Search Results

You are looking at 21 - 30 of 50 items for :

  • All content x
Clear All
Free access

Jennifer A Crookshank, Daniel Serrano, Gen-Sheng Wang, Christopher Patrick, Baylie S Morgan, Marie-France Paré, and Fraser W Scott

the rate-limiting enzyme in phospholipid biosynthesis, was downregulated 2.2 fold, similar to NOD mice ( Lindfors et al. 2009 ). Numerous genes associated with disease resistance were identified that were involved in islet function: Rgs2 , Cyth3

Free access

L Zhao, Z Li, M Kullin, L A H Borg, and F A Karlsson

) 51 –57. Atkinson MA , Maclaren NK & Luchetta R 1990 Insulitis and diabetes in NOD mice reduced by prophylactic insulin therapy. Diabetes 39 933 –937. Bergsten P , Gylfe E, Wesslén N

Free access

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

NOD.scid mice that carry this defect (V Ablamunits & K C Herold, unpublished observations; King et al . 2009 , Pino et al . 2010 ). Alternatively, leptin deficiency may be bred onto Rag1 -deficient, perforin-deficient NOD mice, which have been

Free access

Jorge N Artaza and Keith C Norris

-induced apoptosis in non-obese diabetic (NOD) mice and protects against diabetes . Clinical and Experimental Immunology 112 181 – 187 . Dusso AS Brown AJ 1998 Mechanism of vitamin D action and its regulation . American Journal of Kidney Diseases 32

Free access

Rosalia C M Simmen, Dustin M Brown, Charles M Quick, Iad Alhallak, Tyler Rose, Shi J Liu, and Angela S Kelley

endometriosis: link to ovarian cancer . Endocrinology 626 – 638 . ( https://doi.org/10.1210/en.2018-00794 ) 30657901 Burke SD Dong H Hazan AD Croy BA 2007 Aberrant endometrial features of pregnancy in diabetic NOD mice . Diabetes 2919 – 2926

Free access

Gabriele Wolf, Nicole Aumann, Marta Michalska, Antje Bast, Jürgen Sonnemann, James F Beck, Uwe Lendeckel, Philip Newsholme, and Reinhard Walther

that PrxI expression was dramatically reduced in the islets of diabetogenic NOD mice (data not shown). Here we investigated whether the mitochondrial thioredoxin-2–PRX III system could be helpful in preventing oxidative stress-induced damage or

Free access

José Edgar Nicoletti-Carvalho, Tatiane C Araújo Nogueira, Renata Gorjão, Carla Rodrigues Bromati, Tatiana S Yamanaka, Antonio Carlos Boschero, Licio Augusto Velloso, Rui Curi, Gabriel Forato Anhê, and Silvana Bordin

al . 2003 , Choi et al . 2004 ), and to increase cell death in primary islets treated with FFAs ( Ellingsgaard et al . 2008 ). Paradoxically, it was observed that the incidence of T1DM in non-obese diabetic (NOD) mice decreased when the mice were

Free access

Kouki Mori, Katsumi Yoshida, Ayumi Komatsu, Jun-ichi Tani, Yoshinori Nakagawa, Saeko Hoshikawa, and Sadayoshi Ito

. Green EA , Eynon EE & Flavell RA 1998 Local expression of TNFα in neonatal NOD mice promotes diabetes by enhancing presentation of islet antigens. Immunity 9 733 –743. Guha M & Mackman N 2001 LPS induction of gene

Free access

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

Free access

Jean-Claude Henquin, Myriam Nenquin, Andras Szollosi, Atsutaka Kubosaki, and Abner Louis Notkins

Hendricks W Notkins AL 2004 Targeted disruption of the IA-2β gene causes glucose intolerance and impairs insulin secretion but does not prevent the development of diabetes in NOD mice . Diabetes 53 1684 – 1691 . Kubosaki A Nakamura S Notkins AL