The post-stroke depression (PSD) is one of the common complications of stroke.It can not only delay the recovery of the neurological function in patients, seriously affect the quality of life of patients, but also increase the mortality and morbidity.More and more attention has been paid to the pathogenesis of PSD.Recent studies have confirmed that brain small vessel disease is closely related to the occurrence of PSD.This article reviews relationship between brain small vessel diseases and PSD.

Background: Esophageal variceal bleeding is a clinical emergency and the major cause of death in patients with liver cirrhosis.Aims: To assess the value of platelet count (PC)/spleen diameter (SD) ratio in predicting the presence of esophageal varices (EV) in patients with HBV-related cirrhosis in China.Methods: A total of 91 consecutive HBV-related cirrhosis patients with EV from Aug.2013 to Dec.2015 at Renji Hospital (South Campus),School of Medicine,Shanghai Jiao Tong University were enrolled.Thirty-two HBV-related cirrhosis patients without EV were enrolled as controls.Upper gastrointestinal endoscopy,routine laboratory examinations and abdominal ultrasonography were performed and the related parameters were collected.Binary Logistic regression analysis was carried out to identify independent risk factors associated with EV.ROC curve was used to evaluate the predictive performance of PC/SD ratio for the presence of EV.Results: The PC/SD ratio was significantly lower in EV group than in non-EV group (538.2±327.0 vs.1 105.9±426.6,P=0.001).Binary Logistic regression analysis showed that the PC/SD ratio was independently associated with the presence of EV (OR=57.29,95％ CI: 15～214,P=0.000).In ROC curve analysis,the area under the curve (AUC) of PC/SD ratio in predicting the presence of EV was 0.853;the optimal cutoff value was 842,and the sensitivity,specificity,positive predictive value and negative predictive value were 85.7％,75.0％,90.7％,and 64.9％,respectively.Conclusions: PC/SD ratio can be used as a non-invasive tool for prediction of the presence of EV in patients with HBV-related cirrhosis.It may reduce the number of unnecessary endoscopy.

Background:More and more evidences suggest that microRNA plays an important role in the development of gastric cancer (GC).Expression of miR-129 in GC tissues is found abnormal, however, the mechanism of miR-129 in cell proliferation and invasion is still undefined.Aims:To investigate the expression of miR-129 in GC tissue and GC cell lines and the mechanism of miR-129 in proliferation and invasion of SGC-7901 cells.Methods:Eighty-two GC tissues and corresponding paracancerous tissues were collected, human gastric epithelial cell line and different GC cell lines were cultured, qPCR was conducted to assess miR-129 expression.SGC-7901 cells were transfected with miR-129 mimic or miR-NC, and then were transfected with overexpressed HMGA2 plasmid.Colony formation assay was used to detect cell proliferation ability, and Transwell chamber was used to assess cell invasion ability.Pearson correlation analysis was used to analyze the correlation between miR-129 and HMGA2 mRNA expression.Luciferase assay was performed to determine the activity of luciferase.mRNA and protein expressions of miR-129, HMGA2 were determined by qPCR and Western blotting, respectively.Results:Compared with paracancerous tissues, expression of miR-129 was significantly decreased in GC tissues (P<0.05);when compared with human gastric epithelial cells, expression of miR-129 was significantly decreased in GC cell lines (P<0.05).Compared with miR-NC group, proliferation and invasion abilities of SGC-7901 cells were inhibited in miR-129 mimic group (P<0.05).HMGA2 mRNA expression in GC tissues was significantly upregulated (P<0.05), and was negatively correlated with miR-129 expression (r=-0.543 9, P<0.01).Luciferase activity in wild-type miR-129 mimic group was significantly lower than that in miR-NC group (P<0.05);mRNA and protein expressions of HMGA2 were decreased after transfection with miR-129 mimic (P<0.05).Compared with miR-129+vector group, proliferation and invasion of SGC-7901 cells were significantly increased in miR-129 mimic+HMGA2 group (P<0.05).Conclusions:The expression of miR-129 is decreased in GC tissue and cells;miR-129 inhibits SGC-7901 cells proliferation and invasion by negatively regulating HMGA2.

Background:Activation of hepatic stellate cells( HSCs)plays a pivotal role in development of liver fibrosis. Interleukin-17(IL-17)is the most important effector of T helper 17(Th17)cells that causes inflammatory cell infiltration and tissue damage. Preliminary studies showed that the number of IL-17-positive cells in liver tissue was positively correlated with the severity of liver fibrosis in patients with chronic hepatitis B and autoimmune hepatitis. However,the mechanism of IL-17 in liver fibrosis is not yet clarified. Aims:To investigate the effect of IL-17 on activation of human HSC cell line LX2 and collagen expression. Methods:Human HSC cell line LX2 was treated with different concentrations of IL-17. Viability of LX2 cells was measured by CCK-8 assay. mRNA expressions of α-smooth muscle actin(α-SMA), type Ⅰ collagen(Col-Ⅰ)and Col-Ⅲ were determined by real-time PCR. Protein expressions of α-SMA、Col-Ⅰ and Col-Ⅲ were detected by immunofluorescence. Results: Viability of LX2 cells increased with the increase of IL-17 concentration,but no significant differences were seen between any two groups(P > 0. 05). mRNA expressions of α-SMA, Col-Ⅰ and Col-Ⅲ in IL-17 treatment group(100 ng/ mL)were significantly higher than those in blank control group(P <0. 05). With the increase of IL-17 concentration,protein expressions of α-SMA,Col-Ⅰ and Col-Ⅲ gradually increased. Conclusions:IL-17 can promote the activation of HSCs and expressions of Col-Ⅰ and Col-Ⅲ,thereby contributing to the development of liver fibrosis.

Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.

Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.

Objective To discuss expression of livin genes in colon cancer tissues chip and its correlation with Bcl-2 genes. Methods A total of 60 cases of patients with colon cancer, who chose to be treated with surgical operation in General Surgery Department were selected, and applied with immunohistochemical MaxVisionTM two step method to detect the expression of livin and Bcl-2 genesn in tissues chip. 25 cases of colon tissues chip with normal cutting edge were additionally chosen as control group. Results Positive livin genes expression rates in colon cancer tissues chip (63.33%) were much higher than those in colon tissues with normal cutting edge, which appeared statistical differences (24.00%) (χ2=10.93, P<0.01). Livin genes expression in colon cancer tissues chip had no obvious relevance with gen-der, age, tumor size, differentiation degree, lymphatic metastasis and other pathological characteristics (P>0.05), but ob-vious relevance with invasive depth, Duke’s stages, distant metastasis and other pathological characteristics (P<0.05 or P<0.01). Positive Bcl-2 genes expression rates in colon cancer tissues chip (68.33%)were much higher than those in colon tissues with normal cutting edge, which appeared statistical differences (4.00%) (χ2=29.22, P<0.01). Livin genes expres-sion was positively relatedto Bcl-2 genes in expression in colon cancer tissues chip (P<0.01). The invasive depth, Duke’s stages and distant metastasis were included in meta stasis of dinthe Logistic regression model for livin genes expression (P<0.05). Conclusion Livin genes play important roles in the disease process of colon cancer tissues chip and have close relevance with pathologic process of malignant invasion and transfer of tumor. The expression of Livin genes and Bcl-2 genes may play synergetic roles in process of colon cancer.

ObjectiveTo explore the Apolipoprotein-E （ApoE） gene polymorphism in patients with Alzheimer's disease （AD）, vascular dementia (VD) or mild cognitive impairment (MCI). MethodsPeripheral blood was taken from patient with AD, VD or MCI to determine the ApoE genotypes. ResultsThe most of the patients were ε3/ε3 genotype, while the ε2/ε2 and ε4/ε4 could not be detected. ε3/ε4 genotype （P=0.001） and ApoE ε4 allele （P=0.013） was more frequent in AD than in MCI. ApoE ε4 was more frequent in VD than in MCI （P=0.044）. ConclusionApoE ε4 allele is a risk factor in AD, and may be associated with VD and MCI.

Objective to provide the evidence for inducing the SAP model in rats with proper concentration of sodium taurocholate.Methods 60 SD rats were divided into sham operated group, group of 1.5% in concentration, group of 3.5% in concentration and group of 5% in concentration randomly, while the SAP model was induced by the sodium taurocholate concentration of 1.5%,3.5% and 5% with the method of retrograde injection into the biliopancreatic duct.To calculate the mortality of different groups, measure the serum amylase, tumor necrosis factor -α(TNF -α) and interleukin -6 (IL -6),and to observe the pancreatic pathological scores of HE staining in rats.Results The mortality in group of 5% in concentration has a significant ascending compared with group of 1.5% in concentration, while the serum amylase, tumor necrosis factor -α(TNF -α) , interleukin -6( IL -6), pathological score of hemorrhage and acinar necrosis in group of 5% in concentration have a significant ascending compared with group of 1.5% in concentration and group of 3.5% in concentration.Conclusions A better SAP model may be induced by sodium taurocholate with the concentration of 5% by the method of retrograde injection into the biliopancreatic duct, which may accord with the physiological and pathological manifestation of SAP.

Background:Esophagogastric variceal bleeding is a severe and commonly seen complication of portal hypertension in patients with liver cirrhosis. Prevention of rebleeding remains an important issue in the management of patients suffered from the disease. Aims:To evaluate the efficacy and safety of percutaneous transhepatic variceal embolization(PTVE) combined with partial splenic embolization(PSE)for treatment of esophagogastric variceal bleeding in patients with liver cirrhosis. Methods:Ten liver cirrhosis patients with esophagogastric variceal bleeding were prospectively selected and treated by PTVE combined with PSE. The blood flow of portal system was measured by Doppler ultrasonography pre- and post-operatively;meanwhile peripheral blood cells were counted. A 1-2-year follow-up was carried out and the rebleeding and procedure-related complications were recorded. Results:The postoperative inner diameter of main portal vein,as well as the blood flow velocity of main portal vein and splenic vein were significantly reduced as compared with those before operation(P < 0. 05). Three months after operation,the peripheral white blood cell and platelet were still significantly higher than those before operation(P < 0. 05). During 1-year follow-up,rebleeding appeared in 2 patients,one of them was found having main portal vein thrombosis developed,and was treated by endoscopic esophageal variceal ligation because the gastric varices was not as evident as ever. The rebleeding rate and incidence of portal system thrombosis after the PTVE-PSE procedure was 20. 0% and 10. 0%,respectively. Conclusions:PTVE combined with PSE seemed efficient for alleviating portal hypertension,and might be recommended as a safe and effective interventional therapy for liver cirrhosis patients with esophagogastric variceal bleeding.