ObjectiveTo investigate the effects of different doses of obestatin on amylase secretion of pancreatic acinar and lobules of rats in vitro.MethodsPancreatic acinar cells of rats were separated in vitro and incubated with different doses of obestatin (0,0.1,1,10,30 nmol/L) for 1h,another group of pancreatic acinar ceils was incubated with obestatin for 30 min,then was incubated with 100 pmol/L CCK-8 for another 30 min.Pancreatic lobules,which containing intrapancreatic nerve terminals and islets,were prepared and were incubated with different concentrations of obestatin for 30 min at 37℃ with or without 75 mmol/L KCl.Amylase levels in the supernatants,acinar cells and pancreatic lobules were calculated as a percentage of total amylase content.ResultsObestatin (0,0.1,1,10,30 nmol/L) produced no significant change in basal amylase release of acinar cells [ (3.48 ± 1.44) ％,(3.70 ±- 1.39) ％,(3.36 ± 1.24) ％,(3.86 ± 1.41 ) ％,(4.54 ± 2.01 ) ％ ].CCK-8 significantly increased amylase release of acinar cells [ ( 13.84 ± 2.63 ) ％ vs (3.48 ± 1.44)％,P ＜0.05],but obestatin (0.1,1,10 nmol/L) has no effect on the amylase release inducedby CCK-8 [(14.55 ± 1.7)％,(13.79 ± 1.81)％,(14.39 ± 1.12)％].Obestatin (0.1,1,10,30 nmol/L) did not affect the amylase release of pancreatic lobuole.KCl significantly increased anylase release,which was ( 1.84 ± 0.29 ) folds higher than that of control group ( P ＜ 0.05 ),but obestatin has no effect on the amylase release induced by KCl,which were (2.01 ± 0.30 ),( 1.89 ± 0.41 ),( 1.74 ± 0.14 ),( 1.88± 0.33) folds higher than those of control group.ConclusionsExogenous obestatin has no effects on pancreatic exocrine of acinar cells and lobules of rats in vitro and cannot block or assist the increased amylase release induced by CCK-8 or KCl.

Gastrointestinal stromal tumor( GIST)is the most common gastrointestinal mesenchymal neoplasm and accounts approximately 18% of all mesenchymal neoplasms and 1% of all gastrointestinal neoplasms. Morbidity of GIST is about 1-2 per hundred thousand per year. The recurrence rate 5 years after complete resection of malignant GIST is up to 50%,and the median survival of metastatic GIST is only 9 months. Nowadays,endoscopic ultrasonography(EUS)is the first choice management for upper digestive tract GIST with diameter ≤2 cm,however,because of its high degree malignancy,surgical resection is the choice for GIST with diameter > 2 cm,and adjuvant or neoadjuvant chemotherapy with tyrosine kinase inhibitors can be used in case with high risks and difficulties in surgical removal. This article reviewed the advances in study on treatment of GIST.

Objective To investigate the stent occlusion rate and its risk factor in chronic pancreatitis (CP). Methods From November 2006 to January 2010 a total of 77 pancreatic endoprostheses from 64 patients with CP were tested by simulating the pathophysiologically increased main pancreatic duct (MPD)pressure. The water flow during 15 seconds was recorded 4 times at a pressure of 10 cm water. Kaplan Meier method was used to evaluate the univariate relationship between risk factor and stent occlusion, and Cox regression survival analysis was used to evaluate the multivariate relationship between risk factor and stent occlusion. Results 64 patients with CP were included, with 43 males and 21 females, the mean age was 38 years (range, 4 ～ 80 years). The stents had been placed for a mean of 263 days ( range 26 ～ 759 days).Average stent diameter was 8F (range, 5 ～ 10 F). The overall occlusion rate was 67.5% (52/77), the nonocclusion rates at 90, 180, 360, 540 d were 96. 1% (74/77) , 72.7% (56/77) ,58.4% (45/77) and 35.1% (27/77). In the Cox regression analysis, endoprosthesis diameter ≥8.5F was shown to be the only risk factors for stent occlusion. Conclusions A significant proportion of stents placed after 180 d were not occluded, and were significantly lower than those reported from similar studies overseas. Pancreatic endoprosthesis diameter ≥8. 5F was prone to occlusion.

Objective To investigate the clinical manifestations, etiology and risk factors of chronic pancreatitis guided by the M-ANNHEIM classification of chronic pancreatitis and to evaluate the validity and clinical significance of this classification. Methods A review of clinical data of inpatients in our hospital from December 2007 to December 2009 was conducted. The classification was carried out according to the pancreatitis were enrolled. There were 256 adult patients and 51 children and adolescent patients (age of onset<18 yr). Among these cases, 129(42%) reported a drinking history. 110 cases (35.8%) had a smoking history, 31 cases (10.1%) presented with hyperlipoidemia. 12 cases had some factors related to pancreatic duct such as pancreas divisum, pancreas trauma. There were 231 (75.2%) cases with calcification of pancreas, 45 (14.7%) with exocrine insufficiency (steatorrhea), 58 (18.9%) with endocrine dysfunction (diabetes mellitus), 32 (10.4%) underwent pancreatic surgeries, and 39 (12.7%) with pancreatic pseudocysts, biliary obstruction, pancreatic cancer and other severe complications. The M-ANNHEIM clinical staging of chronic pancreatitis was: no case in stage 0, 220(71.7%) cases in stage Ⅰ , 69(22.5%) cases in stage Ⅱ ,12(3.9%) cases in stage Ⅲ and 6 cases in stage Ⅳ. The mean value of the M-ANNHEIM score and severity index was 7.78,69 (22.5%) cases were in the minor level, 174 (56.7%) were in the increased level,62(20.2%) cases were in the advanced level. Conclusions The M-ANNHEIM classification of chronic pancreatitis is a simple, objective, accurate and noninvasive tool in clinical practice. This new classification system will be helpful for investigating the impact and interaction of various risk factors on the course of the disease.

Objective To investigate the effect of α-tocopherol on fibrosis of chronic pancreatitis (CP) rat and explore its mechanism.MethodsMale Wistar rats were randomly divided into control group,acute necrotizing pancreatitis (ANP) group,α-tocopherol group.CP was induced by dibutyltindich loride ( 8 mg/kg) infusion into the tail vein.Gastric lavage of α-tocopherol (800 mg/kg body weight,daily) was started 24 hours after dibutyhindich loride infusion for 4 weeks.The rats in ANP and control group received 0.6 ml salad oil gastric lavage.The rats were sacrificed 4 weeks later.Pancreatic tissue was harvested for histological examination and collagen staining,and measurement of the levels of hydroxyproline and malondialdehyde (MDA) of the pancreas were performed.The mRNA expression of transforming growth factor (TGF)-β１ was measured by real time PCR.ResultsAfter gastric lavage for 4 weeks,the pancreatic tissue inflammation,fiber deposition and abnormal structure in rats of α-tocopherol group were greatly reduced.The levels of MDA and hydroxyproline in rats of α-tocopherol group were significantly lower than those in ANP group [ (0.40 ±0.20) vs (1.07 ±0.41) nmol/100mg,(402.49 ±27.62) vs (664.92 ±29.04) μg/g,P＜0.05].The expressions of TGF-β1 mRNA in rats of o-tocopherol group were significantly lower than those in ANP group (2.24 ± 0.89 vs 3.35 ± 0.66,P ＜ 0.05 ).Conclusions Tocopherol gamma can improve pancreatic inflammation and fibrosis by reducing the oxidative stress level and down-regulating the expression of TGFβ1mRNA in rats with CP.

Objective to determine the basal levels of several pancreas-related endocrine hormones in patients with chronic pancreatitis.Methods according to inclusion and exclusion criteria,consecutive patients from February 2016 to August 2016 in Department of Gastroenterology,Changhai Hospital,Second Military Medical University and ten healthy control (matched for age and gender) were included.Basal levels of glucagon-like peptide 1,pancreatic polypeptide,Secretin,glucagon,somatostatin between groups of CP vs healthy control,CP with abnormal glycometabolism vs CP with normal glycometabolism and alcoholic CP vs non-alcoholic CP were compared.Results a total of 53 patients with chronic pancreatitis and 8 healthy subjects were included in this study.(1) CP vs healthy controls:the level of secretin in healthy control patients is significant lower than that in CP patients;(2) CP with abnormal glycometabolism vs CP with normal glycometabolism:the level of triglyceride and somatostatin is significant lower than that in CP patients;the prevalence of patients with chronic alcohol consumption and the level of glucagon-like peptide 1 in CP with abnormal glycometabolism is significant higher than that in CP with normal glycometabolism;(3) the prevalence of abnormal glycometabolism in alcoholic CP group is significant higher than that in non-alcoholic CP.The results above are all of statistical significance.Conclusions in addition to dysfunction of islets/3-cells,CP also easily affects the level of other pancreas-related hormones such as secretin,somatostatin and glucagon-like peptide 1.Otherwise,chronic alcohol consumption is also strongly related with abnormal glycometabolism,the mechanism deserves further researches.

Objective To investigate the relationship between alcohol and smoking and the development of pancreatic calcification in chronic pancreatitis (CP) in China. Methods The patients were divided into two groups according to the presence of pancreatic calcification at admission and the data were analyzed; furthermore, the discharged patients without pancreatic calcification were divided into two groups as newly diagnosed pancreatic calcification group and persistent non-pancreatic calcification group. Logistic regression and Cox proportional-hazards model was used for multivariate analysis of the risk factors for pancreatic calcification. Results From January1997 to July 2007, 449 patients with CP were enrolled and followed up successfully. 248 patients presented with pancreatic calcification at admission; among the 201 patients presented without pancreatic calcification, 13 patients developed pancreatic calcification after discharge. Patients with pancreatic calcification had a young age at onset, long CP history, higher incidence of diabetes mellitus and diarrhea. Age at onset ≤ 40, alcohol intake over 20 g/day, and diabetes mellitus and diarrhea were risk factors for pancreatic calcification. The only risk factor of development of pancreatic calcification after discharge was excessive alcohol intake (OR: 3.2). Conclusions Alcohol intake increased the risk of pancreatic calcifications, suggesting the patients abstain from alcohol intake. Further studies are necessary to clarify the role of smoking.

Objective To investigate the incidence of diabetes mellitus and risk factors for the disease in chronic pancreatitis (CP) patients.Methods A historical cohort study on subjects with painful CP who were admitted to hospital from Jan.1997 to July 2007 were conducted.A life-table method was used to estimate the cumulative probability of the development of diabetes mellitus once clinical onset of abdominal pain.Cox proportional-hazards model was used for multivariate analysis of the variables including age,sex,drinking and smoking habits,etiological factor,presence of pancreatic masses,pancreatic calcifications,measure of intervention,diarrhea,weight loss and degree of pain.Results Data were obtained from 354 patients (239 males,mean age at onset of pain (38.1±17.6) years;alcoholic origin 18.1%) with painful CP.The mean follow-up period was (45.2±32.9)months.The rate of diabetes mellitus in CP patients was 16.1%.There was a high incidence (29.8%)of diabetes mellitus 1 year before the episodes of abdominal pain.The cumulative risk of diabetes mellitus in subjects 5 and 10 years after the episodes of pain was 9.3% and 20.7%,respectively.Cox proportional-hazards model selected smoking (＞10 pack years) (hazard rate (HR)= 3.3),mild abdominal pain (HR=5.2),weight loss (HR = 2.6) and pancreatic calcifications (HR = 2.2) as variables identifying subjects with diabetes mellitus in patients with painful CP before they were performed therapeutic endoscopy or surgical intervention.Smoking (＞10 pack years) (HR = 3.0),weight loss (HR= 2.8) and distal pancreatectomy (HR =7.3) were identified with an increased risk of diabetes mellitus in these cases after they received therapeutic endoscopy or surgical intervention.Conclusion The risk factors of diabetes mellitus for CP appears to be independent of smoking (＞10 pack years),mild abdominal pain,weight loss,pancreatic calcifications and distal pancreatectomy.

Objective To investigate the incidence and risk factors of pancreatic cancer in patients with painful chronic pancreatitis (CP). Methods Three hundred and ninty-seven patients with painful CP were recruited between Jan. 1997 to July 2007. A life-table method was used to estimate the cumulative probability of the incidence of pancreatic cancer. Cox proportional-hazards model was used for multivariate analysis of the variables including age, sex, drinking and smoking habits, etiological factor, presence of pancreatic masses, pancreatic calcifications, measure of intervention, diabetes mellitus, diarrhea, weight loss and degree of pain. Results Of 397 patients,346 (87.2%) were follow-up for (34.3±27.1)months with 244 males and 102 females(2.4 :1). The mean age of the patients were (47.7 ±13. 7) years and alcoholic origin accounted for 22. 2%. The incidence of the pancreatic cancer was 8.1 % (28/346). There was a high incidence of cancers during the 4 years after the episodes of abdominal pain. The cumulative risks of pancreatic cancer 1, 5 and 10 years after the episodes of pain were 5 %, 5.6% and 11.6% respectively. Cox proportional-hazards model selected age at onset (≥51 years) [hazard rate(HR) = 3. 1], pancreatic calcifications ( HR = 4.1) ,pancreatic masses ( HR = 7. 1 )], no improvement of abdominal pain ( HR = 3. 8), increased frequency of pain (HR= 6.8), no diarrhea (HR= 15.3) as variables identified with pancreatic cancer in painful CP patients. Conclusions Pancreatic cancer should be suspected in patients with CP. The risk factors of pancreatic cancer are age at onset (≥ 51 years), pancreatic calcifications, pancreatic masses, no improvement of abdominal pain, increased frequency of pain and no diarrhea.

Objective To evaluate the risk factors of failure in pain resolution in chronic pancreatitis(CP)after endoscopic treatment.Methods We undertook a retrospective cohoa study of subjects with pain caused by CP,who underwent endoscopic treatment from January 1997 to December 2006.Cox proportional-hazards model was used for multivariate analysis of the variables that were possibly related to failure of treatment.Results Follow-up data were obtained from 172 patients(114 males and 58 females,mean age 39.4 yr.Pain resolution after endoscopic treatment was achieved in 148(86.0%).Cox proportional-hazards model showed risk factors of failure in pain resolution after endoscopic treatment were onset age(＞36 years,hazard rate(HR)=3.5),mild and moderate abdominal pain before endoscopy(HR=2.4),no decrease in amount alcohol consume(＜50%,HR=1.9)and inappropriate diet(HR=2.8).Conclusion Patients with CP should abstain from alcohol and have low-fat diet,especially for those with pain onset at older ages (＞36 years)and with mild and moderate abdominal pain before endoscopic treatment.