Relevant bibliographies by topics / Inbred mice

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Inbred mice'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Inbred mice"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Inbred mice"

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Langford, Christopher Patrick. "Repeated infection of inbred mice with Heligmosomoides polygyus." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46403.

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Byers, Shannon L. "Use of Inbred Strains of Mice to Study the Genetics and Biology of Sperm Function." Fogler Library, University of Maine, 2006. http://www.library.umaine.edu/theses/pdf/ByersSL2006.pdf.

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Wood, Erin. "A Behavioral Comparison of Four Inbred Strains of Mice." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2224.

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Isogenic, or inbred, mouse strains are currently the experimental subjects of choice in laboratory studies focused on genetics, pharmacology, and psychological issues. Understanding phenotypic differences in isogenic strains is important in order to interpret experimental results obtained from inbred mouse strains. Four commonly used inbred strains, C57BL/6NHsd (C57), DBA/2NHsd (DBA), 129S2/SvHsd (129), and Balb/cAnHsd (Balb/c), are investigated in this study using four different behavioral tasks that measure locomotor activity and cognitive behavior (Morris Water Maze (MWM), T-maze, and operant autoshaping procedures). In the locomotor activity task 129 mice showed significantly less horizontal ambulation than any other strain, while differences in rearing was seen between all strains, with C57 mice producing the most, and 129 showing the least rearing. Thigmotaxia was seen the most in the 129 strain, less so with the Balb/c and DBA strains, and the least in the C57 mice. In the MWM learning across strains was noted but there was no difference between the strains. In the T-maze the Balb/c strain showed the shortest latency to enter an arm, while the 129 strain showed the longest. As expected they also showed the lowest accuracy and the highest percent time-outs compared to all the other strains. In the autoshaping procedure little difference between the strains was observed. Balb/c mice trended graphically towards higher rates however there was no difference with regard to number of contingent responses or number per strain to reach a criterion of 10 or more contingent reinforcers. Finally, locomotor activity was measured again at the end of the study. The activity results were still similar, although the C57 strain showed a decrease in horizontal ambulation as compared to DBA and Balb/c strains; however, the 129 strain still showed the least activity. These results indicate that there are significant differences in locomotor behavior and cognitive processes in these strains that should be considered when interpreting results from studies using these inbred mouse strains.
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Peugh, W. N. "The genetics and immunology of cardiac allograft rejection in inbred mice." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375315.

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Liu, Dien. "Effects of R294C mutation on expression and stability of interferon regulatory factor-8 in BXH-2 mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116090.

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Interferon regulatory factor-8 (Irf-8), a hematopoietic transcriptional regulator, controls myeloid-cell proliferation and coordinates innate and adaptive host immune responses. Mice from the BXH-2 recombinant inbred strain carry an endogenous R294C mutation in Irf-8. This loss-of-function mutation induces clonal infiltration of undifferentiated Mac-1+/Gr-1 + granulocytic precursors in BXH-2 mice, extramedullary hematopoiesis, and splenomegaly similar to those seen in human chronic myeloid leukemia. It also renders the host permissible to the otherwise avirulent Mycobacterium bovis (BCG), and negatively affects survival or recovery of these mice to other infectious pathogens. Here, we generated a polyc1onal anti-Irf-8 antibody to better characterize the effects of the R294C mutation on Irf-8 protein expression, stability, and inducibility in hematopoietic and non-hematopoietic tissues. We found that mutant Irf-8C294-expressing tissues consistently displayed reduced Irf-8 abundance compared to their wild-type counterparts in both primary splenocytes and following transfection into heterologous cells, presumably due to decreased stability or increased rate of degradation of the mutant isoform. Results also indicate that native Irf-8 is also expressed in the heart, and to a lesser extent, in the kidneys. Since neither of these organs is well-known to be associated with hematopoietic or immune functions, this finding strengthens the possibility that Irf-8 may exert additional regulatory functions in other cellular contexts. Taken together, our study provides a better understanding about the molecular features of the mutant Irf-8 C294 protein and contributes to a growing body of evidence in support of Irf-8 expression in non-hematopoietic tissues.
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Cushnie, Duncan Wells. "On the expression and deficiency of 5,10-methylenetetrahydrofolate reductase in murine sperm development." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116083.

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Development of specific DNA methylation patterns is required for normal spermatogenesis. DNA methyltransferases (DNMTs) use S-adenosylmethionine (SAM) produced in a pathway requiring 5,10-methylenetetrahydrofolate reductase (MTHFR). This thesis describes: testicular phenotype differences derived from Mthfr-deficiency in different mouse strains; the cellular Mthfr expression pattern during male germ cell development; and finally, changes to the DNA methylation of Mthfr-deficient sperm. Mthfr-deficient BALB/c, but not C57BL/6, mice have reduced neonatal germ cell proliferation but both have abnormal germ cells as adults. Germ cell MTHFR expression differed developmentally in parallel with DNMTs associated with de novo methylation. Sperm from mice with reduced Mthfr levels or dietary folate deficiency had differential DNA methylation at multiple loci, compared to wildtype mice, indicating that maintenance as well as acquisition of methylation can be altered by SAM-reduction. These results highlight the important role of folate in sperm development throughout life.
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Knock, Erin Heather 1981. "Long-term dietary folate deficiency and intestinal tumor development in mice." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115689.

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Epidemiological evidence linking dietary folate deficiency and risk for colorectal cancer is conflicting. Studies using animal models indicate that timing, dose and presence of pre-malignant lesions will influence whether folate deficiency prevents or promotes tumor formation. In this thesis a new model of spontaneous tumor formation due to long-term dietary folate deficiency alone, in non-transgenic mice and without carcinogen induction, is developed. The mechanisms by which folate deficiency might influence cancer risk are also examined.
BALB/c mice, with or without a null allele in a key folate-metabolizing enzyme, Methylenetetrahydrofolate reductase (Mthfr ), develop intestinal tumors due to dietary folate deficiency alone. On folate-deficient (FD) diets, 12.5% of Mthfr+/+ mice and 28.1% of Mthfr+/- mice developed tumors; mice on control diet (CD) did not. C57B1/6 mice (a strain resistant to other methods of tumor induction) placed on the same diets for the same amount of time did not develop any tumors. To investigate possible mechanisms the levels of DNA damage (dUTP/dTTP ratio and p-H2AX staining) and DNA methylation (thin layer chromatography) were examined. FD BALB/c, but not C57B1/6 mice, had a trend towards increased dUTP/dTTP and DNA double-strand breaks and decreased global DNA methylation compared to CD mice. To determine why the FD diet affects the BALB/c and not the C57Bl/6 strain, the expression of genes involved in folate metabolism was examined. Several changes in gene expression were observed. In particular, BALB/c mice had increased Mthfr expression and MTHFR activity compared to C57Bl/6 mice. Increased MTHFR activity may deplete 5,10-methylenetetrahydrofolate supplies for the dTMP synthesis, increasing the dUMP levels and, possibly, DNA damage. The levels of several DNA repair genes were also examined. Two genes involved in base excision repair, Thymine DNA glycosylase (Tdg) and Apurinic/apyrimidinic endonuclease 1 (Apex1), were increased in FD C57B1/6 compared to FD BALB/c mice suggesting increased DNA repair capacity.
These results support the evidence that dietary folate deficiency promotes intestinal tumor formation possibly through increased DNA damage, with subsequent defects in DNA repair.
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Pereira, Bernardo Acácio Santini. "Leishmania (Leishmania) amazonensis: participação de fatores do hospedeiro e do parasito no curso da infecção experimental em camundongos." reponame:Repositório Institucional da FIOCRUZ, 2010. https://www.arca.fiocruz.br/handle/icict/4112.

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Submitted by Tatiana Oliveira (tsilva@icict.fiocruz.br) on 2012-05-31T16:59:24Z No. of bitstreams: 1 bernardo_as_pereira_ioc_bp_002_2010.pdf: 3428909 bytes, checksum: 68f2b1087a42200dd708a3f10aac479e (MD5)
Made available in DSpace on 2012-05-31T16:59:24Z (GMT). No. of bitstreams: 1 bernardo_as_pereira_ioc_bp_002_2010.pdf: 3428909 bytes, checksum: 68f2b1087a42200dd708a3f10aac479e (MD5) Previous issue date: 2010
Fundação Oswaldo Cruz.Instituto Oswaldo Cruz. Rio de janeiro, RJ, Brasil
A leishmaniose é uma doença antropozoonose que afeta 88 países, o que denota a importância da realização de estudos que permitem o desenvolvimento de novas estratégias de vacinação ou quimioterapias. Os agentes etiológicos dessa doença são espécies do gênero Leishmania, sendo que, no Brasil, a Leishmania (Leishimania) amazonensis está relacionada à forma tegumentar da leishmaniose e está expandindo sua área de distribuição geográfica. O modelo murino de infecção experimental tem sido largamente empregado nos estudos de leishmanioses, por permitir o controle das características do hospedeiro e a análise de aspectos específicos da doença. O presente estudo tem por objetivo verificar a atuação de fatores de interação parasito-hospedeiro nesse modelo de infecção utilizando linhagens de camundongos comdiferentes graus de susceptibilidade. Para tanto, efetuamos o seqüenciamento da extensão COOH-terminal de um tipo específico de cisteína proteinase (CP) do parasito, a CPB, e, em seguida, o mapeamento in silico de epitopos de MHC classe I nessa seqüência. Os epitopos preditos foram então sintetizados e utilizados em ensaios in vivo (vacinação) e in vitro (indução de blastogênese e de expressão de citocinas e efeitos sobre os linfócitos T CD4+ e CD8+). Alguns desses epitopos preditos demonstraram efeitos antigênicos nos ensaios in vitro, porém sem efeitos perceptíveis nos ensaios in vivo. Os epitopos preditos P4 e P5 induziram a blastogênese em culturas de células de camundongos BALB/c (mais susceptíveis a Leishmania), enquanto P2, P8 e P9 o fizeram em células de células de camundongos CBA (menos suscetíveis). Os epitopos P5, P6 e P8 também promoveram alterações nas porcentagens dos linfócitos CD4+ ou CD8+ em culturas de células de camundongos BALB/c. Quanto à indução da expressão de citocinas, os epitopos P1 e P2 (em BALB/c) e P2 e P3 (em CBA) induziram à expressão de citosinas relacionadas à resposta imune tipo Th1; P6 (em BALB/c) e P8 (em CBA) à expressão de citosinas da resposta Th2; e P4 (em BALB/c) e P9 (em CBA) à expressão de citosinas dos dois tipos de resposta imune. Ensaios de Molecular Doking foram utilizados para auxiliar na compreensão dos fenômenos de interação nos complexos epitoppos/MHC, apontando para padrões de interação associados aos padrões de indução da expressão de citocinas. Adicionalmente, foram efetuados ensaios de PCR em tempo real para se analisar os padrões de expressão de genes de moléculas de MHC do hospedeiro e de CPs do parasito ao longo da infecção, que indicam distinções na expressão de genes de MHC classes I e II entre as linhagens murinas e na expressão de CPs pelo parasito, o que pode estar relacionado às diferentes formas de progressão da infecção nessas linhagens. Os resultados obtidos nesse estudo complementam os dados da literatura sobre as interações parasito-hospedeiro na infecção experimental murina e apontam para novas estratégias de análise dessas interações em leishmaniose
Leishmaniasis is a disease that affects anthropozoonosis 88 countries, demonstrating the importance of studies that allow the development of new strategies for vaccination or chemotherapy. The etiologic agents of this disease are species of the genus Leishmania, and in Brazil, Leishmania (Leishimania) amazonensis is related to the cutaneous form of leishmaniasis and is expanding its geographical distribution. The murine model of experimental infection has been widely used in studies of leishmaniasis by allowing the control of the characteristics of the host and analysis of specific aspects of the disease. The present study aims to verify the performance factors of the host-parasite interaction in this infection model using mice strains comdiferentes degrees of susceptibility. Therefore, we performed by sequencing the COOH-terminal extension of a particular type of cysteine ​​proteinase (CP) of the parasite, CPB, and then, the in silico mapping of epitopes on MHC class I that sequence. The predicted epitopes were then synthesized and used in vivo assays (vaccination) and in vitro (induced blastogenesis and expression of cytokines and effects on T lymphocytes CD4 + and CD8 +). Some of these antigenic epitopes predicted effects demonstrated in vitro assays, but without noticeable effects in vivo assays .. The predicted epitopes P4 and P5 induced blastogenesis in cultured cells of BALB / c (most likely Leishmania), while P2, P8 and P9 cells did cell CBA mice (less likely). The epitopes P5, P6 and P8 also induced variations in the percentages of CD4 + or CD8 + cell cultures of BALB / c mice. The induction of expression of cytokines, the epitopes P1 and P2 (in BALB / c) and P3 and P2 (in CBA) to induce expression of cytokines related to Th1 type immune response, P6 (in BALB / c) and P8 (in CBA) to the expression of Th2 cytokines, and P4 (in BALB / c) and P9 (in CBA) to the expression of cytokines of both types of immune response. Molecular tests Doking were used to assist in understanding the complex interaction phenomena in epitoppos / MHC, pointing to patterns of interaction patterns associated with induction of cytokine expression. Additionally, PCR assays were performed in real time to examine the expression patterns of genes of the host MHC molecules and CPs along the parasite infection, indicating distinctions in the gene expression of MHC class I and II between the strains and expression of murine CPs the parasite, which can be related to different forms of progression of the infection in these strains. The results of this study complement the literature on host-parasite interactions in murine experimental infection and point to new strategies for analysis of these interactions in leishmaniasis
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Wang, Chengming Kaltenboeck Bernhard. "Multivariate analysis of Chlamydia pneumoniae lung infection in two inbred mouse strains." Auburn, Ala., 2005. http://hdl.handle.net/10415/1260.

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Wong, Andrew Wai Kit. "Correlations between hippocampal synaptic plasticities and proteins, in inbred mice and in transgenic mice modelling Alzheimer's disease, and behaviour." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408247.

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Books on the topic "Inbred mice"

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Li, Ha-Sheng. Genetic influences on susceptibility of the auditory system to aging and environmental factors. Oslo: Scandinavian University Press, 1992.

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Li, Ha-Sheng. Genetic influences on susceptibility of the auditory system to aging and environmental factors. Oslo: Scandinavian University Press, 1992.

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Festing, Michael F. W. Inbred Strains in Biomedical Research. Palgrave, 2014.

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The Allen Reference Atlas, (Book + CD-ROM) : A Digital Color Brain Atlas of the C57BL/6J Male Mouse. Wiley, 2007.

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Lavooy, Maria Jacoba. Play and motor development in inbred strains and selected lines of Mus musculus. 1988.

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M, Brown Stephen D., Lyon Mary F, Rastan Sohaila, and International Committee on Standardized Genetic Nomenclature for Mice., eds. Genetic variants and strains of the laboratory mouse. 3rd ed. Oxford: Oxford University Press, 1996.

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Seiichirō, Tarui, Tochino Yoshihiro, and Nonaka Kyohei, eds. Insulitis and type I diabetes: Lessons from the NOD mouse. Tokyo: Academic Press, 1986.

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Edward, Leiter, and Atkinson Mark 1961-, eds. NOD mice and related strains: Research applications in diabetes, AIDS, cancer, and other diseases. Austin, Tex: R.G. Landes, 1998.

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(Editor), Edward Leiter, and Mark Atkinson (Editor), eds. Nod Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, And Other Diseases (Molecular Biology Intelligence Unit). Landes Bioscience, 1998.

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Burgess, V. N. Trends in Muscular Dystrophy Research. Nova Biomedical Books, 2006.

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Book chapters on the topic "Inbred mice"

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Sundberg, John P., James G. Fox, Jerrold M. Ward, and Hendrick G. Bedigian. "Idiopathic Focal Hepatic Necrosis in Inbred Mice." In Digestive System, 213–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60473-7_31.

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Sundberg, John P., James G. Fox, Jerrold M. Ward, and Hendrick G. Bedigian. "Idiopathic Focal Hepatic Necrosis in Inbred Mice." In Digestive System, 213–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-25996-2_31.

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Epstein, Randy J., and R. Doyle Stulting. "Immunologically Mediated Corneal Neovascularization in Inbred Mice." In Documenta Ophthalmologica Proceedings Series, 341–48. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3337-8_52.

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Gasser, M., W. Timmermann, and A. Thiede. "Segmental Femoral Artery Allografts: Histomorphological Analysis of the Rejection Response in Inbred Rat Strains." In Organtransplantation in Rats and Mice, 359–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_36.

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Potter, Michael. "Indomethacin Inhibition of Pristane Plasmacytomagenesis in Genetically Susceptible Inbred Mice." In Advances in Experimental Medicine and Biology, 151–56. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4793-8_23.

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Angulo, A. F., A. K. Banerjee, and A. A. Polak-Vogelzang. "Detection of Mycoplasma neurolyticum in a colony of inbred mice: clinically silent infection." In New Developments in Biosciences: Their Implications for Laboratory Animal Science, 447–48. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-3281-4_73.

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Hartman, A. B., L. A. D’Hoostelaere, M. Potter, and S. Rudikoff. "The X-24 VH Gene Family in Inbred Mouse Strains and Wild Mice." In The Wild Mouse in Immunology, 157–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71304-0_19.

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Gottlieb, P. D., R. T. Boyd, P. D. Ponath, and M. M. Goldrick. "Restriction Enzyme Polymorphisms in Vϰ and Jϰ Genes of Inbred and Wild Mice." In The Wild Mouse in Immunology, 186–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71304-0_22.

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Cagiano, R., M. A. De Salvia, M. Tattoli, C. Lacomba, N. Brunello, G. Racagni, and V. Cuomo. "Behavioural and Neurochemical Changes Produced by Lefetamine in Two Inbred Strains of Mice." In Archives of Toxicology, 375–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74117-3_73.

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Caballero, Armando, and Peter D. Keightley. "Inferences on genome-wide deleterious mutation rates in inbred populations of Drosophila and mice." In Mutation and Evolution, 229–39. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5210-5_19.

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Conference papers on the topic "Inbred mice"

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Chan, W. Y., I. M. Martin, K. P. Tao, T. T. J. Li, J. G. S. Tsun, W. W. Y. Yu, G. W. K. Wong, and J. P. Mizgerd. "The Identification of Rhinovirus C Susceptible Inbred Mice." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6169.

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Berndt, Annerose, Clinton L. Cario, Jason E. Devlin, Steven D. Shapiro, Helen McNeil, and John P. Sundberg. "FAT4 In Aging-Related Pulmonary Adenomas Of Inbred Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5291.

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Cozzi, E., M. Prysak, and D. Beier. "Airway Hyperresponsiveness Quantitative Trait Linkage Analyses in Inbred and Outbred Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2749.

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Gladwell II, W., H. Cho, L. Miller Degraff, J. Martin, L. Perrow, and SR Kleeberger. "A Genetic Model of Bronchopulmonary Dysplasia in Neonate Inbred Strains of Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2762.

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Gladwell, Wes, Alexandra Levitt, Dianne Walters, Jessica Martin, Tim Wiltshire, and Steven Kleeberger. "Genetic And Genomic Analysis Of Airway Hyperresponsiveness To Serotonin In Inbred Mice." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4908.

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High, MD, HY Cho, F. Polack, T. Wiltshire, and S. Kleeberger. "Quantitative Trait Loci Associated with Respiratory Syncytial Virus Susceptibility in Inbred Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5985.

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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Rubin, Matthew A., and Iwona Jasiuk. "Multiscale Characterization of the Ultrastructure of Normal and Osteoporotic Human Trabecular Bone." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32591.

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In this paper we characterized hierarchical structure of healthy and osteoporotic human trabecular bone from microscale down to nanoscale. To characterize the hierarchical structure, trabecular bone was investigated at the microstructural level (i.e. trabecula, trabecular packets), sub-microstructural level (lamellar structure) and the nanostructural level (crystal-collagen collagen composite). There was an emphasis on evaluating the sub-microstructure and nanostructure of trabecular bone since detailed descriptions of the lamellar structure and of the crystal-collagen relationship in osteoporotic bone are relatively unknown. The ultrastructure of healthy and osteoporotic human trabecular bone was characterized experimentally by means of transmission electron microscopy (TEM) and scanning electron microscopy (SEM). The experiments also involved studying trabecular bone from C57BL/6J and C3H/HeJ mice. These mice have nearly the same size and weight, but have very different bone density. Thus, they were good candidates for a comparative study of healthy and osteoporotic human trabecular bone. TEM and SEM were used to characterize the hierarchical microstructure of trabecular bone in the inbred mice. The understanding of the hierarchical nature of healthy and osteoporotic bone microstructure is needed for a deeper understanding of the state of bone health and its mechanical properties.
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Krupke, Debra M., Dale A. Begley, Steven B. Neuhauser, Joel E. Richardson, John P. Sundberg, and Carol J. Bult. "Abstract B50: Mouse Tumor Biology (MTB) database–An integrated data resource for GEM, inbred strains, and PDX models of human cancer." In Abstracts: AACR Special Conference: Advances in Modeling Cancer in Mice: Technology, Biology, and Beyond; September 24-27, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.mousemodels17-b50.

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Reports on the topic "Inbred mice"

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Blank, Robert D. Genetics of Bone Mineralization and Morphology in Inbred Mice: Analysis of the HcB/Dem Recombinant Congenic Strains. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada400522.

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