ferritin (12/16) (Young \i et al\i0 ., 1976). Resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). Resistant (11/12) to experimental autoimmune orchitis induced by two or three sc injections with viable syngeneic testicular germ cells without any adjuvants (Tokunaga et al 1993). Anti-BPO IgE monoclonal antibody failed to produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). High expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (Muthing, 1997). \par \i Infection\i0 \par Resistant to infection by \i Salmonella typhimurium \i0 strain C5 (4/7) (Plant and Glynn, 1974). Susceptible to liver fluke \i Opisthorchis felineus \i0 (1/6) (Zelentsov, 1974). Susceptible to natural intestinal helminth infection (9/10) (Eaton, 1972). Develops a chronic non-healing lesion on infection with \i Leishmania tropica, \i0 the parasite causing cutaneous leishmaniasis (Howard et al 1980). Susceptible (7/7) to the induction of dental caries due to infection with \i Streptococcus mutans\i0 (Kurihara et al 1991). Susceptible (3/7) to the development of chronic Chagas' cardiomyopathy in postacute \i Trypanosoma cruzi\i0 infection (Rowland et al 1992). Infection with larval \i Echinococcus multilocularis\i0 by transportal injection of hyatid homogenate results in well developed protoscoleces (cf 4/9) (Nakaya et al, 1997). Highly susceptible to infection with \i Pseudomonas aeruginosa\i0 with rapid accumulation of bacterial burden and high mortailty, in contrast with resistant BALB/c mice (Morissette et al, 1995). Susceptibility is associated with a delay in inflamatory response and the initiation of bacterial clearance (Morisette et al, 1996). Susceptible (2/4) to\i \i0 disseminated \i Cryptococcus neoformans\i0 (Irokanulo et al, 1995). Highly susceptible to infection with \i Candida albicans\i0 (2/6) (Ashman et al,1996). Resistant, with low amylase response to the fungus \i Paracoccidioides brasiliensis\i0 (cf 6/12) (Xidieh et al, 1994). Highly susceptible (1/17), with high mortality following infection with\i Mycoplasma pulmonis\i0 (Cartner et al, 1996). Susceptibile to infection by \i Helicobacter felis\i0 with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). \par \par Low susceptibility to BALB/Tennant leukaemia virus (10/12) (Tennant, 1965). Hyperglycaemia can be induced by encephalomyocarditis virus (cf. 2/6), which also causes diabetes mellitus (cf. 7/14) (Boucher and Notkins, 1973; Boucher \i et al\i0 ., 1975). High susceptibility to develop leukaemia on infection with Friend virus (cf. 5/Il) (Dietz and Rick, 1972). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). \par \i Reproduction\i0 \par Poor breeding performance (18/25). Colony output 0.85 young/female/week. Low litter size at weaning of 4.7 (17/26) (Festing, 1976a). Poor breeding performance (8/8). Litter size 4.2_0.3, sterility 31% (Nagasawa \i et al\i0 ., 1973). Intermediate breeding performance (13/24) (Hansen \i et al\i0 ., 1973). Corpora lutea may persist over many cycles, becoming hyalinised and calcified (Chai and Dickie, 1966). Has shorter and less regular oestrus cycles than C57BL/6J (Nelson et al 1992). Susceptible to foetal resorption resulting from restraint-induced stress when mated to C3H/HeJ males, in contrast with CBA/J and A/J. This was reduced by alloimmunization with C3H cells (McMaster et al 1993). \par \i Miscellaneous\i0 \par Recommended host for the following transplantable tumours: fibrosarcoma SaD2, lymphatic leukaemia P1534 and mammary adenocarcinoma CaD2 (Kaliss, 1972). Hybrids involving DBA/2 are recommended host for transplantable leukaemia L1210, melanoma S91 and MOPC myeloma used as models in screening potential anticancer drugs (E.O.R.T.C. Screening Group, 1972). \par \par The \i Fv2\i0 \i \up8 r\up0 \i0 \i \i0 allele appears to be lethal on the DBA/2 genetic background (Blank and Lilly, 1976). High mortality after neonatal thymectomy (5/6) (Law, 1966a). \par DC \par Inbr (Le) 100. Agouti, +. Origin: mutation to dancer \i Dc\i0 arose in an obese stock outcrossed to a BALB/c x C3H/He hybrid in 1956. One cross to C3H/HeJ, then inbred. Heterozygotes exhibit circling and head tossing behaviour but are not deaf. Homozygotes die at birth with cleft lip and cleft palate. A neurological mutation "scrambler" appeared in 1991. Homozygotes have unstable gait, with phenotype and pathology resembling reeler (Sweet et al, 1996). Maint. by Le. \par DD \par Inbr (A) 91. Albino: \i A,B,c,S.\i0 Origin: From noninbred ddN stock of Cen.Lab. Exp. Animals, Osaka University 1956, to Heston 1957 (Heston et al 1964), to Nara 1959. \par Characteristics \par Mammary tumours 84% at 7.7 months in DD, 4% at 20 months in DDfC57BL and 91% in DDfC3H at 6.7 months (Heston and Vlahakis, 1971). High serum haptoglobin level (2/11) (Peacock \i et al\i0 ., 1967). High erythrocyte catalase (2/18) (Hoffman and Rechcigl, 1971). Host for transplantable androgen-dependent mouse mammary carcinoma SS-115, which only grows in intact males (Bruchovsky and Meakin, 1973). Develop keratinized nodules and squamous cell tumours when given urethan in the drinking water (Imai et al 1984). Low spontaneous locomotor activity (1/9) (Nikulina et al 1991).Carries an incomplete proviral genome of endogenous mammary tumour virus (MMTV) on the Y chromosome (c.f. 4/10) (Nishikawa et al 1991). Clonidene failed to produce an aggressive behavioural response (cf 3/9) (Nikulina and Klimek, 1993). \par DDD \par Inbr: F 50 +. Albino. Genet: \i c\i0 . Origin: According to Tanaka Matsuzawa (1990) "Inbreeding of dd mice maintained at Denken was commenced in 1957 and the resulting inbred strain was named DDD after dd at Denken. The ancestors of dd mice had come from Germany. The process of introduction to Japan and the history of these mice were surveyed in the literatures, since the description concerning them had been confused. As a result, the following history was confirmed: the original colony of mice of an unknown size was introduced from the Hoechst Company, Frankfurt a.m. Main, Germany into the Kitasato Institute, Tokyo, Japan by Dr. Tsuneo Komatsu under the direction of Dr. Sahachiro Hata in autumn, 1928. Dr. Hata and his colleagues bred these mice to use for medical researches and called them "deutsche Maus". Their descendants (one male and one female) were shipped to the Health Institute of Manchuria Railway, Talien (currently called Dalian), China on demand of Dr. Koji Ando in 1934. Two males and eight females from the Talien colony were shipped back to Dr. Saburo Kojima, the Institute for Infectious Diseases, Tokyo, Japan in 1943. They had been maintained without crossing with another colony at the Institute, from which mice were distributed to many institutes throughout Japan between 1944 and 1960, and served as the starting nuclei of many inbred or outbred strains. The "deutsche Maus" was named dd mice after "deutsche Maus at Denken" in 1952. Thus, the mouse strains connected with dd mice usually have D, DD or dd at the head in their names." \par \par Characteristics \par Mammary tumours 8% at 14 months in virgin and 14% at 14 months in force-bred females. Mammary tumour virus carried by the strain is probably of plaque-inducing group found in DD, RIII and BR6 but not in C3H (Matsuzawa \i et al\i0 ., 1974). Develop a high incidence of heritable hydronephrosis, with a higher incidence observed in males and females. This appears to be caused by an abnormally high internal pressure in the renal pelvis leading to incomplete protection against the vesico-urethral reflex (Mannen et al 1991). Host of a very stable, transplantable pregnancy-dependent mammary tumour TPDMT-4 (Matsuzawa and Yamamoto, 1975). Resistant to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). High incidence of lethality among F1 \i Dh/+\i0 male mice resulting from a cross between DDD females and DH-\i Dh/+\i0 males, however, this is not observed in the reciprocal cross (Suto et al, 1996). \par \par DDI \par Inbr. 83. Albino: \i a,B,c,D,S.\i0 Origin: Animals from Lab. Infect. Dis. Tohoku Univ. in 1948 and 1953. Maintained by D.Takasuki (1948-63), by H. Nikaido (1960-65) and by Sadao Ishigaki since 1965. Inbreeding started in 1960, and reached F20 in 1968. Maint. by Tohi \par DDK \par Inbr: F105. Albino. Genet: \i A,B,c,D,s\i0 . Developed by K. Kondo from outbred dd stock from Institute of Infectious Diseases, University of Tokyo, in 1944. \par Characteristics \par DDK females mated to C57BL males are semi-sterile, but the reciprocal cross is fully fertile. The low `fertility' is caused by embryonic death at the morula-blastocyst or pre-egg cylinder stage 3-5 days after fertilisation. A deficit of trophoblast formation was observed. Transplantation experiments show that the defect is the property of the embryos, not the uterine environment. The DDK karyotype appears normal (Wakasugi, 1973). Tendency to diabetes (Nishimura, 1969). Nuclear transplantation experiments between hybrid eggs of BALB/c and DDK strains has shown that failure of F1 (DDK female x BALB/c male) embryos to develop is not due to the combination per se of maternal (DDK) and paternal (BALB/c) genomes but rather to an incompatibility between paternal (BALB/c) genomic contribution and DDK cytoplasm. This incompatibility does not occur between a female BALB/c pronucleus and the DDK cytoplasm, suggesting the involvement of a differential imprinting of parental genomes. (Babinet et al 1990) \par \par DDN \par Inbr. 27. Albino \i A,b,c.\i0 Origin: Outbred Jcl:ddN inbred in 1972 by R.Shoji. Selected for expression of spontaneous forefoot post-axial polydactyly found in the ddN mice. Maintained by Idr \par \par DDP \par Inbr. 52. Albino \i A,B,c.\i0 Origin: Outbred Jcl:ddN mice inbred in 1972 by Shoji. Selected for the expression of postaxial polydactyly, which is now almost 100% in both forefeet of these mice. Maintained by Idr. \par DDY \par Inbr: 72. Genet: \i a, B, c. \i0 Origin: From non-inbred dd of Institute of Infectious Diseases, University of Tokyo, 1953 (Tajima, 1968). Most suitable among 6 strains tested for the culture of (Kim et al 1992). \par DE \par Inbr: 60 +. Off-white. Genet: \i c\i0 \i \up8 e\up0 \i0 \up8 \up0 , \i A. \i0 Origin: Eaton 1940, from cross of CE/Wy x E/Gw, selected for \i c\i0 \i \up8 e\up0 \i0 \i \i0 phenotype. \par Characteristics \par High incidence of amyloidosis; have polydipsia (30-50 ml/day) and polyuria (25-45 ml/day), more noticeable in females; specific gravity of urine is 1.005. \par DF/Wf (now extinct) \par Inbr: 26. Genet: \i a\i0 \i \up8 e\up0 \i0 \i , Df/df (df \i0 is Ames dwarf.) Origin: + \i df \i0 from A. Bartke 1965, crossed with C57BL/6JNlcr, then sib-mated. \par Characteristics \par Large, vigorous; adults as well as young are jumpers. \par DH \par Inbr 32 (Jah, Aug. 1995). Genet. \i a, Dh\i0 , albino. Origin: Institute of Medical Science, University of Tokyo. C57BL/6xC3H/HeF1 mice from J were crossed with BALB/c-nu/nu once and mice with an albino coat colour were selected, and the nu gene was eliminated. Obtained by Jah in 1986. Carries the dominant hemimelia gene \i Dh\i0 (Green 1989). High incidence of lethality among F1 \i Dh/+ \i0 male mice resulting from a cross between DDD females and DH-\i Dh/+\i0 males, however, this is not observed in the reciprocal cross (Suto et al, 1996). \par DHS \par Inbr(Hok) 98. Albino: \i c.\i0 Origin: Germany to Kitasato Inst. 1910 to 1920, to Inst. Infect. Dis.(Univ. Tokyo) in 1944, to Hok 1957. b x s inbreeding started in 1957. High incidence of polydactyly. Maint. by Hok. \par DK \par Inbr (Lm) 28. Brown, non-agouti, yellow \i A\i0 \i \up8 y\up0 \i0 \i /a,b.\i0 Yellow mice turn dark (sable) at first molt. Descended from mice of TOE, By, RW and JUN stocks (Harwell). (Lamoreaux and Galbraith 1986). Maintained by Lm. \par DKI \par Inbr: F61. Albino. Genet: \i a, c\i0 . Strain developed from dd outbred stock of Central Laboratory of Experimental Animals. Inbreeding started by B. Kitasato in 1953. \par Characteristics \par Susceptible to \i Salmonella enteritidis. \i0 A congenic strain in which the gene for resistance found in C3H/He has been backcrossed to DKI has beendeveloped (Kishimoto, 1972). \par DKI-R \par Inbr (Jko) N11F36. Origin: Cross of DKI/Jko x C3H/He, followed by backcrossing to DKI with selection for a gene for relative resistance to \i Salmonella enteritidis.\i0 Maint. by Jko \par DL \par Inbr (Ra) 105. Black: a. Origin: balanced \i se,+/+,d\i0 \i \up8 l\up0 \i0 \up8 \up0 stock from Truslove to E.S.Russell, to Kelton 1958. Inbred by Kelton. Maint. by Ra. \par DLS \par Inbr: 58. Genet: \i a, d\i0 \i \up8 l\up0 \i0 \i + / + se. \i0 Origin: Mutation to \i d\i0 \i \up8 l\up0 \i0 \up8 \up0 (dilute-lethal) occurred in C57BL/Gr in 1950. Truslove to E. S. Russell 1957 as balanced stock. To Lane 1968 at F32. Carries balanced lethal \i se,+/+,d\i0 \i \up8 l\up0 \i0 \i .\i0 \par Characteristics \par Homozygous \i d\i0 \i \up8 l\up0 \i0 \i /d\i0 \i \up8 l\up0 \i0 \up8 \up0 die before weaning. Maint by Le \par DM \par Inbr. F70+10 (Shi). Albino: \i a,B,c,D,S.\i0 Origin: One pair of inbred dd mice (F69) from Ms to Shionogi Research Labs. in 1971. Coat colour genes of DM/Ms are reported to be \i A,b,c \i0 (Exp. Anim. 17:31, 1968), but this substrain is \i a,B.\i0 Maintained by Shi. \par DM/Mk \par Inbr: 42. Genet: \i c\i0 . Origin: Germany; to Kitasato Inst. about 1910-1920, to Institute of Infectious Diseases, University of Tokyo, 1944, to Hokkaido Univ. 1945. \par Characteristics \par Good reproductive performance, good nursing, docile character. substrain DM/Ms separated at F12 (Tajima, 1968). \par DMC \par Inbr: F29. Genet: \i c\i0 . Origin: A single pair obtained by Div. Labs. & Res., State Dept. Health, Albany, in 1930; interstock breeding 1930-1942, b x s 1942-1962. In 1962, two pregnant females were hysterectomised and the progeny were fostered on germ-free NIH mice. \par Characteristics \par Vigorous, prolific, extended breeding life, good longevity. Average litter size greater than seven. No spontaneous tumours; used in tumour immunology; good vehicle for ascites tumours. \par DOPG \par Inbr. 21. Agouti \i A,B,C.\i0 Origin: Wild mice trapped in Pigeon near Windsor, Ontario, Canada by M.L.Petras. Inbred by Moriwaki in 1972. Has never been crossed with wild mice. Carries rare \i H2\i0 haplotype (Sagai et al 1986). Maintained by Ms. \par DRC \par Inbr(Hok) ?+48. Albino (?). Origin: DDD mated to C57BL/6.F1 backcrossed 8 times to DDD then b x s. To Hok 1972 from Univ. Tokyo. Maint. by Hok. \par DSD \par Inbr: 44. Genet: \i A, B, c, S. \i0 Origin: From non-inbred dd stock of Institute of Infectious Diseases, University of Tokyo, in 1953. \par Characteristics \par Docile character, poor at making nest, occasional mammary tumour. (Tajima, 1968). Small litter size and low weaning rate probably due to low pituitary and placental mammotrophin secretion during pregnancy (Nagasawa \i et al\i0 ., 1972). \par DTB \par Inbr: 51. Genet: \i c\i0 . Origin: From Nara Med. Univ., 1960, at F13. substrain of DHT and DD. \par DW \par Inbr: F110 (J). Grey. Genet: \i a, ln. \i0 Carries dwarf \i (dw) \i0 mutation with forced heterozygosity.\i dw\i0 mutation arose in a stock of silver mice obtained by Snell from an English fancier before 1929. Established by Jackson Laboratory in 1966 from stock supplied by Lane. \par Characteristics \par The dwarf mutation causes a reduction in acidophils and thyrotrophin-producing cells of the anterior pituitary. Mutant mice have a variety of anatomical, cytological and physiological defects due to deficiency of anterior pituitary hormone, including reduced growth and organ development and infertility. Pituitary homografts or injections of growth hormone and/or prolactin partially reverse some of these defects. Dwarf mice are almost tumour-free, whereas their normal litter mates have a high incidence of a range of tumours. However, dwarf mice also have a shorter life-span. Deficiencies of RNA metabolism in the liver have been noted (Chen \i et al\i0 ., 1972a). Dwarf DW mice have a lower expression of group-specific antigen to endogenous C-type\i \i0 RNA tumour virus than normal litter mates, which have 45-61% incidence of reticulum cell sarcoma (Chen \i et al\i0 ., 1972b). A complete bibliography of the strain from 1967 to 1973 has been given by\i \i0 Richardson (1973). The effects of prolactin on activity of 17-beta-hydroxysteroid dehydrogenase has been studied by Musto \i et al\i0 . (1972). \par EBT \par Inbr. (Cv) 63. Yellow, belted (?) \i a,bt,e.\i0 Origin: Cross of non-inbred \i bt/bt\i0 x C57BL/Ha-\i e/e.\i0 To Chapman 1974. Maint. by Cv. \par EL \par Inbr (Yok) 84. Albino. \i c.\i0 Origin K.Imaizumi, \i El \i0 (epilepsy) mutation in non-inbred albino mice in 1954. \par Characteristics \par Epilepsy-like behaviour which can be induced by Megamide (Nakano et al, 1996). Phenobarbital suppresses the seizures dose-dependently, but zonisamide is ineffective (Nagatomo et al, 1996a). Seizure susceptibility may be due to a reduced number of nitric oxide-producing cells in the hippocampal area (Nagatomo et al, 1996b) Maint. by Yok. \par F/St \par Inbr: F140. Silver-grey with white blaze on head. Genet: \i a,\i0 \i b, c\i0 \i \up8 ch\up0 \i0 \i , d, s. \i0 Origin: Strong 1926 from a group of unpedigreed Bussey Institute mice. \par Characteristics \par High leukaemia in older mice. Resistant to fibrosarcoma induction by methylchol-anthrene (14/15 in males, 15/15 in females) (Strong, 1952). Low balsa-wood gnawing activity (1/16) Fawdington and Festing (1980). \par FL/1 \par Inbr (Brk) 93. Black \i a\i0 ,\i f, rd\i0 . Origin: \i f,\i0 flexed-tail gene (causing microcytic anaemia) originally obtained from Jay came from Snell's WA linkage testing stock. Seven rounds of cross-intercross to C3H by Jay and E.S. Russell. Outcross to WB/Re by Re, with b x s mating of \i f/f\i0 progeny started in 1956. Charac. Foetuses and new-born \i f/f\i0 mice show a transient siderocytic anaemia which is cured by 14 days. Variable belly spotting and tail flexure. Good breeding performance when young, later impared by obesity. Maint. by Brk. \par FL/4 \par Inbr(Mob): N30F46. Origin: see FL/1. Separated from FL/1Re-\i f/+W/+\i0 at N30 in 1968. In 1980 fostered onto C57BL/6J. Maint. by Mob. \par FM \par Inbr: 31. Genet: Pink-eyed. Origin: From Ueno Zoo to Dept. Zool., Kyushu Univ., to Natl. Inst. Genet., to Inst. Infect. Diseases, Univ. Tokyo. Inbreeding started in 1958. (Supposed to have originated from mongrels of Japanese fancy mice.) \par Characteristics \par High incidence of mammary tumours. (Tajima, 1968). \par FRG \par Inbr. (Tbr) 35: Albino (?). Origin: Non-inbred dd mice Chugai Lab. to Tbr 1981 at F26. Resistant to Friend leukaemia virus. Maint. by Tbr. \par FS \par Inbr (Dn) 77. Fawn: \i b,c\i0 \i \up8 ch\up0 \i0 \i ,fr,p.\i0 Origin: Snell linkage testing stock to M.C Green to Eicher 1971, to Davisson 1983. Carries the pink-eyed dilution gene, \i p\i0 , which is derived from Asian mice of the \i Mus musculus\i0 type (see also strains 129/J, P/J and SJL) (Brilliant et al, 1994). Also carries \i sh1/sh1.\i0 Maint. by Dn. \par FSB \par Inbr (Dn) 98. Black \i a, fs.\i0 Origin: furless mutation \i fs\i0 arose in unpedigreed stock at Ohio State University in 1951. Mutant females mated with C57BL/10 males. Charac. Low fecundity and viability. \i fs/fs\i0 mice grow a normal coat, but this thins at about 19 days. A new coat grows but persists only a short time. Mature mice are partly devoid of hair at all times. All types of hairs are shorter than normal (Green, 1954). Maint. by Dn. \par FTC \par Inbr (U) ?+77. Light-grey with pink eyes: \i a,b,p.\i0 Origin: Formerly called CPB-FT. CPB-TNO (1950) to Vet. Fac. Utrecht in 1973. About 8% of newborn show neonatal jaundice probably due to temporary inability to breakdown bilirubin. About 50% tail kinks. Maint. by U. \par FVB \par Inbr. F38. Albino,\i A,B,c,D,P\i0 . Origin: Outbred N:GP (NIH General Purpose) Swiss mice established at the National Institutes of Health in 1935. In 1966 two strains (HSFS/N and HSFR/N) were selected for sensitivity and resistance, respectively, to challenge with histamine following pertussis vaccination. In the early 1970s a group of mice at the eighth inbred generation of HSFS/N were found to carry the \i Fv1\i0 \i \up8 b\up0 \i0 \up8 \up0 allele for sensitivity to the B strain of Friend leukaemia virus. Homozygous mice were then inbred as strain FVB, without further selection for histamine sensitivity (Taketo et al 1991). Rowe (NIH) to Amsterdam, 1978. \par Characteristics \par Strain is useful for the production of transgenic mice on a fully inbred genetic background. They have a vigorous reproductive performance with large litters. Fertilized eggs contain large and prominant pronuclei which facilitate the microinjection of DNA, and following injection survive as well as C57BL/6 x SJL F1 hybrids, and much better than pure-line C57BL/6 (Taketo et al 1991). The strain has been typed at at least 44 marker loci on 15 chromosomes. Relatively insensitive to the initiation of papillomas following initiation by 7,12-dimethylbenz(a)anthracene and promotion with 12-o-tetradecanoylphorbol-13-acetate (TPA), but a high proportion progress to carcinomas (Hennings et al, 1993). A new strain 129-derived embryonic stem cell line, H3. gives good levels of germ-line transmission in chimeras involving FVB (Kim et al, 1996). \par 60% survival to 24 months of age in both sexes with 55% and 66% gross tumour incidence in males and females, respectively at that time. Most common tumour types were lung alveolar-bronchiolar, hepatocellular, subcutis neural crest and Harderian gland adenomas in males and lung, pituitary, ovarian, lymphomas, histiocytic sarcomas, Harderian gland adenomas and pheochromocytomas in females (Mahler et al, 1996). Maint. by N, A, J. \par G/Gw \par Inbr: 75 +. Origin: Goodale, selected for body weight, to Gowen at Iowa State; b x s inbreeding; to Nash at Colorado State 1967. \par Characteristics \par Hyperglycaemic, with mean plasma glucose levels of 230 mg/100 ml at 60 days, at which time males are about 41 g and females 35 g. Normal response curve following i.p. glucose tolerance test and no gross pathological changes with aging (Nash and Logsdon, 1974). \par GL \par Inbr (Le) 50. Agouti: \i +.\i0 Origin: mutation to grey-lethal (\i gl\i0 ) discovered in a stock segregating for \i c\i0 \i \up8 e\up0 \i0 \up8 \up0 by Gruneberg in 1935. From G to Jay to M.Dickie to P.Lane who inbred to F25, then one outcross to \i dl\i0 \i \up8 J\up0 \i0 \i /dl\i0 \i \up8 J\up0 \i0 \i \i0 (downless, closely linked to \i gl\i0 and used as a linked marker), and b x s mating as a balanced stock. Maint. by Le \par GLF \par Inbr (Y): F65. Agouti, +. Origin: From Jax as bearers of grey lethal mutation; selected for the normal genotype by progeny testing. Maint. by Y. \par GRS \par Inbr (A) 101. Albino \i a,c.\i0 Origin:Formerly called GR/A. Muhlbock 1965 from outbred mice obtained from Grumbach in Zurich. \par Characteristics \par Breeding females have a high incidence of mammary tumours which are highly hormone-responsive. Carries a mammary tumour agent different from MTI, transmitted by milk and gametes, which is not eliminated by foster nursing. Hormone-dependent tumours are also produced in GRS x RIII F\dn8 1\dn0 hybrids (Muhlbock, 1965; van Nie and Thung, 1965; Brcand and Daehnfeldt, 1973). High incidence of hepatomas in mice treated with normal horse serum or horse-anti-mouse antilymphocyte serum (Den Engelese \i et al\i0 ., 1976). Leukosis 11% (Hilgers and Galesloot, 1973). Susceptibility to mammary tumour induction with progesterone and oestrone in ovariectomised mice may be due to a single gene, although linkage with eighteen marker loci could not be established (van Nie and Hilgers, 1976). Resistant to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). \par GT \par Inbr (Le) 28. Breeders are agouti:\i A,gt/+;gt/gt\i0 are light grey with white belly spot and have tremors like myelin deficient mice. Origin: Developed by Lane. \i gt\i0 mutation arose in strain HYIII/Le in 1977 at F55. One outcross to C3HeB/FeJ x C57BL/6-\i A\i0 \i \up8 wJ\up0 \i0 \up8 \up0 F1, then bxs. Has a spontaneous spongiform encephalopathy whose expression is determined by the interaction of genetic factors and an unconventional unrecognised transmissible agent (Sidman et al 1985). The strain is maintained only as frozen embryos by Dr. T Cunliffe-Beamer. \par H1 \par Inbr. F30 (1993). Black agouti. Origin: DeFries from a cross between BALB/c and C57BL/6 followed by selection for high open-field activity. \par H2. \par Inbr. F30 (1993). Black agouti. Replicate of strain H1. \par HC \par Inbr (U) ?+82. Light grey (?): \i b, d, p.\i0 Origin: CPB-TNO (about 1950) to Vet. Fac. Utrecht in 1973. Most females have one pair of supernumary (non-lactating) nipples lateral from pair IV. Hyporesponder to dietary cholesterol. Maint. by U. \par HDA32 \par Inbr (Thb) F22 (Sept. 1995). Albino. Origin: Institut fuer Tierproduktion, Technical University, Berlin (now Institut fuer Grundlagen der Nutztierwissenschaften (now part of Humboldt-University)). From many sources including inbred strains and pet shop mice from Berlin, Bavaria and Denmark (Weiniger et al 1974, Mukherjee et al 1976). One of 15 strains developed from the same base population. Carries a new mutation provisionally designated \i sht\i0 causing short hair. \par HLC \par Inbr 47. Colour ?. Origin: from hybrid stock derived from crosses involving C57BL/6J, C57BR/cd, A/J, BALB/c, LG, and SM. Selected for high leukocyte count (strain LLC was selected for low leukoctye count). Mean total leukocyte count 36,000 in males to 38,000 in females. Thymus and spleen weights much higher than in strain LLC. Maint. by Harrison (J). \par HLG \par Inbr. >30 (1993). Albino, \i A,B,c,D.\i0 An inbred strain in 1938 at the Inst. of Radiology, Univ. of Freiburg. To Heiligernberg in 1945, then returned to Freiburg in 1950. In 1982 to Inst. of Radiation Biology, University Clinic Essen, Germany. Brother x sister mating started in 1985 by Dr. D. Buttner. Defined at 22 biochemical loci. High fat content, especially in older females. Good breeding performance. Used because of its synchrony in early embryonal development (Molls et al 1983). High incidence of spontaneous and radiation-induced congenital malformations (Pampfer and Streffer 1988). High incidence of gastroschisis, a herniation of the abdominal viscera with umbilical ring disruption and intestinal evisceration following X-ray exposure of the zygotes (Hillebrandt et al, 1996). \par HLS \par Inbr. F75. Albino. Origin: Stock from Univ. of California (Dr. Epstein) to Yokohama Univ. to Hok in Jan 1967 at F40. Crossed several times to SWJ/Hok, then sib mating. Hairless. Maintained by Hok. \par HPG \par Inbr (Bm) 21. Agouti.Origin: WG Beamer, 1988 following hysterectomy and fostering on B6D2 of a stock carrying \i hpg\i0 (hypogonadal) mutation obtained from Bruce Cattanach. Maintained by Bm. \par HPT \par Inbr (Le) 26. Agouti, segregating patchy coat; \i A, Hpt/+.\i0 Origin: Priscilla Lane 1988 from a spontaneous mutation (\i Hpt\i0 , hair patches, MNL 65:29) which arose in a segregating hybrid (C57BL/6JxC3HeB/FeJLe-a/a) background at N3 in 1979. \i Hpt\i0 was backcrossed three times to this hybrid, then inbred. Maintained by Le. \par HR/De \par Inbr: F78 +. Pink-eyed dilute strain carrying hairless mutation. Genet: \i p\i0 , \i hr \i0 with forced heterozygosity. Inbred by Deringer from \i hr \i0 stock received from Carnochan in 1948. \par Characteristics \par Haemangioendotheliomas 19-33% (Heston, 1963). Skin papillomas in 3-9% of hairless animals at 18-22 weeks (Murphy, 1966). High incidence of haemangioendotheliomas (54-76%) in mice treated with 4-0- tolylazo-Otoluidine (Heston, 1963). Sensitive to chloroform toxicity (cf. 4/9) (Deringer \i et al\i0 ., 1953). Type B reticulum-cell neoplasms at 20 weeks 12% (haired) and 8% (hairless) (Dunn and Deringer, 1968). \par HRA.HRII-c/+ \par Inbr (Skh) F30N11. Albino and pigmented (thought to be \i a,b,c\i0 or \i C,hr\i0 ). Origin: PD Forbes by backcrossing outbred pigmented mice to the HRA/Skh strain (F?+30, homozygous for hr) with selection for both pigmented and albino hairless offspring. Strain homozygous for the \i hr\i0 gene. Comparative immune responses of HRA/Skh described by Smith et al (1982). \par HRS \par Inbr. F79 (J). Albino, \i b,c,d.\i0 Origin: Hairless (\i hr\i0 ) stock from Crew to Carnochan to Heston to Chase, to E.L.Green 1952, to Les 1956, to M.C.Green 1959, to J 1964. Maintained by mating \i +/hr\i0 females with hr/hr males. \par Characteristics \par Homozygous hairless mice lose their hair at about 10 days. The complete hair is lost from the follicle. After a time a few thin fuzzy hairs grow again, but are soon lost. These are exclusively guard hairs. There is hyperkeratosis of the stratified epithelium and the upper part of the hair canals. Hair club formation is abnormal and the lower part of the follicles tends to separate from the upper part. The isolated lower parts develop into cysts, which may become large and numerous (M. C. Green, 1966). About 45% of \i hrhr \i0 mice develop leukaemia by 8-10 months compared with only 1% in \i hr\i0 /+ mice. Graft versus host assay shows that \i hrhr \i0 mice are immunologically hyporesponsive, which may be associated with the high leukaemia incidence (I'Anson and Gasser, 1973). Similarly, Heiniger \i et al\i0 ., (1974) found 70% leukaemia at 8 months in \i hrhr \i0 mice but only 20% in \i hr\i0 /+. Difference thought to be due to a functional immune deficiency. Large kidney/body weight ratio (1/21) (Schlager, 1968). High lymphocyte phytohaemagglutinin response (13/43) (Heiniger \i et al\i0 ., 1975). \par HSFR \par Inbr ?. Albino \i c.\i0 Origin: N:NIH outbred stock selectively bred for resistance to the action of histamine after treatment with \i Bordetella pertussis.\i0 Maint. by N. \par HSFS \par Inbr. ?. Albino \i c.\i0 Origin: As HSFR, but selected for sensitivity. Maint. by N. \par HTG \par Inbr: F? 131. Cinnamon-coloured. Genet:\i A, b\i0 . Formerly called H-2G. Developed by Gorer about 1937 as an \i H2 \i0 locus recombinant from heterogeneous stock of unstated origin (Gorer and Mikulska, 1959). \par HTH \par Inbr: F?+53. Brown. Genet: \i a, b. \i0 Origin: see HTG. Formerly called H-2H. \par HTI \par Inbr: F? + 54. Black. Genet: \i a\i0 ,. Origin: see HTG. Formerly called H-2I. High incidence of whisker-eating (original observation). \par HYIII \par Inbr (Le) 83. Agouti:\i +.\i0 Origin: Mutation to hydrocephalus-3 discovered in heterogeneous stock by H.Gruneberg. To M.C.Green 1963, then b x s. To Lane 1975. Homozygous \i hy3/hy3\i0 mice die with frank hydrocephalus by 4-5 weeks. Maint. by Le. \par I \par Inbr:(N) F143. Pink-eyed fawn with variable white patches. Genet: \i a, b, d, p, s, \i0 with some substrains carrying \i ln \i0 and/or \i c\i0 \i \up8 ch\up0 \i0 \i . \i0 Origin: Strong 1926 from unpedigreed mice. Carries the b allele at the \i Phk\i0 locus, a sex-linked locus that controls level of activity of the enzyme phosphorylase kinase. This activity is virtually absent in muscle and reduced in the brain,kidney and heart in this strain. \par \i Behaviour\i0 \par Short latency to attack crickets (1/7) (Butler, 1973). High hole-in-the-wall entries (2/7), high Y-maze exploration (1/7), high number of stairs climbed (1/7), high urination (1/7) and defaecation (2/7) (McClearn \i et al\i0 ., 1970). Low alcohol preference (Rodgers, 1966). \par \i Life-span and spontaneous disease\i0 \par Spontaneous adenomatous stomach lesion occurs in nearly all mice (Heston, 1963). \par \i Normal physiology and biochemistry\i0 \par Mammary gland sensitive to oestradiol and progesterone (2/7) (Singh \i et al\i0 ., 1970). Poor growth rate, and no response to fat in diet (4/4) (Fenton and Carr, 1951). Carries \i Phk, \i0 a sex-linked phosphorylase kinase deficiency leading to a 3-4-fold elevation of skeletal muscle glycogen content (Gross \i et al\i0 ., 1975). Acutely sensitive to vitamin B\dn8 6\dn0 depletion. Brief depletion which causes only moderate weight loss in other strains results in hyperactivity and convulsions followed by death. Tissue stores of B\dn8 6\dn0 are not different from normal. Sensitivity not due to malabsorption, rapid excretion or failure to form a cofactor at normal rate (Bell and Haskell, 1971; Bell \i et al\i0 ., 1971). C3HF x I F\dn8 1\dn0 hybrid used as a model of obesity and diabetes. Characterised by moderate obesity at 3-4 months, glycosuria in 50% of males but only 5% of females. Islets of Langerhans enlarged, with increased insulin levels. Abnormalities associated with hyperphagia and may be prevented by food restriction (Bray and York, 1971; Stauffacher \i et al\i0 ., 1971). Pure-line strain I resistant to dietary induction of obesity (Fenton and Dowling, 1953). Thyroid epithelial cells contain crystals in membrane-bounded dense bodies, which may be lysosomes (Neve and Wollman, 1973). Complement undetectable (Staats, 1976). \par \i Anatomy\i0 \par High leukocyte count (1/18), high red blood cell count (4/18), high haematocrit (4/18) (Russell \i et al\i0 ., 1951). Low percent carcass lipid on a high-fat diet (2/9) (West et al 1992). Corpus callosum absent in a high proportion of mice (Wahlsten and Schalomon, 1994). This is associated with slow growth of the medial septum subadjacent to the cavum septi. See also strains BALB/c and CXBG. (Wahlsten and Bulman-Fleming, 1994). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Susceptible to papilloma induction by methylcholanthrene (1/5) (Andervont and Edgcomb, 1956), but resistant to fibrosarcoma induction by methylcholanthrene (15/15 in males, 14/15 in females) (Strong, 1952). \par \i Immunology\i0 \par Low lymphocyte phytohaemagglutinin response (34/43) (Heiniger \i et al\i0 ., 1975). Low immune response to ferritin (13/16) (Young \i et al\i0 ., 1976). \par \i Reproduction\i0 \par Poor reproductive performance, with a high incidence of maternal neglect (Andervont and Edgcomb, 1956). Oocytes display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules (Albertini and Eppig, 1995). \par IAH \par Inbr: 29+. Origin: Bred in Helsinki from commercial Swiss albinos as a hobby by Ilona Ahtinen (Imanishi and M\'8a kel\'8a , 1973). \par IC \par Inbr (Le) 59. Agouti:\i +.\i0 Origin: Ichthyosis (\i ic\i0 ) gene reported by Carter and Philips in 1950, to Snell 1950, to M.C.Green 1970 to Lane 1975. Heterogenious stock crossed once to CBA followed by b x s. A \i +/+\i0 line was separated at F22. Homozygous \i ic/ic\i0 mice show abnormal clumping of chromatin in nuclei, with about 10% more DNA than in \i +/+\i0 mice. Useful as cell marker. Maint. by Le. \par Inbr ?. \par ICFW \par Inbr: F37. Albino. Genet: \i c\i0 . Strain developed from outbred CFW stock by Festing in 1965. \par Characteristics \par Sensitive to Warfarin (2/12) (Lush and Arnold, 1975). Short sleeping time under hexobarbital anaesthetic (2/15 in males, 5/15 in females) (Lovell, 1976), short sleeping time under pentobarbitone anaesthetic (2/23), Lovell (1986). Good reproductive performance (2/25), with colony output 1.5 young/female/wk and litter size at weaning high at 6.1(4/25) (Festing, 1976a). Probably only exists as frozen embryos. \par ICGN \par Inbr. F26 (Asano, 1993). Albino. Origin: Outbred ICR stock inbred by Ogura,Takano, Yamamoto and Asano, Dept. of Veterinary Sci. NIH, Japan. All animals develop glomerular nephritis (Ogura et al 1989, 1990, 1991a,b). Initially, mice develop hyproteinemia and hypoalbuminemia with a progressive rise in urinary protein. Later the concentrations of total cholesterol, triglyceride and betalipoprotein increase. Finally there is a rapid deterioration of renal function with high blood urea nitrogen and creatinine levels (Ogura et al, 1994). \par ICR \par No details. Maint. by Cri. \par ICR/Bc (NB. Duplicate name) \par Inbr 29. Albino. Origin: BLU:Ha(ICR) outbred stock from the Institute of Cancer Research in 1958, to Arbor Scientific Co. Ltd., to UBC, Vancouver in 1977, followed by sib mating. Maint. by Bc. \par ICR/Ha (NB. Duplicate name) \par Inbr: F43 +. Albino. Genet: \i A, B, c, P, rd\i0 \i \up8 +\up0 \i0 \i . \i0 Origin: Hauschka from `Swiss Webster' stock purchased from J. C. Landis in 1947. \par Characteristics \par Litter size 8.3 _ 0.13 with 30% preweaning mortality. High intrastrain aggression. Has been typed at several polymorphic loci (Hauschka and Mirand, 1973). Susceptible to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 3/7) (Evans \i et al\i0 ., 1977). High histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser (3/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Susceptible to the anaphylactic death following an intravenous injection of bovine serum albumin into primed mice (Lei et al, 1996). \par ICRC \par Inbr ?. No details. Maint. by Cri. \par ICW \par Inbr. F44 (1993). Albino. Genet: \i c\i0 . Origin: From Jcl:ICR outbred mice obtained from CLEA, Japan with inbreeding started in 1975. Large litters. Maint. by Dr. M. Miyajima, Wakayama Med. Coll., Japan. \par IDH2 \par Inbr. F?+20 (1993). Black, \i a\i0 . Origin: F2 hybrid of C57BL/6x\i Mus musculus domesticus\i0 from Israel. Mice homozygous for Idh2\up8 b \up0 were backcrossed an unknown number of generations to C57BL/6 to give strain named ID2. Imported to Jackson Laboratory by Dr. Eva Eicher and re-named IDH2, then to Davisson. Homozygous for rare allele at Idh2 (formerly Id2\up8 50\up0 ) locus. \par IF \par Inbr: F70 (A). Black and tan. Genet: \i a\i0 \i \up8 t\up0 \i0 \up8 \up0 . Origin: G. Bonser (Leeds) 1932-1936 by selection for formation of a `wart' after tar application. \par Characteristics \par Now more susceptible than five other strains (including BALB/c and CBA) to tar, methylcholanthrene and 3,4-benzpyrene. No spontaneous mammary tumours (Bonser, 1938). Susceptible to induction of brain tumours by \i N\i0 -ethyl-\i N\i0 -nitrosourea (Searle and Jones, 1972). High incidence of spontaneous pseudopregnancy. Maint. by A. \par IITES \par Inbr: F76 (Nga). Genet: \i a, b, C, d, s. \i0 Origin: Crossbred among CS, DBA/2, NBC and ITES. \par Characteristics \par Carries new endogenous mammary tumour viruses Mtv-42-45 (Wajjwalku et al 1991). Useful for testing colour genes. \par ILS \par Inbr. F35 (1993). Brown, pink-eyed. Origin: DeFries: obtained by inbreeding a heterogeneous stock selectively bred for long duration of loss of righting reflex under ethanol-induced anaesthesia. \par IM \par Inbr. 55 (Dk). Dilute brown; \i a,b,C,d.\i0 Origin: Strain VM crossed with linkage-marker stock from Inst. Animal Genetics, Edinburgh. Inbred by Dickinson in 1969 with selection for dilute, brown, \i Sinc\i0 \i \up8 p7\up0 \i0 \up8 \up0 , and a new "lustre" mutant. \i H2\i0 \i \up8 b\up0 \i0 \i . \i0 (see also MB). Maintained by Dk. \par IOR \par Inbr (Hab) 65. Albino: \i c.\i0 Origin: R. Castillo Menendez from 1970 from outbred albino mice. High fertility, low mortality and rapid growth in tropical conditions. Tumour incidence 32%. Amyloidosis and chronic nephritis seen in old animals. 95% of old animals also develop cataracts which may be caused by a recessive mutation (Menendez and Abdraschitova 1990). Maintaind by Hab. \par IQI \par Inbr ?. Albino c. Origin: Outbred Jcl:ICR mice inbred in 1976 by Y. Yoshimura (Cent. Inst. for Exp. Anim., Japan). Maintained by Shi. \par IS \par Inbr (Dn) 42+13. Agouti: +. Origin: \i Mus musculus praetextus\i0 male caught in Israeli port x \i M.m. musculus\i0 female from laboratory stock carrying \i bt, m, b, \i0 and \i a.\i0 To Roderick, to Eicher 1971 at F42, to Dn 1983. Maint. by Dn. \par ISS \par Inbr. F35 (1993). Albino. Origin: DeFries following inbreeding of a heterogeneous stock selectively bred for duration of loss of righting reflex under ethanol-induced anaesthesia. \par ITES \par Inbr (Nga): 87. Colour ?:\i a,b,d/+,s.\i0 Origin: From cross involving CS, DBA/2, and SII in 1962. Useful for testing colour genes Relatively rediation resistant. Carries new endogenous mammary tumour viruses Mtv-42-45 (Wajjwalku et al 1991). Maint. by Nga. \par ITES \par Inbr (Nga): 87. Colour ?: a,b,d/+,s. Origin:From cross involving CS, DBA/2, and SII in 1962. Useful for testing colour genes Relatively rediation resistant. Maint. by Nga. \par IVCE \par Inbr: 48. Origin: Separated during inbreeding and selection of IVCS. \par Characteristics \par Docile; regular 4 day oestrus cycle; litter size 9; mean body weight at 21 days, females 9.2, males 9.4; at 70 days, females 25.1, males 29.9 (Nobunga, 1973). \par IVCS \par Inbr: F73 (Csk). Albino. Genet: \i a, B, c, S. \i0 Origin: From outbred ddN mice of Cen. Lab. Exp. Anim., Japan, by selective breeding for regular 4 day oestrus cycles, 1960. \par Characteristics \par Litter size averages about 9-10 with 70 day body weight about 24 g in females and 30 g in males. Mice are docile (Nobunga, 1973). Resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). \par IXBL \par Inbr: 51. Genet: \i a, B, C, D, s. \i0 Origin: Crossbred among Japanese and US stocks. \par Characteristics \par Good reproductive performance. \par J/Glw \par Inbr: F92 (Glw). Cinnamon. Genet: \i A, b. \i0 Origin: Falconer. \par Characteristics \par High frequency of cleft palate. \par JBT \par Inbr: F86 (Jd). Chocolate belted. Genet: \i a, b, bt. \i0 Origin: From Falconer's outbred JC stock. \par Characteristics \par Very low incidence of congenital malformations, except for frequent tail kinks. Susceptible to teratogenic effects (exencephaly) of methodone hydrochloride (Jurand, 1973). \par JE \par Inbr (Le) F47. Slate ruby-eyed: \i a,f,ru,je/+.\i0 Also carries \i f.\i0 Origin: Fisher to Snell 1948, to Lane 1969, b x s since 1972. Homozygous jerker (\i je/je\i0 ) females are poor breeders. Maint. by Le. \par JGBF \par Inbr (Ty) F55. Khaki: \i a,jg,+/+,bf.\i0 Origin: mutation to jagged-tail occurred in C3H/HeJ in 1960. Crossed once to C57BL/10 and b x s, then crossed once to C57BL/6J-\i bf\i0 and inbred as a balanced stock. Homozygous \i jg/jg\i0 mice are usually born dead. Ty maintains it as an RI line, Le as a balanced mutant strain. Maint. by Ty. \par JIGR \par Inbr (Dn) F65. Agouti: +. Segregates for \i gr \i0 (grizzled) and \i ji \i0 (jittery). Origin: \i ji\i0 arose in waltzing (\i v\i0 ) stock of Snell before 1957. bxs to F15. To M.C.Green in 1963 and outcrossed to \i gr/gr\i0 stock (F30). Balanced stock bxs. To Eicher 1972, then Davisson 1980.\i gr\i0 from Falconer to Snell 1950. Two crosses to CBA then bxs to F30. Cross to \i ji/+\i0 to make the balanced stock. \i ji/ji\i0 die before weaning. \i gr/gr\i0 often poor breeders. Maint. by Dn. \par JU \par Inbr: F41+60 (Ct). Albino. Genet: \i a, c.\i0 Origin: Falconer 1952, from crosses involving Goodale's and MacArthur's large strains, Bateman's high-lactation strain and various mutant stocks with about 50% of C57BL/Fa ancestry. It was the only survivor from an inbreeding experiment involving twenty lines (Falconer, 1960b). Falconer to Cattanach in 1966. \par Characteristics \par Average first litters 9; high prenatal mortality (50%) in second litters when gestation is concurrent with suckling first litter; low penetrance of \i nil. \i0 (Staats, 1976). Lm maintains a number of substrains with different pigment mutations including a non-albino \i +\i0 \i \up8 c\up0 \i0 \up8 \up0 . Maint. by Ct. \par JU/Ct-\i C\i0 . \par Inbr. N5F59 (Ct). Black, \i a\i0 ,\i C\i0 . Derived from a cross between JU female (F41) with a CBA male, five backcrosses to JU, then selection for the \i CC\i0 genotype upon sib mating. \par JU/Ct-\i C,A\i0 . \par Inbr. N5F59. Agouti, +. Origin: same as JU/Ct-\i C\i0 , but selection for the agouti phenotype upon sib mating. Charac. Background enhances expression of \i Sl \i0 and \i W\i0 \i \up8 v\up0 \i0 \i \i0 with regard to coat colour. \par K \par Inbr ?. Albino \i A,b,c.\i0 Origin: Probably from the Rockefeller Inst. in the 1930's. To Gowen, Ames in about 1937. One of four strains from Rockefeller characterised for bacterial and/or viral resistance. This strain is listed as resistant to both (though this is relative). To D.Grahn, Aregonne in 1963. Moderate resistance to S. typhimurium. Sensitive to irradiation. Long life expectancy. No special neoplasia. \par KC \par Now designated CPB-K. \par KE \par Inbr:F94 (Kw). Genet: \i a, b, c, P. \i0 Origin: Krzanowska 1952, from mice of unknown origin; cross also produced KP. \par Characteristics \par Mean litter size 6.1; low percentage of fertilised ova. 17.6% of spermatozoa have abnormal heads, the inheritance of this character being connected to the Y chromosome and may be due to a rel. deficiency of androgens (Bartke and Krzanowska, 1972). Sperm head shape, the level of sperm abnormalities and fertilizing capacity are determined largely autonomously by genes acting in the germ cells. (Krzanowska et al 1991). \par KF \par Inbr: F48 (Tbr). Albino. Genet: \i a, B, c, S. \i0 Origin. Non-inbred ddN stock of Central Lab. Exp. Anim. to Nara in 1964. \par Characteristics \par Recipient for Leydig cell tumour. \par KI \par Inbr: F141 (Glw). Genet: \i c, Ki\i0 (kink). Origin: Fuki (kinky) stock inbred by Dunn and Gluecksohn-Waelsch. \par Characteristics \par Kinky is an incomplete dominant; heterozygotes show tail abnormalities; homozygotes die before birth. Maint. by Glw. \par KK and KK/Upj-\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 /J \par Inbr: F90 +. Albino. Genet: \i a, B, c, D, S.\i0 Origin: K. Kondo 1944 from Japanese dealer stock (Kasukabe group). Some substrains carry the yellow (\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 ) gene. \par Characteristics \par Strain develops diabetes mellitus associated with insensitivity to insulin and intolerance to glucose without hyperglycaemia. When obesity is induced by nutrition, the yellow obese gene \i A\i0 \i \up8 y\up0 \i0 \up8 \up0 or gold thioglucose treatment, the mice develop hyperglycaemia accompanying marked insensitivity of adipose tissue to insulin (Taketomi \i et al\i0 ., 1973). Mice are inheritantly glucose intolerant with insulin resistance, and develop overt diabetes if they become obese due to dietary manipulation or aging (Ikeda, 1994). Mode of inheritance of glycosuria depends on both genetic and environmental factors with at least two major genes which are dominant in crosses with C57BL (Butler and Gerritsen, 1970; Butler, 1972). Moderate obesity (mature weight about 45 g) occurs by about 2 months and stabilises by 4-5 months. Carcase fat is about 33% of total. Bray and York (1971) state that the diabetes is characterised by hyperglycaemia, hyper-insulinaemia, glucose intolerance and hyperphagia, although the hyperglycaemia abates by about 1 year. Food restriction makes the animals more normal. There is an elevated pituitary growth hormone level, and significant glomerular lesions. Opperman \i et al\i0 . (1975) found that fasting results in impaired glucose tolerance. Glipizide, an oral hypoglycemic compound, improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals. (Reddi et al 1990). Senegrin-II from \i Polygala senegra\i0 significantly lowered blood glucose level in the KK-\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 mice (Kako et al,1995). Oral administration of low doses of argenine reduces kidney collagen accumulation, cross-linking, lipid peroxidation, glyoxidation, kidney weight and albuminuria. Reduction in proteinuria may be due to blocking of lipid peroxidation (Lubec et al, 1997). Weekly or every 2nd. week treatment of KK-\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 mice with Freund's complete adjuvent for 12 weeks reduced fatty changes in the liver and kidney glomerular lesions but pancreatic islet morphology was unchanged. No toxic effects were observed and it was concluded that this treatment could inhibit diabetic glomerular lesions (Muto et al, 1997). \par Interstitial fibrotic heart lesions appear at 15 weeks in untreated KK mice, and progress with age. These were completely suppressed by treatment with diltiazem. These results suggest that hyperglycemia induces an anaerobic state in heart muscle leading to hypertrophy, degeneration and fibrosis which can be ameliorated by calcium antagonists (Shimada, 1993). \par \par Corneal degeneration starts early in life, is progressive with age, tends to be bilateral, and is confined largely to the anterior part of the corneal centre (Huang and Sery, 1971). Using light and electron microscopy, the lenses of KK-\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 mice were normal at 2 months, showed some necrosis and intranuclear lesions of epithelial cells at 4 months with more marked changes at 6 and 12 months (Lu et al, 1993). The obese syndrome is also described by Stauffacher \i et al\i0 . (1971). \par \par Resistant to development of anaphylactic shock from ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). \par KP \par Inbr: F91 (Kw). Fawn (?). Genet: \i a, b, p. \i0 Origin: see KE. \par Characteristics \par Mean litter size 5.0; high embryonal and postembryonal mortality; frequent sterile matings; low sperm production and low libido of males; testis abnormalities: degeneration of some tubules and cells, large amounts of interstitial tissue (Staats, 1976). Maint. by Kw. \par KR \par Inbr: F102 (Nga). Albino. Genet: \i A, B, c, D, S. \i0 Origin: Same as KK, 1952. \par Characteristics \par Good reproductive performance; liver and kidney esterase like DBA/2; imperforate vagina 2%. \par KSB \par Inbr: F80 (Nga). Black, white patches. Genet: \i a, B, C, D, s. \i0 Origin: as KK 1944-1948. \par Characteristics \par Diabetic with consistant glycosuria in females and decreased ability to assimilate glucose in both sexes (Nishimura, 1969). \par KSN \par Inbr (Kuj) F39+23 (June 1995). Albino. Genet.\i c\i0 \i nu\i0 . Origin: A female nude mouse with good nursing ability and her litter mate obtained during the development of a DDD/1-nu/+ congenic strain, with the nude gene originating from a BALB/c-nu strain (Sudo and Suzuki, 1987, Sudo et al, 1989). Congenic strains carrying beige (\i bg\i0 ), X-linked immune deficiency (\i xid\i0 ) and both these have also been developed (Ishigaki et al, 1996). \par KYF \par Inbr. 83. Brown or chocolate with white spotting: \i a,b,C,s.\i0 Origin: KYF/Ms mice to Shoji. Maintained by Idr. \par L1 \par Inbr. F30 (1993). Albino. Origin: DeFries from a cross between BALB/c and C57BL/6 followed by selection for low activity in an open-field (see also H1, H2, C1 and C2). \par L2 \par Inbr. F30 (1993). Albino. Replicate line of L1.FB \par Inbr (Ki) F58. Colour ?. Origin: Kirschbaum, 1942-52 from multiple crosses between A,F and NH. About 50% reticular tissue neoplasms. Some myeloid leukaemia. Maint. by Ki. \par LCS \par Inbr. ?. No details. Maint. by Cri \par LDJ \par Inbr (Le) 72. Black or very black: \i a,mg/+.\i0 Also carries \i ld\i0 \i \up8 J\up0 \i0 \i /+.\i0 Origin: \i ld\i0 \i \up8 J\up0 \i0 \up8 \up0 arose spontaneously in CBA/Ca-\i se\i0 stock (M.C.Green) 1959. One cross to C57BL/10Gn, bxs to F3, outcrossed to an inbred mg/mg stock (F27), and bxs as balanced stock. To Lane 1975. The \i mg\i0 mutation arose in a cross of C3H female x Swiss stock in 1950, with bxs until 1950. Maint. by Le. \par LG \par Inbr (J) 104. Albino. Genet. \i a,c\i0 Origin: Developed by Goodale with selection for large body size begining in 1931 (Chai 1961). Two substrains, J and Ckc were separated at F27. LG/J is \i H2\i0 \i \up8 d\up0 \i0 \i , Pgk2\i0 \i \up8 b\up0 \i0 \up8 \up0 while LG/Ckc is \i H2\i0 \i \up8 ar1,\up0 \i0 \up8 \up0 \i Pgk2\i0 \i \up8 a\up0 \i0 \i .\i0 LG/J should not be confused with MacArthur's large strain which has never been established as an inbred strain and is now extinct. \par Characteristics \par Mean life-span 491 days (Staats, 1976). About 5% incidence of bent or kinked tails (Dagg, 1966). Low kidney arylsulphatase activity (12/12) (Daniel, 1976). Large brain weight (1/25) and spinal cord (1/25) (Roderick \i et al\i0 ., 1973). High serum complement activity (c.f. 8/26) (Ong et al 1989). Low lymphocyte phyto-haemagglutinin response (41/43) (Heiniger \i et al\i0 ., 1975). Large number of granule cells in right area dentata of brain (1/5) (Wimer and Wimer 1982) Maint. by J. Large body weight which differs from that of the small strain SM/J as a result of about seven quantitative trait loci at one week and 17 loci at 10 weeks of age. Each locus has a small effect (Cheverud et al, 1996). \par J substrain develops antinuclear autoantibodies and rheumatoid factor, and develop renal disease including glomerulonephritis, intersticial nephritis and perivasculitis, but not hepatic or cutaneous disease. Strain MRL/Mp has an estimated 75% of genome in common with this strain (Peng et al, 1996). \par LIBP/1 \par Inbr F60 (1993). Origin: Kunming outbred "Swiss" mice obtained from theHaffkin Medical Science Institute to China in 1946. Characterised at 26 loci by Wu et al (1992). High level of delayed hypersensitivity (1/5). Rate of Fc receptor (IgG) positive cells is lower than in C57BL/6, C3H/He or DBA/2. It is relatively sensitive to BCG, \i B. anthracis\i0 , Hantaan virus, Dyssentery bacillus, rabies fixed virus, sarcoma 180, Echerichia's ascites tumour, leukaemia cells L7712 and diabetes. A cross between LIPB/1 and BALB/c produces more and better quality ascites than BALB/c alone (Dr. Ning Lei, personal communication) \par LIS \par Inbr: F101 (A). Albino. Genet: \i c\i0 . Origin: Muhlbock, from Hyg. Inst. Zurich in 1955; closely related to STS and LTS (J. Hilgers, personal communication). \par Characteristics \par Low mammary tumour incidence in females, lung tumours in both sexes. Leukosis 6% (Hilgers and Galesloot, 1973). \par LLC \par Inbr (Ckc) 46. Colour ?. Origin: Chai 1976. Selected for low leukocyte count from a cross involving C57BL/6J, C57BR/cdJ, A/J, BALB/cJ, LG/J, and SM/Ckc (see also HLC). \par Characteristics \par Mean leukocyte count now 4000-5000/cu mm. Mice over 10-18 months have amyloid deposits in the spleen and kidney and most show reticular cell hypoplasia. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in LLC.A/Ckc (Sundberg et al 1991). Maint. by Ckc. \par LM \par Inbr. 82 (Dk). Albino: \i a,b,c,d.\i0 Also carries lustre coat, and \i Sinc\i0 \i \up8 s7\up0 \i0 \i .\i0 Origin: Outbred Moredun Research Inst., Edinburgh stock. Inbred by Dickinson in 1963. Maint. by Dk. \par LMM (was LM) \par Inbr (Bc) 49. Agouti. Origin: "C3H" mice from Rockland Farms in 1966, inbred by J.R.Miller, then outcrossed to SWV at F27, followed by sib mating. Resulting colony 1/8th. SWV, and the rest from the original stock. Homozygous for the \i lg\i0 \i \up8 Ml\up0 \i0 \up8 \up0 mutation resulting in 94% open-eyes at birth.(Note. Name changed by Editor in order to avoid duplicate name. LM above appears to have priority). Maint. by Bc. \par LP \par Inbr (J) 125. Colour: white-bellied agouti with white patches \i A\i0 \i \up8 w\up0 \i0 \i ,s.\i0 Origin: Dunn 1928 from a chinchilla stock from Castle and some coat colour stocks from English fanciers. To Scott, to Dickie 1947, to J 1949. Maint. by J. \par Characteristics \par High emotionality (4/15) (Thompson, 1953). Susceptible to audiogenic seizures (1/11) (Fuller and Sjursen, 1967). Long life-span in conventional conditions (22/22 = 748 days in males, 22/22 = 799 days in females) (Storer, 1966). Overall tumour incidence 26% in males and 30% in females, with a wide range of tumour types, including mammary tumours (14% in females, 3% in males), lymphoma (1% in males, 8% in females), lung tumours (5% in males, 4% in females) and soft-tissue sarcomas (7% in males, 6% in females) (Smith et al. 1973). High plasma cholesterol at 12 and 24 weeks (1/8) (Weibust, 1973). High serum ceruloplasmin levels in females (5/27) and males (8/26) (Meier and MacPike, 1968). Low plasma cholinesterase activity in males (19/22) (Angel \i et al\i0 ., 1967). Low hypoxanthene-guanine phosphoribosyl transferase in thalamus (7/7) (Suran, 1973). Low brain monoamine oxidase (6/7) and catechol-\i O\i0 -methyltransferase activity (7/7) (Tunnicliff \i et al\i0 ., 1973). High mean heart rate adaptation (1/7) (Blizard and Welty, 1971). Large spinal cord (4/25) (Roderick \i et al\i0 ., 1973). Small kidney/body weight ratio (17/21) (Schlager, 1968). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Highly resistant to the induction of catalepsy by haloperidol (8/8) associated with midbrain dopamine D2 receptor density levels (Kanes et al, 1993) \par Low retinal ganglion cell number (5/24) (Williams et al, 1996). \par High lymphocyte phytohaemagglutinin response (9/43) (Heiniger \i et al\i0 ., 1975). Poor immune response to ovomucoid, but good response to ovalbumin (cf. 6/12) (Vaz \i et al\i0 ., 1971). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). \par \par Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher \i et al\i0 ., 1975). \par LPT \par Inbr (Le) 89. Colour: agouti. Origin: Mutation to loop-tail (\i Lp\i0 ) arose in strain A in 1949. From W.Hollander to Snell 1950. Crossed 7 times to C57BL/6J, once to C3H/He, then b x s. To Lane 1969. Loop-tail is a semi-dominant mutation with \i Lp/+\i0 mice having crooked or looped tails and some head wobbling. Homozygotes die at birth. Maint. by Le. \par LS \par Inbr (Le) F80. Black-and-tan, or black and tan with white spots: \i a\i0 \i \up8 t\up0 \i0 \i ,ls/a\i0 \i \up8 t\up0 \i0 \i ,+.\i0 Origin: Mutation to lethal spotting (\i ls\i0 ) occurred in C57BL-\i a\i0 \i \up8 t\up0 \i0 \up8 \up0 mice at Harwell. Phillips to Lane as balanced stock in 1961. Homozygous \i ls/ls\i0 develop megacolon, but some survive and breed. Maint. by Le. \par LST \par Inbr (Bc) 63. Albino. Origin: A tabby/ circling stock from Oak Ridge circa 1957. To Katheryn F.Stein, Mount Holyoke College, Mass. to U.B.C., Vancouver in 1966 at F9. Homozygous for the \i lg\i0 \i \up8 Stn\up0 \i0 \up8 \up0 gene resulting in 99% open-eyes at birth. Maint. by Bc. \par LSXSS- \par Set of 27 recombinant inbred strains developed from a cross between outbred stocks SS and LS, selected for short and long sleeping times, respectively, under ethanol anaesthetic (McClearn and Kakihana, 1981). Mean sleeping time varies from 36 to 171 minutes in the 27 strains (DeFries \i et al\i0 1989). The set of strains has been characterised for sensitivity to pentobarbital, phenobarbital, and flurazepam as measured by sleep times (Wehner et al 1991), and for 118 SSLP genetic markers (Markel et al, 1996) \par LT \par Inbr (Sv) 121. Colour: Light brown \i a,B\i0 \i \up8 lt\up0 \i0 \i .\i0 Origin: MacDowell 1950 from a mutation at the brown locus in strain C58. Outcrossed to BALB/c. To Chase, to Re in 1957 at F28. \par Characteristics \par Ovarian teratomas occur spontaneously in about half of the females. Ultrastructurally the stem cells do not differ from those of testicular or embryo-derived teratomas (Damjanov \i et al\i0 ., 1975). Some tumours begin to develop at about 30 days and the incidence rises to 50% at 90 days. These resemble normal embryos until blastocyst stage and then become disorganised. A small percentage of ovulated eggs also develop parthenogenetically, but die at 5-7 days (Stevens and Varnum, 1974). Oocytes arrest at metaphase of meiosis I rather than progressing to metaphase II like other strains. This is a necessary, but not sufficient condition for parthogenetic activation (Eppig et al, 1996). Metaphase I arrest is frequently followed by parthogenetic activation. Oocytes typically contain a single large centrosome with microtubules being shorter than usual (Albertini and Eppig, 1995). Metaphase I arrest is associated with a sustained elevation of p34 (\i Cdc2\i0 ) kinase activity, sustained in part by restricted degradation of cyclin B (Hampl and Eppig, 1995). Oocytes ovulated at metaphase I are not capable of undergoing normal fertilisation \i in-vitro\i0 . Only 13% of such oocytes penetrated by sperm formed a diploid female pronucleus and a haploid male pronucleus by 4hr. after insemination (Maleszweski and Yanagimachi, 1995). Spontaneously digynic triploid embryos result from the fertilization of primary oocytes. These embryos develop to the forelimb-bud stage but invariably posess neural tube and cardiac abnormalities (Henery and Kaufman, 1993). Treatment with cisplatin reduced the incidence of ovarian teratomas, and those that did develop were not transplantable (Nishida et al, 1995). A locus on chromosome 6 designated \i Ots1\i0 (ovarian teratoma susceptibility) is the single major locus that increases the frequency of teratomas in a semidominant manner (Lee et al, 1997) \par LTS \par Inbr (A) 98. Albino: \i c.\i0 Origin: Muhlbock, from P.Loustalot, Ciba, Basel 1954. Maint. by A. \par Characteristics \par High mammary tumour incidence in both virgin and breeding females; closely related to LIS/A and STS/A, as deduced from isoenzyme patterns. A fostered low-tumour line, LTSfA, is also kept. Leukosis 6% in unfostered substrain and 18% in fostered substrain (Hilgers and Galesloot, 1973). \par MA \par Inbr (J): 132. Albino. Genet. \i c.\i0 Origin: Marsh's strain 3. Started from a pair of mice from the Lathrop-Loeb colony (1903-1915). 32 generations of cousin mating by Marsh, to W.S.Murray who started b x s (Murray 1963). \par Characteristics \par Primary lung tumours 37% in males, 42% in females. Lymphatic leukaemia 1% in males and breeding females, zero in virgin females. Mammary tumours zero (Hoag, 1963). Low gross tumour incidence (22/22) (Storer, 1966). Polydipsia-polyuria (Bernstein, 1966), which may be associated with cysts pressing on posterior lobe of pituitary (Russell and Meier, 1966). Life-span intermediate in both sexes (7/22 = 459 days in males, 12/22 = 585 days in females) (Storer, 1966). \par \par High metabolic rate (3/18) (Storer, 1967). High plasma cholinesterase activity in females (4/22) but low in males (18/22) (Angel \i et al\i0 ., 1967). Low liver arylsulphatase activity (11/12) (Daniel, 1976). Only strain out of 29 tested that carries the mannosephosphate isomerase \i Mpi 1\i0 \i \up8 a\up0 \i0 \i \i0 allele (Nichols \i et al\i0 ., 1973). \par \par Small spinal cord (23/25) (Roderick \i et al\i0 ., 1973). Large kidney/body weight ratio (4/21) (Schlager, 1968). Large hippocampus (2/9) (Wimer \i et al\i0 ., 1969). Fusion between left part of median lobe and left lateral lobe of liver is common (Bunker, 1959). \par \par Resistant to X-irradiation (2/27 in J substrain, 7/27 in My substrain) (Roderick, 1963). Resistant to pulmonary hyaline-membrane formation (1/10) and long survival in 90% oxygen (3/10) (Lieberman and Kellog, 1967). \par \par Highly susceptible to the mammary tumour virus, which is not normally carried by the strain (Murray and Little, 1967). \par MAS \par Inbr (A) 98. Albino. Genet. \i c\i0 . Origin: Muhlbock from same stock as GRS, and is similar to it at 48/50 biochemical loci. Maint. by A. \par Characteristics \par Low mammary tumour incidence in females, high lung tumour in both sexes. As is BALB/c, this strain is susceptible to both C3H mammary tumour virus and GRS mammary tumour virus. Very similar to GRS/A: of over 50 genetic markers, only two are different. Leukosis 22% (Hilgers and Galesloot, 1973). \par MB \par Inbr. 48 (Dk) Dilute brown; \i a,b,C,d.\i0 Origin: Strain VM crossed with linkage-marker stock from Inst. Animal Genetics, Edinburgh. Inbred by Dickinson in 1969 with selection for dilute, brown, \i Sinc\i0 \i \up8 p7\up0 \i0 \i ,\i0 and a new "lustre" mutant. \i H2\i0 \i \up8 m\up0 \i0 \i .\i0 Maintained by Dk. \par MH/Re \par Inbr: 40. Genet: \i mk\i0 /+. Origin: Jax mutant No. 63-36, B6D2F\dn8 1\dn0 -\i mk\i0 from M. M. Dickie to E. S. Russell 1963. \par Characteristics \par Segregates for compensating microcytic anaemia. All \i mk/mk \i0 are born alive; one-third to one-half die before 3 weeks, developing skin lesions and tail amputation, but surviving \i mk/mk \i0 are fertile and appear normal except for supernormal numbers of very small erythrocytes. Haematology well characterised (Staats, 1976). \par MIG \par Inbr 40 (Tif). Albino; \i c.\i0 Origin: Outbred mice from Naval Med. Res. Inst., Bethesda (NMRI) to Thubingen, 1964 to Ivanovas to Ciba-Geigy. Inbred by M.Hammerli in 1968. Good reproductive performance, docile. Maintained by Tif. \par MIW \par Inbr. 35 (Ciba-Geigy). Albino \i c.\i0 Origin: Outbred mice from Charles River, USA to Ciba-Geigy in 1967. Inbred by M. Hammerli. Maintained by Tif. \par MK \par Inbr (Ty) 78. Colour ?. Origin: Mutation to \i mk \i0 (microcytic anaemia) in descendents of a cross between C57BL/6J and DBA/2J. From M.M.Dickie to Re in 1963. Segregates for a gene, \i mk,\i0 causing microcytic anaemia in homozygotes apparently due to a generalised impairment of cellular iron uptake. Maint. by Ty. \par MM \par Inbr 84 (Dk). Albino; \i a,b,c,D.\i0 Origin: Outbred Moredun Inst. (Edinburgh) colony inbred by Dickinson in 1963. High incidence of pyelonephritis associated with \i Proteus sp.\i0 and \i Streptococcus sp.\i0 (Taylor and Fraser, 1975). \i Sinc\i0 \i \up8 s7\up0 \i0 \i ,\i0 \i H2\i0 \i \up8 a\up0 \i0 \i .\i0 Maintained by Dk. \par MO/Ko \par Inbr: 75. Origin: Kobozieff 1949, from local mice of unknown ancestry which had corneal opacity, since shown not to be hereditary. \par Characteristics \par Used for the study of longitudinal hemimelia, alopecia, periodic hypotrichosis. \par MOA \par Inbr. 50. White-bellied agouti \i A\i0 \i \up8 w\up0 \i0 \i ,B,C.\i0 Origin: Wild mice trapped in Anjo-City, Aichi Prefecture, Japan. Has not been crossed to laboratory mice. Inbred by K.Kondo in 1967. Maintained by Ms. \par MOC \par Inbr (U) ?+61. Albino: \i c.\i0 Origin: Inst. Trop. Hygiene, Amsterdam (?) to CPB-TNO in about 1957. To Vet. Fac. Utrecht in 1973. Has skeletal deformities with brachypodism. Maint. by U. \par MOLC. \par Inbr 46 (1989). Agouti. Origin: \i Mus musculus molussinus\i0 inbred by Roderick at the Jackson Lab. and originally designated MOL 3-I. Genetically distinct from common inbred strains of mice (Hilgers et al 1988). Maint. by Rk (?), A. \par MOLD. \par Inbr 50 (1989). Origin: As for MOLC. Developed from wild \i Mus musculus molussinus\i0 without any intercrossing with laboratory mice. Differs from laboratory mice at many biochemical loci and also in skeletal morphology (Festing and Roderick 1989). Low retinal ganglion cell number (1/24) (Williams et al, 1996). Maint. by Rk. \par MOLE \par Substrain of MOLD selected from F23 for intensity of white spotting phenotypes. \par MOLG/Dn \par Inbr. F17+14. White-bellied agouti , A\up8 w \up0 . Derived by Davisson from an incipient inbred strain MOLC/Rk (now extinct) at F14, itsself derived from \i Mus musculus molussinus\i0 imported from Dr. Michael Potter to the Jackson Laboratory in 1969. These mice were said to be "within one to three generations of [mice] captured in the wild." Has a very large probable duplication of heterochromatin C-band near the centromere of chr. 2. which provides a cytological marker for gene mapping of proximal end of this chromosome. \par MOM \par Inbr. 30. White-bellid agouti \i A\i0 \i \up8 w\up0 \i0 \i ,B,C.\i0 Origin: Wild \i Mus musculus molussinus\i0 mice trapped in Mizuho-District, Nagoya City, Aichi Prefecture, Japan. Inbred by K.Kondo in 1972. Has never been crossed with laboratory mice. Maintained by Ms. \par MOR2 \par Inbr (Cv) 44. Black: \i a.\i0 Origin: Wild mice trapped in Ohio by Bruell, to Shows, to Chapman 1972. Carries \i Mor1\i0 \i \up8 b\up0 \i0 \up8 \up0 gene, a mitochondrial malate dehydrogenase variant. Maint. by Cv. \par MRL and MRL/Mp-\i lpr\i0 \par Inbr (J) 65. Albino: \i a,c.\i0 Origin: Murphy from crosses started in about 1960 involving a number of standard inbred strains. Now estimated to have a composite genome of LG (75%), AKR/J (12.6%), C3H (12.1%) and C57BL/6 (0.3%). A mutation \i lpr\i0 (lymphoproliferation) was found in the 12th. generation of b x s. Homozygotes develop massive generalised enlargement of the lymph nodes and autoimmunity, and usually die at 14-16 weeks of age. \par Characteristics \par Origin and characteristics reviewed by Murphy (1981). Theofilopoulos et al (1980) have compared immune function in this and other autoimmune strains. Behavioural differences between MRL and MRL-\i lpr\i0 mice can be detected before the onset of immunological symptoms in the latter congenic strain (Sakic et al 1992). The \i lpr\i0 mutation is caused by the insertion of of the early transposable element ETn in the \i Fas\i0 gene. This causes a striking reduction in \i Fas\i0 mRNA expression and is associated clinically with marked acceleration of the lupus-like disease (Drappa et al, 1993). Diethyldithiocarbamate (DTC), an immunomodulative agent which may enhance T cells, prolongs life in autoimmune MRL-\i lpr/lpr \i0 mice, but not in autoimmune NZBxNZWF1 hybrids (Halpern and Yocum 1991). Mice with systemic lupus erythematosus (SLE) have unusual patterns of lymphocyte traffic characterised by diminished uptake of intravenously injected autoimmune cells into lymph nodes. This appears to result from defects intrinsic to the lymphocyte population and not the micro-environment. (Manolios et al 1990). Levels of circulating immune complexes rise enormously from about three months of age in MRL\i -lpr/lpr \i0 but not in MRL mice. These results corresponded to histopathological glomerular findings. (Hewicker et al 1990). Ultrastructural pathology of the thymic reticulum revealed several features in common with NZB and \i BXSB\i0 in varying degrees according to sex and age of the mice. Main anomalies included vacuolized aspect of the thymic epithelium, an increased number of macrophages, interdigitating cells and cystic cavities, the presence of a great number of plasmocytes and mastocytes and extensive interstitial fibrosis and arteriosclerosis. The most intriguing finding was the presence of crystal-like inclusions in epithelial cells (Nabarra et al 1990). Renal thrombrexane is increased in \i lpr/lpr \i0 mice, and this is temporally associated with a decrease in glomerular thrombexane binding sites without a change in receptor affinity (Spurney et al, 1993). Homozygous \i lpr\i0 mice spontaneously develop lacrimal gland inflamatory lesions and are a model of human Sjogren's syndrome. These lesions were not decreased by monoclonal anti-CD4 antibodies, though the morphology was different (Jabs et al, 1996). Serum has high concentrations of nitrite/nitrate and peritoneal cells produce markedly higher levels of interleukin 12 (IL-12) than in MRL-+/+ controls. The high capacity to produce an enhanced responsiveness to IL-12 leads to the production of high levels of NO. These are important contributory factors in the development of autoimmunity (Huang et al, 1996). \par High susceptibility of MRL-\i lpr \i0 to \i Mycobacterium leprae\i0 (contrast NOD) (Yogi et al 1989). Molecular heterogeneity of auto-anti-idiotypic antibodies has been studied by Koisumi et al (1991). \par Develop a mild spontaneous arthritis which can be enhanced by intradermal injection of complete Freund's adjuvant. This appears to be due largely to background genes rather than \i lpr\i0 (Ratkay et al, 1994). \par Embryonic stem cell lines have been established (Kawase et al, 1994). \par MRL/Mp-+/+ mice develop pancreatitis and sialoadenitis from seven months of age and also drastic thymic involution. Transplantation of allogeneic foetal thymus (from C57BL/6 mice) plus either foetal bone marrow or hematopoetic cells resulted in normal T and B cell function, and the pancreatitis and sialoadenitis was also fully corrected (Hosaka et al, 1996). \par Maint. by J, Ola. \par MS \par Inbr (A) 30. Albino. Origin: \i A,U.\i0 Aeschbacher before 1973, from 4 males of a Swiss CD-1 stock treated with methylurea. Selection based on high incidence of foetal death. Now more susceptible than other strains to several mutagens/ carcinogens. Highly susceptible to the induction of micronuclei by many chemical compared with other strains (Collaborative Study Group, 1988, Hayashi et al, 1982). Maint. by A. \par MSM \par Inbr. 20. White-bellied agouti \i A\i0 \i \up8 w\up0 \i0 \i ,b,c.\i0 Origin: Wild mice trapped in Mishima City, Shizuoka Prefecture, Japan and inbred in 1979 by Moriwaki. Has not been crossed with laboratory mice. Previously called M.MOL-MSM. Resistant to the development of lymphoma, due to at least two loci in crosses involving strain SL/Kh (Pataer et al, 1996). Fibroblast-like cells from the brains of these mice immortalise in tissue culture in a similar way to those of other strains (Yuasa et al, 1996). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-\i ras\i0 and p53, respectively (Masui et al, 1997). \par MT \par Inbr. 124. Albino \i A,B,c.\i0 Origin: Albino \i Mus musculus\i0 from Univ. Tokyo to Hok in 1946. Crossed with \i Mus molussinus,\i0 and an albino substrain separated. Inbred by S.Makino. To Idr in 1972, and maintained by R.Shoji. Various congenital abnormalities have been found including 7% exencephaly (Shoji et al, 1984). Maintained by Idr. \par MTH \par Inbr. 20. Albino: \i A,c.\i0 Origin: MT/Hok inbred in 1972 to Shoji. Carries unnamed hypotrichosis mutation. Maintained by Idr. \par MWT \par Inbr (Le) 59. Colour ?. Genet. \i a\i0 \i \up8 t\up0 \i0 \i /a\i0 \i \up8 t\up0 \i0 \i Mi\i0 \i \up8 wh\up0 \i0 \up8 \up0 / + \i W\i0 \i \up8 v\up0 \i0 \up8 \up0 / + \i T\i0 / +. Origin: M.C.Green from a heterogeneous background about 1959. Useful for linkage testing. Maint. by Le. \par MY \par Inbr (Le) 98. Chocolate: \i a,b. \i0 Origin\i :\i0 C57BR/cd female x line 85 F71 male from MacDowell in 1948. F8 male outcrossed to C3HeB/HuJ; selected for \i aa,bb\i0 in F2 generation. Carries \i my/my,\i0 but the only visible effect is missing eyes, though kidneys may also be missing. Poor breeders. Maint. as frozen embryos by J. \par MYD \par Inbr (Le) MYD is N7F12, MYD-\i +/+\i0 is F71. Agouti: \i +.\i0 Origin Mutation to \i myd \i0 (myodystrophy) occurred in 1963 in \i ls \i0 (lethal spotting) stock from R.Phillips in 1961. Crossed to C57BL/6J-\i A\i0 \i \up8 wJ\up0 \i0 \i ,\i0 then b x s. \i Os\i0 from ROP crossed \i to +/+\i0 and to \i myd/+ \i0 (N7). Maintained as \i Os,+/+,myd\i0 balanced stock. A \i +/+\i0 substrain was derived at F35. \i myd\i0 homozygotes have a progressive and diffuse myopathy of all skeletal muscles and die between 5 wks. and 5 months. Maint. by J as frozen embryos.. \par N \par Inbr (Ao): 119. Colour: dilute with white patches \i a,b,d,s.\i0 Origin: Strong, about 1926 from a group of unpedigreed mice. Ancestral to strain PBR. Resistant to carcinogens. Maint. by Ao. \par NAKED \par Inbr: 20. Genet: \i N\i0 . Origin: Falconer, Edinburgh, to Genet. Inst. Nijmegen 1958; outcrossed then inbred. \par NBL \par Inbr: 91. Genet: \i a\i0 . Origin: Probable contamination of C57BL/10Sc; should not be considered a C57BL substrain. \i N\i0 IH \i Black. \i0 \par Characteristics \par Low erythrocyte catalase activity (18/18) (Hoffman and Rechigl, 1971). Susceptible to amyloid induction (1/10) (Ram \i et al\i0 ., 1969). Good reproductive performance with 2.4 young/female/ month (3/24) (Hansen \i et al\i0 ., 1973). \par NBR \par Inbr: 61. Genet: \i a, b. \i0 Origin: From hybrids of Japanese fancy mice (Nishiki-Nezumi group) between 1944 and 1949. \par Characteristics \par Poor reproductive performance; liver and kidney esterase like DBA/2. \par NC \par Inbr: F112 (Nga). Cinnamon. Genet: \i A, b, C, D, S. \i0 Origin: K. Kondo, from Japanese fancy mice (Nishiki-Nezumi). \par Characteristics \par Leukocyte count 2.95 x 10\up8 3\up0 /ml, erythrocyte count 9.06 x 10\up8 6\up0 /ml, haematocrit 50, haemoglobin 19 g/100 ml. Liver and kidney esterase like DBA/2. Susceptible to X-irradiation; LD\dn8 50/30\dn0 547 R (Tajima, 1968). Highly susceptible to anaphylactic shock from ovalbumin (cf. 2/13) (Tanioka and Esaki, 1971). \par NCU/CpbU \par Inbr (U) ?+80. Light grey (?):\i a,b,p.\i0 Origin: CPB-TNO (1950) to Vet. Fac. Utrecht in 1973. Poor breeders, obese. Maint. by U. \par ND2/Rij \par Inbr: 29 +. Origin: Non-inbred germ-free Swiss mice from Lobund Inst., Notre Dame, 1963. \par NFR \par Inbr (N) 59. Albino. Origin: From NIH outbred stock as multiple-branch inbred from 1936, then random breeding in the 1960s. Inbred as HSFR with selection for resistance to the action of histamine after treatment with \i Bordetella pertussis\i0 in 1966, then separated as NFR in 1972. Maint. by N. \par NFS \par Inbr (N) 57. Albino a,c. As for NFR, but selectively bred for sensitivity to the action of histamine after treatment with \i Bordetella pertussis.\i0 Carries an incomplete proviral genome of endogenous mammary tumour virus (MMTV) on the Y chromosome (c.f. 4/10) (Nishikawa et al 1991). Susceptible to both acute and chronic cadmium toxicity (contrast BALB/c) (Abshire and Waalkes, 1994). A mutant substrain NFS/NJic has a mutation \i sld\i0 causing sublingual gland differentiation arrest (Kojima and Hata, 1988). When these mice are thymectomised at 3 days of age they develop autoimmune sialadenitis, a model of human Sjogren's disease (Hayashi et al, 1996). \par Maint. by A,N. \par NGP \par Inbr: F69 (N). Albino. Genet:\i a\i0 , \i c\i0 . Origin: A randomly selected litter from the NIH General Purpose outbred stock N:GP(S). \par Characteristics \par High intrastrain aggression and a high incidence of amyloidosis (Page and Glenner, 1972). \par NH \par Inbr: F109 (Ao). Dilute spotted. Genet: \i a, d, p, s.\i0 Origin: Strong, from crosses involving CBA, N and JK. \par Characteristics \par Low tumour incidence; resistant to induction of leukaemia by Moloney virus (1/9) (Law, 1966b). Nodular hyperplasia and adrenal adenomas in at least 10% of old mice; gonadectomy at 6 weeks enhances adenomas; some obesity; breeding ceases at approximately 9 months. \par \par NIH/Ola \par Inbr (Ola) ?+27. Albino: \i a,b,c.\i0 Origin: Pitman at NIH from N:NIH(S) stock to Natl. Inst. Biol. Standards, Hampstead, England in 1968. To Burroughs Welcome 1970 and Ola in 1975. \par Characteristics \par Good reproductive performance, and able to breed at high ratios of females per male (Peters and Festing 1985). Carries gene \i rd\i0 causing retinal degeneration (Stirling \i et al \i0 1983). Highly susceptible to infection with the helminth \i Mesocestoides corti \i0 . Larval burdens at 21 days after infection with 100 tetrathyridia being considerably higher (greater than 1000) than all other strains except SJL, which was comparable. (Lammas et al 1990). Maint. by Ola \par NJS \par Inbr (Jing-fang, 1996) F20. Albino: \i A,B,c,D. \i0 Origin: Inbred by Sun Jing-fang, Medical Animal Experimental Center, Nanjing, P.R. China, from four pairs of KM outbred mice, starting in 1989, with selection for high serum cholesterol from the 6th. generation. \par Characteristics \par Athersclerosis in aortic sac and/or ascending aorta at 8-months is 100%. Serum cholesterol at 70 days about double that of the original base population, though no special diet has been used. Typed at 26 biochemical loci. \par NLC \par Inbr: 51. Origin: Lab. Genet., Fond. Curie. \par Characteristics \par Mammary tumours 15% in virgins, 60% in breeders. \par NMRI \par Inbr: F50 (Lac). Albino. Genet: \i c\i0 . Origin: Non-inbred Swiss mice from Lynch to Poiley 1937. Inbred by Poiley known as NIH/PI. To US Naval Med. Res. Inst. at F51, known as NMRI (but not histocompatible on arrival at Laboratory Animals Centre). NOTE: Many colonies of NMRI, particularly European, are random or pen-bred. \par Characteristics \par Poor water-escape learning (5/6) (Festing, 1973b). Low preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (26/26) (Lush 1988). High brain glutamic acid decarboxylase (1/10) (Gaitonde and Festing, 1976). Short sleeping time under hexobarbital anaesthetic in females (4/15) (Lovell, 1976), short sleeping time under pentobarbitone anaesthetic (5/23), Lovell (1986). Good primary immune response to bacteriophage fd (1/7) (outbred) (Kolsch \i et al\i0 ., 1971). Good reproductive performance (1/25) with colony output 1.5 young/female/week and litter size 7.3 (1/25) (Festing, unpublished). \par NOD \par Inbr (Komeda) 22. Albino: \i c.\i0 Origin: A substrain developed by selection for diabetes (high fasting blood glucose) from F6 of the CTS strain, which was derived from outbred Jcl:ICR mice (Makino \i et al\i0 1980). At F13 a non-diabetic substrain now designated NON was separated from the main diabetic colony, though care should be taken in using this as a control strain (Leiter 1993), and at F20 a female was found with spontaneous insulin-dependent diabetes mellitus (IDDM). The origin and characteristics of this strain has been reviewed by Kikutani and Makino (1992) and Leiter (1993), and there is now an extensive literature on the characteristics of the strain. There is some evidence that substrains exist which differ in the incidence of IDDM even when maintained in a common environment (see Leiter 1993) \par Characteristics \par About 80% of females and 20% of males develop insulin-dependent diabetes by the age of 30 weeks, though this is dependent on environmentazl conditions. This is associated with insulitis, a leukocyte infiltration of the pancreas with a marked decrease in pancreatic insulin content by about 12 weeks of age in females. Genetic analysis suggests that the diabetes is dependent on multiple recessive loci including one associated with the H2, and another with the Thy1/Apoa1 loci (Prochazka et al 1989, Wicker et al 1989). Has a unique MHC class II haplotype (Acha-Orbea and Scarpellino 1991). Type I insulin-dependent diabetes is associated with overexpression of class I major histocompatibility complex proteins on pancreatic islet cells and is prevented by anti-interferon-gamma antibody (Kay \i et al\i0 1991). Develops Coombs'-positive hemolytic autoimmune anaemia (Baxter and Mandel 1991). Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed (Sundberg et al 1991). Defect in the expression of the alloantigen, Ly6C, which is not detectable on spleen or lymph node cells (c.f. NZB and ST but contrast most other strains) and may be due to an interruption in the flanking region of the Ly6C gene at a point 475 bp upstream of the transcription initiation site (Philbrick et al 1990). NOD mice may have abnormalities in IFN-gamma production. (Tsumura et al 1989). Newborn pinealectomy accelerates the development of diabetes in females while exogenous melatonin protects the mice though it results in an increase in insulin autoantibodies (Conti and Maestroni, 1996). \par Low susceptibility to \i Mycobacterium leprae\i0 (contrast MRL-\i lpr\i0 ) (Yogi et al 1989). Lymphoid cells are resistant to several signals known to induce apoptosis in other mouse strains, suggesting that they have a defect in mechanisms mediating programmed cell death (Leijon et al, 1994). Do not differ significantly from mice of other strains in antioxidant enzyme profiles, suggesting that it is unlikely that any adverse effect of oxygen radicals on beta cells is a result of antioxidant enzyme deficiency (Cornelius et al, 1993). Mice are C5-complement deficient (Hc\up8 0\up0 ) (Baxter and Cooke, 1993). \par Maint. by Jic, Wak. \par NON \par Inbr (Komeda) 27. Albino: \i c.\i0 Origin: A non-diabetic substrain with the same origin as NOD. Has a unique MHC class II haplotype (Acha-Orbea and Scarpellino 1991). Anti-BPO IgE monoclonal antibody failed to produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). Maint. by Wak. \par NOR1/Lt (Reserved symbol, Lt) \par Inbr F16. Albino. Origin: Accidental genetic outcross-backcross of NOD with C57BL/KsJ, followed by b x s mating (Prochazka et al (1992) \par Characteristics \par The strain is an insulin-resistant and diabetes-free strain which carries the diabetogenic \i H2\i0 \i \up8 g7\up0 \i0 \up8 \up0 complex on chromosome 17. Although completely resistant to cyclophosphamide-induced diabetes, the mice have peripheral T-lymphocyte accumulation characteristic of NOD/Lt. Similarly, the peritoneal macrophages show the depressed interleukin-1 secretion seen in NOD, but the T-suppressor lymphocyte function is more robust. The strain may be regarded as an MHC-matched diabetes-resistant control strain for NOD/Lt (Prochazka et al 1992). \par NOR2/Lt-\i or\i0 \i \up8 2J\up0 \i0 \i /+\i0 (Reserved symbol, Dn) \par Inbr. F14. Origin: As NOR1/Lt, but separated before F20. Carries mutation \i or\i0 \i \up8 2J\up0 \i0 \up8 \up0 \par NOXCB-1 \par Inbr. F20. Single recombinant inbred strain developed by Herberg in about 1992 from a corss between NOD/Shi and CBA/LsLt. \par NRH \par Inbr (Nrs) 71. Albino. \i a,b,c.\i0 Origin: CF-1 from Carworth Farms to Takeda Chem. Industries Ltd. to Jmo to Nrs. Inbreeding started Sept. 1960 without selection. Foster nursed on germ-free NDII in 1972. Maint. by Nrs. \par NSY \par Inbr F47 (Sept. 1996). Albino. Origin: From Jcl:ICR mice in 1975 with selective breeding for glucose intolerance. Develop spontaneous non-insulin-dependent diabetes mellitus in an age-dependent manner, reaching 98% in males and 31% in females at 48 weeks of age. Neither severe obesity nor extreme hyperinsulinemia is seen at any age (Ueda et al, 1995). \par NX129- \par Inbr circa 20. Set of 8 recombinant inbred strains developed by B.A.Taylor from NZB/BlNJ X 129/J. Maint. by Ty. \par NXSM- \par Inbr circa 20. Set of 17 recombinant inbred strains developed by Eva M. Eicher from NZB/BlNJ x SM/J. Typed at 58 loci on 16 autosomes and the X chromosome (Eicher and Lee 1990). Maint. by Ei. \par NYLR \par Inbr (Nya) 89. Albino: \i c.\i0 Origin: outbred colony from a single pair of unknown origin obtained from a breeder in Albany, NY in 1930. b x s matings started in 1942. Maint. by Nya. \par NZB \par Inbr: F121 (J). Black. Genet: \i a\i0 . Origin: Outbred mice from Imp. Cancer Research Fund, London, to Univ. of Otago Med. School 1930. Inbred by Bielschowsky 1948. A number of other strains, including NZO, NZC, NZX and NZY, were developed from the same stock. (Bielschowsky and Goodall, 1970). Strain NZW was derived from the same outbred stock, but was inbred independently by Hall (Hall and Simpson, 1975). \par Life-span, spontaneous disease and immunology \par Develops autoimmune haemolytic anaemia of the Coombs-positive, warm antibody type (Simpson, 1976; Howie and Simpson, 1974) as well as a nephropathy which is variable in expression and unpredictable in progress, but is probably an immune-complex-induced glomerulonephritis. Burnet (1972a, b) considered that at least two genes are involved, one of which is also present in NZC. Genetic linkage to chromosomes 1, 4, 7, 10, 13 and 19 imply that multiple genes in different combinations contribute to the severe renal disease (Drake et al, 1995). \par A virus may also be involved, although Simpson (1976) considered that: `. . .the case for a viral aetiology is unproven, although the possibility exists that virus may be present in incomplete form'. According to Burnet, NZB mice have an abnormally high immunological vigour and resistance to induction of immunological tolerance or paralysis, which is manifested before the animals become Coombs-positive. The condition may be transferred to young isogenic mice by cells from the spleen, but not from other lymphoid organs. Thus, the condition appears to depend on stem cells of immunocyte lines. Autoimmune plaque-forming cells, active against mouse erythrocytes, are present in old mice. Onset and severity of the condition can be influenced by diet (Fernandes \i et al\i0 ., 1972). Theofilopoulos et al (1980) have compared immune function in this and other autoimmune strains. Only NZB splenic lymphocytes from autoimmune donors inoculated into pre-autoimmune NZB or in BALB/c mice could evoke a positive Coombs test (Jenkinson and East (1980). Diethyldithiocarbamate (DTC), an immunomodulative agent which may enhance T cells, prolongs life in autoimmune MRL-lpr/lpr mice, but not in autoimmune NZBxNZWF1 hybrids (Halpern and Yocum 1991). Defect in the expression of the alloantigen, Ly6C, which is not detectable on spleen or lymph node cells (c.f. NOD and ST but contrast most other strains) and may be due to an interruption in the flanking region of the Ly6C gene at a point 475 bp upstream of the transcription initiation site, as found in NOD (Philbrick et al 1990). Ultrastructural pathology of the thymic reticulum revealed several features in common with BXSB and MRL-\i lpr\i0 in varying degrees according to sex and age of the mice. Main anomalies included vacuolized aspect of the thymic epithelium, an increased number of macrophages, interdigitating cells and cystic cavities, the presence of a great number of plasmocytes and mastocytes and extensive interstitial fibrosis and arteriosclerosis. The most intriguing finding was the presence of crystal-like inclusions in epithelial cells (Nabarra et al 1990). Natural autoantibodies are involved in the heamolytic anaemia (Hentati et al, 1994). \par \par Pure-line mice have a high level of natural thymocytotoxic autoantibodies (Auer \i et al\i0 ., 1974), a low immune response to Dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972), a low lymphocyte phytohaemagglutinin response (30/43) (Heiniger \i et al\i0 ., 1975), a high 25% incidence of serum antinuclear factor (4/17) (Barnes and Tuffrey, 1967) and a poor immune response to DNP-keyhole limpet haemo-cyanin (9/11) (Borel and Kilham, 1974), and are discriminators between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). Mean life-span short (2/17 = 459 days in males, 441 days in females) in SPF fostered conditions (Festing and Blackmore, 1971). Median life-span short (4/4 = 280 days males, 4/4 = 270 days females) (Stutman, 1974). Males resistant but females more susceptible to immunosuppression of contact hypersensitivity by ultraviolet B light (Noonan and Hoffman, 1994) \par \par Hypertrophy of the pituitary in 80% of survivors to 1 year and pituitary tumours in 25% of aged breeders (Russfield, 1966). \par \b Hybrids with NZB\b0 \par In hybrids with C57BL there is a late-appearing positive direct Coombs test. Hybrids with NZW develop an autoimmune disease resembling human systemic lupus erythematosus (Talal \i et al\i0 ., 1972), with high titres of natural thymocyto-toxic autoantibody in many animals (Shirai and Mellors, 1972). NZBxNZWF1 hybrid B cells apparently differ from normal murine B cells in their capacity to produce IgG antibodies upon T cell-dependent antigenic stimulation. (Riley et al 1991). Genetic analysis of a backcross to NZW shows that one set of loci regulate serum levels of IgG antibodies to double-stranded DNA, single-stranded DNA, total histones and chromatin, and these overlap with loci that control autoantibodies to the viral glycoprotein gp70. These latter loci are most strongly linked with renal disease. A locus on distil chromosome 4 was linked with nephritis but not with any of the autoantibodies measured (Vyse et al, 1996). Daily intraperitoneal injections of DNase from 4-7 months of age resulted in reduced proteinuria and serum creatinine and strikinly less severe renal pathology (Macanovic et al, 1996). Autoimmunity is associated with increased anxiety and less exploratory behaviour (Schrott and Crnic, 1996). Caloric restriction and supplementation with fish oil increases life span and diminishes histological evidence of glomerulonephritis. This is associated with decreased expression of platelet-derived growth factor-A (Troyer et al, 1997).. \par \par Other characteristics \par High balsa-wood gnawing activity (12/16) (Fawdington and Festing 1980). High coumarin hydroxylating ability (cf. 4/13) (Lush and Arnold, 1975). Pentobarbital i.p. induces hepatic epoxide hydrase (cf. 4/7) (Oesch \i et al\i0 ., 1973). Sensitive to lethal effects of ozone (2/21) (Goldstein \i et al\i0 ., 1973). Mineral oil injected i.p. induces plasmacytomas (Potter, 1972). High plasma triglyceride (9/11) and cholesterol (11/11) levels (Jiao et al 1990). \par \par Susceptible to mouse hepatitis virus type 3 infection (cf. 5/14) (Le Prevost \i et al\i0 ., 1975). No transmission of murine leukaemia virus (Scripps) to succeeding generations (Jenson \i et al\i0 ., 1976). Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). In contrast to ten other strains, it does not carry type I and II endogenous type-c viruses (cf. SWR) (Stephenson \i et al\i0 ., 1975). Totally refractory to infection by \i Leishmania tropica \i0 parasite (Howard \i et al \i0 1980) and to \i Leishmania major mexicana\i0 (Lazama-Davila, 1997). Low immune response to ganglio-series gangliosides (c.f. 4/10) Kawashima et al (1992). \par About 30-40% develop neocortical ectopias due to a recessive gene with incomplete penetrance (Sherman et al, 1994) \par Poor reproductive performance (24/25). Litter size 3.8 at weaning, colony output 0.5 young/female/week (Festing, 1976a). First litter size high (1/6) but fourth litter low (6/6). Low proportion of females produce four or more litters (6/6) and low percentage of fertile matings (6/6) (Fernandes \i et al\i0 ., 1973). Intermediate breeding performance (17/24) (Hansen \i et al\i0 ., 1973). High bone density of femur (2/11) (Beamer et al, 1996). \par NZBR \par Inbr ?. Chocolate brown \i a,b.\i0 Origin: Presumed mutation to brown (\i b\i0 ) in NZB/Bl at F73. \par Characteristics \par Develops autoimmune anaemia like NZB. Maint. by Wehi. \par NZC \par Inbr: F137 (Wehi). Chocolate-brown. Genet: \i a, b. \i0 Origin: see NZB. \par Characteristics \par High incidence of ovarian granulosa cell tumours (Bielschowsky and D'Ath, 1973). High incidence of spontaneous hydronephrosis (56% in males, 81% in females) (Warner, 1971). Has excessively high endogenous spleen colony forming activity with a marked reduction in spleen haematopoietic colony formation in isogenic transplantation experiments. In \i in vitro \i0 studies it has reduced immunological response to sheep red blood cells, phytohaemagglutinin and pokeweed. This may be due to a defect in the number of progenitor cells for the immune system, possibly involving only one component cell population (Herrod and Warner, 1972; Burnet, 1972a, b). \par NZM-38-4479. \par Set of 26 inbred strains, at F24-F30. All the mice originated in NZB x NZW mice, either F2 or backcrosses to NZW, in the Wadsworth Center for Laboratories and Research, Albany, NY (WCLR). The stocks came from UMC (University of Minnesota) in 1973 and had been strictly inbred at WCLR. For 12-15 months the mice were pen-bred for coat colour: chocolate brown, tan and grey. Inbreeding was started from single pairs in 1981 by CT Olsen. At F4-F5 AE Gabrielsen took over and abandoned the colour criterion for the grey mice and selected for continuation lines-to-be in which lupus nephritis deaths had already been documented. Inbreeding continued in WCLR and at All Children's Hospital (ACH), St. Petersburg, Florida. All are maintained at WCLR since 1990. Since March 1989 the colony has been maintained by UH Rudofsky and BD Evans. There are 26 strains, 24 descended from grey coated mice and one each from tan and chocolate. \par Characteristics \par Many lines at F13-F18 resembled NZBxNZWF1 in lifespan and pathology. One had accelerated disease, and others had delayed disease. In a few, males sickened almost as early as females. 3-4 strains had delayed or no disease. (AE Gabrielsen and UH Rudofsky, personal communication 2nd. July 1991). \par NZO \par Inbr: F128 (Wehi). Agouti. Genet: +. Origin: see NZB. \par Characteristics \par Intermediate to low incidence of ovarian granulosa cell tumours (Bielschowsky and D'Ath, 1973). Median life-span about 460 days in males and 530 days in females. High incidence (15-20%) of malignant lymphomas of Peyer's patches and high incidence of duodenal and lung tumours (Goodall \i et al\i0 ., 1972, 1973; Rappaport \i et al\i0 ., 1971). \par \par Very obese. Fat collects mainly in the abdomen, starting about 4 weeks, although divergence of growth curves is not detectable before about 2-4 months. At maturity 50-74% of body weight is fat. Animals are hyperglycaemic but not hyperinsulinaemic (Bray and York, 1971). Blood glucose levels, plasma insulin levels, body weight and glucose tolerance return to normal after implantation of pancreatic islets from normal albino mice. The genetic lesion therefore appears to be situated within the islets of Langerhans (Gates \i et al\i0 ., 1972). Obesity is largely caused by an increase in adipose cell numbers, although cell size is slightly increased (Johnson and Hirsch, 1972). Obesity may be at least partly due to an abnormality in the cyclic AMP system which controls lipolysis in adipose tissue (Lovell-Smith and Sneyd, 1973). Obese syndrome also reviewed by Stauffacher \i et al\i0 . (1971). Develop non-insulin-dependent diabetes mellitus (NIDDM) with active liver glycogen synthase (GS) reduced to 54% and 36% in neonates and adults, respectively. However, total GS was 65% higher in adults than in NZC controls. Glycogen phosphorylase was not different from NZC controls (Thorburn et al, 1995). Increased hepatic glucose production is present at an early age and is associated with impared suppression of the gluconeogenic enzyme fructose-1,6-bisphosphatase (Andrikopoulos et al, 1996). \par NZW \par Inbr: F 70. Albino. Genet: \i b, c, p.\i0 Origin: see NZB. \par Characteristics \par High within-strain aggression. Litter mate males housed together often fight severely by 6-8 weeks (original observation). High balsa-wood gnawing activity (15/16) (Fawdington and Festing 1980). Long life-span in both sexes (17/17 = 802 days in males, 16/17 = 733 days in females) in SPF fostered conditions. Lung tumours 2-24%, lymphatic leukaemia 3-29% and heart defects 2-24% (Festing and Blackmore, 1971). Short sleeping time under hexobarbital anaesthetic (3/15 in males, 1/15 in females) (Lovell, 1976), short sleeping time under pentobarbitone anaesthetic (3/23), Lovell (1986). Phenobarbital i.p. induces hepatic epoxide hydrase (cf. 4/7) (Oesch \i et al\i0 ., 1973). High incidence of exencephaly reported by Vogelwide et al (1993). High retinal ganglion cell number (20/24) (Williams et al, 1996). \par Serum antinuclear factor found in 12% of animals (6/17) (Barnes and Tuffrey, 1967). The TCR beta-chain locus of NZW mice carries an 8.8-kb deletion which encompasses the C beta 1, D beta 2, and all six J beta 2 gene segments Studies suggest that D beta 2 and J beta 2 gene segments are required to maintain a diverse T cell repertoire and that their deletion from the genome may confer a significant selective disadvantage in the wild.(Woodland et al 1990). Resistant to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 4/18) (Noonan and Hoffman, 1994). Deficient in eosinophil peroxidase, one of the enzymes in the eosinophil-specific granules, resembling the similar condition in humans (Ohmori et al, 1996). \par Intermediate breeding performance (13/25), colony output 1.00 young/female/ week, litter size at weaning low (23/25) at 4.1 (Festing 1976a). Poor breeding performance (19/24) (Hansen \i et al\i0 ., 1973). \par Strain widely used as the NZB x NZW F1 hybrid (also known as the B x W hybrid), giving a model of systemic lupus erythematosus (see also NZB). Syndrome includes typical lupus erythematosus cells, antinuclear antibody, haemolytic anaemia, proteinuria with casts and terminal nephrosis with renal failure before 8 months (see Milich and Gershwin 1981). Incidence and severity of the disease is greater in females than males (Dubois \i et al\i0 ., 1966). \par NZW x BXSB F1 male mice develop systemic autoimmunity involving autoantibodies, thrombocytopenia, lupus nephritis and coronary vascular disease with myocardial infarction. These effects can be modulated by diet, and may be mediated by anti-cardiolipin autoantibodies (Mizutani et al, 1994), and can be treated effectively by ACE inhibitors such as imidapril and captopril (Ogiku et al, 1994). \par NZX \par Inbr: F90 (Wehi). Origin: see NZB. From an NZC female (F33) and an NZY male (F27), offspring b x s mated. \par Characteristics \par From F13, some females have shown congenital imperforate vagina, and both sexes have a low incidence of megacolon. \par NZY \par Inbr: F120 (Wehi). Cinnamon piebald (?). Genet: \i b, s.\i0 Origin: see NZB; a piebald male appeared at F2 which was mated with a tan sister; at F4 a piebald brother-sister appeared; b x s mating with selection for piebald gene\i , s\i0 led to fixation of the coat pattern at F7. \par Characteristics \par High incidence of mammary tumours and pituitary adenomas. Megacolon 10%, associated with the \i s\i0 gene (Bielschowsky and Schofield, 1962). Highly susceptible to induction of connective tissue tumours by 4-nitroquinone \i N\i0 -oxide (1/5) (Searle and Spencer, 1966). A subline has been developed: NZYf/Bu Inbr: 65 since fostering. Origin: NZY at F26 were fostered on NZC. A marked reduction in mammary cancer but pituitary tumour incidence unchanged. \par O20 \par Inbr (A) 194. Albino: \i a,c.\i0 Origin: R.Kortweg, 1931, from Amsterdam petshop mice. \par Characteristics \par Mammary tumours 0% in virgins, 5% in breeders, 13% in force-bred; believed not to carry the milk agent, but susceptible to it and can transmit it to offspring (Muhlbock and Rijssel, 1954). Leukosis 8% (Hilgers and Galesloot, 1973). Maint. by A. \par OIR \par Inbr. G12F90. Colour ?. Origin: Muhlbock 1959. A strain partly congenic with O20 developed by cross-intercross matings with selection for resistance to transplanted mammary tumour of O20 following outcross to DBA/LiA. Maint. by A. \par OUBCr \par Inbr: F10 since mutation. Origin: In Oct. 1969 a mutation occurred in NZB/Bl to creamy ventral surface; mutants b x s mated. \par Characteristics \par Similar to NZB, but survival time about 100 days longer; mice develop strongly positive direct Coombs tests but do not become severely anaemic (Hall and Simpson, 1975). \par OUBW \par Inbr: F40 +. Origin: Varicoloured outbred mice taken to Dunedin from California by R. Ortman in 1957. At F\dn8 6\dn0 a pair selected for black and white coats were mated. \par Characteristics \par A small number have shown minor kidney pathology (Hall and Simpson, 1975). \par OUCW Syn: NZCW. \par Inbr: F45 +. Origin: As OUBW; at F\dn8 6\dn0 a chocolate and white male was mated with a black and white littermate. From this pair a pair of chocolate and white siblings was selected. \par Characteristics \par Average life-span: males 640, females 540 days. Average litter size 6; increase in amount of lymphoid tissue, thymic enlargement common; hybrids with NZB have enlarged abdominal lymph nodes (Hall and Simpson, 1975). \par OUF \par Inbr: F60 +. Origin: Random-bred fawn-coloured mice, selected for coat colour, 1953. \par Characteristics \par Average survival times about 580 days for females and 700 days for males; nephritis and liver tumours (Hall and Simpson, 1975). \par OUGW \par Inbr: F20 +. Origin: As OUBW; a grey and white male was mated to a black and white female. In the F\dn8 2\dn0 a grey and white pair was obtained. \par Characteristics \par Lacks a characteristic pathology (Hall and Simpson, 1975). \par OUW Syn: NZW. \par See NZW. \par OUYW \par Inbr: 20 +. Origin: Varicoloured random-bred mice from UK in 1939; a pair of ginger and white mice produced yellow and white offspring, which were inbred; dwarfism appeared at F\dn8 4\dn0 (Hall and Simpson, 1975). \par P/A \par Inbr: 91. Origin: P. Kortweg 1934; DBA female x C57BL male, then N20 to C57BL, then b x s inbred. \par P/J \par Inbr: F153. Pink-eyed fawn. Genet: \i a, b, d, p, rd, se. \i0 Origin: Snell from a cross involving strain BDP. Carries the pink-eyed dilution gene, \i p\i0 , which is derived from Asian mice of the \i Mus musculus\i0 type (see also strains SJL, 129/J and FS/Ei) (Brilliant et al, 1994) \par \i Characteristics\i0 \par Lymphatic leukaemia 22% in males and 29% in breeding, and 58% in virgin females. Primary lung tumours zero in males and 3% in females (Hoag, 1963). Life-span short (3/22 = 384 days in males and 8/22 = 510 days in females) in conventional conditions (Storer, 1966). Low metabolic rate (15/18) (Storer, 1967). High serum ceruloplasmin levels in females (4/27) (Meier and MacPike, 1968). High susceptibility to audiogenic and electroconvulsive seizures (1/6) (Deckard \i et al\i0 ., 1976). Large brain weight (15/18 in males, 14/18 in females) (Storer, 1967). Large brain/body weight ratio (1/20) and large spinal cord (2/25) (Roderick \i et al\i0 ., 1973). Resistant to X-irradiation (5/27) (Roderick, 1963). Short survival in 90% oxygen (3/10) (Lieberman and Kellog, 1967). Low lymphocyte phytohaemagglutinin response (37/43) (Heiniger \i et al\i0 ., 1975). Intermediate breeding performance (15/24) (Hansen \i et al\i0 ., 1973). \par \par High degree of genetic distinctiveness (8/27) (Taylor, 1972). Susceptible to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 3/7) (Evans \i et al\i0 ., 1977). \par PAA \par Inbr 45. Colour: Agouti (?). Origin: Wild pair trapped in Philadelphia factory (see also PAB,PAC,PAD). Maint. by Henderson, Oberlin College. \par PAB \par Inbr(42) Colour: Agouti, but 91% white head spot. Origin, Maint.: see PAA. \par PAC \par Inbr (42) Colour: Agouti (?). Origin, Maint.: See PAA \par \par PAD \par Inbr (45) Colour: Agouti (?). Origin, Maint.: see PAA. \par PBA \par Inbr: F20 +. Albino. Genet: c. Origin: P. C. Bailey from a pair of pet shop mice purchased in Birmingham, Alabama, in 1958. \par Characteristics \par Litter size 6.1; 6 week weight 21 g (both sexes); mean life-span 317 days in males, 268 days in females. Spontaneous lymphomas 100%, mammary tumours 74%, pulmonary adenomas 77% in animals over 1 year (Bailey \i et al\i0 ., 1970). Development of spontaneous adenomas associated with increased serum concentration of IgG\dn8 1\dn0 and IgG\dn8 2\dn0 immunoglobulins (Schrohenloher and Bailey, 1972). \par PBB \par Inbr: F20+. Black. Genet: \i a\i0 . Origin: P. C. Bailey from multicoloured pet shop stock, in about 1972. \par Characteristics \par Become obese on a standard diet. Maximum body weight of about 65-75g is achieved at about 12 months. Blood glucose normal, but glucose tolerance abnormal. Serum insulin elevated. No histological abnormalities of pancreatic islets seen, although mild fatty infiltration of the liver is common. Breeding performance good and life-span normal (18-22 months). Obesity may be analogous to mature onset obesity in man (Hunt \i et al\i0 ., 1972), and equivalent in many respects to the mutants \i ob\i0 (obese) and \i A\i0 \i \up8 y\up0 \i0 \i \i0 (yellow) and the NZO inbred strain. The diabetes in this case has a polygenic mode of inheritance (Hunt \i et al\i0 ., 1976). \par PE \par Inbr (Rl) 90+. Colour: Agouti and pearl: \i +,pe.\i0 Origin: Pearl mutation causing dilution of black and yellow pigments arose in C3H/HeRl mice before 1954. Maintained by \i pe/+\i0 x \i pe/pe\i0 matings. \par Characteristics \par Homozygotes have elevated levels of some kidney lysosomal enzymes. Maint. by Rl. \par PERA \par Inbr. F40-F50 (1989). Origin: Seven breeders trapped by Olga Atteck in 1961 in Peru for Dr. Margaret Wallace. At about generation 15 in 1971 stock was passed to Drs. T.H. Roderick and Eva Eicher, who maintained separate stocks, PERA/CanRk and PERA/CamRk. Moderate susceptibility to experimental allergic encephalomyelitis with late onset (10/10), high severity (2/10), high mortality (1/10) and high incidence of spontaneous relapse (3/10) (Lindsey, 1996). \par PERU-COPPOCK W4. \par Inbr. 20 Agouti: \i A,B,C.\i0 . Origin: Wild mice trapped in Nana village, in Rimac valley in Peru. Inbred by M.E.Wallace in 1972. Has never been crossed with laboratory mice. Produces an unusually high frequency of visible mutants and nestling lethals (Wallace 1985). Maintained by Ms. \par PET \par Inbr: 66. Origin: From mixed stock of C3H and black pet shop mice, Med. Coll. Va. 1956, to W. M. Reams 1958. \par Characteristics \par Name from Pigmented Extra-epidermal Tissues; occasional mammary tumours in older females. \par PF \par Inbr: F35 (Fo). Agouti piebald. Genet: \i a, s, + /Lst. \i0 Origin: Selection for high expression of hindfoot polydactyly. \par Characteristics \par High expression of forefoot and hindfoot polydactyly and occasional moderate tibial hemimelia in heterozygotes caused by Strong's luxoid mutation \i Lst\i0 , with great reduction of radius and tibia in homozygotes\i .\i0 Maint. by Fo. \par PH/Re \par Inbr: 77. Genet: \i Ph/ +. \i0 Origin: Spontaneous mutation \i Ph\i0 (patch) in C57BL/6J. Truslove to E. S. Russell 1957, as non-inbred stock. \par Characteristics \par White- spotted agouti; \i Ph/Ph \i0 is lethal. \par PHH \par Inbr: f95 (wE). Grey. Genet: \i a, ln.\i0 Origin: Weir, from MacArthur outbred stock obtained from Butler 1949; b x s inbreeding with selection for high blood pH (Weir and Clark, 1955; Wolf, 1959). \par Characteristics \par Blood pH 7.48 _ 0.004, blood lactic acid 3.6 _ 0.2 umol/ml, CO\dn8 2\dn0 output 5.90 _ 0.01 mg h\up8 -1\up0 g\up8 -1\up0 body weight, sex ratio 52.8 _ 1.00% males (Weir, 1962). Overall fertility low. \par PHL \par Inbr: F97 (We). Genet: \i a\i0 \i \up8 t\up0 \i0 \i , b, In.\i0 Origin: Same as PHH, selected for low blood pH. \par Characteristics \par Blood pH 7.43 _ 0.004, blood lactic acid 5.4 _ 0.3 mol/ml, CO\dn8 2\dn0 output 5.90 _ 0.03 mg h\up8 -1\up0 g\up8 -1\up0 body weight, sex ratio 41.8 _ 0.93% males. Overall fertility high. (Weir, 1962). \par PIC \par Inbr. 46. Albino: \i c.\i0 Origin: Jcl:ICR mice inbred by Ichiro Narusex in 1977. \par Characteristics \par Carries the dominant \i Pdn\i0 gene causing preaxial polydactyly, and arhinencephaly and exencephaly in homozygotes (Naruse and Kameyama 1982), Hagasaka \i et al\i0 (1980). Naruse and Kemeyama (1980). Maintained by Idr. \par PL \par Inbr: F130 (J). Albino. Genet: \i c, rd. \i0 Origin: Developed by Lynch from 200 non-inbred `Princeton' stock purchased from a dealer in 1922, and developed as a high-leukaemia strain. \par Characteristics \par Leukaemia 50% in females and 19% in males (Staats, 1976), 80-90% (Heston, 1968). Life-span intermediate in males (10/22 = 517 days) and short in females (4/22 = 448 days) in conventional conditions (Storer, 1966). High incidence of leukaemia (Albert \i et al\i0 ., 1965). High gross tumour incidence in females (5/22) (Storer, 1966). \par \par High plasma cholinesterase activity (3/22 in females, 5/22 in males) (Angel \i et al\i0 ., 1967). Large brain weight (4/25) (Roderick \i et al\i0 ., 1973). Small spleen/body weight (9/9 to 6/9, depending on age) (Albert \i et al\i0 ., 1966). Large relative thymus weight (2/8 at 14,49 and 90 days) (Albert \i et al\i0 ., 1965). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). High lymphocyte phytohaemagglutinin response (1/43) (Heiniger \i et al\i0 ., 1975). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). High degree of genetic distinctiveness (7/27) (Taylor, 1972). Develop antiphospholipid antibody syndrome with reduced litter size following immunisation with beta(2)-glycoprotein (Garcia et al, 1997). Moderate susceptibility to experimental allergic encephalitis with late onset (2/10) and high mortality (4/10) (Lindsey, 1996). \par PM \par Inbr 80. Colour ?. Origin: C. Biancifiori, Perugia, from C3HbxBALB/cfC3H. Descendents b x s mated with selection for high incidence of mammary tumours. \par Characteristics \par Now has high mammary tumour incidence and inherited polycystic kidneys. Maint. by Perugia. \par PN \par Inbr 52. Albino \i c.\i0 Origin: Albino mice from pet shop in New Zealand in 1948. From Palmerston North Hosp. to Massey Univ. as 'NOS outbred'. To Glaxo Labs of New Zealand as 'GW outbred'. Back to Palmerston North as 'PN'. Maintained by Wigley in Med. Res Dept. and inbred starting in 1964, with selection for positive ANA (anti nuclear antibody) in first three generations. \par Characteristics \par Antinuclear antibodies appear at about 5 months, and 80% are positive by 10 months. Develops lupus erythematosus with glomerular depositis of IgG, IgM and IgA (Wigley \i et al\i0 ., 1975). Maint. by Hm, Mac. \par PRO \par Inbr: F61 (Brk). Genet: \i a, c\i0 \i \up8 ch\up0 \i0 \i , p.\i0 Origin: E. S. Russell, 129/ReJ x C57BL/6J. Sib-mating with selection for \i a,\i0 \i c\i0 \i \up8 ch\up0 \i0 \up8 \up0 and \i p.\i0 Mutation to \i Pro1\i0 \i \up8 b\up0 \i0 \i \i0 (proline oxidase-1) which controls activity level of proline oxidase in liver, kidney, and brain, which is about 20% of normal in this strain. 7 and 50 fold elevation of proline in blood and urine, respectively. \par Characteristics \par Hyperprolinaemia and prolinuria with increased taurine excretion (Blake \i et al\i0 ., 1974); sluggish movements, 50% generalised hair loss (Kanwar \i et al\i0 ., 1975). Hyperprolinaemia due to a deficiency in the activity of component 1 of mitochondrial proline dehydrogenase (Blake \i et al\i0 ., 1976), and associated with a decreased liver proline oxidase activity (Blake, 1972). High lymphocyte phyto-haemagglutinin response (8/43) (Heiniger \i et al\i0 ., 1975). \par PT \par Inbr (Kist) 54 (1993). Near-white: \i a,b,c\i0 \i \up8 ch\up0 \i0 \i ,d,p,s, se.\i0 Origin: Seven-locus stock from Dr.Mary Lyon, Harwell in 1969. Inbred since then. Also carries \i se\i0 and \i Ty/+.\i0 Maint. by Osaka Univ., Ms, and Kist (Korea) \par PUC \par Inbr 25 (Fre). Agouti. Origin: Wild mice from Rimach valley in Peru, captured by Coppock. To M.Wallace, Cambridge, to J. Peters, to Von Deimling in 1977. Inbred by Von Deimling. Large ears. Maintained by Von Deimling,Fre. \par PUH \par Inbr (Cam) 50. Agouti. Origin: wild mouse from Rimach valley in Peru (Peru-Harland) x CBA. Inbred by M.E.Wallace. Many mutations present in this strain. Maint. by Cam (?). \par PWD \par Inbr 33 (Ph). Agouti. Origin: \i Mus musculus musculus \i0 (?), Prague inbred by Forejt in 1974. Maint. by Ph. \par PWK \par Inbr. 38 (1989). Origin: Wild Mus musculus musculus trapped in Lhotka near Prague, Czechoslovakia in 1974. Similar to PWD except at the Es13 locus. \par QC \par Inbr (U) ?+94. Off-white (?) \i a,c\i0 \i \up8 e\up0 \i0 \i .\i0 Origin: Hagedoorn to Hirschfeld (1937) to CPB (1949), to Vet. Fac. Utrecht (1973). Susceptible to tuberculosis. Maint. by U. \par QF-5612 \par Inbr: 51. Genet: \i a\i0 . \par Characteristics \par Selected for early sexual maturity of males. Mean age of first fertile mating 49.9 days; mean body weight at 100 days, 35.9 g. \par QF-5604 \par Inbr: 51. Genet: \i A\i0 \i \up8 w\up0 \i0 \i , b, ln.\i0 \par Characteristics \par Selected for early sexual maturity of males. Mean age of first fertile mating 51.7 days; mean body weight at 100 days 39.6 g. \par RAP/Ko \par Inbr: 70 +. Origin: Kobozieff, 1951, from a pair of Rockland (USA) mice. \par Characteristics \par Used for the study of longitudinal hemimelia and periodic hypo-trichosis; the mutation cataract appeared in this line. \par RB/1 \par Inbr (Bg) 45. Albino; \i c.\i0 Origin: Swiss albino stock from dealer selected for high incidence of audiogenic seizures (Frings and Frings 1953). Susceptible to audiogenic seizures. Inbred since 1959. Maintained by Bg. \par RB/2 \par Inbr (Bg) 55. Albino; \i c.\i0 Origin: as for RB/1, but selected for resistance to audiogenic seizures. Maintained by Bg. \par RBA \par Inbr (Dn) ? +25. Agouti. Origin: from wild mice captured near Mutten, Albula Valley, Grisons, S.E. Switzerland by A.Gropp and H.winking. To Davisson and Roderick 1977, to Davisson 1981. Homozygous for Robertsonian translocation Rb(4.12)9Bnr. Has never been outcrossed to a laboratory strain. Maint. by Dn. \par RBB \par Inbr (Dn) ? +35. Agouti. Origin: wild mice captured near Bondo, Val Bregaglia, Grisons, S.E. Switzerland by A.Gropp and H.Winking. To Davisson and Roderick 1977, to Davisson 1981. Homozygous for Robertsonian translocation Rb(1.10)10Bnr. Probably has never been crossed to a laboratory strain, but is not as wild as RBA. Maint. by Dn \par RBC \par Inbr (Dn) ?+ 33. Albino. Origin: Robertsonian translocation Rb(8.17)1Iem arose in a colony of white mice at the Inst. Exp. Med., Leningrad. From Rappolovo Nursery of Acad. Med. Sci of USSR to Gropp, to Davisson and Roderick 1977, to Davisson 1981. Maint. by Dn. \par RBD \par Inbr (Dn) 60. Albino: \i A,E\i0 \i \up8 tob\up0 \i0 \i ,c.\i0 Origin: derived from crosses of Swiss mice (probably Han:NMRI, A.Gropp personal communication to Dn) with wild mice captured in the Valle di Poschiavo in SE Switzerland. The wild population was originally known as the 'tobacco' mouse because of their dark coat colour (\i E\i0 \i \up8 tob\up0 \i0 \up8 \up0 ). They also appear in the literature as \i Mus\i0 \i poschiavinus \i0 (Gropp et al, 1970). To Fls from Gropp (probably via F.Ruddle) to T.Roderick in 1970, b x s ever since. To M. Davisson in 1981. Homozygous for the Robertsonian chromosomes Rb(5.15)3Bnr, Rb(11.13)4Bnr and Rb(16.17)7Bnr. Maint. by Dn. \par RBE \par Inbr (Dn) 36. Albino. \i A,c.\i0 Origin: constructed by Davisson by crossing together two stocks originally derived from F1 hybrids between wild mice captured in the Valle di Poschiavo in SE Switzerland and Swiss laboratory mice (probably Han:NMRI, A.Gropp, personal communication to Dn) or a B6D2F1 female. F1s from A.Gropp to F.H.Ruddle to T.H.Roderick in 1970. Stocks to M.T.Davisson in 1974. Homozygous for the Robertsonian chromosomes Rb(1.3)1Bnr, Rb(4.6)2Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. Maint. by Dn (now extinct). \par RBF \par Inbr (Dn) 60. Albino \i c,E\i0 \i \up8 tob\up0 \i0 \i .\i0 Origin: Swiss mice (probably Han:NMRI) crossed with wild mice captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. They also appear in the literature as \i Mus poschiavinus\i0 Fatio and more recently as \i Mus musculus poschiavinus.\i0 Gropp to Roderick 1970 at F1. To Davisson 1981. Homozygous for Robertosonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. Maint. by Dn,J. \par RBG \par Inbr (Dn) 30. Cinnamon; \i b,A.\i0 Origin: Muriel Davisson 1978 from a mating of NMRI females x wild males subsequently crossed to laboratory stocks involving strains C57BL/6J, AEJ/Gn and DBA/2. Homozygous for Rb(3.8)2Rma, Rb(4.15)4Rma and Rb(10.11)5Rma. The Y chromosome comes from DBA/2J. Maintained by Dn \par RBJ (reserved symbol) \par Inbr (Dn) 14. Tobacco: \i A,E\i0 \i \up8 tob\up0 \i0 \i .\i0 Origin: Muriel Davisson 1984 from crosses between 1) a stock derived from an "Orobie" male captured near Bergamo, N. Italy x a 129/- female (note that the Orobie stock was developed with crosses involving C57BL/6J, DBA/2J and AEJ/Gn) and 2) an inbred strain RBD (see above). Homozygous for Rb(2.8)2Lub, Rb(5.15)3Bnr, Rb(11.13)4Bnr, Rb(16.17)7Bnr and has a Y chromosome from the Orobie wild population. Maintained by Dn. \par RC \par Inbr (U) ?+75. Albino; \i c.\i0 Origin: Formerly CPB-R. Rhodesfarm, S.Africa (?) to Compton to Hagedoorn to CPB-TNO (1949), to Vet. Fac. Utrecht (1973). High frequency of hydrocephalus. Maint. by U. \par RF \par Inbr: F113 (J). Albino. Genet: \i a, c.\i0 Origin: Furth 1928 from Rockefeller Institute general-purpose stock. Transferred to Oak Ridge. History somewhat questionable. \par \i Behaviour\i0 \par High spontaneous bar pressing (1/14), high open-field activity (2/14) and high social grooming during aggressive encounters (1/14), but low tail rattling during such encounters (14/14) (Southwick and Clark, 1968). \par \i Life-span and spontaneous disease\i0 \par Intermediate life-span in males (15/22 = 651 days) but short in females (5/22 = 452 days) in conventional conditions. High gross tumour incidence in males (4/22) (Storer, 1966). Necrotising arteritis involving the aorta, its major branches and other arteries and arterioles seen in 10-20% of aged mice. Disease may involve an autoimmune mechanism (Upton \i et al\i0 ., 1967). Mean life- span 619_7 days. Leukaemia 66%, glomerulosclerosis 63% and reticulum cell sarcoma 52% (Yuhas and Clapp, 1972). Spontaneous glomerular hyalinisation and glomerrnlosclerosis develops at 8-20 months (Russell and Meier, 1966). Leukaemia 46% (Myers \i et al\i0 ., 1970) \par \i Normal physiology and biochemistry\i0 \par Low plasma cholesterol at 12 weeks (7/8), but intermediate by 24 weeks (Weibust, 1973). High serum ceruloplasmin levels (2/26 in males, 1/27 in females) (Meier and MacPike, 1968). High systolic blood pressure (6/19) (Schlager and Weibust, 1967). Low plasma cholinesterase activity (21/22) (Angel \i et al\i0 ., 1967). High liver tyrosine aminotransferase level in fasted mice (2/10) (Blake, 1970). High kidney (1/12) and liver (2/12) arylsulphatase activity (Daniel, 1976). \par \i Anatomy\i0 \par Large brain weight in females (15/18) (Storer, 1967). Small brain/body weight ratio (20/20) (Roderick \i et al\i0 ., 1973). Large brain weight (5/25) (Roderick \i et al\i0 ., 1973). Large neocortex (1/9) (Wimer \i et al\i0 ., 1969). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Sensitive to lethal effects of ozone (5/21) (Goldstein \i et al\i0 ., 1973). Sensitive to hyperbaric oxygen (5/18) (Hill \i et al\i0 ., 1968). Resistant to X-irradiation as judged by the LD50 (3/8) (Yuhas and Storer, 1969). \par \i Immunology\i0 \par Resistant to experimental allergic encephalomyelitis (cf. 7/18) (Levine and Sowinski, 1973). Erythrocytes have a low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). \par \i Infection\i0 \par Encephalomyocarditis virus causes diabetes mellitus (cf. 7/14) (Boucher \i et al\i0 ., 1975). \par \i Reproduction\i0 \par High post-implantation loss of embryos (2/8) (Leonard \i et al\i0 ., 1971). \par RFM \par Inbr 120 +. Albino \i a,c.\i0 Origin: Furth, to Oak Ridge 1949. Strain has been found to be segregating for \i H2\i0 \i \up8 f\up0 \i0 \up8 \up0 and \i H2\i0 \i \up8 k\up0 \i0 \up8 \up0 and substrains also differ in other respects, so genetic contamination of some substrains must be suspected. Maint. by N. \par Characteristics \par Leukaemia low (5%), but highly susceptible to induction of both myeloid and lymphoid leukaemia by X-irradiation and chemical carcinogens (Walburg and Cosgrove, 1971). Spalding and Brooks (1971) found that the strain was segregating for \i H2\i0 \i \up8 k\up0 \i0 \i \i0 and \i H2\i0 \i \up8 f\up0 \i0 \i . \i0 Two substrains were developed with a mean life-span of 655 _ 8 days in the \i H2\i0 \i \up8 k\up0 \i0 \i \i0 substrain and 604 _ 10 days in the \i H2\i0 \i \up8 f\up0 \i0 \i \i0 substrain, implying that the \i H2 \i0 locus may affect survival. The substrains also differed in radiation resistance and spontaneous activity. The presence of genetic variation within this strain may imply that some substrains have become genetically contaminated by a non-strain mating. Develops a spontaneous myelogenous leukaemia that is transplantable into non-leukaemic mice of the same strain (Huseini \i et al\i0 ., 1976). Reticulum cell sarcomas 57% in males and 70% in females. Lung tumours 24% in males and 19% in females, and non-neoplastic moderate to severe glomerular lesions in more than 50% of animals (Zurcher \i et al\i0 ., 1976). \par RHJ \par Inbr (Le) 72. Albino: \i a,b,c.\i0 Origin: Mutation to rhino-J (\i hr\i0 \i \up8 rhJ\up0 \i0 \up8 \up0 ) in a Carworth Farms stock received by E.P.Nagler, then back to Carworth, then to M.M.Dickie 1951. To Lane 1960. Crosses to BALB/cHu 6 times, b x s to F16, then outcrossed to albino stock followed by b x s. \par Characteristics \par Homozygotes begin to lose hair at about 10 days. Skin becomes thickened and more wrinkled than \i hr/hr\i0 animals, and females do not nurse young. Maint. by J. \par RIII \par Inbr 80+. Albino: \i A,c.\i0 Origin: Dobrovolskaia-Zavadskaia, Inst. du Radium, Paris 1928, then see below. High mammary tumour incidence in unfostered substrains. \par The following substrains are recognised: \par \par RIII. \par Origin as above. \par RIII/An. \par Dobrovolskaia-Zavadskaia to Andervont. \par RIII/SeA. \par From Severi (Perugia) to Muhlbock (Amsterdam) 1964. Differs from the other substrains at the \i Hbb \i0 and \i Mup \i0 loci \par \i Behaviour\i0 \par Short latency to emerge from home cage (2/7), high rearing in Y-maze (2/7), high hole-in-the-wall entries (1/7), high exploration in Y-maze (2/7), high number of stairs climbed (2/7) and low urination score (7/7) (McClearn \i et al\i0 ., 1970). \par \i Life-span and spontaneous disease\i0 \par Long life-span in conventional conditions (19/22 = 685 days in males, 16/22 = 655 days in females) (Storer, 1966). High incidence (88%) of mammary tumours in breeding females (Heston, 1963), but a low proportion are of the acinar type (7/7) (Tengbergen, 1970). Ovarian tumours 60% in breeding females, 50% in virgin females (Murphy, 1966). Mammary tumours 96% at 9 months (Schlom \i et al\i0 ., 1973), 70% at 12 months (Seman and Dmochowski, 1973). Has been known to loose the mammary tumour virus spontaneously (Andervont and Dunn, 1962). \par \i Normal physiology and biochemistry\i0 \par High plasma cholinesterase activity (6/22 in females, 4/22 in males) (Angel \i et al\i0 ., 1967). Mammary gland sensitive to oestradiol and progesterone (1/7) (Singh \i et al\i0 ., 1970). High brain cholinesterase activity (1/5) (Pryor \i et al\i0 ., 1966). \par \i Anatomy\i0 \par Small kidney/body weight ratio (18/21) (Schlager, 1968). Low total leukocyte count (17/18), low erythrocyte count (15/18), high mean corpuscular volume (4/18) (Russell \i et al\i0 ., 1951). High proportion of basophilic cells in adenohypophysis (1/5) (Keramidas and Symeonidis, 1973). Adrenal gland has a small X zone (8/8), with a low incidence of vacuolisation (6/6) (Delost and Chirvan-Nia, 1958). \par \i Drugs\i0 \par Sensitive to X-irradiation (24/27) (Roderick, 1963). Low susceptibility to endotoxin lipopolysaccharide (5/5) (Heppner and Weiss, 1965). \par \i Immunology\i0 \par High lymphocyte phytohaemagglutinin response (5/43) (Heiniger \i et al\i0 ., 1975). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). \par \i Reproduction\i0 \par Poor reproductive performance (7/8), litter size 6.1 _ 0.2 and sterility 31% (Nagasawa \i et al\i0 ., 1973). \par RIIIS \par In 1967 both RIII and RIII/An maintained at The Jackson Laboratory failed to produce viable young. RIII/2J was developed from a cross between the two substrains. Name later changed to RIIIS. High serum complement activity (c.f. 8/26) (Ong et al 1989) \par \i Characteristics\i0 \par RIIIS carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). High ED50 to behavioural effects of nicotine (16/19) (Marks et al 1989). Has the largest known deletion of the T cell receptor (TCR) V beta genes, having lost approximately 130 kb of V beta chromosome and with it 13 V beta genes out of the known 21 V beta genes of the TCR. The deletion is marked by the presence of V beta 10 gene upstream and V beta 3 gene downstream. (Haqqi et al 1989). \par Develops a condition resembling human type I von Willebrand's disease characterised by a prolonged bleeding time, normal von Willebrand factor multimer (VWF) distribution, autosomal dominant inheritance and proportionally decreased plasma von Willebrand factor antigen and factor VIII activity. The disease is caused by a genetic defect at a locus distinct from the murine von Willebrand factor gene (Nichols et al, 1994). A single dominant modifier locus (\i Mvwf\i0 ) on distil chromosome 11 accounted for 63% of variation in plasma VWF levels in a cross with CASA/Rk. This is distinct from the \i Vwf \i0 locus on chromosome 6 (Mohlke et al, 1996). \par Resistant to the induction of arthritis by type II collagen (Ortman et al, 1994). Carries two mutations causing defects in cortosteroid-binding globulin (Orava et al, 1994). \par RLC \par Inbr. F20+?. Albino. Genet. \i rlc/rlc.\i0 Origin: A spontaneous autosomal recessive mutation with rupture of the lens capsule and dislocation of the lens nucleus, designated \i rlc\i0 occurred in the CXSN/A strain. This was crossed with BALB/c followed by more than 20 generations of sib mating. \par Characteristics \par Opacity of the lens of both eyes develops spontaneously at 35-60 days of age. Histologically there is irregular swelling, condensation, degeneration and fragmentation of lens fibers in the deep cortex, leading to rupture of the lens capsule at the posterior pole at 45-100 days of age. Following rupture, the lens nucleus dislocates behind the lens or occasionally in the anterior chamber (Iida et al, 1997). The gene maps to the middle section of chromosome 14 near D14Mit39 at about position 30.0 (Matsushima et al, 1996). \par RNC \par Inbr 50+. Colour ?. Origin: R.C.Roberts, Edinburgh 1968. Three pairs carrying \i Re \i0 (Rex), \i Tr \i0 (trembler) and \i nu \i0 (nude). \i Tr\i0 was lost. Recombinant \i Re,nu/+,+\i0 were mated b x s. Homozygous \i nu/nu \i0 (nude) mice are athymic and have defective cell-mediated immune response. \par ROP \par Inbr (Le) 67. Agouti: \i +.\i0 Origin: Heterogenious stock maintained by M.C.Green in 1960, to Lane 1975. Carries \i Ra/+ \i0 (Ragged), \i Os/+ \i0 (oligosyndactyly) and \i Pt/+ \i0 (pintail). Maint. by Le. \par RR \par Inbr: 40. Genet: \i a, b, C, S. \i0 Origin: Japanses fancy mice from dealer in Sendai to Dept. Pathol., Tohoku Univ. School of Med., 1949, to Dept. Anim. Breed., Fac. Agr., Tohoku Univ. Inbreeding started by T. Ino 1963. \par Characteristics \par Poor breeding performance (Tajima, 1968). \par RSV \par Inbr (Le) 66. Agouti: \i +.\i0 Origin: Carter's Stock 1 (Edinburgh linkage testing stock E1) to Woodworth 1950. Outcrossed to C57BL/6, CBA and C3H. To Lane 1967. b x s thereafter. Carries \i Re/Re\i0 (Rex) \i Sd/+ \i0 (Danforth's short-tail) and \i Va/+ \i0 (varitint-waddler). Maint. by Le. \par RW \par Inbr (W) 82. Albino: \i a,B,c,D.\i0 Origin: Albino mice from the University of Wroclaw, Poland. Inbred since 1960. No known crosses with other strains. \par Characteristics \par Mammary tumours 41% in virgin and 74% in breeding females at 300-400 days. Haematopoetic tumours 41-49% at same age. Maint. by W. \par S \par Inbr ?. Albino \i A,B,c.\i0 Origin: Dept. of Genetics, Ames, Iowa. Probably one of the original lines selected by Lambert in the 1930's for resistance to bacterial infection. To D.Grahn, Argonne in 1963. \par Characteristics \par Very resistant to \i S. typhimurium.\i0 Moderate life expectancy. Good litter size but poor fertility. Usual spectrum of neoplasia. \par SAMP1 \par Inbr. F?+59 (1993). Origin: Dr. Toshio Takeda, Dept. of Senescence Biology, Chest Disease Research Institute, Kyoto University, Sakyo-ku, Kyoto 606, Japan, from AKR/J mice imported from J in 1968 and crossed (?) with mice of an unknown strain, followed by sib mating since 1975. Albino (\i c\i0 ). All SAMP mice have been defined at approx. 20 loci. There is only minor variation among the strains restricted to the \i Idh1, Mod1\i0 and \i Car2 \i0 loci. The origin, history and characteristics of the SAM family of strains has been summarised by Takeda (1994), Higuchi (1997) and Takeda et al (1997). \par Characteristics \par All mice over 8 months show amyloid deposition of AApoAII protein (Higuchi et al 1986) due to an amino acid substitution in a precursor of apoA-II (Yonezu et al 1987, Higuchi et al 1991). About 75% of mice over 10 months have kideny defects. Autoimmunity develops early in life (Yoshida et al 1989). There is an age-related increase in the frequency of chromosomal abberations in bone marrow cells (Nisitani et al 1990). Strain has accelerated aging with median survival time of 374 days (Takeda et al 1991). \par SAMP10 \par Inbr ?+50. Origin: as SAMP1. Albino (\i c\i0 ). \par Characteristics: \par Shows accelerated aging.All mice over 8 months have amyloidosis and about 78% of mice over 10 months have contracted kidneys. Median survival time in conventional conditions is 333 days. (Takeda et al 1991). Spontaneous brain atrophy with advancing age. This is most marked in the frontal cortex, and other neocortical regions develop diffuse atrophy. Age-related loss of neocortical neurones is evident (Shimada et al 1992), and correlates with deficits in learning (Shimada et al 1993). Aged garlick oil prevents the development of atrophic changes in the frontal brain at 12 months (Moriguchi et al, 1997). \par SAMP2 \par Inbr. ?+62. Origin: as SAMP1. Albino (\i c\i0 ) \par Characteristics \par Shows accelerated aging (Takeda et al 1991). All mice over 7 months have amyloidosis in which AApoAII often co-exists with AA amyloid protein (Higuchi et al 1983). The incidence of contracted kidney is about 73% at over 10 months of age. Median survival is 304 days in conventional conditions. \par Appears to be a suitable model for studies of senile lung (Teramoto et al, 1994). \par SAMP3 \par Inbr ?+56. Origin: as SAMP1. Albino (\i c\i0 ). \par Characteristics: \par Shows accelerated aging (Takeda et al 1991). The first of the SAMP series to show degenerative changes in the condyle of the temporomandibula joint, reaching approx 50% at 7-9 months and 100% at over 12 months (Chen et al 1989). Median survival time is 507 days in conventional conditions. \par SAMP6 \par Inbr ?+56. Origin: as SAMP1. Albino (\i c\i0 ). \par Characteristics: \par Shows accelerated aging (Takeda et al 1991). Has a significantly lower peak bone mass than other SAMP strains, but rate of decrease is similar to other strains. Mineral and collagen contents per dry weight of bone show little difference between strains. This suggests that osteopenia is not due to osteomalacia but rather to osteoporosis (Matsuchita et al 1986). Median survival is 321 days in conventional conditions. \par SAMP7 \par Inbr ?+57. Origin: as SAMP1. Albino (\i c\i0 ). \par Characteristics: \par Shows moderate to severe accelerated aging (Takeda et al 1991). About 43% of the mice aged 3 to 12 months have thymic lymphoma. Median survival time is 326 days in conventional conditions. \par SAMP8 \par Inbr ?+59. Origin: as SAMP1. Albino (\i c\i0 ). \par Characteristics: \par Shows accelerated aging (Takeda et al 1991). Deterioration in passive and active avoidance tasks progresses with advancing age and becomes significant at 4 and 8 months of age, respectively (Yagi et al 1988, Ohta et al 1989). Age-related massive occurrence of PAS-positive granular structures often observed in the hippocampus and spongiform degeneration of the reticular formation of the brain stem are unusual neuropathological findings (Akiyama et al 1986). Hippocampal glutamic acid content is higher than in SAMP1 (Nomura et al 1991). Median survivial time is 364 days in conventional conditions. \par SAMR1 \par Inbr. F?+49. Albino, \i c\i0 . \i Origin\i0 : Dr. Toshio Takeda, Dept. of Senescence Biology, Chest Disease Research Institute, Kyoto University, Sakyo-ku, Kyoto 606, Japan, from AKR/J mice imported from J in 1968 and crossed (?) with mice of an unknown strain, followed by sib mating since 1975 with selection for normal life-span. \par \i Characteristics\i0 : \par About 25% and 22% of the mice aged over 16 months which die naturally have lymphocytic and histiocytic neoplasia, respectively. About 68% of females which die after 20 months of age have ovarian cysts. Median survival is 568 days in conventional conditions. Good passive avoidance skills up to 22 months of age. Used as a normally-aging control strain for the SAMP (Senescence-Accelerated Mouse) strains (see Takeda et al 1981, Hosokawa et al 1984, Takeda et al 1991) \par SB \par Inbr (Le) 101. Pale grey. \i sa,bg,A\i0 \i \up8 w\up0 \i0 \i .\i0 Origin: mutations to \i sa\i0 and \i bg,\i0 possibly rediation-induced, occurred independently in stocks used for mutation rate studies at Oak Ridge. Rl to Le 1961, then sib-mated. \par Characteristics \par Develops progressive infectious pneumonitis associated with the beige gene. Also has a high incidence of lymphadenopathy, including reticulum cell neoplasms and atypical lympho-proliferative lesions. Beige mice have giant lysosomal granules in the leukocytes and pigment dilution closely analogous to the Chediak-Higashi syndrome in man and similar disorders in mink and cattle. These mice appear to be a suitable model for the study of the increased susceptibility to infection seen with this syndrome (Lane and Murphy, 1972). \par SC \par Inbr (U) ?+93. Albino: \i c.\i0 Origin: A "Bagg Swiss" from Rockefeller Inst. to Laidlow (Hampstead, England), to Hagedoorn, to CPB-TNO (1949), to Vet. Fac. Utrecht in 1973. Probably same origin as BRVR and BRVS. \par Characteristics \par Males are rather aggressive. Selected for "bacillary resistant, virus susceptible" (like BSVS ?). Hyporesponder to dietary cholesterol. Maint. by U. \par SD \par Inbr (Glw) 122. Albino: \i c.\i0 Origin: Dunn and Gluecksohn-Waelsch. Carries \i Sd \i0 (Danforth's short-tail) gene. \par Characteristics \par Homozygotes and some heterozygotes develop urogenital abnormalities, and die shortly after birth. Heterozygotes have short tails and other abnormalities. Maint. by Glw. \par SEA \par Inbr (J) 142. Grey \i b,d,+/d,se.\i0 Origin: EL and MC Green from BALB/c x P. Carries se (short-ear) gene causing short ears, skeletal abnormalities. \par Characteristics \par Host for transplantable rhabdomyosarcoma T811. Low lymphocyte phytohaemagglutinin response (40/43) (Heiniger \i et al\i0 ., 1975). \par SEC \par Pale brown: \i a,b,c\i0 \i \up8 ch\up0 \i0 \i .\i0 Origin: Green prior to 1946 from a cross between NB and BALB/c. Carries \i se \i0 (short-ear) gene causing short ears and skeletal abnormalities. Substrains as follows: \par SEC/Rl \par Inbr (Rl) 100 +. Colour ?: \i a,b,c\i0 \i \up8 ch\up0 \i0 \i ,d,se \i0 .Origin: E.L.Green 1948 to Rl at F20-F21. Maint. by J. \par \par SEC/1Gn \par Inbr (Le) 149. Gets multiple lung cysts, especially in \i se/se\i0 . \par \par SEC/1Re \par Inbr (J) 138. From SEC/1Gn, but short-ear eliminated by E.S.Russell. \par Characteristics \par High shuttle-box avoidance (2/5) (Messeri \i et al\i0 ., 1972). High plasma cholinesterase activity (7/22 in females, 2/22 in males) (Angel \i et al\i0 ., 1967). High hepatic delta-aminolaevulinic acid synthetase activity after DDC treatment (3/15) (Gross and Hutton, 1971). Low sensitivity of females to X-irradiation (5/5) (Ehling, 1964). Low lymphocyte phytohaemagglutinin response (31/43) (Heiniger \i et al\i0 ., 1975). Good reproductive performance (1/5) (Ehling, 1964). \par SELH \par Inbr. F20+. Non-agouti, black, chinchilla (\i aaBBc\i0 \i \up8 ch\up0 \i0 \i c\i0 \i \up8 ch\up0 \i0 \up8 \up0 ). Origin: A partially inbred stock of mixed background, including BALB/cGa, 129/- and CBA/- and homozygous for the lidgap-Gates (\i lgG\i0 \i \up8 a\up0 \i0 \up8 \up0 ) was backcrossed to N3 in 1977 with outbred BLU:Ha(ICR) mice from Arbor Scientific Company, Ontario, Canada. A new recessive mutation spherocytosis-British Columbia\i (sph\i0 \i \up8 2Bc\up0 \i0 \up8 \up0 ) appeared at the second intercross (N3xN3), and was selected for during brother x sister mating with the elimination of the lidgap-Gates mutation. Exencephaly was observed in 1981 at F5. Exencephaly producing parents were selected in subsequent generations, and all animals trace back to a single breeding pair at F6. The strain has been typed at 28 polymorphic loci (Juriloff et al, 1989). See also Gunn et al (1992). \par Characteristics \par High incidence of exencephaly at birth which has been attributed to two or three additive genetic loci which differ between SELH and the closely-related normal strain ICR/Bc. Defects may be related to abnormal cranial neural tube closure mechanism with a lack of the initiation of contact and fusion of the cranial neural tube at the prosencephalon/mesencephalon boundary (Closure 2). SELH mice undergo closure by extension of a more rostral site of fusion (Gunn et al, 1995) leading to 10-20% exencephaly, cleft cerebellum and 5-10% ataxia in young adults, which all appear to be causally related (Juriloff et al, 1993, Gunn et al, 1995, Harris et al, 1994). More sensitive to retinoic acid (Tom et al, 1991) and valproic acid-induced (Hall et al, 1997) exencephaly than SWV/Bc and ICR/Bc. The strain appears to have a high incidence of spontaneous mutations, including three at the albino locus (Juriloff et al, 1994). \par SEN \par Inbr (Or) 20. Albino \i c.\i0 Origin: From outbred "SENCAR" mice produced by Boutwell (1964) using Rockland-derived mice from A.Sutter, Springfield Mo. Selected for skin tumors following initiation by DMBA and promotion with croton oil. Later crossed with outbred CD-1 mice. To McArdale Lab. for Cancer Research, to Oak Ridge. Inbred by Sloga in 1979 with further selection to F9 for skin tumors following treatment with DMBA and TPA. Maint. by Or. \par SF \par Inbr (Dn) 42+32. Agouti \i +.\i0 Origin: wild mice trapped in coal mine and sib-mated by M.Barnawell (Berkeley CA) as 'Corte Madera' to Cambridge 1959. Maint. by Dn. \par SF-5613 \par Inbr: 45. Genet: \i a\i0 . \par Characteristics \par Selected for late sexual maturity of males. Mean age of first fertile mating formerly 58.8 days, now 52 days; mean body weight at 100 days, 28.9 g. \par SF-5621 \par Inbr: 36. Genet: \i A, b. \i0 \par Characteristics \par Selected for late sexual maturity in males. Mean age of first fertile mating. 58.2 days; mean weight body at 100 days, 32.3 g. \par SF/Cam \par Inb : 42 + 8. Genet: +. Origin: Wild mice trapped in a coal mine and sib-mated to F10 by M. Barnawell (Berkeley, Calif.) as `Corte Madera', to Cambridge 1959. \par Characteristics \par Adrenal X zone relatively and absolutely large in females; very poorly developed zona glomerulosa (Wallace, 1970). High serum complement activity (c.f. 8/26) (Ong et al 1989) \par SHI \par Inbr (Le) 78. Agouti chinchilla: \i cc\i0 \i \up8 h.\up0 \i0 \up8 \up0 Origin: Snell's FS stock to M.C.Green. Outcrossed to C57BL/10Gn then b x s. To Lane 1975. Carries \i sh1 \i0 (shaker-1) gene. \par Characteristics \par Homozygotes show circling, head tossing, deafness and hyperactivity. Maint. by Le. \par SHM/2Gn \par Inbr: 35. Genet: + \i /shm. \i0 Origin: \i shm \i0 (shambling) mutation arose in random-bred stock in March 1960. This strain descended from (SHM/Gn x C57BL/6J) x C3HeB/FeJ (SHM/Gn discontinued at F35 in 1970). \par Characteristics \par Homozygotes have abnormal gait, small body size, phospholipidosis, sterility, low viability (Green, 1967). \par SHN \par Inbr: F51 (Mei). Genet: \i c, A, b. \i0 Origin: Swiss albino mice from the City of Hope Medical Centre, California. Inbred as SWM/Ms by Natl. Inst. Genet. Misima. Selected for high early mammary tumour incidence with full-sib mating starting in 1964, and F20 in 1972. \par Characteristics \par Have mammary tumour virus locus \i Mtv4\i0 which is genetically transmitted rather than being passed through the milk (Imai \i et al\i0 1983). Tumour incidence 90-100% in breeders and virgins at 6.6 months. Litter size 7.6, weaning rate 89% (Nagasawa \i et al\i0 ., 1976a, b). See also SLN. \par SHR \par Inbr (Dn) 59. Colour ?. Origin: E.L.Green from \i shm\i0 (shambling) mutation which arose in outbred stock in 1960. Crossed with C57BL/6J, C3HeB/FeJ and finally to a \i Re\i0 (rex) stock. Strains SHM and SHM/2 from same cross discontinued in 1970 and 1977. \par Characteristics \par Homozygotes have abnormal gait, small body size, are infertile, and have phospholipid-like material deposited in the central nervous system. Maint. by Dn. \par SIIT \par Inbr: F39. Genet: \i a, b, s. \i0 Origin: From hybrids between KSB and NBR in 1964. Characteristics Brown, piebald, to be used as a marker-testing strain. \par SIM [Sandos Inbred Mice] \par Inbr: F 20 + (?). Albino. Origin: A strain of Swiss mice highly susceptible to Friend virus. Congenic line SIM.R has been developed by backcrossing resistance gene from C57BL/6 (Ware and Axelrad, 1972). (NOTE: This is not the SIMPSON strain.) \par SJL \par Inbr: F104 (J). Albino. Genet: \i c, p, rd. \i0 Origin: Swiss Webster outbred stock from three sources that were brought to The Jackson Laboratory between 1938 and 1943, and pen-bred until 1955, when sib-mating was started. Although the strain has been developed relatively recently, it has rapidly become widely used owing to the high incidence of reticulum cell sarcomas resembling Hodgkin's disease. General biological data on the strain have been reviewed by Crispens (1973). Carries the pink-eyed dilution gene, \i p\i0 , which is derived from Asian mice of the \i Mus musculus\i0 type (see also strains 129/J, P/J and FS/Ei) (Brilliant et al, 1994) \par \i Behaviour\i0 \par High spontaneous fighting (Page and Glenner, 1972). Severe fighting among males housed together, beginning at about 8 weeks. Most males will be killed by 4-5 months unless caged separately (Crispens, 1973). \par \i Life-span and spontaneous disease\i0 \par Short life-span in conventional conditions (8/22 = 472 days in males, 3/22 = 395 days in females). High gross tumour incidence (4/22 females, 6/22 males) (Storer, 1966). Reticulum cell sarcomas appear in about 90% of animals at an average age of about 13 months (Murphy, 1963; Crispens, 1973; Fujinaga \i et al\i0 ., 1970). These first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes (Crispens, 1973). Most of the tumours are pleomorphic or mixed-cell types commonly called type-B reticulum cell neoplasms by Dunn, but a few are type-A histiocytomas. The unusual feature of the SJL reticulum cell tumours is their regular and early appearance, with the preneoplastic lesion detectable as early as 22 days (Potter, 1972). Tumour development as well as autoimmunity may result from an effective amplification of the immune response (Owens and Bonavida, 1976). Leukaemia 83% (Myers \i et al\i0 ., 1970). High incidence of spontaneous amyloidosis, possibly associated with fighting (Page and Glenner, 1972). Develops gamma-l and gamma-2 paraproteinaemia (Wanebo \i et al\i0 ., 1966). Hyperplastic neuroretinopathy and disorders of pigment epithelial cells with a high incidence of subretinal tumor is present at 9 days (Caffe et al 1993). \par \i Normal physiology and biochemistry\i0 \par Low plasma cholesterol at 24 weeks (7/8 males, 8/8 females) (Weibust, 1973). High metabolic rate (2/18) (Storer, 1967). Low serum ceruloplasmin levels in females (23/27) but intermediate in males (Meier and MacPike, 1968). High systolic blood pressure (5/19) (Schlager and Weibust, 1967). Low plasma cholinesterase activity in males (20/22) (Angel \i et al\i0 ., 1967). High mean heart rate (1/7), but low mean heart rate adaptation (7/7) (Blizard and Welty, 1971). High brain sphingosine (1/5) and low brain sterol (5/5) (Sampugna \i et al\i0 ., 1975). Low hepatic delta-aminolaevulinic acid synthetase activity after DDC treatment (13/15) (Gross and Hutton, 1971). Venous blood has a low pH (9/10) (Dagg, 1966). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). High intrinsic myogenicity of muscle cells both in-vivo and in-vitro (Maley et al, 1994, Mitchell et al, 1995)). \par \i Anatomy\i0 \par Low brain weight (17/18 in males, 16/18 in females) (Storer, 1967). Low brain weight (22/25), small spinal cord (24/25) (Roderick \i et al\i0 ., 1973). Cerebellum has no intraculminate fissure between vermian lobule IV and vermian lobule V (the ventral and dorsal lobules of the culmen) (contrast DBA/2) (Cooper et al 1991). Low percent carcass lipid on a high-fat diet (3/9) (West et al 1992). Low retinal ganglion cell number (6/24) (Williams et al, 1996). High bone density of femur (4/11) (Beamer et al, 1996). \par \i Drugs\i0 \par Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to induction of subcutaneous tumours by 3-methylcholanthrene (11/14) (Kouri \i et al\i0 ., 1973), (9/12) (Whitmire \i et al\i0 ., 1971). Resistant to X-irradiation (3/27) (Roderick, 1963). Poor ovulatory response to 3 I.U. (5/6) and 7 I.U. (5/6) of PMS, but response facilitated by exposure to males at latter dose rate only (Zarrow \i et al\i0 ., 1971). Resistant to hyperbaric oxygen (14/18) (Hill \i et al\i0 ., 1968) Short survival in 90% oxygen (2/10) (Lieberman and Kellog, 1967). Resistant to X-irradiation as judged by the LD\dn8 50\dn0 (Yuhas and Storer, 1969). Susceptible to induction of splenic amyloidosis by injection of casein (1/7) (Clerici, 1972). Susceptible to induction of lymphoid and myeloid leukaemia by DMBA (Crispens, 1973). Resistant to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (4/4) (Bhathal et al 1990). Airways hyporeactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995). Low voluntary comsumption of morphine in two-bottle choice situation (12/15) (Belknap et al, 1993). Susceptible to weight loss induced by cocaine, but this is attenuated by anisomycin (cf C3H, CBA) (Shimosato et al, 1994). \par \par \i Immunology\i0 \par Susceptible to induction of experimental allergic encephalomyelitis (EAE) (1/18) (Levine and Sowinski, 1973). High susceptibility to induction of EAE (1/10) but moderate mortality (Lindsey, 1996). Low lymphocyte phytohaemagglutinin response (29/43) (Heiniger \i et al\i0 ., 1975). Poor immune response to small doses of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to DNP-keyhole-limpet haemocyanin (11/11) (Borel and Kilham, 1974). No immune response to GAT (random terpolymer of Glu\up8 60\up0 , Ala\up8 30\up0 , Tyr\up8 10\up0 ) (10/10) (Dorf \i et al\i0 ., 1974). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18) (McCarthy and Dutton, 1975). Very sensitive to anaphylactic shock (Treadwell, 1969). Resistant to induction of immunological tolerance (1/14) (Fujiwara and Cinader, 1974). Poor immune response to (Pro\up8 66\up0 , Gly\up8 34\up0 )n (7/7) (Fuchs \i et al\i0 ., 1974). High (3/12) susceptibility to IgE- and IgG\dn8 1\dn0 -mediated passive cutaneous anaphylaxis (De Souza \i et al\i0 ., 1974). Erythrocytes have a high agglutinability (cf. 14/25) (Rubinstein \i et al\i0 ., 1974). Low response to Dextran (cf. 6/10) (Blomberg \i et al\i0 ., 1972). Immune response to type-III pneumococcal polysaccharide declines by 42 weeks, in contrast to BALB/c and C3H (Smith, 1976). Susceptible to induction of experimental autoimmune thyroiditis (cf. 2/5) (Vladutiu and Rose, 1971a). Thymocytes exhibit a periodicity (5-9 days)in their response to hormonal stimulation with isoproterenol. This is expressed in large changes in the intensity of the response (peak levels of intracellular cAMP which vary approximately 6-fold), and in the response pattern, i.e., in the occurrence or non-occurrence of an immediate hormone-induced desensitization. In contrast, C57BL/6 thymocytes have a homogeneous response pattern (Riven-Kreitman et al 1990). Resistant to immunosuppression of contact hypersensitivity by ultraviolet B light (cf 4/18) (Noonan and Hoffman, 1994). Low natural killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (6/6) (Pope et al, 1994). Has defective T cell receptor-induced interleukin-4 production and absence of T-cells with the NK1.1 antigen. However, natural-killer-like T-cells develop nromally in spite of these defects (Beutner et al, 1997). Mast cells grow faster in culture and have more than twice the amount of histamine and TNF-alpha in their granules than BALB/c (Bebo et al, 1996). High level of serum complement C5 (Lynch and Kay, 1995). \par \par \i Infection\i0 \par Encephalomyocarditis virus causes diabetes mellitus (cf. 7/14) (Boucher \i et al\i0 ., 1975). High susceptibility to develop leukaemia on infection with Friend virus (cf. 5/11) (Dietz and Rich, 1972). Resistant to measles virus (1/6) (Rager-Zisman \i et al\i0 ., 1976). Develop flaccid paralysis and survivors develop a distinct neurological disorder associated with marked mononuclear cell infiltration and active demyelination in spinal cord after intracerebral inoculation with Theiler's encephalomyelitis virus. Incubation period may be 2-3 months (Lipton and Dal Canto, 1976). Resistant to street rabies virus (SRV) injected via the intraperitoneal route (Perry and Lodmell 1991). Develops herpes simplex encephalitis (HSE) resembling the human condition, following intranasal infection with a neurovirulent clinical isolate of herpes simplex virus type 1 (contrast 9 other strains) (Hudson et al 1991). Resistant to carditis on infection with Lyme borreliosis (\i Borrelia burgdorferi) (contrast C3H, SWR, BALB/c)\i0 (Barthold et al 1990). High eosinophilia on infection with the helminth \i Mesocestoides corti \i0 (1/12) and highly susceptible to infection with the parasite. Larval burdens at 21 days after infection with 100 tetrathyridia being considerably higher (greater than 1000) than all other strains except NIH, which was comparable. (Lammas et al 1990). Susceptibile to infection by \i Helicobacter felis\i0 with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). \par \par SK \par Inbr: F?+38 (Dn). Origin: From three mice trapped on Skokholm Island off Pembrokeshire in 1962 by R. J. Berry; inbred by M. Wallace (Wallace, 1970). Then to Rk, Dn, and Ei. \par Characteristics \par Fairly large litters, the size of which dropped little on inbreeding. \par SL \par Inbr(A) ?+90. Albino: \i A,B,c.\i0 Origin: Outbred Swiss mice to Keio University in 1941, University of Tokyo in 1944, then Hokkaido University at an unknown date and Misima in 1951. Derived as a high-leukaemia strain by K. Tsuchikawa in Misima. Transferred to Kyushu University in 1954 from where the four current substrains are derived. These differ in leukaemia incidence, ecotropic virus expression, as well as for a number of genetic markers (Hiai et al 1987). A detailed genetic analysis of the four substrains designated SL/QDj, SL/Am, SL/Ni and SL/Kh using 100 microsatellite markers showed that the Am and Ni substrains were almost identical, though they differ in biological characteristics with the Am strain having a high incidence of lymphoma not found in the Ni substrain. SL/Kh has probably been contaminated by AKR, and the QDj substrain seems to be a recombinant between the Am and Kh substrains. All four substrains have the\i H2\i0 \i \up8 q\up0 \i0 \up8 \up0 haplotype. The Ni and Am substrains carry the type 1 \i Mx\i0 gene conferring resistance to influenza virus, also found in strain A2G (Abujiang et al, 1996). \par Characteristics \par In Misima leukaemia incidence is low (Tajima, 1968). Kh substrain develops B-lymphomas associated with a gene in the H2 complex (Yamada et al, 1994), and ecotrophic murine leukemia viruses (Pataer et al, 1996). High and early incidence of nonthymic lymphomas at an unusually early age, with a cumulative incidence of 88% in females and 48% in males by the age of six months, rising to 100% in females and 94% in males by 12 months. Two types of poorly differentiated leukemias were seen with the major type proliferating in lymph nodes and the spleen and the minor type in the bone marrow, causing paraplegia by spinal compression with many host and epigenetic factors favourable for lymphoma development (Hiai, 1996). Other papers describing SL/Kh include Hial et al, (1992), Shimada et al, (1993) and Lu et al, (1997). \par SLN \par Inbr (Mei) 45. Colour ?. Origin: see SHN. This is the high-late mammary tumour line. \par Characteristics \par Mammary tumour incidence is about 50-60% in breeders, 9-10% in virgins at 10 months. Litter size 5.8, weaning rate 60%. Maint. by Mei. \par SM/J \par Inbr (J) 112. White-bellied agouti or black \i A\i0 \i \up8 w\up0 \i0 \i /a\i0 or \i a/a.\i0 Origin: MacArthur, 1939 by crossing seven stocks including DBA and selecting for small body size. To Runner 1948, who began b x s mating. Small body size at birth and weaning, but this relatively small size tends to disappear as the animals mature. Very low tumour incidence. Carries a number of relatively rare polymorphic alleles. Maint. by A,J. \par Characteristics \par Intermediate life-span in conventional conditions (13/22 = 572 days in males, 14/22 = 591 days in females). Low gross tumour incidence (20/22) (Storer, 1966). Life-span, sexes combined, 422 days (Chai, 1959). High incidence of amyloidosis (Russell and Meier, 1966). High porphyrin content of Harderian gland (4/16) (Margolis, 1971). High spermatazoal beta-glucuronidase activity (2/9) (Erickson, 1976). Low brain weight in males (15/18) (Storer, 1969). Large brain/body weight ratio (4/20) (Roderick \i et al\i0 ., 1973). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Long survival on Warfarin (10/12) (Lush and Arnold, 1975). Low lymphocyte phytohaemagglutinin response (39/43) (Heiniger \i et al\i0 ., 1975). Susceptible to the development of atherosclerosis on a semi-synthetic high fat diet but in contrast with C57BL/6 and SWR they had the same level of high-density lipoprotein cholesterol levels as on chow and high fat diets (3/9) (Nishina et al, 1993). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid did not cause a high incidence of cholesterol gallstones (like AKR, DBA/2 contrast C57L, SWR, A) (Faulkner et al, 1995). Small body weight which differs from that of the large strain LG/J as a result of about seven quantitative trait loci at one week and 17 loci at 10 weeks of age. Each locus has a small effect (Cheverud et al, 1996). \par SM/JH \par Inbr ? +16 (H). White-bellied agouti substrain \i A\i0 \i \up8 w\up0 \i0 \i /A\i0 \i \up8 w\up0 \i0 \i .\i0 Chai to Bateman (Edinburgh) 1958, to Dickinson 1961, to Lush in early 1970's, to Peters (Harwell), to Nash, to Peters again in 1979. Identical wth SM/J at seventeen loci, but differs in being \i Gpi1\i0 \i \up8 b\up0 \i0 \up8 \up0 while SM/J is \i Gpi1\i0 \i \up8 a\up0 \i0 \i .\i0 This is believed to be due to residual heterozygosity or mutation rather than genetic contamination (Peters and Lyon 1986). \par SMXA \par Inbr. F32-40 (1995). Set of recombinant inbred strains derived from a cross between SM/J and A/J (Goto et al 1993). Inbreeding started in 1985, and a total of 26 strains have been developed, designated SMXA1 to SMXA30 (strains 2, 13, 20 and 28 are extinct). So far, the strains have been typed at 158 marker loci (Nishimura et al, 1995). \par SPE \par Inbr. 23 (1989). Origin: Wild \i Mus spretus\i0 trapped in Santa Fe (near Granada, Spain) by Louis Thaler in 1978, then maintained as a closed colony by Bonhomme. Later inbred at the Pasteur Institute. \par SRH \par Inbr: F63 (Crusio). Dilute brown: \i a, b, d.\i0 Origin: van Abeelen, C57BL/6J x DBA/2J, backcrossed to DBA/2 five generations, followed by b x s (from 1966) with selection for behavioural traits. \par Characteristics \par High frequency of exploratory rearing responses and high locomotor activity (Abeelen, 1975). Maint. Crusio, Nmg. \par SRL \par Inbreeding, genetics and Origin: As SRH. \par Characteristics \par Differs from SRH in developmental-age dependent behavioural characters, and in hippocampal anatomy. Low frequency of exploratory rearing and low locomotor activity. \par SS \par Inbr. 86. Albino: \i A,B,c.\i0 Origin: Japanese laboratory mice from a dealer (Umemori) in 1963. Inbred by S.Nishida. \par Characteristics \par Good reproductive performance. Homogeneous reaction to \i Staph. aureus \i0 E 46Y, and high incidence of diabetes after alloxan. Good reproductive performance, good nursing (Tajima, 1968). \par SSIN \par Inbr (Utsp) 22+. Albino. Origin: 1970's, from outbred SENCAR (sensitive to carcinogens) selected for high skin tumour number following challenge for 10 generations with a topical application of dimethylbenz(a)anthracene followed by repetitive application of the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Inbred in 1986. \par Characteristics \par Hardy animals with low spontaneous tumour incidence; useful in chemical carcinogenesis studies because of extreme sensitivity to TPA (Fischer \i et al\i0 1987). Low LD50 following injection of butylated hydroxytoluene (BHT) (4/4) (Kehrer and DiGiovanni 1990) \par \par \par SSL \par Inbr (Le) 60. White spotted, heavy spotting or black-eyed white depending on genotype: \i a, s/s\i0 or \i s/s\i0 \i \up8 l\up0 \i0 \i ,\i0 or \i s\i0 \i \up8 l\up0 \i0 \i /s\i0 \i \up8 l\up0 \i0 \i .\i0 Origin: Developed by Le. \i s\i0 \i \up8 l\up0 \i0 \up8 \up0 arose in the F2 from a cross of C3H/HeSn x C57BL/6J. b x s to F18. In 1968 outcrossed to \i a/a,\i0 \i s/s\i0 stock (F19) and maintained by sib mating of \i s/s\i0 \i \up8 l\up0 \i0 \up8 \up0 to present. The \i s \i0 gene came from a multiple recessive stock of Holman to Runner before 1955. Outcrossed to C57BL/6J and b x s to F19. In 1968 crossed to a \i a/a hr+/+s\i0 \i \up8 l\up0 \i0 \up8 \up0 to make \i s/s\i0 \i \up8 l\up0 \i0 \i .\i0 \i s\i0 \i \up8 l\up0 \i0 \i /s\i0 \i \up8 l\up0 \i0 \up8 \up0 get megacolon and generally die though a few live to breed. Maint. by Le. \par ST \par Inbr.(J) 143. Albino \i a,b,c.\i0 Origin: Englebreth-Holm from outbred Danish white mice in about 1940. To Heston in 1947 at F23. Two major substrains are known which differ at the \i H2\i0 locus. These were separated after more than eight generations of sib-mating. \par \par ST/a \par See above. This is the \i H2\i0 \i \up8 b\up0 \i0 \up8 \up0 substrain which is not so widely used. \par \par ST/b \par See above. \i H2\i0 \i \up8 k\up0 \i0 \up8 \up0 substrain. Maint. by J,N. \par Characteristics \par Life-span in conventional conditions short (5/22 = 433 days in males, 9/22 = 511 days in females), but low gross tumour incidence (21/22 in females, 19/22 in males) (Storer, 1966). \par High preference for sweet tasting substances (saccharin, sucrose,dulcin and acesulfame, averaged) (2/26) (Lush 1988). Low metabolic rate (17/18) (Storer, 1967). Low serum ceruloplasmin levels in females (27/27), but intermediate levels in males (Meier and MacPike, 1968). Large spinal cord (3/25) (Roderick \i et al\i0 ., 1973). Low thyroid weight (5/5) (Mendoza \i et al\i0 ., 1967). Low haemoglobin per ml blood (18/18) (Russell \i et al\i0 ., 1951). Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas \i et al\i0 ., 1973). Resistant to X-irradiation (4/27) (Roderick, 1963). Short survival in 90% oxygen (10/10), but high susceptibility to pulmonary hyaline-membrane formation (2/10) (Lieberman and Kellog, 1967). Resistant to chloroform toxicity (cf. 5/9) (Deringer \i et al\i0 ., 1953). Resistant to experimental allergic encephalomyelitis (cf. 7/18) (Levine and Sowinski, 1973). Erythrocytes have low agglutinability (cf. 11/25) in b substrain (Rubinstein \i et al\i0 ., 1974). Susceptible to \i Plasmodium berghei \i0 infection (2/8) (Most \i et al\i0 ., 1966). Resistant to seizures induced by nicotine (1/19) (Marks et al 1989). Low self-selection of nicotine (6/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996). Resistance may be related to brain alpha-bungarotoxin binding, which is significantly higher in ST/b than in sensitive DBA/2 mice (Marks et al, 1996). Defect in the expression of the alloantigen, Ly6C, which is not detectable on spleen or lymph node cells (c.f. NOD and NZB but contrast most other strains) and may be due to an interruption in the flanking region of the Ly6C gene at a point 475 bp upstream of the transcription initiation site, as found in NOD (Philbrick et al 1990). \par STAR \par Inbr (N) 83. Albino: \i c.\i0 Origin: Gotchevsky (Austria) who obtained a stock of albino mice from Bittner in the early 1930's, to NIH in 1972. Homozygous for a dominant cataract. Maint. by N. \par STR \par Inbr (N) 145. Brown \i a,b.\i0 Origin: Strong from a stock treated with methylcholanthrene between generations F4 and F27. \par Characteristics \par Susceptible to periodontal disease. Polydipsia with the daily water intake of the polydipsic STR/N of both sexes being between five and eight times that of nonpolydipsic controls: STR/1N, and Swiss-Webster (S/W) mice. Polydipsia may depend, at least in part, on the angiotensin II system in the brain. (Katafuchi et al 1991). Susceptible to periodontal disease (Baer \i et al\i0 ., 1961); polydipsic. \par STR/1 and STR/Ort \par Inbr (N) 138. Piebald brown. \i a,b,s.\i0 Origin: piebald mutation in STR at F29 in 1961. Develops osteoarthropathy of the knee joints, and obstructive uropathy in males before 16 months. Maint. by N. \par Characteristics \par Osteoarthropathy of the knee joints (Russell and Meier, 1966). The condition has been considered in detail by Walton 1977a, b, 1979 a, b, c). Oseroarthrosis is a non-inflammatory disease in which there is degeneration if the articulating surfaces of a joint with associated thickening of the underlying bone. By around 12 months of age 60% of males and 30% of females have osteoarthrosis as assessed radiologically. Medial patella dislocation, which can be prevented by surgical stabilization of the patella leading to a reduction in the disease, is a common feature of the condition. Eventually, the conditions becomes so severe as to impair joint movement. \par Up to 90% of male mice develop osteoarthritis which is related to changes in monoamine oxidase activity and distribution, and catecholamine metabolism. Simultaneous treatment with both diclofenac sodium and tribenoside resulted in 7/9 mice having no sign of osteoarthritis (Chayen et al, 1996). \par Changes in the patellar tendon of males were observed at five months using magnetic resonance imaging. Other degenerative features were seen at nine months (Munasinghe et al, 1996). \par High level of plasma phospholipids, cholesterol, cholesterol ester and total lipids, but no excessive obesity (Yamamoto \i et al\i0 ., 1963). Sokoloff et al (1962) considered that the mice become obese, but Walton (1979a) found that males were not obese when compared with CBA, though females were, and did not consider that obesity was associated with the osteoarthropathy. Polydipsia (Bernstein, 1966) and obstructive uropathy constantly seen at less than 16 months (Russell and Meier, 1966). Urine has low osmolality (7/7) (Silverstein, 1961). \par STS \par Inbr (A) 100. Albino: \i c.\i0 Origin: Muhlbock, from albino mice from the Hyg. Inst. Zurich in 1955. \par Characteristics \par In contrast with five other strains, STS is resistant to mammary tumour induction by hypophysial isografts (van der Gugten et al 1985). No mammary tumours but lung tumours in both sexes; closely related to LIS/A and LTS/A. Leukosis 8% (Hilgers and Galesloot, 1973). High preference for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame, averaged) (3/26) (Lush 1988). Carries an incomplete proviral genome of endogenous mammary tumour virus (MMTV) on the Y chromosome (c.f. 4/10) (Nishikawa et al 1991). Higher proliferative response in the mixed lymphocyte culture than BALB/c when tested with cells from eleven other mouse strains with 10 MHC types (Holan et al, 1996). \par STU \par Inbr: 60 +. Origin: Swiss; Gonnert, Bayer-Leverkusen, to Max-Planck-Inst. fur Virusforsch. (Tubingen) 1950. (Figueroa et al 1982). \par Characteristics \par Used for passage of Ehrlich ascites tumour and Rous sarcoma virus-induced fibrosarcomas, and for transplantation experiments with Rous sarcomas. \par STX \par Inbr (Le) 59. Black: \i E\i0 \i \up8 so\up0 \i0 \i .\i0 Origin: sombre (\i E\i0 \i \up8 so\up0 \i0 \up8 \up0 ) mutation in C3H held by N.Bateman before 1961, to M.Foster, to M.C.Green 1966. Crossed with \i Tw \i0 (twirler) from M.Lyon in 1967, then b x s. Also carries \i Xt\i0 \i \up8 J\up0 \i0 \i \i0 (extra-toes). Has been well characterised at many polymorphic loci and is useful for linkage testing. Maint. by Dr. Taisei Nomura, Osaka University, Osaka 530. \par SUMS \par Inbr (Weller) ?+20. Colour ?. Origin: spontaneous hydrocephalic mutation in a stock at Guy's Hospital, London. To R.O.Weller in 1973 and b x s mating. Carries autosomal recessive unnamed mutation causing hydrocephalus in homozygotes which is lethal by 2-6 weeks of age. It is probably not obstructive hydrocephalus. Maintained by T.Richards, Southampton General Hospital, U.K. \par Swiss. \par Various lines from mainly commercial sources, inbred in different laboratories, as SWJ/Mk, SWM/Ms, etc. Characteristics may vary widely between strains. \par SWJ \par Inbr. 106. Albino \i c.\i0 Origin: City of Hope Medical Center to Inst. Genetics (Mishima) in May 1953, to Hok in March 1956 at F ?+9. Maintained by Hok. \par SWM/Ms \par Inbr: ? + 50. Genet: \i c\i0 . Origin: City of Hope Medical Center, Calif., to Moriwaki, Misima 1953. \par SWR \par Inbr: F148 (J). Albino. Genet: \i c, rd. \i0 Origin: Swiss mice from A. de Coulon of Lausanne, inbred by Lynch from about 1926 (Lynch, 1969). Now widely used in research as a general-purpose strain. Develops extreme polydipsia and polyuria on ageing. Maint. by J, Ola. \par \i Anatomy\i0 \par Low percent carcass lipid on a high-fat diet (1/9) (West et al 1992). \par \i Behaviour\i0 \par Low intrastrain aggression (11/14) (Southwick and Clark, 1966). High avoidance conditionability (1/9) (Royce, 1972). Poor T-maze learning (5/6) (Stasik, 1970). Low spontaneous bar-pressing activity (14/14) (Southwick and Clark, 1968). Ten "non-taster" congenic strains on the SWR "taster" genetic background have been developed by repeated backcrossing with selection for inability to taste bitter compounds including raffinose undecaacetate, glucose pentaacetate and brucine (Harder et al, 1996). \par \i Life-span and spontaneous disease\i0 \par Life-span in conventional conditions intermediate in males (14/22 = 616 days) but short in females (7/22 = 496 days) (Storer, 1966). Pulmonary tumours 80% in mice living to 18 months (Heston, 1963). Mammary tumours 7-28% (Deringer, 1970). Develops extreme polydipsia and polyuria (nephrogenic diabetes insipidus) on ageing (Kutscher \i et al\i0 ., 1975; Kutscher and Schmalback, 1975). Low gross tumour incidence in females (19/22) (Storer, 1967). One or more tumours found in 62% of mice. Lung tumours 36%, mammary tumours 30% (Rabstein \i et al\i0 ., 1973). Arteriosclerosis common (Russell and Meier, 1966). About 10-25% of SWRxSWXJ-9 F1 hybrid mice spontaneously develop granulosa cell tumours. These secrete inhibin, which can be used as a marker for tumour-bearing animals (Gocze et al, 1997). \par \i Normal physiology and biochemistry\i0 \par High metabolic rate (4/18) (Storer, 1967). High serum ceruloplasmin levels (7/27 in females, 7/26 in males) (Meier and MacPike, 1968). High systolic blood pressure (1/19) (Schlager and Weibust, 1967). Low plasma cholesterol levels (3/11) but high triglyceride levels (10/11) (Jiao et al 1990). Low sensitivity to thyrotropin (18/21) (Levy \i et al\i0 ., 1965). Low erythrocyte catalase (15/18) (Hoffman and Rechcigl, 1971). High kidney and liver arylsulphatase activity (3/12) (Daniel, 1976). High spermatazoal beta-glucuronidase activity (1/9) (Erickson, 1976). Arterial blood has a high pH (1/10) (Bernstein, 1966). Low hepatic delta-aminolaevulinic acid synthetase activity after DDC treatment (12/15) (Gross and Hutton, 1971). Resistant to the development of obesity assocaited with adipocyte insensitivity to insulin (contrast AKR/J) (Eberhart et al, 1994). Consume 30% fewer calories than susceptible AKR mice,with a significantly higher intake of carbohydrate (62 vs 24%) (Smith et al, 1997). \par \i Drugs\i0 \par High susceptibility to transplacental tumour induction by 1-ethyl-1-nitrosourea (2/5) (Diwan \i et al\i0 ., 1973). Resistant to skin ulceration by DMBA (cf. 9/22) (Thomas \i et al\i0 ., 1973). Resistant to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Susceptible to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 3/7) (Evans \i et al\i0 ., 1977). Resistant to teratogenic effects of acetazolamide (6/6) (Green \i et al\i0 ., 1973). Susceptible to `CNS syndrome' from high doses of X-irradiation (5/5) (Yuhas, 1968). Long survival in 90% oxygen (2/10) (Lieberman and Kellog, 1967). Low LD50 to X-irradiation (8/9) (Yuhas and Storer, 1969). Sensitive to X-irradiation (9/10 females, 7/10 males) (Storer, 1966). Susceptible to toxic effects of isoniazid (9/10) (Taylor, 1976b). Sensitive to seizures induced by nicotine (17/19) (Marks et al 1989). Low voluntary comsumption of morphine in two-bottle choice situation (15/15) (Belknap et al, 1993). A diet containing 15% dairy fat, 1% cholesterol and 0.5% cholic acid caused a high incidence of cholesterol gallstones (like C57L, A, contrast SM, AKR, DBA/2) (Faulkner et al, 1995). Prolonged administration of 2mg 5-aminolevulinic acid/ml of drinking water resulted in uroporphyrinogen decarboxylase insufficiency (11% of controls) and uroporphyria within eight weeks (contrast DBA/2) (Constantin et al, 1996). \par \i Immunology\i0 \par Susceptible to experimental allergic encephalomyelitis (EAE) (2/18) (Levine and Sowinski, 1973). High susceptibility to EAE (2/10) with high severity (1/10) and mortality (2/10) and spontaneous relapse (4/10) (Lindsey, 1996).Low lymphocyte phytohaemmagglutinin response (36/43) (Heiniger \i et al\i0 ., 1975). Poor immune response to low doses of bovine gammaglobulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to ovomucoid, but good response to ovalbumin (cf. 6/12) (Vaz \i et al\i0 ., 1971). Large quantity of antibody produced (2/7), but only intermediate relative affinity (4/7) (Alpers \i et al\i0 ., 1972). Erythrocytes have low agglutinability (cf. 11/25) (Rubinstein \i et al\i0 ., 1974). Susceptible to induction of experimental autoimmune thyroiditis (cf. 3/5) (Vladutiu and Rose, 1971a). Resistant to the induction of arthritis by type II collagen (Ortman et al, 1994). Develop allergic conjunctivitis and specific anti-ragweel IgE following topical exposure of the nasal and conjunctival mucosa ragweed. The effects were reduced in mice treated with nedocromil sodium (Marayo-Lloves et al, 1996). \par \i Infection\i0 \par Susceptible to herpes simplex virus (10/11) (Lopez, 1975). Susceptible to LCM virus infection (5/5) (Oldstone and Dixon, 1968). Encephalomyocarditis virus causes diabetes mellitus (cf. 7/14) (Boucher \i et al\i0 ., 1975). In contrast to ten other strains, it does not carry type I and II endogenous type C viruses (cf. NZB) (Stephenson \i et al\i0 ., 1975). Carries no detectable endogenous ecotropic MuLV DNA sequences (Jenkins et al 1982). Susceptible to immune-mediated central nervous system demyelination following infection with Theiler's murine encephalomyelitis virus. This is genetically dominant. One copy of \i H2\i0 \i \up8 q\up0 \i0 \up8 \up0 is sufficient for the disease, but an additional non-\i H2\i0 gene is also implicated (Nicholson et al, 1995). \par Rapid immunological expulsion of \i Trichinella spiralis \i0 worms (Wakelin and Donachie 1980). Susceptible to Lyme borreliosis (\i Borrelia burgdorferi) \i0 when inoculated at 3 weeks of age (2/5) and as adults. Mice inoculated at age 3 weeks also developed polyarthritis. (Barthold et al 1990). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). An ecotropic murine leukemia virus (MuLV) isolate can infect the thecal cells surrounding the follicles in the ovary and the Leydig cells in the testis. Both types actively synthesize viral RNA and express a viral antigen and can infect the germ line or the early embryo or both when inoculated at birth (Panthier et al 1989). \par Pattern of infection with Leishmania major depends on site of innoculation of parasite, in contrast with BALB/c and most other mouse strains, where route of infection is not critical (Nabors and Farrell, 1994). \par Develop severe myocarditis following infection with Coxsackie virus B3 (Zhang et al, 1994). \par Reproduction \par Prolific ovulators in response to exogenous hormones and the one-cell embryos have large and prominant pronuclei with good resistance to lysis following microinjection. The strain, like strain FVB, is highly suitable for the propogation of transgenes particularly as it is genetically well defined (Osman et al, 1997) \par \i Miscellaneous\i0 \par High degree of genetic distinctiveness (1/27) (Taylor, 1972). Large brain/body weight ratio (5/20) (Roderick \i et al\i0 ., 1973). \par SWV \par Inbr (Bc) 73. Albino: \i A,c,\i0 plus unknown dilution gene. Origin: Outbred animals from Defense Research Bd. Suffield, Alberta to Cent. Animal Depot, Univ. Brit. Columbia. Inbreeding started in 1959. Develops nephrogenic diabetes insipidus with a progressive and unique kidney defect. Maint. by Bc. \par Characteristics \par Females over 8 months have a hereditary polydipsia-polyuria defect with a severe increase in water turnover and with hypotonic urine that contains no glucose, blood or protein: i.e. nephrogenic diabetes insipidus. They are vasopressin-resistant. Females also have a progressive kidney defect which, although it resembles nephronophthisis in some aspects and hypokalaemia in others, is unique. Males have a milder form of the defect at an older age and show no signs of histopathology (Virgo and Miller, 1974). Resistant to acetazolamide-induced teratogenesis (Hackman and Hurley 1983). \par SWXJ- \par Inbr (28-32). Set of 14 recombinant inbred strains developed by Beamer from a cross of SWR x SJL (MNL 75:34,1986). Maint. by Bm. \par SWXL- \par Inbr. ?. Set of 7 recombinant inbred strains maintained at the Jackson Laboratory. \par SWXL-4 mice exhibit tonic-clonic and generalised seizures similar to the commonest epilepsy in humans. Seizures are observed in routine handling from about 80 days of age, and are due to a dominant gene\i Szf1\i0 on chromosome 7 which accounts for about 32% of the variation in susceptibility (Frankel et al, 1994). \par SXC \par Inbr. 30 (1992). Origin: S.M. Singh from a cross between "true-breeding" Swiss Webster (SW) mice (Charles River, Quebec) and acatalasemic C3H/HeAnl-\i Cas1\i0 \up8 b\up0 . A spontaneous belted mutation was found in 1983. Genet. \i Cas1\i0 \i \up8 b\up0 \i0 \i , bt\i0 \i \up8 w\up0 \i0 \up8 \up0 . All animals are negative for blood catalase activity. \par SZA \par Inbr 16-26 (Wim). albino \i a,B,c,D.\i0 Origin: R and C Wimer, 1981 from a cross between NZB/BlNJ and RF/J. Spontaneous seizures appeared at F6, and the strain has been maintained with selection for seizures. \par Characteristics \par Exhibit apparently spontaneous non-fatal convulsions from the age of 8-12 weeks, possibly triggered by olfactory stimuli. No reduction in fertility or viability. Maintained by Wim. \par SZB \par Inbr 16-26. As for SZA, but separated at F13. \par SZC \par Inbr 16-26. As for SZA, but separated from SZA at F9, and has lost the spontaneous convulsions. \par T739 (provisional name). \par Inbr. F74 (Dec. 1991). Cinnamon, \i A, b, C, D\i0 . \i Origin\i0 : Prof. Sun Wenyi, Inst. of Medical and Pharmaceutical Science, PO Box 300070, 96 Gui Zhou Rd., Heping District, Tianjin, China. From a cross in 1973 between a female albino KUNMING mouse with a male of strain 615, followed by sib mating. \par Characteristics \par Average litter size 5.7 at birth and 5.5 at weaning. Mammary tumours in multiparous mice 3.4%. Pulmonary adenoma and leukaemia by 23 months of age is 29.8% and 1.3%, respectively. \par TA1 \par Inbr. 90. Albino: \i a,b,c.\i0 Origin: Outbred mice from Tianjin (China) in June 1956. Inbred since then. Well characterised at polymorphic loci. Maint. by A. \par TA2 \par Inbr. 66. Albino: \i a,B,c,d.\i0 Origin: Outbred 'Kun Ming' mice from Bioproducts Institute, Peking in 1962. Inbred since then. \par Characteristics \par Mammary tumours 81% in breeding females, 41% in virgins. Well characterised at polymorphic loci. Maint. by A. \par TB \par Inbr: 20+. Genet: \i c, p\i0 . Origin: Pasteur Inst. \par TF \par Inbr. (Le) 77. Black: \i a.\i0 Origin: M.C.Green from \i T tf/t\i0 \i \up8 6\up0 \i0 \up8 \up0 stock received from M.F.Lyon in 1961, then outcrossed to C57BL/10Gn to obtain \i +\i0 \i \up8 tf\up0 \i0 \up8 \up0 chromosome in 1962, followed by b x s. To Lane 1975. Has good chromosome 17 markers. Maint. by Le. \par TFH \par Inbr (H) 33. Agouti: \i +.\i0 Origin: Outbred \i T,tf/+,tf\i0 stock. Sib mating started in 1972. Homozygous \i tf/tf,\i0 but forced segregation of \i T/+.\i0 Maint. by H. \par TFM \par Inbr F24. Agouti: \i Ta \i0 (carried in balance with \i Tfm\i0 ). Origin: Carol M Wilson 1979 from a 1971 cross between \i Tfm/+\i0 females from S. Ohno and Ta/Y males from J. \i Tfm\i0 is carried in balance with \i Ta\i0 to facilitate the identification of female carriers from males which are phenotypically females. There may be some residual heterozygosity in the region of the X chromosome that lies between these two loci. \i Ren2\i0 \i \up8 n\up0 \i0 \i ,\i0 \i Tfm\i0 \i \up8 H\up0 \i0 \i ,\i0 \i Thy1\i0 \i \up8 b\up0 \i0 \i ,\i0 \i Ly2\i0 \i \up8 b\up0 \i0 \i ,\i0 \i B2m\i0 \i \up8 b\up0 \i0 \i ,\i0 \i I-Ad.\i0 Maintained by Wil. \par TH \par Inbr (Wl) 93. Black-and-tan: \i a\i0 \i \up8 t\up0 \i0 \i .\i0 Origin: H.G.Wolfe before 1961 with selection for high blood pH. Good reproductive performance. Arterial blood pH 7.34. Sex ratio at birth 57% males. Maint. by Wl. \par TKDU \par Inbr (Dn) 69. Grey: \i a,d.\i0 Also carries \i du \i0 (ducky) and \i tk \i0 (tail kinks). Origin: \i du\i0 from C.Keeler to G.D.Snell 1948, to M.C.Green 1956, to Eicher 1972, to Davisson 1980. Cross to DBA then bxs to F10, crossed to BALB/c then bxs to F4. Crossed to DBA/1 then bxs to F2. Crossed to C57BL/10 then bxs to F2. Crossed to BALB/c-\i tk \i0 (from Gruneberg 1961) and maintained as balanced stock. \i tk\i0 arose in BALB/c (probably An substrain) in 1953 at the Chester Beatty R.Inst. Maint. by Dn. \par TL \par Inbr (Wl) 96. Brown with white-belly: \i A\i0 \i \up8 w\up0 \i0 \i ,b.\i0 Origin: as for TH, but with selection for low blood pH. Arterial blood pH 7.30, sex ratio at birth 51% males. Maint. by Wl. \par TM \par Inbr 90+. Albino. Origin: Casas, 1948 from unpedigreed Swiss mice inbred since 1948. Maint. by Szepsenwol (Univ. Puerto Rico). \par Characteristics \par Lung tumours 48%, fore-stomach papillomas 27%, pyloric tumours 13%, brain nerve cell tumours 11%. Low mammary cancer. A low incidence of heart tumours has also been observed (Szepsenwol and Boschetti, 1975). \par TP \par Inbr (Rl) 68+. Black or slate-grey. \i a,tp/+ .\i0 Origin: Jackson Laboratory. Taupe mutation in C57BL/10J in 1948. Six generations of backcross-intercross to C57BL/10, then b x s. Homozygous \i tp\i0 mice viable, but females have difficulties during gestation and can not rear young due to abnormal nipples. Maint. by Rl. \par TPS \par Inbr (Y) 38. Black:\i a.\i0 Origin: Heterogenious stock synthesised from A/Sn, BALB/c, CBA/Ca, C57BL/6J, DBA/2, GLF, I/St, and 101/H, with selection for high sensitivity to cytogenetic effect of thiotepa in bone marrow cells. \par Characteristics \par Extremely sensitive to thioTEPA, mitomycin C, phtoraphur, and cyclophosphamide. Maint. by Y. \par TR \par Inbr (Dn) 81. Irregular patches of full-coloured and very lightly coloured fur: \i Mo\i0 \i \up8 to\up0 \i0 \i .\i0 Origin: Dickie 1952 from tortoise (\i Mo\i0 \i \up8 to\up0 \i0 \up8 \up0 ) mutation in non-inbred obese stock. Maintained by matings of \i Mo\i0 \i \up8 to\up0 \i0 \up8 \up0 females with normal males. Line has been maintained by trio matings for 21 years as offspring do not survive as well from pair matings. \par Characteristics \par Mottled females with much white in coat do not usually mature. Darker ones survive well. Maint. by Dn. \par TRE/Ko \par Inbr: 64+. Origin: Kobozieff 1937, from waltzing mice of unknown origin. \par Characteristics \par Malformation of one or both ears in low incidence. \par TS/Wf (now extinct) \par Inbr: 23. Genet: + \i a\i0 \i \up8 t\up0 \i0 \i /A\i0 \i \up8 s\up0 \i0 \i A\i0 \i \up8 w\up0 \i0 \i \i0 Origin: From R. J. S. Phillips 1965. \par TSI \par Inbr. (A) ?+72. Albino: \i a,c.\i0 Origin: Muhlbock, from stock supplied by P.Schafer (Tubingen) in 1958. High incidence of leukosis in both sexes. Maint. by A. \par TSJ \par Inbr (Le) 64. Cinnamon. \i b.\i0 Origin: mutation to \i Ts \i0 (tail-short) arose at NCI in 1946. From Morgan to G.D.Snell 1950. Crossed to C57BL/6, C57BR/cd and BALB/cSn then b x s. Homozygous lethal before 6 days of gestation. \par Characteristics \par Heterozygotes have short kinked tails with numerous other skeletal abnormalities, and a transient anaemia. Maint. by Le. \par TT6 \par Inbr (Le) 85. Agouti. Origin: 'TR' stock from M.F.Lyon to M.C.Green in 1961, to Le 1970. One cross to jittery-grizzled stock, b x s to F7, one cross to B6CBAF1-\i A\i0 \i \up8 wJ\up0 \i0 \i /A\i0 in 1972, then b x s. Carries \i T \i0 (brachyury), \i t\i0 \i \up8 6\up0 \i0 \i ,\i0 and \i tf \i0 (tufted). Useful for study of t-alleles. Maint. by Le. \par UMB \par Inbr. F114 (1994). Albino, c. Origin: Developed between 1960 and 1962 from outbred stock UMPOP which was founded from stock II (later NMRI) and III of the Bundesforschungsanstalt fur Viruskrankheiten (Tubingen), and described by Gehring (1956). Selected for high lifetime reproductive performance using mother x son or grandson as well as brother x sister mating. Later strict full sib mating was used (Kluge et al 1994, Wunsch 1992). \par UMB/a \par Inbr. F101 (1994). Albino, c. Origin same as UMB \par UMB/b \par Inbr. F111 (1994). Albino, c. Origin same as UMB \par UMC \par Inbr. F98 (1994). Albino, c. Origin same as UMB \par UMCBE \par Inbr. F71. Albino, c. Origin: 1971, from a cross of undefined strain E and CBA/J \par UMDH/+ \par Inbr. F25. Agouti, C, A, B, D. Origin: Charles River Germany, kept as a separate subline. Carries dominant hemimelia (Dh) mutation found in about 42% of offspring. (Kluge and Meyer 1994). \par UMG \par Inbr. F45. Dilute brown C, a,b,d. Origin: from a cross between outbred stock UMPOP (see UMB) and CBA/J (Kluge and Meyer 1994, Wunsch 1992). \par UMS \par Inbr. F65. Black, C, a, B, D. Origin: inbred in 1972 from an outbred stock UMPH-c which was selected for high phagocytosis (Buschmann and Meyer 1981) \par UMZ \par Inbr. F114 (1994). Albino, c. Origin same as UMB. \par UMZ/a \par Inbr. F114 (1994). Albino, c. Origin same as UMB \par UW \par Inbr (Pas) N9 (1994). Under white,\i uw\i0 . Origin: Wild allele of under white found segregating in a Corsican mouse, backcrossed 9 times to 129/Sv. \par V \par Inbr (Le) 63. Leaden and leaden-piebald \i a,fz,ln/fz ln, s,v/+.\i0 Origin: G.D.Snell from a stock carrying \i v \i0 (waltzer), \i s \i0 (piebald) and \i ln \i0 (leaden) from Ludwin in 1947. Crossed to C57BL/10, then to \i fz \i0 (fuzzy) stock in 1960 and non-sib mated. To Lane 1969, then b x s. Homozygous waltzer females are poor mothers. Maint. by Le. \par VC \par Inbr (U) ?+86. Chinchilla (?): \i c\i0 \i \up8 ch\up0 \i0 \i .\i0 Origin: Formerly CPB-V. Hagedoorn (?) to CPB-TNO in 1949, to Vet. Fac. Utrecht in 1973. Relatively low concentration of major urinary protein in males. No sex difference in response to hexobarbital. Maint. by U. \par VL \par Inbr. 82 (Dk). Leaden: \i a,B,C,D,ln.\i0 Origin: Random-bred albino stock (pre 1960) at ARC Compton crossed with leaden-carrying marker stock from Inst. Anim. Genetics, Edinburgh. Inbred by Dickinson in 1963. \i Sinc\i0 \i \up8 s7\up0 \i0 \up8 \up0 , \i H2\i0 \i \up8 b\up0 \i0 \up8 \up0 . Maintained by Dk. \par VM and VM-Sincs7 \par Inbr. 81 (Dk). Albino. Genet. \i a,b,c,d.\i0 , \i H2\i0 \i \up8 b\up0 \i0 \i , Mls\i0 \i \up8 a\up0 \i0 \i . \i0 Origin: Inbred as `5M' from Moredun Inst. stock (Dickinson and Mackay, 1964), and name later changed to conform with nomenclature rules (Dickinson \i et al\i0 ., 1968). Congenic mouse strains VM/Dk and VM-Sincs7/Dk differ at the Sinc gene, which controls the incubation period of scrapie in mice; VM/Dk mice are Sincp7p7 and VM-Sincs7/Dk mice are Sincs7s7. Restriction fragment length polymorphism and DNA sequencing analysis demonstrated that the PrP genes also differ in these strains (Hunter et al 1992) \par Characteristics \par Long incubation of ME 7 scrapie agent and short incubation of 22A compared with most other strains (Dickinson and Meikle, 1971). Spontaneous astrocytomas occur at 1.5% incidence. Tumours are largely confined to white matter areas, and have not been seen in sixteen other strains. Also has high incidence (1/6) of developmental defects, including cleft palate, subcutaneous blebs, facial and tail defects and cranial meningocoele (Fraser, 1971), including spina bifida (Dickinson, 1977). \par VP/Wf (now extinct) \par Inbr: 30. Genet: \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 \i \up8 e\up0 \i0 \i B/b P/p DSe/dse. \i0 Origin: Female \i A\i0 \i \up8 vy\up0 \i0 \i x \i0 male \i a\i0 \i \up8 v\up0 \i0 \i .\i0 Sib-mating with forced heterozygosis at five loci. \par VY \par Inbr (Nctr) 74. Variable yellow to agouti and black: \i A\i0 \i \up8 vy\up0 \i0 \i /a, a/a.\i0 Origin: The \i A\i0 \i \up8 vy\up0 \i0 \up8 \up0 mutation occurred in C3H/HeJ in 1960. Crossed with a C57BL/6J male, then backcrossed to C57BL/6J. One N3 male and two N1 females from M.M.Dickie, Jackson Lab. to Inst. Cancer Research in 1962. These were mated and the offspring sib mated. Maintained by \i A\i0 \i \up8 vy\up0 \i0 \i /a, a/a\i0 matings since then. To the Nctr in 1972 at F35. Caesarian derived and fostered on C3Hf in 1977 at F47. Pseudoagouti phenotype about 10% of \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 mice. Spontaneous hepatocellular tumours in 24% of male yellow mice but only 13% of black mice. Phenotypically yellow mice differ from agouti ones in a range of biological properties (Wolff et al 1990). Maint. by Nctr. \par WB \par Inbr (J) 119. Black or black-eyed white: \i a,W.\i0 Origin: \i W \i0 (dominant spotting) heterozygotes from S.J.Holman and S.G.Waelsch. Sib-mating started in 1948. \par Characteristics \par \i WW\i0 homozygotes are anaemic, sterile, lack pigmentation in coat; heterozygotes have normal blood picture and fertility, but white ventral spotting; anaemics die at approximately 11 days. Many other anaemia-producing mutant alleles are maintained congenic with this strain. Resistant to lethal effects of ozone (19/22) (Goldstein \i et al\i0 ., 1973). High lymphocyte phytohaemagglutinin response (4/43) (Heiniger \i et al\i0 ., 1975). Abnormal azygos vein which varied from a single unpaired vein on the right side that connected to the right anterior vena cava through bilaterally symmetrical and paired veins to the expected unpaired vein on the left side found in most strains (Biddle et al 1991). Develop a high frequency of subcutaneous edema in day 15 fetuses when mothers are treated with acetazolamide. A transient edema is also seen in 56% of control mice. The condition appears to be due to more than one gene (Biddle 1990). Carry a single recessive gene different from that found in BALB/cBy and C57BL/6J, causing age-related hearing loss (Willott et al, 1995). \par WC \par Inbr (J) N58F37. Colour grey, white or black depending on genotype: \i a,Sl.\i0 Origin:\i Sl \i0 (steel) mutation backcrossed to strain WB-\i +/+.\i0 Phenotype of \i SlSl\i0 homozygotes rather similar to \i WW\i0 homozygotes, but defect is due to abnormal environment for stem-cell development. Maint. by J. \par WH \par Inbr: 90. Genet and Origin: As WB. \par Characteristics \par As WB, except that anaemics die at approximately 5 days. \par WHT \par Inbr:F125 (Gy). Albino, \i c\i0 . Origin: Hewitt, London. \par Characteristics \par Hardy, breeds well; origin of a spontaneous squamous carcinoma which metastasises to the lymph nodes (Sakamoto and Sakka, 1973). Diminished expression of neutral glycosphingolipid GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (Muthing, 1997). \par WK \par Inbr: 74. Genet and Origin: As WB. \par Characteristics \par As WB, except that anaemics die at approximately 10 days. The mutant \i dy\i0 \i \up8 2J\up0 \i0 \i \i0 arose in this strain. \par WLA \par Inbr. 27 (1989). Origin: Wkild mice trapped in 1976 near Toulouse (France) by Jean-Louis Guenet, and sib-mated since then. \par WLHR/Le \par Inbr: F92 (Le). chocolate. Genenet: \i a, b, wl\i0 + / + \i hr. \i0 Origin: Mutation to \i wl\i0 (wabbler-lethal) occurred in pirouette stock in 1948. Crossed to \i hr \i0 from Hummel in 1947, Dickie to Lane 1958 and inbred as balanced stock. \par Characteristics \par Homozygous \i wl/wl \i0 die before weaning. \par WLL \par Inbr: F?+112 (A). Albino. Genet: \i c\i0 . Origin: Kreyberg 1929, from a commercial dealer in Oslo. In 1934 `White Label' mice were sent to Leeds, becoming WLL, and some stayed in Oslo, becoming WLO (not reported). Leukosis 4% (Hilgers and Galesloot, 1973). \par WMP \par Wild mice trapped in Monastir (Tunisia) by G. Lefranc in 1080 and maintained at the Institut Pasteur by sib mating. Homozygous for nine pairs of metacentric chromosomes. \par WN \par Inbr: F60 (Nga). Colour depends on genotype. Genet: \i a, B, C, D, S, W\i0 \i \up8 n\up0 \i0 \i . \i0 Origin: New mutant at W locus. \i W\i0 \i \up8 n\up0 \i0 \i /W\i0 \i \up8 n\up0 \i0 \up8 \up0 die at 16-18 days gestation with anaemic syndrome, seldom survive birth, but die in a few days. Heterozygote has normal blood, viable and fertile. Amount of white spotting is greater than in \i Wv\i0 / +. \par WR \par Inbr (Y) 36. Black spotted: \i a,W\i0 \i \up8 y\up0 \i0 \i /+.\i0 Origin: Developed by selection for dilution of pigmentation of \i a/a, W\i0 \i \up8 y\up0 \i0 \i /+\i0 mice and a high incidence of somatic reversion of \i W\i0 \i \up8 y\up0 \i0 \up8 \up0 to + in a cross of 129 and 129xC57BL/6-\i W\i0 \i \up8 y\up0 \i0 \i /+.\i0 Inbred since 1975. Anaemic \i W\i0 \i \up8 y\up0 \i0 \i /W\i0 \i \up8 y\up0 \i0 \up8 \up0 die at birth. \i W\i0 \i \up8 y\up0 \i0 \i /+\i0 mice have light coat colour, 25% with black spots. Maint. by Y. \par X \par Inbr: F89. Albino. Genet: \i a, B/b, c.\i0 Origin: Unknown, but maintained by Goldfeder since 1953. \par Characteristics \par No spontaneous tumours of any kind. They are resistant to the induction of tumours by urethane, producing only 3% tumours at dose levels that would induce 80-90% in other strains. Also resistant to tumour induction by X-rays. Combined X-ray and urethane produces only 6% tumours. The mice do not produce murine leukaemia virus antigens in their milk, and are resistant to polyoma virus, Friend leukaemia virus and FBJ osteosarcoma virus. They also have high immune response against sheep erythrocytes, pronounced splenic phagocytic activity, high levels of antibody to mammary tumour virus and a tendency to spontaneous amyloidosis. The low tumour incidence is attributed to high immune competence and absence of an apparent oncogenic virus as revealed by electron microscopy (Goldfeder \i et al\i0 ., 1966; Goldfeder, 1972). Resistance to carcinogens does not appear to be due to differences in biochemiceal response to such chemicals (Grantham \i et al\i0 ., 1976). \par XLII \par Inbr (Orl) 50+. Cinnamon (?): \i b.\i0 Origin: Dobrovolskaia-Zavadskaia from a cross between C57L and C57BL. Biochemical polymorphisms characterised (Moutier, 1968). Very low tumour incidence. Maint. by Orl. \par XVII \par Inbr: F80 (Rd). Albino. Genet: \i c\i0 . Origin: Dobrovolskaia-Zavadskaia 1928; b x s inbreeding since 1943. \par Characteristics \par No mammary tumours or leukaemia; pulmonary adenomas 19.5% after 13 months; mammary tumours 1.3%, leukaemia females 0.4%, males 1.6%; lung tumour females 5.1%, males 8.8%; sensitive to Graffi leukaemia agent (Krischke and Graffi, 1962); blood catalase has low specific activity (7/7) (Magdon, 1962); strong reactivity against specific antigens of carcinogen-induced sarcomas (Pasternak, 1963); very susceptible to lung oncogenesis by chemical agents. \par YBR \par Inbr (Ki) 132. Colour brown or yellow. Genet. \i A\i0 \i \up8 y\up0 \i0 \i /a,b.\i0 Origin: Little to Andervont 1936, to Heston 1946 at An's F30. Amyloid at least 50% in both sexes and genotypes. Obesity in crosses with other strains. Low tumour incidence. Lacks microsomal glucuronidases. Maint. by Ki. \par YPC \par Inbr. F46 (Asano, 1993). Albino, A, B, c. Origin: Non-inbred Swiss albino inbred by Ogura, Koura, Noguchi and Asano, NIH, Japan. Carries a mutant "poor coat". Hair bulbs and hair papillae are poorly developed at anagen stage of the hair cycle. As a result the hairs are thin and short (Kurosawa et al 1991). \par YS \par Inbr (Nctr) 84. Mottled yellow, pseudoagouti,black, piebald, depending on genotype. \i A\i0 \i \up8 vy\up0 \i0 \i /a, \i0 or\i a/a,s.\i0 Origin: Jackson Laboratory to Chase in 1942. Crossed to get mice with a B/b and ss genotype to develop a strain designated Y\dn8 z57\dn0 . Chase to Inst. of Cancer Research 1959 at F38-39. In 1962 outcrossed to an N3 male from a (C3H/HeJxC57BL/6)xC57BL/6 cross. \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 mice were backcrossed to the YS strain to N35. To Nctr in 1972, then caesarian derived and fostered on C3Hf. \par Characteristics \par Strain has impared glucose tolerance on which the impairment of glucose tolerance due to obesity of \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 mice is superimposed. High level of serum-glutamyltranspeptidase activity. Pseudoagouti phenotype in about 16% of \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 mice. Hepatoma incidence in males at 12-16 months: 11% in \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 , 3% in \i a/a\i0 . Large testes weight (1/8) (Shire and Bartke, 1972). Maint. by Nctr. \par YT \par Inbr (Y) 45. Near-white. \i a,b,c\i0 \i \up8 ch\up0 \i0 \i ,p,d,ln.\i0 Origin: From crosses involving C57L, DBA/2, C57BL-\i go,\i0 129/J. Inbred since 1967. Carries multiple recessive genes including \i go \i0 (angora), producing long-hair. Used for mutagenesis studies. Maint. by Y. \par YX \par Inbr 50. Colour: Yellow: \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 x\up0 \i0 \i .\i0 Origin: From an \i A\i0 \i \up8 y\up0 \i0 \i /a\i0 \i \up8 x\up0 \i0 \up8 \up0 stock of L.B.Russell crossed with an \i A\i0 \i \up8 vy\up0 \i0 \i /a\i0 male in 1968. Homozygous \i a\i0 \i \up8 x\up0 \i0 \up8 \up0 is lethal. Maint. by R. Pederson, San Francisco. \par \par \par References \par Abshire M. K. and Waalkes M. P. (1994) Cadmium-induced oxidative tissue damage in mice: Role of mouse strain and tissue metallothionein levels. \i Toxic Substances Journal\i0 \b 13\b0 , 141-152. \par \par Abujiang P., Yamada Y., Haller O., Kobayashi H., Kamoto T., Lu L. M., Ogawa M., Ishimoto A., Katoh H., Kanehira K., Ikegami S., Fukumoto M., and Hiai H. (1996) The origin of SL family mice. \i Lab. Animal Sci.\i0 \b 46\b0 , 410-417. \par \par Acha-Orbea H. and Scarpellino L. (1991) Nonobese diabetic and nonobese nondiabetic mice have unique MHC class II haplotypes. \i Immunogenet.\i0 \b 34\b0 , 57-59. \par \par Acton R. T., Blankenhorn E. P., Douglas T. C., Owen R. D., Hilgers J., Hoffman H. A., and Boyse C. A. (1973) Variations among sublines of inbred AKR mice. \i Nature New Biol.\i0 \b 245\b0 , 8-10. \par \par Adam-Rodwell G., Morse M. A., and Stoner G. D. (1993) The effects of phenethyl isothiocyanate on benzo(a)pyrene-induced tumors and DNA adducts in A/J mouse lung. \i Cancer Lett.\i0 \b 71\b0 , 35-42. \par \par Adinolfi M., Beck S. E., Seller M. J., Fedor T., and McLaren A. (1990) Alpha-fetoprotein levels in different strains of mice during development. \i Exp. Clin. Immunogenet.\i0 \b 7\b0 , 123-128. \par \par Adkison D. L. and Sundberg J. P. (1991) "Lipomatous" hamartomas and choristomas in inbred laboratory mice. \i Vet. Pathol.\i0 \b 28\b0 , 305-312. \par \par Ahmed S. A., Boone J., and Verthelyi D. (1993) Anticardiolipin antibodies in autoimmune-prone BXSB and MRL/lpr mice, and estrogen-treated normal C57BL/6J mice crossreact with other phospholipids. \i International Journal of Immunopathology and Pharmacology\i0 \b 6\b0 , 135-147. \par \par Akiyama H., Kameyama M., Akiguchi I., Sugiyama H., Kawamata T., Fukuyama H., Kimura H., Matsuchita M., and Takeda T. (1986) Periodic acid-Schiff (PAS)-positive, granular structures increase in the brain of senescence accelerated mouse (SAM). \i Acta Neuropathol.\i0 \b 72\b0 , 124-129. \par \par Al-Ani A. T., Tunnicliff G., Rick J. T., and Kerkut G. A. (1970) GABA production, acetylcholinesterase activity and biogenic amine levels in brain for mouse strains differing in spontaneous activity and reactivity. \i Life Sci.\i0 \b 9\b0 , 21-27. \par \par Albert S., Wolf P. L., Pryjma I., and Moore W. (1965) Thymus development in high and low-leukemic mice. \i J. Reticuloendothel. Soc.\i0 \b 2\b0 , 218-237. \par \par Albert S., Wolf P. L., Loud A. V., Pryjma I., Potter R., and Moore W. (1966) Spleen development in mice of high and low leukemic strains. \i J. Reticuloendothel. Soc.\i0 \b 3\b0 , 176-201. \par \par Albertini D. F. and Eppig J. J. (1995) Unusual cytoskeletal and chromatin configurations in mouse oocytes that are atypical in meiotic progression. \i Developmental Genetics\i0 \b 16\b0 , 13-19. \par \par Almeida R. M. A., Correa B., Xavier J. G., Mallozzi M. A. B., Gambale W., and Paula C. R. (1996) Acute effect of aflatoxin B-1 on different inbred mouse strains. \i Mycopathologia\i0 \b 133\b0 , 23-29. \par \par Alpers J. H., Steward M. W., and Southill J. E. (1972) Differences in immune elimination in inbred mice. The role of low affinity antibody. \i Clin. Exp. Immunol.\i0 \b 12\b0 , 121-132. \par \par Ammassari-Teule M., Hoffman H. J., and Rossi-Arnaud C. (1993) Learning in inbred mice: strain-specific abilities across three radial maze problems. \i Behav. Genet.\i0 \b 23\b0 , 405-412. \par \par Ammassari-Teule M., Tozzi A., Rossi-Arnaud C., Save E., and Thinus-Blanc C. (1995) Reactions to spatial and nonspatial change in two inbred strains of mice: Further evidence supporting the hippocampal dysfunction hypothesis in the DBA/2 strain. \i Psychobiology\i0 \b 23\b0 , 284-289. \par \par Amor S., Baker D., Groome N., and Turk J. L. (1993) Identification of a major encephalitogenic epitope of proteolipid protein (residues-56-70) for the induction of experimental allergic encephalomyelitis in Biozzi AB/H and Non-obese diabetic mice. \i J. Immunol.\i0 \b 150\b0 , 5666-5672. \par \par Amor S., Groome N., Linington C., Morris M. M., Dornmair K., Gardinier M. V., Matthieu J. M., and Baker D. (1994) Identification of epitopes of myelin oligodendrocyte glycoprotein for the induction of experimental allergic encephalomyelitis in SJL and Biozzi AB/H mice. \i J. Immunol.\i0 \b 153\b0 , 4349-4356. \par \par Amsbaugh D. F., Hansen C. T., Prescott B., Stashak P. W., Barthold D. R., and Baker P. J. (1972) Genetic control of the antibody response to type III pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. \i J. Exp. Med.\i0 \b 136\b0 , 931-949. \par \par Anderson G. W. and Osterman J. V. (1980a) Host defenses in experimental rickettsialpox: genetics of natural resistance to infection. \i Infect. Immun.\i0 \b 28\b0 , 132-136. \par \par Anderson G. W. and Osterman J. V. (1980b) Host defenses in experimental rickettsialpox: resistance of C3H mouse sublines. \i Acta Virol.\i0 \b 24\b0 , 294-296. \par \par Anderson G. W., Palmer G. A., Rowland R. R. R., Even C., and Plagemann P. G. W. (1995) Infection of central nervous system cells by ecotropic murine leukemia virus in C58 and AKR mice and in in utero-infected CE/J mice predisposes mice to paralytic infection by lactate dehydrogenase- elevating virus. \i Journal of Virology\i0 \b 69\b0 , 308-319. \par \par Anderson L. M., Jones A. B., and Kovatch R. M. (1990) Effect of pretreatment with beta-naphthoflavone on tumorigenesis by N-nitrosoethylurea in five mouse strains. \i Cancer Lett.\i0 \b 16\b0 , 91-94. \par \par Andervont H. B. and Dunn T. B. (1962) Studies of the mammary tumor agent of strain RIII mice. \i J. Natl. Cancer Inst.\i0 \b 28\b0 , 159-185. \par \par Andervont H. B. and Edgcomb J. H. (1956) Responses of seven inbred strains of mice to percutaneous applications of 3-methylcholanthrene. \i J. Natl. Cancer Inst.\i0 \b 17\b0 , 481-495. \par \par Andrikopoulos S., Rosella G., Kaczmarczyk S. J., Zajac J. D., and Proietto J. (1996) Impaired regulation of hepatic fructose-1,6-bisphosphatase in the New Zealand obese mouse: An acquired defect. \i Metabolism: Clinical and Experimental\i0 \b 45\b0 , 622-626. \par \par Angel C. R., Mahin D. T., Farris R. D., and Woodward K. T. (1967) Heritability of plasma cholinesterase activity in inbred mouse strains. \i Science\i0 \b 156\b0 , 529-530. \par \par Angel J. M., Morizot D. C., and Richie E. R. (1993) Localization of a novel chromosome 7 locus that suppresses development of N-methyl-N-nitrosourea-induced murine thymic lymphomas. \i Molecular Carcinogenesis\i0 \b 7\b0 , 151-156. \par \par Armsby C. C., Stuarttilley A. K., Alper S. L., and Brugnara C. (1996) Resistance to osmotic lysis in BXD-31 mouse erythrocytes -association with up-regulated K-Cl cotransport. \i American Journal of Physiology-Cell Physiology\i0 \b 39\b0 , C866-C877. \par \par Arnesen K. (1963) The cytology of the adrenal cortex in mice with spontaneous adrenocortical lipid depletion. \i Acta Pathol. Microbiol. Scand.\i0 \b 58\b0 , 212-218. \par \par Artz K., Hamburger L., and Flaherty L. (1977) H39, a histocompatibility locus closely linked to the T/t complex. \i Immunogenet.\i0 \b 5\b0 , 477-480. \par \par Asada Y., Varnum D. S., Frankel W. N., and Nadeau J. H. (1994) A mutation in the Ter gene causing increased susceptibility to testicular teratomas maps to mouse chromosome 18. \i Nature Genet.\i0 \b 6\b0 , 363-368. \par \par Ashman R. B. and Bolitho E. M. (1993) Strain differences in the severity of lesions in murine systemic candidiasis correlate with the production of functional gamma interferon by Candida-activated lymphocytes in vitro. \i Lymphokine and Cytokine Research\i0 \b 12\b0 , 471-476. \par \par Ashman R. B., Bolitho E. M., and Papadimitriou J. M. (1993) Patterns of resistance to Candida albicans in inbred mouse strains. \i Immunology and Cell Biology\i0 \b 71\b0 , 221-225. \par \par Ashman R. B., Fulurija A., and Papadimitriou J. M. (1996) Strain-dependent differences in host response to \i Candida albicans\i0 infection in mice are related to organ susceptibility and infectious load. \i Infect. Immun.\i0 \b 64\b0 , 1866-1869. \par \par Auer I. O., Tomasi T. B. Jr., and Milgrom F. (1974) Natural thymocytolytic autoantibodies in NZB and other strains of mice. \i Cell. Immunol.\i0 \b 10\b0 , 404-414. \par \par Autenrieth I. B., Beer M., Bohn E., Kaufmann S. H. E., and Heesemann J. (1994) Immune responses to \i Yersinia enterocolitica\i0 in susceptible BALB/c and resistant C57BL/6 mice: An essential role for gamma interferon. \i Infect. Immun.\i0 \b 62\b0 , 2590-2599. \par \par Babbini M., Pong S. F., King W. T., and White C. L. (1974) Mobility of mice after amphetamine: effects of strain aggregation and illumination. \i Pharmacol. Biochem. Behav.\i0 \b 2\b0 , 803-809. \par \par Babinet C., Richoux V., Guenet J. L., and Renard J. P. (1990) The DDK inbred strain as a model for the study of interactions between parental genomes and egg cytoplasm in mouse preimplantation development. \i Development - Supplement\i0 \b 1990\b0 , 81-87. \par \par Badr F. M. (1975) Prostaglandin levels in tissues of the male reproductive system in six strains of mice. \i Endocrinol.\i0 \b 96\b0 , 540-543. \par \par Baer P. N., Crittenden L. B., Jay G. E. Jr., and Lieberman J. E. (1961) Studies on periodontal disease in the mouse. II. Genetic and maternal effects. \i J. Dental Res.\i0 \b 40\b0 , 23-33. \par \par Bailey P. C., Leach W. B., and Hartley M. W. (1970) Characteristics of a new inbred strain of mice (PBA) with a high tumor incidence: preliminary report. \i J. Natl. Cancer Inst.\i0 \b 45\b0 , 59-73. \par \par Baker D., O'Neil J. K., Gschmeissner S. E., Wilcox C. E., Butter C., and Turk J. L. (1990) Induction of chronic relapsing experimental allergic encephalomyelitis in Biozzi mice. \i J. Neuroimmunol.\i0 \b 28\b0 , 261-270. \par \par Baker D., Rosenwasser O. A., O'Neill J. K., and Turk J. L. (1995) Genetic analysis of experimental allergic encephalomyelitis in mice. \i J. Immunol.\i0 \b 155\b0 , 4046-4051. \par \par Bang F. B. and Warwick A. (1960) Mouse macrophages as host cells for the mouse hepatitis virus and the genetic basis of their susceptibility. \i Proc. Natl. Acad. Sci. USA\i0 \b 46\b0 , 1065-1071. \par \par Barber R. P., Vaughn J. T., Wimer R. E., and Wimer C. C. (1974) Genetically associated variations in the distribution of dentate granule cell. Synapses upon the pyramidal cell dendrites in mouse hippocampus. \i J. Comp. Neurol.\i0 \b 156\b0 , 417-434. \par \par Barnes R. D. and Tuffrey M. (1967) Serum antinuclear factor and the influence of environment in mice. \i Nature\i0 \b 214\b0 , 1136-1138. \par \par Barone F. C., Knudsen D. J., Nelson A. H., Feuerstein G. Z., and Willette R. N. (1993) Mouse strain differences in susceptibility to cerebral ischemia are related to cerebral vascular anatomy. \i Journal of Cerebral Blood Flow and Metabolism\i0 \b 13\b0 , 683-692. \par \par Barrett C. P., Donati E. J., Volz J. E., and Smith E. B. (1975) Variations in serum calcium between strains of inbred mice. \i Lab. Animal Sci.\i0 \b 25\b0 , 638-640. \par \par Barthold S. W., Beck D. S., Hansen G. M., Terwilliger G. A., and Moody K. D. (1990) Lyme borreliosis in selected strains and ages of laboratory mice. \i J. Infect. Dis.\i0 \b 162\b0 , 133-138. \par \par Bartke A. and Krzanowska H. (1972) Spermatogenesis in mouse strains with high and low abnormal spermatazoa. \i J. Hered.\i0 \b 63\b0 , 172-174. \par \par Baxter A. G. and Cooke A. (1993) Complement lytic activity has no role in the pathogenesis of autoimmune diabetes in NOD mice. \i Diabetes\i0 \b 42\b0 , 1574-1578. \par \par Baxter A. G. and Mandel T. E. (1991) Hemolytic anemia in non-obese diabetic mice. \i Eur. J. Immunol.\i0 \b 21\b0 , 2051-2055. \par \par Beamer W. G., Donahue L. R., Rosen C. J., and Baylink D. J. (1996) Genetic-variability in adult bone-density among inbred strains of mice. \i Bone\i0 \b 18\b0 , 397-403. \par \par Beauchamp G. K. and Fisher A. S. (1993) Strain differences in consumption of saline solutions by mice. \i Physiol. Behav.\i0 \b 54\b0 , 179-184. \par \par Bebo B. F., Lee C. H., Orr E. L., and Linthicum D. S. (1996) Mast cell-derived histamine and tumor-necrosis-factor - differences between SJL/J and BALB/c inbred strains of mice. \i Immunology and Cell Biology\i0 \b 74\b0 , 225-230. \par \par Bechensteen A. G., Halvorsen S., Abdelnoor M., and Skottner A. (1993) Growth hormone treatment and development of malignancy: Recombinant human growth hormone does not induce leukemia in AKR/O-mice. \i Pediatric Hematology and Oncology\i0 \b 10\b0 , 41-47. \par \par Bedigian H. G., Shepel L. A., and Hoppe P. C. (1993) Transplacental transmission of a leukemogenic murine leukemia virus. \i Journal of Virology\i0 \b 67\b0 , 6105-6109. \par \par Belinsky S. A., Devereux T. R., Foley J. F., Maronpot R. R., and Anderson M. W. (1992) Role of the alveolar type II cell in the development and progression of pulmonary tumors induced by 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone in the A/J mouse. \i Cancer Res.\i0 \b 52\b0 , 3164-3173. \par \par Belinsky S. A., Stefanski S. A., and Anderson M. W. (1993) The A/J mouse lung as a model for developing new chemointervention strategies. \i Cancer Res.\i0 \b 53\b0 , 410-416. \par \par Belknap J. K., Crabbe J. C., Riggan J., and O'Toole L. A. (1993) Voluntary consumption of morphine in 15 inbred mouse strains. \i Psychopharmacology\i0 \b 112\b0 , 352-358. \par \par Bell R. R. and Haskell B. E. (1971) Metabolism of vitamin B6 in the I-strain mouse. I. Absorption, excretion and conversion of vitamin to enzyme co-factor. \i Arch. Biochem. Biophys.\i0 \b 147\b0 , 588-601. \par \par Bell R. R., Blanchard C. A., and Haskell B. E. (1971) Metabolism of vitamin B6 in the I-strain mouse. II. Oxidation to pyridoxal. \i Arch. Biochem. Biophys.\i0 \b 147\b0 , 602-611. \par \par Bellini O., Casazza A. M., and Di Marco A. (1976) Histological and histochemical studies of myocardial lesions in BALB/cCr mice. \i Lab. Animal Sci.\i0 \b 26\b0 , 329-333. \par \par Belyaev D. K., Gruntenko E. V., and Videlets I. Y. (1970) Genetic differentiation of the thymus in mice of different strains with respect to malignant growth communication. II. Differences in the weight of the thymus in various strains of mice. \i Sov. Genet.\i0 \b 6\b0 , 47-51. \par \par Bennett L. M., Farnham P. J., and Drinkwater N. R. (1995) Strain-dependent differences in DNA synthesis and gene expression in the regenerating livers of C57BL/6J and C3H/HeJ mice. \i Molecular Carcinogenesis\i0 \b 14\b0 , 46-52. \par \par Bentvelzen P., Daams J. H., Hageman P., and Calafat J. (1970) Genetic transmission of viruses that incite mammary tumors in mice. \i Proc. Natl. Acad. Sci. USA\i0 \b 67\b0 , 377-384. \par \par Bergeron A. J. and Yohe H. C. (1996) Reclassification of the BXH11/Ty mouse as an endotoxin-hyporesponsive strain. \i Journal of Endotoxin Research\i0 \b 3\b0 , 165-168. \par \par Bergman R. K. and Munoz J. (1968) Action of the histamine sensitizing factor from Bordetella pertussis on inbred and random bred strains of mice. \i Int. Arch. Allergy\i0 \b 34\b0 , 331-338. \par \par Bernadini G. L., Gu X., and German D. C. (1991) Nucleus A10 dopaminergic neurons in inbred mouse strains: firing rate and autoreceptor sensitivity are independent of the number of cells in the nucleus. \i Brain Res. Bull.\i0 \b 27\b0 , 163-168. \par \par Bernstein S. E. (1966) Physiological characteristics, in \i Biology of the Laboratory Mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 337-350. McGraw-Hill, New York. \par \par Berry C. L. and Nickols C. D. (1979) The effects of aspirin on the development of the mouse 3rd. molar. \i Arch. Toxicol.\i0 \b 42\b0 , 185-190. \par \par Beutner U., Launois P., Ohteki T., Louis J. A., and MacDonald H. R. (1997) Natural killer-like T cells develop in SJL mice despite genetically distinct defects in NK1.1 expression and in inducible interleukin-4 production. \i Eur. J. Immunol.\i0 \b 27\b0 , 928-934. \par \par Bhathal P. S., Jordan T. W., and Mackay I. R. (1990) Mouse strain differences in susceptibility to sporidesmin-induced biliary tract injury. \i Liver\i0 \b 10\b0 , 193-204. \par \par Bhol K. C., Mukherjee R. M., Mehra S., Jalan K. N., Maitra T. K., and Haldar D. P. (1990) Experimental hepatic amoebiasis in inbred mice. \i Indian Journal of Pathology & Microbiology\i0 \b 33\b0 , 364-367. \par \par Biddle F. G., Jung J. D., and Eales B. A. (1991) Genetically determined variation in the azygos vein in the mouse. \i Teratology\i0 \b 44\b0 , 675-683. \par \par Biddle FG (1990) Genetically determined transient edema found in the WB/ReJ mouse strain in a teratogenic survey with acetazolamide. \i Teratology\i0 \b 42\b0 , 659-670. \par \par Bielschowsky M. and D'Ath E. F. (1973) Spontaneous granulosa cell tumours in mice of strains NZC/Bl, NZO/Bl, NZY/Bl and NZB/Bl. \i Pathology\i0 \b 5\b0 , 303-310. \par \par Bielschowsky M. and Goodall C. M. (1970) Origin of inbred NZ mouse strains. \i Cancer Res.\i0 \b 30\b0 , 834-836. \par \par Bielschowsky M. and Schofield G. C. (1962) Studies on megacolon in piebald mice. \i Aust. J. Exp. Biol. Med. Sci.\i0 \b 40\b0 , 395-404. \par \par Blake R. L. (1970) Regulation of liver tyrosine amino transferase activity in inbred strains and mutant mice. I. Strain variance in fasting enzyme levels. \i Int. J. Biochem.\i0 \b 1\b0 , 361-370. \par \par Blake R. L. (1972) Animal model for hyperprolinaemia: deficiency of mouse proline oxidase activity. \i Biochem. J.\i0 \b 129\b0 , 987-989. \par \par Blake R. L., Grillo R. V., and Russell E. S. (1974) Increased taurine excretion in hereditary hyperprolinemia of the mouse. \i Life Sci.\i0 \b 14\b0 , 1285-1290. \par \par Blake R. L., Hall J. G., and Russell E. S. (1976) Mitochondrial proline dehydrogenase deficiency in hyperprolinemic PRO/Re mice: Genetic and enzymatic analyses. \i Biochem. Genet.\i0 \b 14\b0 , 739-757. \par \par Blank K. J. and Lilly F. (1976) Lethality of the Fv-2 resistance allele in with a DBA/2 background. \i Genetics\i0 \b 83\b0 , 58. \par \par Blizard D. A. and Welty R. (1971) Cardiac activity in the mouse: strain differences. \i J. Comp. Physiol. Psychol.\i0 \b 77\b0 , 337-344. \par \par Blomberg B., Geckeler W. R., and Weigert M. (1972) Genetics of the antibody response to Dextran in mice. \i Science\i0 \b 177\b0 , 178-180. \par \par Boehm G. W., Sherman G. F., Hoplight II B. J., Hyde L. A., Waters N. S., Bradway D. M., Galaburda A. M., and Denenberg V. H. (1996a) Learning and memory in the autoimmune BXSB mouse: Effects of neocortical ectopias and environmental enrichment. \i Brain Res.\i0 \b 726\b0 , 11-22. \par \par Boehm G. W., Sherman G. F., Rosen G. D., Galaburda A. M., and Denenberg V. H. (1996b) Neocortical ectopias in BXSB mice: Effects upon reference and working memory systems. \i Cerebral Cortex\i0 \b 6\b0 , 696-700. \par \par Boehme D. H. (1970) Resistance to Salmonella infections in inbred mouse strains. \i Bull. N.Y. Acad. Med.\i0 \b 46\b0 , 499-508. \par \par Bonhomme F., Britton-Davidian J., Catalan J., and Thaler L. (1982) New inbred strain: BFM/2Mpl. \i Mouse N.L.\i0 \b 66\b0 , 71-72. \par \par Bonner J. J. and Slavkin H. C. (1975) Cleft palate susceptibility linked to histocompatibility-2 (H-2) in the mouse. \i Immunogenet.\i0 \b 2\b0 , 213-218. \par \par Bonser G. M. (1938) The hereditary factor in induced skin tumours in mice: establishment of a strain specially sensitive to carcinogenic agents applied to the skin. \i J. Pathol. Bacteriol.\i0 \b 46\b0 , 581-602. \par \par Borel Y. and Kilham L. (1974) Carrier-determined tolerance in various strains of mice: the role of isogenic IgG in the induction of hapten specific tolerance. \i Proc. Soc. Exp. Biol. Med.\i0 \b 145\b0 , 470-474. \par \par Bornstein S., Trasler D. G., and Fraser F. C. (1970) Effect of the uterine environment on the frequency of spontaneous cleft lip in CL/Fr mice. \i Teratology\i0 \b 3\b0 , 295-298. \par \par Boucher D. W. and Notkins A. L. (1973) Virus-induced diabetes mellitus. I. Hyperglycemia and hyperinsulinemia in mice infected with encephalomyo-carditis virus. \i J. Exp. Med.\i0 \b 137\b0 , 1226-1239. \par \par Boucher D. W., Hayashi K., Rosenthal J., and Notkins A. L. (1975) Virus-induced diabetes mellitus. III. Influence of sex and strain of host. \i J. Infect. Dis.\i0 \b 131\b0 , 462-466. \par \par Boutwell R. K. (1964) Some biological aspects of skin carcinogenesis. \i Prog. Exp. Tumor Res.\i0 \b 4\b0 , 207-250. \par \par Bovet D., Bovet-Nitti F., and Oliverio A. (1966) Effects of nicotine on avoidance conditioning of inbred strains of mice. \i Psychopharmacologia\i0 \b 10\b0 , 1-5. \par \par Bovet D., Bovet-Nitti F., and Oliverio A. (1969) Genetic aspects of learning and memory in mice. \i Science\i0 \b 163\b0 , 139-149. \par \par Brackertz D., Mitchell G. F., Vadas M. A., Mackay I. R., and Miller J. F. A. P. (1977) Studies on antigen-induced arthritis in mice. II. Immunological correlates of arthritis susceptibility in mice. \i J. Immunol.\i0 \b 118\b0 , 1639-1644. \par \par Braley H. C. and Freeman M. J. (1971) Strain differences in antibody plaque- forming cell responses in inbred mice to pneumococcal polysaccharide. \i Cell. Immunol.\i0 \b 2\b0 , 73-81. \par \par Bray G. A. and York D. A. (1971) Genetically transmitted obesity in rodents. \i Physiol. Rev.\i0 \b 51\b0 , 598-646. \par \par Brcand P. and Daehnfeldt J. L. (1973) Enzyme patterns of glucose catabolism in hormone-dependent and independent mammary tumours of GR mice. \i Eur. J. Cancer\i0 \b 9\b0 , 763-770. \par \par Brenner G. J., Cohen N., and Moynihan J. A. (1994) Similar immune response to nonlethal infection with herpes simplex virus-1 in sensitive (BALB/c) and resistant (C57BL/6) strains of mice. \i Cell. Immunol.\i0 \b 157\b0 , 510-524. \par \par Brieland J., Freeman P., Kunkel R., Chrisp C., Hurley M., Fantone J., and Engleberg C. (1994) Replicative Legionella pneumophila lung infection in intratracheally inoculated A/J mice: A murine model of human Legionnaires' disease. \i Am. J. Pathol.\i0 \b 145\b0 , 1537-1546. \par \par Briles D. E., Krause R. M., and Davie J. M. (1976) Genetic control of non-H-2 linked T-dependent antibody response defects of the BSVS mouse. \i Fed. Proc.\i0 \b 35\b0 , 824. \par \par Brilliant M. H., Ching A., Nakatsu Y., and Eicher E. M. (1994) The original pink-eyed dilution mutation (p) arose in asiatic mice: Implications for the H4 minor histocompatibility antigen, Myod1 regulation and the origin of inbred strains. \i Genetics\i0 \b 138\b0 , 203-211. \par \par Briody B. A. (1966) The natural history of mouse pox. \i National Cancer Institute Monograph\i0 \b 20\b0 , 105-116. \par \par Brooke M. S. (1965) Natural haemogglutinins in mice: their occurrence and properties. \i Immunol.\i0 \b 8\b0 , 375-383. \par \par Brown A. M. (1965) Pharmacogenetics of the mouse. \i Lab. Anim. Care\i0 \b 15\b0 , 111-118. \par \par Brown D. M. and Hughes B. O. (1962) Practical aspects of strain variation in relation to pharmacological testing. \i J. Pharm. Pharmacol.\i0 \b 14\b0 , 397-428. \par \par Bruchovsky N. and Meakin J. W. (1973) The metabolism and binding of testosterone in androgen-dependent and autonomous transplantable mouse mammary tumors. \i Cancer Res.\i0 \b 33\b0 , 1689-1695. \par \par Bruell J. H. (1964) Inheritance of behavioural and physiological characters of mice and the problem of heterosis. \i Am. Zool.\i0 \b 4\b0 , 125-138. \par \par Bruell J. H. (1969) Genetics and adaptive significance of emotional defecation in mice. \i Ann. NY Acad. Sci.\i0 \b 159\b0 , 825-830. \par \par Bruell J. H., Daroczy A. F., and Hellerstein H. K. (1962) Strain and sex differences in serum cholesterol levels in mice. \i Science\i0 \b 135\b0 , 1071-1072. \par \par Brunnert S. R. (1997) Morphologic response of myocardium to freeze-thaw injury in mouse strains with dystrophic cardiac calcification. \i Lab. Animal Sci.\i0 \b 47\b0 , 11-18. \par \par Bunker L. E. (1959) Hepatic fusion, a new gene in linkage group I of the mouse. \i J. Hered.\i0 \b 50\b0 , 40-44. \par \par Burnet F. M. (1972a) The New Zealand mice, in \i Auto-immunity and auto-immune disease\i0 (Burnet M., ed), pp. 109-119. Davis, Philadelphia. \par \par Burnet F. M. (1972b) A re-assessment of the forbidden clone hypothesis of auto-immune disease. \i Aust. J. Exp. Biol. Med. Sci.\i0 \b 50\b0 , 1-9. \par \par Buschmann H. and Meyer J. (1981) Resistenzzuch bei der Maus. Etablieriung von zwei Mauselinien, welche auf hohes und niedriges Phagozytosevermogen selektiert worden sing. \i Zbl. Vet. Med. B.\i0 \b 28\b0 , 713-732. \par \par Butler A. and Whitehead A. S. (1994) Resistance to secondary amyloidosis in A/J mice is not significantly associated with allelic variants linked to the serum amyloid A gene cluster. \i Scand.J. Immunol.\i0 \b 40\b0 , 355-358. \par \par Butler K. (1973) Predatory behaviour in laboratory mice. Strain and sex comparisons. \i J. Comp. Physiol. Psychol.\i0 \b 85\b0 , 243-249. \par \par Butler L. (1972) The inheritance of glucosuria in the KK and AY mouse. \i Can. J. Genet. Cytol.\i0 \b 14\b0 , 265-269. \par \par Butler L. and Gerritsen G. C. (1970) A comparison of the modes of inheritance of diabetes in the Chinese hamster and the KK mouse. \i Diabetologia\i0 \b 6\b0 , 163-167. \par \par Cabib S. and Bonaventura N. (1997) Parallel strain-dependent susceptibility to environmentally-induced stereotypies and stress-induced behavioral sensitization in mice. \i Physiol. Behav.\i0 \b 61\b0 , 499-506. \par \par Caffe A. R., Szel A., Juliusson B., Hawkins R., and vanVeen T. (1993) Hyperplastic neuroretinopathy and disorder of pigment epithelial cells precede accelerated retinal degeneration in the SJL/N mouse. \i Cell & Tissue Research\i0 \b 271\b0 , 297-307. \par \par Cartner S. C., Simecka J. W., Briles D. E., Cassell G. H., and Lindsey J. R. (1996) Resistance to Mycoplasmal lung-disease in mice is a complex genetic trait. \i Infect. Immun.\i0 \b 64\b0 , 5326-5331. \par \par Casley W. L., Menzies J. A., Girard M., Larocque L., Mousseau N., Whitehouse L. W., and Moon T. W. (1997a) Differences in caffein 3-demethylation activity among inbred mouse strains: a comparison of hepatic \i Cyp1a2\i0 gene expression between two inbred strains. \i Fundam. Appl. Toxicol.\i0 \b 40\b0 , 228-237. \par \par Casley W. L., Menzies J. A., Mousseau N., Girard M., Moon T. W., and Whitehouse L. W. (1997b) Increased basal expression of hepatic \i Cyp1a1\i0 and \i Cyp1a2\i0 genes in inbred mice selected for susceptibility to acetaminophen-induced hepatotoxicity. \i Pharmacogenetics\i0 \b 7\b0 , 283-293. \par \par Castonguay A. and Packer L. (1993) Pulmonary carcinogenesis and its prevention by dietary polyphenolic compounds. \i Annals of the New York Academy of Sciences\i0 \b 686\b0 , 177-185. \par \par Castro A. P., Aguas A. P., and Silva M. T. (1993) Adjuvant treatment increases the resistance to Mycobacterium avium infection of Mycobacteria-susceptible BALB/c mice. \i Clin. Exp. Immunol.\i0 \b 92\b0 , 466-472. \par \par Cerny J., McAlack R. F., Sajid M. A., and Friedman H. (1971) Genetic differences in the immunocyte response of mice to separate determinants on one bacterial antigen. \i Nature New Biol.\i0 \b 230\b0 , 247-248. \par \par Chai C. K. (1959) Lifespan in inbred and hybrid mice. \i J. Hered.\i0 \b 50\b0 , 203-208. \par \par Chai C. K. (1961) Analysis of quantitative inheritance of body size in mice. IV an attempt to isolate polygenes. \i Genet. Res.\i0 \b 2\b0 , 25-32. \par \par Chai C. K. and Dickie M. M. (1966) Endocrine variations, in \i Biology of the laboratory mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 387-403. McGraw-Hill, New York. \par \par Chai C. K., Amin A., and Reineke E. P. (1957) Thyroidal iodine metabolism in inbred and F1 hybrid mice. \i Am. J. Physiol.\i0 \b 188\b0 , 499-502. \par \par Chan C. C., Gery I., Kohn L. D., Nussenblatt R. B., Mozes E., and Singer D. S. (1995) Periocular inflammation in mice with experimental systemic lupus erythematosus: A new experimental blepharitis and its modulation. \i J. Immunol.\i0 \b 154\b0 , 4830-4835. \par \par Chaouat G., Kolb J.-P., Kiger N., Stanislawski M., and Wegmann T. G. (1985) Immunologic consequences of vaccination against abortion in mice. \i J. Immunol.\i0 \b 134\b0 , 1594-1598. \par \par Chayen J., Bitensky L., and Chambers M. G. (1996) Modulation of murine osteoarthritis. \i Cell Biochemistry and Function\i0 \b 14\b0 , 57-61. \par \par Chen B., You L., Wang Y., Stoner G. D., and You M. (1994) Allele-specific activation and expression of the K-ras gene in hybrid mouse lung tumors induced by chemical carcinogens. \i Carcinogenesis\i0 \b 15\b0 , 2031-2035. \par \par Chen H. W., Hamer D. H., Heiniger H. J., and Meier H. (1972a) Stimulation of hepatic RNA synthesis in dwarf mice by ovine prolactin. \i Biochim. Biophys. Acta\i0 \b 287\b0 , 90-97. \par \par Chen H. W., Meier H., Heiniger H. J., and Huebner R. J. (1972b) Tumorigenesis in strain DW/J mice and induction by prolactin of the group-specific antigen of endogenous C-type RNA tumour virus. \i J. Natl. Cancer Inst.\i0 \b 49\b0 , 1145-1154. \par \par Chen W. H., Hosokawa M., Tsuboyama T., Ono T., Iizuka T., and Takeda T. (1989) Age-related changes in the temporomandibular joint of the senescence accelerated mouse (SAM): SAM-P/3 as a new murine model of degenerative joint disease. \i Am. J. Pathol.\i0 \b 135\b0 , 379-385. \par \par Cheverud J. M., Routman E. J., Duarte F. A. M., Van Swinderen B., Cothran K., and Perel C. (1996) Quantitative trait loci for murine growth. \i Genetics\i0 \b 142\b0 , 1305-1319. \par \par Chiodini R. J. and Buergelt C. D. (1993) Susceptibility of Balb/c, C57/B6 and C57/B10 mice to infection with \i Mycobacterium paratuberculosis\i0 . \i J. Comp. Pathol.\i0 \b 109\b0 , 309-319. \par \par Christensen L. R., Wolf G. L., Matanic B., Bond E., and Wright E. (1963) Accidental chloroform poisoning of BALB/cAnNIer mice. \i Z. Versuchstierk.\i0 \b 2\b0 , 135-140. \par \par Ciranello R. D., Barchas R., Kessler S., and Barchas J. D. (1972) Catecholamines: strain differences in biosynthetic enzyme activity in mice. \i Life Sci.\i0 \b 11\b0 , 565-572. \par \par Clark D. A., Banwatt D., and Chaouat G. (1993) Stress-triggered abortion in mice prevented by alloimmunization. \i American Journal of Reproductive Immunology\i0 \b 29\b0 , 141-147. \par \par Clement Y., Martin B., Venault P., and Chapouthier G. (1995) Involvement of regions of the 4th and 7th chromosomes in the open-field activity of mice. \i Behavioural Brain Research\i0 \b 70\b0 , 51-57. \par \par Clement Y., Kia K. H., Daval G., and Verge D. (1996) An autoradiographic study of serotonergic receptors in a murine genetic model of anxiety-related behaviors. \i Brain Res.\i0 \b 709\b0 , 229-242. \par \par Clerici E. (1972) Induction of amyloidosis in mice upon treatment with polypeptidylcaseins and DNP-casein. Relation to antigenicity. \i Acta Pathol. Microbiol. Scand.\i0 \b Suppl., 233\b0 , 167-171. \par \par Collaborative Study Group for the Micronucleus Test (1988) Strain differences in the micronucleus test. \i Mutation Res.\i0 \b 204\b0 , 307-316. \par \par Collins G. R., Goodheart C. R., and Henson D. (1971) Spontaneous heritable hydronephrosis in inbred mice. I. Description, incidence and distribution of lesions. \i Lab. Animal Sci.\i0 \b 22\b0 , 333-338. \par \par Constantin D., Francis J. E., Akhtar R. A., Clothier B., and Smith A. G. (1996) Uroporphyria induced by 5-aminolaevulinic acid alone in \i Ahr\i0 \i \up8 d\up0 \i0 \up8 \up0 SWR mice. \i Biochemical Pharmacology\i0 \b 52\b0 , 1407-1413. \par \par Conti A. and Maestroni G. J. M. (1996) Melatonin rhythms in mice and its role in autoimmune diseases. \i Periodicum Biologorum\i0 \b 98\b0 , 451-457. \par \par Cook M. J. and Vlcek A. (1961) Sex ratio in mice. \i Nature\i0 \b 191\b0 , 89. \par \par Cooper P. A., Benno R. H., Hahn M. E., and Hewitt J. K. (1991) Genetic analysis of cerebellar foliation patterns in mice (\i Mus musculus\i0 ). \i Behav. Genet.\i0 \b 21\b0 , 405-419. \par \par Cornelius J. G., Luttge B. G., and Peck A. B. (1993) Antioxidant enzyme activities in IDD-prone and IDD-resistant mice: A comparative study. \i Free Radical Biology and Medicine\i0 \b 14\b0 , 409-420. \par \par Coulson P. S. and Wilson R. A. (1989) Portal shunting and resistance to \i Shistosoma mansoni\i0 in 129 strain mice. \i Parasitology\i0 \b 99\b0 , 383-389. \par \par Courtenay J. S., Dallman M. J., Dayan A. D., Martin A., and Mosedale B. (1980) Immunization against heterologous type II collagen induces arthritis in mice. \i Nature\i0 \b 283\b0 , 666-668. \par \par Coutinho A. (1976) Genetic control of B-cell responses. II. Identification of the spleen B-cell defect in C3H/HeJ mice. \i Scand.J. Immunol.\i0 \b 5\b0 , 129-140. \par \par Creighton W. D., Zinkernagel R. M., and Dixon F. J. (1979) T cell-mediated immune responses of lupus-prone BXSB mice and other murine strains. \i Clin. Exp. Immunol.\i0 \b 37\b0 , 181-189. \par \par Crispens C. G. (1973) Some characteristics of strain SJL/JDg mice. \i Lab. Animal Sci.\i0 \b 23\b0 , 408-413. \par \par Csiza C. K. and McMartin D. N. (1976) Apparent acaridal dermatitis in a C57BL/6 Nya mouse colony. \i Lab. Animal Sci.\i0 \b 26\b0 , 781-787. \par \par Curtis H. J. (1971) Genetic factors in aging. \i Adv. Genet.\i0 \b 16\b0 , 305-324. \par \par Cutroneo K. R., Guzman N. A., and Liebelt A. G. (1973) Elevation of peptidylproline hydroxylase activity and collagen synthesis in spontaneous primary mammary cancers of inbred mice. \i Cancer Res.\i0 \b 32\b0 , 2828-2833. \par \par Czarnomska A. and Wezykowa J. (1971) Some genetic characteristics of BN/a and BN/b inbred strains of mice. \i Genet. Polon.\i0 \b 12\b0 , 529-536. \par \par Dagg C. P. (1966) Teratogenesis, in \i Biology of the laboratory mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 309-328. McGraw-Hill, New York. \par \par Dagg C. P., Schlager G., and Doerr A. (1966) Polygenic control of the teratogenicity of 5-fluorouracil in mice. \i Genetics\i0 \b 53\b0 , 1101-1117. \par \par Dains K., Hitzemann B., and Hitzemann R. (1996) Genetics, neuroleptic response and the organization of cholinergic neurons in the mouse striatum. \i J. Pharmacol. Exp. Therapeut.\i0 \b 279\b0 , 1430-1438. \par \par Damjanov I., Katic V., and Stevens L. C. (1975) Ultrastructure of ovarian teratomas in LT mice. \i Z. Krebsforsch.\i0 \b 83\b0 , 261-267. \par \par Daniel W. L. (1976) Genetics of murine liver and kidney arylsulfatase B. \i Genetics\i0 \b 82\b0 , 477-491. \par \par Darnell M. B., Koprowski H., and Lagerspatz K. (1974) Genetically determined resistance to infection with group B arboviruses. I. Distribution of the resistance gene among various mouse populations and characteristics of gene expression in vivo. \i J. Infect. Dis.\i0 \b 129\b0 , 240-247. \par \par Davis W. M. and King W. T. (1967) Pharmacogenetic factor in the convulsive responses of mice to flurothyl. \i Experientia\i0 \b 23\b0 , 214-215. \par \par Davis W. M., King W. T., and Rabbini M. (1967) Placebo effect of saline on locomotor activity in several strains of mice. \i J. Pharmaceut. Sci.\i0 \b 56\b0 , 1347-1349. \par \par De Beer M. C., De Beer F. C., McCubbin W. D., Kay C. M., and Kindy M. S. (1993) Structural prerequisites for serum amyloid A fibril formation. \i J. Biol. Chem.\i0 \b 268\b0 , 20606-20612. \par \par Deckard B. S., Lieff B., Schlesinger K., and DeFries J. C. (1976) Developmental patterns of seizure susceptibility in inbred strains of mice. \i Devel. Psychobiol.\i0 \b 9\b0 , 17. \par \par DeFries J. C., Wilson J. R., Erwin V. G., and Peterson D. R. (1989) LSXSS Recombinant inbred strains of mice: Initial characterization. \i Alcoholism: Clin. Exp. Res.\i0 \b 13\b0 , 196-200. \par \par DeFries J. L. and McClearn G. E. (1970) Social dominance and Darwinian fitness in the laboratory mouse. \i Am. Naturalist\i0 \b 104\b0 , 408-411. \par \par Delker D. A., Bammler T. K., and Rosenberg D. W. (1996) A comparative-study of hepatic and colonic metabolic enzymes in inbred mouse lines before and after treatment with the colon carcinogen, 1,2-dimethylhydrazine. \i Drug Metab. Disp.\i0 \b 24\b0 , 408-413. \par \par Delost P. and Chirvan-Nia P. (1958) Differences raciales dans l'involution de la zone x multi surrenalienne chez la souris adulte vierge. \i C. R. Soc. Biol.\i0 \b 152\b0 , 453-455. \par \par de Macario E. C. and Macario A. J. L. (1980) Immunosuppression associated with erythropoiesis in genetic low responder mice. \i Ann. Immunol (Inst. Pasteur)\i0 \b 131C\b0 , 397-404. \par \par Den Engelese L., Misdorp W., and Emmelot P. (1976) Hepatomas in GRS/A male mice treated with horse serum or horse anti-mouse antilymphocyte serum. \i Eur. J. Cancer\i0 \b 12\b0 , 101-106. \par \par Deringer M. K. (1959a) Necrotizing arteritis in strain BL/De mice. \i Lab. Invest.\i0 \b 8\b0 , 1461-1465. \par \par Deringer M. K. (1959b) Occurrence of tumors, particularly mammary tumors in agent-free strain C3HeB mice. \i J. Natl. Cancer Inst.\i0 \b 22\b0 , 995-1002. \par \par Deringer M. K. (1970) Mammary tumors in strains BL/LyDe and SWR/LyDe mice. \i J. Natl. Cancer Inst.\i0 \b 45\b0 , 215-218. \par \par Deringer M. K., Dunn T. B., and Heston W. E. (1953) Results of exposure of strain C3H mice to chloroform. \i Proc. Soc. Exp. Biol. Med.\i0 \b 83\b0 , 474-479. \par \par De Souza C. M., Maia L. C. S., and Vaz N. M. (1974) Susceptibility to cutaneous anaphylaxis in inbred strains of mice. \i J. Immunol.\i0 \b 112\b0 , 1369-1372. \par \par Dickie M. M. and Atkinson W. B. (1957) Increased sensitivity to estrogen in uterine hyperplasia in DBA x CE and reciprocal hybrid mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 96\b0 , 415-417. \par \par Dickie M. M., Atkinson W. B., and Fekete E. (1957) The ovary, estrus cycle and fecundity of DBA x CE and reciprocal hybrid mice in relation to age and the hyperovarian syndrome. \i Anat. Rec.\i0 \b 127\b0 , 187-199. \par \par Dickinson A. G. Personal communication. \par \par Dickinson A. G. and Mackay J. M. K. (1964) Genetical control of the incubation period in mice of the neurological disease, scrapie. \i Heredity\i0 \b 19\b0 , 279-288. \par \par Dickinson A. G. and Meikle V. M. H. (1971) Host -genotype and agent effects in scrapie incubation: change in allelic interaction with different strains of agent. \i Molec. Gen. Genet.\i0 \b 112\b0 , 73-79. \par \par Dickinson A. G., Meikle V. M. H., and Fraser H. (1968) Identification of a gene which controls the incubation period of some strains of scrapie agent in mice. \i J. Comp. Pathol.\i0 \b 78\b0 , 293-299. \par \par Dietz M. and Rick M. A. (1972) Effect of host strain and H-2 type on spontaneous regression of murine leukemia virus. \i Int. J. Cancer\i0 \b 10\b0 , 99-104. \par \par Dileto C. L. and Travis E. L. (1996) Fibroblast radiosensitivity in-vitro and lung fibrosis in-vivo -comparison between a fibrosis-prone and fibrosis-resistant mouse strain. \i Radiation Res.\i0 \b 146\b0 , 61-67. \par \par Di Paola J. A., Strong L. C., and Moore G. E. (1964) Calcareous pericarditis in mice of several genetically related strains. \i Proc. Soc. Exp. Biol. Med.\i0 \b 115\b0 , 496-497. \par \par Di Pauli R. (1972) Genetics of the immune response. I. Differences in the specificity of antibodies to lipopolysaccharides among different strains of mice. \i J. Immunol.\i0 \b 109\b0 , 394-400. \par \par Diwan B. A. (1974) Strain-dependent teratogenic effects of 1-ethyl-1- nitrosourea in inbred strains of mice. \i Cancer Res.\i0 \b 34\b0 , 151-157. \par \par Diwan B. A., Meier H., and Huebner R. J. (1973) Transplacental effects of 1- ethyl-1-nitrosourea in inbred strains of mice. III. Association between infectious or subinfectious endogenous type-C-RNA tumour virus expression and chemically induced tumorigenesis. \i J. Natl. Cancer Inst.\i0 \b 51\b0 , 1965-1970. \par \par Diwan B. A., Meier H., and Huebner R. J. (1974) Transplacental effect of 1- -ethyl-1-nitrosourea in inbred strains of mice. IV. Rapid tumoe induction in strain crosses. \i J. Natl. Cancer Inst.\i0 \b 52\b0 , 893-895. \par \par Dorf M. E., Dunham E. K., Johnson J. P., and Benacerraf B. (1974) Genetic control of the immune response: the effect of non-H-2 linked genes on antibody production. \i J. Immunol.\i0 \b 112\b0 , 1329-1336. \par \par Dostal M. and Jelinek R. (1973) Sensitivity of embryos and intraspecies differences in mice in response to prenatal administration of corticoids. \i Teratology\i0 \b 8\b0 , 245-252. \par \par Doyle D. and Schimke R. T. (1969) The genetic and developmental regulation of hepatic -aminolaevulinate dehydratase in mice. \i J. Biol. Chem.\i0 \b 244\b0 , 5449-5459. \par \par Dragani T. A., Manenti G., Gariboldi M., De Gregorio L., and Pierotti M. A. (1995a) Genetics of liver tumor susceptibility in mice. \i Toxicol. Lett.\i0 \b 82-83\b0 , 613-619. \par \par Dragani T. A., Manenti G., Gariboldi M., Degregorio L., and Pierotti M. A. (1995b) Genetics of liver-tumor susceptibility in mice. \i Toxicol. Lett.\i0 \b 82-3\b0 , 613-619. \par \par Drake C. G., Rozzo S. J., Hirschfeld H. F., Smarnworawong N. P., Palmer E., and Kotzin B. L. (1995) Analysis of the New Zealand black contribution to lupus-like renal disease: Multiple genes that operate in a threshold manner. \i J. Immunol.\i0 \b 154\b0 , 2441-2447. \par \par Drappa J., Brot N., and Elkon K. B. (1993) The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL lpr/lpr. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 90\b0 , 10340-10344. \par \par Drasher M. L. (1965) Strain differences in the response of the mouse uterus to estrogens. \i J. Hered.\i0 \b 46\b0 , 190-192. \par \par Dubois E. L., Horowitz R. E., Demopaulos H. B., and Teplitz R. (1966) NZB/NZW mice as a model of systemic lupus erythematosus. \i J. Am. Med. Assoc.\i0 \b 195\b0 , 285-289. \par \par Dunn T. B. and Deringer M. K. (1968) Reticulum cell neoplasm, type B, or `Hodgkin's-like lesion' of the mouse. \i J. Natl. Cancer Inst.\i0 \b 40\b0 , 771-821. \par \par Eaton G. J. (1972) Intestinal helminths in the mouse. \i Lab. Animal Sci.\i0 \b 22\b0 , 850-853. \par \par Ebbesen P. (1971) Reticulosarcoma and amyloid development in BALB/c mice inoculated with syngeneic cells from young and old donors. \i J. Natl. Cancer Inst.\i0 \b 47\b0 , 1241-1245. \par \par Eberhart G. P., West D. B., Boozer C. N., and Atkinson R. L. (1994) Insulin sensitivity of adipocytes from inbred mouse strains resistant or sensitive to diet-induced obesity. \i American Journal of Physiology - Regulatory Integrative and Comparative Physiology\i0 \b 266\b0 , R1423-R1428. \par \par Ehling U. H. (1964) Strain variation in reproductive capacity and radiation response of female mice. \i Radiation Res.\i0 \b 23\b0 , 603-610. \par \par Eicher E. M. and Lee B. K. (1990) The NXSM recombinant inbred strains of mice: genetic profile for 58 loci including the Mtv proviral loci. \i Genetics\i0 \b 125\b0 , 431-446. \par \par Eicher E. M., Beamer W. G., Washburn L. L., and Whitten W. K. (1980) A cytogenetic investigation of inherited true hermaphroditism in BALB/cWt mice. \i Cytogenet. Cell Genet.\i0 \b 28\b0 , 104-115. \par \par Elmer G. I. and George F. R. (1995) Genetic differences in the operant rate-depressant effects of ethanol between four inbred mouse strains. \i Behavioural Pharmacology\i0 \b 6\b0 , 794-800. \par \par Elmer G. I., Pieper J. O., Goldberg S. R., and George F. R. (1995) Opioid operant self administration, analgesia, stimulation and respiratory depression in mu-deficient mice. \i Psychopharmacology\i0 \b 117\b0 , 23-31. \par \par Enomoto T., Weghorst C. M., Ward J. M., Anderson L. M., Perantoni A. O., and Rice J. M. (1993) Low frequency of H-ras activation in naturally occurring hepatocellular tumors of C3H/HeNCr mice. \i Carcinogenesis\i0 \b 14\b0 , 1939-1944. \par \par EORTC Screening group (1972) Handbook of materials and methods. \i Eur. J. Cancer\i0 \b 8\b0 , 185-196. \par \par Epe C., Sabel T., Schnieder T., and Stoye M. (1994) The behavior and pathogenicity of Toxacara canis larvae in mice of different strains. \i Parasitology Research\i0 \b 80\b0 , 691-695. \par \par Eppig J. J., Wigglesworth K., Varnum D. S., and Nadeau J. H. (1996a) Genetic-regulation of traits essential for spontaneous ovarian teratocarcinogenesis in strain LT/Sv mice - aberrant meiotic cell-cycle, oocyte activation, and parthenogenetic development. \i Cancer Res.\i0 \b 56\b0 , 5047-5054. \par \par Eppig J. J., Wigglesworth K., Varnum D. S., and Nadeau J. H. (1996b) Genetic regulation of traits essential for spontaneous ovarian teratocarcinogenesis in strain LT/Sv mice: Aberrant meiotic cell cycle, oocyte activation, and parthenogenetic development. \i Cancer Res.\i0 \b 56\b0 , 5047-5054. \par \par Erickson R. P. (1974) Erythrocyte nicotinamide - adenine dinucleotide phosphate levels and the genetic regulation of erythrocyte glucose 6-phosphate dehydrogenase activity in the inbred mouse. \i Biochem. Genet.\i0 \b 11\b0 , 33-40. \par \par Erickson R. P. (1976) Strain variation in spermatazoal -glucuronidase in mice. \i Genet. Res.\i0 \b 28\b0 , 139-145. \par \par Erway L. C., Shiau Y. W., Davis R. R., and Krieg E. F. (1996) Genetics of age-related hearing-loss in mice .3. Susceptibility of inbred and F1-hybrid strains to noise-induced hearing-loss. \i Hearing Research\i0 \b 93\b0 , 181-187. \par \par Evans J. G., Collins M. A., Lake B. G., and Butler W. H. (1992) The histology and development of hepatic nodules and carcinoma in C3H/He and C57BL/6 mice following chronic phenobarbitone administration. \i Toxicologic Pathology\i0 \b 20\b0 , 585-594. \par \par Evans J. T., Hauschka T. S., and Mittelman A. (1974) Differential susceptibility of four mouse strains to induction of multiple large-bowel neoplasms by 1,2,-dimethylhydrazine. \i J. Natl. Cancer Inst.\i0 \b 52\b0 , 999-1000. \par \par Evans J. T., Shows T. B., Sproul E. E., Paolini N. S., Mittelman A., and Hauschka T. S. (1977) Genetics of colon carcinogenesis in mice treated with 1, 2-dimethylhydrazine. \i Cancer Res.\i0 \b 37\b0 , 134-136. \par \par Fahey J. L. (1965) Differences in the electrophoretic mobility of antibody from inbred strains of mice. \i J. Immunol.\i0 \b 94\b0 , 819-823. \par \par Fairchild S., Baker D., and Turk J. L. (1993a) Characterization of experimental allergic encephalomyelitis- susceptible Biozzi AB/H(H-2(dq1)) mice which express H-2A(nod): Analysis of T-cell receptor expression and the detection of a deletion ligand encoded by Mtv-7. \i Immunol.\i0 \b 78\b0 , 260-265. \par \par Fairchild S., Baker D., and Turk J. L. (1993b) Characterization of experimental allergic encephaolmyelitis-susceptible, Biozzi AB/H (H-2\up8 dq1\up0 ) mice which express H-2\up8 NOD\up0 . Analysis of T-cell receptor expression and the detection of a ligand encoded by MTV-7. \i Immunol.\i0 \b 78\b0 , 260-265. \par \par Falconer D. S. (1960) The genetics of litter size in mice. \i J. Cell. Comp. Physiol.\i0 \b 56\b0 , S153-S168. \par \par Falconer D. S. and Bloom J. L. (1962) A genetic study of induced lung tumours in mice. \i Brit. J. Cancer\i0 \b 16\b0 , 665-685. \par \par Faulkner C. B., Davidson M. K., Davis J. K., Schoeb T. R., Simecka J. W., and Lindsey J. R. (1995) Acute Mycoplasma pulmonis infection associated with coagulopathy in C3H/HeN mice. \i Lab. Animal Sci.\i0 \b 45\b0 , 368-372. \par \par Fawcett L. B., Buck S. J., Beckman D. A., and Brent R. L. (1996) Is there a no-effect dose for corticosteroid-induced cleft palate? The contribution of endogenous corticosterone to the incidence of cleft palate in mice. \i Pediatric Research\i0 \b 39\b0 , 856-861. \par \par Fawdington E. and Festing M. F. W. Mouse strain differences in balsa wood gnawing. Unpublished data. \par \par Fawl R. L., Gesser R. M., Valyinagi T., and Fraser N. W. (1996) Reactivation of herpes-simplex virus from latently infected mice after administration of cadmium is mouse-strain-dependent. \i J. Gen. Virol.\i0 \b 77\b0 , 2781-2786. \par \par Fenton P. F. and Carr C. J. (1951) The nutrition of the mouse. XI. Response of four strains to diets differing in fat content. \i J. Nutrit.\i0 \b 45\b0 , 225-233. \par \par Fenton P. F. and Dowling M. T. (1953) Studies on obesity. I. Nutritional obesity in mice. \i J. Nutrit.\i0 \b 49\b0 , 319-331. \par \par Fernandes G., Yunis J., Smith J., and Good R. A. (1972) Dietary influence on breeding behaviour, hemolytic anemia and longevity in NZB mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 139\b0 , 1189-1196. \par \par Fernandes G., Yunis E. J., and Good R. A. (1973) Reproductive deficiency of NZB male mice. Possibility of a viral basis. \i Lab. Invest.\i0 \b 29\b0 , 278-281. \par \par Fernandez J. L., Peters A. G., Cossens I. A., Weeks M., and Festing M. F. W. (1989) CBXC: a set of recombinant inbred strains between CBA/Ca and BALB/c. \i Lab. Anim.\i0 \b 23\b0 , 200-202. \par \par Festing M. F. W. (1969) Inbred mice in research. \i Nature\i0 \b 221\b0 , 716. \par \par Festing M. F. W. (1972) Mouse strain identification. \i Nature\i0 \b 238\b0 , 351-352. \par \par Festing M. F. W. (1973) Water escape learning in mice. I. Strain differences and biometrical considerations. \i Behav. Genet.\i0 \b 3\b0 , 13-24. \par \par Festing M. F. W. (1974) Footpad bristles: a convenient metric character in mice. \i Genet. Res.\i0 \b 24\b0 , 315-321. \par \par Festing M. F. W. Absence of the 3rd. molar in A2G mice. Unpublished data. \par \par Festing M. F. W. Breeding performance of mouse colonies at the MRC Laboratory Animals Centre. Unpublished data. \par \par Festing M. F. W. (1976b) Effects of marginal malnutrition on the breeding performance of inbred and F1 hybrid mice-a diallel study, in \i The Laboratory Animal in the Study of Reproduction\i0 (Antikatzides T., Ericksen S., and Spiegel A., eds), pp. 99-114. Gustav Fischer, Stuttgart. \par \par Festing M. F. W. (1977) Wheel activity in 26 strains of mouse. \i Lab. Anim.\i0 \b 11\b0 , 257-258. \par \par Festing M. F. W. (1980) Inbred strains and the factorial experimental design in toxicological screening, in \i Animal Quality and Models in Biomedical Research. Proceeding of the 7th. ICLAS Symposium, Utrecht\i0 (Spiegel A., Erichsen S., and Solleveld H. A., eds), pp. 59-66. Gustav Fischer, Stuttgart. \par \par Festing M. F. W. and Blackmore D. K. (1971) Life span of specified-pathogen-free (MRC category 4) mice and rats. \i Lab. Anim.\i0 \b 5\b0 , 179-192. \par \par Festing M. F. W. and Roderick T. H. (1989) Correlation between genetic distances based on single loci and on skeletal morphology in inbred mice. \i Genet. Res.\i0 \b 53\b0 , 45-55. \par \par Figueroa F., Tewarson S., Neufeld E., and Klein J. (1982) H-2 haplotypes of strains DBR7, B10.NZW, NFS, BQ2, STU, TO1 and TO2. \i Immunogenet.\i0 \b 15\b0 , 431-436. \par \par Fingerote R. J., Leibowitz J. L., Rao Y. S., and Levy G. A. (1995) Treatment of resistant A/J mice with methylprednisolone (MP) results in loss of resistance to murine hepatitis strain 3 (MHV-3) and induction of macrophage procoagulant activity (PCA). \i Advances in Experimental Medicine and Biology\i0 \b 380\b0 , 89-94. \par \par Finn D. A., Roberts A. J., Lotrich F., and Gallaher E. J. (1997) Genetic differences in behavioral sensitivity to a neuroactive steroid. \i J. Pharmacol. Exp. Therapeut.\i0 \b 280\b0 , 820-828. \par \par Fischer S. M., O'Connell J. F., Conti C. J., Tacker K. C., Fries J. W., Patrick K. E., Adams L. A., and Slaga T. J. (1987) Characterization of an inbred strain of the SENCAR mice that is highly sensitive to phorbol esters. \i Carcinogenesis\i0 \b 8\b0 , 421-424. \par \par Fiske R. D. and Klein P. A. (1975) Effect of immunosuppression on the genetic resistance of A2G mice to neurovirulent influenza virus. \i Infect. Immun.\i0 \b 11\b0 , 576-587. \par \par Flaks A. (1968) The susceptibility of various strains of neonatal mice to the carcinogenic effects of 9, 1 0-dimethyl- 1, 2-benzanthracene. \i Eur. J. Cancer\i0 \b 4\b0 , 579-585. \par \par Fox J. G., Li X., Cahill R. J., Andrutis K., Rustgi A. K., Odze R., and Wang T. C. (1996) Hypertrophic gastropathy in \i Helicobacter felis\i0 -infected wild-type C57BL/6 mice and p53 hemizygous transgenic mice. \i Gastroenterology\i0 \b 110\b0 , 155-166. \par \par Frankel W. N., Taylor B. A., Noebels J. L., and Lutz C. M. (1994) Genetic epilepsy model derived from common inbred mouse strains. \i Genetics\i0 \b 138\b0 , 481-489. \par \par Franko A. J. and Sharplin J. (1994) Development of fibrosis after lung irradiation in relation to inflammation and lung function in a mouse strain prone to fibrosis. \i Radiation Res.\i0 \b 140\b0 , 347-355. \par \par Fraser H. (1971) Astrocytomas in an inbred mouse strain. \i J. Pathol.\i0 \b 103\b0 , 266-270. \par \par Freund R., Dubensky T., Bronson R., Sotnikov A., Carroll J., and and Benjamin T. (1992a) Polyoma tumorigenesis in mice: evidence for dominant resistance and dominant susceptibility genes of the host. \i Virology\i0 \b 191\b0 , 724-731. \par \par Freund R., Dubensky T., Bronson R., Sotnikov A., Carroll J., and Benjamin T. (1992b) Polyoma tumorigenesis in mice: Evidence for dominant resistance and dominant susceptibility genes of the host. \i Virology\i0 \b 191\b0 , 724-731. \par \par Frings H. and Frings M. (1953) The production of stocks of albino mice with predictable susceptibilities to audiogenic seizures. \i Behav.\i0 \b 5\b0 , 305-319. \par \par Frith C. H., Haley T. J., and Seymore B. W. (1975) Spontaneous epicardial mineralization in BALB/cStCrl mice. \i Lab. Animal Sci.\i0 \b 25\b0 , 787. \par \par Fuchs P. C. (1962) Attempts to alter incidence of leukemia, and mammary cancer in C3H/Fg mice. \i Anat. Rev.\i0 \b 142\b0 , 233. \par \par Fuchs S., Mozes E., Maoz A., and Sela M. (1974) Thymus independence of a collagen-like synthetic polypeptide and of collagen, and the need for thymus and bone marrow-cell cooperation in the immune response to gelatin. \i J. Exp. Med.\i0 \b 139\b0 , 148-158. \par \par Fujinaga S., Poel W. E., Williams W. C., and Dmochowski L. (1970) Biological and morphological studies of SJL/J strain reticulum cell neoplasms induced and transmitted serially in low leukemia-strain mice. \i Cancer Res.\i0 \b 30\b0 , 729-742. \par \par Fujiwara M. and Cinader B. (1974) Cellular aspects of tolerance. IV. Strain variations of tolerance inducibility. \i Cell. Immunol.\i0 \b 12\b0 , 11-29. \par \par Fuller J. L. (1964) Measurement of alcohol preference in genetic experiments. \i J. Comp. Physiol. Psychol.\i0 \b 57\b0 , 85-88. \par \par Fuller J. L. and Sjursen F. H. (1967) Audiogenic seizures in eleven mouse strains. \i J. Hered.\i0 \b 58\b0 , 135-140. \par \par Furney S. K., Roberts A. D., and Orme I. M. (1990) Effect of rifabutin on disseminated Mycobacterium avium infections in thymectomized, CD4 T-cell-deficient mice. \i Antimicrobial Agents & Chemotherapy\i0 \b 34\b0 , 1629-1632. \par \par Furney S. K., Skinner P. S., Farrer J., and Orme I. M. (1995) Activities of rifabutin, clarithromycin, and ethambutol against two virulent strains of Mycobacterium avium in a mouse model. \i Antimicrobial Agents & Chemotherapy\i0 \b 39\b0 , 786-789. \par \par Gabridge M. G., Abrams G. D., and Murphy W. H. (1972) Lethal toxicity of Mycoplasma fermentens in mice. \i J. Infect. Dis.\i0 \b 125\b0 , 153-160. \par \par Gaines S., Currie J. A., and Tully J. G. (1965) Factors affecting formation of incomplete Vi antibody in mice. \i J. Bacteriol.\i0 \b 90\b0 , 635-642. \par \par Gaitonde M. K. and Festing M. F. W. (1976) Brain glutamic acid decarboxylase and open field activity in ten inbred strains of mice. \i Brain Res.\i0 \b 103\b0 , 617-621. \par \par Gannon K. S. and Contreras R. J. (1995) Sodium intake linked to amiloride-sensitive gustatory transduction in C57BL/6J and 129/J mice. \i Physiol. Behav.\i0 \b 57\b0 , 231-239. \par \par Garber A. T., Winkler C., Shringhara T., King C. R., Inana G., Piatigorsky J., and Gold R. M. (1985) Selective loss of a family of gene transcripts in a hereditary murine cataract. \i Science\i0 \b 227\b0 , 74-77. \par \par Garcia C. O., KanbourShakir A., Tang H., Molina J. F., Espinoza L. R., and Gharavi A. E. (1997) Induction of experimental antiphospholipid antibody syndrome in PL/J mice following immunization with beta(2)GPI. \i American Journal of Reproductive Immunology\i0 \b 37\b0 , 118-124. \par \par Gasser D. L. and Silvers W. K. (1971) Genetic basis of male skin rejection in mice. \i Transplant.\i0 \b 12\b0 , 412-414. \par \par Gates R. J., Hunt M. I., Smith R., and Lazarus N. R. (1972) Return to normal of blood-glucose, plasma-insulin, and weight gain in New Zea1and obese mice after implantation of islets of Langerhans. \i The Lancet\i0 \b ii\b0 , 567-570. \par \par Gebran S. J., Yamamoto Y., McHugh S., Newton C., Klein T. W., and Friedman H. (1994) Differences and similarities in permissive A/J versus non-permissive BALB/c murine macrophages infected with Legionella pneumophila: The role of iron. \i FEMS Immunology and Medical Microbiology\i0 \b 9\b0 , 7-14. \par \par Gehrung K (1956) Zur Zucht und Haltung der weissen Maus. I. Beibachtung zur Fortpflanzungsphysiologie. \i Zbl. Vet. Med.\i0 \b 3\b0 , 742-766. \par \par Gershon R. K. and Kondo K. (1976) Deficient production of a thymus- dependent high affinity antibody subset in mice (CBA/N) with an X-linked B lymphocyte defect. \i J. Immunol.\i0 \b 117\b0 , 701-702. \par \par Ghaffar A. and James K. (1973) The effect of antilymphocyte antibody on the humoral immune response in different strains of mice. \i Immunol.\i0 \b 24\b0 , 455-465. \par \par Gilbert D. J., Neumann P. E., Taylor B. A., Jenkins N. A., and Copeland N. G. (1993) Susceptibility of AKXD recombinant inbred mouse strains to lymphomas. \i Journal of Virology\i0 \b 67\b0 , 2083-2090. \par \par Gilmore G. L. (1997) Recovery from retrovirus-induced immune suppression in BDP/J mice: Dominance of the 'regressor' phenotype. \i Immunol.\i0 \b 90\b0 , 7-13. \par \par Glant T. T., Mikecz K., Thonar E. J.-M. A., and Kuettner K. E. (1993) Immune responses to cartilage proteoglycans in inflammatory animal models and human disease, in \i Joint Cartilage Degradation\i0 (Woessner J. Jr. and Howell D. S., eds), pp. 435-473. Marcel Dekker, Inc, New York, Basel, Hong Kong. \par \par Gocze P. M., Beamer W. G., De Jong F. H., and Freeman D. A. (1997) Hormone synthesis and responsiveness of spontaneous granulosa cell tumors in (SWR x SWXJ-9) F1 mice. \i Gynecologic Oncology\i0 \b 65\b0 , 143-148. \par \par Goldfeder A. (1972) Urethan and X-ray effects on mice of a tumor-resistant strain, X/Gf. \i Cancer Res.\i0 \b 32\b0 , 2771-2777. \par \par Goldfeder A., Kauffman S. L., and Ghosh A. K. (1966) Carcinogenesis in naturally tumour-resistant mice. X-irradiation versus urethan as a carcinogenic agent. \i Brit. J. Cancer\i0 \b 20\b0 , 361-374. \par \par Goldstein B. D., Lai L. Y., Ross S. R., and Cuzzi-Spada R. (1973) Susceptibility of inbred mouse strains to ozone. \i Arch. Environ. Health\i0 \b 27\b0 , 412-413. \par \par Gonnerman W. A., ElliottBryant R., Carreras I., Sipe J. D., and Cathcart E. S. (1995a) Linkage of protection against amyloid fibril formation in the mouse to a single, autosomal dominant gene. \i Journal Of Experimental Medicine\i0 \b 181\b0 , 2249-2252. \par \par Gonnerman W. A., Elliott-Bryant R., Carreras I., Sipe J. D., and Cathcart E. S. (1995b) Linkage of protection against amyolid fibril formation in the mouse to a single, autosomal dominant gene. \i J. Exp. Med.\i0 \b 181\b0 , 2249-2252. \par \par Gonnerman W. A., Kandel R., and Cathcart E. S. (1996) Amyloid enhancing factor is produced by rats and amyloid-resistant CE/J mice. \i Lab. Invest.\i0 \b 74\b0 , 259-264. \par \par Gonzalez C. R., Mejia M. V., Paniagua J., OrttzNavarrete V., Ramirez G., and Isibasi A. (1995) Immune response to porins isolated from \i Salmonella typhi\i0 in different mouse strains. \i Archives of Medical Research\i0 \b 26\b0 , S99-S103. \par \par Goodall C. M., Bielschowsky M., and Forster D. R. (1972) Incidence and metastatic pattern of lymphoreticular neoplasms in untreated NZO/Bl mice. \i Lab. Anim.\i0 \b 6\b0 , 85-94. \par \par Goodall C. M., Bielschowsky M., Forster D. R., and D'Ath E. F. (1973) Oncological and survival reference data for NZO/Bl inbred mice. \i Lab. Anim.\i0 \b 7\b0 , 65-71. \par \par Goodrick C. L. (1975) Lifespan and the inheritance of longevity of inbred mice. \i J. Gerontol.\i0 \b 30\b0 , 257-263. \par \par Gorer P. A. and Mikulska Z. B. (1959) Some further data on the H-2 system of antigens. \i Proc. R. Soc. Lond. (Biol.)\i0 \b 151\b0 , 57-69. \par \par Goto N., Yamaoka A., Sudo T., Mannen H., Fukuta K., and Nishimura M. (1993) Morphometric profiles of the mandible of SMXA recombinant inbred strains of mice and strain identification on the basis of mandible measurements. \i Exp. Animals (Japan)\i0 \b 42\b0 , 41-50. \par \par Gout O. and Dubois-Dalcq M. (1993) Directed migration of transplanted glial cells toward a spinal cord demyelinating lesion. \i International Journal of Developmental Neuroscience\i0 \b 11\b0 , 613-623. \par \par Granholm N. A. and Cavallo T. (1995) Enhancement of renal disease in BXSB lupus prone mice after prior exposure to bacterial lipopolysaccharide. \i Lupus\i0 \b 4\b0 , 339-347. \par \par Grantham P. H., Mohan L. C., and Weisburger E. K. (1976) Metabolism of N-2-fluorenylacetamide in X/Gf mice: lack of correlation between biochemical interaction and carcinogenicity. \i J. Natl. Cancer Inst.\i0 \b 56\b0 , 649-651. \par \par Green E. L. (1954) The genetics of a new hair deficiency, furless, in the house mouse. \i J. Hered.\i0 \b 45\b0 , 115-118. \par \par Green E. L. (1967) Shambling, a neurological mutant of the mouse. \i J. Hered.\i0 \b 58\b0 , 65-68. \par \par Green M. C. (1989) Catalog of mutant genes and polymorphic loci, in \i Genetic variants and strains of the laboratory mouse, 2nd ed.\i0 (Lyon M. F. and Searle A. G., eds), pp. 12-403. Oxford University Press, Oxford, New York, Tokyo. \par \par Green M. C. and Kaufer K. A. (1965) A test for histocompatibility between sublines of the CBA strain of mice. \i Transplant.\i0 \b 3\b0 , 767-768. \par \par Green M. C., Azar C. A., and Maren T. H. (1973) Strain differences in susceptibility to the teratogenic effect of acetazolamide in mice. \i Teratology\i0 \b 8\b0 , 143-145. \par \par Green R. C. and Seyfried T. N. (1991) Kindling susceptibility and genetic seizure predisposition in inbred mice. \i Epilepsia\i0 \b 32\b0 , 22-26. \par \par Griem P., Scholz E., Turfeld M., Zander D., Wiesner U., Dunemann L., and Gleichmann E. (1997) Strain differences in tissue concentrations of mercury in inbred mice treated with mercuric chloride. \i Toxicol. Appl. Pharmacol.\i0 \b 144\b0 , 163-170. \par \par Gropp A., Tettenborn U., and vonLehmann E. (1970) Chromosome variations of the Robertson type in the tobacco mouse, M poschiavinus, and its hybrids with the laboratory mouse. \i Cytogenetics\i0 \b 9\b0 , 9. \par \par Groschel D. and Koprowski H. (1965) Development of a virus-resistant inbred mouse strain for the study of innate resistance to arbo B virus. \i Arch. Ges. Virusforsch.\i0 \b 17\b0 , 379-391. \par \par Gross S. and Hutton J. (1971) Induction of hepatic -aminolaevulinic acid synthetase activity in strains of inbred mice. \i J. Biol. Chem.\i0 \b 246\b0 , 606-614. \par \par Gross S. R., Longshore M. A., and Pangburn S. (1975) The phosphorylase kinase deficiency (Phk) locus in the mouse: evidence that the mutant allele codes for an enzyme with an abnormal structure. \i Biochem. Genet.\i0 \b 13\b0 , 567-584. \par \par Guhad F. A., Jensen H. E., Aalbaek B., Rycroft A., and Hau J. (1995) A murine model for the study of mycotic mastitis. \i J. Comp. Pathol.\i0 \b 113\b0 , 315-325. \par \par Guida J. D., Fejer G., Pirofski L. A., and Brosnan C. F. (1995) Mouse adenovirus type 1 causes a fatal hemorrhagic encephalomyelitis in adult C57BL/6 but not BALB/c mice. \i Journal of Virology\i0 \b 69\b0 , 7674-7681. \par \par Gunn T. M., Juriloff D. M., and Harris M. J. (1992) Further genetic studies of the cause of exencephaly in SELH mice. \i Teratology\i0 \b 45\b0 , 679-686. \par \par Gunn T. M., Juriloff D. M., and Harris M. J. (1995) Genetically-determined absence of an initiation site of cranial neural-tube closure is causally related to exencephaly in SELH/Bc mouse embryos. \i Teratology\i0 \b 52\b0 , 101-108. \par \par Gunn T. M., Juriloff D. M., and Harris M. J. (1996) Exencephaly and cleft cerebellum in SELH/Bc mouse embryos are alternative developmental consequences of the same underlying genetic defect. \i Teratology\i0 \b 54\b0 , 230-236. \par \par Gupta R., Ganguly N. K., Ahuja V., Joshi K., and Sharma S. (1995) An ascending non-obstructive model for chronic pyelonephritis in BALC/c mice. \i J. Med. Microbiol.\i0 \b 43\b0 , 33-36. \par \par Hackman R. M. and Hurley L. S. (1983) Interaction of dietary zinc, genetic strain, and acetazolamide in teratogenesis in mice. \i Teratology\i0 \b 28\b0 , 355-368. \par \par Hagasaka I., Nakatsuka T., Fujii T., Naruse I., and Oda S.-I. (1980) Polydactyly Nagoya, Pdn: A new mutant gene in the mouse. \i Exp. Animals (Japan)\i0 \b 29\b0 , 391-395. \par \par Halevy S. and Altura B. M. (1974) Genetic factors influencing resistance to trauma. \i Circulatory Shock\i0 \b 1\b0 , 287-293. \par \par Hall J. L., Harris M. J., and Juriloff D. M. (1997) Effect of multifactorial genetic liability to exencephaly on the teratogenic effect of valproic acid in mice. \i Teratology\i0 \b 55\b0 , 306-313. \par \par Hall W. H. and Simpson L. 0 (1975) The origins of some hitherto undescribed inbred mouse strains. \i Lab. Anim.\i0 \b 9\b0 , 139-142. \par \par Haller O., Frese M., Rost D., Nuttall P. A., and Kochs G. (1995) Tick-borne Thogoto virus infection in mice is inhibited by the orthomyxovirus resistance gene product Mx1. \i Journal of Virology\i0 \b 69\b0 , 2596-2601. \par \par Halpern M. D. and Yocum D. E. (1991) The paradoxical effects of diethyldithiocarbamate: comparisons between New Zealand black/white F1 hybrid and Balb/c mice. \i Clin. Immunol. Immunopathol.\i0 \b 58\b0 , 69-79. \par \par Hampl A. and Eppig J. J. (1995) Analysis of the mechanism(s) of metaphase I arrest in maturing mouse oocytes. \i Development\i0 \b 121\b0 , 925-933. \par \par Hampl R., Ivanyi P., and Starka L. (1971) Testosterone and testosterone binding in murine plasma. \i Steroidologia\i0 \b 2\b0 , 113-120. \par \par Hancock R. L. and Dickie M. M. (1969) Biochemical, pathological and genetic aspects of spontaneous mouse hepatoma. \i J. Natl. Cancer Inst.\i0 \b 43\b0 , 407-415. \par \par Hanford W. C., Nep R. L., and Arfin S. M. (1974) Genetic variation in histidine ammonia-lyase activity in the mouse. \i Biochem. Biophys. Res. Comm.\i0 \b 61\b0 , 1434-1437. \par \par Hansen C. T., Judge F. J., and Whitney R. A. (1973) \i Catalog of NIH rodents\i0 . National Institutes of Health. DHEW publication (NIH) 74-606, Bethesda. \par \par Haqqi T. M., Banerjee S., Anderson G. D., and David C. S. (1989) RIII S/J (H-2r). An inbred mouse strain with a massive deletion of T cell receptor V beta genes. \i J. Exp. Med.\i0 \b 169\b0 , 1903-1909. \par \par Haqqi T. M., Qu X. M., and Banerjee S. (1995a) Limited heterogeneity in T-cell receptor Vbeta chain gene expression in arthritic joints of BUB/BnJ (H-2(q)) mice - A T-cell receptor Vbetaa strain. \i Annals of the New York Academy of Sciences\i0 \b 756\b0 , 221-224. \par \par Haqqi T. M., Qu X. M., Sy M. S., and Banerjee S. (1995b) Restricted expression of T cell receptor Vbeta and lymphokine genes in arthritic joints of a TCR Vbeta\up8 a\up0 (H-2\up8 q\up0 ) mouse strain-BUB/BnJ-with collagen-induced arthritis. \i Autoimmunity\i0 \b 20\b0 , 163-170. \par \par Harada M., Nagata M., Takeuchi M., Ohara T., Makino S., and Watanabe A. (1991) Age-dependent difference in susceptibility to IgE antibody- and IgG1 antibody-mediated passive anaphylactic shock in the mouse. \i Immunological Investigations\i0 \b 20\b0 , 515-523. \par \par Haran-Ghera N., Peled A., Brightman B. K., and Fan H. (1993) Lymphomagenesis in AKR.Fv-1b congenic mice. \i Cancer Res.\i0 \b 53\b0 , 3433-3438. \par \par Haran-Ghera N., Peled A., Wu L., Shortman K., Brightman B., and Fan H. (1995) The effects of passive antiviral immunotherapy in AKR mice: I. The susceptibility of AKR mice to spontaneous and induced T cell lymphomagenesis. \i Leukemia\i0 \b 9\b0 , 1199-1206. \par \par Harder D. B., Gannon K. S., and Whitney G. (1996) SW. B6-Soab nontaster congenic strains completed and a sucrose octaacetate congenic quartet tested with other bitters. \i Chemical Senses\i0 \b 21\b0 , 507-517. \par \par Hare W. V. and Stewart H. L. (1956) Chronic gastritis of the glandular stomach, adenomatous polyps of the duodenum, and calcareous pericarditis in strain DBA mice. \i J. Natl. Cancer Inst.\i0 \b 16\b0 , 889-911. \par \par Harris M. J., Juriloff D. M., Gunn T. M., and Miller J. E. (1994) Development of the cerebellar defect in ataxic SELH/Bc mice. \i Teratology\i0 \b 50\b0 , 63-73. \par \par Harvey M., McArthur M. J., Montgomery C. A., Bradley A., and Donehower L. A. (1993) Genetic backgound alters the spectrum of tumors that develop in p53-deficient mice. \i FASEB\i0 \b 7\b0 , 938-943. \par \par Haston C. K., Amos C. I., King T. M., and Travis E. L. (1996) Inheritance of susceptibility to bleomycin-induced pulmonary fibrosis in the mouse. \i Cancer Res.\i0 \b 56\b0 , 2596-2601. \par \par Hauschka T. S. (1952) Mutilation patterns and hereditary (?) cannibalism. \i J. Hered.\i0 \b 43\b0 , 117-123. \par \par Hauschka T. S. and Mirand E. A. (1973) \i The `Breeder: HA (ICR)' Swiss mouse, a multipurpose stock selected for fecundity\i0 . Liss, In Perspectives in Cancer Research and Treatment (ed. Murphy, G.P.), Alan R. \par \par Hayashi m, Sofuni T., and Ishidate M. J. (1982) High sensitivity in micronucleus induction of a mouse strain (MS). \i Mutation Res.\i0 \b 105\b0 , 253-256. \par \par Hayashi Y., Haneji N., Hamano H., Yanagi K., Takahashi M., and Ishimaru N. (1996) Effector mechanism of experimental autoimmune sialadenitis in the mouse model for primary Sjogren's syndrome. \i Cell. Immunol.\i0 \b 171\b0 , 217-225. \par \par Hecht S. S. (1995) Chemoprevention by isothiocyanates. \i J. Cell. Biochem.\i0 \b 58\b0 , 195-209. \par \par Hegmann J. P. (1972) Physiological function and behavioural genetics. I. Genetic variance for peripheral nerve conduction velocity in mice. \i Behav. Genet.\i0 \b 2\b0 , 55-67. \par \par Heiniger H. J., Chen H. W., Meier H., Taylor B. A., and Commerford L. S. (1972) Studies on the genetic control of cell proliferation. 1. Clearance of DNA-bound radioactivity in 19 inbred strains and hybrid mice. \i Life Sci.\i0 \b 11\b0 , 87-98. \par \par Heiniger H. J., Meier H., Kaliss N., Cherry M., Chen H. W., and Stoner R. D. (1974) Hereditary immunodeficiency and leukemogenesis in HRS/J mice. \i Cancer Res.\i0 \b 34\b0 , 201-211. \par \par Heiniger H. J., Taylor B. A., Hards E. J., and Meier H. (1975) Heritability of the phytohaemagglutinin responsiveness of lymphocytes and its relationship to leukemogenesis. \i Cancer Res.\i0 \b 35\b0 , 825-831. \par \par Hellman A. and Fowler A. K. (1972) Studies of the blastogenic response of murine lymphocyte. III. Specific viral transformation. \i Proc. Soc. Exp. Biol. Med.\i0 \b 141\b0 , 106-109. \par \par Henderson N. D. (1970) Genetic influences on the behaviour of mice can be obscured by laboratory rearing. \i J. Comp. Physiol. Psychol.\i0 \b 72\b0 , 505-511. \par \par Henery C. C. and Kaufman M. H. (1993) Cellular and nuclear volume of primitive red blood cells in digynic and diandric triploid and control diploid mouse embryos. \i European Journal of Morphology\i0 \b 31\b0 , 237-249. \par \par Hennings H., Glick A. B., Lowry D. T., Krsmanovic L. S., Sly L. M., and Yuspa S. H. (1993) FVB/N mice: An inbred strain sensitive to the chemical induction of squamous cell carcinomas in the skin. \i Carcinogenesis\i0 \b 14\b0 , 2353-2358. \par \par Henry K. R. and McGinn M. D. (1992) The mouse as a model for human audition. A review of the literature. \i Audiology\i0 \b 31\b0 , 181-189. \par \par Hentati B., PayelleBrogard B., Jouanne C., Avrameas S., and Ternynck T. (1994) Natural autoantibodies are involved in the haemolytic anaemia of NZB mice. \i Journal of Autoimmunity\i0 \b 7\b0 , 425-439. \par \par Heppner G. and Weiss D. W. (1965) High susceptibility of strain A mice to endotoxin and endotoxin-red blood cell mixtures. \i J. Bacteriol.\i0 \b 90\b0 , 696-703. \par \par Herr W. and Gilbert W. (1982) Germ-line MuLV reintegrations in AKR/J mice. \i Nature\i0 \b 296\b0 , 865-868. \par \par Herrod H. G. and Warner N. L. (1972) Defects in the immune response of NZC mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 140\b0 , 1254-1258. \par \par Heston W. E. (1963) Genetics of neoplasia, in \i Methodology in mammalian genetics\i0 (Burdette W. J., ed), pp. 247-268. Holden-Day, San Francisco. \par \par Heston W. E. (1968) Genetic aspects of experimental animals in cancer research. \i Japanese Cancer Assoc. Gann Monograph\i0 \b 5\b0 , 3-15. \par \par Heston W. E. and Vlahakis G. (1971) Mammary tumours, plaques and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumour virus. \i Int. J. Cancer\i0 \b 7\b0 , 141-148. \par \par Heston W. E., Vlahakis G., and Tsubura Y. (1964) Strain DD, a new high mammary tumor strain, and comparison of DD with strain C3H. \i J. Natl. Cancer Inst.\i0 \b 32\b0 , 237-251. \par \par Hewicker M., Kromschroder E., and Trautwein G. (1990) Detection of circulating immune complexes in MRL mice with different forms of glomerulonephritis. \i Z. Versuchstierk.\i0 \b 33\b0 , 149-156. \par \par Hiai H. (1996) Genetic predisposition to lymphomas in mice. \i Pathology International\i0 \b 46\b0 , 707-718. \par \par Hiai H., Kaneshima H., Nakamura H., Oguro Y. B., Moriwaki K., and Nishizuka Y. (1982) Unusually early and high rate of spontaneous occurrence of nonthymic leukemias in SL/Kh mice, a subline of SL strain. \i Gann\i0 \b 73\b0 , 704-712. \par \par Hiai H., Buma Y. O., Ikeda H., Moriwaki K., and Nishizuka Y. (1987) Epigenetic control of endogenous ecotropic virus expression in SL/No mice. \i J. Natl. Cancer Inst.\i0 \b 79\b0 , 781-787. \par \par Hiai H., Yokota Y., and Buma Y. (1992) Epigenetic control of endogenous MuLV expression and lymphomagenesis by maternal resistance factor, in \i Molecular approaches to study and treatment of human diseases\i0 (Yoshida T. O. and Wilson J. M., eds), pp. 171-175. Elsevier Science Publishers B.V., Amsterdam. \par \par Higuchi K. (1997) Genetic characterization of senescence-accelerated mouse (SAM). \i Exp. Gerontol.\i0 \b 32\b0 , 129-138. \par \par Higuchi K., Matsumura A., Honma A., Takeshita S., Hashimoto K., Hosokawa M., Yasuhira K., and Takeda T. (1983) Systemic senile amyloid in senescence-accelerated mice: A unique fibril protein demonstrated in tissue from various organs by the unlabelled immunoperoxidase method. \i Lab. Invest.\i0 \b 48\b0 , 231-240. \par \par Higuchi K., Kitagawa K., Naiki H., Hanada K., Hosokawa M., and Takeda T. (1991) Polymorphism of apolipoprotein A-II (apoA-II) among inbred strains of mice. Relationship between the molecular type of apoA-II and mouse senile amyloidosis. \i Biochem. J.\i0 \b 279\b0 , 427-433. \par \par Higushi K., Yonezu T., Kogishi K., Matsumura A., Takeshita S., Higuchi K., Kohno A., Matsushita M., Hosokawa M., and Takeda T. (1986) Purification and characterization of a senile amyloid-related antigenic substance (apoSAMSAM) from mouse sera. \i J. Biol. Chem.\i0 \b 261\b0 , 12834-12840. \par \par Hilgers J. and Arends J. W. A. (1985) A series of recombinant inbred strains between BALB/cHeA and STS/A strains. \i Curr. Top. Microbiol. Immunol.\i0 \b 122\b0 , 31-37. \par \par Hilgers J. and Galesloot J. (1973) Genetic control of MuLV-gs expression in crosses between high and low leukemia incidence strains. \i Int. J. Cancer\i0 \b 11\b0 , 780-793. \par \par Hilgers J., van Nie R., Ivanyi D., Hilkens J., Michalides R., de Moes J., Poort-Keesom R., Kroezen V., von Deimling O., Kominami R., and Holmes R. (1985) Genetic differences in BALB/c sublines. \i Curr. Top. Microbiol. Immunol.\i0 \b 122\b0 , 19-30. \par \par Hilgers J., von Deimling O., van Zutphen L. F. M., ten Berg R., Anand R., and Festing M. F. W. (1988) Esterase alleles of inbred mouse strains maintained in the Netherlands. \i Genet. Res.\i0 \b 51\b0 , 29-40. \par \par Hill G. B., Osterhout S., and O'Fallon W. M. (1968) Variation in response to hyperbaric oxygen among inbred strains of mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 129\b0 , 687-689. \par \par Hill R. N., Clemens T. L., Liu D. K., and Vesell E. S. (1975) Genetic control of chloroform toxicity in mice. \i Science\i0 \b 190\b0 , 159-161. \par \par Hillebrandt S., Streffer C., and Muller W. U. (1996) Genetic analysis of the cause of gastroschisis in the HLG mouse strain. \i Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis\i0 \b 372\b0 , 43-51. \par \par Hilton J., Dearman R. J., Boylett M. S., Fielding I., Basketter D. A., and Kimber I. (1996) The mouse IgE test for the identification of potential chemical respiratory allergens: Considerations of stability and controls. \i J. Appl. Toxicol.\i0 \b 16\b0 , 165-170. \par \par Hirasawa K., Ogiso Y., Takeda M., Lee M. J., Itagaki S., and Doi K. (1995) Protective effects of macrophage-derived interferon against encephalomyocarditis virus-induced diabetes mellitus in mice. \i Lab. Animal Sci.\i0 \b 45\b0 , 652-656. \par \par Hoag W. G. (1963) Spontaneous cancer in mice. \i Ann. NY Acad. Sci.\i0 \b 108\b0 , 805-831. \par \par Hoffman H. A. and Rechcigl M. Jr. (1971) Erythrocyte catalase in inbred mice. \i Enzyme\i0 \b 12\b0 , 219-225. \par \par Holan V., Lipoldova M., and Demant P. (1996) Identical genetic-control of MLC reactivity to different MHC incompatibilities, independent of production of and response to IL-2. \i Immunogenet.\i0 \b 44\b0 , 27-35. \par \par Hopkins W. J., GendronFitzpatrick A., McCarthy D. O., Haine J. E., and Uehling D. T. (1996) Lipopolysaccharide-responder and nonresponder C3H mouse strains are equally susceptible to an induced Escherichia coli urinary tract infection. \i Infect. Immun.\i0 \b 64\b0 , 1369-1372. \par \par Hosaka N., Nose M., Kyogoku M., Nagata N., Miyashima S., Good R. A., and Ikehara S. (1996) Thymus transplantation, a critical factor for correction of autoimmune disease in aging MRL/+ mice. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 93\b0 , 8558-8562. \par \par Hosokawa M., Kasai R., Higuchi K., Takeshita S., Shimizu K., Hamamoto H., Honma A., Irino M., Toda K., Matsumura A., Matsushita T., and Takeda T. (1984) Grading score system: A method for evaluation of the degree of senescence in senescence accelerated mouse (SAM). \i Mech. Ageing Dev.\i0 \b 26\b0 , 91-102. \par \par Howard J. G., Hale C., and Chan-Liew W. L. (1980) Immunological regulation of experimental cutaneous leishmaniasis 1. Immunogenetic aspects of susceptibility to Leishmania tropica in mice. \i Parasite Immunol.\i0 \b 2\b0 , 303-314. \par \par Huang F. P., Feng G. J., Lindop G., Stott D. I., and Liew F. Y. (1996) The role of interleukin 12 and nitric oxide in the development of spontaneous autoimmune disease in MRL/MP-\i lpr/lpr\i0 mice. \i Journal Of Experimental Medicine\i0 \b 183\b0 , 1447-1459. \par \par Huang L. H. and Sery T. W. (1971) Corneal degeneration in a congenitally diabetic inbred strain of mouse. \i Brit. J. Ophthalmol.\i0 \b 55\b0 , 266-271. \par \par Hudson S. J., Dix R. D., and Streilein J. W. (1991) Induction of encephalitis in SJL mice by intranasal infection with herpes simplex virus type 1: a possible model of herpes simplex encephalitis in humans. \i J. Infect. Dis.\i0 \b 163\b0 , 720-727. \par \par Huff S. D. and Chaykin S. (1967) Genetic and androgenic control of N- methylnicotinamide oxidase activity in mice. \i J. Biol. Chem.\i0 \b 242\b0 , 1265-1270. \par \par Hultcrantz M. and Li H. S. (1993) Inner ear morphology in CBA/Ca and C57BL/6J mice in relationship to noise, age and phenotype. \i European Archives of Oto-Rhino-Laryngology\i0 \b 250\b0 , 257-264. \par \par Hummel K. P. and Chapman D. B. (1959) Visceral inversion and associated anomalies in the mouse. \i J. Hered.\i0 \b 50\b0 , 9-13. \par \par Hummel K. P., Richardson F. L., and Fekete E. (1966) Anatomy, in \i Biology of the Laboratory Mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 247-307. McGraw-Hill, New York. \par \par Hunt C. E., Lindsey J. R., MaxField L. M., and Fox O. J. (1972) Obesity in a new strain of mouse. \i Fed. Proc.\i0 \b 31\b0 , 244. \par \par Hunt C. E., Lindsey J. R., and Walkley S. U. (1976) Animal models of diabetes and obesity, including the PBB/Ld mouse. \i Fed. Proc.\i0 \b 35\b0 , 1206-1217. \par \par Hunter N., Dann J. C., Bennett A. D., Somerville R. A., McConnell I., and Hope J. (1992) Are Sinc and the PrP gene congruent? Evidence from PrP gene analysis in Sinc congenic mice. \i J. Gen. Virol.\i0 \b 73\b0 , 2751-2755. \par \par Huseini S., Fried W., Knospe W. H., and Trobaugh F. E. Jr. (1976) Dynamics of leukaemia and normal stem cells in leukaemic RFM mice. \i Cancer Res.\i0 \b 36\b0 , 1784-1789. \par \par Hutton J. J. (1971) Genetic regulation of glucose-6-phosphate dehydrogenase activity in the inbred mouse. \i Biochem. Genet.\i0 \b 5\b0 , 315-331. \par \par Hutton J. J. and Gross S. R. (1970) Chemical induction of hepatic porphyria in inbred strains of mice. \i Arch. Biochem. Biophys.\i0 \b 141\b0 , 284-292. \par \par I'Anson V. A. and Gasser D. L. (1973) Relationship between graft-vs-host reactivity and possession of the high leukaemia genotype hr/hr. \i J. Immunol.\i0 \b 111\b0 , 1604-1609. \par \par Ichihara M., Hara T., Takagi M., Cho L. C., Gorman D. M., and Miyajima A. (1995) Impaired interleukin-3 (IL-3) response of the A/J mouse is caused by a branch point deletion in the IL-3 receptor alpha subunit gene. \i EMBO Journal\i0 \b 14\b0 , 939-950. \par \par Iida F., Matsushima Y., Hiai H., Uga S., and Honda Y. (1997) Rupture of lens cateract: a novel hereditary recessive cateract model in the mouse. \i Exp. Eye Res.\i0 \b 64\b0 , 107-113. \par \par Iizawa Y., Wagner R. D., and Czuprynski C. J. (1993) Analysis of cytokine mRNA expression in Listeria-resistant C57BL/6 and Listeria-susceptible A/J mice during Listeria monocytogenes infection. \i Infect. Immun.\i0 \b 61\b0 , 3739-3744. \par \par Ikeda H. (1994) KK mouse. \i Diabetes Research and Clinical Practice\i0 \b 24\b0 , S313-S316. \par \par Imai S., Tsubura Y., Hilgers J., and Michalides R. (1983) A new locus (Mtv-4) for endogenous mammary tumor virus expression and early mammary tumor development in the SHN mouse strain. \i J. Natl. Cancer Inst.\i0 \b 71\b0 , 517-521. \par \par Imai S., Tsubura Y., and Hilgers J. (1984) Urethan-induced mammary tumorigenesis in a murine mammary tumor virus (MuMTV)-positive mouse strain: evidence for a keratinized nodule as an MmMTV-negative precursor lesion for squamous cell tumors. \i J. Natl. Cancer Inst.\i0 \b 73\b0 , 935-941. \par \par Imanishi T. and M\'8a kel\'8a O. (1975) Inheritance of antibody specificity. II. Anti- (4-hydroxy-5-bromo-3-nitrophenyl) acetyl in the mouse. \i J. Exp. Med.\i0 \b 141\b0 , 840-854. \par \par Irokanulo E. A. O. and Akueshi C. O. (1995) Virulence of \i Cryptococcus neoformans\i0 serotypes A, B, C and D for four mouse strains. \i J. Med. Microbiol.\i0 \b 43\b0 , 289-293. \par \par Ishigaki Y., Hayakawa J. I., Hashimoto N., Nikaido H., and Nikaido O. (1996) New immunodeficient mouse strains bred by introducing beige and xid mutations into the KSN nude strain. \i Lab. Animal Sci.\i0 \b 46\b0 , 418-424. \par \par Ishii A. I. and Sano M. (1989) Strain-dependent differences in susceptibility of mice to experimental Angiostrongylus costaricennsis infection. \i J. Helminthology\i0 \b 63\b0 , 302-306. \par \par Iwakawa M., Ando K., Ohkawa H., Koike S., and Chen Y. (1994) A murine model for bone marrow metastasis established by an i.v. injection of C-1300 neuroblastoma in A/J mice. \i Clinical and Experimental Metastasis\i0 \b 12\b0 , 231-237. \par \par Jabs D. A., Burns W. H., and Prendergast R. A. (1996) Paradoxic effect of anti-CD4 therapy on lacrimal gland disease in MRL/Mp-\i lpr/lpr\i0 mice. \i Investigative Ophthalmology & Visual Science\i0 \b 37\b0 , 246-250. \par \par James K. and Milne I. (1972) The effect of anti-lymphocytic antibody on the humoral immune response in different strains of mice. I. The response to bovine serum albumin. \i Immunol.\i0 \b 23\b0 , 897-909. \par \par Jenkins N. A., Copeland N. G., Taylor B. A., and Lee B. K. (1982) Organization, distribution, and stability of endogenous ecotropic murine leukemia virus DNA sequences in chromosomes of Mus musculus. \i J. Virol.\i0 \b 43\b0 , 26-36. \par \par Jenkinson A. M. and East J. (1980) The cellular basis of autoimmunity: precocious immunological maturity in NZB mice. \i J. Clin. Lab. Immunol.\i0 \b 3\b0 , 145-152. \par \par Jenson A. B., Groff D. E., McConahey P. J., and Dixon F. J. (1976) Transmission of murine leukemia virus (Scripps) from parent to progeny mice as determined by P30 antigenemia. \i Cancer Res.\i0 \b 36\b0 , 1228-1232. \par \par Jiao S., Cole T. G., Kitchens R., Pfleger B., and Schonfeld G. (1990) Genetic heterogeneity of lipoproteins in inbred strains of mice: analysis by gel-permeation chromatography. \i Metabolism\i0 \b 39\b0 , 155-160. \par \par John S. W. M., Hagaman J. R., MacTaggart T. E., Peng L., and Smithes O. (1997) Intraocular pressure in inbred mouse strains. \i Investigative Ophthalmology & Visual Science\i0 \b 38\b0 , 249-253. \par \par Johnson A. P., Tuffrey M., and Taylor-Robinson D. (1989) Resistance of mice to genital infection with Neisseria gonorrhoeae. \i J. Med. Microbiol.\i0 \b 30\b0 , 33-36. \par \par Johnson P. R. and Hirsch J. (1972) Cellularity of adipose depots in six strains of genetically obese mice. \i J. Lipid Res.\i0 \b 13\b0 , 2-11. \par \par Johnston C. J., Piedboeuf B., Baggs R., Rubin P., and Finkelstein J. N. (1995) Differences in correlation of mRNA gene expression in mice sensitive and resistant to radiation-induced pulmonary fibrosis. \i Radiation Res.\i0 \b 142\b0 , 197-203. \par \par Jungmann P., Guenet J. L., Cazenave P. A., Coutinho A., and Huerre M. (1996) Murine acariasis: I. Pathological and clinical evidence suggesting cutaneous allergy and wasting syndrome in BALB/c mouse. \i Research in Immunology\i0 \b 147\b0 , 27-38. \par \par Jurand A. (1973) Teratogenic activity of methadone hydrochloride in mouse and chick embryos. \i J. Embryol. Exp. Morphol.\i0 \b 30\b0 , 449-458. \par \par Juriloff D. M. (1993) Current status of genetic-linkage studies of a major gene that causes CL(p) in mice - exclusion map. \i Journal of Craniofacial Genetics and Developmental Biology\i0 \b 13\b0 , 223-229. \par \par Juriloff D. M. (1995) Genetic analysis of the construction of the AEJ.A congenic strain indicates that nonsyndromic CL(P) in the mouse is caused by two loci with epistatic interaction. \i Journal of Craniofacial Genetics and Developmental Biology\i0 \b 15\b0 , 1-12. \par \par Juriloff D. M., MacDonald K. B., and Harris M. J. (1989) Genetic analysis of the cause of exencephaly in the SELH/Bc mouse stock. \i Teratology\i0 \b 40\b0 , 395-405. \par \par Juriloff D. M., Harris M. J., Harrod M. L., Gunn T. M., and Miller J. E. (1993) Ataxia and a cerebellar defect in the exencephaly-prone SELH/Bc mouse stock. \i Teratology\i0 \b 47\b0 , 333-340. \par \par Juriloff D. M., Porter S. D., and Harris M. J. (1994) 3 spontaneous mutations at the albino locus in SELH/Bc mice. \i Genome\i0 \b 37\b0 , 190-197. \par \par Kagiyama N., Takakura A., Koyoma K., Terada E., and Sakuria Y. (1991) Detection of mouse hepatitis virtus antibody by protein A-ELISA in 6 prevalent inbred strains or outbred stocks of mice. \i Lab. Anim.\i0 \b 25\b0 , 106-109. \par \par Kako M., Miura T., Usami M., Nishiyama Y., Ichimaru M., Moriyasu M., and Kato A. (1995) Effect of senegin-II on blood glucose in normal, and NIDDM mice. \i Biol. Pharmaceut. Bull.\i0 \b 18\b0 , 1159-1161. \par \par Kalcheva I. D., Matsuda Y., Plass C., and Chapman V. M. (1995) Isolation and characterization of a pseudoautosomal region-specific genetic-marker in C57BL/6 mice using genomic representational difference analysis. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 92\b0 , 12352-12356. \par \par Kaliss N. Transplanted tumors. Jax Notes 410, Jackson Laboratory, Bar Harbor, Maine. \par \par Kalter H. (1965) Interplay of intrinsic and extrinsic factors, in \i Teratology\i0 (Wilson J. G. and Warkany J., eds) University of Chicago Press, Chicago. \par \par Kalter H. (1968) Sporadic congenital malformations of newborn inbred mice. \i Teratology\i0 \b 1\b0 , 193-200. \par \par Kalter H. (1981a) Dose response studies with genetically homogeneous lines of mice as a teratology testing and risk assessment procedure. \i Teratology\i0 \b 24\b0 , 79-86. \par \par Kalter H. (1981b) Dose-response studies with genetically homogeneous lines of mice as a teratology testing and risk-assessment procedure. \i Teratology\i0 \b 24\b0 , 79-86. \par \par Kanes S. J., Hitzemann B. A., and Hitzemann R. J. (1993) On the relationship between D2 receptor density and neuroleptic-induced catalepsy among eight inbred strains of mice. \i J. Pharmacol. Exp. Therapeut.\i0 \b 267\b0 , 538-547. \par \par Kano K. and Mizuma Y. (1974) Comparison of the total blood volume in four inbred strains of mice with different hemoglobin types. \i Exp. Animals (Japan)\i0 \b 23\b0 , 123-127. \par \par Kanwar Y. S., Krakower C. A., Manaligod J. R., Justice P., and Wong P. W. K. (1975) Biochemical, morphological and hybrid studies in hyperprolinemic mice. \i Biomedicine\i0 \b 22\b0 , 209-216. \par \par Kapoor A. K., Nash A. A., Wildy P., Phelan J., Henney S., Rebello P., and Blaskovic D. (1992) Relative role of B and T lymphocytes in pathogenesis of a murine herpes virus. \i Ind. J. Exp. Biol.\i0 \b 30\b0 , 690-695. \par \par Katafuchi T., Hattori Y., Nagatomo I., Koizumi K., and Silverstein E. (1991) Involvement of angiotensin II in water intake of genetically polydipsic mice. \i Am. J. Physiol.\i0 \b 260\b0 , R1152-R1158. \par \par Kataoka Y., Haritani M., Mori M., Kishima M., Sugimoto C., Nakazawa M., and Yamamoto K. (1991) Experimental infections of mice and pigs with Streptococcus suis type 2. \i J. Vet. Med. Sci.\i0 \b 53\b0 , 1043-1049. \par \par Katiyar S. K., Agarwal R., and Mukhtar H. (1993) Protective effects of green tea polyphenols administered by oral intubation against chemical carcinogen-induced forestomach and pulmonary neoplasia in A/J mice. \i Cancer Lett.\i0 \b 73\b0 , 167-172. \par \par Kawase E., Suemori H., Takahashi N., Okazaki K., Hashimoto K., and Nakatsuji N. (1994) Strain difference in establishment of mouse embryonic stem (ES) cell lines. \i International Journal of Developmental Biology\i0 \b 38\b0 , 385-390. \par \par Kawashima I., Nakamura O., and Tai T. (1992) Antibody responses to ganglio-series gangliosides in different strains of inbred mice. \i Molecular Immunology\i0 \b 29\b0 , 625-632. \par \par Kay T. W. H., Campbell I. L., Oxbrow L., and Harrison L. C. (1991) Overexpression of class I major histocompatibility complex accompanies insulinitis in the non-obese diabetic mouse and is prevented by anti-interferon-gamma antibody. \i Diabetologia\i0 \b 34\b0 , 779-785. \par \par Kaye M. and Kusy P. (1995) Genetic lineage, bone mass, and physical activity in mice. \i Bone\i0 \b 17\b0 , 131-135. \par \par Keetch D. W., Humphrey P., and Ratliff T. L. (1994) Development of a mouse model for nonbacterial prostatitis. \i Journal of Urology\i0 \b 152\b0 , 247-250. \par \par Kehrer J. P. and DiGiovanni J. (1990) Comparison of lung injury induced in 4 strains of mice by butylated hydroxytoluene. \i Toxicol. Lett.\i0 \b 52\b0 , 55-61. \par \par Kennedy B. P., Payette P., Mudgett J., Vadas P., Pruzanski W., Kwan M., Tang C., Rancourt D. E., and Cromlish W. A. (1995) A natural disruption of the secretory group II phospholipase A2 gene in inbred mouse strains. \i J. Biol. Chem.\i0 \b 270\b0 , 22378-22385. \par \par Keramidas G. D. and Symeonidis A. (1973) Characteristic microscopic differences in the adenohypophysis of high and low mammary tumour strains of mice. \i Pathol. Eur.\i0 \b 8\b0 , 35-36. \par \par Khanuja B., Cheah Y. C., Hunt M., Nishina P. M., Wang D. Q. H., Chen H. W., Billheimer J. T., Carey M. C., and Paigen B. (1995) Lith1, a major gene affecting cholesterol gallstone formation among inbred strains of mice. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 92\b0 , 7729-7733. \par \par Kikutani H. and Makino S. (1992) The murine autoimmune diabetes model: NOD and related strains. \i Adv. Immunol.\i0 \b 52\b0 , 285-322. \par \par Kim D., Park D. H., Kang N. G., Namkoong Y., and Shin H. S. (1996) A new embryonic stem-cell line with germ-line competence in the FVB/N background. \i Molecules and Cells\i0 \b 6\b0 , 577-581. \par \par Kim J. I., Chung D. I., and Choi D. W. (1992) Egg production of Clonorchis sinensis in different strains of inbred mice. \i Korean Journal of Parasitology\i0 \b 30\b0 , 169-175. \par \par Kimura M., Takahasi H., Ohtake T., Sato T., Hishida A., Nishimura M., and Honda N. (1993) Interstrain differences in murine daunomycin-induced nephorsis. \i Nephron\i0 \b 63\b0 , 193-198. \par \par Kirk E. A., Moe G. L., Caldwell M. T., Lernmark J. A., Wilson D. L., and LeBoeuf R. C. (1995) Hyper- and hypo-responsiveness to dietary fat and cholesterol among inbred mice: Searching for level and variability genes. \i J. Lipid Res.\i0 \b 36\b0 , 1522-1532. \par \par Kishimoto Y. (1972) Breeding of coisogenic mice for studying natural resistance to infection. \i Exp. Animals (Japan)\i0 \b 21\b0 , 47-55. \par \par Kleeberger S. R., Levitt R. C., and Zhang L. Y. (1993) Susceptibility to ozone-induced inflammation. I. Genetic control of the response to subacute exposure. \i American Journal of Physiology - Lung Cellular and Molecular Physiology\i0 \b 264\b0 , L15-L20. \par \par Kluge R., Meyer J., and Rapp K. G. (1994) Genetic characterization of the mouse strains of the Institute for Animal Breeding of the Veterinary Faculty of the University of Munich, Germany. \i J. Exp. Anim. Sci.\i0 \b 36\b0 , 179-188. \par \par Kodama Y. and Bock F. G. (1970) Benz [] pyrene-metabolizing enzyme activity of livers of various strains of mice. \i Cancer Res.\i0 \b 30\b0 , 1846-1849. \par \par K\'9a lsch E., Diller E., Weber G., and Davies A. J. S. (1971) Genetics of the immune response. I. The immune response to the phage fd in high and low responding inbred strains of mice. \i Eur. J. Immunol.\i0 \b 1\b0 , 201-210. \par \par Koizumi T., Puccetti A., Migliorini P., Barrett K. J., and Schwartz R. S. (1991) Molecular heterogeneity of auto-anti-idiotypic antibodies in MLR-lpr/lpr mice. \i Eur. J. Immunol.\i0 \b 21\b0 , 2185-2193. \par \par Kojima a and Hata M. (1988) New mutant: sublingual gland differentiation arrest in the NFS/N subline. \i Mouse N.L.\i0 \b 80\b0 , 147. \par \par Konno S., Adachi M., Matsuura T., Sunouchi K., Hoshino H., Okazawa A., Kobayashi H., and Takahashi T. (1993) Bronchial reactivity to methacholine and serotonin in six inbred mouse strains. [Japanese]. \i Japanese Journal of Allergology\i0 \b 42\b0 , 42-47. \par \par Kosobud A. E., Cross S. J., and Crabbe J. C. (1992) Neural sensitivity to pentylenetetrazol convulsions in inbred and selectively bred mice. \i Brain Res.\i0 \b 592\b0 , 122-128. \par \par Kouri R. E., Salerno R. A., and Whitmire C. E. (1973) Relationships between arylhydrocarbon hydroxylase inducibility and sensitivity to chemically induced subcutaneous sarcomas in various strains of mice. \i J. Natl. Cancer Inst.\i0 \b 50\b0 , 363-368. \par \par Krischke W. V. and Graffi A. (1962) Weitere versuch zur abhangigkeit der Wirkung des virus der myeloischen leukamie der Maus von versuchiedenen biologischen Bedingangen der infizierten tiere. \i Arch. Geschwulstforsch.\i0 \b 20\b0 , 22-29. \par \par Krzanowska H., Wabik-Sliz B., and Rafinski J. (1991) Phenotype and fertilizing capacity of spermatozoa of chimaeric mice produced from two strains that differ in sperm quality. \i J. Reprod. Fertil.\i0 \b 91\b0 , 667-676. \par \par Kulikov A. V., Kozlachkova E. Y., Maslova G. B., and Popova N. K. (1993) Inheritance of predisposition to catalepsy in mice. \i Behav. Genet.\i0 \b 23\b0 , 379-384. \par \par Kunstyr I. and Leuenberger H. G. W. (1975) Gerontological data on C57BL/6 mice. I. Sex differences in survival curves. \i J. Gerontol.\i0 \b 30\b0 , 157-162. \par \par Kurihara Y., Naito T., Obayashi K., Hirasawa M., Kurihara Y., and Moriwaki K. (1991) Caries susceptibility in inbred mouse strains and inheritance patterns in F1 and backcross (N2) progeny from strains with high and low caries susceptibility. \i Caries Res.\i0 \b 25\b0 , 341-346. \par \par Kurosawa S., Ogura A., Koura M., Noguchi A., Noguchi Y., Yamamoto Y., and Takano K. (1991) A histological study on the skin and hairs of PC (poor coat) mice. \i Exp. Animals (Japan)\i0 \b 40\b0 , 259-261. \par \par Kutscher C. L. and Schmalbach N. L. (1975) Effects of water deprivation, NaCl injection, and seven aversive taste stimuli on drinking in two normal mouse strains and one with diabetes insipidus. \i Physiol. Behav.\i0 \b 15\b0 , 659-667. \par \par Kutscher C. L., Miller M., and Schmalbach N. L. (1975) Renal deficiency associated with diabetes insipidus in the SWR/J mouse. \i Physiol. Behav.\i0 \b 14\b0 , 815-818. \par \par Lammas D. A., Mitchell L. A., and Wakelin D. (1990) Genetic influences upon eosinophilia and resistance in mice infected with Mesocestoides corti. \i Parasitology\i0 \b 101\b0 , 291-299. \par \par Lamoreaux M. L. and Galbraith D. B. (1986) DK/Lm: A strain of laboratory mouse with an unusual expression of the lethal yellow (Ay) phenotype. \i Genet. Res.\i0 \b 48\b0 , 35-50. \par \par Lane P. W. and Murphy E. D. (1972) Susceptibility to spontaneous pneumonitis in an inbred strain of beige and satin mice. \i Genetics\i0 \b 72\b0 , 451-460. \par \par Laskay T., Diefenbach A., Rollinghoff M., and Solbach V. (1995) Early parasite containment is decisive for resistance to Leishmania major infection. \i Eur. J. Immunol.\i0 \b 25\b0 , 2220-2227. \par \par Law L. W. (1966a) Studies of thymic function with emphasis on the role of the thymus in oncogenesis. \i Cancer Res.\i0 \b 26\b0 , 551-574. \par \par Law L. W. (1966b) Transmission studies of a leukemogenic virus, MLV, in mice, in \i Conference on Murine Leukemia\i0 (Rich M. A. and Moloney J. B., eds) National Cancer Institute Monograph 22, . \par \par Le A. D., Ko J., Chow S., and Quan B. (1994) Alcohol consumption by C57BL/6, BALB/c, and DBA/2 mice in a limited access paradigm. \i Pharmacol. Biochem. Behav.\i0 \b 47\b0 , 375-378. \par \par Lee B. K. and Eicher E. M. (1990) Segregation patterns of endogenous mouse mammary tumor viruses in five recombinant inbred strain sets [published erratum appears in J Virol 1991 Mar;65(3):1666]. \i J. Virol.\i0 \b 64\b0 , 4568-4572. \par \par Lee G. H., Bugni J. M., Obata M., Nishimori H., Ogawa K., and Drinkwater N. R. (1997) Genetic dissection of susceptibility to murine ovarian teratomas that originate from parthenogenetic oocytes. \i Cancer Res.\i0 \b 57\b0 , 590-593. \par \par Lei H. Y., Lee S. H., and Leir S. H. (1996) Antigen-induced anaphylactic death in mice. \i International Archives of Allergy and Immunology\i0 \b 109\b0 , 407-412. \par \par Leijon K., Hammarstrom B., and Holmberg D. (1994) Non-obese diabetic (NOD) mice display enhanced immune responses and prolonged survival of lymphoid cells. \i International Immunology\i0 \b 6\b0 , 339-345. \par \par Leiter E.H. (1993) The NOD mouse: A model for analyzing the interplay between heredity and environment in development of autoimmune disease. \i ILAR News\i0 \b 35\b0 , 4-14. \par \par Leonard A. and Deknudt G. (1967) A new marker for chromosome studies in the mouse. \i Nature\i0 \b 214\b0 , 504-505. \par \par Leonard A., Deknudt G., and Linden G. (1971) Ovulation and prenatal losses in different strains of mice. \i Exp. Anim. (France)\i0 \b 4\b0 , 1-6. \par \par Le Prevost C., Virelizier J. L., and Dupuy J. M. (1975) Immunopathology of mouse hepatitis virus type 3 infection. III. Clinical and virologic observation of a persistent viral infection. \i J. Immunol.\i0 \b 115\b0 , 640-643. \par \par Les E. P. (1972) A disease related to cage population density: tail lesions of C3H/HeJ mice. \i Lab. Animal Sci.\i0 \b 22\b0 , 56-60. \par \par Leslie K. B., Jalbert S., Orban P., Welham M., Duronio V., and Schrader J. W. (1996) Genetic basis of hypo-responsiveness of A/J mice to interleukin-3. \i Blood\i0 \b 87\b0 , 3186-3194. \par \par Levine B. B. and Vaz N. M. (1970) Effect of combinations of inbred strain, antigen and antigen dose on immune responsiveness and reagin production in the mouse. \i Int. Arch. Allergy\i0 \b 39\b0 , 156-171. \par \par Levine S. and Sowinski R. (1973) Experimental allergic encephelomyelitis in inbred and outbred mice. \i J. Immunol.\i0 \b 110\b0 , 139-143. \par \par Levy R. P., McGuire W. L., Shaw R. K., and Bartsch G. E. (1965) Effect of species differences of mice on the bioassay of thyrotropin. \i Endocrinol.\i0 \b 76\b0 , 890-894. \par \par Lewis J. B., Cobb R. R., and Whitney JB I. I. I. (1993) Recombination and genetic polymorphism at the mouse alpha-globin locus. \i Genomics\i0 \b 18\b0 , 432-434. \par \par Lewis W. H. P. and Truslove G. M. (1969) Electrophoretic heterogeneity of mouse erythrocyte peptidase. \i Biochem. Genet.\i0 \b 3\b0 , 493-498. \par \par LezamaDavila C. M. (1997) Vaccination of different strains of mice against cutaneous leishmaniosis: Usefulness of membrane antigens encapsulated into liposomes by intraperitoneal and subcutaneous administration. \i Archives of Medical Research\i0 \b 28\b0 , 47-53. \par \par Li H. S. (1992) Genetic influences on susceptibility of the auditory system to aging and environmental factors. \i Scandinavian Audiology, Supplement\i0 \b 21\b0 , 1-39. \par \par Li H. S. and Borg E. (1993) Auditory degeneration after acoustic trauma in two genotypes of mice. \i Hearing Research\i0 \b 68\b0 , 19-27. \par \par Li H. S., Hultcrantz M., and Borg E. (1993) Influence of age on noise-induced permanent threshold shifts in CBS/Ca and C57BL/6J mice. \i Audiology\i0 \b 32\b0 , 195-204. \par \par Liebelt A. G., Liebelt R. A., and Dmochowski L. (1971) Cytoplasmic inclusion bodies in primary and transplanted hepatomas of mice of different strains. \i J. Natl. Cancer Inst.\i0 \b 47\b0 , 413-427. \par \par Liebelt R. A., Suzuki S., Liebelt A. G., and Lane M. (1970) Virus-like particles in chemically induced sarcomas in high- and low-leukemia strains of mice. \i Cancer Res.\i0 \b 30\b0 , 2438-2448. \par \par Lieberman J. and Kellog F. (1967) Hyaline-membrane formation and pulmonary plasminogen-activator activity in various strains of mice. \i Pediatrics\i0 \b 39\b0 , 75-81. \par \par Lijinsky W., Thomas B. J., and Kovatch R. M. (1991) Differences in skin carcinogenesis by methylnitrosourea between mice of several strains. \i Cancer Lett.\i0 \b 61\b0 , 1-5. \par \par Lilly F. and Pincus T. (1973) Genetic control of murine viral leukemogenesis. \i Adv. Cancer Res.\i0 \b 17\b0 , 231-277. \par \par Lindenman J., Lane C. A., and Hobson D. (1963) The resistance of A2G mice to myxoviruses. \i J. Immunol.\i0 \b 90\b0 , 942-951. \par \par Lindsay D. S., Lenz S. D., Cole R. A., Dubey J. P., and Blagburn B. L. (1995) Mouse model for central nervous system \i Neospora caninum\i0 infections. \i Journal of Parasitology\i0 \b 81\b0 , 313-315. \par \par Lindsey J. W. (1996) Characteristics of initial and reinduced experimental autoimmune encephalomyelitis. \i Immunogenet.\i0 \b 44\b0 , 292-297. \par \par Lipton H. L. and Dal Canto M. C. (1976) Chronic neurologic disease in Theiler's virus infection of SJL/J mice. \i J. Neurol. Sci.\i0 \b 30\b0 , 201-207. \par \par Liu G. Y., Baker D., Fairchild S., Figueroa F., Quartey-Papafio R., Tone M., Healey D., Cooke A., Turk J. L., and Wraith D. C. (1993) Complete characterization of the expressed immune response genes in Biozzi AB/H mice: structural and functional identity between AB/H and NOD A region molecules. \i Immunogenet.\i0 \b 37\b0 , 296-300. \par \par Livy D. J. and Wahlsten D. (1997) Retarded formation of the hippocampal commissure in embryos from mouse strains lacking a corpus callosum. \i Hippocampus\i0 \b 7\b0 , 2-14. \par \par Lopez C. (1975) Genetics of natural resistance to herpes virus infections in mice. \i Nature\i0 \b 258\b0 , 152-153. \par \par Loscher W., Czuczwar S. J., and Wolff G. L. (1986) AE mice-an inbred mouse strain with interesting features for epilepsy research. \i Epilepsia\i0 \b 27\b0 , 657-664. \par \par Lovell D. P. Hexobarbital sleeping time in mice. Unpublished data. \par \par Lovell D.P. (1986) Variation in pentobarbitone sleeping time in mice. I. strain and sex differences. \i Lab. Anim.\i0 \b 20\b0 , 85-90. \par \par Lovell-Smith C. J. and Sneyd J. G. T. (1973) Lipolysis and adenosine 3', 5'- cyclic monophosphate in adipose tissue of the New 2ealand obese mouse. \i J. Endocrinol.\i0 \b 56\b0 , 1-11. \par \par Lu G., Uga S., Miyata M., and Ishikawa S. (1993) Histopathological study of congenitally diabetic yellow KK mouse lens. \i Japanese Journal of Ophthalmology\i0 \b 37\b0 , 369-378. \par \par Lu L.-M., Ogawa M., Kamoto T., Yamada Y., Abujiang P., and Hiai H. (1997) Expression of LECAM-1 and LFA-1 on pre-B lymphomaz cells but not on preneoplastic pre-B cells in SL/Kh mice. \i Leuk. Res.\i0 \b 21\b0 , 337-342. \par \par Lu X., Skamene E., and Richardson P. M. (1994) Studies of axonal regeneration in C57BL/6J and A/J mice. \i Brain Res.\i0 \b 652\b0 , 174-176. \par \par Lubec B., Aufricht C., Amann G., Kitzmuller E., and Hoger H. (1997) Arginine reduces kidney collagen accumulation, cross-linking, lipid peroxidation, glycoxidation, kidney weight and albuminuria in the diabetic KK mouse. \i Nephron\i0 \b 75\b0 , 213-218. \par \par Lukacher A. E., Ma Y., Carroll J. P., AbromsonLeeman S. R., Laning J. C., Dorf M. E., and Benjamin T. L. (1995) Susceptibility to tumors induced by polyoma virus is conferred by an endogenous mouse mammary tumor virus superantigen. \i Journal Of Experimental Medicine\i0 \b 181\b0 , 1683-1692. \par \par Lunde M. N. and Gelderman A. H. (1971) Resistance of AKR mice to lymphoid leukemia associated with a chronic protozoan infection, Besnoitia jellisoni. \i J. Natl. Cancer Inst.\i0 \b 47\b0 , 485-488. \par \par Lush I. E. and Arnold C. J. (1975) High coumarin 7-hydroxylase activity does not protect mice against Warfarin. \i Heredity\i0 \b 35\b0 , 279-281. \par \par Lush I.M. (1988) The genetics of tasting in mice. VI. Saccharin, acesulfame, dulcin and sucrose. \i Genet. Res.\i0 \b 53\b0 , 95-99. \par \par Lynch C. B. and Hegmann J. P. (1973) Genetic differences influencing behavioural temperature regulation in small mammals. II. Genotype- environment interactions. \i Behav. Genet.\i0 \b 3\b0 , 145-154. \par \par Lynch C. J. (1969) The so-called Swiss Mouse. \i Lab. Anim. Care\i0 \b 19\b0 , 214-220. \par \par Lynch D. M. and Kay P. H. (1995) Studies on the polymorphism of the fifth component of complement in laboratory mice. \i Exp. Clin. Immunogenet.\i0 \b 12\b0 , 253-260. \par \par Macanovic M., Sinicropi D., Shak S., Baughman S., Thiru S., and Lachmann P. J. (1996) The treatment of systemic lupus erythematosus (SLE) in NZB/W F1 hybrid mice; studies with recombinant murine DNase and with dexamethasone. \i Clin. Exp. Immunol.\i0 \b 106\b0 , 243-252. \par \par Macario A. J. L., Stahl W., and Miller R. M. (1980) Lymphocyte subpopulations and function in chronic murine toxaplasmosis. II. Cyclic immunosuppression in genetic-low-responder mice. \i Cell. Immunol.\i0 \b 56\b0 , 235-239. \par \par Macario de E. C. and Macario A. J. L. (1980) Immunosuppression associated with erythropoiesis in genetic low responder mice. \i Ann. Immunol (Inst. Pasteur)\i0 \b 131C\b0 , 397-404. \par \par Machleder D., Ivandic B., Welch C., Castellani L., Reue K., and Lusis A. J. (1997) Complex genetic control of HDL levels in mice in response to an atherogenic diet - Coordinate regulation of HDL levels and bile acid metabolism. \i J. Clin. Invest.\i0 \b 99\b0 , 1406-1419. \par \par Magdon E. von (1962) Untersuchungen der katalaseaktivitat des Blutes vershiedener Mausestamme. \i Z. Versuchstierk.\i0 \b 1\b0 , 173-178. \par \par Mahler J. F., Stokes W., Mann P. C., Takaoka M., and Maronpot R. R. (1996) Spontaneous lesions in aging FVB/N mice. \i Toxicologic Pathology\i0 \b 24\b0 , 710-716. \par \par Maia A. L., Berry M. J., Sabbag R., Harney J. W., and Larsen P. R. (1995) Structural and functional differences in the \i dio1\i0 gene in mice with inherited type 1 deiodinase deficiency. \i Molec. Endocrinol.\i0 \b 9\b0 , 969-980. \par \par Makino S., Kunimoto K., Muraoka Y., Mizushima Y., Katagiri K., and Tochino Y. (1980) Breeding of a non-obese, diabetic strain of mice. \i Exp. Animals (Japan)\i0 \b 29\b0 , 1-13. \par \par Maleszewski M. and Yanagimachi R. (1995) Spontaneous and sperm-induced activation of oocytes in LT/Sv strain mice. \i Development Growth & Differentiation\i0 \b 37\b0 , 679-685. \par \par Maley M. A. L., Fan Y., Beilharz M. W., and Grounds M. D. (1994) Intrinsic differences in MyoD and myogenin expression between primary cultures of SJL/J and BALB/C skeletal muscle. \i Exp. Cell Research\i0 \b 211\b0 , 99-107. \par \par Mannen H., Tsuji S., and Goto N. (1991) Incomplete protection mechanism against vesico-urethral reflex and hydronephrosis in the inbred mouse strain DDD. \i Lab. Anim.\i0 \b 25\b0 , 156-161. \par \par Manolios N., Geczy C. L., and Schrieber L. (1990) Aberrant lymphocyte migration patterns in systemic lupus erythematosus (MRL/l, MRL/n) mice are independent of the micro-environment. \i Autoimmunity\i0 \b 7\b0 , 139-148. \par \par Marek P., Yirmiya R., and Liebeskind J. C. (1990) Genetic influences on brain stimulation-produced analgesia in mice: II. Correlation with brain opiate receptor concentration. \i Brain Res.\i0 \b 507\b0 , 155-157. \par \par Margolis F. L. (1971) Regulation of porphyrin biosynthesis in the Harderian gland of inbred mouse strains. \i Arch. Biochem. Biophys.\i0 \b 145\b0 , 373-381. \par \par Markel P. D., Bennett B., Beeson M. A., Gordon L., Simpson V. J., and Johnson T. E. (1996a) Strain distribution patterns for genetic markers in the LSXSS recombinant-inbred series. \i Mamm. Genome\i0 \b 7\b0 , 408-412. \par \par Markel P. D., Bennett B., Beeson M. A., Gordon L., Simpson V. J., and Johnson T. E. (1996b) Strain distribution patterns for genetic-markers in the lsxss recombinant-inbred series. \i Mamm. Genome\i0 \b 7\b0 , 408-412. \par \par Marks M. J., Stitzel J. A., and Collins A. C. (1989) Genetic influences on nicotine responses. \i Pharmacol. Biochem. Behav.\i0 \b 33\b0 , 667-678. \par \par Marks M. J., Pauly J. R., Grun E. U., and Collins A. C. (1996) ST/b and DBA/2 mice differ in brain alpha-bungarotoxin binding and alpha-7 nicotinic receptor subunit messenger-RNA levels - a quantitative autoradiographic analysis. \i Molecular Brain Research\i0 \b 39\b0 , 207-222. \par \par Marley S. B., Hadley C. L., and Wakelin D. (1994) Effect of genetic variation on induced neutrophilia in mice. \i Infect. Immun.\i0 \b 62\b0 , 4304-4309. \par \par Marshall J. D., Mu J.-L., Cheah Y.-C., Nesbitt M. N., Frankel W. N., and Paigen B. (1992) The AXB and BXA set of recombinant inbred mouse strains. \i Mamm. Genome\i0 \b 3\b0 , 669-680. \par \par Martin S. E. and Martin W. J. (1975) X chromosome-linked defect of CBA/HN mice in production of tumor-reacting naturally occurring IgM antibodies. \i J. Immunol.\i0 \b 115\b0 , 502-507. \par \par Massey A. C., Coppola M. A., and Thomas C. Y. (1990) Origin of pathogenic determinants of recombinant murine leukemia viruses: analysis of Bxv-1-related xenotropic viruses from CWD mice. \i J. Virol.\i0 \b 64\b0 , 5491-5499. \par \par Massey A. C., Lawrenz-Smith S. C., Innes D. J., and Thomas C. Y. (1994) Origins of enhancer sequences of recombinant murine leukemia viruses from spontaneous B- and T-cell lymphomas of CWD mice. \i Journal of Virology\i0 \b 68\b0 , 3773-3783. \par \par Masui T., Tezuka N., Nakanishi H., Inada K. I., Miyashita N., and Tatematsu M. (1997) Induction of invasive squamous cell carcinomas in the forestomach of (C3H x MSM)F1, MSM, and C3H mice by N-methyl-N-nitrosourea and mutational analysis of the H-\i ras\i0 and p53 genes. \i Cancer Lett.\i0 \b 111\b0 , 97-104. \par \par Matsuchita M., Tsuboyama T., Kasai R., Okumura H., Yamamuro T., Higuchi K., Higuchi K., Kohono A., Yonezu T., Utani A., Umezawa M., and Takeda T. (1986) Age-related changes in bone mass in the senescence accelerated mouse (SAM): SAM-R/3 and SAM-P/6 as new murine models for senile osteoporosis. \i Am. J. Pathol.\i0 \b 125\b0 , 276-283. \par \par Matsushima Y., Kamoto T., Iida F., Abujiang P., Honda Y., and Hiai H. (1996) Mapping of rupture of lens cataract (rlc) on mouse chromosome 14. \i Genomics\i0 \b 36\b0 , 553-554. \par \par Matsuzawa A. and Yamamoto T. (1975) Response of a pregnancy-dependent mammary tumour to hormones. \i J. Natl. Cancer Inst.\i0 \b 55\b0 , 447-456. \par \par Matsuzawa A., Yamamoto T., and Suzuki K. (1974) Pregnancy dependence of mammary tumors in strain DDD mice. \i J. Natl. Cancer Inst.\i0 \b 52\b0 , 449-453. \par \par Matyniak J. E. and Reiner S. L. (1995) T helper phenotype and genetic susceptibility in experimental lyme disease. \i Journal Of Experimental Medicine\i0 \b 181\b0 , 1251-1254. \par \par Mayberry L. F., Conder G. A., Bristol J. R., Johnson S. S., and Modric S. (1993) Absence of typical Nippostrongylus brasiliensis self-cure in putative BALB/c mice. \i Journal of Parasitology\i0 \b 79\b0 , 962-963. \par \par McCarthy M. M. and Dutton R. W. (1975) The humoral response of mouse spleen cells to two types of sheep erythrocytes. \i J. Immunol.\i0 \b 115\b0 , 1316-1321. \par \par McClearn G. E. (1965) Genotype and mouse behavior, in \i Genetics Today\i0 (Geerts J. J., ed) Proc. XI Int. Genetics Congress, The Hague, Sept. 1993, . \par \par McClearn G. E. and Kakihana R. (1981) Selective breeding for ethanol sensitivity: short-sleep and long-sleep mice, in \i Development of animal models as pharmacogenetic tools, (DHHS publication No. ADM 81-1133) ed.\i0 (McClearn G. E., Deitrich R. A., and Erwin V. G., eds), pp. 147-159. Government Printing Office, Washington, DC. \par \par McClearn G. E., Wilson J. R., and Meredith W. (1970) The use of isogenic and heterogenic mouse stocks in behavioral research, in \i Contribution to behavior genetic analysis. The mouse as a prototype\i0 (Lindzey G. and Thiessen D. D., eds), pp. 3-32. Appleton-Century-Crofts, New York. \par \par McClive P. J., Huang D., and Morahan G. (1994) C57BL/6 and C57BL/10 inbred mouse strains differ at multiple loci on chromosome 4. \i Immunogenet.\i0 \b 39\b0 , 286-288. \par \par McLaren A. and Tait A. (1969) Cytoplasmic isocitrate dehydrogenase variation within the C3H inbred strain. \i Genet. Res.\i0 \b 14\b0 , 93. \par \par Medvedev N. N. (1969) Inbreeding, fertility and viability. \i Sov. Genet.\i0 \b 5\b0 , 376-387. \par \par Meier H. and Hoag W. G. (1966) Blood coagulation, in \i Biology of the laboratory mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 373-376. McGraw-Hill, New York. \par \par Meier H. and MacPike A. D. (1968) Levels and heritability of serum ceruloplasmin activity in inbred strains of mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 128\b0 , 1185-1190. \par \par Melo J. A., Shendure J., Pociask K., and Silver L. M. (1996) Identification of sex-specific quantitative trait loci controlling alcohol preference in C57BL/6 mice. \i Nature Genet.\i0 \b 13\b0 , 147-153. \par \par Mendoza L. A., Hamburg M., and Fuld H. (1967) Differences in thyroid activity in several inbred strains of mice. \i Anat. Rec.\i0 \b 158\b0 , 275-280. \par \par Menendez R. C. and Abdraschitova E. (1990) Development and characterization of the IOR/Hab inbred mouse strain. \i Lab. Anim.\i0 \b 24\b0 , 303-307. \par \par MerayoLloves J., Zhao T. Z., Dutt J. E., and Foster C. S. (1996) A new murine model of allergic conjunctivitis and effectiveness of nedocromil sodium. \i Journal of Allergy and Clinical Immunology\i0 \b 97\b0 , 1129-1140. \par \par Merino R., Iwamoto M., Fossati L., Muniesa P., Araki K., Takahashi S., Huarte J., Yamamura K. I., Vassalli J. D., and Izui S. (1993) Prevention of systemic lupus erythematosus in autoimmune BXSB mice by a transgene encoding I-E alpha chain. \i Journal Of Experimental Medicine\i0 \b 178\b0 , 1189-1197. \par \par Messeri P., Oliverio A., and Bovet D. (1972) Relations between avoidance and activity. A diallel study in mice. \i Behav. Biol.\i0 \b 7\b0 , 733-742. \par \par Mewissen D. J. (1971) Natural tumor incidence in a population of mice as a reference index. \i Fed. Proc.\i0 \b 30\b0 , 311. \par \par Milich D. R. and Gershwin M. E. (1981) The pathogenesis of autoimmunity in New Zealand mice, in \i Immunologic defects in laboratory animals\i0 (Gershwin M. E. and Merchant B., eds), pp. 77-142. Plenum Press, New York, London. \par \par Mills E., Kuhn C. M., Feinglos M. N., and Surwit R. (1993) Hypertension in CB57BL/6J mouse model of non-insulin-dependent diabetes mellitus. \i Am. J. Physiol.\i0 \b 264\b0 , R73-R78. \par \par Misra M., Rodriguez R. E., North S. L., and Kasprzak K. S. (1991) Nickel-induced renal lipid peroxidation in different strains of mice: concurrence with nickel effect on antioxidant defense systems [published erratum appears in Toxicol Lett 1992 60:239]. \i Toxicol. Lett.\i0 \b 58\b0 , 121-133. \par \par Mitchell C. A., Grounds M. D., and Papadimitriou J. M. (1995) The genotype of bone marrow-derived inflammatory cells does not account for differences in skeletal muscle regeneration between SJL/J and BALB/c mice. \i Cell & Tissue Research\i0 \b 280\b0 , 407-413. \par \par Miyake T., Cameron A. M., and Hall B. K. (1996a) Detailed staging of inbred C57BL/6 mice between Theiler's [1972] stages 18 and 21 (11-13 days of gestation) based on craniofacial development. \i Journal of Craniofacial Genetics and Developmental Biology\i0 \b 16\b0 , 1-31. \par \par Miyake T., Cameron A. M., and Hall B. K. (1996b) Stage-specific onset of condensation and matrix deposition for Meckel's and other first arch cartilages in inbred C57BL/6 mice. \i Journal of Craniofacial Genetics and Developmental Biology\i0 \b 16\b0 , 32-47. \par \par Miyamoto H., Maruta K., Ogawa M., Beckers M. C., Gros P., and Yoshida S. I. (1996) Spectrum of Legionella species whose intracellular multiplication in murine macrophages is genetically controlled by Lgn1. \i Infect. Immun.\i0 \b 64\b0 , 1842-1845. \par \par Mizutani H., Engelman R. W., Kinjoh K., Kurata Y., Ikehara S., Matsuzawa Y., and Good R. A. (1994) Calorie restriction prevents the occlusive coronary vascular disease of autoimmune (NZW x BXSB)F1 mice. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 91\b0 , 4402-4406. \par \par Mohammadi M., Redline R., Nedrud J., and Czinn S. (1996) Role of the host in pathogenesis of Helicobacter-associated gastritis: \i H. felis\i0 Infection of inbred and congenic mouse strains. \i Infect. Immun.\i0 \b 64\b0 , 238-245. \par \par Mohlke K. L., Nichols W. C., Westrick R. J., Novak E. K., Cooney K. A., Swank R. T., and Ginsburg D. (1996) A novel modifier gene for plasma von Willebrand factor level maps to distal mouse chromosome 11. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 93\b0 , 15352-15357. \par \par Mokler C. M. and Iturrian W. B. (1973) Strain differences in subcellular calcium distribution in striated muscle of the mouse. \i Proc. Soc. Exp. Biol. Med.\i0 \b 142\b0 , 919-923. \par \par Molls M., Zamboglu N., and Streffer C. (1983) A comparison of the cell kinetics of preimplantation mouse embryos from two different mouse strains. \i Cell Tissue Kinet.\i0 \b 16\b0 , 277-283. \par \par Monroy-Ostria A., Fuentes-Fraga I., Garcia-Flores C., and Favila-Castillo L. (1994) Infection of BALB/c, C57Bl/6 mice and F1 hybrid CB6F1 mice with strains of \i Leishmania mexicana\i0 isolated from Mexican patients with localized or diffuse cutaneous leishmaniasis. \i Archives of Medical Research\i0 \b 25\b0 , 401-406. \par \par Mori A. (1968) Hereditary hydrocephalus in C57BL mouse. \i Brain and Nerve\i0 \b 20\b0 , 695-700. \par \par Moriguchi T., Saito H., and Nishiyama N. (1997) Anti-ageing effect of aged garlic extract in the inbred brain atrophy mouse model. \i Clin. Exp. Pharmacol. Physiol.\i0 \b 24\b0 , 235-242. \par \par Morissette C., Skamene E., and Gervais F. (1995) Endobronchial inflammation following \i Pseudomonas aeruginosa\i0 infection in resistant and susceptible strains of mice. \i Infect. Immun.\i0 \b 63\b0 , 1718-1724. \par \par Morissette C., Francoeur C., Darmondzwaig C., and Gervais F. (1996) Lung phagocyte bactericidal function in strains of mice resistant and susceptible to \i Pseudomonas aeruginosa\i0 . \i Infect. Immun.\i0 \b 64\b0 , 4984-4992. \par \par Moskow J. J., Bullrich F., Huebner K., Daar I. O., and Buchberg A. M. (1995) Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice. \i Molecular and Cellular Biology\i0 \b 15\b0 , 5434-5443. \par \par Most H., Nussenzweig R. S., Vanderberg J., Herman R., and Yoeli M. (1966) Susceptibility of genetically standardized (JAX) mouse strains to sporozoite and blood-induced Plasmodium berghei infections. \i Mil. Med.\i0 \b 131\b0 , 915-918. \par \par Moumaris M., Sestier C., Miltgen F., Halbreich A., Gentilini M., and Sabolovic D. (1995) Effect of fatty acid treatment in cerebral malaria-susceptible and nonsusceptible strains of mice. \i Journal of Parasitology\i0 \b 81\b0 , 997-999. \par \par Moutier R. (1968) D\'8e termination de quelques charact\'8e ristiques g\'8e n\'8e tiques chez des souris de souche XLII/GIF. \i Exp. Anim. (France)\i0 \b 1\b0 , 261-267. \par \par Mu J. L., Cheah Y. C., and Paigen B. (1992) Strain distribution pattern of 25 simple sequence length polymorphisms in the AXB and BXA recombinant inbred strains. \i Mamm. Genome\i0 \b 3\b0 , 705-708. \par \par M\'9f hlbock O. (1965) A note on a new inbred mouse strain GR/A. \i Eur. J. Cancer\i0 \b 1\b0 , 123-124. \par \par M\'9f hlbock O. and Rijsse1 T. G. van (1954) Studies on mammary tumors in the O20 Amsterdam strain of mice. \i J. Natl. Cancer Inst.\i0 \b 15\b0 , 73-93. \par \par Muggleton-Harris A. L., Festing M. F. W., and Hall M. (1987) A gene location for the inheritance of the Cataract Fraser (CatFr) mouse congenital cataract. \i Genet. Res.\i0 \b 49\b0 , 235-238. \par \par Muhlbock O. and Tengbergen W. P. Jr. (1971) Instability of characteristics in inbred strains of mice, in \i Defining the laboratory animal\i0 (Schneider H. A., ed), pp. 230-249. Proc. IV ICLAS Symposium, . \par \par Mukherjee et al. (1976) Effect of stress on the quantitative levels of certain enzymesin mice. \i J. Anim. Breed. Geneti.\i0 \b 93\b0 , 48-59. \par \par MullerSieburg C. E. and Riblet R. (1996a) Genetic control of the frequency of hematopoietic stem cells in mice: Mapping of a candidate locus to chromosome 1. \i Journal Of Experimental Medicine\i0 \b 183\b0 , 1141-1150. \par \par Mullersieburg C. E. and Riblet R. (1996b) Genetic-control of the frequency of hematopoietic stem-cells in mice - mapping of a candidate locus to chromosome-1. \i Journal Of Experimental Medicine\i0 \b 183\b0 , 1141-1150. \par \par Mullink J. W. M. A., Antonisse H. W., and van Ham B. M. Blood pressure in inbred mice. Personal communication. \par \par Munasinghe J. P., Tyler J. A., Hodgson R. J., Barry M. A., Gresham G. A., Evans R., and Hall L. D. (1996) Magnetic resonance imaging, histology, and X-ray of three stages of damage to the knees of SRT/ORT mice. \i Investigative Radiology\i0 \b 31\b0 , 630-638. \par \par Murphy E. D. (1963) SJL/J, a new inbred strain of mouse with a high, early incidence of reticulum-cell neoplasms. \i Proc. Am. Assoc. Cancer Res.\i0 \b 4\b0 , 46. \par \par Murphy E. D. (1966) Characteristic tumors, in \i Biology of the laboratory mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 521-562. McGraw-Hill, New York. \par \par Murphy E. D. (1981) Lymphoproliferation (lpr) and other sinbgle-locus models for murine lupus, in \i Immunologic defects in laboratory animals Vol. I\i0 (Gershwin M. E. and Merchant B., eds), pp. 143-173. Plenum Press, New York,London. \par \par Murphy E. D. and Roths J. B. (1979) A Y chromosome associated factor in strain BXSB producing accelerated autoimmunity and lymphoproliferation. \i Arthritis Rheum.\i0 \b 22\b0 , 1188-1194. \par \par Murphy E.D. (1981) \i Lymphoproliferation (lpr) and other sinbgle-locus models for murine lupus. pp 143-173 in M.E. Gershwin and B. Merchant (eds) Immunologic defects in laboratory animals\i0 . Plenum Press, New York, London. \par \par Murray W. S. (1963) MA/My strain of the Marsh albino mouse. \i J. Natl. Cancer Inst.\i0 \b 30\b0 , 605-610. \par \par Murray W. S. and Little C. C. (1967) Genetic studies of carcinogenesis in mice. \i J. Natl. Cancer Inst.\i0 \b 38\b0 , 639-656. \par \par Musto N., Hafiez A. A., and Bartke A. (1972) Prolactin increases 17 - hydroxysteroid dehydrogenase activity in the testis. \i Endocrinol.\i0 \b 91\b0 , 1106-1108. \par \par Muthing J. (1997) Neutral glycosphingolipids and gangliosides from spleen T lymphoblasts of genetically different inbred mouse strains. \i Glycoconjugate Journal\i0 \b 14\b0 , 241-248. \par \par Muto Y., Satoh J., Muto G., Masuda T., Sagara M., Fukuzawa M., Miyaguchi S., Qiang X. L., Sakata Y., Nakazawa T., Ikehata F., and Toyota T. (1997) Effect of long-term treatment with complete Freund's adjuvant on KK-\i A\i0 \i \up8 y\up0 \i0 \up8 \up0 mouse, a model of non-insulin-dependent diabetes mellitus. \i Clin. Immunol. Immunopathol.\i0 \b 83\b0 , 53-59. \par \par Myers D. D., Meier H., and Huebner R. J. (1970) Prevalence of murine C-type RNA virus group specific antigen in inbred strains of mice. \i Life Sci.\i0 \b 9\b0 , 1071-1080. \par \par Nabarra B., Dardenne M., and Bach J. F. (1990) Thymic reticulum of autoimmune mice. II: Ultrastructural studies of mice with lupus-like syndrome (NZB, BXSB, MRL/l). \i Journal of Autoimmunity\i0 \b 3\b0 , 25-36. \par \par Nabors G. S. and Farrell J. P. (1994) Site-specific immunity to Leishmania major in SWR mice: The site of infection influences susceptibility and expression of the antileishmanial immune response. \i Infect. Immun.\i0 \b 62\b0 , 3655-3662. \par \par Nagasawa H., Yanai R., and Miyamoto M. (1972) Differences in mammary development and pituitary and placental mammotropin levels of two inbred strains of mice (DDD and DSD) established from the common ancestor (dd). \i Exp. Animals (Japan)\i0 \b 21\b0 , 205-210. \par \par Nagasawa H., Miyamoto M., and Fujimoto M. (1973) Reproductivity in inbred strains of mice and project for their efficient production. \i Exp. Animals (Japan)\i0 \b 22\b0 , 119-126. \par \par Nagasawa H., Tokuzen R., and Nakahara W. (1976a) Growth of mammary tumors in a high and a low mammary tumor strains of mice established from the same basal stock of Swiss albino. \i Gann\i0 \b 67\b0 , 913-915. \par \par Nagasawa H., Yanai R., Taniguchi H., Tokuzen R., and Nakahara W. (1976b) Two-way selection of a stock of Swiss albino mice for mammary tumorigenesis: Establishment of two new strains (SHN and SLN). \i J. Natl. Cancer Inst.\i0 \b 57\b0 , 425-430. \par \par Nagatomo I., Akasaki Y., Kuchiiwa S., Nakagawa S., and Takigawa M. (1996a) Sparse distribution of NADPH diaphorase neurons in the hippocampal-formation of the inbred mutant strain EL mouse. \i Brain Res.\i0 \b 730\b0 , 223-226. \par \par Nagatomo I., Akasaki Y., Nagase F., Nomaguchi M., and Takigawa M. (1996b) Relationships between convulsive seizures and serum and brain concentrations of phenobarbital and zonisamide in mutant inbred strain EL mouse. \i Brain Res.\i0 \b 731\b0 , 190-198. \par \par Nagy Z. M. and Misanin J. R. (1970) Visual perception in the retinal degenerate C3H mouse. \i J. Comp. Physiol. Psychol.\i0 \b 72\b0 , 306-310. \par \par Nakamura M., Nishimura M., Koide Y., and Yoshida T. O. (1996) Analysis of pathogenesis of autoimmune insulitis in nod mice -adoptive transfer experiments of insulitis in ILI and nod nude-mice. \i Exp. Anim.\i0 \b 45\b0 , 233-238. \par \par Nakano A., Kita E., and Kashiba S. (1995) Different sensitivity of complement to \i Salmonella typhimurium\i0 accounts for the difference in natural resistance to murine typhoid between A/J and C57BL/6 mice. \i Microbiology and Immunology\i0 \b 39\b0 , 95-103. \par \par Nakano H., Saito K., and Suzuki K. (1996) Clinico-ECoG correlate of megimide-induced epileptic seizures in epilepsy-prone EL and its mother strain nonepileptic ddY mice. \i Physiol. Behav.\i0 \b 60\b0 , 809-816. \par \par Nakaya K., Nakao M., and Ito A. (1997) \i Echinococcus multilocularis\i0 : Mouse strain difference in hydatid development. \i J. Helminthology\i0 \b 71\b0 , 53-56. \par \par Nakayama M., Yazaki K., Kusano A., Nagata K., Hanai N., and Ishihama A. (1993) Structure of mouse Mx1 protein. Molecular assembly and GTP-dependent conformational change. \i J. Biol. Chem.\i0 \b 268\b0 , 15033-15038. \par \par Nandi J., Bern H. A., Biglieri E. G., and Pieprzyk J. K. (1967) In vitro steroidogenesis by the adrenal glands of mice. \i Endocrinol.\i0 \b 80\b0 , 576-582. \par \par Naruse I. and Kameyama Y. (1982) Morphogenesis of genetic preaxial polydactyly, polydactyly-Nagoya, Pdn, in mice. \i Congenit. Anom.\i0 \b 22\b0 , 137-144. \par \par Naruse I. and Kemeyama Y. (1980) Developmental abnormalities of the mouse brain in hereditary polydactyly (polydactyly Nagoya, \i Pdn\i0 ). \i Teratology\i0 \b 22\b0 , 17A. \par \par Nash D. J. and Logsdon D. F. (1974) Characteristics of a new hyperglycemia in an inbred strain of mice. \i Am. Zool.\i0 \b 14\b0 , 1277. \par \par Neal R. A. and Harris W. G. (1975) Attempts to infect inbred strains of rats and mice with Entamoeba histolytica. \i Trans. R. Soc. Trop. Med. Hyg.\i0 \b 69\b0 , 429-430. \par \par Nelson J. F., Karelus K., Felicio L. S., and Johnson T. E. (1990) Genetic influences on the timing of puberty in mice. \i Biol. Reprod.\i0 \b 42\b0 , 649-655. \par \par Nelson J. F., Karelus K., Felicio L. S., and Johnson T. E. (1992) Genetic influences on oestrous cyclicity in mice: evidence that cycle length and frequency are differentially regulated. \i J. Reprod. Fertil.\i0 \b 94\b0 , 261-268. \par \par Nemirovsky T. and Trainin N. (1973) Leukemia induction in C3H mice following their inoculation with normal AKR lymphoid cells. \i Int. J. Cancer\i0 \b 11\b0 , 172-177. \par \par Nesbitt M. N. and Skamene E. (1984) Recombinant inbred mouse strains derived from A/J and C57BL/6J: a tool for the study of genetic mechanisms in host resistance to infection and malignancy. \i J. Leukocyte Biol.\i0 \b 36\b0 , 357-364. \par \par Nesnow S., Ross J. A., Nelson G., Wilson K., Roop B. C., Jeffers A. J., Galati A. J., Stoner G. D., Sangaiah R., Gold A., and Mass M. J. (1994) Cyclopenta(cd)pyrene-induced tumorigenicity, Ki-ras codon 12 mutations and DNA adducts in strain A/J mouse lung. \i Carcinogenesis\i0 \b 15\b0 , 601-606. \par \par Neve P. and Wollman S. H. (1973) Crystals in dense bodies in the typical thyroid epithelial cell of the I mouse. \i J. Natl. Cancer Inst.\i0 \b 51\b0 , 659-665. \par \par Ng G. Y. K., Odowd B. F., and George S. R. (1996) Genotypic differences in mesolimbic enkephalin gene-expression in DBA/2J and C57BL/6J inbred mice. \i Eur. J. Pharmacol.\i0 \b 311\b0 , 45-52. \par \par Nichols E. A., Chapman V. M., and Ruddle F. H. (1973) Polymorphism and linkage for mannosephosphate isomerase in Mus musculus. \i Biochem. Genet.\i0 \b 8\b0 , 47-53. \par \par Nichols W. C., Cooney K. A., Mohlke K. L., Ballew J. D., Yang A., Bruck M. E., Reddington M., Novak E. K., Swank R. T., and Ginsburg D. (1994) von Willebrand disease in the RIIIS/J mouse is caused by a defect outside of the von Willebrand factor gene. \i Blood\i0 \b 83\b0 , 3225-3231. \par \par Nicholson S. M., Jokinen D. M., Dal Canto M. C., Kim B. S., and Melvold R. W. (1995) Genetic analysis of susceptibility to Theiler's murine encephalomyelitis virus-induced demyelinating disease in the SWR strain. \i J. Neuroimmunol.\i0 \b 59\b0 , 19-28. \par \par Niewiesk S., Brinckmann U., Bankamp B., Sirak S., Liebert U. G., and Ter Meulen V. (1993) Susceptibility to measles virus-induced encephalitis in mice correlates with impaired antigen presentation to cytotoxic T lymphocytes. \i Journal of Virology\i0 \b 67\b0 , 75-81. \par \par Nikulina E. M. and Klimek V. (1993) Strain differences in clonidine-induced aggressiveness in mice and its interaction with the dopamine system. \i Pharmacol. Biochem. Behav.\i0 \b 44\b0 , 821-825. \par \par Nikulina E. M., Skrinskaya J. A., and Popova N. K. (1991) Role of genotype and dopamine receptors in behaviour of inbred mice in a forced swimming test. \i Psychopharmacology\i0 \b 105\b0 , 525-529. \par \par Nishi Y., Hasegawa M. M., and Inui N. (1993) Genetic variations in baseline and ultraviolet light-induced sister chromatid exchanges in peritoneal lymphocytes among different mouse strains. \i Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis\i0 \b 286\b0 , 145-154. \par \par Nishida T., Sugiyama T., Kataoka A., Ushijima K., Ueyama T., and Yakushiji M. (1995) Cytotoxic impacts on the tumorigenesis and transplantability of ovarian teratoma in LT/Sv mouse. \i Oncology Reports\i0 \b 2\b0 , 1045-1048. \par \par Nishikawa R., Okumoto M., Iwai M., Iwai Y., Takamori Y., Imai S., and Hilgers J. (1991) Incomplete proviral genome of mouse mammary tumour virus is present on chromosome Y of NIH Swiss and some genetically related mouse strains. \i Lab. Anim.\i0 \b 25\b0 , 4-8. \par \par Nishimura M. (1969) Breeding of mice strains for diabetes mellitus. \i Exp. Animals (Japan)\i0 \b 18\b0 , 147-157. \par \par Nishimura M., Hirayama N., Serikawa T., Kanehira K., Matsushima Y., Katoh H., Wakana S., Kojima A., and Hiai H. (1995) The SMXA: a new set of recombinant inbred strain of mice consisting of 26 substrains and their genetic profile. \i Mamm. Genome\i0 \b 6\b0 , 850-857. \par \par Nishina P. M., Wang J., Toyofuku W., Kuypers F. A., Ishida B. Y., and Paigen B. (1993) Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. \i Lipids\i0 \b 28\b0 , 599-605. \par \par Nishioka Y. (1987) Y-chromosomal DNA polymorphism in mouse inbred strains. \i Genet. Res.\i0 \b 50\b0 , 69-72. \par \par Nisitani S., Hosokawa M., Sasaki M. S., Yasuoka K., Naiki H., Matsuchita T., and Takeda T. (1990) Acceleration of chromosome abberations in senescence-accelerated strains of mice. \i Mutation Res.\i0 \b 237\b0 , 221-228. \par \par Nobunga T. (1973) Establishment by selective inbreeding of the IVCS strain and related sister strains of the mouse, demonstrating regularly repeated 4-day estrus cycles. \i Lab. Animal Sci.\i0 \b 23\b0 , 803-811. \par \par Nomura Y., Kitamura Y., and Zhao X. H. (1991) Aging in the glutamergic system with special reference to the NMDA receptor/ion channel complex in the brains of senescence accelerated mice, in \i NMDA Receptor related agents: Biochemistry, Pharmacology and Behavior\i0 (Kameyama T., Domino F., and Nabeshima T., eds), pp. 287-298. NPP Books, Ann Arbor, MI. \par \par Nonoyama S., Smith F. O., Bernstein I. D., and Ochs H. D. (1993) Strain-dependent leakiness of mice with severe combined immune deficiency. \i J. Immunol.\i0 \b 150\b0 , 3817-3824. \par \par Noonan F. P. and Hoffman H. A. (1994) Susceptibility to immunosuppression by ultraviolet B radiation in the mouse. \i Immunogenet.\i0 \b 39\b0 , 29-39. \par \par Norga K., Paemen L., Masure S., Dillen C., Heremans H., Billiau A., Carton H., Cuzner L., Olsson T., Van Damm J., and Opdenakker G. (1995) Prevention of acute autoimmune encephalomyelitis and abrogation of relapses in murine models of multiple sclerosis by the protease inhibitor D-penicillamine. \i Inflam. Res.\i0 \b 44\b0 , 529-534. \par \par Oesch F., Morris N., and Daly J. W. (1973) Genetic expression of the induction of epoxide hydrase and aryl hydrocarbon hydroxylase activities in the mouse by phenobarbital or 3-methylcholanthrene. \i Molec. Pharmacol.\i0 \b 9\b0 , 692-696. \par \par Ogiku N., Sumikawa H., Nishimura T., Narita H., and Ishida R. (1994) Reduction of the mortality rate by imidapril in a small coronary artery disease model, (NZW x BXSB)F1 male mice. \i Jpn. J. Pharmacol.\i0 \b 64\b0 , 129-133. \par \par Ogunremi O. and Tabel H. (1995) Genetics of resistance to \i Trypanosoma congolense\i0 in inbred mice: Efficiency of apparent clearance of parasites correlates with long-term survival. \i Journal of Parasitology\i0 \b 81\b0 , 876-881. \par \par Ogura A., Asano T., Matuda J., Nakagawa M., and Fukui M. (1989) Characteristics of mutant mice (ICGN) with spontaneous renal lesions: a new model for human nephrotic syndrome. \i Lab. Anim.\i0 \b 23\b0 , 169-174. \par \par Ogura A., Asano T., Matuda J., Noguchi Y., Yamamoto Y., and Nakagawa M. (1990) Development of nephritic ICGN mice- the origin, reproductive ability and incidence of glomerulonephritis. \i Exp. Animals (Japan)\i0 \b 38\b0 , 349-352. \par \par Ogura A., Asano T., Matuda J., and Fujimura H. (1991a) Evolution of glomerular lesions in nephrotic ICGN mice: Serial biopsy with electron microscopy. \i J. Vet. Med. Sci.\i0 \b 53\b0 , 513-515. \par \par Ogura A., Asano T., Matuda J., Koura M., Nakagawa M., Kawaguchi H., and Yamaguchi Y. (1991b) An electron microscope study of glomerular lesions in hereditary nephrotic mice (ICGN strain). \i Virchows Archiv. A\i0 \b 417\b0 , 223-228. \par \par Ogura A., Asano T., Suzuki O., Yamamoto Y., Noguchi Y., Kawaguchi H., and Yamaguchi Y. (1994) Hereditary nephrotic syndrome with progression to renal failure in a mouse model (ICGN strain): Clinical study. \i Nephron\i0 \b 68\b0 , 239-244. \par \par Ogura A., Yamamoto Y., Suzuki O., Takano K., Wakayama T., Mochida K., and Kimura H. (1996) In-vitro fertilization and microinsemination with round spermatids for propagation of nephrotic genes in mice. \i Theriogenology\i0 \b 45\b0 , 1141-1149. \par \par Ohmori J., Tokunaga H., Ezaki T., Maruyama H., and Nawa Y. (1996) Eosinophil peroxidase deficiency in New Zealand White mice. \i International Archives of Allergy and Immunology\i0 \b 111\b0 , 30-35. \par \par Ohta A., Hirano T., Yagi H., Tanaka S., Hosokawa M., and Takeda T. (1989) Behavioural characteristics of the SAM-P/8 strain in Sidman active avoidance taks. \i Brain Res.\i0 \b 498\b0 , 195-198. \par \par Ohtori H., Yoshida T., and Inuta T. (1968) . \i Exp. Animals (Japan)\i0 \b 17\b0 , 91-98. \par \par Oldstone M. B. A. and Dixon F. J. (1968) Susceptibility of different mouse strains to lymphocytic choriomeningitis virus. \i J. Immunol.\i0 \b 100\b0 , 355-357. \par \par Oldstone M. B. A. and Dixon F. J. (1973) Change in susceptibility of C3H/He mice to LCM virus infection. \i J. Immunol.\i0 \b 111\b0 , 1613-1615. \par \par O'Neill J. K., Baker D., and Turk J. L. (1992) Inhibition of chronic relapsing experimental allergic encephalomyelitis in the Biozzi AB/H mouse. \i J. Neuroimmunol.\i0 \b 41\b0 , 177-187. \par \par O'Neill J. K., Baker D., Davison A. N., Allen S. J., Butter C., and Waldmann H. (1993) Control of immune-mediated disease of the central-nervous-system with monoclonal (CD4-specific) antibodies. \i J. Neuroimmunol.\i0 \b 45\b0 , 1-14. \par \par Ong G. L. and Mattes M. J. (1989) Mouse strains with typical mammalian levels of complement activity. \i J. Immunol. Methods\i0 \b 125\b0 , 147-158. \par \par Ong G. L., Baker A. E., and Mattes M. J. (1992) Analysis of high complement levels in Mus hortulanus and BUB mice. \i J. Immunol. Methods\i0 \b 154\b0 , 37-45. \par \par Oppermann W., Iwatsuka H., Reddi A. S., and Camerini-Davalos R. A. (1975) Prolonged fasting in mice: a more sensitive approach to genetic diabetes. \i Hormone Res.\i0 \b 6\b0 , 150-156. \par \par Orava M., Zhao X. F., Leiter E., and Hammond G. L. (1994) Structure and chromosomal location of the gene encoding mouse corticosteroid-binding globulin: Strain differences in coding sequence and steroid-binding activity. \i Gene\i0 \b 144\b0 , 259-264. \par \par Ortman R. A., Holderbaum D., Qu X. M., Banerjee S., and Haqqi T. M. (1994) BUB/BnJ (H-2(q)) is a TCR deletion mutant mouse strain (TCR Vbetaa, KJ16- ) that is susceptible to type II collagen-induced arthritis. \i J. Immunol.\i0 \b 152\b0 , 4175-4182. \par \par Osman G. E., Jacobson D. P., Li S. W., Hood L. E., Liggitt H. D., and Ladiges W. C. (1997) SWR: An inbred strain suitable for generating transgenic mice. \i Lab. Animal Sci.\i0 \b 47\b0 , 167-171. \par \par Otterness D. M. and Weinshilboum R. M. (1987a) Mouse thiopurine methyltransferase pharmacogenetics: biochemical studies and recombinant inbred strains. \i J. Pharmacol. Exp. Therapeut.\i0 \b 240\b0 , 180-186. \par \par Otterness D. M. and Weinshilboum R. M. (1987b) Mouse thiopurine methyltransferase pharmacogenetics: Monogenic inheritance. \i J. Pharmacol. Exp. Therapeut.\i0 \b 240\b0 , 817-824. \par \par Owens H. M. and Bonavida B. (1976) Immune functions characteristic of SJL/J mice and their association with age and spontaneous reticulum cell sarcoma. \i Cancer Res.\i0 \b 36\b0 , 1077-1083. \par \par Page D. L. and Glenner G. G. (1972) Social interaction and wounding in the genesis of spontaneous murine amyloidosis. \i Am. J. Pathol.\i0 \b 67\b0 , 555-570. \par \par Pagel J., Pegram V., Vaughn S., Donaldson P., and Bridgers W. (1973) The relationship of REM sleep with learning in mice. \i Behav. Biol.\i0 \b 9\b0 , 383-388. \par \par Pampfer S. and Streffer C. (1988) Prenatal death and malformations after irradiation of mouse zygotes with neutrons or X-rays. \i Teratology\i0 \b 37\b0 , 599-607. \par \par Panthier J. J., Gounon P., Condamine H., and Jacob F. (1989) Pattern of expression of ecotropic murine leukemia virus in gonads of inoculated SWR/J mice. \i J. Virol.\i0 \b 63\b0 , 2134-2142. \par \par Paquette N. C., Zhang L. Y., Ellis W. A., Scott A. L., and Kleeberger S. R. (1996) Vitamin A deficiency enhances ozone-induced lung injury. \i American Journal of Physiology - Lung Cellular and Molecular Physiology\i0 \b 270\b0 , L475-L482. \par \par Park E. I., Paisley E. A., Mangian H. J., Swartz D. A., Wu M. X., O'Morchoe P. J., Behr S. R., Visek W. J., and Kaput J. (1997) Lipid level and type alter stearoyl CoA desaturase mRNA abundance differently in mice with distinct susceptibilities to diet-influenced diseases. \i J. Nutrit.\i0 \b 127\b0 , 566-573. \par \par Pasternak G. (1963) Die unterschiedliche Reaktionsf\'8a higkeit zweier Mausein-zuchtstamme gegen spezifische Antigens isolog transplantabler Carcinogentu-moren. \i Acta Biol. Med. Germ.\i0 \b 10\b0 , 572-578. \par \par Pataer A., Kamoto T., Lu L. M., Yamada Y., and Hiai H. (1996) Two dominant host-resistance genes to pre-B lymphoma in wild-derived inbred mouse strain MSM/Ms. \i Cancer Res.\i0 \b 56\b0 , 3716-3720. \par \par Paul W. E., Yoshida T., and Benacerraf B. (1970) Genetic control of the specificity of anti-DNP antibodies. II. Differences in the specificity of anti-DNP antibody produced by several inbred strains of mice. \i J. Immunol.\i0 \b 105\b0 , 314-321. \par \par Peacock A. C., Gelderman A. H., Ragland R. H., and Hoffman H. A. (1967) Haptoglobin levels in serum of various strains of mice. \i Science\i0 \b 158\b0 , 1703-1704. \par \par Peng S. L., Madaio M. P., and Craft J. (1996) Systemic autoimmunity in LG/J mice. \i Immunology Letters\i0 \b 53\b0 , 153-155. \par \par Pennycuik P. R. (1967) A comparison of the effects of a variety of factors on the metabolic rate of the mouse. \i Aust. J. Biol. Med. Sci.\i0 \b 45\b0 , 331-346. \par \par Perry L. L. and Lodmell D. L. (1991) Role of CD4+ and CD8+ T cells in murine resistance to street rabies virus. \i J. Virol.\i0 \b 65\b0 , 3429-3434. \par \par Peters A. G. and Festing M. F. W. (1985) NIH/Ola: a highly productive inbred strain of the laboratory mouse. \i Lab. Anim.\i0 \b 19\b0 , 320-327. \par \par Peters J. and Lyon M. F. (1986) New substrain of SM, SM/JH. \i Mouse N.L.\i0 \b 76\b0 , 6. \par \par Petty R. E., Steward M. W., and Soothill J. F. (1972) The heterogeneity of antibody affinity in inbred mice and its possible immunopathologic significance. \i Clin. Exp. Immunol.\i0 \b 12\b0 , 231-241. \par \par Philbrick W. M., Maher S. E., Bridgett M. M., and Bothwell A. L. (1990) A recombination event in the 5' flanking region of the Ly-6C gene correlates with impaired expression in the NOD, NZB and ST strains of mice. \i EMBO Journal\i0 \b 9\b0 , 2485-2492. \par \par Pinchuck P. and Maurer P. H. (1965) Antigenicity of polypeptides (poly alpha amino acids). XVI. Genetic control of immunogenicity of synthetic polypeptides in mice. \i J. Exp. Med.\i0 \b 122\b0 , 673-679. \par \par Plant J. and Glynn A. A. (1974) Natural resistance to Salmonella infection, delayed hypersensitivity and Ir genes in different strains of mice. \i Nature\i0 \b 248\b0 , 345-347. \par \par Poiley S. M. (1972) Growth, tables for 66 strains and stocks of laboratory animals. \i Lab. Animal Sci.\i0 \b 22\b0 , 759-779. \par \par Poirier L. A., Stoner G. D., and Shimkin M. B. (1975) Bioassay of alkyl halides and nucleotide base analogs by pulmonary tumor response in strain A mice. \i Cancer Res.\i0 \b 35\b0 , 1411-1415. \par \par Polanski Z (1990) Different response of maturing oocytes from two inbred strains of mice to sperm penetration. \i Folia Biol.\i0 \b 38\b0 , 13-19. \par \par Poletaeva I. I., Lilp I. G., Irisova O. A., Ivanov V. I., and Bizikoeva F. Z. (1992) An unusual type of locomotion in mice of line 101/Hy [Russian]. \i Genetika\i0 \b 28\b0 , 147-149. \par \par Pollard M. (1973) Multinucleated acinar cells in the pancreases of AKR and C58 mice. \i Experientia\i0 \b 29\b0 , 596-597. \par \par Poole T. M. and Drinkwater N. R. (1996) Strain-dependent effects of sex-hormones on hepatocarcinogenesis in mice. \i Carcinogenesis\i0 \b 17\b0 , 191-196. \par \par Pope B. L., Chourmouzis E., MacIntyre J. P., Lee S., and Goodman M. G. (1994) Murine strain variation in the natural killer cell and proliferative responses to the immunostimulatory compound 7-Allyl-8-oxoguanosine: Role of cytokines. \i Cell. Immunol.\i0 \b 159\b0 , 194-210. \par \par Potter M. (1972) Immunoglobulin-producing tumors and myeloma proteins of mice. \i Physiol. Rev.\i0 \b 52\b0 , 631-719. \par \par Potter M., Mushinski E. B., Wax J. S., Hartley J., and Mock B. A. (1994) Identification of two genes on chromosome 4 that determine resistance to plasmacytoma induction in mice. \i Cancer Res.\i0 \b 54\b0 , 969-975. \par \par Potter M (1985) \i (ed) The BALB/c mouse. Current Topics in Microbiol. Immunol. 122\i0 . Springer-Varlag, Berlin, New York, Tokyo. \par \par Powers J. M., Wisniewski H., and Terry R. D. (1976) Lack of amyloidosis and renal disease in A-strain mice. \i Arch. Pathol. Lab. Med.\i0 \b 100\b0 , 69-73. \par \par Preece N. E., Amor S., Baker D., Gadian D. G., O'Neill J. K., and Urenjak J. (1994) Experimental encephalomyelitis modulates inositol and taurine in the spinal cord of biozzi mice. \i Magnetic Resonance in Medicine\i0 \b 32\b0 , 692-697. \par \par Price P., Eddy K. S., Papadimitriou J. M., Faulkner D. L., and Shellam G. R. (1991) Genetic determination of cytomegalovirus-induced and age-related cardiopathy in inbred mice. Characterization of infiltrating cells. \i Am. J. Pathol.\i0 \b 138\b0 , 59-67. \par \par Prochazka M., Serrez D. V., Worthen S. M., and Leiter E. H. (1989) Genetic control of diabetogenesis in NOD/Lt mice.# Development and analysis of congenic stocks. \i Diabetes\i0 \b 38\b0 , 14-46. \par \par Prochazka M., Serreze D. V., Frankel W. N., and Leiter E. H. (1992) NOR/Lt mice: MHC-matched diabetes-resistant control strain for NOD mice. \i Diabetes\i0 \b 41\b0 , 98-106. \par \par Prud'homme G. J., Sanders R., Parfrey N. A., and Ste-Croix H. (1991) T-cell maturation and clonal deletion in cyclosporine-induced autoimmunity. \i Journal of Autoimmunity\i0 \b 4\b0 , 357-368. \par \par Pryor G. T., Schlesinger K., and Calhoun W. H. (1966) Differences in brain enzymes among five inbred strains of mice. \i Life Sci.\i0 \b 5\b0 , 2105-2111. \par \par Qiao J. H., Fishbein M. C., Demer L. L., and Lusis A. J. (1995) Genetic determination of cartilaginous metaplasia in mouse aorta. \i Arteriosclerosis, Thrombosis, and Vascular Biology\i0 \b 15\b0 , 2265-2272. \par \par Quezada-Calvillo R., Senchyna M., and Underdown B. J. (1993) Characterization of intestinal gamma-glucoamylase deficiency in CBA/Ca mice. \i American Journal of Physiology - Gastrointestinal and Liver Physiology\i0 \b 265\b0 , G1150-G1157. \par \par Quock R. M., Mueller J. L., Vaughn L. K., and Belknap J. K. (1996) Nitrous-oxide antinociception in BXD recombinant inbred mouse strains and identification of quantitative trait loci. \i Brain Res.\i0 \b 725\b0 , 23-29. \par \par Rabstein L. S., Peters R. L., and Spahn G. J. (1973) Spontaneous tumors and pathologic lesions in SWR/J mice. \i J. Natl. Cancer Inst.\i0 \b 50\b0 , 751-758. \par \par R\'87 dl J. and Hollander C. F. (1974) Homogeneous immunoglobulins in sera of mice during aging. \i J. Immunol.\i0 \b 112\b0 , 2272-2273. \par \par Rager-Zisman B., Ju G., and Udem S. (1976) Resistance and susceptibility of mice to infection with measles virus. \i Fed. Proc.\i0 \b 35\b0 , 391. \par \par Ram J. S., Dehellis R. A., and Glenner G. G. (1969) Amyloid. VIII on strain variation in experimental murine amyloidosis. \i Proc. Soc. Exp. Biol. Med.\i0 \b 130\b0 , 462-464. \par \par Ranadive K. J., Sunanda V., Gothoskar S. V., and Fernandes G. (1969) A new inbred strain of mouse C17/Icrc developed for testing weak carcinogens. \i Ind. J. Med. Res.\i0 \b 57\b0 , 521-527. \par \par Rank W. R., Flugge U., and DiPauli R. (1969) Inheritance of the lipoid A- induced 19S-plaque-forming cell-response in mice. Evidence for three antigen-recognition mechanisms. \i Behringwirk- Mitt.\i0 \b 49\b0 , 222-229. \par \par Rao J. V., Swamy A. N., and Yamin S. (1991) In vitro brain acetylcholinesterase response among three inbred strains of mice to monocrotophos. \i Journal of Environmental Science & Health - Part B: Pesticides Food Contaminants & Agricultural Wastes\i0 \b 26\b0 , 449-458. \par \par Rappaport H., Bielschowsky M., D'Ath E. F., and Goodall C. M. (1971) Malignant lymphomas arising in Peyer's patches and other organs of untreated NZ0/Bl mice. \i Cancer Res.\i0 \b 31\b0 , 2047-2053. \par \par Ratkay L. G., Tait B., Tonzetich J., and Waterfield J. D. (1994) Lpr and MRL background gene involvement in the control of adjuvant enhanced arthritis in MRL-lpr mice. \i Journal of Autoimmunity\i0 \b 7\b0 , 561-573. \par \par Rebuffe-Scrive M., Surwit R., Feinglos M., Kuhn C., and Rodin J. (1993) Regional fat distribution and metabolism in a new mouse model (C57BL/6J) of non-insulin-dependent diabetes mellitus. \i Metabolism: Clinical and Experimental\i0 \b 42\b0 , 1405-1409. \par \par Reddi A. S., Velasco C. A., Reddy P. R., and Khan M. Y. (1990) Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis. \i Exp. Mol. Path.\i0 \b 53\b0 , 140-151. \par \par Reue K., PurcellHuynh D. A., Leete T. H., Doolittle M. H., Durstenfeld A., and Lusis A. J. (1993) Genetic variation in mouse apolipoprotein A-IV expression is determined pre- and post-transcriptionally. \i J. Lipid Res.\i0 \b 34\b0 , 893-903. \par \par Richardson D. M. DW/J. Jax Notes 414, The Jackson Laboratory, Bar Harbor, Maine. \par \par Rikke B. A., Zhao Y., Daggett L. P., Reyes R., and Hardies S. C. (1995) Mus spretus LINE-1 sequences detected in the Mus musculus inbred strain C57BL/6J using LINE-1 DNA probes. \i Genetics\i0 \b 139\b0 , 901-906. \par \par Riley R. L., Kruger M. G., Landa B., Elia J., and Ringel A. (1991) B cells in autoimmune (NZB x NZW)F1 mice show altered IgG isotype switching upon T cell-dependent antigenic stimulation in vitro. \i Clin. Immunol. Immunopathol.\i0 \b 58\b0 , 33-45. \par \par Riley V. (1975) Mouse mammary tumors: alteration of incidence as an apparent function of stress. \i Science\i0 \b 189\b0 , 465-467. \par \par Rings R. W. and Wagner J. E. (1971) Incidence of cardiac and other soft tissue mineralized lesions in DBA/2 mice. \i Lab. Animal Sci.\i0 \b 22\b0 , 344-352. \par \par Riven-Kreitman R., Tauber-Finkelstein M., Zipori D., and Shaltiel S. (1990) A periodicity in the response of SJL/J thymocytes to isoproterenol. Simulation by cell lines. \i Molecular & Cellular Endocrinology\i0 \b 73\b0 , 211-216. \par \par Roach M. L., Stock J. L., Byrum R., Koller B. H., and McNeish J. D. (1995) A new embryonic stem cell line from DBA/1lacJ mice allows genetic modification in a murine model of human inflammation. \i Exp. Cell Research\i0 \b 221\b0 , 520-525. \par \par Roberts A. and Thompson J. S. (1976) Inbred mice and their hybrids as an animal model for atherosclerosis research, in \i Atherosclerosis Drug Discovery\i0 (Day C. E., ed), pp. 313-327. Plenum Press, New York. \par \par Robinson M. L., Holmgren A., and Dewey M. J. (1993) Genetic control of ocular morphogenesis: Defective lens development associated with ocular anomalies in C57BL/6 mice. \i Exp. Eye Res.\i0 \b 56\b0 , 7-16. \par \par Robinson S. F., Marks M. J., and Collins A. C. (1996) Inbred mouse strains vary in oral self-selection of nicotine. \i Psychopharmacology\i0 \b 124\b0 , 332-339. \par \par Robson H. G. and Vas S. I. (1972) Resistance of mice to Salmonella typhimurium. \i J. Infect. Dis.\i0 \b 126\b0 , 378-380. \par \par Roderick T. H. (1963) The response of twenty-seven inbred strains of mice to daily doses of whole-body X-irradiation. \i Radiation Res.\i0 \b 20\b0 , 631-639. \par \par Roderick T. H., Wimer R. E., Wimer C. C., and Schwartzkroin P. A. (1973) Genetic and phenotypic variation in weight of brain and spinal cord between inbred strains of mice. \i Brain Res.\i0 \b 64\b0 , 345-353. \par \par Rodgers D. A. (1966) Factors underlying differences in alcohol preference among inbred strains of mice. \i Psychosomat. Med.\i0 \b 28\b0 , 498-513. \par \par Rose N. R., Vladutiu A. O., David C. S., and Shreffier D. C. (1973) Autoimmune murine thyroiditis. V. Genetic influence on the disease in BSVS and BRVR mice. \i Clin. Exp. Immunol.\i0 \b 15\b0 , 281-287. \par \par Rosenstreich D. L. and Glode L. M. (1975) Differences in cell nitrogen responsiveness between closely related strains of mice. \i J. Immunol.\i0 \b 115\b0 , 777-780. \par \par Rosner A., Peled A., HaranGhera N., and Canaani E. (1993) Analysis of Ly-1+ B-cell populations and IgH rearrangements in 'normal' spleens and in lymphomas of AKR/J and AKR Fv-1b mice. \i Cancer Res.\i0 \b 53\b0 , 2147-2153. \par \par Roubertoux P. L., Martin B., Leroy I., Beau J., Marchaland C., Perezdiaz F., Cohensalmon C., and Carlier M. (1996) Vocalizations in newborn mice - genetic-analysis. \i Behav. Genet.\i0 \b 26\b0 , 427-437. \par \par Rowland E. C., Lozykowski M. G., and McCormick T. S. (1992) Differential cardiac histopathology in inbred mouse strains chronically infected with \i Trypanosoma cruzi\i0 . \i Journal of Parasitology\i0 \b 78\b0 , 1059-1066. \par \par Rowlatt C., Chesterman F. C., and Sheriff M. U. (1976) Lifespan, age changes and tumour incidence in an ageing C57BL mouse colony. \i Lab. Anim.\i0 \b 10\b0 , 419-442. \par \par Royce J. R. (1972) Avoidance conditioning in nine strains of inbred mice using optimal stimulus parameters. \i Behav. Genet.\i0 \b 2\b0 , 107-110. \par \par Royce J. R., Yeudall L. T., and Poley W. (1971) Diallel analysis of avoidance conditioning in inbred strains of mice. \i J. Comp. Physiol. Psychol.\i0 \b 76\b0 , 353-358. \par \par Rubinstein P., Liu N., Strenn E. W., and Decary F. (1974) Electrophoretic mobility and agglutinability of red blood cells: a `new' polymorphism in mice. \i J. Exp. Med.\i0 \b 139\b0 , 313-322. \par \par Russell E. S. and Meier H. (1966) Constitutional diseases, in \i Biology of the Laboratory Mouse, 2nd. ed.\i0 (Green E. L., ed), pp. 571-587. McGraw-Hill, New York. \par \par Russell E. S., Neufeld E. F., and Higgins C. T. (1951) Comparison of normal blood picture of young adults from 18 inbred strains of mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 78\b0 , 761-766. \par \par Russfield A. B. (1966) \i Tumors of endocrine glands and secondary sex organs\i0 . US Dept. of Health, Education & Welfare, Pub. Health Service Publ. 1332, Washington, DC. \par \par Sadarangani C., Skamene E., and Kongshaven P. A. L. (1980) Cellular basis for genetically determined enhanced resistance of certain mouse strains to Listeriosis. \i Infect. Immun.\i0 \b 28\b0 , 381-386. \par \par Sagai T., Shiroishi T., Moriwaki K., Bonhomme F., Petras M. L., Thohari m, Yu Z. C., Lu D. Y., and Chow W. S. (1986) Characterization of newly isolated monoclonal antibodies against MHC of Japanese wild mouse. \i Immunogenet.\i0 \b 24\b0 , 361-367. \par \par Sager M. A., Lawton J. W. M., and Murphy W. H. (1973) Serum transmissibility of immune polioencephalomyelitis in C58 mice. \i J. Immunol.\i0 \b 110\b0 , 219-226. \par \par St. John R. D. (1973) Genetic analysis of tail rattling in the mouse. \i Nature\i0 \b 241\b0 , 550. \par \par Saito N. and Natori T. (1985) Low responsiveness to MLM bacilli associated with an impaired macrophage function in CBA/JK mice. \i Exp. Clin. Immunogenet.\i0 \b 2\b0 , 24-35. \par \par Sakagami T., Dixon M., ORourke J., Howlett R., Alderuccio F., Vella J., Shimoyama T., and Lee A. (1996) Atrophic gastric changes in both \i Helicobacter felis\i0 and \i Helicobacter pylori\i0 infected mice are host dependent and separate from antral gastritis. \i Gut\i0 \b 39\b0 , 639-648. \par \par Sakamoto K. and Sakka M. (1973) Survival of clonogenic cells of a murine epithelioma treated with neocarzinostatin. \i Eur. J. Cancer\i0 \b 9\b0 , 829-831. \par \par Sakic B., Szechtman H., Keffer M., Talangbayan H., Stead R., and Denburg J. A. (1992) A behavioral profile of autoimmune lupus-prone MRL mice. \i Brain Behav. & Immunity\i0 \b 6\b0 , 265-285. \par \par Sampugna J., Clements J., Carter T. P., and Campagnoni A. T. (1975) Comparison of lipids in total brain tissue from five mouse genotypes. \i J. Neurobiol.\i0 \b 6\b0 , 259-266. \par \par Sangster M. Y., Heliams D. B., MacKenzie J. S., and Shellam G. R. (1993) Genetic studies of flavivirus resistance in inbred strains derived from wild mice: evidence for a new resistance allele at the flavivirus resistance locus (Flv). \i J. Virol.\i0 \b 67\b0 , 340-347. \par \par Sass B., Peters R. L., and Kelloff G. J. (1976) Differences in tumor incidence in two substrains of claude BALB/c (BALB/CfCd) mice, emphasizing renal, mammary, pancreatic and synovial tumors. \i Lab. Animal Sci.\i0 \b 26\b0 , 736-741. \par \par Sato S., Kitajima K., Konishi S., Takizawa H., and Inui N. (1987) Mouse strain differences in the induction of micronuclei by polycyclic aromatic hydrocarbons. \i Mutation Res.\i0 \b 192\b0 , 185-187. \par \par Sato S. I., Takizawa H., and Inui N. (1993) Mouse strain differences in induction of micronuclei by base analogues and nucleosides. \i Mutation Research - Mutation Research Letters\i0 \b 301\b0 , 45-49. \par \par Satoh M., Kumar A., Kanwar Y. S., and Reeves W. H. (1995) Anti-nuclear antibody production and immune-complex glomerulonephritis in BALB/c mice treated with pristane. \i Proceedings of the National Academy of Sciences of the United States of America\i0 \b 92\b0 , 10934-10938. \par \par Scheller L. F., Wirtz R. A., and Azad A. F. (1994) Susceptibility of different strains of mice to hepatic infection with Plasmodium berghei. \i Infect. Immun.\i0 \b 62\b0 , 4844-4847. \par \par Scheller T., Orgacka H., Szumlanski C. L., and Weinshilboum R. M. (1996) Mouse liver nicotinamide N-methyltransferase pharmacogenetics: Biochemical properties and variation in activity among inbred strains. \i Pharmacogenetics\i0 \b 6\b0 , 43-53. \par \par Schlager G. (1968) Kidney weight in mice: strain differences and genetic determination. \i J. Hered.\i0 \b 59\b0 , 171-174. \par \par Schlager G. (1974) Selection for blood pressure levels in mice. \i Genetics\i0 \b 76\b0 , 537-549. \par \par Schlager G. (1981) Genetic hypertension in different strains of mice, in \i New trends in arterial hypertension\i0 (Worcel M., Bonvalet J. P., and Langer S. Z., eds), pp. 321-331. Elsevier/North Holland, Amsterdam. \par \par Schlager G. (1994) Genetic hypertension in the mouse, in \i Handbook of Hypertension Vol. 16 Experimental and Genetic Models of Hypertension\i0 (Ganten D. and de Jong W., eds), pp. 158-172. Elsevier, Amsterdam, New York, Oxford. \par \par Schlager G. and Dickie M. M. (1967) Spontaneous mutations and mutation rates in the house mouse. \i Genetics\i0 \b 57\b0 , 319-330. \par \par Schlager G. and Weibust R. S. (1967) Genetic control of blood pressure in mice. \i Genetics\i0 \b 55\b0 , 497-506. \par \par Schlager G (1974) Selection for blood pressure levels in mice. \i Genetics\i0 \b 76\b0 , 537-549. \par \par Schlesinger K. and Wimer R. (1967) Genotype and conditioned avoidance learning in the mouse. \i J. Comp. Physiol. Psychol.\i0 \b 63\b0 , 139-141. \par \par Schlom J., Michalides R., Kufe D., Hehlmann R., Spiegelman S., Bentvelzen P., and Hageman P. (1973) A comparative study of the biological and molecular basis of murine mammary carcinoma. A model for human breast cancer. \i J. Natl. Cancer Inst.\i0 \b 51\b0 , 541-551. \par \par Schmid F. A., Dickey P. A., Stanco G. A., and Tarnowski G. S. (1966) Toxicity of intraperitoneal injections of 7,1 2-dimethylbenz (a) anthracene (DMBA) and other agents in inbred mice.# Proc. Am. Assoc. \i Cancer Res.\i0 \b 7\b0 , 62. \par \par Schneider N. A., Lee J. M., and Olitsky P. K. (1957) Effect of nutrition on the production of acute disseminated encephelomyelitis in mice. \i J. Exp. Med.\i0 \b 105\b0 , 319-334. \par \par Schoenmakers C. H. H., Pigmans I. G. A. J., Poland A., and Visser T. J. (1993) Impairment of the selenoenzyme type I iodothyronine deiodinase in C3H/He mice. \i Endocrinol.\i0 \b 132\b0 , 357-361. \par \par Schrohenloher R. E. and Bailey P. C. (1972) Atypical immunoglobulins associated with spontaneous lymphomas in an inbred strain of mice. \i J. Natl. Cancer Inst.\i0 \b 49\b0 , 1027-1037. \par \par Schrott L. M. and Crnic L. S. (1996) Anxiety behavior, exploratory behavior, and activity in NZB x NZW F1 hybrid mice: Role of genotype and autoimmune disease progression. \i Brain Behav. & Immunity\i0 \b 10\b0 , 260-274. \par \par Schwartz R. H., Jackson L., and Paul W. E. (1975) T-lymphocyte-enriched murine peritoneal exudate cells. I. A reliable assay for antigen-induced T- lymphocyte proliferation. \i J. Immunol.\i0 \b 115\b0 , 1330-1338. \par \par Schwartz W. J. and Zimmerman P. (1990) Circadian timekeeping in BALB/c and C57BL/6 inbred mouse strains. \i Journal of Neuroscience\i0 \b 11\b0 , 3685-3694. \par \par Scott P., Eaton A., Gause W. C., Zhou X. D., and Hondowicz B. (1996) Early IL-4 production does not predict susceptibility to \i Leishmania major\i0 . \i Experimental Parasitology\i0 \b 84\b0 , 178-187. \par \par Searle C. E. and Jones E. L. (1972) Tumours of the nervous system in mice treated neonatally with N-ethyl-N-nitrosourea. \i Nature\i0 \b 240\b0 , 559-560. \par \par Searle C. E. and Spencer A. T. (1966) Induction of tumours of connective tissue by repeated applications of 4-nitroquinoline N-oxide to mouse skin. \i Brit. J. Cancer\i0 \b 20\b0 , 877-885. \par \par Sekirina G. G. and Neganova I. E. (1995) The microenvironment created by nonblocking embryos in aggregates may rescue blocking embryos via cell-embryo adherent contacts. \i Zygote\i0 \b 3\b0 , 313-324. \par \par Seller M. J. and Adinolfi M. (1981) The curley-tail mouse: an experimental model for human neural tube defects. \i Life Sci.\i0 \b 29\b0 , 1607-1615. \par \par Seller M. J., Beck S. E., Adinolfi M., and Polani P. E. (1981) Maternal environment and the expression of murine neural tube defects. \i Prenatal Diagnosis\i0 \b 1\b0 , 103-105. \par \par Seman G. and Dmochowski L. (1973) Viropexis of type B particles in reticulum cell sarcoma of RIII/Om strain mice. \i Cancer Res.\i0 \b 33\b0 , 1238-1246. \par \par Shaikh Z. A., Jordan S. A., and Tewari P. C. (1993) Cadmium disposition and metallothionein induction in mice: Strain-, sex-, age- and dose-dependent differences. \i Toxicology\i0 \b 80\b0 , 51-70. \par \par Shepard C. C. and Habas J. A. (1967) Relation of infection to tissue temperature in mice infected with Mycobacterium marinum and Mycobacterium leprae. \i J. Bacteriol.\i0 \b 93\b0 , 790-796. \par \par Sheppard J. R., Albersheim P., and McClearn G. E. (1968) Enzyme activities and ethanol preference in mice. \i Biochem. Genet.\i0 \b 2\b0 , 205-212. \par \par Sherman G. F., Stone L. V., Denenerg V. H., and Beier D. R. (1994) A genetic analysis of neocortical ectopias in New Zealand black autoimmune mice. \i Neuroreport\i0 \b 5\b0 , 721-724. \par \par Shih D. M., Gu L., Hama S., Xia Y. R., Navab M., Fogelman A. M., and Lusis A. J. (1996) Genetic-dietary regulation of serum paraoxonase expression and its role in atherogenesis in a mouse model. \i J. Clin. Invest.\i0 \b 97\b0 , 1630-1639. \par \par Shimada A., Ohta A., Akiguchi I., and Takeda T. (1993) Age-related deterioration in condition avoidance taks in the SAM-P/10 mouse, an animal model for spontaneous brain atrophy. \i Brain Res.\i0 \b 608\b0 , 266-272. \par \par Shimada M. O., Yamada Y., Nakakuki Y., Okamoto K., Fukumoto M., Honjo T., and Hiai H. (1993) SL/Kh strain mice: a novel animal model of pre B lymphomas. \i Leuk. Res.\i0 \b 17\b0 , 573-578. \par \par Shimada T. (1993) Correlation between metabolic and histopathological changes in the myocardium of the KK mouse. Effect of diltiazem on the diabetic heart. \i Jpn. Heart J.\i0 \b 34\b0 , 617-626. \par \par Shimkin M. B. and Stoner G. D. (1975) Lung tumours in mice: application to carcinogenesis bioassay. \i Adv. Cancer Res.\i0 \b 21\b0 , 1-58. \par \par Shimosato K., Saito T., and Marley R. J. (1994) Genotype-specific blockade of cocaine-induced weight loss by the protein synthesis inhibitor, anisomycin. \i Life Sciences\i0 \b 55\b0 , PL293-PL299. \par \par Shirai T. and Mellors R. C. (1972) Natural cytotoxic autoantibody against thymocytes in NZB mice. \i Clin. Exp. Immunol.\i0 \b 12\b0 , 133-152. \par \par Shire J. G. M. and Bartke A. (1972) Strain differences in testicular weight and spermatogenesis with special reference to C57BL/10J and DBA/2J mice. \i J. Endocrinol.\i0 \b 55\b0 , 163-171. \par \par Shoji R. R., Kimura R., Matsuda M., Yamada O., and Inouye E. (1984) Gene-environment interaction in MT mice manifesting exencephalia. \i Teratology\i0 \b 30\b0 , 19A. \par \par Sidman R. L., Kinney H. C., and Sweet H. O. (1985) Transmissable spongiform encephalopathy in the gray tremor mutant mouse. \i Proc. Natl. Acad. Sci. USA\i0 \b 82\b0 , 253-257. \par \par Silverstein E. (1961) Urine specific gravity and osmolality in inbred strains of mice. \i J. Appl. Physiol.\i0 \b 16\b0 , 194-196. \par \par Simpson E. M., Linder C. C., Sargent E. E., Davisson M. T., Mobraaten L. E., and Sharp J. J. (1997) Genetic variation among 129 substrains and its importance for targeted mutagenesis in mice. \i Nature Genet.\i0 \b 16\b0 , 19-27. \par \par Simpson L. O. (1976) An NZB virus or NZB mice with viral infections? \i Lab. Anim.\i0 \b 10\b0 , 249-260. \par \par Singh D. V., DeOme K. B., and Bern H. A. (1970) Strain differences in response of the mouse mammary gland to hormones in vitro. \i J. Natl. Cancer Inst.\i0 \b 45\b0 , 657-675. \par \par Sinha Y. M., Salocks C. B., and Vanderlaan W. P. (1975) Prolactin and growth hormone levels in different inbred strains of mice: patterns in association with estrous cycle, time of day and perphenazine stimulation. \i Endocrinol.\i0 \b 97\b0 , 1112-1122. \par \par Sipe J. D., Carreras I., Gonnerman W. A., Cathcart E. S., De Beer M. C., and De Beer F. C. (1993) Characterization of the inbred CE/J mouse strain as amyloid resistant. \i Am. J. Pathol.\i0 \b 143\b0 , 1480-1485. \par \par Slingsby J. H., Hogarth M. B., Simpson E., Walport M. J., and Morley B. J. (1996) New microsatellite polymorphisms identified between C57BL-6, C57BL- 10, and C57BL-KsJ inbred mouse strains. \i Immunogenet.\i0 \b 43\b0 , 72-75. \par \par Smith A. G. and Francis J. E. (1993) Genetic variation of iron-induced uroporphyria in mice. \i Biochem. J.\i0 \b 291\b0 , 29-35. \par \par Smith A. M. (1976) The effects of age on the immune response to type III pneumococcal polysaccharide (SIII) and bacterial lipopolysaccharide (LPS) in BALB/c, SJL/J and C3H mice. \i J. Immunol.\i0 \b 116\b0 , 469-474. \par \par Smith B. K., West D. B., and York D. A. (1997) Carbohydrate versus fat intake: Differing patterns of macronutrient selection in two inbred mouse strains. \i American Journal of Physiology-Regulatory Integrative and Comparative Physiology\i0 \b 41\b0 , R357-R362. \par \par Smith G. S. and Pilgrim H. I. (1971) Spontaneous neoplasms in germfree BALB/cPi mice.# Proc. Soc. Exp. Biol. Med., 138,542-544 # Smith, A.M. (1976). The effects of age on the immune response to type III pneumococcal polysaccharide (SIII) and bacterial lipopolysaccharide (LPS) in BALB/c, SJL/J and C3H mice. \i J. Immunol.\i0 \b 116\b0 , 469-474. \par \par Smith G. S., Walford R. L., and Mickey R. M. (1973) Lifespan and incidence of cancer and other diseases in selected long-lived inbred mice and their F1 hybrids. \i J. Natl. Cancer Inst.\i0 \b 50\b0 , 1195-1213. \par \par Smith R. M., Morgan A., and Wraith D. C. (1994) Anticlass-II MHC antibodies prevent and treat EAE without depletion. \i Immunol.\i0 \b 83\b0 , 1-8. \par \par Smith S. M., Forbes P. D., and Linna T. J. (1982) Immune responses in nonhaired mice. \i Int. Arch. Allergy Appl. Immunol.\i0 \b 67\b0 , 254. \par \par Sokoloff L. and Haberman R. T. (1958) Idiopathic necrosis of bone in small animals. \i Arch. Pathol.\i0 \b 65\b0 , 323-330. \par \par Sokoloff L., Crittenden L., Yamamoto R., and Jay G. E. (1962) The genetics of degenerative joint disease in mice. \i Arthritis Rheum.\i0 \b 5\b0 , 531-564. \par \par Southwick C. H. and Clark L. H. (1966) Aggressive behaviour and exploratory activity in fourteen mouse strains. \i Am. Zool.\i0 \b 6\b0 , 559. \par \par Southwick C. H. and Clark L. H. (1968) Interstrain differences in aggressive behaviour and exploratory activity of inbred mice. \i Commun. Behav. Biol. Part A\i0 \b 1\b0 , 49-59. \par \par Spalding J. F. and Brooks M. R. (1971) The possible influence of a single gene locus on lifespan and its relationship to radiation resistance and activity. \i Proc. Soc. Exp. Biol. Med.\i0 \b 136\b0 , 1091-1093. \par \par Spurney R. F., Onorato J. J., Ruiz P., Pisetsky D. S., and Coffman T. M. (1993) Characterization of glomerular thromboxane receptors in murine lupus nephritis. \i J. Pharmacol. Exp. Therapeut.\i0 \b 264\b0 , 584-590. \par \par Srivastava R. A. K. (1995) Increased apoB100 mRNA in inbred strains of mice by estrogen is caused by decreased RNA editing protein mRNA. \i Biochemical and Biophysical Research Communications\i0 \b 212\b0 , 381-387. \par \par Staats J. (1976) Standardized nomenclature for inbred strains of mice: Sixth listing. \i Cancer Res.\i0 \b 36\b0 , 4333-4377. \par \par Stasik J. H. (1970) Inheritance of T-maze learning in mice. \i J. Comp. Physiol. Psychol.\i0 \b 71\b0 , 251-257. \par \par Stauffacher W., Orci L., Cameron D. P., Burr I. M., and Renold A. E. (1971) Spontaneous hyperglycemia and/or obesity in laboratory rodents: an example of the possible usefulness of animal disease models with both genetic and environmental components. \i Recent Prog. Horm. Res.\i0 \b 27\b0 , 41-91. \par \par Steinberg A. D., Pincus T., and Talal N. (1971) The pathogenesis of autoimmunity in New Zealand mice. III. Factors influencing the formation of anti-nucleic acid antibodies. \i Immunol.\i0 \b 20\b0 , 523-531. \par \par Stephenson J. R., Reynolds R. K., Tronick S. R., and Aaronson S. A. (1975) Distribution of three classes of endogenous type-C RNA viruses among inbred strains of mice. \i Virology\i0 \b 67\b0 , 404-414. \par \par Stevens L. C. (1973) A new inbred subline of mice (129/ter, Sv) with a high incidence of spontaneous congenital testicular teratomas. \i J. Natl. Cancer Inst.\i0 \b 50\b0 , 235-242. \par \par Stevens L. C. and Varnum D. S. (1974) Development of teratomas from parthenogenetically activated ovarian mouse eggs. \i Devel. Biol.\i0 \b 37\b0 , 369-380. \par \par Stewart-Phillips J. L. and Lough J. (1991) Pathology of atherosclerosis in cholesterol-fed, susceptibile mice. \i Atherosclerosis\i0 \b 90\b0 , 211-218. \par \par Stirling P., Tullo A. B., Blyth W. A., and Hill T. J. (1983) Retinal degeneration in NIH (inbred) mice. \i Exp. Eye Res.\i0 \b 36\b0 , 761-763. \par \par Storer J. B. (1966) Longevity and gross pathology at death in 22 inbred strains of mice. \i J. Gerontol.\i0 \b 21\b0 , 404-409. \par \par Storer J. B. (1967) Relation of lifespan to brain weight, body weight and metabolic rate among inbred mouse strains. \i Exp. Gerontol.\i0 \b 2\b0 , 173-182. \par \par Stranden A. M., Staeheli P., and Pavlovic J. (1993) Function of the mouse Mx1 protein is inhibited by overexpression of the PB2 protein of influenza virus. \i Virology\i0 \b 197\b0 , 642-651. \par \par Stravoravdi P., Toliou T., and Polyzonis M. B. (1991) A new approach combining interferon and bromocriptine LA to prevent spontaneous mouse mammary carcinoma. \i Journal of Interferon Research\i0 \b 11\b0 , 49-51. \par \par Strong L. C. (1952) Differences in response among mice of fifteen inbred strains to the subcutaneous injection of methylcholanthrene. \i Yale J. Biol. Med.\i0 \b 25\b0 , 34-43. \par \par Strozik E. and Festing M. F. W. (1981) Whisker trimming in mice. \i Lab. Anim.\i0 \b 15\b0 , 309-312. \par \par Stutman O. (1974) Cell-mediated immunity and aging. \i Fed. Proc.\i0 \b 33\b0 , 2028-2032. \par \par Styrna J., Imai H. T., and Moriwaki K. (1991) An increased level of sperm abnormalities in mice with a partial deletion of the Y chromosome. \i Genet. Res.\i0 \b 57\b0 , 195-199. \par \par Sudo K. and Suzuki K. (1987) Establishment of new inbred nude strain. \i Mouse N.L.\i0 \b 79\b0 , 13. \par \par Sudo K., Suzuki K., Matsumoto K., Furuya T., and Kurokawa W. (1989) Characteristics of the KSN inbred mice: a strain of self-perpetuating nude mice, in \i Immune-Defficient Animals in Experimental Medicine\i0 (Wu B.-Q. and Zheng J., eds), pp. 45-49. Karger, Basil. \par \par Sundberg J. P., Adkison D. L., and Bedigian H. G. (1991a) Skeletal muscle rhabdomyosarcomas in inbred laboratory mice. \i Vet. Pathol.\i0 \b 28\b0 , 200-206. \par \par Sundberg J. P., Hanson C. A., Roop D. R., Brown K. S., and Bedigian H. G. (1991b) Myoepitheliomas in inbred laboratory mice. \i Vet. Pathol.\i0 \b 28\b0 , 313-323. \par \par Suran A. A. (1973) Hypoxanthine-guanine phorphoribosyl transferase in brains of mice. Regional distribution in seven inbred mouse strains. \i Life Sci.\i0 \b 13\b0 , 1779-1788. \par \par Surwit R. S., Seldin M. F., Kuhn C. M., Cochrane C., and Feinglos M. N. (1991) Control of expression of insulin resistance and hyperglycemia by different genetic factors in diabetic C57BL/6J mice. \i Diabetes\i0 \b 40\b0 , 82-87. \par \par Surwit R. S., Feinglos M. N., Rodin J., Sutherland A., Petro A. E., Opara E. C., Kuhn C. M., and Rebuffe-Scrive M. (1995) Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and A/J mice. \i Metabolism: Clinical and Experimental\i0 \b 44\b0 , 645-651. \par \par Suto J., Wakayama T., Imamura K., Goto S., and Fukuta K. (1996) High lethality of F1 (dh/+) male-mice from the cross between DDD female and Dh (Dh/+) male. \i Exp. Anim.\i0 \b 45\b0 , 99-101. \par \par Sweet H. O., Bronson R. T., Johnson K. R., Cook S. A., and Davisson M. T. (1996) Scrambler, a new neurological mutation of the mouse with abnormalities of neuronal migration. \i Mamm. Genome\i0 \b 7\b0 , 798-802. \par \par Szabo K. T. and Steelman B. A. (1967) Effects of thalidomide treatment of inbred female mice on pregnancy, fetal development, and mortality of offspring. \i Am. J. Vet. Res.\i0 \b 28\b0 , 1829-1835. \par \par Szepsenwol J. and Boschetti N. V. (1975) Primary and secondary heart tumors in mice maintained on various diets. \i Oncology\i0 \b 32\b0 , 58-72. \par \par Tajima Y. (1968) Stansardized nomenclature for inbred strains of mice. Experimental animals in cancer research. \i Japanese Cancer Association Gann Monograph\i0 \b 5\b0 , 123-128. \par \par Takahashi M., Kleeberger S. R., and Croxton T. L. (1995) Genetic control of susceptibility to ozone-induced changes in mouse tracheal electrophysiology. \i American Journal of Physiology - Lung Cellular and Molecular Physiology\i0 \b 269\b0 , L6-L10. \par \par Takeda T., ed (1994) \i The SAM model of senescence\i0 . Excerpta Medica, Amsterdam, New York, Oxford, Tokyo. \par \par Takeda T., Hosokawa M., Takeshita S., Irino M., Higuchi K., Matsushita T., Tomita Y., Yasuhira K., Hamamoto H., Shimizu K., Ishii M., and Yamamuro T. (1981) A new murine model of accelerated senescence. \i Mech. Ageing Dev.\i0 \b 17\b0 , 183-194. \par \par Takeda T., Hosokawa M., and Higuchi K. (1991) Senescence-accelerated mouse (SAM): A novel murine model of accelerated senescence. \i J. Amer. Geriatr. Soc.\i0 \b 39\b0 , 911-919. \par \par Takeda T., Hosokawa M., and Higuchi K. (1997) Senescence-accelerated mouse (SAM): A novel murine model of senescence. \i Exp. Gerontol.\i0 \b 32\b0 , 105-109. \par \par Taketo M., Schroeder A. C., Mobraaten L. E., Gunning K. B., Hanten G., Fox R. R., Roderick T. H., Stewart C. L., Lilly F., Hansen C. T., and Overbeek P. A. (1991) FVB/N: An inbred mouse strain preferable for transgenic analyses. \i Proc. Natl. Acad. Sci. USA\i0 \b 88\b0 , 2065-2069. \par \par Taketomi S., Tsuda M., Matsuo T., Iwatsuka H., and Suzuoki Z. (1973) Alterations of hepatic enzyme activities in KK and yellow KK mice with various diabetic states. \i Hormone Metab. Res.\i0 \b 5\b0 , 333-339. \par \par Talal N., Sternberg A. D., and Staples P. L. (1972) Immunological hyperactivity in New Zealand mice, in \i Tolerance, Autoimmunity and Aging\i0 (Sigel M. M. and Good R. A., eds), pp. 127-131. Thomas, Springfiled, Ill. \par \par Tam P. E. and Messner R. P. (1996) Genetic-determinants of susceptibility to coxsackievirus B1-induced chronic inflammatory myopathy - effects of host background and major histocompatibility complex genes. \i Journal of Laboratory and Clinical Medicine\i0 \b 128\b0 , 279-289. \par \par Tanaka S. and Matsuzawa A. (1990) The history of the "deutsche maus", the origin of the dd mouse group. [Review] [Japanese]. \i Jikken Dobutsu - Experimental Animals\i0 \b 39\b0 , 141-153. \par \par Tanaka S., Sato M., Taniguchi T., and Yokomizo Y. (1994) Histopathological and morphometrical comparison of granulomatous lesions in BALB/c and C3H/HeJ mice inoculated with Mycobacterium paratuberculosis. \i J. Comp. Pathol.\i0 \b 110\b0 , 381-388. \par \par Tanioka Y. and Esaki K. (1971) Strain differences in mortality of anaphylactic shock in mice-challenging by intravenous injection. \i Exp. Animals (Japan)\i0 \b 20\b0 , 127-130. \par \par Tankersley C. G., Fitzgerald R. S., and Kleeberger S. R. (1994) Differential control of ventilation among inbred strains of mice. \i American Journal of Physiology - Regulatory Integrative and Comparative Physiology\i0 \b 267\b0 , R1371-R1377. \par \par Tankersley C. G., Fitzgerald R. S., Levitt R. C., Mitzner W. A., Ewart S. L., and Kleeberger S. R. (1997) Genetic control of differential baseline breathing pattern. \i J. Appl. Physiol.\i0 \b 82\b0 , 874-881. \par \par Tateda K., Takashima K., Miyazaki H., Matsumoto T., Hatori T., and Yamaguchi K. (1996) Noncompromised penicillin-resistant pneumococcal pneumonia CBA/J mouse model and comparative efficacies of antibiotics in this model. \i Antimicrobial Agents & Chemotherapy\i0 \b 40\b0 , 1520-1525. \par \par Taylor B. A. (1972) Genetic relationship between inbred strains of mice. \i J. Hered.\i0 \b 63\b0 , 83-86. \par \par Taylor B. A. (1976) Genetic analysis of susceptibility to isoniazid-induced seizures in mice. \i Genetics\i0 \b 83\b0 , 373-377. \par \par Taylor B. A., Navin A., and Phillips S. J. (1994) PCR-amplification of simple sequence repeat variants from pooled DNA samples for rapidly mapping new mutations of the mouse. \i Genomics\i0 \b 21\b0 , 626-632. \par \par Taylor D. M. and Fraser H. (1973) Hydronephrosis in inbred strains of mice with particular reference to the BRVR strain. \i Lab. Anim.\i0 \b 7\b0 , 229-236. \par \par Taylor D. M. and Fraser H. (1975) The association of Proteus mirabilis with pylonephritis in male MM mice. \i Proc. Soc. Gen. Microbiol.\i0 \b 3\b0 , 15. \par \par Teague P. O., Friou G. J., Yunis E. J., and Good R. A. (1972) Spontaneous autoimmunity in aging mice, in \i Tolerance, Autoimmunity and Aging\i0 (Sigel M. M. and Good R. A., eds), pp. 36-61. Thomas, Springfield, Ill. \par \par Tengbergen W. J. P. R. van E. (1970) Morphological classification of mammary tumours in the mouse. \i Path. Eur.\i0 \b 5\b0 , 260-272. \par \par Tennant J. R. (1965) Susceptibility and resistance to viral leukemogenesis in the mouse. I. Biological definition of the virus. \i J. Natl. Cancer Inst.\i0 \b 34\b0 , 625-632. \par \par Teramoto S., Fukuchi Y., Uejima Y., Teramoto K., Oka T., and Orimo H. (1994) A novel model of senile lung: Senescence-accelerated mouse (SAM). \i American Journal of Respiratory and Critical Care Medicine\i0 \b 150\b0 , 238-244. \par \par Theofilopoulos A. N., McConahey P. J., Izui S., Eisenberg R. A., Pereira A. B., and Creighton W. D. (1980) A comparitive immunologic analysis of several murine stains with autoimmune manifestations. \i Clin. Immunol. Immunopathol.\i0 \b 15\b0 , 258-278. \par \par Thimme R., Frese M., Kochs G., and Haller O. (1995) Mx1 but not MxA confers resistance against tick-borne Dhori virus in mice. \i Virology\i0 \b 211\b0 , 296-301. \par \par Thomas P. E., Hutton J. J., and Taylor B. A. (1973) Genetic relationship between aryl hydrocarbon hydroxylase inducibility and chemical carcinogen induced skin ulceration in mice. \i Genetics\i0 \b 74\b0 , 655-659. \par \par Thompson J. S. (1968) Atherosclerosis in inbred strains of mice. \i Anat. Res.\i0 \b 160\b0 , 440. \par \par Thompson W. R. (1953) The inheritance of behaviour: behavioural differences in fifteen mouse strains. \i Can. J. Psychol.\i0 \b 7\b0 , 145-155. \par \par Thorburn A., Andrikopoulos S., and Proietto J. (1995) Defects in liver and muscle glycogen metabolism in neonatal and adult New Zealand obese mice. \i Metabolism: Clinical and Experimental\i0 \b 44\b0 , 1298-1302. \par \par Threadgill D. W., Yee D., Matin A., Nadeau J. H., and Magnuson T. (1997) Genealogy of the 129 inbred strains: 129/SvJ is a contaminated inbred strain. \i Mamm. Genome\i0 \b 8\b0 . \par \par Toda S., Kimura M., and Tohya K. (1989) Strain differences in histamine release from mouse peritoneal mast cells induced by compound 48/80 or A23187. \i Jikken Dobutsu - Experimental Animals\i0 \b 38\b0 , 135-137. \par \par Tokunaga Y., Hiramine C., Itoh M., Mukasa A., and Hojo K. (1993) Genetic susceptibility to the induction of murine experimental autoimmune orchitis (EAO) without adjuvant. I. Comparison of pathology, delayed type hypersensitivity, and antibody. \i Clin. Immunol. Immunopathol.\i0 \b 66\b0 , 239-247. \par \par Tom C., Juriloff D. M., and Harris M. J. (1991) Studies of the effect of retinoic acid on anterior neural-tube closure in mice genetically liable to exencephaly. \i Teratology\i0 \b 43\b0 , 27-40. \par \par Treadwell P. E. (1969) The inheritance of susceptibility to anaphylaxis in inbred mice and their hybrid progenies. \i J. Reticuloendothel. Soc.\i0 \b 6\b0 , 343-353. \par \par Troyer D. A., Chandrasekar B., Barnes J. L., and Fernandes G. (1997) Calorie restriction decreases platelet-derived growth factor (PDGF)-A and thrombin receptor mRNA expression in autoimmune murine lupus nephritis. \i Clin. Exp. Immunol.\i0 \b 108\b0 , 58-62. \par \par Trune D. R., Kempton J. B., and Mitchell C. (1996) Auditory function in the C3H/HeJ and C3H/HeSnJ mouse strains. \i Hearing Research\i0 \b 96\b0 , 41-45. \par \par Tsao J. W., Brown M. C., Carden M. J., McLean W. G., and Perry V. H. (1994) Loss of the compound action potential: An electrophysiological, biochemical and morphological study of early events in axonal degeneration in the C57BL/Ola mouse. \i European Journal of Neuroscience\i0 \b 6\b0 , 516-524. \par \par Tsubura A., Senzaki H., Oyaizu T., Fujita Y., and Morii S. (1993) Strain differences in neoplastic response to DMBA-induced uterine vascular tumors in mice. \i International Journal of Oncology\i0 \b 2\b0 , 927-930. \par \par Tsumura H., Komada H., Ito Y., and Shimura K. (1989) In vitro and in vivo interferon production in NOD mice. \i Lab. Animal Sci.\i0 \b 39\b0 , 575-578. \par \par Tucker P. K., Lee B. K., Lundrigan B. L., and Eicher E. M. (1992) Geographic origin of the Y chromosomes in "old" inbred strains of mice. \i Mamm. Genome\i0 \b 3\b0 , 254-261. \par \par Tunnicliff G., Wimer C. C., and Wimer R. E. (1973) Relationships between neurotransmitter metabolism and behaviour in seven inbred strains of mice. \i Brain Res.\i0 \b 61\b0 , 428-434. \par \par Turusov V. S., Morozova O. V., and Samoilov D. V. (1994) Estrogen modification of 1,2-dimethylhydrazine carcinogenesis in C3HA mice. \i Cancer Lett.\i0 \b 83\b0 , 51-58. \par \par Ueda H., Ikegami H., Yamato E., Fu J., Fukuda M., Shen G., Kawaguchi Y., Takekawa K., Fujioka Y., Fujisawa T., Nakagawa Y., Hamada Y., Shibata M., and Ogihara T. (1995) The NSY mouse: A new animal model of spontaneous NIDDM with moderate obesity. \i Diabetologia\i0 \b 38\b0 , 503-508. \par \par Upton A. C., Conklin J., Cosgrove G., Gude W. D., and Darden E. B. (1967) Necrotizing polyarteritis in aging RF mice. \i Lab. Invest.\i0 \b 16\b0 , 483-487. \par \par Vadasz C., Fleischer A., Lafrancois J., and Mao R. F. (1996) Self-administration of ethanol - towards the location of predisposing polygenes in quasi-congenic animal-models. \i Alcohol\i0 \b 13\b0 , 617-620. \par \par Valatx J. L. and Bugat R. (1974) Facteurs g\'8e n\'8e tiques dans le determinisme du cycle veille-sommeil chez la souris. \i Brain Res.\i0 \b 69\b0 , 315-330. \par \par van Abeelen J. H. F. (1975) Genetic analysis of behavioural responses to novelty in mice. \i Nature\i0 \b 254\b0 , 239-241. \par \par Van den Broek F. A. R., Omitzigt C. M., and Beynen A. C. (1993) Whisker trimming behaviour in A2G mice is not prevented by offering means of withdrawal from it. \i Lab. Anim.\i0 \b 27\b0 , 270-272. \par \par van der Gugten A. A., Ropcke G., van Nie R., and Hilgers J. (1985) Mouse strain (STS/A) resistant to mammary tumor induction by hypophysial isografts. \i Cancer Res.\i0 \b 45\b0 , 3448-3453. \par \par Van Heyningen H. E. (1961) Differences in thyroid function of several strains of mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 106\b0 , 37-40. \par \par Van Iersel M., Walters D. G., Price R. J., Lovell D. P., and Lake B. G. (1994) Sex and strain differences in mouse hepatic microsomal coumarin 7- hydroxylase activity. \i Food and Chemical Toxicology\i0 \b 32\b0 , 387-390. \par \par van Nie R. and Hilgers J. (1976) Genetic analysis of mammary tumor induction and expression of mammary tumor virus antigen in hormone- treated ovariectomized GR mice. \i J. Natl. Cancer Inst.\i0 \b 56\b0 , 27-32. \par \par van Nie R. and Thung P. J. (1965) Responsiveness of mouse mammary tumours to pregnancy. \i Eur. J. Cancer\i0 \b 1\b0 , 41-50. \par \par Vaz N. M., Phillips-Quagliata J. M., Levine B. B., and Vaz E. M. (1971) H-2 linked genetic control of immune responsiveness to ovalbumin and ovomucoid. \i J. Exp. Med.\i0 \b 134\b0 , 1335-1348. \par \par Verley F. A., Grahn D., Leslie W. P., and Hamilton K. F. (1967) Sex ratio of mice as possible indicator of mutation rate for sex-linked lethals. \i J. Hered.\i0 \b 58\b0 , 285-290. \par \par Vesell E. S. (1968) Factors altering the responsiveness of mice to hexobarbital. \i Pharmacology\i0 \b 1\b0 , 81-97. \par \par Vetvicka V., Vonkova J., and Rihova B. (1993) Effect of age on antibody responses in low responder C57BL/10ScSn and high responder A/J strains of mice. \i Mechanisms of Ageing and Development\i0 \b 71\b0 , 131-141. \par \par Vieten G., Grams B., Muller M., Hartung K., and Emmendorffer A. (1996) Examination of the mononuclear phagocyte system in lupus-prone male BXSB mice. \i J. Leukocyte Biol.\i0 \b 59\b0 , 325-332. \par \par Viklicky V. (1967) High frequency of mast cells in spleens of A-strain mice. \i Experientia\i0 \b 23\b0 , 194-195. \par \par Villalpandofierro I., Villafanmonroy H., and Pacheco P. (1996) Delayed expression of the insulin-like growth-factor-I (IGF-I) gene in the XY sex-reversed female mouse ovary. \i International Journal of Developmental Biology\i0 \b 40\b0 , 477-482. \par \par Virgo N. S. and Miller J. R. (1974) Hereditary vasopressin-resistant diabetes insipidus in SWV mice. \i Can. J. Physiol. Pharmacol.\i0 \b 52\b0 , 995-1011. \par \par Vladutiu A. O. and Rose N. R. (1971) Genetic influence on experimental autoimmune thyroiditis in mice. \i Fed. Proc.\i0 \b 30\b0 , 306. \par \par Vlahakis G., Heston W. E., and Smith G. H. (1970) Strain C3H-AvyfB mice: ninety percent incidence of mammary tumours transmitted by either parent. \i Science\i0 \b 170\b0 , 185-187. \par \par Vogel S. N., Weinblatt A. C., and Rosenstreich D. L. (1981) Inherent macrophage defects, in \i Immunologic defects in laboratory animals Vol. 1\i0 (Gershwin M. E. and Merchant B., eds), pp. 327-357. Plenum Press, New York, London. \par \par Vogelweid C. M., Vogt D. W., Besch-Williford C. L., and Walker S. E. (1993) New Zealand white mice: an experimental model of exencephaly. \i Lab. Animal Sci.\i0 \b 43\b0 , 58-60. \par \par von Krischke W. and Graffi A. (1962) Weitere versuche zur abhangigkeit der Wirkung des virus der myeloischen leukamie der Maus von versuchiedenen biologischen Bedingangen der infizierten tiere. \i Arch. Geschwulstforsch.\i0 \b 20\b0 , 22-29. \par \par von Magdon E. (1962) Untersuchungen der katalaseaktivitat des Blutes vershiedener Mausestamme. \i Z. Versuchstierk.\i0 \b 1\b0 , 173-178. \par \par Vyse T. J., Drake C. G., Rozzo S. J., Roper E., Izui S., and Kotzin B. L. (1996) Genetic linkage of IgG autoantibody production in relation to lupus nephritis in New Zealand hybrid mice. \i J. Clin. Invest.\i0 \b 98\b0 , 1762-1772. \par \par Waalkes M. P. and Rehm S. (1994) Carcinogenic and chronic toxic effects of single and multiple subcutaneous doses of cadmium chloride in male BALB/c mice. \i Toxic Substances Journal\i0 \b 13\b0 , 97-111. \par \par Wahlsten D. (1973) Contribution of the genes albinism (c) and retinal degeneration (rd) to a strain-by-training procedure interaction in avoidance learning. \i Behav. Genet.\i0 \b 3\b0 , 303-316. \par \par Wahlsten D. (1974) Heritable aspects of anomalous myelinated fibre traits in the forebrain of the laboratory mouse. \i Brain Res.\i0 \b 68\b0 , 1-18. \par \par Wahlsten D. and BulmanFleming B. (1994) Retarded growth of the medial septum: A major gene effect in acallosal mice. \i Developmental Brain Research\i0 \b 77\b0 , 203-214. \par \par Wahlsten D. and Schalomon P. M. (1994) A new hybrid mouse model for agenesis of the corpus callosum. \i Behavioural Brain Research\i0 \b 64\b0 , 111-117. \par \par Wahlsten D., Hudspeth W. J., and Bernhardt K. (1975) Implications of genetic variation in mouse brain structure for electrode placement by stereotoxic surgery. \i J. Comp. Neurol.\i0 \b 162\b0 , 519-532. \par \par Wajjwalku W., Takahashi M., Miyaishi O., Lu J., Sakata K., Yokoi T., Saga S., Imai M., Matsuyama M., and Hoshino M. (1991) Tissue distribution of mouse mammary tumor virus (MMTV) antigens and new endogenous MMTV loci in Japanese laboratory mouse strains. \i Jpn. J. Cancer Res.\i0 \b 82\b0 , 1413-1420. \par \par Wakasugi N. (1973) Studies on fertility of DDK mice: reciprocal crosses between DDK and C57BL/6J strains and experimental transplantation of the ovary. \i J. Reprod. Fertil.\i0 \b 33\b0 , 283-291. \par \par Wakelin D. and Donachie A. M. (1980) Genetic control of immunity to parasites: adoptive transfer of immunity between inbred strains of mice characterized by rapid and slow immune expulsion of Trichinella spiralis. \i Parasite Immunol.\i0 \b 2\b0 , 249-260. \par \par Walburg H. E. and Cosgrove G. E. (1971) Methycholanthrene-induced neoplasms in germfree RFM mice. \i Int. J. Cancer\i0 \b 8\b0 , 338-343. \par \par Wallace M. E. (1970) An unprecedented number of mutants in a colony of wild mice. \i Environmental Pollution\i0 \b 1\b0 , 175-184. \par \par Wallace M. E. (1985) An inherited agent of mutation with chromosome damage in wild mice. \i J. Hered.\i0 \b 76\b0 , 271-278. \par \par Walton J. P., Frisina R. D., and Meierhans L. R. (1995) Sensorineural hearing loss alters recovery from short-term adaptation in the C57BL/6 mouse. \i Hearing Research\i0 \b 88\b0 , 19-26. \par \par Walton M. (1979) Obesity as an aetiological factor in the development of osteoarthrosis. \i Gerontol.\i0 \b 25\b0 , 36-41. \par \par Walton M. (1977a) Degenerative joint disease in the mouse knee; histological observations. \i J. Pathol.\i0 \b 123\b0 , 109-122. \par \par Walton M. (1977b) Degenerative joint disease in the mouse knee; radiological and morphological observations. \i J. Pathol.\i0 \b 123\b0 , 97-107. \par \par Walton M. (1979a) Bone thickening in osteoarthrosis. \i Acta Orthop. Scand.\i0 \b 50\b0 , 501-506. \par \par Walton M. (1979b) Patella displacement and osteoarthrosis of the knee joint in mice. \i J. Pathol.\i0 \b 127\b0 , 165-172. \par \par Wanebo H. J., Gallmier W. M., Boyse E. A., and Old L. J. (1966) Paraproteinemia and reticulum cell sarcoma in an inbred mouse strain. \i Science\i0 \b 154\b0 , 901-903. \par \par Wang Y., Burnier M., Detrick B., and Hooks J. J. (1996) Genetic predisposition to coronavirus-induced retinal disease. \i Investigative Ophthalmology & Visual Science\i0 \b 37\b0 , 250-254. \par \par Ware L. M. and Axelrad A. A. (1972) Inherited resistance to N- and B-tropic murine leukemia viruses in vitro: evidence that congenic mouse strains SIM and SIM.R differ at the Fv-1 locus. \i Virology\i0 \b 50\b0 , 339-348. \par \par Warner N. L. (1971) Spontaneous hydronephrosis in the inbred mouse strain NZC. \i Aust. J. Exp. Biol. Med. Sci.\i0 \b 49\b0 , 477-486. \par \par Waters N. S., Sherman G. F., Galaburda A. M., and Denenberg V. H. (1997) Effects of cortical ectopias on spatial delayed-matching-to-sample performance in BXSB mice. \i Behavioural Brain Research\i0 \b 84\b0 , 23-29. \par \par Waymouth C. (1973) Erythrocyte sodium and potassium levels in normal and anaemia mice. \i Comp. Biochem. Physiol.\i0 \b 44A\b0 , 751-766. \par \par Webster L. T. (1933a) Inheritance and acquired factors in resistance to infection. I. Development of resistant and susceptible lines of mice through selective breeding. \i J. Exp. Med.\i0 \b 57\b0 , 793-817. \par \par Webster L. T. (1933b) Inheritance and acquired factors in resistance to infection. II. A comparison of mice inherently resistant or susceptible to Bacillus enteritidis infection with respect to fertility, weight and susceptibility to various routes and types of infection. \i J. Exp. Med.\i0 \b 57\b0 , 819-843. \par \par Webster L. T. (1937) Inheritance of resistance of mice to enteric bacterial and neurotropic virus infections. \i J. Exp. Med.\i0 \b 65\b0 , 261-286. \par \par Weghorst C. M., Devor D. E., Henneman J. R., and Ward J. M. (1994) Promotion of hepatocellular foci and adenomas by di(2-ethylhexyl) phthalate and phenobarbital in C3H/HeNCr mice following exposure to N-nitrosodiethylamine at 15 days of age. \i Experimental and Toxicologic Pathology\i0 \b 45\b0 , 423-431. \par \par Wehner J. M., Pounder J. I., and Bowers B. J. (1991) The use of recombinant inbred strains to study mechanisms of drug action. \i J. Addict. Dis.\i0 \b 10\b0 , 89-107. \par \par Weibust R. S. (1973) Inheritance of plasma cholesterol levels in mice. \i Genetics\i0 \b 73\b0 , 303-312. \par \par Weir J. A. (1962) Hereditary and environmental influences on the sex ratio of PHH and PHL mice. \i Genetics\i0 \b 47\b0 , 881-897. \par \par Weir J. A. and Clark R. D. (1955) Production of high and low blood-pH lines of mice by selection with inbreeding. \i J. Hered.\i0 \b 46\b0 , 125-132. \par \par Weniger et al. (1974) Modellversuche zur Selektion auf Belastbarkeit in ihrer Beziehung zum Wachstum. \i J. Anim. Breed. Geneti.\i0 \b 91\b0 , 265-270. \par \par West D. B., Boozer C. N., Moody D. L., and Atkinson R. L. (1992) Dietary obesity in nine inbred mouse strains. \i Am. J. Physiol.\i0 \b 262\b0 , R1025-R1032. \par \par West D. B., Waguespack J., and McCollister S. (1995) Dietary obesity in the mouse: Interaction of strain with diet composition. \i American Journal of Physiology - Regulatory Integrative and Comparative Physiology\i0 \b 268\b0 , R658-R665. \par \par White B. J. and Tjio J.-H. (1975) AL/N: A homozygous Robertsonian translocation mouse strain identical to TlWh. \i Cytologia\i0 \b 40\b0 , 249-252. \par \par Whitmire C. E. and Salerno R. A. (1972) RNA tumour virus antigen and tumour induction by various doses of 3-methylcholanthrene in various strains of mice treated as weanlings. \i Cancer Res.\i0 \b 32\b0 , 1129-1132. \par \par Whitmire C. E., Salerno R. A., Rabstein L. S., Heubner R. J., and Turner H. C. (1971) RNA tumour-virus antigen expression in chemically induced tumours. Virus-genome specified common antigens detected by complement fixation in mouse tumours induced by 3-methylcholanthrene. \i J. Natl. Cancer Inst.\i0 \b 47\b0 , 1255-1265. \par \par Wicker L. S., Miller B. J., Fischer P. A., Pressey A., and Peterson L. B. (1989) Genetic control of diabetes and insulitis in the nonobese diabetic mouse. Pedigree analysis of a diabetic H-2\up8 nod\up0 /b heterozygote. \i J. Immunol.\i0 \b 142\b0 , 781-784. \par \par Wigley R. D., Craig A. S., Williamson K. I., and Couchman K. G. (1975) Spontaneous arteritis and glomerulitis in mice: a comparison of light and electron microscope renal changes in PN/n, NZB/Bl, 101/Mac and CBA/Mac mice. \i Lab. Invest.\i0 \b 33\b0 , 8-15. \par \par Willerson J. T., Asofsky R., and Barth W. F. (1969) Experimental murine amyloid. IV amyloidosis and immunoglobulins. \i J. Immunol.\i0 \b 103\b0 , 741-749. \par \par Williams N. M. and Timoney P. J. (1994) Variation in susceptibility of ten mouse strains to infection with a strain of Ehrlichia risticii. \i J. Comp. Pathol.\i0 \b 110\b0 , 137-143. \par \par Williams R. W., Strom R. C., Rice D. S., and Goldowitz D. (1996) Genetic and environmental-control of variation in retinal ganglion-cell number in mice. \i Journal of Neuroscience\i0 \b 16\b0 , 7193-7205. \par \par Willott J. F., Aitkin L. M., and McFadden S. L. (1993) Plasticity of auditory cortex associated with sensorineural hearing loss in adult C57BL/6J mice. \i J. Comp. Neurol.\i0 \b 329\b0 , 402-411. \par \par Willott J. F., Erway L. C., Archer J. R., and Harrison D. E. (1995) Genetics of age-related hearing loss in mice. II. Strain differences and effects of caloric restriction on cochlear pathology and evoked response thresholds. \i Hearing Research\i0 \b 88\b0 , 143-155. \par \par Wimer R. E. and Wimer C. C. (1982) A geneticists map of the mouse brain, in \i Genetics of the brain\i0 (Lieblich I., ed), pp. 395-420. Elsevier, Oxford. \par \par Wimer R. E., Wimer C. C., and Roderick T. H. (1969) Genetic variability in forebrain structures between inbred strains of mice. \i Brain Res.\i0 \b 16\b0 , 257-264. \par \par Wolf H. G. (1959) Blood-pM differences in two inbred strains of mice. \i J. Hered.\i0 \b 50\b0 , 155-158. \par \par Wolff G. L., Greenman D. L., Frigeri L. G., Morrissey R. L., Suber R. L., and Felton R. P. (1990) Diabetogenic response to streptozotocin varies among obese yellow and among lean agouti (BALB/c x VY)F1 hybrid mice. \i Proc. Soc. Exp. Biol. Med.\i0 \b 193\b0 , 155-163. \par \par Woodland D. L., Kotzin B. L., and Palmer E. (1990) Functional consequences of a T cell receptor D beta 2 and J beta 2 gene segment deletion. \i J. Immunol.\i0 \b 144\b0 , 379-385. \par \par Wragg L. E. and Speirs R. S. (1952) Strain and sex differences in response of inbred mice to adrenal cortical hormones. \i Proc. Soc. Exp. Biol. Med.\i0 \b 80\b0 , 680-684. \par \par Wu X., Wang C., Katoh H., Xing R., Zhang X., Yao G., Zhu B., and Moriwaki K. (1992) Genetic profile of LIBP/1 inbred strain derived from the Kunming outbred stock of the mouse. [Japanese]. \i Exp. Animals (Japan)\i0 \b 41\b0 , 541-543. \par \par Wunsch AB (1992) \i Zuchtgeschichte von sechs Mause-Inzuchtstammen. Diss. Vet. Med. Fak\i0 . Munchen, Uni. \par \par Wysocki C. J., Whitney G., and Tucker D. (1977) Specific anosmia in the laboratory mouse. \i Behav. Genet.\i0 \b 7\b0 , 171-188. \par \par Xidieh C. F., Singer-Vermes L. M., Calich V. L. G., and Burger E. (1994) Plasma amylase levels as a marker of disease severity in an isogenic murine model of paracoccidioidomycosis. \i Journal of Medical and Veterinary Mycology\i0 \b 32\b0 , 37-45. \par \par Yagi H., Katoh S., Akiguchi I., and Takeda T. (1988) Age-related deterioration of ability of aquisition in memory and learning in senescence accelerated mouse: SAM-P/8 as an animal model of disturbances in recent memory. \i Brain Res.\i0 \b 474\b0 , 86-93. \par \par Yamada Y., Shisa H., Matsushiro H., Kamoto T., Kobayashi Y., Kawarai A., and Hiai H. (1994) T lymphomagenesis is determined by a dominant host gene thymic lymphoma susceptible mouse-1 (Tlsm-1) in mouse models. \i Journal Of Experimental Medicine\i0 \b 180\b0 , 2155-2162. \par \par Yamamoto R. S., Crittenden L. B., Sokoloff L., and Jay G. E. (1963) Genetic variations in plasma lipid content in mice. \i J. Lipid Res.\i0 \b 4\b0 , 413-418. \par \par Yamamoto Y., Saito H., Setogawa T., and Tomioka H. (1991) Sex differences in host resistance to Mycobacterium marinum infection in mice. \i Infect. Immun.\i0 \b 59\b0 , 4089-4096. \par \par Yang G. M., Kitagawa K., Matsushita K., Mabuchi T., Yagita Y., Yanagihara T., and Matsumoto M. (1997) C57BL/6 strain is most susceptible to cerebral ischemia following bilateral common carotid occlusion among seven mouse strains: Selective neuronal death in the murine transient forebrain ischemia. \i Brain Res.\i0 \b 752\b0 , 209-218. \par \par Yano T., Ishikawa G., and Ichikawa T. (1993) Oxidative stress as a modulating factor of pulmonary tumorigenesis in mice; comparative study on two different strains. \i Comparative Biochemistry and Physiology - C Pharmacology Toxicology and Endocrinology\i0 \b 104\b0 , 407-410. \par \par Yano T., Ishikawa G., and Ichikawa T. (1994a) Comparative study on factors regulating the level of oxidative stress toward pulmonary nuclei in two different strains of mice. \i Int. J. Biochem.\i0 \b 26\b0 , 121-125. \par \par Yano T., Obata Y., Yano Y., Otani S., and Ichikawa T. (1994b) Vitamin E acts as a useful chemopreventive agent to reduce spontaneous lung tumorigenesis in mice. \i Cancer Lett.\i0 \b 87\b0 , 205-210. \par \par Yogi Y., Nakamura K., and Suzuki A. (1989) The experimental inoculation with Mycobacterium leprae in autoimmune mice: results of MRL/lpr mice inoculated into the right hind foot. \i Japanese Journal of Leprosy\i0 \b 58\b0 , 235-240. \par \par Yonezu T., Tsunasawa S., Higuchi K., Kogishi K., Naiki H., Hanada K., Sakiyama F., and Takeda T. (1987) A molecular-pathologic approach to murine senile amyloidosis. Serum precursor-apolipoprotein A-II variant (Pro5-Gln) present only in the senile amyloidosis-prone SAM-P/2 mice. \i Lab. Invest.\i0 \b 57\b0 , 65-70. \par \par Yoshida K., Natsume N., Kinoshita H., Tsunoda N., Takahashi H., and Kawai T. (1996) Experimental-study on cleft-lip and/or palate - fetuses ofA/J mice in uteri of F1-hybrid mothers using ovarian transplantation. \i Cleft Palate-Craniofacial Journal\i0 \b 33\b0 , 291-296. \par \par Yoshioka H., Yoshida H., Doi T., Muso E., Ohshio G., Higuchi K., Inada M., Miyake T., Kita T., Hamashima Y., and Takeda T. (1989) Autoimmune abnormalities in a murine model of accelerated senescence. \i Clin. Exp. Immunol.\i0 \b 75\b0 , 129-135. \par \par Young C. R., Deacon N. J., Ebringer A., and Davis D. A. L. (1976) Genetic control of the immune response to ferritin in mice. \i J. Immunogenet.\i0 \b 3\b0 , 199-205. \par \par Yuasa T., Abe E., Oshimura M., and Namba M. (1996) Immortalization of cells from brains derived from a strain (MSM/MSfB6C3F1) of wild mouse. \i Acta Medica Okayama\i0 \b 50\b0 , 319-324. \par \par Yuhas J. M. (1968) The central nervous system syndrome of the mouse: effects of strain, age, and conditioning exposure. \i Radiation Res.\i0 \b 35\b0 , 714-721. \par \par Yuhas J. M. and Clapp N. K. (1972) Incidence of leukemia and nonlymphatic tumors in mice with glomerulosclerosis and allied disorders. \i J. Natl. Cancer Inst.\i0 \b 48\b0 , 367-373. \par \par Yuhas J. M. and Storer J. B. (1969) On mouse strain differences in radiation resistance: hematopoietic death and the endogenous colony-forming unit. \i Radiation Res.\i0 \b 39\b0 , 608-622. \par \par Yun T. K., Kim S. H., and Lee Y. S. (1995) Trial of a new medium-term model using Benzo(a)pyrene induced lung tumor in newborn mice. \i Anticancer Research\i0 \b 15\b0 , 839-845. \par \par Yunis E. J., Fernandes G., Teague G., Stutman O., and Good R. A. (1972) The thymus, autoimmunity and the involution of the lymphoid system, in \i Tolerance, Autoimmunity and Aging\i0 (Sigel M. M. and Good R. A., eds), pp. 62-119. Thomas, Springfiled, Ill. \par \par Zaharia M. D., Kulczycki J., Shanks N., Meaney M. J., and Anisman H. (1996) The effects of early postnatal stimulation Morris water-maze acquisition in adult mice: Genetic and maternal factors. \i Psychopharmacology\i0 \b 128\b0 , 227-239. \par \par Zarrow M. X., Christenson C. M., and Eleftheriou B. C. (1971) Strain differences in the ovulatory response of immature mice to PMS and to the pheromonal facilitation of PMS-induced ovulation. \i Biol. Reprod.\i0 \b 4\b0 , 52-56. \par \par Zelentsov A. G. (1974) Susceptibility of inbred mice to helminths. II. Development of Opisthorchis felineus in A/He, CBA/Lac, CC57W/Mv, C57BL/6J, DBA/2J and SWR/J mice [in Russian]. \i Med. Parazit. (Mosk.).\i0 \b 43\b0 , 95-98. \par \par Zhang H., Yousef G. E., Ouyang X., and Archard L. C. (1994) Characterization of a murine model of myocarditis induced by a reactivated Coxsackievirus B3. \i International Journal of Experimental Pathology\i0 \b 75\b0 , 99-110. \par \par Zhang L. Y., Levitt R. C., and Kleeberger S. R. (1995) Differential susceptibility to ozone-induced airways hyperreactivity in inbred strains of mice. \i Experimental Lung Research\i0 \b 21\b0 , 503-518. \par \par Zschiesche W. (1972) Spontaneous amyloidosis of the mouse. \i Acta Pathol. Microbiol. Scand.\i0 \b A 80 Suppl. 233\b0 , 135-140. \par \par Zurcher C., Nooteboom A. L., and Hollander C. F. Neoplastic and non-neoplastic lesions in aging male C57BL/Ka mice. Ann. Rep. Organisation for Health Research, TNO, Rijswijk. pp 252-254. \par \par Zurcher C., van Zwieten M. J., and Hollander C. F. Neoplastic and non-neoplastic lesions in aged RFM mice. Personal communication. \par \par \par INBRED STRAINS OF MICE \par Updated April 9, 1998 \par Michael FW Festing\par \par \qc MRC Toxicology Unit, University of Leicester, Hodgkin Building, \par PO Box 138, Lancaster Road, Leicester, UK \par \par FAX +44 (0)116 252 5616 \par email mfwf1@leicester.ac.uk\par \par


The database is protected by copyright ©essaydocs.org 2016
send message

    Main page