gallstones/protease

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Possible role of hepatic bile mucus glycoprotein in development of intrahepatic gallstones.

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To study the role played by hepatic bile mucus glycoprotein in the development of hepatolithiasis, mucus glycoprotein, isolated from the bile of patients with intrahepatic gallstones by gel filtration and ultracentrifugation, was examined for precipitability in control hepatic bile obtained

Secretory pancreatic stone protein messenger RNA. Nucleotide sequence and expression in chronic calcifying pancreatitis.

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The pancreatic stone protein and its secretory form (PSP-S) are inhibitors of CaCO3 crystal growth, possibly involved in the stabilization of pancreatic juice. We have established the structure of PSP-S mRNA and monitored its expression in chronic calcifying pancreatitis (CCP). A cDNA encoding

Change of pancreatic enzymes, pancreatic stone protein (PSP), and plasma alpha(2)-macroglobulin-trypsin complex-like substance (MTLS) in the activation of pancreatic juice.

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To characterize the activation of pancreatic zymogens (trypsinogen, chymotrypsinogen, and proelastase 1) in acute pancreatitis, we studied the activation of pancreatic juice with porcine enteropeptidase in vitro, and then enzymatic activities and the generation of pancreatic stone protein (PSP) S1

Complete amino acid sequence of an immunoreactive form of human pancreatic stone protein isolated from pancreatic juice.

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The primary structure of a pancreatic stone protein form has been elucidated for the first time. The protein studied was the lowest-Mr form prepared from human pancreatic juice (PSP S1). The N-terminal sequence up to residue 65 had already been determined. The five peptides obtained after

Rat pancreatic stone protein messenger RNA. Abundant expression in mature exocrine cells, regulation by food content, and sequence identity with the endocrine reg transcript.

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We used a cDNA encoding the human pancreatic stone protein (PSP-S), the secretory inhibitor of CaCO3 crystal growth, as a probe for cloning rat PSP-S messenger RNA. Overlapping clones gave a mRNA sequence of 783 nucleotides encoding a preprotein of 165 amino acids including a prepeptide of 21 amino

Effect of short-term pancreatico-biliary duct obstruction with intraductal hypertension on subcellular organelle fragility and pancreatic adenylate energy metabolism in rats: protective effect of a new protease inhibitor, E-3123.

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Blockage of the rat pancreatico-biliary duct (PBDO) for 4 hours and secretin infusion (0.2 CU [Clinical Unit]/kg/hr) caused significant rises in portal serum amylase, cathepsin B levels, pancreatic water content, and pancreatic amylase content as well as lysosomal and mitochondrial fragility.

Mannan-binding lectin and mannan-binding lectin-associated serine protease 2 in acute pancreatitis.

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OBJECTIVE Complement activation may play a prominent role in acute pancreatitis (AP). Mannan-binding lectin (MBL) and MBL-associated serine protease 2 (MASP-2) participate in complement activation. The objective of the present study was to evaluate the role of MBL and MASP-2 as markers in AP with

Evidence for oxidative stress in the gall bladder mucosa of gall stone patients.

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BACKGROUND There is considerable evidence indicating that gall stone patients have altered gall bladder functions with respect to secretion and absorption and inflammation in mucus membrane when compared with gall stone free subjects. Increased levels of accelerated generation of reactive oxygen

Biochemical and physicochemical changes in collagen isolated from the gall bladder of gall stone patients.

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Abnormal gall bladder motor function with delayed emptying and stasis are the contributory factors of gall stone formation. Since collagen is the major contractile protein, this study was designed to find out whether the biochemical and physicochemical changes of collagen contribute to the

Lysosomal enzyme activities in gallbladder mucosa of gallstone-free subjects and patients with gallstones.

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OBJECTIVE Gallstone patients have a reduced cellular lysosome content in the gallbladder mucosa cells compared with gallstone-free subjects. The purpose of the study was to further evaluate the possible role of lysosomes in the pathogenesis of cholesterol gallstone formation in

Digestive enzymes and protease inhibitors in plasma from patients with acute pancreatitis.

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The plasma levels of certain digestive enzymes and protease inhibitors were determined in 40 patients with severe acute pancreatitis diagnosed as gallstone-induced (GP), alcoholic (AP), or idiopathic (IP). On admission, plasma levels of amylase and immunoreactive cationic trypsin(ogen) (IRCT) and

Protein-X, Pancreatic Stone-, Pancreatic thread-, reg-protein, P19, lithostathine, and now what? Characterization, structural analysis and putative function(s) of the major non-enzymatic protein of pancreatic secretions.

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Reg protein was first found in pancreatic stones. It was named Pancreatic Stone Protein and later renamed lithostathine, as it was assumed to prevent stone formation. The 144 amino acid protein is O-glycosylated on Thr-5. The glycan chain is variable in length and in charge. Lithostathine 3-D

Immunochemical and functional properties of biliary alpha-1-antitrypsin.

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Alpha-1-antitrypsin (AAT), the archetype of the serpin (serine proteinase inhibitor) superfamily, is synthesized by hepatocytes and excreted to some extent into bile. The role of intact biliary AAT in gallstone pathogenesis is unsettled, but its 36-residue C-terminal peptide was found to promote

Plasma alpha 2-macroglobulin-trypsin complexlike substance (MTLS) in pancreatic disease.

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alpha 2-macroglobulin-trypsin complexlike substance (MTLS) was determined in plasma of pancreatic and nonpancreatic diseases using a two-step enzyme immunoassay to study the diagnostic and pathophysiological significance of MTLS. Plasma levels of MTLS in acute pancreatitis (mean +/- SD = 265.6 +/-

Incidence, etiology and prognosis of first-time acute pancreatitis in young patients: a population-based cohort study.

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OBJECTIVE The etiology of acute pancreatitis (AP) seems to have changed during the last two decades, and since detection of mutations in the gene for cationic trypsinogen(PRSS1) causing hereditary pancreatitis some patients formerly diagnosed with idiopathic AP (IAP) turn out to have a genetic

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