These findings suggest that some of the therapeutic actions of somatostatin on acute pancreatitis might be mediated by reducing local IL-6 secretion in the pancreas.
To elucidate the mechanisms mediating the therapeutic actions of somatostatin on acute pancreatitis, we investigated how somatostatin affects the tumor necrosis factor (TNF)-alpha-induced interleukin (IL)-6 and IL-8 secretion from pancreatic myofibroblasts.
The mouse stress-induced protein (SIP) mRNA is activated in the pancreas with acute pancreatitis and in several cell lines in response to various stress agents.
The aim of the present study was: (1) to assess plasma leptin levels in rats with caerulein-induced pancreatitis (CIP) and humans with acute pancreatitis; and (2) to determine the effects of exogenous leptin on the course of acute CIP in rats.
Further studies are warranted to evaluate the frequency and role of rare ('mild') CFTR gene point mutations in subjects suffering from severe acute pancreatitis.
In conclusion, the similarities in the immunoreactivity of anti-ErbB2 antibodies in recurrent acute pancreatitis and chronic pancreatitis support the hypothesis that acute pancreatitis can be a forerunner of chronic pancreatitis.
The functional GSTT-1*A genotype was more prevalent in severe (96%) compared with mild attacks of AP (78%; odds ratio [OR], 5.9; 95% confidence interval [CI ], 2-17; P < 0.0001) and controls (76%; OR, 6.6; 95% CI, 2.3-18.7; P < 0.0001).
DNA from 320 patients with AP (90 severe) and 263 controls was genotyped for glutathione S-transferase (Mu-1 [M-1], theta-1 [T-1], and pi-1 [P-1: Ile-105Val]), manganese superoxide dismutase (Ala-9Val), and catalase (C-260T) polymorphisms.
DNA from 320 patients with AP (90 severe) and 263 controls was genotyped for glutathione S-transferase (Mu-1 [M-1], theta-1 [T-1], and pi-1 [P-1: Ile-105Val]), manganese superoxide dismutase (Ala-9Val), and catalase (C-260T) polymorphisms.
Increased soluble CD14 expression is associated with the systemic inflammatory response to acute pancreatitis and an expansion of the proinflammatory CD14+/CD16+ monocyte subset.
Increased soluble CD14 expression is associated with the systemic inflammatory response to acute pancreatitis and an expansion of the proinflammatory CD14+/CD16+ monocyte subset.
Increased soluble CD14 expression is associated with the systemic inflammatory response to acute pancreatitis and an expansion of the proinflammatory CD14+/CD16+ monocyte subset.
We studied whether polymorphisms of the tumor necrosis factor alpha (TNF-alpha), heat shock protein 70-2 (HSP70-2), and CD14 genes correlate with the severity of acute pancreatitis.
We studied whether polymorphisms of the tumor necrosis factor alpha (TNF-alpha), heat shock protein 70-2 (HSP70-2), and CD14 genes correlate with the severity of acute pancreatitis.
We studied whether polymorphisms of the tumor necrosis factor alpha (TNF-alpha), heat shock protein 70-2 (HSP70-2), and CD14 genes correlate with the severity of acute pancreatitis.
We studied whether polymorphisms of the tumor necrosis factor alpha (TNF-alpha), heat shock protein 70-2 (HSP70-2), and CD14 genes correlate with the severity of acute pancreatitis.
We studied whether polymorphisms of the tumor necrosis factor alpha (TNF-alpha), heat shock protein 70-2 (HSP70-2), and CD14 genes correlate with the severity of acute pancreatitis.