Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the role of nitric oxide (NO) in the development and progression of acute pancreatitis, we investigated the effect of different NO synthase inhibitors and NO donors on experimental pancreatitis in rats. Closed duodenal loop (CDL)-induced pancreatitis was produced in male Wistar rats, and the animals were treated with normal saline, the NO-synthase substrate L-arginine, the NO donor S-nitroso-N-acetylpenicillamine, aminoguanidine, which is a more powerful inhibitor of inducible NO synthase (iNOS) than is endothelial NO synthase (eNOS), and N-nitro-L-arginine methyl ester (L-NAME), a more powerful inhibitor of eNOS than of iNOS. All drugs were infused intravenously during a period of 6 or 12 h in each group. Pancreatic tissue was removed at 6 and 12 h after creating the CDL. L-Arginine, S-nitroso-N-acetyl-penicillamine, and aminoguanidine treatment had no effect on the elevation of serum pancreatic enzymes, whereas L-NAME administration significantly exacerbated their elevation. Pathologically, L-NAME treatment resulted in a significantly worse histologic score at 6 and 12 h, especially in terms of the degree of hemorrhage, acinar cell necrosis, and microvascular thrombosis. Addition of L-arginine clearly reversed the effect of L-NAME. Neither the NO substrate nor NO donor could inhibit the progression of hemorrhagic pancreatitis in CDL-induced pancreatitis. Aminoguanidine had no effect on the severity of the pancreatitis. We therefore concluded that NO production by eNOS may play a significant role in preventing the development and progression of acute pancreatitis.
Pancreas 1999 Nov
PMID:An endothelial nitric oxide synthase inhibitor aggravates CDL-induced acute pancreatitis in rats. 1054

Visceral organs display differential sensitivity to ischemia and reperfusion injury, but the cellular mechanisms underlying these differential responses are not completely understood. A significant response to ischemia identified in brain is stress to the endoplasmic reticulum (ER), as indicated by PKR-like endoplasmic reticulum eIF2alpha kinase (PERK)-mediated phosphorylation of eIF2alpha. To determine the generality of this response, we evaluated the PERK pathway in brain, GI tract, heart, liver, lung, kidney, pancreas and skeletal muscle following a clinically relevant, 10 min cardiac arrest-induced whole body ischemia and either 10 or 90 min reperfusion. The potential role of nitric oxide (NO) on PERK activation was investigated by conducting ischemia and reperfusion in the presence and absence of the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME). Organ stress could be ranked with respect to the degree of eIF2alpha phosphorylation at 10 min reperfusion. Brain, kidney and GI tract were reactive organs, showing 15 to 20-fold increases in eIF2alpha(P) compared to controls. Moderately reactive organs included liver and heart, showing <10-fold increases in eIF2alpha(P). Pancreas, lung and skeletal muscle were nonreactive. Although treatment of cultured neuroblastoma 104 cells with the NO-donor S-nitroso-N-acetyl-penicillamine (SNAP) activated PERK, administration of L-NAME had no effect on PERK activation or eIF2alpha phosphorylation in organs following ischemia and reperfusion. Thus, PERK is activated differentially in reperfused organs independent of NO. These results suggest that ER stress may play a role in differential responses of viscera to ischemia and reperfusion. ER stress in viscera may contribute to the pathophysiology of resuscitation from cardiac arrest and during organ transplantation procedures.
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PMID:PERK is activated differentially in peripheral organs following cardiac arrest and resuscitation. 1602 20

The 3 International Conference for Cancer Metabolism and Therapy was successfully held at the South Hospital Conference Center of Shanghai First People's Hospital, nearly 200 international experts from the field of cancer metabolism and therapy and about two thousand local scientists attended the conference. The conference was sponsored by the Yangtze River Delta City Group Hospital Synergistic Development Strategic Alliance, the China Anti-Cancer Association Cancer Metabolism Professional Committee, the Chinese Association for Cancer Metabolism and Therapy under Chinese Medical Doctoral Association-Clinical Precision Medicine, and co-organized by the First People's Hospital Affiliated to Shanghai Jiaotong University, and Shanghai Jiao Tong University School of Basic Medicine Undertake, Translational Medicine Network, Shanghai Anti-Cancer Association Youth Council, Fudan University Affiliated Tumor Hospital, University of California, Los Angeles, Agi Hirshberg Center for Pancreatic Diseases and Hirshberg Foundation for Pancreatic Cancer Research, Dalian University of Technology, New York-Presbyterian, American Cancer Research Association (AACR). The theme of the conference was 'Inheritance, Innovation, Excellence, Leading' and its aim is to create a high-end academic exchange platform to discuss new technologies, new methods, and new products in tumor metabolism, tumor immunity, tumor markers and other fields. The conference involves cancer metabolism reprogramming, metabolism and tumor microenvironment, lipid metabolism, non-metabolic function of metabolic enzymes, metabolism and epigenetics, clinical transformation, new technologies for tumor immunotherapy, clinical application of tumor immunotherapy, emerging targeted therapy, PD-1/PD-L1 technology, CAR-T technology, novel tumor protein markers, novel tumor methylation markers, ctDNA, CTC, etc. The meeting ended in a lively discussion among scientists from different levels who truly benefit from the sessions about cancer metabolism and treatment. The next meeting is planned to be held October 2 through October 6, 2019 in Los Angeles, Calif. The meeting venue will be announced accordingly in the meeting web site (www.cmt.org).
Pancreas 2020 02
PMID:Proceedings of the 3rd International Conference for Cancer Metabolism and Therapy, October 12-14, 2018, Shanghai, China. 3204 50