Disease relevance of Pancreatitis, Acute Necrotizing

• CONCLUSION: Melatonin is an antioxidant that is able to counteract some of the L-Arg-induced changes during acute pancreatitis, and may therefore be helpful in the supportive therapy of patients with acute necrotizing pancreatitis [1].
• METHODOLOGY: Acute necrotizing pancreatitis was induced by intraperitoneal injection of 500 mg/100 g body weight of L-arginine in male Wistar rats [2].
• This is the second case of this rare condition, in which acute necrotizing pancreatitis followed an ACTH-dependent hypercortisolism [3].

High impact information on Pancreatitis, Acute Necrotizing

• Caerulein, a decapeptide cholecystokinin analogue, induces acute necrotizing pancreatitis in mice when given in high doses (50 micrograms/kg per h) over a period of 6 h [4].
• The potential protective role of IL-10 in a model of acute necrotizing pancreatitis in mice was tested [5].
• BACKGROUND/AIMS: Induction of acute necrotizing pancreatitis with cerulein causes profound pancreatic glutathione depletion in the mouse [6].
• Caerulein-induced acute necrotizing pancreatitis in mice: protective effects of proglumide, benzotript, and secretin [7].
• OBJECTIVE: To analyze the involvement of connective tissue growth factor (CTGF) in the transforming growth factor-beta (TGF-beta) pathway during acute necrotizing pancreatitis (ANP) in humans and rats [8].

Chemical compound and disease context of Pancreatitis, Acute Necrotizing

• METHODS: Severe acute necrotizing pancreatitis was induced in rats by a combination of low-dose controlled intraductal infusion of glycodeoxycholic acid superimposed on intravenous cerulein hyperstimulation [9].
• In two groups, acute necrotizing pancreatitis was induced by retrograde intraductal infusion of 3% sodium taurocholate [10].
• BACKGROUND: Bacterial infection of pancreatic necrosis is thought to be a major determinant of outcome in acute necrotizing pancreatitis [11].
• CONCLUSIONS: Early pancreatic infection after acute necrotizing pancreatitis can be reduced with a full-gut decontamination regimen or with an antibiotic concentrated by the pancreas (imipenem) but not by unconcentrated antibiotics of similar spectrum (cefotaxime) or by oral antibiotics alone [9].
• Twelve patients suffering from acute necrotizing pancreatitis were treated with imipenem-cilastatin (0.5 g), mezlocillin (2 g), gentamicin (0.08 g), amikacin (0.5 g), pefloxacin (0.4 g), and metronidazole (0.5 g) [12].

Biological context of Pancreatitis, Acute Necrotizing

• The effect of glucagon-like peptide 2 on intestinal permeability and bacterial translocation in acute necrotizing pancreatitis [13].
• We compared the usefulness of proliferating cell nuclear antigen immunostaining and the incorporation of 5-bromodeoxyuridine to demonstrate acinar cell proliferation in the pancreas of rats with acute necrotizing pancreatitis [14].
• The effect of antibiotic and probiotic combination therapy on secondary pancreatic infections and oxidative stress parameters in experimental acute necrotizing pancreatitis [15].

Anatomical context of Pancreatitis, Acute Necrotizing

• RESULTS: l-Arginine treatment induced acute necrotizing pancreatitis in the rat at 24 hours. l-Arginine (24 hours) increased FLI in the dorsal horn of the spinal cord, with a peak effect at L1 [16].
• AIMS: To measure the release of NEFA in the blood stream, pancreatic tissue, and peritoneal cavity during taurocholate-induced acute necrotizing pancreatitis in rats [17].

Gene context of Pancreatitis, Acute Necrotizing

• Recombinant human interleukin-11 decreases severity of acute necrotizing pancreatitis in mice [18].
• OBJECTIVE: To study the potential roles of lipopolysaccharide (LPS) signaling molecules, LPS-binding protein (LBP), CD14, and Toll-like receptor 4 (TLR4) in mice with acute necrotizing pancreatitis (ANP) [19].
• The plasminogen activator/plasmin system is up-regulated after acute necrotizing pancreatitis in human beings [20].
• In this study we analyzed the expression and distribution of the urokinase plasminogen activator (uPA), its membrane receptor (urokinase plasminogen activator receptor [uPAR]), and its inhibitor (plasminogen activator inhibitor-1 [PAI-1]) in acute necrotizing pancreatitis in human beings [20].
• Relationship between overexpression of NK-1R, NK-2R and intestinal mucosal damage in acute necrotizing pancreatitis [21].

Analytical, diagnostic and therapeutic context of Pancreatitis, Acute Necrotizing

• Control group: 54 case-control matched patients with acute necrotizing pancreatitis and pulmonary failure, who had not been treated with octreotide [22].
• PURPOSE: This study was conducted to determine whether continuous regional arterial infusion (CRAI) of the protease inhibitor, nafamostat mesylate, in acute necrotizing pancreatitis, would reduce mortality [23].
• The aim of this study was to investigate the influence of a small amount of enteral nutrition along with parenteral nutrition on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats in the early phase of disease [24].

References