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thy-nephritis

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https://www.readbyqxmd.com/read/26125859/decreased-tim-3-mrna-expression-in-peripheral-blood-mononuclear-cells-from-nephropathy-patients
#1
X Z Cai, N Liu, Y Qiao, S Y Du, Y Chen, D Chen, S Yu, Y Jiang
Increasing evidence shows that TIM-1 and TIM-3 in-fluence chronic autoimmune diseases, and their expression levels in immune cells from nephritic patients are still unknown. Real-time transcription-polymerase chain reaction analysis was used to deter-mine expression levels of TIM-1 and TIM-3 mRNA in peripheral blood mononuclear cells (PBMCs) from 36 patients with minimal change glo-merulopathy (MCG), 65 patients with lupus nephritis (LN), 78 patients with IgA nephropathy (IgAN), 55 patients with membranous nephropa-thy (MN), 22 patients with crescentic glomerulonephritis (CGN), 26 patients with anaphylactoid purpura nephritis (APN), and 63 healthy controls...
June 12, 2015: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/25871528/glomerular-damage-in-experimental-proliferative-glomerulonephritis-under-glomerular-capillary-hypertension
#2
Pei-Rong Wang, Hiroshi Kitamura, Akira Shimizu, Nobuaki Yamanaka
BACKGROUND/AIMS: Immunologically and hemodynamically mediated the destruction of glomerular architecture is thought to be the major causes of end-stage renal failure. The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular sclerosis after Thy-1 nephritis was induced. METHOD: Thy-1 nephritis was induced in the stroke-prone spontaneously hypertensive rat strain (SHR-SP) (group SP) and in age-matched Wistar-Kyoto (WKY) (group WKY) rats, following unilateral nephrectomy (UNX), and a vehicle was injected alone in UNX SHR-SP as control (group SC)...
2015: Kidney & Blood Pressure Research
https://www.readbyqxmd.com/read/25656369/anti-inflammatory-role-of-dpp-4-inhibitors-in-a-nondiabetic-model-of-glomerular-injury
#3
Yoshiki Higashijima, Tetsuhiro Tanaka, Junna Yamaguchi, Shinji Tanaka, Masaomi Nangaku
Dipeptidyl peptidase (DPP)-4 is an enzyme that cleaves and inactivates incretin hormones capable of stimulating insulin secretion from pancreatic β-cells. DPP-4 inhibitors are now widely used for the treatment of type 2 diabetes. Experimental studies have suggested a renoprotective role of DPP-4 inhibitors in various models of diabetic kidney disease, which may be independent of lowering blood glucose levels. In the present study, we examined the effect of DPP-4 inhibitors in the rat Thy-1 glomerulonephritis model, a nondiabetic glomerular injury model...
April 15, 2015: American Journal of Physiology. Renal Physiology
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