Objective To explore the effectiveness and safety of endoscopic sphincterotomy(EST)plus endoscopic pap-illary balloon dilation (EPBD) for the removal of common bile duct stones. Methods One hundred patients who re-ceived endoscopic retrograde pancreatic angiography(ERCP)in the first hospital of shanxi medical university from June 2012 to March 2014 were randomly divided into EST group and ESBD group. ESBD group in advance nipples small in-cision after balloon expansion; EST group used normal operation. The successful rate of stone clear-ance,operation time,the rate of mechanical lithotripsy and related complications were observed.Results After one time,all stones were removed one time from 46 cases(92%) assigned EST and 48 cases(96%) assigned EPBD(P>0.05); Mechanical lithotripsy was used to fragment stones 8 cases(16%) in EST group and 2 cases(4%) in ESBD group(P<0.05); EST group had 4 cases of high amylase levels,2 cases of acute pancreatitis,hemorrhage in 1 case; ESBD group had 2 cases with high blood amylase occurred,1 case of acute pancreatitis, early complications of total incidence were 14% and 6% respectively(P>0.05); Average operation time,respectively (45.3±13.0) min and (30.5±9.2) min(P<0.05). Con-clusion Endoscopic papillary sphincter small incision combined with balloon dilatation lithotomy success rate and post-operative complication rates comparable to conventional sphincterotomy is similary,but the average operation time and the use of mechanical lithotripsy probability compared with EST were low,so EST combined with EPBD to treat com-mon bile stone is a safe and effective method.

Objective To study the effects of butylphthalide on cognitive function,apoptosis and pp38MAPK in hippocampus of rat model of vascular dementia.Methods The vascular dementia (VD) model was established by two vascular (2VO) method,and then sixty male Wistar rats were randomly divided into VD group,sham operation group and NBP (butylphthalide) group.Rats in NBP group were given 120 mg · kg-1 · day-1 dose butylphthalide by gavage,and rats in VD group and sham operation group were given the same dose vegetable oil.The cognitive function of each rat was tested by Morris water maze.The expression of p-p38MAPK in the hippocampus was observed by Western blot;and the apoptosis was observed in hippocampal CAl region by TUNEL staining.Results The hidden platform escape latency of NBP group ((48.72 ± 7.01) s,(42.41 ± 4.06) s,(40.34 ± 2.46) s)was significantly shortened compared with those of VD group((82.71±8.27) s,(80.36±9.65) s,(77.74±6.33) s)(P＜ 0.01) ; and the former platform quadrant time and the number of passing through the platform of NBP group ((26.45±4.66)s,(1.84±0.82) times) were significantly prolonged (P＜0.01) compared with those of VD group ((18.67±5.39) s,(1.32±0.61) times);the apoptosis and the expression of p38MAPK phosphorylation in hippocampus in NBP group ((153.65±9.85),(0.42±0.04)) significantly reduced (P＜0.01) compared with those of VD group ((209.46±11.49),(0.88±0.10)).Conclusion Butylphthalide can improve the learning and memory ability of VD rats,the reduce apoptosis in the hippocampus by the inhibition of the P38MAPK pathway.This may be one of the ways by which butylphthalide can treat vascular dementia.

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.