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NOEL S. STURM ANN MARIE HUTZLER CLINTON S. DAVID BASSEM Y. AZIZEH DEV TRIVEDI VICTOR J. HRUBY 《Chemical biology & drug design》1997,49(4):293-299
We have designed and synthesized eight compounds 2-9 which incorporate neutral, hydrophobic amino acid residues in positions 9, 11 and 16 of the glucagon molecule: (2) [desHis1,Va19,11e11,16] glucagon amide, (3) [desHis1,Val9,11,16]glucagon amide, (4) [desHis1,Va19,Leu11,16]glucagon amide, (5) [desHis1,Nle9,11e11,16]glucagon amide, (6) [desHis1,Nle9,Val11,16]glucagon amide, (7) [desHis1,Nle9,Leu11,16]glucagon amide, (8) [desHis1,Val9,Leu11,16,Lys17,18,Glu21]glucagon amide and (9) [desHis1,Nle9,Leu11,16,Lys17,18,Glu21]glucagon amide. The effect of neutral, hydrophobic residues at positions 9, 11 and 16 led to good binding to the glucagon receptor. Compared to glucagon (IC50= 1.5 nM), analogues 2-9 were found to have IC50 values of 6.0, 6.0, 11.0, 9.0, 2.5, 2.8, 6.5 and 7.0 nM, respectively. When these compounds were tested for their ability to block adenylate cyclase (AC) activity, they were found to be antagonists having no stimulation of adenyl cyclase, with PA2, values of 6.15, 6.20, 6.30, 7.25, 6.10, 7.30, 6.25 and 7.25, respectively. © Munksgaard 1997. 相似文献
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SANGHAMITRA MOHANTY M.D. M.S. F.H.R.S. PRASANT MOHANTY M.B.B.S. M.P.H. LUIGI DI BIASE M.D. Ph.D. F.H.R.S. RONG BAI M.D. F.H.R.S. CHINTAN TRIVEDI M.D. M.P.H. PASQUALE SANTANGELI M.D. FRANCESCO SANTORO M.D. RICHARD HONGO M.D. STEVEN HAO M.D. SALWA BEHEIRY R.N. DAVID BURKHARDT M.D. JOSEPH G. GALLINGHOUSE M.D. RODNEY HORTON M.D. JAVIER E. SANCHEZ M.D. SHANE BAILEY M.D. PATRICK M. HRANITZKY M.D. JASON ZAGRODZKY M.D. ANDREA NATALE M.D. F.H.R.S. F.E.S.C. F.A.C.C. 《Journal of cardiovascular electrophysiology》2014,25(9):930-938
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ALEXANDER DELVECCHIO HEATHER A. TRIVEDI JOHN D. FISHER SOO G. KIM KEVIN J. FERRICK JAY N. GROSS EUGEN C. PALMA 《Pacing and clinical electrophysiology : PACE》2005,28(S1):S260-S262
Opinions vary regarding the need to perform defibrillation testing prior to hospital discharge in recipients of state-of-the-art cardioverter defibrillators (ICDs). Our protocol is to perform predischarge ICD testing 1 day after implant. This report includes 682 consecutive implants. Adverse observations at testing were grouped into (1) risk of defibrillation failure, (2) surgical complications, (3) sensing/pacing issues or narrow defibrillation margin warranting closer follow-up, or (4) findings correctable by device reprogramming. Among the 682 patients, 63% had single-chamber and 37% dual-chamber or biventricular ICDs. In 48 patients (7%) there were 69 concerns and/or interventions, with overlaps among the four categories, including one failure to defibrillate (0.15%), and six other patients at risk. Surgical complications included 11 hematomas (1.6%), and six lead dysfunctions. Closer follow-up was indicated in 19 patients (2.7%), for high pacing thresholds in seven, sensing issues in seven, and <10 J defibrillation margin in five. Device reprogramming was needed in 31 patients (4.5%), for tachycardia detection and therapy settings in 12, and for pacing/sensing functions in 22 patients. In eight patients ventricular fibrillation could not be induced. There was no morbidity or mortality due to testing. The state-of-the-art ICDs delivering biphasic shocks are remarkably reliable. The routine pre-hospital discharge defibrillation testing of such ICDs may be optional and left to the physicians' discretion. 相似文献
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This paper reports the synthesis and the biological activities of six new glucagon analogues. In these compounds N-terminal modifications of the glucagon sequence were made, in most cases combined with changes in the C-terminal region which had been shown previously to enhance receptor affinity. The design of these analogues was based on [Lys17.18,Glu21]glucagon,1 a superagonist, which binds five times better than glucagon to the glucagon receptor, and on the potent glucagon antagonist [d -Phe4,Tyr5,Arg12]glucagon, which does not stimulate adenylate cyclase system even at very high concentrations. The N-terminal modifications involved substitution of His1 by the unnatural conformationally constrained residue, 4,5,6,7-tetrahydro-1H-imidazo[c]pyridine-6-carboxylic acid (Tip) and by desaminohistidine (dHis). In addition we prepared two analogues (6 and 7), in which we deleted the Phe6 residue, which was suggested to be part of a hydrophobic patch and involved in receptor binding. The following compounds were synthesized: [Tip1, Lys17.18,Glu21]glucagon (2); [Tip1,d -Phe4,Tyr5,Arg12,Lys17.18,Glu21 glucagon (3); [dHis1,d -Phe4,Tyr5,Arg12, Lys17.18,Glu21 glucagon (4); [dHis1,Asp3,d -Phe4,Tyr5,Arg12,Lys17.18,Glu21]glucagon (5); des-Phe6-[Tip1,D-Phe4,Tyr5Arg12,Glu21 glucagon (6); des-Phe6-[Asp3,d -Phe4,Tyr5,Arg12,Glu21]glucagon (7) The binding potencies of these new analogues relative to glucagon (= 100) are 3.2 (2), 2.9 (3), 10.0 (4), 1.0 (5), 8.5 (6), and 1.7 (7). Analogue 2 is a partial agonist (maximum stimulation of adenylate cyclase (AC) approximately 15% and a potency 8.9% that of glucagon, while the remaining compounds 3-7 are antagonists unable to activate the AC system even at concentrations as high as 10?5m . In addition, in competition experiments, analogues 3-7 caused a right-shift of the glucagon stimulated adenylate cyclase dose-response curve. Hence these compounds are glucagon receptor antagonists with respect to the glucagon receptor coupled to the adenylate cyclase system. 相似文献
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Culture of sinusoidal endothelial cells from rat liver 总被引:3,自引:0,他引:3
DEV A SAMARASINGHE 《Journal of gastroenterology and hepatology》1998,13(8):851-854
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MADHURI S. GOKHALE DEEPAK H. SHAH ZEENAT HAKIM DEV D. SANTANI RAMESH K. GOYAL 《Pharmacological research》1998,37(6):455-459
We have investigated the effects of amlodipine on streptozotocin- (STZ) induced neonatal non-insulin-dependent diabetes mellitus (NIDDM) rats. NIDDM was induced by intraperitoneal injection of STZ (70 mg kg−1) to 5-day-old rat pups. The animals were weaned at 30 days and maintained with food and waterad libitumfor 3 months. Amlodipine (5 mg kg−1p.o.) was administered for 6 weeks after the animals were confirmed diabetic (3 months after the STZ injection). A group of control animals were also maintained and this group received citrate buffer 5 days after birth. Fasting- and fed-glucose levels in NIDDM rats were significantly higher than control rats. Treatment with amlodipine reduced the elevated fasting- and fed-glucose levels significantly. Results of the oral glucose tolerance test (OGTT) revealed that glucose tolerance is impaired in the NIDDM rats. There was a marked increase in glucose levels after oral administration of glucose in the control NIDDM rats. Increased glucose levels were found to be associated with increased insulin levels. Treatment with amlodipine in the NIDDM rats caused a decrease in insulin release, however, glucose levels were found to be lowered significantly indicating that amlodipine causes an increase in insulin sensitivity. In conclusion, our data indicated that amlodipine increases insulin sensitivity in neonatal-STZ NIDDM rats. 相似文献
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