Objective To evaluate curative effect and related prognosis factors of synchronous colorectal cancer with liver metastasis.Methods The clinicopathological and follow-up data of 47 patients undergoing surgical treatment with synchronous colorectal cancer with liver metastasis at Shanghai Jiaotong University Affiliated Sixth People's Hospital and Tongji University Affiliated Yangpu Hospital from Jun 2013 to Jan 2018 were retrospectively analyzed.Results All 47 patients were followed up and themedian followup time was 38 months (2-65 months),after simultaneous colorectal and hepatic neoplasm radical surgery,added in 41 patients by postoperative chemotherapy.There was no perioperative mortality and the postoperative complication rate was 34％.The 1-,3-,and 5-year overall-survival rates were 87％,53％,and 15％,respectively.The disease-free survival rates were 81％,43％,and 9％,respectively.Multivariate results showed tumor differentiation,serum CEA level and adjuvant chemotherapy are independent prognostic factors for patients with synchronous colorectal cancer liver metastasis (P ＜ 0.05).Conclusions Colorectal cancer with synchronous liver metastasis treated by simultaneous resection of colorectal cancer and liver metastases are the widerly adopted treatments.Long-term survival is closely related to the degree of primary neoplasm differentiation,serum CEA level at diagnosis,and postoperative adjuvant chemotherapy.

Objective To compare the clinical results of laparoscopic spleen-preserving distal pancreatectomy (LSPDP) and open spleen-preserving distal pancreatectomy (OSPDP).Methods From Jan 2014 to Aug 2017,the clinical results of 30 patients undergoing LSPDP were compared with those of 20 OSPDP patients.The postoperative pancreatic fistula rate was the main observation index.Results There was significant difference in operation time [(140.33 ±55.93) min vs.(182.71 ±43.51)min],blood loss [(175.61 ± 180.78) ml vs.(253.51 ± 176.06) ml],postoperative hospital stay [(6.16 ± 7.22) d vs.(8.85 ± 9.36) d],postoperative exhaust [(2.17 ± 1.43) d vs.(3.10 ± 1.89) d],and postoperative feeding time [(2.26 ± 1.78)d vs.(3.42 ±2.01)d] between LSPDP and OSPDP.LSPDP group was better than OSPDP group (all P ＜ 0.05).The rate of postoperative pancreatic fistula (66.7％ vs.70.0％) and overall complications (80％ vs.90.0％) were not statistically different between the two groups.Pancreatic leakage occurred in 20 cases,lung infection in 1 case,peritoneal infection in 1 case and chylous leakage in one case in LSPDP group,while pancreatic leakage in 14 cases,lung infection in 2 cases,and peritoneal infection in 2 cases in OSPDP group,all were cured by conservative therapy.Conclusions LSPDP is a safe,effective,less traumatic and more economic surgical approach for benign cystic tumors located at the body or tail of the pancreas.

Objective To explore the clinical efficacy and safety of complex splenectomy.Methods The retrospective cohort study was adopted.The clinical data of 235 patients including 135 from Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine,67 from Shanghai Jiaotong University Affiliated First People's Hospital,26 from Shanghai Jiaotong University Affiliated Sixth People's Hospital,7 from 85 Hospital of PLA who underwent complex splenectomy from January 2005 to December 2015 were collected.All the patients received total splenectomy after splenic artery ligation.The observation indexes included:(1) surgical situations,(2) major complications including intraperitoneal hemorrhage,pulmonary complication,left subphrenic abscess and peritoneal effusion,(3) follow-up situations:portal vein (PV) complications (splenic venous thrombophlebitis,thrombosis of splenic vein and main portal vein thrombosis),survival of patients.The follow-up using outpatient examination and telephone interview was performed up to March 2016,and patients received regularly ultrasound reexamination,computed tomography (CT) rescan,routine blood retest and coagulation function.Measurement data with normal distribution were presented as-x ± s,and count data were analyzed using the chisquare test.Results (1) Surgical situations:of 235 patients,200 patients underwent secondary spleen pedicle severance and 35 patients underwent non-secondary spleen pedicle severance.Volume of intraoperative blood loss and duration of splenic resection were (268 ± 103) mL and (82 ± 29) minutes.(2) Major complications:of 31 patients with postoperative complications,intraperitoneal hemorrhage was detected in 12 patients,pulmonary complication in 17 patients,left subphrenic abscess in 3 patients and massive peritoneal effusion in 21 patients.Some patients were combined with multiple symptoms.The patients with above complications were cured after reoperations and non-operative treatments.(3) Follow-up situations:PV complications:splenic venous thrombophlebitis was detected in 16 patients,thrombosis of splenic vein in 17 patients,thrombosis of splenic vein combined with main portal vein thrombosis in 7 patients,and they were improved after the treatments of antiinflammation,anti-coagulation and thrombolysis.The thrombi rate after splenectomy was 32.4％ (12/37) in patients with schistosoma-related cirrhosis and 8.1％ (12/149) in patients with HBV-related cirrhosis,with a statistically significant difference (x2 =10.9,P ＜ 0.05).Survival of patients:of 235 patients,228 were followed up for (7.9 ± 4.2) years,with good survival.Conclusion Complex splenectomy is safe and effective,and the key procedure determining the safety of complex splenectomy includes careful preoperative evaluation,delicate surgical technique,proper splenic pedicle severance and peritoneal wounds.

Objective To evaluate the outcome of surgical approaches in patients of gastric cancer with portal hypertension.Methods The clinical data of 80 patients with portal hypertension undergoing curative surgery for gastric cancer or simultaneous surgery for portal hypertension were retrospectively analyzed.Results The radical gastrectomy alone had no tremendous impact on postoperative liver function.But simultaneous surgery for portal hypertension affected patients' liver function dramatically (P =0.018).For those who underwent surgery for portal hypertension simultaneously,the incidence of complications in Child B patients was much higher than that in Child A patients (P =0.018).However,the incidence of complications did not differ between Child A and B patients who underwent radical gastrectomy alone.In addition,patients undergoing simultaneous surgery for portal hypertension had more severe complications than those who underwent radical gastrectomy only (P =0.042).Age ＞ 50 (P =0.012),tumor stage (P =0.015),and simultaneous surgery for portal hypertension (P =0.007) were the independent risk factors for postoperative liver dysfunction.The survival time of patients undergoing simultaneous surgery for portal hypertension was significantly shorter than that of patients undergoing radical gastrectomy only (in Child A patients,P =0.009,in Child B patients,P =0.000).Conclusions Individualized surgical approaches for the treatment of gastric cancer with portal hypertension should be decided by preoperative liver function.Simultaneous management of portal hypertension was not recommended.

ObjectiveTo investigate the effect of anti hepatitis B virus (HBV) therapy on patients with HBV associated hepatocellular carcinoma (HCC) after resection.MethodsClinical data of 87 patients with HBV associated HCC after resection treated in Shanghai Jiao Tong University Afifliated Sixth People's Hospital, Afifliated First People's Hospital and Ruijin Hospital, Shanghai Jiaotong University from January 2008 to January 2013 were retrospectively analyzed. There were 40 males and 47 females, 32 cases were<55 years old and 55 cases were≥55 years old. The informed consents of all patients were obtained and the local ethical committee approval was received. According to the tumor diameter, the patients were divided into the tumor diameter≤3 cm group (n=36) and>3 cm group (n=51). According to whether the patients had received anti HBV therapy, each group was divided into anti HBV subgroup and non-anti HBV subgroup. Patients with anti HBV therapy began to receive treatment of entecavir 14 d after operation. The changes of alanine aminotransferase (ALT) and inhibition rate of hepatitis B virus-deoxyribonucleic acid (HBV-DNA) 6 months after operation were observed in each group. The ALT and inhibition rate of HBV-DNA were compared usingt test, survival analysis was conducted using Kaplan-Meier method and Log-rank test, and influencing factors analysis was conducted using Cox proportional hazard regression model.ResultsIn the tumor diameter≤3 cm group, the inhibition rate of HBV-DNA in the anti HBV subgroup was (47±6) %, which was higher than (9±3) % in the non-anti HBV subgroup (t=3.142,P<0.05). And in the anti HBV subgroup, the ALT level decreased from (46±10) U/L before treatment to (34±8) U/L after treatment, where signiifcant difference was observed (t=-2.339, P<0.05). In the tumor diameter≤3 cm group, the median of disease-free survival (DFS) time of the patients in the anti HBV subgroup was 48 months, and was 35 months in the non-anti HBV subgroup, and signiifcant difference was observed between two groups (χ2=13.09,P<0.05). Anti HBV therapy after operation and serum alpha-fetoprotein (AFP) level>400 μg/L were the independent factors for the DFS of patients with tumor diameter≤3 cm (OR=0.220, 2.657;P<0.05). ConclusionsPostoperative anti HBV therapy is an independent inlfuencing factor for the DFS of patients with small HCC. Anti HBV therapy can raise the survival rate by improving the residual liver function of patients.

Objective To study the regulation mechanism of bone mesenchymal stem cell (MSC)combined co-translation of islets in differentiation of Follicular Helper T cell (Tfh),and its roll on immunotolerence induction in non-obese diabetic (NOD) mice transplantation model.Methods The NOD mice were divided into 4 groups:Group A with islet transplantation alone;Group B with MSC co-transplantation with islets (MSC:0.5 × 106);Group C with MSC co-transplantation with islets (MSC:2 × 106);Group D with MSC co-transplantation with islets (MSC:3 × 106).ELISA was used to test the expression level of diabetes autoantibody GAD65Ab and IAA.Tfh cell count was detected by FACS.Results The survival time of transplantation groups was much longer in MSCs co-transplantation group than islet-alone group;the level of GAD65Ab,IAA and Tfh cell count were much lower in MSCs co-transplantation group than islet-alone group.Conclusion MSC may protect the islet transplants by regulating the Tfh cell differentiation.

ObjectiveTo explore the correlation between hepatitis C virus infection and the risk of cholangiocarcinoma (CCA) through Meta-analysis.MethodsLiteratures that were formally published prior to August, 2013 were searched on National Knowledge Infrastructure (CNKI), PubMed, EMBASE and MEDLINE databases using English, Chinese terms mainly including hepatitis C virus, HCV, cholangiocarcinoma, bile duct cancer, intrahepatic, extrahepatic. Moreover, associated literatures were also searched by manual searching. Data from the literatures were merged and the correlation between hepatitis C virus and risk of CCA, intrahepatic cholangiocarcinoma (ICC), extrahepatic cholangiocarcinoma (ECC) was analyzed respectively. Heterogeneity test was conducted usingQ test.RR value of each study and pooled data were calculated and forest graph was drawn to display the results and features of each study. Funnel plot and Egger test were used to identify the publication bias.ResultsA total of 16 case-control studies and 2 cohort studies (total 873 501 patients) were included in the ifnal analysis. Meta-analysis showed that hepatitis C virus infection was not associated with the occurrence of CCA (RR=2.36,P>0.05) and hepatitis C virus infection was the risk factor for the occurrence of ICC and ECC (RR=4.10, 1.48;P<0.05).Funnel plot and Egger test showed no evidence for publication bias.ConclusionHepatitis C virus infection is associated with the risks of ICC and ECC, especially ICC.

Objective To investigate the clinical significance of silent mating-type information regulation 2 homologue 1 (SIRT1) in hepatocellular carcinoma (HCC).Method We analyzed p53 mutation by gene sequencing and activation of SIRT1 and AMP-actived protein kinase (AMPK) using western-blot in 252 patients with hepatitis B virus-positive HCC.Results A higher proportion of tissues with mutant p53 were demonstrated to harbor activated SIRT1 (64.8％ vs 31.8％ ; P ＜ 0.01).Activated SIRT1 predicted a longer relapse-free survival.On multivariate analysis,activated SIRT1 remained significant (OR:0.339,CI:0.160-0.720,P =0.005).Analysis of 252 paired specimens revealed a significant correlation between activated SIRT1 and activated AMPK in HCC tissues harboring mutant p53 (P =0.007).Conclusion SIRT1 exerted anti-carcinogenic effects through the AMPK pathway in HCC in the context of mutant p53.

Objective To understand how SIRT1 differently regulates oncogenesis in hepatocellular carcinoma (HCC) with wild type and mutant type p53.Methods HCC cell line PLC5 cells (249 site mutated p53),and HepG2 cells (wild type p53) were infected with lentivirus containing shSIRT1.Western blotting was used for signaling pathway detection.Cell growth and proliferation assay,colony formation assay and tumor xenograft assay were performed to test the tumor growth ability of HepG2 cells,HepG2-shSIRT1 cells,PLC5 cells and PLC5-shSIRT1 cells respectively.Results SIRT1 silencing resulted in significant inhibition of cell proliferation in HepG2 cells but stimulating cell proliferation in PLC5 cells (t =3.595,P ＜0.01).Acetylation of p53 was found in HepG2 (HepG2-shSIRT1) and p21 was up-regulated,however,in PLC5 (PLC5-shSIRT1) cells,acetylation of p53 was found but p21 was not induced despite of p53 activation.Silence of SIRT1 resulted in no change of AMPK function in HepG2 cells but a lower activity of AMPK in PLC5 cells (t =4.268,P ＜ 0.01).Conclusions In HCC cell lines the function following SIRT1 activation is largely determined by p53 mutant status.

Humans ; Lymph Node Excision ; standards ; Pancreatic Ducts ; pathology ; surgery