Methods: We induced DM in twenty vervet monkeys (Chlorocebus aethiops) by intravenous administration of either 45 (n = 8, ST7-45) or 55 mg/kg STZ (n = 12, STZ-55); ten control (CTL) monkeys received saline. Results: Overall there was 15% mortality, likely secondary to renal toxicity. Twice-daily insulin therapy was initiated to maintain comparable glycemic control, confirmed by comparable glycated hemoglobin levels. Exogenous insulin requirements increased rapidly for 4 weeks; STZ-45 insulin doses stabilized thereafter while STZ-55 doses

continued to increase through 16 weeks. Glucose tolerance testing and arginine-stimulated insulin secretion confirmed 80-90% reduction GNS-1480 datasheet in pancreatic beta cell function in both groups. Body weight was reduced in all STZ monkeys, with return to baseline only in STZ-45 at DZNeP research buy 16 wks. Elevated blood urea nitrogen (BUN) and creatinine were noted in the STZ-55 group. Alkaline phosphatase (ALKP) was also increased with STZ-55 (p < 0.05 vs. CR) whereas ST7-45 ALKP elevation resolved by study end. Red cell parameters were reduced in all STZ monkeys, but more severely in the STZ-55 group. Discussion: We have demonstrated that a model of DM can be induced and maintained in vervets with a single dose of STZ. The lower

dose of STZ (45 mg/kg) significantly improved the toxicity profile without altering efficacy in inducing DM. Finally, sufficient time following induction is recommended to allow transient renal, hepatic and hematologic parameters to resolve. (C) 2011 Elsevier Inc. All rights reserved.”
“The fate of notochord cells during disc development and aging is still a subject of debate. Cells with the typical notochordal morphology disappear from the disc within the first decade of life. However, the pure morphologic differentiation of notochordal from non-notochordal disc cells can be difficult,

prompting the use of cellular markers. Previous reports on these notochordal cell markers only explored the occurrence in young age groups without considering changes during Proteasome inhibitor disc degeneration. The aim of this study, therefore, was to investigate presence, localization, and abundance of cells expressing notochordal cell markers in human lumbar discs during disc development and degeneration. Based on pilot studies, cytokeratins CK-8, -18 and -19 as well as Galectin-3 were chosen from a broad panel of potential notochordal cell markers and used for immunohistochemical staining of 30 human lumbar autopsy samples (0-86 years) and 38 human surgical disc samples (26-69 years). In the autopsy group, 80% of fetal to adolescent discs (0-17 years) and 100% of young adult discs (18-30 years) contained many cells with positive labeling.