Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histopathological study was made of 12 Merino sheep - five splenectomized and seven intact - experimentally infected with Babesia ovis. Non-purulent encephalitis; initially exudative and subsequently interstitial pneumonia; pericarditis, myocarditis and haemorrhagic endocarditis; centrilobular necrotic hepatitis; hyperplasia of the lymphoreticular system; necrosis and vascular changes in adrenal glands were observed. The kidney was the most severely affected organ, exhibiting acute tubular necrosis typical of kidney shock syndrome. The lesions observed were suggestive of hypovolemic shock culminating in haemorrhagic diathesis owing to consumptive coagulopathy. Additionally, the massive release of catabolites from lysis and necrosis apparently produced endotoxic shock.
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PMID:Histopathological changes in sheep experimentally infected with Babesia ovis. 202 25

Renal ischemia/reperfusion (I/R) injury is one of the main causes of postoperative renal failure. Activated neutrophils are implicated in the development of I/R-induced renal failure. JTE-607 has been reported to be a potent inhibitor of the multiple inflammatory cytokines in the endotoxic shock mouse model and heart Langendorff perfusion model. In this study, we examined whether JTE-607 attenuates I/R-induced renal injury by reducing neutrophil activation. Male wistar rats were intravenously administered JTE-607 (JTE group, 30 mg/kg) or 5% mannitol (control group) 30 min before ischemia. JTE-607 reduced the I/R-induced increases in the serum concentrations of blood urea nitrogen and creatinine, and improved the histopathologic changes, including acute tubular necrosis. I/R-induced an increase in neutrophil activation, reflected by increases in renal cytokine-induced neutrophil chemoattractant (CINC)-1 and myeloperoxidase (MPO) concentrations which were significantly reduced by JTE-607. These findings indicate that JTE-607 attenuates I/R-induced acute renal injury, probably by inhibiting neutrophil activation. JTE-607 might be a novel therapeutic strategy for the protection of postoperative renal failure in surgery associated with renal ischemia as well as renal transplantation.
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PMID:JTE-607, an inflammatory cytokine synthesis inhibitor, attenuates ischemia/reperfusion-induced renal injury by reducing neutrophil activation in rats. 1869 26