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pancreatitis/proline
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Tumor necrosis factor-alpha mediates pancreatitis responses in acinar cells via protein kinase C and proline-rich tyrosine kinase 2.
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OBJECTIVE
Although tumor necrosis factor alpha is implicated as an important mediator of the inflammatory response in acute pancreatitis, its role in other pathologic features of the disease remains unknown. We investigated the role for tumor necrosis factor alpha in cytoskeletal responses and the
[Changes serum proline levels after gelatin loading in patients with chronic pancreatitis].
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A serum metabolomic investigation on lipoprotein lipase-deficient mice with hyperlipidemic pancreatitis using gas chromatography/mass spectrometry.
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Hypertriglyceridemia (HTG) is often associated with acute pancreatitis. The relationship between these diseases and the role that hypertriglyceridemia plays in acute pancreatitis pathogenesis remains to be elucidated. In the present study, in order to investigate the mechanisms of hyper-lipidemic
[Changes in collagen and non-collagen protein metabolisms in rat acute pancreatitis induced by ethionine].
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Collagen and non-collagen protein metabolisms in rat acute pancreatitis induced by ethionine were investigated with an incorporation study of 3H-proline to those proteins. Enhanced collagen metabolism, which may provide a basis for parenchymal cells regeneration, was observed in the initial phase of
Amyloidogenesis of feline amylin and plasma levels in cats with diabetes mellitus or pancreatitis
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Amylin is a pancreatic hormone cosecreted along with insulin and involved in pancreatic amyloidosis and β-cell apoptosis in diabetic cats and humans. Amylin is usually elevated in early stages of type 2 diabetes but recently was found to be increased in acute and chronic pancreatitis in humans.
Effect of new oligopeptide inhibitors of elastase on acute experimental pancreatitis in the rat.
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Acute experimental pancreatitis was induced in male Wistar rats by retrograde injection of 0.4 ml 2% sodium taurocholate into the common choledochopancreatic duct. Prophylactic intraperitoneal injection of 20 mg glutaryl-trialanine-ethylamide, Glt-(Ala)3-NH-Et, 30 min. before induction of
Clusterin and Pycr1 alterations associate with strain and model differences in susceptibility to experimental pancreatitis.
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Acute pancreatitis has several underlying etiologies, and results in consequences ranging from mild to complex multi-organ failure. The wide range of pathology suggests a genetic predisposition for progression. We compared the susceptibility to acute pancreatitis in BALB/c and FVB/N mice, coupled
The effect of hypothalamic peptides, neurohormone C and proline-rich peptide-1on the Ca p>2+ p>-handling system in heartin pathophysiological conditions
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Atthe Institute of Biochemistry named after H. Buniatyan we discovered and studied hypothalamic peptides with coronary dilatory and antioxidant activities:neurohormone C (NC) and proline-rich peptide-1 (PRP-1). Both NC and PRP-1 exhibit cardioprotective effects, in part by restoring the calcium
A fast protein liquid chromatography (FPLC) method for study of thyrotropin-releasing hormone (TRH) and its metabolite histidyl-proline diketopiperazine (CHP) in human blood: degradation in liver and pancreatic diseases.
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We have developed a convenient method combining fast protein liquid chromatography (FPLC) with sensitive radioimmunoassay (RIA) for thyrotropin-releasing hormone (TRH) to separate and identify TRH and its metabolite histidyl-proline diketopiperazine (CHP) and applied this to study inactivation of
Alterations in plasma amino acid levels in chronic pancreatitis.
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BACKGROUND
Dietary proteins and amino acids can modulate pancreatic function.
OBJECTIVE
Our aim was to estimate the levels of plasma amino acids in chronic pancreatitis patients and study their relationship with disease characteristics as well as exocrine and endocrine insufficiency.
METHODS
One
Cathepsin B inhibition prevents trypsinogen activation and reduces pancreatitis severity.
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Intrapancreatic activation of trypsinogen is believed to play a critical role in the initiation of acute pancreatitis, but mechanisms responsible for intrapancreatic trypsinogen activation during pancreatitis have not been clearly defined. In previous in vitro studies, we have shown that
Does chronic ethanol intake cause chronic pancreatitis?: evidence and mechanism.
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OBJECTIVE
To demonstrate the relationship between prolonged alcohol intake and chronic pancreatitis.
METHODS
Wistar rats were fed diet containing 25% concentration (vol/vol) of ethanol for 6 months. Cholecystokinin (CCK) was quantified by radioimmunoassay. Immunohistochemistry was used to detect
Fibroblast structure and function during regeneration from hormone-induced acute pancreatitis in the rat.
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The regeneration of the rat exocrine pancreas from a hormone-induced pancreatitis was investigated. In a previous study it was shown that the [3H]thymidine labeling index of interstitial cells increases 20- to 30-fold on day 1.5 after the induction of pancreatitis. Here we show by electron
A novel mutation of the calcium sensing receptor gene is associated with chronic pancreatitis in a family with heterozygous SPINK1 mutations.
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BACKGROUND
The role of mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene in chronic pancreatitis is still a matter of debate. Active SPINK1 is thought to antagonize activated trypsin. Cases of SPINK1 mutations, especially N34S, have been reported in a subset of patients with
Pancreatic stellate cells respond to inflammatory cytokines: potential role in chronic pancreatitis.
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BACKGROUND
It is now generally accepted that chronic pancreatic injury and fibrosis may result from repeated episodes of acute pancreatic necroinflammation (the necrosis-fibrosis sequence). Recent studies suggest that pancreatic stellate cells (PSCs), when activated, may play an important role in
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