Relevant bibliographies by topics / C57BL/6 wild-type 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 'C57BL/6 wild-type mice'

Author: Grafiati
Published: 5 June 2025
Last updated: 1 August 2025

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Journal articles on the topic "C57BL/6 wild-type mice"

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Durmus, Nedim, Wen-Chi Chen, Sung-Hyun Park та ін. "Resistin-like Molecule α and Pulmonary Vascular Remodeling: A Multi-Strain Murine Model of Antigen and Urban Ambient Particulate Matter Co-Exposure". International Journal of Molecular Sciences 24, № 15 (2023): 11918. http://dx.doi.org/10.3390/ijms241511918.

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Pulmonary hypertension (PH) has a high mortality and few treatment options. Adaptive immune mediators of PH in mice challenged with antigen/particulate matter (antigen/PM) has been the focus of our prior work. We identified key roles of type-2- and type-17 responses in C57BL/6 mice. Here, we focused on type-2-response-related cytokines, specifically resistin-like molecule (RELM)α, a critical mediator of hypoxia-induced PH. Because of strain differences in the immune responses to type 2 stimuli, we compared C57BL/6J and BALB/c mice. A model of intraperitoneal antigen sensitization with subseque
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Kenyon, Nicholas J., Albert van der Vliet, Bettina C. Schock, Tatsuya Okamoto, Gabrielle M. McGrew, and Jerold A. Last. "Susceptibility to ozone-induced acute lung injury in iNOS-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 3 (2002): L540—L545. http://dx.doi.org/10.1152/ajplung.00297.2001.

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Mice deficient in inducible nitric oxide synthase (iNOS; C57Bl/6Ai-[KO] NOS2 N5) or wild-type C57Bl/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclea
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SINGH, Uma, Shumei ZHONG, Momiao XIONG, Tong-bin LI, Allan SNIDERMAN, and Ba-Bie TENG. "Increased plasma non-esterified fatty acids and platelet-activating factor acetylhydrolase are associated with susceptibility to atherosclerosis in mice." Clinical Science 106, no. 4 (2004): 421–32. http://dx.doi.org/10.1042/cs20030375.

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Animal models provide vital tools to explicate the pathogenesis of atherosclerosis. Accordingly, we established two atherosclerosis-prone mice models: (i) mice lacking the LDL (low-density lipoprotein) receptor (LDLR) and the ability to edit apo (apolipoprotein) B mRNA (Apobec1; designated LDb: LDLR-/-Apobec1-/-), and (ii) mice with the LDb background, who also overexpressed human apoB100 (designated LTp: LDLR-/-Apobec1-/-ERhB+/+). Both LDb and LTp mice had markedly elevated levels of LDL and increased levels of NEFAs (non-esterified fatty acids) compared with C57BL/6 wild-type mice. However,
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Pappo, Jacques, Deirdre Torrey, Lillian Castriotta, Anneli Savinainen, Zita Kabok, and Alexander Ibraghimov. "Helicobacter pylori Infection in Immunized Mice Lacking Major Histocompatibility Complex Class I and Class II Functions." Infection and Immunity 67, no. 1 (1999): 337–41. http://dx.doi.org/10.1128/iai.67.1.337-341.1999.

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ABSTRACT The role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pyloriinfection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pylori SS1 resulted in significantly greater (P ≤ 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization with H. pylori whole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude of H. pylori infection in C57BL/6 wild-type (P = 0.0083) and MHC class I knockout mice (P = 0.0048), but it had no effect
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Akoum, J., K. Tahiri, F. Etienne, M. T. Corvol, F. Rannou, and C. Nguyen. "AB0063 AGING CARTILAGE IN WILD-TYPE MICE: AN OBSERVATIONAL STUDY." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1333.2–1333. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5989.

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Background:Many animal models of osteoarthritis (OA) have been used to study the pathogenesis of cartilage degeneration1. In mice, spontaneous OA can occur in wild-type or genetically modified animals. The first report of spontaneous OA developing in wild-type mice was published in 19562and changes affecting the knee joint were further related to OA by using ultrastructural- histochemical analyses. However, a quantitative assessment of age-related evolution of OA-type cartilage lesions is lacking. The OA Research Society International (OARSI) grading score was adapted to semi-quantify histopat
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Zhong, Zifu, João Paulo Portela Catani, Séan Mc Cafferty, et al. "Immunogenicity and Protection Efficacy of a Naked Self-Replicating mRNA-Based Zika Virus Vaccine." Vaccines 7, no. 3 (2019): 96. http://dx.doi.org/10.3390/vaccines7030096.

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To combat emerging infectious diseases like Zika virus (ZIKV), synthetic messenger RNAs (mRNAs) encoding viral antigens are very attractive as they allow a rapid, generic, and flexible production of vaccines. In this work, we engineered a self-replicating mRNA (sr-mRNA) vaccine encoding the pre-membrane and envelope (prM-E) glycoproteins of ZIKV. Intradermal electroporation of as few as 1 µg of this mRNA-based ZIKV vaccine induced potent humoral and cellular immune responses in BALB/c and especially IFNAR1-/- C57BL/6 mice, resulting in a complete protection of the latter mice against ZIKV infe
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Curran, Shelly, and Joseph Kovacs. "Altered Trained immunity in AID−/− versus wild type mice following infection with Pneumocystis murina." Journal of Immunology 208, no. 1_Supplement (2022): 58.12. http://dx.doi.org/10.4049/jimmunol.208.supp.58.12.

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Abstract Pneumocystis pneumonia continues to be a life-threatening infection in immunocompromised individuals. Dendritic cells are key antigen presenters to CD4+ T cells, which are critical to controlling Pneumocystis infection along with B cells. β-1,3 glucans are found in the cell wall of the cyst form of Pneumocystis. Glucans derived from other fungi have been shown to induce trained immunity. Therefore, we explored if Pneumocystis infection can induce a trained immunity response in C57Bl/6 (wild type) mice following exposure via a natural route of infection. We also tested activation-induc
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Kopić, Alexandra, Karima Benamara, Maria Schuster, et al. "Coagulation phenotype of wild-type mice on different genetic backgrounds." Laboratory Animals 53, no. 1 (2018): 43–52. http://dx.doi.org/10.1177/0023677218811059.

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Genetically engineered mouse models are used to investigate beneficial treatment in haemophilia by comparison with wild-type mice. It has been recognized that wild-type and haemophilic mice of different genetic backgrounds show different bleeding phenotypes. We assessed ex-vivo coagulation parameters in nine wild-type substrains of 129S1/Sv, BALB/c and C57BL/6 mice applying thromboelastography (TEG), activated partial thromboplastin time (aPTT), prothrombin time (PT) and fibrinogen levels. The comprehensive ex-vivo data are discussed in view of results from a tail-tip bleeding assay. Time to f
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Hertz, Cheryl J., Hanna Filutowicz та John M. Mansfield. "Resistance to the African Trypanosomes Is IFN-γ Dependent". Journal of Immunology 161, № 12 (1998): 6775–83. http://dx.doi.org/10.4049/jimmunol.161.12.6775.

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Abstract The role of variant surface glycoprotein (VSG)-specific Th cell responses in determining resistance to the African trypanosomes was examined by comparing Th cell responses in relatively resistant and susceptible mice as well as in cytokine gene knockout mice infected with Trypanosoma brucei rhodesiense. Resistant B10.BR and C57BL/6 mice expressed Th1 cell cytokine responses to VSG stimulation during infection, while susceptible C3H mice produced weak or no Th1 cell cytokine responses. Neither resistant B10.BR and C57BL/6 mice nor susceptible C3H mice made detectable Th2 cell cytokine
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Boesteanu, Alina C., Jillian A. Norton, Martin Turner, and Peter D. Katsikis. "The role of p110delta in the immunopathology of influenza virus infection (130.12)." Journal of Immunology 182, no. 1_Supplement (2009): 130.12. http://dx.doi.org/10.4049/jimmunol.182.supp.130.12.

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Abstract Infection of C57Bl/6 mice with influenza virus is accompanied by morbidity manifested as weight loss and lung pathology. We have found that mice that have an inactivating mutation in the leucocyte-specific phosphoinositide kinase 3 (PIK3) isoform p110delta (p110delta-/- on a C57BL/6 background manifest significantly reduced morbidity after influenza virus infection compared to C57BL/6 mice. RAG-/- mice also showed reduced morbidity compared to wild type animals, indicating a role for lymphocytes in this pathology. At day 6 postinfection activated pulmonary T cells and NK cells were gr
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Dissertations / Theses on the topic "C57BL/6 wild-type mice"

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Vulin, Johann. "Caractérisation des agents infectieux responsables de deux maladies à prion : l'ESB atypique de type H chez les bovins et la tremblante de type "CH1641" chez les petits ruminants." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10210.

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Nous avons entrepris la caractérisation de la protéine prion pathologique par Western blot à partir d’isolats de petits ruminants et de bovins atteints d’Encéphalopathie Spongiforme Subaiguë Transmissible (ESST) afin d’identifier des signatures moléculaires divergeant de la signature associée à l’ESST affectant habituellement ces animaux ; la tremblante classique pour les petits ruminants et l’ESB classique (ESB-C) pour les bovins. Cette étude a permis d’évaluer la fréquence de phénotypes inhabituels et a contribué à envisager les formes d’ESB atypiques comme sporadiques. Ensuite la transmissi
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BERNARDO, Ana Karolina de Santana Nunes. "Avaliação dos efeitos do inibidor de fosfodiesterase-5 sobre os mecanismos regulatórios da neuroinflamação, em modelo de desmielinização induzido em camundongos C57BL/6 wild type e knockout para iNOS." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/17352.

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Submitted by Isaac Francisco de Souza Dias (isaac.souzadias@ufpe.br) on 2016-07-13T17:12:13Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Tese completa final.pdf: 16433373 bytes, checksum: 4fb5e2d57332bcee63dcfd63d64a9b42 (MD5)<br>Made available in DSpace on 2016-07-13T17:12:13Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Tese completa final.pdf: 16433373 bytes, checksum: 4fb5e2d57332bcee63dcfd63d64a9b42 (MD5) Previous issue date: 2016-02-19<br>O Sildenafil (Viagra®) é um inibido
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NUNES, Ana Karolina de Santana. "Avaliação dos efeitos do inibidor de fosfodiesterase-5 sobre as células gliais e a re-mielinização, em modelo de desmielinização induzido em camudongos C57BL/6 WILD TYPE e KONCKOUT para iNOS." Universidade Federal de Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/12599.

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Submitted by Chaylane Marques (chaylane.marques@ufpe.br) on 2015-03-13T18:16:16Z No. of bitstreams: 2 Dissertação completa final 2.pdf: 2784660 bytes, checksum: 15ae7aeb47a5c6076dc1ce82e7adefad (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5)<br>Made available in DSpace on 2015-03-13T18:16:16Z (GMT). No. of bitstreams: 2 Dissertação completa final 2.pdf: 2784660 bytes, checksum: 15ae7aeb47a5c6076dc1ce82e7adefad (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2012-02-10<br>CNPQ; FACEPE<br>O Sildenafil (V
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Books on the topic "C57BL/6 wild-type mice"

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Hesse, Lautaro Daniel. Estudio del impacto de la ausencia de Kir6.2/K-ATP en la regeneración hepática posterior a una hepatectomía parcial. Teseo, 2022. http://dx.doi.org/10.55778/ts878848969.

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&lt;p&gt;Comprender los mecanismos que rigen la regeneración hepática es crucial para el manejo apropiado de los procesos regenerativos y el desarrollo de nuevas terapias en situaciones donde es necesario recuperar la masa hepática perdida. Se plantea la siguiente pregunta: ¿Existe alguna relación entre la expresión de Kir6.2 y la regeneración hepática posterior a una hepatectomía parcial (HP)? Se utilizaron ratones de las cepas C57BL/6 (WT, &lt;i&gt;wild-type&lt;/i&gt;) como animales control, y ratones &lt;i&gt;knockout&lt;/i&gt; para Kir6.2 (Kir-/-), los cuales fueron sometidos a HP de dos t
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Book chapters on the topic "C57BL/6 wild-type mice"

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Pyo, Hyun Mi, Jie Yun Park, Sue Nie Park, Hyun Su Kim, Kee Sun Shin, and Har Young Poo. "Immunization with Virus-Like Particle of Human Papillomavirus Type 16 L1 Elicits CTL Immune Response in C57BL/6 Mice." In Key Engineering Materials. Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-958-x.119.

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Jana, Rishika, Souvik Karmakar, Bishal Hazra, Subhadeep Roy, and Jayasri Das Sarma. "Mice as an Experimental Model to Understand the Pathobiology of Diseases." In Rodents and Their Role in Ecology, Medicine and Agriculture [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.1001835.

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Murine models are widely used in scientific research because they share many genetic similarities with humans, making them a valuable tool for studying various diseases. C57BL/6 is an experimental mouse model to study the demyelination and inflammation etiology of Multiple Sclerosis (MS). Intracranial inoculation of neurotropic murine β-coronavirus strain of Mouse hepatitis virus in C57BL/6 mice induces demyelination with or without axonal loss, providing many insights regarding the mechanism of MS as well as SARS-CoV-2 mediated pulmonary and neuro pathology in humans. By selectively using kno
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Kaur, Harpreet, Svetlana Golovko, Mikhail Y. Golovko, Surjeet Singh, Diane C. Darland, and Colin K. Combs. "Effects of Probiotic Supplementation on Short Chain Fatty Acids in the AppNL–G–F Mouse Model of Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220028.

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Background: The intestinal microbiota and its metabolites, particularly short-chain fatty acids (SCFAs), have been implicated in immune function, host metabolism, and even behavior. Objective: This study was performed to investigate whether probiotic administration influences levels of intestinal microbiota and their metabolites in a fashion that may attenuate brain changes in a mouse model of Alzheimer’s disease (AD). Methods: C57BL/6 wild-type (WT) mice were compared to AppNL–G–F mice. The animals were treated with either vehicle or probiotic (VSL#3) for 8 weeks. Fecal microbiome analysis al
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Sahu, Bijayani, Amy R. Mackos, Angela M. Floden, Loren E. Wold, and Colin K. Combs. "Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210013.

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Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and neuronal death. There are several well-established genetic and environmental factors hypothesized to contribute to AD progression including air pollution. However, the molecular mechanisms by which air pollution exacerbates AD are unclear. Objective: This study explored the effects of particulate matter exposure on AD-related brain changes using the APP/PS1 transgenic model of disease. Methods: Male C57BL/6;C3H wild type and APP/PS
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Armstrong, Tyler D., Usa Suwannasual, Conner L. Kennedy, et al. "Exposure to Traffic-Generated Pollutants Exacerbates the Expression of Factors Associated with the Pathophysiology of Alzheimer’s Disease in Aged C57BL/6 Wild-Type Mice." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210017.

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Background: Multiple studies report a strong correlation between traffic-generated air pollution-exposure and detrimental outcomes in the central nervous system (CNS), including Alzheimer’s disease (AD). Incidence of AD is rapidly increasing and, worldwide, many live in regions where pollutants exceed regulatory standards. Thus, it is imperative to identify environmental pollutants that contribute to AD, and the mechanisms involved. Objective: We investigated the effects of mixed gasoline and diesel engine emissions (MVE) on the expression of factors involved in progression of AD in the hippoc
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de la Monte Suzanne M., Lyn-Cook Jr. Lascelles E., Lawton Margot, et al. "Hepatic Ceramide May Mediate Brain Insulin Resistance and Neurodegeneration in Type 2 Diabetes and Non-alcoholic Steatohepatitis." In Advances in Alzheimer’s Disease. IOS Press, 2011. https://doi.org/10.3233/978-1-60750-733-8-179.

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Background: Obesity, type 2 diabetes mellitus (T2DM), and non-alcoholic steatohepatitis (NASH) can lead to cognitive impairment and neurodegeneration. Experimental high fat diet (HFD) induced obesity with T2DM causes neurodegeneration with brain insulin resistance. Objective: Since ceramides are neurotoxic, cause insulin resistance, and are increased in T2DM, we investigated their potential role in neurodegeneration. Methods: C57BL/6 mice were pair-fed HFD or control diets for 4-20 weeks. Pro-ceramide genes and biochemical indices of neurodegeneration were measured. In vitro experiments direct
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Dymecki, Susan M. "Site-specific recombination in cells and mice." In Gene Targeting. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199637928.003.0006.

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The use of site-specific recombinase systems has revolutionized our ability to genetically manipulate embryonic stem (ES) cells and mice. Recent advances using the Cre-loxP and Flp-FRT systems have now made it possible to generate ‘clean’ germline mutations following a single gene targeting event, as well as to (in)activate genes in a conditional manner in the living mouse. Not only can target gene mutations be induced in a spatially and temporally restricted fashion, but lineage tracers can be activated in specific progenitor populations to chart cell fate directly in the wild-type or mutant
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"E." In Genetic variants and strains of the Laboratory mouse, edited by Mary F. Lyon, Sohaila Rastan, and S. D. M. Brown. Oxford University PressOxford, 1996. http://dx.doi.org/10.1093/oso/9780198548690.003.0007.

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Abstract This locus is probably homologous with the extension locus which occurs in several other mammals and governs the extension of eumelanin with the opposite effects on phaeomelanin. In this series of alleles, in contrast to those of the agouti locus, the dominant alleles produce partial or full extension of black, the wild-type allele produces normal extension of yellow and black as in the agouti pattern, and the recessive alleles produce partial or full extension of yellow (7). Because the skin cells of e/e mutant mice produce eumelanin after treatment with dibutyryl cyclic AMP, it was
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Conference papers on the topic "C57BL/6 wild-type mice"

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Dalenogare, Diéssica Padilha, Diulle Spat Peres, Maria Fernanda Pessano Fialho, and Gabriela Trevisan dos Santos. "Periorbital nociception in a progressive multiple sclerosis mouse model is dependent on TRPA1 channel activation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.610.

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Background: Headache is one of the main painful symptoms described by multiple sclerosis patients. Previously, it was described that neuropathic pain-like behaviors were dependent on transient receptor potential ankyrin 1 (TRPA1) activation in a progressive multiple sclerosis model induced by experimental autoimmune encephalomyelitis (PMS- EAE) in mice. Objective: Here, we aimed to investigate if periorbital mechanical allodynia induced by PMS-EAE was also related to TRPA1 activation. Design and setting: Federal University of Santa Maria, Santa Maria, RS, Brazil. Methods: To induce a PMS-EAE w
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Tur, Dariya, Oleg Shevelev, and Andrey Akulov. "COMPARATIVE MRI STUDY OF THE BRAIN MICE GENETIC LINES: C57BL/6, CD1, NOD.SCID IN A PHARMACOLOGICAL MODEL OF TYPE 1 DIABETES MELLITUS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2354.sudak.ns2021-17/375-376.

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Myers, Kristin M., and Thao D. Nguyen. "Modeling the Inflation Response of C57BL/6 Mouse Sclera." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53181.

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Small rodent models have become increasingly useful to investigate how the mechanical properties of soft tissues may influence disease development. These animal models allow access to aged, diseased, or genetically-altered tissue samples, and through comparisons with wild-type or normal tissue it can be explored how each of these variables influence tissue function. The challenges to deriving meaningful material parameters for these small tissue samples include designing physiologically-relevant mechanical testing protocols and interpreting the experimental load-displacement data in an appropr
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Mutoh, Michihiro, Naoya Teraoka, Shinji Takasu, et al. "Abstract 2837: Adiponectin knockout enhances intestinal carcinogenesis in Min and wild-type mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2837.

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Bryan, Andrea, Amy Sung, Ian Lian, and Jeffrey Omens. "The Role of Tropomodulin in Cardiac Function and Remodeling." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61363.

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Tropomodulin is an actin-capping protein in cardiac muscle, and is associated with both sarcomeric and cytoskeletal actin filaments. Homozygous knockout of erythrocyte tropomodulin (E-Tmod) is embryonically lethal, but heterozygous knockout (+/-) mice survive. Heterozygous E-Tmod knockout resulted in smaller right ventricle (RV) cavities and free walls compared to wild type. To investigate the effect of heterozygous tropomodulin knockout on mouse cardiac function and remodeling, mice (n=6 to 9) were subjected to 5 weeks of hypoxia to increase loading conditions on the RV via pulmonary hyperten
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Peterson, Sherket B., Zannatul Ferdous, Magnus Höök, and K. Jane Grande-Allen. "Decorin Deficient Cells Demonstrate Increased Proliferation and Altered Phenotypic Properties." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176043.

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Decorin (DCN), a class I member of the small leucine-rich proteoglycan (SLRP) family, is composed of a protein core of approximately 40kDa [1, 2] substituted with a single glycosaminoglycan (GAG) chain of chondroiton/dermatan sulfate on the N-terminal site [3]. DCN has been reported to interact with collagen [4,5] via its core protein, influence collagen fibrillogenesis [6], and inhibit the growth rates of various cell types when added exogenously to cell cultures [5,6]. There has recently been growing interest and studies in DCN related research using the knockout (KO) mice model which provid
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Reports on the topic "C57BL/6 wild-type mice"

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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease obser
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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in esta
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