Objective To determine the serum KL-6 level in patients with pancreatic carcinoma and investigate its diagnostic value. Methods The data of 53 pancreatic carcinoma (PC) patients; 68 chronic pancreatitis (CP) patients and 51 patients with high risks of pancreatic cancer (HR) with complete follow-up data were studied, and 50 healthy volunteers were used as controls. ELISA was used to measure the serum levels of KL-6, MUC4, and CA50. Radioimmunoassay methods were used to measure the serum CA19-9 levels. The sensitivity and specificity of KL-6 for the diagnosis of PC were determined, and the relationship between its levels and clinicopathologic parameters, patients' outcome were analyzed. Results The serum KL-6 levels were (753±548), (135±93), (105±55) and (99±50) U/ml in PC group, CP group, HR group and control group, and the value in PC group was significantly higher than those in other 3 groups (P <0.01). Using >232 U/ml as the cut-off point, the sensitivity and specificity of KL-6 for the diagnosis of PC was 96% and 94%. Using >244 U/ml as the cut-off point, the sensitivity and specificity of KL-6 for the diagnosis of PC was 97% and 91%. The clinical value of KL-6 was higher than those of CA19-9, CASO and MUC4. The serum level of KL-6 was not associated with clinicopathologic parameters. The median survival of patients with serum level of KL-6 =300 U/ml was (9.3 ±1.2) months, which was significantly longer than that in patients with serum level of KL-6 >300 U/ml [ (4.6 ±0.7) months, P =0.006]. Conclusions KL-6 might be a useful serological marker of pancreatic cancer, and it may play a role in the differential diagnosis between pancreatic cancer and chronic pancreatitis.

Objective To investigate the effect of tumor necrosis factor receptor-p55/p75(TNFR-p55/ TNFR-p75) on the pathogenesis of severe acute pancreatitis (SAP) in rats. Methods Thirty-six male Sprague-Dawley rats were divided into 2 groups: SAP group and control group. SAP model was ~induced by injection of 5% sterile sodium taurocholate into biliopancreatic duct, while control group was only given sham operation. Rats were sacrificed at 3, 6, and 12 hours after the onset of operation. Blood sample and pancreatic tissues were collected. The severity of pancreatitis was assessed according to the level of serum amylase and histological scoring. The serum levels of tumor necrosis factor-?(TNF-?) were examined by ELISA. Expressions of TNFR-p55 mRNA and ~TNFR-p75 mRNA in pancreatic tissues and peripheral blood mononuclear cells (PBMC) were measured by semi-quantitative RT-PCR. Results The levels of serum amylase and TNF-? in SAP group were both significantly higher than those in the control group at each time point (P

Objective To investigate the relationship between acute biliary pancreatitis (ABP) and anomalous pancreaticobiliary duetal union (APBDU). Methods 131 patients with ABP were enrolled to test the serum total bilirubin (TB), alanine amintransferase (ALT), aspartate amintransferase (AST), alkaline phosphates (ALP), γ-glutamyl transferase (γ-GT). All the patients received medical treatment, and then these tests were performed again. Thereafter, all the patients underwent selective surgery and intra-operative cholangiography was performed to observe the pancreaticobiliary duetal union. Results 27 patients (20.6%) with APBDU were found in 131 patients. Among them, 8 cases (29.6%) was B-P subtype (TypeⅠ), 16 cases (59.3%) was P-B subtype (TypeⅡ) , and the remaining 3 cases was mixed subtype (TypeⅢ). A significant decrease of ALT, AST, ALP, γ-GT after non-surgical treatment in both group of APBDU and NAPBDU was noted (P＜0.05). The serum levels of ALT, AST,γ-GT in APBDU patients were (71.81± 23.19) U/L, (47.85±27.87) U/L, (52.86±31.49) U/L, respectively; and in NAPBDU patients were (51.96±15.40) U/L, (40.77±16.58) U/L, (34.86±26.47) U/L. The difference was statistically significant (P＜0.05). Condusions APBDU is an important etiology of ABP.

Objective To analyze the relationship between blood glucose level, blood pressure and weight with pancreatic cancer genesis. Then to explore the metabolism associated risk factors in pancreatic cancer genesis. Methods Form December 2002 to September 2009 in Ruijin Hospital, 548 pancreatic cancers with pathology diagnosis after pancreatectomy were collected for the study with retrospective analysis method. The association of pancreatic cancer with blood glucose level, blood pressure, weight and other metabolic factors were analyzed. Results With principal component analysis, it suggested that there were strong correlation between blood glucose level, blood pressure and weight index (BMI) increasing with pancreatic cancer. The contribution rates were 3. 614%,25. 236%, 15. 418% and 12. 918%, respectively. Single factor analysis indicated that the association between pancreatic cancers and new onset diabetes mellitus (duration≤ 2 years) was stronger than that of long-term diabetes mellitus. The occurrence rate of pancreatic cancer in patients with long-term diabetes whose blood glucose level was not well controlled recently while well controlled previously (44.6 % ) was significant hister than that in patients without diabetes (5. 6% , P＜0.05). The fasting blood glucose level of these PC patients ( 13.87± 3. 49 mmol/L) was significantly higher than new onset and other long-term diabetes patients, the comparative risk was 13.46 (95% CI 4. 560,39. 731). BMI increasing was a risk factor of pancreatic cancer, but there was no significant statistical difference between risk degree and BMI increasing level. All above metabolic diseases were risk factors of pancreatic cancer, but for pathology, location and stage of pancreatic cancer there was no statistical difference in theses factors. Conclusion This study suggested diabetes, BMI increasing and hypertension were high risk factors of pancreatic cancer genesis. New onset and long-term diabetes patients whose blood glucose not controlled well recently should be watched carefully for pancreatic cancer. Early treatment and intensive follow-up of metabolic disease might be helpful to early diagnosis and prognosis of pancreatic cancer.

Objective To investigate the role of connexin 43(Cx43)in the apoptosis of pancreatic cancer cell line BxPC and its possible mechanism.Methods pcDNA-Cx43,pcDNA-Cx43N,pcDNA3.0,siRNA-Cx43 and siRNA-NC were transfected into BxPC3 cells via liposome method.Cx43 protein and Cytochrome C(Cyt C)concentration was determined by Western blot,and the apoptosis was analyzed by Annexin V/PI binding assay.The mitechondria apoptosis pathway involved in Cx43 associated apoptosis was examined which contains the depolarization of mitechondrial membrane potential (MMP);fluorospectrophotometer was used to measure the activities of caspase-3 and caspase-9. Gap junction intercellular communication(GJIC) was determined by dye-transfer method.Results Cx43 protein expression increased after BxPC3 transfeetion,apoptosis rate increased from(6.35±0.43)%in empty vector transfection group to(14.29±1.24)%;after H202 treatment,apoptosis rate increased from(20.34±2.47)%to(31.27±2.56)%(P<0.05).Meanwhile,mitochondrial membrane potential was decreased,Cyt C was increasingly released from mitochondria,caspases activities were increased;after siRNA43 interference,apoptosis rate decreased from(7.42±0.47)% to(5.19±1.37)%,after H_2O_2 treatment,apoptosis rate decreased from (19.43±1.71)%to(11.67±1.97)%(P<0.05).Decreased mitochondrial membrane potential and Cyt C release were observed,caspases activities were decreased.GJIC of pcDNA-Cx 43 transfection group increased from 14.52±0.57 to 23.05±3.84.and it increased from 1.70 ±0.24 to 3.84 ±0.45 in the presence of β-GA(P<0.05).But the apoptosis rate was not significantly different.Conclusions Cx43 could promote BxPC3 apoptosis via mitochondrial apoptotic signal pathway,and the possible mechanism included signal pathway other than GJIC.

Objective To investigate the relationship between expression of nuclear factor kappa B p65 ( NF-κB p65) and hippocampal neuronal apoptosis in acute necrotizing pancreatitis (ANP) rats with brain injury. Methods Sixty-four SD rats were randomized into normal saline group (NS) and ANP group. The ANP rat model was induced by retrograde injection of 4% sodium taurocholate into the pancreaticobiliary duct of SD rats. Nissle stain was used to detect the brain injury. Neuronal apoptosis was determined by TUNEL.NF-κB p65 expression was detected by immunohistochemistry and RT-PCR. Results Hippocampal neuron was absent, karyopyknosis, unclear nucleolus and decreased Nissl bodies were found, the injuries was aggravated with time. The apoptosis index at the 3, 6 and 12 h in ANP group was 10.63 ±0.24, 21.02±0.25, 17.12±0.36, respectively, while they were 0.33±0.19,0.71±0.67, 0.45 ± 0. 33 in NS group, and the difference was statistically significant ( P ＜ 0. 01 ). The expressions of NF-κB p65 mRNA were 0. 63 ± 0.05,1.05 ±0.06,0.92 ±0.05, which were significantly higher than those in the NS group (0.11 ±0.01,0.12±0.01,0.08±0.01,P＜0.05).The chatge of expression of NF±κB p65 protein was consistent with that of NF-κB p65 mRNA. Conclusions The brain injury of ANP rats was highly correlated with neuronal apoptosis at the early and middle phase of ANP, and its mechanism may be related with NF-κB p65 activation.

Objective To investigate the relationship between the activity of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway in cerulein-induced pancreatic acinar cell line AR42J. Methods The in vivo model of AP was induced by cerulean treated pancreatic acinar cell line AR42J, then RPM and AG490 were given for intervention. Western blot was used to determine theexpressions of JAK1 and phosphorylation JAK1 ( P JAK1 ) , STAT1, PSTAT1 and TNFα, IL-1β, IL-6. The expressions of IL-6, IL-1 β, and TNFα mRNA were measured by RT-PCR. Survival rate of cells was evaluated by trypan blue stain. Results The relative expressions of JAK1, P JAK1, STAT1, P STAT1 and TNF-o, IL-1β, IL 6 without cerulean treatment were 0.09 ±0.04,0.14 ±0.08,0.21 ±0.09,0.12 ±0.12,0.10 ±0.02,0.08 ± 0.03,0.02 ± 0.02. After cerulean treatment, the expressions of abovementioned protein increased in a time-dependant manner, the expressions at 24h were 0.53 ± 0.09,0.53 ± 0.13,0.56 ± 0.09,0.55 ± 0.10,0.25 ± 0.04,0.25 ±0.09,0.27 ±0.07, which were significantly higher than those in the control group (P ＜0.05). 2 4 h after RPM and AG 4 9 0 inhibition, the expressions of TNF-α, IL-1 β, IL-6 proteins significantly decreased to 0.17 ± 0.03and 0.17 ± 0.01,0.15 ± 0.05 and 0.14 ± 0.07,0.19 ± 0.04 and 0.19 ± 0.05; their expressions of mRNA significantly decreased ( P ＜ 0.05 ). The cell survival rates in RPM and AG490 treatment group were (72.4 ± 11.2) %, (69.7 ± 9.8 ) %, and in cerulein-stimulated cells (42.2 ± 12.3 ) % ( P ＜ 0.05 ).Conclusions The JAK1/STAT1 signaling pathway was involved in pancreatic inflammatory response with cerulein stimulation. Early treatment with inhibitors to the JAK1/STAT1 signaling pathway might control the inflammatory response in acute pancreatitis.

Objective:To prepare poly-L-lactic acid(PLLA)electrospun nanofibers carrying icariin(ICA)(ICA /PLLA)and to evaluate the effects of the ICA /PLLA on MC3T3-E1 cells.Methods:ICA solution was dispersed into PLLA solution,and electrospun fibers were fabricated by W/O emulsion method.The morphology of ICA /PLLA was observed by SEM.The in vitro release kinetics of ICA /PLLA was examined.The attachment of MC3T3-E1 cells on ICA /PLLA was examined by propidiumiodide(PI)labling and ob-served under fluorescent microscope.The proliferation of the cells was measured by MTT assay.The differentiation of the cells was ob-served by alkaline phosphatase (ALP)assay.Results:In vitro,ICA was effectively released from ICA /PLLA for 22 days,cells were attached well on the surface in all groups,ICA did not affect the proliferation of MC3T3-E1 cells(P >0.05),but increased the ALP activity(P <0.05)of the cells.Conclusion:ICA /PLLA can effectively control the release of ICA and promote the differentiation of MC3T3-E1 cells.

AIM:To investigate the effects of peroxiredoxin 4 ( Prdx4) protein expression levels on the migra-tion and invasion of human cervical cancer HeLa cells.METHODS:The plasmid pcDNA3.0-HA-Prdx4 was transfected into HeLa cells.The HeLa cells were infected with LV-Prdx4 RNAi vector to establish stable Prdx4 shRNA HeLa cells. The change in the expression of Prdx4 protein was validated by Western blotting.The wound-healing assay, and Transwell migration and invasion assays were performed to detect the migration and invasion of HeLa cells, respectively.RESULTS:The expression of Prdx4 protein was up-regulated in the HeLa cells after transfection with pcDNA3.0-HA-Prdx4 plasmid ( P<0.05), whereas it was down-regulated in the Prdx4 shRNA HeLa cells (P<0.05).The abilities of migration and inva-sion were significantly increased in Prdx4-overexpressing HeLa cells compared with non-transfected and mock plasmid trans-fected control groups ( P<0.01) .When Prdx4 was knocked down by shRNA, the migration and invasion of the HeLa cells were remarkably repressed compared with blank control group and negative control group ( P<0.01 ) .CONCLUSION:The up-regulation of Prdx4 expression facilitates the migration and invasion of HeLa cells, and the down-regulation of Prdx4 expression inhibits the migration and invasion of HeLa cells, indicating that Prdx4 may be a potential molecular target for cervical cancer therapy.

Objective To describe the clinical and pathological features and survival of juvenile patients with pancreatic carcinoma ( age ≤ 40 years old ) and to explore whether pancreatic carcinoma in young patients was a particular subtype. Methods As a case control study, the clinical data and follow-up data of sporadic 29 cases diagnosed as juvenile pancreatic carcinoma in Ruijin hospital from January, 2000 to December, 2007 were analyzed and compared with randomly selected 89 cases of senile eases (age≥ 61 years old) with pancreatic carcinoma. Results The percentage of juvenile pancreatic carcinoma was 3.6% (29/811 ) and the male/female ratio was 2.5: 1. The incidence rate of abdominal pain was significantly higher in the juvenile patients than in the senile patients (72.4% vs 48.3% , P < 0.05 ) ;the incidence of malnutrition was significantly lower in juvenile patients than that in senile patients ( 13.8% vs 38.0%, P <0.05 ) ;and the rate of patients with advanced stage disease ( Ⅲ～Ⅳ ) was significantly higher in juvenile patients than in senile patients (69.0% vs 55. 1%, P < 0.05). The percentage of radical operation in juvenile patients was not statistically different from that in senile patients ( 34.5% vs 30.34%, P > 0.05 ), and analysis using the Kaplan-Meier method and log-rank test revealed no significant difference in overall survival between the two groups ( median survival time : 7.0 vs 8.0 months, P > 0.05 ). Conclusions The age onset of the pancreatic carcinoma tended to be younger. The predominant clinical manifestations of juvenile pancreatic carcinoma were abdominal pain or back pain. Juvenile pancreatic carcinoma may be a particular subtype of pancreatic cancer.