Objective To analyze relevant factors causing pancreatic fistula post pancreaticoduodenectomy with ex-ternal drainage of pancreatic duct. Methods Altogether 133 patients who underwent pancreaticoduodenectomy with exter-nal drainage of pancreatic duct in our hospital from 1999 to 2011 were retrospectively analyzed. Logistic regression analysis was used to analyze the relevance of pancreatic fistula with age, gender, combined diseases, pancreatic duct diameter, patho-logical types, preoperative total bilirubin (TBIL), albumin (ALB) levels, drainage of the bile duct before operation, obstruc-tion of the pancreatic duct drainage and postoperative application of growth somatostatin. Then we also analyzed the relation-ship between those risk factors and the severity of pancreatic fistula. Results Postoperative pancreatic fistula occurred in 24 cases (3 cases were of grade A,13 cases were of grade B and 8 cases were of grade C) among the 133 patients. Logistic re-gression analysis showed that obstruction of the pancreatic duct drainage is a major risk factor of pancreatic fistula in these patients(OR=4.529,P=0.005). The patients whose pancreatic duct drainage was obstructed had a significantly higher pan-creatic fistula rate than the patients whose drainage was not obstructed (30.8%vs 12.8%, P＜0.05). The occurrence of pan-creatic fistula has no significant correlation with age, gender, combined diseases, pancreatic duct diameter, pathological types, preoperative TBIL, ALB level, preoperative bile duct drainage and postoperative application of somatostatin. What’s more, in those pancreatic fistula patients, the pancreatic fistulas were more severe in the obstructed ones than those in the un-obstructed ones. Conclusion The obstruction of the pancreatic duct drainage is a major risk factor of pancreatic fistula post pancreaticoduodenectomy with external drainage of pancreatic duct. If adequate preventive measures were employed during operation , the incidence of pancreatic fistula and pancreatic fistula severity will be significantly reduced.

Objective To analyze the relevant factors of portal vein thrombosis in patients after splenectomy for portal hypertension due to cirrhosis resulting from hepatitis. Methods The clinical data of 226 patients with hypertension due to cirrhosis resulting from hepatitis receiving simple splenectomy or splenectomy and portal-azygous devascularization in our hospital from August 2000 to June 2007 were retrospectively analyzed. Effective results were found in 154 of the patients. The 154 cases were divided into the thrombosis group and non-thrombosis group. The relation of portal vein thrombosis to the descendent level of portal vein pressure after operation,the prothrombin ratio (PTR) and fibrinogen(FIB) before operation, platelet count before and 1, 7, 14 days after operation, diameter of main portal vein and bilirubin level before operation and blood loss in operation were determined by logistic regression analysis. Results Portal vein thrombosis occurred in 31 patients. Regression univariate analysis showed that portal vein thrombosis was related to the descendent level of portal vein pressure after operation but not to the PTR and FIB, platelet count, diameter of main portal vein, bilirubin level and blood loss. Multivariate analysis demonstrated the same results. Conclusion The descended level of portal vein pressure is an important factor in portal vein thrombosis in patients after splenectomy for portal hypertension due to cirrhosis resulting from hepatitis.

Objective To study the correlation between the coagulation factor Ⅶ (F Ⅶ) and progressive hemorrhage after brain contusion in mice and provide the experimental evidence for the clinical application of recombinant human FⅦa.Methods Twelve male BALB/c mice were given liposomeencapsulated FⅦsiRNA via tail vein at doses of 1,3,5 and 10 mg/kg with 3 mice per dosage.The other 3 mice received equivalent volume of normal saline as controls.Two days after the injection,mice blood sampling was used to detect FⅦ mRNA expression in liver using real-time PCR,level of plasma FⅦ using ELISA method,and activity of plasma FⅦ using chromogenic substrate assay.The optimal dose at which F Ⅶ expression was inhibited was determined.Thirty BALB/c male mice were assigned to two groups (n =15 per group) according to the random number table:FⅦ-suppressing group,mice were injected with FⅦsiRNA at the optimal dose and control group,mice were injected with same volume of negative control vector.The model of brain contusion was established in both groups.Volume of hemorrhage following brain contusion was measured at 3,24 and 72 h postinjury,and hematoma volume at 24 and 48 h postinjury.Results Liposome-encapsulated siRNA delivery down-regulated FⅦ expression in the mouse liver.Level and activity of plasma FⅦ were also reduced significantly.The optimal siRNA dose was 3 mg/kg.At 3,24 and 72 h postinjury,relative volume of brain hemorrhage in FⅦ-suppressing group was 1.46 ± 0.10,1.82 ± 0.23 and 2.28 ± 0.15 respectively,significantly higher than that in control group (1.00 ± 0.25,1.20 ± 0.31 and 1.20 ± 0.22 respectively) (P ＜ 0.05).At 24 and 48 h postinju-ry,volume of hematoma in FⅦ-suppressing group was (6.7 ± 1.5)mm3 and (9.8 ± 1.0) mm3,significantly higher than that in control group [(5.2 ± 1.2) mm3 and (5.5 ± 1.5) mm3] (P ＜0.01).Conclusions Level of FⅦ in vivo relates closely to the progressive hemorrhage of brain contusion in mice.Administration of FⅦ is effective to reduce the incidence of progressive hemorrhage.

This article was aimed to study the antioxidant and antihyperlipidemic effect of total phenolic composition prepared from pineapple (A nanas comosus L.) leave. It had a rapid absorption after intragastric administration and the principle ingredient, p-coumaric acid, reached the peak concentration after 5 minutes of administration. The mice model with single intragastric administration of lipid and glucose were used in the observation of changes on postprandial glucose, lipid and intestinal lipase at different time points after drug administration. The results showed that phenols of pineapple leave can inhibit triglyceride and glucose absorption in certain extent. No significant effect was observed on inhibition at 30 minutes after the phenol administration. However, the intestinal lipase activity was obviously inhibited in normal mice and the intestinal lipase activity decline caused by acute lipid consumption can be reversed. It was concluded that the phenols pineapple leave may inhibit the absorption of lipids with correlation to lipase activity. It had certain regulation effect on the high postprandial glucose and fat absorption.

OBJECTIVETo study the 3, 4- dinitro-furazan-based oxidation furazan (DNTF) of sub-acute toxicity and chronic toxicity, to determine the acute toxicity classification DNTF, the nature of toxic effects and major target organ for the development provide the basis for occupational exposure limits.

METHODS( 1) Acute toxicity: The oral gavage method once infected, symptoms of poisoning of animals observed to calculate the LD50DNTF and 95% confidence limits. ( 2) sub-chronic experiment: selection of 96 healthy SD rats were randomly divided into four groups, doses of 25, 56.2, 125 mg/kg and the negative control group, Exposure for ninety days,five days a week, once a day, The rats were killed at end of Exposure, heart, liver, spleen, lung, kidney, brain,testis, uterus were taken to observe the pathological changes.

RESULTS( 1) Acute oral toxicity test results indicate that DNTF rat oral LD50 greater than 5000 mg/kg, DNTF mice treated by oral LD50 4589 mg/kg, 95%confidence limit for the 4026-5230 mg/kg, Acute toxicity grade level is low toxicity compounds. (2) Sub-chronic toxicity experiment, the high-dose male rats, high, medium and low-dose group female rats weight gain than the negative control group, compared with the control group, the difference was statistically significant (P<0.05).125 mg/kg of serum alanine aminotransferase, aspartate aminotransferase was significantly higher. 125 mg/kg dose groups, liver, kidney, lung, testicular factor was significantly higher. Liver, kidney, lung histological examination showed obvious morphological changes.

CONCLUSIONAcute toxicity grade DNTF low toxicity level compounds, target organ toxicity of liver, kidney and lung.

Animals ; Female ; Lethal Dose 50 ; Male ; Mice ; Nitrofurazone ; analogs & derivatives ; toxicity ; Oxadiazoles ; toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests

OBJECTIVETo study the teratogenicity of new high-energy compounds, 3, 4 two furazan-based oxidation furazan (DNTF) and the impact on human health, occupational exposure limits were provided for the following research.

METHODSPregnant SD rats were randomly divided into five groups by Standard teratogenicity test, including three dose groups (5.0, 15.8, 50.0 mg/kg), the negative control (vegetable oil), and the positive control group (CP 10.0 mg/kg). Each 10 to 15 rats were in one group. Gavage was consecutive for rats during pregnancy 7 ∼ 12 d and then sacrifice after 20 d.

RESULTSThere were no significantly difference between the three dose groups and negative controls in the pregnancy rate, the weight of pregnant rats, fetal weight, fetal growth, fetal malformation rate and internal organs,

CONCLUSIONThere were no maternal toxicity, embryo toxicity and teratogenicity for rats when DNTF in the range 5.0 ∼ 50.0 mg/kg.

Animals ; Female ; Nitrofurazone ; toxicity ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Teratogens

OBJECTIVETo study the mutagenicity and teratogenicity induced by ammonium dinitramide(ADN).

METHODSAccording to technical specifications for toxicity determination of chemicals, Salmonella typhimurium reverse mutation assay (Ames assay), in vivo mammalian erythrocyte micronucleus test, sperm malformation test and teratogenesis test were used to detect the mutagenicity and teratogenicity induced by AND.

RESULTSWhen the exposure doses of AND were 8-5000 pg/plate, the result of Ames assay was negative. As compared with control group, the micronucleus rate of mice exposed to 113.8 mg/kg AND significantly increased(P<0.05), the sperm malformation rates of mice exposed to 54.4-272.0 mg/kg AND did not increased significantly. The survival rate of fetuses decreased, the rate of assimilated fetuses increased, the rate of fetus sternum agenesis enhanced in mice exposed to 319 mg/kg AND, as compared with controls. The rates of in the 4th-6th fetus sternum agenesis in groups exposed to 21.3, 79.7 and 319 mg/kg AND were higher than that in control group. The malformation rate of fetus bowels in groups exposed to 319 mg/kg AND was higher than that in control group. The teratogenic index of ADN was 30.

CONCLUSIONAND may be a mutagen and induce the teratogenic effect.

Animals ; Embryo, Mammalian ; drug effects ; pathology ; Female ; Male ; Mice ; Mice, Inbred Strains ; Micronucleus Tests ; Mutagenicity Tests ; Nitrites ; toxicity ; Pregnancy ; Quaternary Ammonium Compounds ; toxicity ; Spermatozoa ; drug effects ; pathology ; Sternum ; drug effects ; pathology

OBJECTIVETo study the acute, subacute and subchronic toxicity induced by ammonium dinitramide (ADN), and to ascertain the gradation and target organs of acute toxicity induced by AND.

METHODSAccording to technical specifications for toxicity determination of chemicals, the oral tests for acute, subacute and subchronic toxicity induced by AND were performed for 90 days.

RESULTSThe oral LDx for mouse and rat was 568.9 mg/kg and 616.6 mg/kg ADN respectively. The gradation of acute toxicity induced by AND was low level. The results of oral subacute and subchronic toxicity tests (for 28 and 90 days) showed that a gain in weight in group exposed to 123 mg/kg AND was significantly lower than that in control group (P<0.05), the TBIL and ALT in group exposed to 61.6 and 123 mg/kg AND significantly increased and the ratio of liver weight to body weight obviously decreased, as compared with control group, the number of animals with hepatic pathological changes in group exposed to 61.6 and 123 mg/kg AND was significantly higher than that in control group (P<0.05).

CONCLUSIONThe gradation of acute toxicity induced by ADN was low level. When the exposure dose of AND was 30.8 mg/kg, the adverse effect was not observed, and the target organ was liver.

Animals ; Body Weight ; Female ; Liver ; drug effects ; pathology ; Male ; Mice ; Mice, Inbred Strains ; Nitrites ; toxicity ; Quaternary Ammonium Compounds ; toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests, Acute ; Toxicity Tests, Subchronic

OBJECTIVETo investigate the role of stromal cell derived factor 1 (SDF-1) on the proliferation of hepatic oval cells, and the influencing factors.

METHODSFlow cytometry was used to detect the expression of CXCR4 on the cell surface when WB-F344 cells were growing in the culture medium with and without transforming growth factor β1 (TGF-β1) respectively. Western bolt was used to detect the expression of β-catenin and its phosphorylation level. The translocation of β-catenin was shown by confocal microscopy analysis. Q-RT-PCR was used in detecting the β-catenin downstream gene expression such as Ccnd1 and c-Myc. MTT was used to detect the proliferation of WB-F344 cells which were treated by SDF-1 + TGF-β1 and those cells exposed to SDF-1 or TGF-β1 only, as well as of the negative control group.

RESULTWB-F344 cells rarely express CXCR4 under conventional circumstance, but this receptor can be up-regulated when the culture medium contain a modest amount of TGF-β1 (the rate of CXCR4 positive cell increased by 39.5%). The bond of SDF-1 to CXCR4 results in the phosphorylation of β-catenin, and its inactivation. SDF-1 alone didn't affect the proliferation of WB-F344 cells (0.512 ± 0.010 vs. 0.513 ± 0.008, t = 0.337, P > 0.05), while TGF-β1 group show a slight decrease of cell population (0.393 ± 0.007,t = 28.001, P < 0.05). But when TGF-β1 combined with SDF-1, the proliferation of WB-F344 was more weakened than TGF-β1 group, and the difference was statistically significant (0.272 ± 0.009,t = 32.204, P < 0.05).

CONCLUSIONSTGF-β1 can up-regulate the expression of CXCR4 in hepatic oval cells, and then inhibit the proliferation of hepatic oval cells via inactivating β-catenin in vitro.

Cell Line ; Cell Proliferation ; Chemokine CXCL12 ; metabolism ; Hepatocytes ; metabolism ; Humans ; Receptors, CXCR4 ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; beta Catenin ; metabolism

OBJECTIVETo investigate the effect of sphingosine kinase 1 (SphK1) on the proliferation, apoptosis, migration and invasion of colon cancer TH-29 cells and to explore its molecular mechanisms.

METHODSPhorbol 12-myristate 13-acetate (PMA) was used to induce the activity of SphK1 and N, N-dimethylsphingosine (DMS) was used to suppress the activity of SphK1. Cell prolieration and apoptosis were detected by MTT assay and flow cytometry, respectively. The migration and invasion capabilities of the cells were assessed in Transwell chambers. The activity of SphK1 was assayed by autoradiography. Western blot was used to evaluate the protein expression of SphK1, p38, phosphorylated p38 (p-p38) and SAPK/JNK.

RESULTSPMA and DMS were able to induce and suppress the activity and protein expression of SphK1 in a time-dependent manner, respectively. PMA enhanced and DMS suppressed the cell viability in a time- and dose-dependent manner. Being treated with 100 nmol/L PMA or 50 µmol/L DMS for 0, 6, 12, 24 h, the cell apoptosis rates of PMA group were (9.35 ± 0.84)%, (7.61 ± 0.48)%, (5.53 ± 0.76)% and (0.56 ± 0.33)%, contrastly, that of DMS group were (9.18 ± 0.94)%, (12.06 ± 1.41)%, (19.80 ± 2.36)% and (31.85 ± 3.60)%, respectively. Compared with the control group, the cell migration and invasion capabilities of the PMA group were significantly enhanced, and that of the DMS group were significantly suppressed. The migration cell number of control, PMA and DMS groups were 68.75 ± 6.15, 109.33 ± 11.63 and 10.83 ± 2.48, the invasion cell number of control, PMA and DMS groups were 55.42 ± 4.50, 90.58 ± 7.06 and 9.58 ± 2.39, respectively. With the elevating activity and expression of SphK1, the protein expressions of p38, p-p38 and SAPK/JNK were strikingly suppressed. On the contrary, after treating with DMS the protein expressions of p38, p-p38 and SAPK/JNK were enhanced.

CONCLUSIONSSphK1 potently enhances the prolieration, migration and invasion of colon cancer HT-29 cells, meanwhile suppresses the cell apoptosis. The suppressing of the p38 and SAPK/JNK signalling pathways may be one of its molecular mechanisms.

Apoptosis ; drug effects ; Carcinogens ; administration & dosage ; pharmacology ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Enzyme Inhibitors ; administration & dosage ; pharmacology ; HT29 Cells ; Humans ; MAP Kinase Kinase 4 ; metabolism ; Neoplasm Invasiveness ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor) ; metabolism ; physiology ; Sphingosine ; administration & dosage ; analogs & derivatives ; pharmacology ; Tetradecanoylphorbol Acetate ; administration & dosage ; analogs & derivatives ; pharmacology ; Time Factors ; p38 Mitogen-Activated Protein Kinases ; metabolism