AIM： Pancreatic regenerating protein （reg Ⅰ ） stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and 13-cells. This suggests that reg Ⅰand its receptor may play a role in recovery ...AIM： Pancreatic regenerating protein （reg Ⅰ ） stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and 13-cells. This suggests that reg Ⅰand its receptor may play a role in recovery after pancreatic injury. We hypothesized that reg Ⅰ and its receptor are induced in acute pancreatitis. METHODS： Acute pancreatitis was induced in male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 hours after injection and from normal controls （4 rats/group）. Reg Ⅰ receptor mRNA, serum reg Ⅰ protein, and tissue reg Ⅰ protein levels were determined by Northern analysis, enzymelinked immunosorbent assay （ELISA）, and Western analysis, respectively. Immunohistochemistry was used to localize changes in reg Ⅰ and its receptor. RESULTS： Serum amylase levels and histology confirmed necrotizing pancreatitis in taurocholate treated rats. There was no statistically significant change in serum reg Ⅰ concentrations from controls. However, Western blot demonstrated increased tissue levels of reg Ⅰ at 24 and 36 h. This increase was localized primarily to the acinar cells and the ductal cells by immunohistochemistry. Northern blot demonstrated a significant increase in reg Ⅰ receptor mRNA expression with pancreatitis. Immunohistochemistry localized this increase to the ductal cells, islets, and acinar cells. CONCLUSION： Acute pancreatitis results in increased tissue reg Ⅰ protein levels localized to the acinar and ductal cells, and a parallel threefold induction of reg Ⅰ receptor in the ductal cells, islets, and acinar cells. These changes suggest that induction of reg Ⅰand its receptor may be important for recovery from acute pancreatitis.展开更多
Hepatic encephalopathy(HE)is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases.The precise pathophysiology of HE is still under discussion;the leading hypothesis focus...Hepatic encephalopathy(HE)is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases.The precise pathophysiology of HE is still under discussion;the leading hypothesis focus on the role of neurotoxins,impaired neurotransmission due to metabolic changes in liver failure,changes in brain energy metabolism,systemic inflammatory response and alterations of the blood brain barrier.HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations.Minimal HE is diagnosed by abnormal psychometric tests.Clinically overt HE includes personality changes,alterations in consciousness progressive disorientation in time and space,somnolence,stupor and,finally,coma.Except for clinical studies,no specific tests are required for diagnosis.HE is classified according to the underlying disease,the severity of manifestations,its time course and the existence of precipitating factors.Treatment of overt HE includes supportive therapies,treatment of precipitating factors,lactulose and/or rifaximin.Routine treatment for minimal HE is only recommended for selected patients.展开更多
基金Supported by NIDDK R01 DK.54511 (MZ), R01 DK060106 (BD) NIH Digestive Disease Research Core Center (DDRCC) grant P30 DK52574 (BD)
文摘AIM： Pancreatic regenerating protein （reg Ⅰ ） stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and 13-cells. This suggests that reg Ⅰand its receptor may play a role in recovery after pancreatic injury. We hypothesized that reg Ⅰ and its receptor are induced in acute pancreatitis. METHODS： Acute pancreatitis was induced in male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 hours after injection and from normal controls （4 rats/group）. Reg Ⅰ receptor mRNA, serum reg Ⅰ protein, and tissue reg Ⅰ protein levels were determined by Northern analysis, enzymelinked immunosorbent assay （ELISA）, and Western analysis, respectively. Immunohistochemistry was used to localize changes in reg Ⅰ and its receptor. RESULTS： Serum amylase levels and histology confirmed necrotizing pancreatitis in taurocholate treated rats. There was no statistically significant change in serum reg Ⅰ concentrations from controls. However, Western blot demonstrated increased tissue levels of reg Ⅰ at 24 and 36 h. This increase was localized primarily to the acinar cells and the ductal cells by immunohistochemistry. Northern blot demonstrated a significant increase in reg Ⅰ receptor mRNA expression with pancreatitis. Immunohistochemistry localized this increase to the ductal cells, islets, and acinar cells. CONCLUSION： Acute pancreatitis results in increased tissue reg Ⅰ protein levels localized to the acinar and ductal cells, and a parallel threefold induction of reg Ⅰ receptor in the ductal cells, islets, and acinar cells. These changes suggest that induction of reg Ⅰand its receptor may be important for recovery from acute pancreatitis.
文摘Hepatic encephalopathy(HE)is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases.The precise pathophysiology of HE is still under discussion;the leading hypothesis focus on the role of neurotoxins,impaired neurotransmission due to metabolic changes in liver failure,changes in brain energy metabolism,systemic inflammatory response and alterations of the blood brain barrier.HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations.Minimal HE is diagnosed by abnormal psychometric tests.Clinically overt HE includes personality changes,alterations in consciousness progressive disorientation in time and space,somnolence,stupor and,finally,coma.Except for clinical studies,no specific tests are required for diagnosis.HE is classified according to the underlying disease,the severity of manifestations,its time course and the existence of precipitating factors.Treatment of overt HE includes supportive therapies,treatment of precipitating factors,lactulose and/or rifaximin.Routine treatment for minimal HE is only recommended for selected patients.
