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Vitaly Ablamunits, Simon Klebanov, Sharon Y Giese, and Kevan C Herold

recipient mice are on C57BL/6 background known to have relatively high NK activity compared with NOD strain ( Poulton et al . 2001 ). This may be overcome by breeding an inactivated allele of common cytokine receptor γ chain: human PBMC readily expand in

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S Morimoto, C A Mendoza-Rodríguez, M Hiriart, M E Larrieta, P Vital, and M A Cerbón

-cell death in STZ-diabetic mice and nonobese diabetic (NOD) mice. NOD mice spontaneously develop auto-immune diabetes with remarkable similarity to human insulin-dependent diabetes mellitus (IDDM) ( O’Brien et al. 1997 ). Injection of STZ induces

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Tsutomu Wada, Akari Ishikawa, Eri Watanabe, Yuto Nakamura, Yusuke Aruga, Hayate Hasegawa, Yasuhiro Onogi, Hiroe Honda, Yoshinori Nagai, Kiyoshi Takatsu, Yoko Ishii, Masakiyo Sasahara, Daisuke Koya, Hiroshi Tsuneki, and Toshiyasu Sasaoka

exacerbate local chronic inflammation. Interestingly, macrophages from myeloid-specific MR knockout mice exhibit the transcriptional profile of M2 macrophage ( Usher et al. 2010 ). Currently, however, the expression of MR in M1- and M2-adipose tissue

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Jessica R Mader, Zachary T Resch, Gary R McLean, Jakob H Mikkelsen, Claus Oxvig, Ronald J Marler, and Cheryl A Conover

Gerontology 45 366 – 374 . ( doi:10.1016/j.exger.2010.02.009 ) Tack I Elliot SJ Potier M Rivera A Striker GE Striker LJ 2002 Autocrine activation of the IGF-I signaling pathway in mesangial cells isolated from diabetic NOD mice . Diabetes

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Diana Choi, Stephanie A Schroer, Shun Yan Lu, Erica P Cai, Zhenyue Hao, and Minna Woo

shown the integral role of caspases-3 and -8 in pancreatic β-cell apoptosis in experimental models of diabetes. Mice lacking caspase-3 are protected from β-cell apoptosis and diabetes induced by both streptozotocin (STZ; Liadis et al . 2003 ) and c

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Jian Ma, Xin He, Yan Cao, Kienan O’Dwyer, Katherine M Szigety, Yuan Wu, Buddha Gurung, Zijie Feng, Bryson W Katona, and Xianxin Hua

:// ) Rui J Deng S Lebastchi J Clark PL Usmani-Brown S Herold KC 2016 Methylation of insulin DNA in response to proinflammatory cytokines during the progression of autoimmune diabetes in NOD mice

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M Fraenkel, J Caloyeras, S-G Ren, and S Melmed

1997 ). pttg -null male mice develop hyperglycemia secondary to hypoinsulinemia starting at 6 months of age ( Wang et al. 2003 ). By 1 year, >80% of male pttg −/− mice are diabetic with hypoinsulinemia secondary to reduced post-natal β

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Hamzeh Karimkhanloo, Stacey N Keenan, Emily W Sun, David A Wattchow, Damien J Keating, Magdalene K Montgomery, and Matthew J Watt

small-molecule CTSS inhibitors in mice improved glucose tolerance by reducing hepatic glucose production (HGP) ( Lafarge et al. 2014 ) and attenuated the onset of type 1 diabetes ( Hsing et al. 2010 ). While these studies are informative, the direct

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Ashley Patton, Tyler Church, Caroline Wilson, Jean Thuma, Douglas J Goetz, Darlene E Berryman, Edward O List, Frank Schwartz, and Kelly D McCall

MC Benencia F Malgor R Schwartz FL 2013 Phenylmethimazole suppresses dsRNA-induced cytotoxicity and inflammatory cytokines in murine pancreatic beta cells and blocks viral acceleration of type 1 diabetes in NOD mice . Molecules 18 3841

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Eva Kassi and Athanasios G Papavassiliou

obesity . Nature Medicine 7 941 – 946 . Yoon JW Yoon CS Lim HW Huang QQ Kang Y Pyun KH Hirasawa K Sherwin RS Jun HS 1999 Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells . Science 284