摘要:

Caerulein-induced pancreatitis (CIP) in rats is characterized by oedema and cell necrosis followed by spontaneous regeneration. The ras protein as well as ornithine decarboxylase (ODC) play a central role in the transmission of signals induced by growth factors. Therefore, we analyzed these gene products during the course of CIP and during the regeneration of the gland. Growth and biochemical parameters (pancreatic weight, total DNA, RNA and proteins) were determined along with ODC activity and quantitative reverse-transcrip-tase polymerase chain reaction measurements of mRNA levels. During CIP, the significant increases in pancreatic weight were the result of oedema. During that period, maximal increases in ODC activity were observed at 3 h, in ODC mRNA expression at 2, 3, and 4 h, and in Ki-ras mRNA expression at 1 h. During the 3-day resting period within which no treatment was given, pancreatic weight exhibited its maximal reduction after 2 days in the CIP group. In that same group, the ODC activity reached its maximal level above control after 3 days and ODC and Ki-ras mRNA expression after 1 and 2 days. During the regeneration period of 5 days, the pancreata of the untreated pancreatitis rats did not totally recover, whereas those of the animals receiving the small dose of caerulein (1 μg) showed full recovery and even a significant increase above control after 5 days. During that period, maximal increases in ODC activity and Ki-ras mRNA expression occurred after 1 day of caerulein treatment; ODC mRNA expression was also significantly increased after 3 and 5 days in the pancreatitis animals with no effect of caerulein treatment. The positive effect of caerulein on Ki-ras mRNA suggests that the cholecysto-kinin analogue can induce the expression of essential growth-promoting genes

ISSN:0012-2823    

DOI:10.1159/000201374

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

In this study, 72 patients with chronic hepatitis C virus (HCV) were followed prospectively for a mean period of 27 months after interferon treatment. Fifty-seven percent (20/35) of the patients with complete response, 18/20 with HCV-RNA-negative serum, had a sustained biochemical remission. Reactivation was seen in 43% of these patients after a mean follow-up of 7.3 months. A late relapse after more than 12 months of follow-up occurred in only 2/15 patients. Patients with a long-term complete response had significantly lower pretreatment serum HCV RNA levels than complete responders with relapse (106,239 vs. 345,649 mEq/ml, p = 0.0213). A delayed sustained biochemical remission was seen in 3/37 patients with partial or no response. Thus, long-term response is achieved in 32% of the patients treated with interferon, clearly associated with a suppression of serum HCV RNA. Patients with normal ALT values and undetectable levels of HCV RNA for more than 12 months of follow-up may usually be considered as sustained responders. Thus, for the first time, the pretreatment HCV RNA level in serum was identified as predictive of long-term response.

ISSN:0012-2823    

DOI:10.1159/000201375

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

The activity of platelet-activating factor (PAF) acetylhydrolase in biopsy specimens of intestinal mucosa was compared in patients with Crohn’s disease (n = 11) and controls (n = 6). In addition, PAF acetylhydrolase activity was determined in the plasma of Crohn patients (n = 30) and healthy subjects (n = 35). The activity of PAF acetylhydrolase in mucosal samples from the distal ileum was significantly lower in Crohn patients than in control patients (p 150) had a significantly lower PAF acetylhydrolase activity in plasma, as compared to patients in clinical remission (symptomatic index < 150; p < 0.02), and as compared to healthy subjects (p < 0.001). PAF acetylhydrolase activity in plasma increased within 4 months after bowel resection (P < 0.05). These findings indicate that the PAF acetylhydrolase activity is decreased in the ileal mucosa of patients with Crohn’s disease and that PAF acetylhydrolase activity in plasma is inversely related to disease activity in Crohn’s disease. The possibility that PAF acetylhydrolase is one factor of importance for protecting the intestinal mucosa against PAF-mediated inflammation is inf

ISSN:0012-2823    

DOI:10.1159/000201376

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Intrinsic neurons containing serotonin (5-HT) are involved in the regulation of gastrointestinal motor function and are also thought to be important in the modulation of visceral sensory function. We have evaluated the effect of a specific 5-HT3 antagonist (ondansetron, O) on visceral sensation and rectal compliance in a randomized, double-blind, cross-over, placebo (P) controlled study of·16 mg 3 times/day, in healthy volunteers and patients with irritable bowel syndrome (IBS). Symptoms were also evaluated in the latter group. A 2-week run-in period was followed by two 2-week treatment arms of P and O, separated by a 2-week wash-out period. Twelve healthy subjects and 9 patients with IBS were recruited. Assessment was by daily symptom and bowel function diary, and physiological tests of anal manometry, rectal sensory testing to distension and electrical stimulation, and rectal compliance. Ten healthy subjects completed the entire study, and 6 IBS patients completed the diary card evaluation, including 5 who also completed the physiological evaluation.·caused significantly (p < 0.01) firmer stools when considering both subject groups together. In the healthy subjects no physiological parameters were altered by O. In IBS patients the rectal sensory threshold to electrical stimulation tended to increase with·(20 vs. 28 mA, P vs. O, median, p = 0.06) while the urge (80 vs. 60 ml, p = 0.05) and maximum tolerated volumes (130 vs. 90, p = 0.03) to distension tended to decrease with O. Patients with IBS experienced significantly fewer daily episodes of pain while on·(2 vs. 1, p = 0.03). Serotonin-3 antagonism (O) causes firmer bowel actions in all subjects, and may affect gut sensitivity and pain in patients with

ISSN:0012-2823    

DOI:10.1159/000201377

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:0012-2823    

DOI:10.1159/000201378

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:0012-2823    

DOI:10.1159/000201379

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:0012-2823    

DOI:10.1159/000201380

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:0012-2823    

DOI:10.1159/000201363

出版商:S. Karger AG    

年代:1996

数据来源: Karger