Reoperation on biliary tract diseases is a kind of complex and difficult surgery,with the high risk and recurrence rate.Benign biliary tract diseases included residual and recurrence of bile duct stone,bile duct injury and benign biliary stricture,which are still the most common causes for reoperation.The common causes,application of the precision surgery and new mode of multidisciplinary team (MDT) for the reoperation on benign biliary diseases were explored in this paper.With the techniques developments of minimal invasive and precision surgery,the new mode of MDT for the reoperation on benign biliary diseases will provide the best individual diagnosis and treatment to the patients.

Intraductal papillary neoplasm of the bile duct (IPNB) is a variant of bile duct tumors characterized by papillary growth within the dilated bile duct lumen and secretion with a large amount of mucins.IPNB is an intraductal papillary cancer of the bile duct or a preinvasive lesion classified by the 2010 World Health Organization (WHO) classification.Although the specific etiology and pathogenesis are unclear,IPNB is known to two major risk factors:hepatoliathiasis and clonorchiasis.The clinical manifestations of IPNB include intermittent abdominal pain,acute cholangitis and obstructive jaundice.Results of laboratory test show abnormal liver function resulting from obstruction of bile duct,but it's not specific.The most common imaging findings for IPNB are bile duct dilatation and intraductal masses.Computed tomography,magnetic resonance image and cholangiography are usually performed to access tumor location and extension.According to morphology of the tumor epithelial cells,IPNB are classified into the pancreticbiliary,intestinal,gastric and oncocytic types.The surgical resection is a major treatment of IPNB.In principle,IPNB should be resected in a manner similar to that employed for other types of intrahepatic cholangiocarcinomas and extrabepatic bile duct carcinomas.The type of surgical procedure for IPNB depends upon tumor location and extension.Although several investigations have been conducted for illuminating molecular genetic changes during the development and progression of IPNB,the specific mechanism is still not clear,and further study is needed.

The function of hepatic stellate cell (HSC)in liver fibrosis has been well recognized.In recent years,the role of HSC in the liver tumor microenvironment have been paid increasing attention.Platelet derived growth factor (PDGF) is the most important mitogen of hepatic stellate cell,and plays an important role in the activation of hepatic stellate cell.Hepatic stellate cell is not only the target cells of PDGF,but also PDGF-secreting cells.Thus a bi-directional cycle mode of PDGF activating hepatic stellate cell has been established.The signaling pathways of HSC activation include MAPK,PI-3K,Ca2+ and JAK pathways.To explore PDGF activating hepatic stellate cell in liver tumor microenvironment and to find the new methods of targeting PDGF and hepatic stellate cell,may help us find a new direction for the treatment of hepatocellular carcinoma.

Objective To summarize the causes and the prevention of bile duct injuries during laparoscopic cholecystectomy (LC). Methods Clinical records of 1 000 cases of LC were analyzed retrospectively. Results Conversions to open cholecystectomy were required in 15 cases(1.5%). Complications took place in 6 cases(0.6%), involving 3 cases of common bile duct injury, 1 case of stomach puncture, 1 case of port hemorrhage, and 1 case of bile leakage. No long-term complications were seen. Conclusions The most frequent cause leading to bile duct injuries is pulling the bile duct to be angulated.

Objective To construct a adenovirus vector containing human NRP-1 gene and 3Flag gene to interaction between tumor and interstitial cell.Methods Plasmid containing NRP-1 gene was digested by AgeⅠand NheⅠ restriction endonuclease.Then the DNA was ligated into linearized pDC315-3Flag vector.After having been constructed,the pDC3 1 5-NRP-1-3 Flag plasmid was co-transfected with framework plasmid pBHGlox△E1 , 3Cre into HEK 293 cells to obtain the homologous recombinant adenovirus,which was then amplified and purified its titer tested.Expression of NRP-1 protein was detected using Western blot.Results Polymerase chain reaction and sequencing analysis confirmed that the shuttle plasmid pDC3 1 5-NRP-1-3 Flag and design were consistent. Cytopathic effect was observed by inverted phase contrast after transfecting HEK2 9 3 cells with shuttle plasmid pDC315-NRP-1-3Flag.95-130 ku was detected by Western lot after transfecting HEK293 cells with shuttle plasmid pDC315-NRP-1-3Flag and recombinant adenovirus,the size being consistent with the NRP-1-3Flag fusion protein (104 ku),with a titer of 2.00E+11PFU/mL.Conclusion The recombinant adenovirus vector for human NRP-1 gene was successfully constructed expressed in HEK 2 9 3 cells.

Gallbladder cancer (GBC) is the most common malignancy of the biliary tract.Most patients are diagnosed at the advanced stage,missing the optimal chance for curative surgery,thus leading to the fact that GBC is usually associated with poor prognosis.It is very crucial to strengthen the basic research on GBC,which may further improve the diagnosis and treatment.The research updates on the related genes in the initiation and progression,molecular mechanism of lymphatic metastasis,and tumor microenvironment of GBC in recent years were reviewed in this paper.

Objective To analyse the clinical data of 77 patients with unsuspected gallbladder carcinoma,and to determine the impact of TNM stage and the timing of the second operation on postoperative survival.Methods A retrospectively analysis of 77 patients operated between January 2008 and January 2013 in our hospital for unsuspected gallbladder carcinoma was carried out.The case inclusion criteria was in strict accordance with the medical records which described without preoperative diagnosis,or cholecystectomy for benign gallbladder diseases,or intraoperative or postoperative pathological diagnosis of gallbladder cancer.References to previous published medical literature and the intervals from initial cholecystectomy to further treatment were analyzed to see whether the prognosis and survival varied depending on the TNM staging and whether secondary radical surgery was carried out.Results For the 77 patients in this study,they all had high risk factors associated with gallbladder cancer which included:women,aged ＞ 50 and gallbladder stones.The initial surgery included laparoscopic cholecystectomy (n =53),and open cholecystectomy (n =24).In 26 patients,intraoperative frozen section confirmed the diagnosis and they were treated according to the TNM staging (radical operation n =7,palliative surgery n =17).The postoperative 1-,2-,3-year cumulative survival rates were 65％,45％ and 20％,respectively.For the 54 patients who underwent radical or extended radical cholecystectomy within a short interval from the first operation,the 1-,2-,3-year cumulative survival rates were 82.5％,62.5％ and 45.7％,respectively.Conclusions For resectable gallbladder cancer,the prognosis of unsuspected gallbladder carcinoma was related not only to the clinical staging,but also to the timing of the radical operation.The shorter time interval,the longer the survival,and the better the prognosis.There was no significant difference in prognosis for the group of patients with time intervals between the two operations of less than two weeks when compared with the group with immediate radical surgery.For advanced stages of gallbladder cancer,palliative surgery should be given according to the patient's general condition,aiming to improve quality of life.

Objective To investigate the relativity between c.553G/T polymorphism in exon 4 of Apolipoprotein A5 gene and hypertriglyceridemia (HTG) in Zunyi Han Nationality. Methods c.553G/T polymorphism of 103 HTG patients and 165 healthy individuals were tested by polymerase chain reaction and restriction fragment length (PCR-RFLP) assay. The distributions of genotypes and allele frequencies in HTG patients and healthy group were analyzed between Zunyi population and others. Results The genotype frequency of the Apo A5 gene c.553G/T showed statistical difference between patients group and normal groups (P < 0.05). The distribution of ApoA5 c.553T gene in HTG was higher than the normal group significantly (P < 0.05), and it had effect on triglyceridemia level independently (OR = 15.768, 95%CI: 5.916 ~ 42.025, P < 0.001). In the normal Han nationality groups, gene frequency of Zunyi was lower than that in Taiwan, Jiangsu and Hubei (P < 0.05), but similar to that in Hunan and Xinjiang (P > 0.05). In HTG groups, gene frequency of Zunyi was similar to that in Jiangsu (P>0.05), but higher than that in Xinjiang (P<0.05) and lower than that in Taiwan (P > 0.05). Conclusion There is relativity between Apo A5 gene c.553G/T polymorphisms and HTG in Zunyi Han nationality and the differences vary across different areas. It could be an independent risk factor for HTG.

Objective: To examine whether the progression of early diabetic renal disease with normotension can be slowed by ACE inhibitors(ACEI). Methods: MEDLINE and Chinese Biological Medicine Disk were searched for randomized controlled trials about the effect of ACE inhibitors on patients with normotensive early diabetic renal disease from January, 1990 to April, 1999. According to included criteria, 10 studies were chosen at last.Data were combined by RevMan 3.1 software. Results: The pooled effect sizes of urinary microalbuminuria excretion rate, systolic blood pressure, diastolic blood pressure and mean arterial blood pressure were -77.502 mg/24 h[-100.748,-54.256], -5.002 mmHg [-9.630, -0.685 ], -2.949 mmHg[-4.005, -1.892], -4.284 mmHg[-5.444, -3.123] respectively. Regarded progression to clinical albuminuria as end point,the pooled OR(odds ratio) was 0.27[0.18,0.40]. The sub category analysis showed no differences between type 1 and type 2 diabetes.There were no significant correlations between the pooled effect of urinary microalbuminuria excretion rate and systolic blood pressure, diastolic blood pressure or mean arterial blood pressure. Conclusion: ACE inhibitors can decline urinary microalbuminuria excretion rate in patients with normotensive early diabetic renal disease and delay the progression of early diabetic renal disease to clinical albuminuria, and the effects may not depend on its blood pressure reduction effect. [

Objective To investigate the effects and mechanisms of sorafenib on hepatic stellate cell viability and activation in the microenvironment of liver tumor.Methods The effects of LX2 cells on HepG2 cell proliferation were observed by coculture of LX2 and HepG2 cells.MTT assay was used to observe the effects of sorafenib on LX2 proliferation,and expression of α-smooth muscle actin (α-SMA) was measured immunocytochemically in LX2 cells treated with different concentrations of sorafenib.Changes in PDGF-BB and TGF-β1 concentrations were detected in LX2 supernatant using ELISA.Expression of ERK1,ERK2,and AKT signaling pathways were measured using Western blot.Furthermore,LX2 cells were cocultured with HepG2 cells for 24 hours to observe their effects on the invasive ability of HepG2 cells.Result After coculture of LX2 and HepG2 cells,HepG2 cells increased in the experimental group more than those of in the control group.After treatment with various concentrations of sorafenib for 12,24,36 or 48 hours,the viability of treated LX2 cells was lower than the controls in a concentration-and time-dependent manner.As sorafenib concentration and time of exposure increased,α-SMA expression became weaker in treated cells.PDGF-BB and TGF-β1 concentrations decreased with higher sorafenib concentrations and with longer exposure under the same concentration.ERK1,ERK2 and Akt expression was identical between treated and control groups,but their phosphorylated expression decreased with increased concentrations of sorafenib.The invasive ability of HepG2 cells induced by LX2 gradually decreased as sorafenib concentrations increased.Conclusions Sorafenib suppressed α-SMA expression,inhibited PDGF-dependent signaling pathways in HSCs,downregulated PDGF-BB and TGF β1 expression in the supernatant of HSCs,and restrained the viability and activation of HSCs.Sorafenib treatment therefore resulted in suppressed proliferation and invasion of HepG2 cells.