Stat3 is a member of the STAT (signal transducer and activator of transcription) protein family. It can be activated by many cytokines, growth factors and carcinogens. Activation of Stat3 in the cytoplasm leads to its dimerization, translocation into the nucleus, DNA binding and gene transcription. Constitutively activated Stat3 is associated with cellular transformation, invasion, metastasis, angiogenesis, chemoresistance and radioresistance, and therefore suppress apoptosis of cancer.

Pancreatic cancer is a frequent malignant tumor in digestive tract with extremely poor prognosis,characterized by difficult early diagnosis,high malignancy,poor resective,limited response to chemotherapy and radiotherapy and an intense fibrotic reaction known as tumor desmoplasia.Pancreatic stellate cells play an important role in this reaction and can stimulate pancreatic cancer cells proliferation,invasion and metastasis through the interaction with pancreatic cancer cells.This review describes the role of pancreatic stellate cells in the process of pancreatic cancer progression.

Loss of epithelial characteristics and acquisition of a mesenchymal phenotype are the main features of epithelial-mesenchymal transition (EMT). EMT plays an important role in tumor invasion and metastasis through increasing cell migration, invasion and anti-apoptotic capacity. Several mechanisms involved in EMT regulate invasion and metastasis of pancreatic cancer,including cadherin switch, growth factors, transcription factors, microRNA and signaling pathways.

Objective To investigate the indications and results of combined liver-kidney transplantation.Methods From Jan. 2001 to Dec. 2003, 15 patients were subjected to combined liver-kidney transplantation in our department. The underlying diseases included hepatitis B viral cirrhosis complicated by HRS ( n= 8), hepatitis B viral cirrhosis complicated by uremia ( n =2), hepatitis B viral cirrhosis complicated by diabetic nephropathy ( n =1), polycystic liver and kidney disease ( n =2), Caroli's disease and polycystic kidney ( n =1), alcoholic liver cirrhosis complicated by uremia ( n =1). The surgical procedure, perioperative complications, acute and chronic rejection, the recurrence of hepatic viral B hepatitis, and the result of follow-up were analyzed.Results The graft function in 15 cases of combined liver-kidney transplantation was restored well after operation. The 6-month and one-year survival rate was 100%. One patient was supported by respiration machine for 48 days. The complications occurred in 3 patients after operation, including one case of gastroenternal bleeding repeatedly and one case of postoperative wound bleeding subject to non-surgical treatment, and one case of stenosis of biliary anastomosis subject to ERCP. Only one patient experienced a rejection episode of the liver. No acute rejection of the kidney graft occurred. One patient was died from liver graft function failure by recurrence of hepatitis B after 30 months.Conclusions Combined liver-kidney transplantation is only radical treatment method for patients with end-stage liver disease with chronic renal dysfunction or chronic renal failure. In the patients with hepatitis B,lamividine and hepatitis B immunoglobin can prevent the recurrence of hepatitis B.

Objective To investigate effects of CO_2 pneumoperitoneum on cytokines and peritoneal macrophages in a rat model with implanted liver tumor.Methods A total of 32 Wistar rats with implanted liver tumor were randomly divided into 4 groups((n=8)): Control Group(anesthesia only),Laparotomy Group,Gasless Group(gasless laparoscopy),and Pneumoperitoneum Group(laparoscopy under CO_2 pneumoperitoneum).Serum samples were collected at the 2nd and 24th hours after the procedure respectively for the detection of levels of interleukin-1?(IL-1?) and interleukin-6(IL-6).Samples of peritoneal macrophages were collected and incubated for the detection of levels of tumor necrosis factor-?(TNF-?),a product of macrophages.Results At the 2nd and 24th hours after surgery,levels of serum IL-6 in the Laparotomy Group(57.92?2.06 pg/ml and 35.49?1.15 pg/ml) were significantly greater than those in the Pneumoperitoneum Group(14.64?0.34 pg/ml and 15.39?0.86 pg/ml),the Gasless Group(24.75?1.53 pg/ml and 17.10?0.97 pg/ml),and the Control Group(17.75?1.60 pg/ml and 14.55?0.25 pg/ml)(P

Objectives: To evaluate the feasibility, safety and validity of the early enteral nutrition in severe acute pancreatitis(SAP). Methods: 15 patients of SAP during April 2002 and June 2003 had received early enteral nutrition through naso jejunal tube. The nutrition and immune index and the rates of complications were analyzed. Results: 2～3 days after nutrition tube placed to stomach, the tube heads in 11 cases reached the jejunum automatically, while 3 cases needed the help of X ray and 1 case needed the help of gastroscopy. All of 15 cases tolerated the enteral nutrition well, and there was no relapse of SAP. The nutrition and immune measurement were improved after 2 weeks' enteral nutrition, without infection of pancreatic necrosis. Conclusions: It is safe, efficient and feasible of the early enteral nutrition in severe acute pancreatitis(SAP) through naso jejunal tube. Early enteral nutrition can improve the nutrition, immune function and prognosis.

Objective To screen the genes related with signal transducers and activators of transcription 3 (STAT3) regulating pancreatic cancer invasion and metastasis by gene chips.Methods Human pancreatic cancer cell line SW1990 stably expressing low level of Stat3 was established by lentivirus transfection,while cells transfected with mock plasmid and cells without transfection served as control groups.The differences of invasion and metastasis related genes expression among the three groups were screened by gene chips.STAT3 mRNA and protein expression was measured by real-time PCR and Western blot.Three differentially expressed genes (MMP-7,IL-1β and IgTα7) were verified.ResultsThe expression level of STAT3 mRNA was 0.391 ± 0.037 after pancreatic cancer SW1990 cell trarsfected with STAT3 targeted lentivirus,which was significantly lower than those in mock plasmid group (1.002 ± 0.015) and nontransfected group ( 1.206 ± 0.042,P ＜ 0.05 ) ; the expression level of STAT3 protein was 182.38 ± 65.32,which was significantly lower than those in mock plasmid group (223.40 ±58.40) and non-transfected group (212.33 ±53.69).Eight invasion and metastasis related genes of SW1990 lowly expressing Stat3 were upregulated,while 3 genes were down-regulated.By verification,the mRNA level of MMP-7 and IL-1β were lower than in control group transfected with mook plassmid(0.287 ± 0.115 vs 1.010 ± 0.124,t =19.45,P =0.000;0.490 ± 0.10 vs 1.002 ± 0.002,t =13.83,P =0.000),but the mRNA level of IgTα7 was not decreased (1.173 ±0.280 vs 0.998 ±0.003,t =4.236,P =0.094).Meanwhile,the protein level of MMP-7 was significantly down-regulated when Stat3 was knocked down.ConclusionsStat3 causes changes of expressions of many invasion and metastasis-related genes of SW1990,and MMP-7 may be the main target gene regulated by Stat3.

Background and purpose:Micro-environmental hypoxia is a common phenomenon in most human solid tumors,and this investigation is done to observe the expression of HIF-1? and chemo-resistance-associated genes in human colon cancer cell line under hypoxic micro-environment in vitro,and study the influence of micro-environmental hypoxia on chemo-resistance and the possible mechanisms in human colon cancer.Methods:Human colon cancer cell line SW620 was cultured under hypoxia for 12,24,48 hr,with normoxia as control.Then the expression of HIF-1? and chemo-resistance-associated genes mdr1/P-Gp、LRP were investigated by RT-PCR and western-blot.Results:With prolongation of the hypoxic time,the mRNA expressions of HIF-1? and LRP remained at the same level,but the mRNA expressions of mdr1 showed a time-dependent increase(P

Objective To investigate the effects and mechanism of IL-6 on the epithelial to mesenchymal transition of human pancreatic cancer cells.Methods IL-6 was added into the culture media of human pancreatic cancer cells Capan-2,SW1990,and STAT3-siRNA-SW1990.Cell growth was measured by MTT assays.STAT3,p-STAT3,Snail,Twist,and E-cadherin mRNA and protein expression were examined using real-time fluorescence quantitative polymerase chain reaction (RT-PCR)and Western blot,respectively.The invasion abilities of SW1990 and Capan-2 cells were determined by a cell invasion assay in vitro.Results Our results showed that 100 μg/L of IL-6 significantly promoted the growth and invasion abilities of Capan-2 and SW1990 cells (P＜0.05).The use of IL-6 not only markedly increased the protein expression of P-STAT3 and Snail,but also greatly decreased the mRNA and protein expression of E-cadherin.The use of IL-6 can not change the mRNA and protein expression of Snail and E-cadherin.Conclusion Activation of the STAT3 signal transducer pathway with IL-6 can promote the epithelial to mesenchymal transition of pancreatic cancer cells in vitro through up-regulation of Snail and down-regulation of E-cadherin expression.Therefore the STAT3 signal transducer may provide a novel therapeutic target for the treatment of pancreatic cancer.

Objectives:To investigate if enteral nutrition can reduce pancreatic infection of severe acute pancreatitis(SAP) in rats. Methods:32 SD rats were divided into 4 groups.SAP was induced in rats of A group and C group, and rats fo B group and D group underwent laparotomy without induction of SAP. A group and B group received total parenteral nutrition(TPN),and C group and D group received enteral nutrition(EN) beginning from the 3rd postoperative day.The samples of blood,MLN,pancreas,liver,kidney and lung were detected for bacteria at the end of the study.Blood sugar,albumin and amylase were also detected. Results:None of the rats died.The positive rates of bacteria cultures in MLN and pancreas were significantly lower in C group(37.5%) than those in A group(87.5%)( P =0.033).The species of cultured bacteria were mainly those seen in the gut. Conclusions:Enteral nutrition can reduce the pancreatic infection of severe acute pancreatitis in rats.