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Статті в журналах з теми "Inbred mice"

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Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 6 лютого 2022

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1

Nishioka, Yutaka. "The origin of common laboratory mice." Genome 38, no. 1 (February 1, 1995): 1–7. http://dx.doi.org/10.1139/g95-001.

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The house mouse is one of the model organisms in genetics and more than 400 inbred strains have been established. However, many of the strains are related and their ancestry can be traced back to European fancy mice inbred in the 1920s. Recent molecular studies corroborate the early historical records that assert that Japanese fancy mice were introduced into European stocks and thus contributed to the development of "old" inbred strains. Consequently, many inbred strains have genomic DNA derived from more than one subspecies of Mus musculus. The subspecific hybrid origin of common inbred strains has important bearings on the interpretation of genetic data, and the limitations that history imposes upon the currently available strains make it necessary to establish new inbred strains representing specific wild populations.

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2

West, John D., and Graham Fisher. "Inherited cataracts in inbred mice." Genetical Research 46, no. 1 (August 1985): 45–56. http://dx.doi.org/10.1017/s0016672300022448.

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SUMMARYExamination of the eyes with a slit lamp revealed that 101/H mice had a coloured cataract. Crosses to C3H/HeH indicated that this was inherited as a single recessive gene which we have designated lop-2 (lens opacity-2). The related strain 129/Sv-SlJ-CP had a phenotypically identical cataract and presumably also carries the lop-2 gene. CBA/H, CBA/CaH- + /p, CBA/H-kd and CBA/H-T6 mice had a bright white or white/green cataract that typically extended from the nucleus to the anterior cortex of the lens. Crosses to C3H/HeH indicated that this was inherited as a semi-dominant gene. However, other crosses raise the possibility that the CBA cataract is also caused by lop-2. If so, the expressivity (and penetrance of the heterozygote) is affected by genetic background. Neither lop-2 nor the gene responsible for the CBA cataract was linked to contrasted (Slcon) on chromosome 10, so these are distinct from the Lop (lens opacity) gene. Further studies of genetic linkage are needed to clarify whether lop-2 is responsible for both the 101/H and CBA/H cataracts.

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3

Sundberg, J. P., C. A. Hanson, D. R. Roop, K. S. Brown, and H. G. Bedigian. "Myoepitheliomas in Inbred Laboratory Mice." Veterinary Pathology 28, no. 4 (July 1991): 313–22. http://dx.doi.org/10.1177/030098589102800408.

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4

Passino, Enrica, and Martine Ammassari–Teule. "Visual Discrimination in Inbred Mice." Physiology & Behavior 67, no. 3 (September 1999): 393–99. http://dx.doi.org/10.1016/s0031-9384(99)00076-1.

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5

Iwasaki, Akiko. "Antiviral responses of inbred mice." Nature Reviews Immunology 16, no. 6 (April 25, 2016): 339. http://dx.doi.org/10.1038/nri.2016.44.

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6

Galkin, O. Yu, A. G. Komar, and O. B. Besarab. "Different mice inbred strains humoral immune response against human prostate-specific antigen." Ukrainian Biochemical Journal 91, no. 1 (January 28, 2019): 30–37. http://dx.doi.org/10.15407/ubj91.01.030.

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7

Darlington, T. M., M. A. Ehringer, C. Larson, T. L. Phang, and R. A. Radcliffe. "Transcriptome analysis of Inbred Long Sleep and Inbred Short Sleep mice." Genes, Brain and Behavior 12, no. 2 (February 22, 2013): 263–74. http://dx.doi.org/10.1111/gbb.12018.

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8

Dagnaes-Hansen, Frederik, Jacob M. Moser, Thomas Smith-John, and Mie Aarup. "Sudden death in lactating inbred mice." Lab Animal 39, no. 7 (July 2010): 205. http://dx.doi.org/10.1038/laban0710-205.

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9

Liebelt, Robert A. "Inbred mice fed only bee pollen." Journal of ApiProduct and ApiMedical Science 2, no. 4 (October 1, 2010): 156–60. http://dx.doi.org/10.3896/ibra.4.02.4.04.

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10

Haimrich, B., H. Schwegler, W. E. Crusio, and W. Buselmaier. "Substrain divergence in C3H inbred mice." Behavior Genetics 18, no. 6 (November 1988): 671–74. http://dx.doi.org/10.1007/bf01066849.

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11

Beau, Jacques. "Activity rhythms in inbred mice. I. Genetic analysis with recombinant inbred strains." Behavior Genetics 21, no. 2 (March 1991): 117–29. http://dx.doi.org/10.1007/bf01066331.

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12

Grasperge, Britton J., Kathryn E. Reif, Timothy D. Morgan, Piyanate Sunyakumthorn, Joseph Bynog, Christopher D. Paddock, and Kevin R. Macaluso. "Susceptibility of Inbred Mice to Rickettsia parkeri." Infection and Immunity 80, no. 5 (March 5, 2012): 1846–52. http://dx.doi.org/10.1128/iai.00109-12.

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ABSTRACTRickettsia parkeri, a member of the spotted fever groupRickettsia, is the causative agent of American boutonneuse fever in humans. Despite the increased recognition of human cases, limited information is available regarding the infection of invertebrate and vertebrate hosts for this emerging tick-borne disease. Toward the development of a viable transmission model and to further characterize the pathology associated withR. parkeriinfection, inbred mouse strains (A/J, BALB/c, C3H/HeJ, and C3H/HeN) were intravenously and intradermally inoculated with 105low-passage-numberR. parkeri(Portsmouth strain), and infection, gross pathology, and histopathology were scored. Additionally, a quantitative real-time PCR (qPCR) was performed to estimate rickettsial load in heart, lung, spleen, and liver tissues of infected mice at 19 days postinoculation. Of the A/J, BALB/c, and C3H/HeN mice, none displayed universal pathology consistent with sustained infection. Compared to age-matched control mice, the intravenously inoculated C3H/HeJ mice exhibited marked facial edema and marked splenomegaly upon gross examination, while the intradermally inoculated mice developed characteristic eschar-like lesions. The C3H/HeJ mice also exhibited the greatest concentrations of rickettsial DNA from heart, lung, liver, and spleen samples when examined by qPCR. The similarity of the pathology of human disease and sustained infection suggests that the C3H/HeJ strain of mice is a promising candidate for subsequent experiments to examine the tick transmission, dissemination, and pathology ofR. parkeririckettsiosis.

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13

Salcedo, Tovah, Armando Geraldes, and Michael W. Nachman. "Nucleotide Variation in Wild and Inbred Mice." Genetics 177, no. 4 (December 2007): 2277–91. http://dx.doi.org/10.1534/genetics.107.079988.

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14

Stevens, James C., Gareth T. Banks, Michael F. W. Festing, and Elizabeth M. C. Fisher. "Quiet mutations in inbred strains of mice." Trends in Molecular Medicine 13, no. 12 (December 2007): 512–19. http://dx.doi.org/10.1016/j.molmed.2007.10.001.

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15

Liu, Wing-Keung, Nai-Ki Mak, and Chuen-Chuen Wong. "Immunomodulatory Effect of Methimazole on Inbred Mice." Immunobiology 180, no. 1 (November 1989): 23–32. http://dx.doi.org/10.1016/s0171-2985(89)80027-0.

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16

Lewin, R. "Why do inbred mice evolve so quickly?" Science 228, no. 4704 (June 7, 1985): 1187. http://dx.doi.org/10.1126/science.4039848.

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17

Sundberg, J. P., D. L. Adkison, and H. G. Bedigian. "Skeletal Muscle Rhabdomyosarcomas in Inbred Laboratory Mice." Veterinary Pathology 28, no. 3 (May 1991): 200–206. http://dx.doi.org/10.1177/030098589102800303.

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18

Eisen, H. N., and E. B. Reilly. "Lambda Chains and Genes in Inbred Mice." Annual Review of Immunology 3, no. 1 (April 1985): 337–65. http://dx.doi.org/10.1146/annurev.iy.03.040185.002005.

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19

Pratte, Michel, and Marc Jamon. "Detection of social approach in inbred mice." Behavioural Brain Research 203, no. 1 (October 2009): 54–64. http://dx.doi.org/10.1016/j.bbr.2009.04.011.

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20

Alexander, R. C., J. Duda, D. Garth, W. Vogel, and W. H. Berrettini. "Morphine and cocaine preference in inbred mice." Psychiatric Genetics 3, no. 1 (1993): 33–38. http://dx.doi.org/10.1097/00041444-199321000-00006.

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21

Maeda, Nobuko, Satoshi Arai, Akira Ozaki, Tsutomu Oowada, Akiko Takahashi, Hiroshi Fujita, and Takeo Mizutani. "Experimental Dental Caries on Gnotobiotic Inbred Mice." Microbiology and Immunology 39, no. 1 (January 1995): 71–73. http://dx.doi.org/10.1111/j.1348-0421.1995.tb02171.x.

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22

Otobe, Takayuki, and Junshiro Makino. "Impulsive choice in inbred strains of mice." Behavioural Processes 67, no. 1 (July 2004): 19–26. http://dx.doi.org/10.1016/j.beproc.2004.02.001.

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23

Elmer, Gregory I., Richard A. Meisch, and Frank R. George. "Oral ethanol reinforced behavior in inbred mice." Pharmacology Biochemistry and Behavior 24, no. 5 (May 1986): 1417–21. http://dx.doi.org/10.1016/0091-3057(86)90204-2.

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24

Crow, James F. "C. C. Little, Cancer and Inbred Mice." Genetics 161, no. 4 (August 1, 2002): 1357–61. http://dx.doi.org/10.1093/genetics/161.4.1357.

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25

Kirillicheva, G. B., M. S. Solov'eva, I. G. Baturina, T. N. Shchukovskaya, and G. A. Maslennikov. "Immunomodulating action of histamine in inbred mice." Bulletin of Experimental Biology and Medicine 113, no. 3 (March 1992): 386–88. http://dx.doi.org/10.1007/bf00783122.

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26

Hamada, Akiko, Kiyotoshi Inenaga, Shuichi Nakamura, Masamichi Terashita, and Hiroshi Yamashita. "Disorder of salivary secretion in inbred polydipsic mouse." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (April 1, 2000): R817—R823. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r817.

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Анотація:

To find mechanisms of an extreme polydipsia in an inbred strain of mice, STR/N, this study was undertaken using Institute of Cancer Research (ICR) mice as a control. During food deprivation, daily water intake of both strains decreased. The decrement in the STR/N mice was larger than that in the ICR mice. During dehydration, daily food intake of the STR/N mice was smaller than that of the ICR mice. These data indicate that prandial drinking was more severely affected for the STR/N mice. Under anesthesia, the stimulated salivary secretion by pilocarpine of the STR/N mice was significantly smaller than that of the ICR mice. The submandibular gland of the STR/N mice was lighter and harder than that of the ICR mice. After desalivation from the major three salivary glands, the ICR mice drank as much as the STR/N mice. Young STR/N mice with undeveloped polydipsia did not show different salivary secretion stimulated by pilocarpine from the young ICR mice. These findings indicate a dysfunction with age in the salivary glands of the STR/N mice, and they suggest that the decreased saliva induces thirst and triggers extraordinary drinking in the polydipsic mice.

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27

Chebib, Jobran, Benjamin C. Jackson, Eugenio López-Cortegano, Diethard Tautz, and Peter D. Keightley. "Inbred lab mice are not isogenic: genetic variation within inbred strains used to infer the mutation rate per nucleotide site." Heredity 126, no. 1 (August 31, 2020): 107–16. http://dx.doi.org/10.1038/s41437-020-00361-1.

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AbstractFor over a century, inbred mice have been used in many areas of genetics research to gain insight into the genetic variation underlying traits of interest. The generalizability of any genetic research study in inbred mice is dependent upon all individual mice being genetically identical, which in turn is dependent on the breeding designs of companies that supply inbred mice to researchers. Here, we compare whole-genome sequences from individuals of four commonly used inbred strains that were procured from either the colony nucleus or from a production colony (which can be as many as ten generations removed from the nucleus) of a large commercial breeder, in order to investigate the extent and nature of genetic variation within and between individuals. We found that individuals within strains are not isogenic, and there are differences in the levels of genetic variation that are explained by differences in the genetic distance from the colony nucleus. In addition, we employ a novel approach to mutation rate estimation based on the observed genetic variation and the expected site frequency spectrum at equilibrium, given a fully inbred breeding design. We find that it provides a reasonable per nucleotide mutation rate estimate when mice come from the colony nucleus (~7.9 × 10−9 in C3H/HeN), but substantially inflated estimates when mice come from production colonies.

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28

Eveleigh, J. R. "Murine cage density: cage ammonia levels during the reproductive performance of an inbred strain and two outbred stocks of monogamous breeding pairs of mice." Laboratory Animals 27, no. 2 (April 1, 1993): 156–60. http://dx.doi.org/10.1258/002367793780810432.

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The Laboratory Animal Breeders Association guidelines recommend a minimum floor area of 300 cm2 for a monogamous pair of inbred/outbred mice or a trio of inbreds. The mean level of ammonia produced during lactation from BALB/c, TO and CD-1 breeding pairs housed in M2 cages with a floor area of 300 cm2 on Day 4 after cleaning was 30 ppm, 87 ppm and 92 ppm, respectively. All 3 strains of mice, particularly the outbred strains, were subjected to high levels of ammonia as compared with human long-term health and safety occupational exposure limits (25 ppm). However, there is a gradient of ammonia within an M2 breeding cage from the nest (19 ppm), to the food hopper, 77 ppm. By housing CD-1 pairs of mice in RM2 cages which have more than double the floor area of M2 cages (676 cm2), the mean level of ammonia during lactation on Day 4 after cleaning was reduced to 26 ppm. The reproductive performance on inbred/outbred strains of mice has to be equated with cage size (floor area) to maintain acceptable levels of ammonia. It is suggested that the recommended minimum floor areas for breeding mice be reviewed.

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29

Ishii, Akira I., and Motohito Sano. "Strain-dependent differences in susceptibility of mice to experimental Angiostrongylus costaricensis infection." Journal of Helminthology 63, no. 4 (December 1989): 302–6. http://dx.doi.org/10.1017/s0022149x00009196.

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ABSTRACTExperimental Angiostrongylus costaricensis infection was carried out in inbred strains of mice (C57BL/6, BALB/c, DBA/2 and C3H/He). All strains became infected with this parasite. Marked differences in mortality and in worm burden were found among inbred strains of mice tested. A significant reduction was shown in worm length from mice compared to that from cotton rats.

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30

DiGiovanni, John, Akira Imamoto, Masashi Naito, Susan E. Walker, Linda Beltrán, Kristine J. Chenicek, and Loren Skow. "Further genetic analyses of skin tumor promoter susceptibility using inbred and recombinant inbred mice." Carcinogenesis 13, no. 4 (1992): 525–31. http://dx.doi.org/10.1093/carcin/13.4.525.

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31

Rogers, Arlin B. "Stress of Strains: Inbred Mice in Liver Research." Gene Expression 19, no. 1 (December 14, 2019): 61–67. http://dx.doi.org/10.3727/105221618x15337408678723.

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Inbred mice are the most popular animals used for in vivo liver research. These mice are genetically defined, readily available, less expensive to maintain than larger animals, and enjoy a broad array of commercial reagents for scientific characterization. C57BL/6 mice are the most commonly used strain. However, other strains discussed, including BALB/c, C3H, A/J, and FVB/N, may be better suited to a particular disease model or line of investigation. Understanding the phenotypes of different inbred mouse strains facilitates informed decision making during experimental design. Model systems influenced by strain-dependent phenotype include tissue regeneration, drug-induced liver injury (DILI; e.g., acetaminophen), fibrosis (e.g., carbon tetrachloride, CCl4), Fas-induced apoptosis, cholestasis, alcohol-induced liver disease and cirrhosis, nonalcoholic fatty liver disease and steatohepatitis (NAFLD/NASH), and hepatocellular carcinoma (HCC). Thoughtful consideration of the strengths and weaknesses of each inbred strain in a given model system will lead to more robust data and a clearer understanding of translational relevance to human liver disease.

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32

Kruckeberg, WC, DI Doorenbos, and PO Brown. "Genetic differences in hemoglobin influence on erythrocyte oxidative stress hemolysis." Blood 70, no. 4 (October 1, 1987): 909–14. http://dx.doi.org/10.1182/blood.v70.4.909.909.

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Abstract The RBC from mice of certain inbred strains hemolyzed under oxidative stress (2.0 mmol/L hydrogen peroxide), whereas red cells from mice of other strains did not. In the experimental system human erythrocytes did not hemolyze. The rate of formation of malonyldialdehyde (a fatty acid oxidative breakdown product) was fourfold higher in hemolytic v nonhemolytic red cells. There was insufficient variation in the levels of glutathione, peroxidase activity or its substrate, reduced glutathione, to explain these hemolysis differences. On the other hand, the antioxidants butylated hydroxyanisole and hydroxytoluene, and histidine protected the hemolysis-prone red cells from breaking open. The hemolysis trait demonstrated autosomal recessive Mendelian inheritance. When using inbred, recombinant inbred, and congenic inbred mice, this hemolysis/nonhemolysis trait correlated 1:1 with the type of hemoglobin beta chain in the RBC. This experimental system is a potential model for investigating the role of hemoglobin in prehemolytic events.

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33

Kruckeberg, WC, DI Doorenbos, and PO Brown. "Genetic differences in hemoglobin influence on erythrocyte oxidative stress hemolysis." Blood 70, no. 4 (October 1, 1987): 909–14. http://dx.doi.org/10.1182/blood.v70.4.909.bloodjournal704909.

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Анотація:

The RBC from mice of certain inbred strains hemolyzed under oxidative stress (2.0 mmol/L hydrogen peroxide), whereas red cells from mice of other strains did not. In the experimental system human erythrocytes did not hemolyze. The rate of formation of malonyldialdehyde (a fatty acid oxidative breakdown product) was fourfold higher in hemolytic v nonhemolytic red cells. There was insufficient variation in the levels of glutathione, peroxidase activity or its substrate, reduced glutathione, to explain these hemolysis differences. On the other hand, the antioxidants butylated hydroxyanisole and hydroxytoluene, and histidine protected the hemolysis-prone red cells from breaking open. The hemolysis trait demonstrated autosomal recessive Mendelian inheritance. When using inbred, recombinant inbred, and congenic inbred mice, this hemolysis/nonhemolysis trait correlated 1:1 with the type of hemoglobin beta chain in the RBC. This experimental system is a potential model for investigating the role of hemoglobin in prehemolytic events.

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34

Fiette, L., C. Aubert, U. Müller, S. Huang, M. Aguet, M. Brahic, and J. F. Bureau. "Theiler's virus infection of 129Sv mice that lack the interferon alpha/beta or interferon gamma receptors." Journal of Experimental Medicine 181, no. 6 (June 1, 1995): 2069–76. http://dx.doi.org/10.1084/jem.181.6.2069.

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The Daniels strain of Theiler's virus causes a persistent infection of the white matter of spinal cord of susceptible mice, with chronic inflammation and primary demyelination. Inbred 129Sv mice are resistant to this infection; they present with mild encephalomyelitis and clear the infection within a matter of days. A very different outcome was observed with inbred 129Sv mice whose receptors for interferon alpha/beta or interferon gamma had been inactivated by homologous recombination. The former presented severe encephalomyelitis with acute infection of neurons, particularly in brain and hippocampus, and extensive infection with necrosis of the choroid plexus. Most animals died of this acute disease. The latter, presented the same early encephalomyelitis as the control 129Sv mice. However, they remained persistently infected and developed a very severe late infection of the white matter with extensive primary demyelination. This late disease looked like an exacerbated form of the chronic demyelinating disease observed in susceptible inbred mice such as the SJL/J or FVB strains. Our results show that the two interferon systems play nonredundant roles in the resistance of the 129Sv mouse to the infection by Theiler's virus. They also lend support to the notion that the Ifg gene is involved in the resistance/susceptibility of inbred strains of mice to persistent infection by this picornavirus.

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35

Hata, Hidekazu, and Somei Kojima. "Susceptibility of Inbred Mice to Paragonimus miyazakii Infection." Journal of Parasitology 75, no. 3 (June 1989): 463. http://dx.doi.org/10.2307/3282607.

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36

Postan, Miriam, James A. Dvorak, James J. Bailey, Erik W. Pottala, and James P. McDaniel. "Studies of Trypanosoma cruzi Clones in Inbred Mice." American Journal of Tropical Medicine and Hygiene 37, no. 3 (November 1, 1987): 541–49. http://dx.doi.org/10.4269/ajtmh.1987.37.541.

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37

Gatti, Daniel M., Lu Lu, Robert W. Williams, Wei Sun, Fred A. Wright, David W. Threadgill, and Ivan Rusyn. "MicroRNA expression in the livers of inbred mice." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 714, no. 1-2 (September 2011): 126–33. http://dx.doi.org/10.1016/j.mrfmmm.2011.05.007.

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38

Katafuchi, T., Y. Hattori, and K. Koizumi. "Mechanism of water intake in inbred polydipsic mice." Appetite 12, no. 3 (June 1989): 217. http://dx.doi.org/10.1016/0195-6663(89)90203-1.

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39

Kiupel, Matti, Kathy S. Brown, and John P. Sundberg. "Bulbourethral (Cowper's) gland abnormalities in inbred laboratory mice." Journal of Experimental Animal Science 40, no. 4 (January 2000): 178–88. http://dx.doi.org/10.1016/s0939-8600(00)80010-3.

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40

Tuttle, Alexander H., Vivek M. Philip, Elissa J. Chesler, and Jeffrey S. Mogil. "Comparing phenotypic variation between inbred and outbred mice." Nature Methods 15, no. 12 (November 30, 2018): 994–96. http://dx.doi.org/10.1038/s41592-018-0224-7.

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41

Frelier, P. F., J. W. Templeton, M. Estes, H. W. Whitford, and R. D. Kienle. "Genetic Regulation ofMycobacterium paratuberculosisInfection in Recombinant Inbred Mice." Veterinary Pathology 27, no. 5 (September 1990): 362–64. http://dx.doi.org/10.1177/030098589002700509.

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42

Adkison, D. L., and J. P. Sundberg. "“Lipomatous” Hamartomas and Choristomas in Inbred Laboratory Mice." Veterinary Pathology 28, no. 4 (July 1991): 305–12. http://dx.doi.org/10.1177/030098589102800407.

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43

Downing, Chris, Christina Balderrama-Durbin, Hali Broncucia, David Gilliam, and Thomas E. Johnson. "Ethanol Teratogenesis in Five Inbred Strains of Mice." Alcoholism: Clinical and Experimental Research 33, no. 7 (July 2009): 1238–45. http://dx.doi.org/10.1111/j.1530-0277.2009.00949.x.

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