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Oldal 1 tól től 141 eredmények
Acute hemorrhagic pancreatic necrosis in mice. Intraparenchymal activation of zymogens, and other enzyme changes in pancreas and serum.
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A new experimental model has been found whereby acute hemorrhagic pancreatic necrosis with fat necrosis is induced in 100% of young female mice fed a choline-deficient diet supplemented with 0.5% DL-ethioine. The onset of the pancreatic necrosis has been shown to follow accumulation, and subsequent
Acute hemorrhagic pancreatitis (massive necrosis) with fat necrosis induced in mice by DL-ethionine fed with a choline-deficient diet.
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Female, albino mice were fed a choline-deficient diet containing 0.5% DL-ethionine. All animals died within 5 days due to the development of an acute hemorrhagic pancreatis with fat necrosis throughout the peritoneal cavity. The apancreatitis was characterized by a massive necrosis of the exocrine
Thrombin and tumor necrosis factor alpha synergistically stimulate tissue factor expression in human endothelial cells: regulation through c-Fos and c-Jun.
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Tissue factor is critically important for initiating the activation of coagulation zymogens leading to the generation of thrombin. Quiescent endothelial cells do not express tissue factor on their surface, but many stimuli including cytokines and coagulation proteases can elicit tissue factor
Outbreak of infectious pancreatic necrosis virus (IPNV) in farmed rainbow trout in China.
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Infectious pancreatic necrosis virus (IPNV) is a member of the Aquabirnavirus genus, which caused mass mortality (nearly 100%) in farmed rainbow trout (Oncorhynchus mykiss) in aquaculture farms in 2016, China. Major clinical signs included decreased appetite, mucous-like stools, and darkened
Anti-ICAM-1 antibody modulates late onset of acinar cell apoptosis and early necrosis in taurocholate-induced experimental acute pancreatitis.
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The hallmark of severe acute pancreatitis (SAP) is massive acinar cell death by necrosis. However, programmed, apoptotic acinar cell death has also been observed. Little is known about the dynamics, localization, and inductive factors of acinar cell apoptosis in SAP. We therefore induced SAP in rats
Coumarin necrosis, neonatal purpura fulminans, and protein C deficiency.
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Protein C (PC), a 62,000-molecular weight vitamin K-dependent serine protease zymogen, is a natural anticoagulant that occurs in plasma at 4 mg/L. Activated PC inactivates clotting factors V and VIII and is also profibrinolytic. Activated PC is enhanced in its anticoagulant activity by protein S
Genetic inhibition of protein kinase Cε attenuates necrosis in experimental pancreatitis.
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Understanding the regulation of death pathways, necrosis and apoptosis, in pancreatitis is important for developing therapies directed to the molecular pathogenesis of the disease. Protein kinase Cε (PKCε) has been previously shown to regulate inflammatory responses and zymogen activation in
Inhibition of the tumor necrosis factor-alpha-converting enzyme by its pro domain.
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Tumor necrosis factor-alpha-converting enzyme (TACE) is a disintegrin metalloproteinase that processes tumor necrosis factor and a host of other ectodomains. TACE is biosynthesized as a zymogen, and activation requires the removal of an inhibitory pro domain. Little is known about how the pro domain
Local and systemic zymogen activation in human acute pancreatitis.
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BACKGROUND
Activation of trypsinogen and phospholipase A(2) is an early event in pancreatic inflammation, but little is known about zymogen activation and the severity of human pancreatitis.
METHODS
Using a new fluoroimmunoassay we measured trypsinogen activation peptide (TAP) and phospholipase A(2)
Pancreatic acinar cell necrosis with intact storage of digestive enzymes in selenomethionine treated rats.
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Morphological and biochemical changes were observed in the pancreas and serum of rats after the intraperitoneal administration of selenomethionine, sodium selenite and methionine. Selenomethionine caused rapidly developing acinar cell necrosis. The first pathological changes were mitochondrial
Pancreatic effects of ethionine: blockade of exocytosis and appearance of crinophagy and autophagy precede cellular necrosis.
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Young female mice fed a choline-deficient, ethionine-supplemented (CDE) diet for 24 h develop hemorrhagic pancreatic necrosis with a 5-day mortality rate of approximately 50%. At the end of the diet administration, the in vivo discharge of digestive enzymes is blocked, images of exocytosis and
In-vitro anti-inflammatory and immunomodulatory effects of grepafloxacin in zymogen A- or Staphylococcus aureus-stimulated human THP-1 monocytes.
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The effects of grepafloxacin on the release of cytokines, chemical mediators, hydrolytic enzyme activities, and lipoxygenation in zymogen A- or Staphylococcus aureus-stimulated human THP-1 monocytes were evaluated. Initially, consistent with stimulation of phagocytic mechanisms of the monocytes,
The TACE zymogen: re-examining the role of the cysteine switch.
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Belépés Regisztrálás
The tumor necrosis factor-alpha-converting enzyme (TACE) is a member of the disintegrin family of metalloproteinases (ADAMs) that plays a central role in the regulated shedding of a host of cell surface proteins. TACE is biosynthesized as a precursor protein with latent proteolytic activity
Changes in both the membrane and the enzyme content of individual zymogen granules are associated with sodium taurocholate-induced pancreatitis in rats.
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1. After monitoring the changes associated with necrotizing acute pancreatitis in rats from early stages to 24 h after infusion of 5% sodium taurocholate in the choledocus, we characterized by flow cytometry the zymogen granules that still remained in the pancreas 18 h after sodium taurocholate
Ligation-induced acute pancreatitis in opossums: acinar cell necrosis in the absence of colocalization.
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Acute necrotizing pancreatitis in opossums after bile and pancreatic duct ligation (BPDL) is a useful experimental corollary of gallstone-induced acute pancreatitis in humans. In experimental and human acute pancreatitis, a loss of segregation of the lysosomal enzyme cathepsin B and the zymogen
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