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zymogen/خیز

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مقالاتآزمایشات بالینیحق ثبت اختراع
صفحه 1 از جانب 70 نتایج

Generation of active fragments from human zymogens in the bradykinin-generating cascade by extracellular proteases from Vibrio vulnificus and V. parahaemolyticus.

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Vibrio vulnificus is an opportunistic human pathogen causing septicemia, and the infection is characterized by formation of the edematous skin lesions on limbs. This pathogenic species secretes a thermolysin-like metalloprotease as a virulence determinant. The metalloprotease was confirmed to

The recovery of acute pancreatitis depends on the enzyme amount stored in zymogen granules at early stages.

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Little is known about the changes in pancreatic enzyme storage in acute pancreatitis. We have performed flow cytometric studies of zymogen granules from rats with acute pancreatitis induced by hyperstimulation with caerulein. A comparison was made with rats treated with hydrocortisone (10 mg/kg/day)

Peptide leukotriene receptor antagonist diminishes pancreatic edema formation in rats with cerulein-induced acute pancreatitis.

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BACKGROUND This study was designed to evaluate the protective effect of a peptide leukotriene receptor antagonist, pranlukast hydrate, against pancreatic injuries during acute pancreatitis. METHODS Acute pancreatitis was induced in rats by intravenous infusion of a supramaximal dose of cerulein (5

Experimental acute pancreatitis induced by platelet activating factor in rabbits.

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This study indicates that a single injection of platelet activating factor (PAF, 50-500 ng) into the superior pancreaticoduodenal artery of rabbits induces dose-dependent morphologic alterations of pancreatic tissue and increases serum amylase levels, both consistent with the development of an acute

Effects on endogenous acetaldehyde production by disulfiram and ethanol feeding on rat pancreas.

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Exogenous acetaldehyde infusion can induce pancreatitis-like injury of the pancreas in some isolated pancreas models, whereas in vivo such treatment has failed to induce pancreatitis. In vivo exogenous acetaldehyde may not be effective because it is rapidly metabolized. The aim of this study was to

A rat model to study hypercalcemia-induced acute pancreatitis.

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Hypercalcemia causes acute pancreatitis in humans, a phenomenon reproduced experimentally in cats and guinea pigs. Because the rat is the most frequently used animal for the study of experimental pancreatitis, the present studies were performed to evaluate the effects of hypercalcemia in the rat. In

Glucocorticoids effects on exocrine pancreatic secretion in caerulein-induced acute pancreatitis in the rat.

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The present work reports on exocrine pancreatic secretion in control rats, adrenalectomized rats and hydrocortisone-treated (10 mg/Kg/d) rats during 7 days, under normal conditions and after induction of acute pancreatitis with caerulein (20 micrograms/Kg) by 4 subcutaneous injections at hourly

Cellular alterations of parotid gland of rats with acute pancreatitis induced by cerulein.

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To explore the cellular and subcellular alterations of the parotid gland during acute pancreatitis, we examined the redistribution of lysosomal enzyme, cathepsin B, along with the discharge of the LDH and cathepsin B from parotid acini of rats with acute pancreatitis induced by a supramaximal dose

Histologic and biochemical alterations in experimental acute pancreatitis induced by supramaximal caerulein stimulation.

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We studied the histologic and biochemical alterations in experimental acute pancreatitis induced by supramaximal caerulein stimulation in rats. All rats received 4 subcutaneous injections of various doses of caerulein (5-50 micrograms/kg body weight) at hourly intervals over 3 h, and 9 h after the

Early development of experimental biliary pancreatitis and its amelioration by CCK-receptor blockade.

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OBJECTIVE Development of pancreatitis has extensively been studied in models using CDE-diet and cerulein. This study analyzes early alterations and effects of CCK-receptor blockade in a model of biliary pancreatitis which better reflects the pathogenesis of human pancreatitis. METHODS The common

Enteropeptidase, a type II transmembrane serine protease.

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Enteropeptidase, a type II transmembrane serine protease, is localized to the brush border of the duodenal and jejunal mucosa. It is synthesized as a zymogen (proenteropeptidase) that requires activation by another protease, either trypsin or possibly duodenase. Active enteropeptidase then converts

Spontaneous activation of pancreas trypsinogen in heat shock protein 70.1 knock-out mice.

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OBJECTIVE Heat shock proteins (Hsp's) protect cellular proteins in response to injury, and the role of Hsp70 in experimental pancreatitis was recently described. To find out the possible role of Hsp70 in pancreatitis, we used Hsp70 knock-out mice (Hsp70.1-/-) and wild-type mice

Biliary acute pancreatitis in mice is mediated by the G-protein-coupled cell surface bile acid receptor Gpbar1.

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OBJECTIVE The mechanisms by which reflux of bile acids into the pancreas induces pancreatitis are unknown. We reasoned that key events responsible for this phenomenon might be mediated by Gpbar1, a recently identified and widely expressed G-protein-coupled, cell surface bile acid

Glucagon ameliorates pancreatic subcellular redistribution of lysosomal enzyme in rats with acute pancreatitis of closed duodenal loop.

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The protective effects of glucagon on the exocrine pancreas were investigated in rats with a closed duodenal loop (CDL). A CDL in rats caused marked hyperamylasemia, pancreatic edema and pancreatic histological damage such as acinar cell vacuolization and interstitial edema. A CDL also caused

Mucosal fine structure in experimental sinusitis.

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Rabbit maxillary sinuses were inoculated with Streptococcus pneumoniae and Bacteroides fragilis, and the histologic response in the sinus mucosa was observed over a 12-week period. An increased height of the cylindric cells and hyperplasia of the basal cells were frequent findings irrespective of
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