Objective To investigate the association of the SNP in miRNA146A with genetic prediposion and earlier recurrence after resection for hepatocellular carcinoma (HCC).Methods In the casecontrol study including 173 HCC cases,DNA were exacted from cancer tissue embedded with paraffin and were amplificated by PCR,SNP was explored in gene sequence of miRNA146a (385 base pair including extron).The outcome were analyzed with genetic prediposion and clinical features.Result Only hsa-mir-146a rs2910164 was found.The genetype frequence of C/C 、G/G and C/G at rs2910164 gene locus were separately 61 (35.3％),21 (15％) and 86(49.7％) in cases.Compared to G/G genetype,C/C and C/G genetype were danger factor to onset risk of HCC (OR =3.086,95％ CI:1.289-7.390) ; C/G was danger factor to earlier recurrence after resection(OR =8.179,95％ CI:2.248-29.759).Conclusion rs2910164 may be associated with genetic prediposion and earlier recurrence after resection of HCC in Jiangxi hans

Hepatocellular carcinoma(HCC)has high incidence rate,recurrence rate after surgecal treat-ment,as well as fatality rate in China .HCC is not sensitive to radiotherapy or chemotherapy and no effective treat-ment is available for HCC patients at advanced stage .Sorafenib is the first effective molecularly targeted drug for the treatment of HCC,which represents a milestone in the treatment of HCC .However,it also shows drug resist-ance during clinical application .Therefore,it is important to investigate the mechanism of drug resistance and its molecular markers for HCC .In this review ,we summarize the current status of the studies in these fields .

Objective To explore the deafness-causing underlying mechanisms of CX26 gene recessive mutations through functional analyzing nine missense mutations (p.S19T,p.R32H,p.E47K,p.V84L,p.V95M,p.R143W,p.R165W,p.S199F,p.L214P) in exogenous expression system Hela cells.Methods The nine recessive missense mutations of CX26,which are in the different domains of CX26 protein,and the wild type CX26 were subcloned into pEGFP-N1 vector directively,following to transfect into HeLa cells by the liposome complex method.The expressions of the mutated proteins were analyzed using western blot method.The localizations of the mutated proteins and whether there were gap junction-plaques formation were observed under confocal microscopy with immunofluorescence technique.Results The nine constructs were all expressed in HeLa cells.In which,the mutated proteins of p.S19T,p.E47K,p.V84L,p.V95M and p.R165W localized at the cytoplasmic membrane of HeLa cells and formed gap junction-plaques at contact points between two cells,and the mutated proteins of p.R32H,p.R143W,p.S199F and p.L214P accumulated and localized only intracellularly and did not form gap junction-plaques on cell membrenes.Conclusion The mutations of p.S19T,p.E47K,p.V84L,p.V95M and p.R165W do not interfere the mutated connxins trafficking and inserting into the plasma membrane.The mutations of p.R32H,p.R143W,p.S199F and p.L214P impared the proteins trafficking to the cell surface.The deafness-causing mechanisms of different missense mutations might not be identical and no correlation could be observed between the mutation and the topological domain of the mutated protein.

Objective Galactosialidosis(GS) is an autosomal recessive lysosomal storage disease caused by a combined deficiency of lysosomal ?-galactosidase and neuraminidase as a result of a primary defect in the protective protein/cathepsin A(PPCA).Mouse model of GS has been generated by targeted deletion of PPCA gene and closely resembled the phenotypes in human conditions.However,it remains to be determined whether hearing loss observed in human also occurs in the mouse model.In this study,we observed their alterations of the auditory function and morphology of the ear,and explored pathophysiological mechanisms of hearing impairment.Methods PPCA homozygous(PPCA-/-) mice at 1 and 2 months of age,and their wildtype littermates(PPCA+/+) were examined for auditory thresholds through auditory brainstem responses(ABR) to click,tone pips 8,16,and 32 kHz stimuli.Morphological analyses in ears were performed by series temporal bone section and light microscopy.Results PPCA-/-mice at 1 month of age showed a normal threshold and the morphology of ears.Up to 2months of age,their thresholds were elevated 40～45 dB SPL above those of PPCA+/+ mice.There were distinct pathological changes of middle and inner ear in PPCA-/-mice of 2 months old.The severe otitis media and the vacuolation associated with lysosomal storage were observed within ossicles and cochlear bone cells,stria vascularis cells,spiral ganglion neurons,spiral limbus,Reissner's membrane cells,and the mesothelial cells of the perilymphatic scala and basilar membrane,but not within the organ of Corti.Vestibular organ did not show vacuolation.Conclusion The deficiency of lysosomal protective protein/cathepsin A may result in hearing loss and morphological alterations of ear.The otitis media and ossicle changes,and the defects in lysosomal storage of neurons,stria vascularis,spiral limbus,Reissner's membrane and basilar membrane cells may contribute to the conductive and sensorineural hearing loss respectively.

Objective To study the cytotoxicity of the membrane material of heart assist pump. Methods The membrane materials tested incladed polyurethane (group A) and medical polychloroethylene (group B),and a blank control group with none of the material. L-929 cells (the mouse fibroblasts) were cultured on either material in groups A and B,and 6 cell cultures were without any material. After 24,48 and 72 hours,the growth of cell in groups A,B and the control was observed,and the number was counted. Educts of two materials used in groups A and B was respectively added to culture medium,then the OD was measured every 24h and proliferation rate was determined by MTT test. Results L-929 cells grew very well in groups A and B with less death. The cell counts showed no difference between 2 groups at each time. The OD of group A was always higher than that of group B after 24,48 and 72h ( P

Objective To investigate the maneuver of dividing Arantius duct to expose the posterior of left hepatic vein.Methods Based on the anatomy of Arantius duct on 33 cadavers,exposure of posterior of left hepatic vein was carried out in 43 patients by dividing the Arantius ligament.Results The posterior of left hepatic vein was dissected to expose the left hepatic vein in 43 patients.The operations and the recovery of the patients were smooth and uneventful.Conclsion Cutting the Arantius ligament allows safe exposure and extrahepatic division of left hepatic vein.

Objective To evaluate the safety and efficacy of transcatheter closure of perimembranous ventricular septal defects(VSD) using domestic symmetric double-disk occluders.Methods From March 2003 to July 2007,689 VSD patients were treated with transcatheter intervention using domestic symmetric double-disk occluders and received clinical follow up at 1 month,3 months,6months after the procedure and annually thereafter.Complications including residual shunt,heart rhythm changing,shape of the occluder and the presence of tricuspid/aortic regurgitation were observed thoroughly.Results The overall technical success rate was 98.8%.One patient died of cerebral bleeding 7 days after intervention.One patient suffered complete A-V block and required permanent pacemaker implantation and another patient conversed to open surgery because of moderate tricuspid regurgitation.Asymmetric Amplatzer occluders were used in 6 patients but the intervention failed in 2 patients whom required an open conversion.Comorbidities such as atrial septum defect,patent foramen ovale were treated concomitantly.No other complications were observed during the follow-up period.Conclusion Complication associated with transcatheter closure of perimembranous VSD using domestic symmetric double-disk occluders was relatively low.The procedure was safe and applicable.Meanwhile,it is necessary to stick to the procedural indications and avoid complications such as tricuspid regurgitation etc.

Objective:To investigate the expression and clinical significance of Nusap1 in hepatical carcinoma. Methods:The expression of Nusap1 protein in 61 specimens of hepatical carcinoma was examined by immunohistochemistry. Based on the levels of Nusap1 expression, the 61 specimens were divided into a high Nusap1 expression group and a low Nusap1 expression group. The correlation between Nusap1 expression with clinicopathologic features and prognosis of hepatical carcinoma was analyzed. Results:TherateofhighNusap1expressionwas54.1%inhepaticalcarcinoma.TherateofhighNusap1 expression was 21.3%in noncarcinoma, with signiifcant difference between the 2 groups (P<0.01).Nusap1 overexpression had signiifcant correlation with histological differentiation, tumor size, liver cirrhosis,lymphaticmetastasis,tumorthrombiandearlyrecurrence(P<0.05),butnotwithsex,age,AFP level,tumornumber,TNMclassificationandtumorencapsulation(P>0.05).Survivalanalysissuggested thatthe6monthand12monthnoncarcinomasurvivalratewassignificantlylowerinthehighNusap1 expression group [33.3%(11/33), 17.9%(5/33)] than that in the low Nusap1 expression group [89.3%(25/28), 53.6%(15/28);P<0.005]. Conclusion:Nusap1 is overexpressed in hepatical carcinoma and is a valuable prognostic factor for hepatical carcinoma.

Objective:To investigate the expression of TAZ and KLF5 and their clinical significance in hepatocellular carcinoma ( HCC).Methods:We freshly collected 76 samples of surgically resected HCC and matched normal tumor-adjacent tissues and detected TAZ and KLF5 expression in these samples using immunohistochemical staining.The clinical significance of TAZ and KLF5 protein expression were analysed.Results:The protein expression of TAZ and KLF5 in HCC tissues was significantly higher than those in matched normal tumor-adjacent tissues ( P=0.001;P=0.035 ).Clinicopathological analysis suggested that TAZ and KLF5 protein expression were associated with histopathological differentiation ( P=0.007;P=0.047 ) and TNM stage ( P=0.009;P=0.040).TAZ was positively correlated with KLF5 protein in HCC tissues (r=0.651,P=0.003).Conclusion:The high-expression of TAZ and KLF5 are correlated with poor clinicopathological characteristics,and TAZ is positively associated with KLF5 in HCC tissues, suggesting that TAZ may promote tumor progression through inhibition of KLF5 protein degradation in HCC.

Objective To analyze the relationship between the estimated glomerular filtration rate (eGFR) and 10-year car‐diovascular disease risk (10y CVDR) in Chongqing college staff .Methods The physical examination data of the staff in two univer‐sities including 2630 persons were collected in April 2013 .The eGFR and 10y CVDR of each staff were calculated according to the standardized formula .The differences of 10y CVDR among different eGFR level groups were analyzed .Results The average age of all the staff were (51 .76 ± 14 .53) years old ,which in males was significant higher than that in females (P<0 .01) .The smokers , hypertension patients and diabetes patients accounted for 16 .00% ,15 .20% and 4 .10% respectively .The smokers ,hypertension and diabetes patients in males were significantly more than than those in females (P<0 .05) .The height ,weight ,BMI ,systolic pressure , diastolic pressure ,serum creatinine ,triglyceride ,LDL and blood glucose in males were significantly higher than those in females (P=0 .000) ,while HDL in males was significantly lower than that in females (P=0 .000) .The median of 10y CVDR was 1 .25% , males were significantly higher than females (2 .85% vs .0 .40% ,P<0 .01) .The median of 10y CVDR for the following groups were 0 .74% ,2 .25% ,5 .58% and 14 .39% respectively :eGFR≥90 mL · min-1 · 1 .73 m2 ,75 mL · min-1 · 1 .73 m2 ≤eGFR<90 mL · min-1 · 1 .73 m2 ,60 mL · min-1 · 1 .73 m2 ≤eGFR<75 mL · min-1 · 1 .73 m2 ,and eGFR<60 mL · min-1 · 1 .73 m2 .The results of the one‐way analysis of variance showed that compared to the 10y CVDR of the group with eGFR≥90 mL · min-1 · 1 .73 m2 ,which of the other three groups were all significantly increased .Conclusion eGFR is a significant factor impacting 10y CVDR . The lower the eGFR level ,the higher the risk of the 10y CVDR .