The morbidity and mortality associated with vascular cognitive impairment (VCI) generally increase steeply, and health systems will face increasing demand for services. The present study aims to screen key genes to give new insight into the mechanisms and treatment of VCI based on bioinformatic approaches combined with biological experiments in rats. The gene expression data of VCI patients contained in the GSE122063 data set were downloaded from the Gene Expression Omnibus. We performed a weighted gene co-expression network analysis to identify a hub module and 44 hub genes. Two hundred and seventy-seven differentially expressed genes (DEGs) were analyzed using R software by the "limma" package. STRING database was used to construct protein-protein interaction (PPI) network, after which 36 hub genes were identified through Cytoscape. Functional enrichment analysis revealed that these genes from the yellow module and 277 DEGs were mainly associated with these pathways, such as Staphylococcus aureus infection, complement, and coagulation cascades. These biological functions are related to inflammatory cell activation and inflammatory response. The key genes of VCI were the overlapping hub genes from the yellow module and the PPI network. The expressions of hub genes in rats were determined by quantitative reverse transcription-polymerase chain reaction, Western blot, immunohistochemistry, and immunofluorescence. In conclusion, C1QA, C1QB, C1QC, CD163, and FCGR2A were highly expressed in the hippocampus of VCI rats, and they can serve as candidate biomarkers for the diagnosis and prognosis of VCI. Finally, molecular docking results suggested that 5 genes interact with Bisphenol A. These findings open a new avenue to investigate molecular mechanisms for preventing or treating VCI.

目的:讨论瞬感血糖监测在糖尿病治疗中的辅助效果.方法:将40例糖尿病患者随机分为对照组(指尖血糖监测)与研究组(瞬感血糖监测)各20例,观察干预前后各临床指标、各临床指标变化差值.结果:干预后两组患者的体质量、空腹血糖、甘油三酯、胰岛素、尿酸指标均有所下降,且糖尿病自我管理行为量表指标均有所升高,P<0.05.干预后研究组患者的血糖标准差、平均血糖波动幅度指标均明显小于对照组,P<0.05.研究组患者的体质量、体质量指数、腰围、空腹血糖、甘油三酯、胰岛素指标下降幅度明显比对照组高,尿酸指标下降幅度明显比对照组低,糖尿病自我管理行为量表指标升高幅度明显比对照组高,P<0.05.结论:瞬感血糖监测在糖尿病治疗中的应用可有效帮助患者了解血糖及形成良好的行为,以起到降低血糖及血脂,改善胰岛素功能的效果.

Objective:To investigate the clinical characteristics and risk factors for the progression of acute-on-chronic liver failure(ACLF)associated with hepatitis B in elderly patients.Methods:A total of 168 elderly patients with hepatitis B-related acute-on-chronic liver failure(HBV-ACLF)at Tianjin Third Central Hospital who met the diagnostic criteria of the Asian Pacific Association for the Study of the Liver(APASL)-ACLF were enrolled, 176 non-elderly HBV-ACLF patients served as the control group during the same period, and their baseline and progression data were recorded.At the same time, the elderly group was divided into the progressive subgroup and the non-progressive subgroup based on the diagnostic criteria of the European Society for the Study of the Liver(EASL)-ACLF, and their baseline and progression data were recorded.Independent risk factors for HBV-ACLF progression in the elderly were analyzed using multivariate Cox proportional risk model regression.Results:Compared with non-elderly patients with HBV-ACLF, elderly patients were more likely to progress to meet the EASL-ACLF diagnostic criteria and have higher mortality.Multivariate Cox proportional risk model regression analysis showed that baseline arterial lactic acid levels( HR=1.77, 95% CI: 1.36-2.30, P<0.01), secondary nosocomial infections( HR=13.90, 95% CI: 3.73-51.87, P<0.01), rates of change in maximum total bilirubin( HR=1.08, 95% CI: 1.01-1.15, P=0.04), rates of change in maximum MELD( HR=4.06, 95% CI: 1.53-10.77, P=0.01)and rates of change in maximum CLIF-SOFA( HR=12.74, 95% CI: 2.46-66.08, P<0.01)were independent risk factors for progression of HBV-ACLF in elderly patients. Conclusions:Compared with non-elderly patients, elderly patients with HBV-ACLF have more advanced disease and higher mortality.Therefore, risk factors should be identified as soon as possible and treatment plans should be formulated as soon as possible to further reduce the mortality.

ObjectiveTo investigate the influencing factors for rebleeding after gastroscopy in patients with liver cirrhosis and esophagogastric variceal bleeding. Methods A retrospective analysis was performed for the clinical data of the patients with liver cirrhosis and esophagogastric variceal bleeding who were hospitalized in Tianjin Third Central Hospital from January 1, 2017 to December 31, 2018, and according to the presence or absence of rebleeding and bleeding time, the patients were divided into non-bleeding group (n=148) and bleeding group (n=119). The risk factors for rebleeding after gastroscopy were analyzed. The t-test or the Mann-Whitney U test was used for comparison of continuous data between two groups, and the chi-square test was used for comparison of categorical data between two groups. The Cox regression model was used for univariate and multivariate analyses. The receiver operating characteristic (ROC) curve was used to evaluate the accuracy of Child-Turcotte-Pugh (CTP), fibrosis-4 (FIB-4), and albumin-bilirubin (ALBI) scores in predicting rebleeding after gastroscopy, and MedCalc was used to compare the area under the ROC curve (AUC). ResultsA total of 267 patients with liver cirrhosis and esophagogastric variceal bleeding were enrolled, among whom 53 (19.9%) had liver cancer. A total of 119 patients suffered from rebleeding, with an overall rebleeding rate of 44.6% and a median time to rebleeding of 11.0 (0-39.0) months. The univariate Cox regression analysis showed that liver cancer (hazard ratio ［HR］=0.377, P＜0.001), aspartate aminotransferase (AST) (HR=1002, P=0.025), serum Na (HR=0.935, P=0.004), and FIB-4 (HR=1.030, P=0.049) were associated with rebleeding, and the multivariate Cox regression analysis showed that liver cancer (HR=0.357, P＜0.001), AST (HR=1.003, P=0.030), prothrombin time (PT) (HR=0.196, P=0.001), CTP score (HR=1.289, P=0.014), FIB-4 (HR=1.062, P=0.033), and ALBI score (HR=0.433, P=0.011) were independent risk factors for rebleeding. CTP, FIB-4, and ALBI scores had an AUC of 0.711 (95% confidence interval ［CI］: 0.647-0776), 0.705 (95% CI: 0.640-0.770), and 0.730 (95% CI: 0.667-0.793), respectively, in predicting rebleeding. There was no significant difference in AUC between CTP, FIB-4, and ALBI scores (P＞0.05). ConclusionLiver cancer, AST, PT, CTP score, FIB-4 score, and ALBI score are associated with rebleeding after gastroscopy in patients with liver cirrhosis and esophagogastric variceal bleeding, among which CTP, FIB-4, and ALBI scores have a good value in predicting rebleeding outcome, while there is no significant difference in predictive ability between them.

目的 通过对部分脾动脉栓塞和脾切除治疗脾功能亢进症的治疗费用、疗效及并发症进行分析,评价两种方法治疗脾功能亢进症的特点.方法 92例脾功能亢进症行部分脾动脉栓塞治疗患者作为脾栓塞组,208例脾功能亢进症行脾切除治疗患者作为脾切除组.比较两组患者住院天数及住院费用;术前、术后的白细胞(WBC)、红细胞(RBC)、血小板(PLT)水平;并发症发生情况.结果 两组患者手术均安全、顺利、成功.脾栓塞组住院天数(23.39±10.15)d短于脾切除组的(31.54±11.08)d,住院费用中位数2.77万元少于脾切除组的4.82万元,差异均具有统计学意义(P<0.05).术前,两组患者的WBC、RBC、PLT水平比较,差异均无统计学意义(P>0.05);脾栓塞组术后3、7、14、21 d的WBC、PLT水平均低于脾切除组,术后3 d的RBC水平高于脾切除组,差异均具有统计学意义(P<0.05);两组患者术后7、14、21 d的RBC水平比较,差异均无统计学意义(P>0.05).脾栓塞组患者的腹水感染、脾周脓肿、门静脉血栓形成、发热、肝性脑病、腹泻发生率分别为25.00％、2.17％、0、88.04％、1.09％、2.17％,与脾切除组的42.79％、0、25.00％、98.08％、19.71％、0比较,差异均具有统计学意义(P<0.05);两组患者的腹水、腹痛、左下肺不张、肺炎、腹腔血肿、其他发生率比较,差异均无统计学意义(P>0.05).结论 部分脾动脉栓塞和脾切除均为治疗脾功能亢进症的有效方法,近期治疗效果明确.部分脾动脉栓塞更适合肝功能差、不能耐受外科手术的患者.

Diffuse large B-cell lymphoma (DLBCL) is the most prevalent type of diffuse B-cell lymphoma in non-hodgkin lymphoma (NHL). The progressive enlarging lymphonodus is the most common clinical manifestation of this disease. DLBCL often appears heterogeneous presentations. It is easy to be misdiagnosed. Here, we reviewed a case of DLBCL with liver cirrhosis, in which the initial symptom was upper gastrointestinal hemorrhage, and the endoscopic examination showing gastric ulcer. We hope to improve the understanding and diagnosis and treatment levels of DLBCL by analyzing this case.

[ ABSTRACT] AIM:To investigate the role of Janus kinase/signal transducer and STAT) signaling pathway in propofol ( Pro)-induced reduction of kidney injury after liver c METHODS:Sprague-Dawley rats were assigned randomly to 4 groups ( n=8 each group group);liver cold ischemia/reperfusion model group ( I/R group);propofol group ( Pro gr ·kg-1 ·h-1 was infused continuously for 30 min via right femoral vein 5 min before rep group ( AG490 group):AG490 at dose of 10 mg/kg was applied by intraperitoneal injectio model. The rats were sacrificed at 6 h after reperfusion. Blood samples and kidney tissues concentrations of creatinine ( Cr ) , blood urea nitrogen ( BUN ) , interleukin-6 ( IL-6 ) ( TNF-α) , and the tissue levels of malondialdehyde ( MDA) and superoxide dismutase ( S the renal tissues and nephritic cell apoptosis were analyzed, the damage of the renal tubule (AI) was calculated. The protein levels of p-JAK2, p-STAT1 and p-STAT3 were det SULTS:Compared with sham group, the levels of Cr, BUN, IL-6, TNF-αand MDA, AI were significantly increased, the SOD activity was decreased, and the protein levels of p were up-regulated in I/R group (P<0. 05). Compared with I/R group, the levels of Cr, AI, and renal tubular damage score were significantly decreased, the SOD activity was inc activator of transcription ( JAK/old ischemia/reperfusion in rats. ): sham operation group ( sham oup):propofol at dose of 20 mg erfusion; JAK2 inhibitor AG490 n 30 min before establishing the were obtained to detect the serum and tumor necrosis factor-alpha OD) . The pathologic changes of s was scored and apoptotic index ermined by Western blot. RE-, and renal tubular damage score-JAK2, p-STAT1 and p-STAT3 BUN, IL-6, TNF-α and MDA, reased, and the protein levels of&nbsp;p-JAK2, p-STAT1 and p-STAT3 was down-regulated in Pro group and AG490 group (P<0. 05). CONCLUSION:Propo-fol reduces kidney injury induced by liver cold ischemia/reperfusion, and the mechanism is possibly associated with inhibi-ting the JAK/STAT pathway activation.

液体治疗是围术期管理非常重要的一部分，也是争论最多的问题之一。适当的液体治疗对患者术中循环稳定和术后恢复具有积极作用。由于肝移植患者具有特殊的病理生理学特点，液体治疗可以直接影响患者预后。随着人们对不同种类液体生化性质和生物学特点的深入了解，容量监测方法的进一步完善，围术期容量管理发生了新变化。合理的围术期液体管理对于减少术后并发症具有重要意义。

Objective To evaluate the effect of propofol on Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the hippocampus of rats undergoing orthotopic liver transplantation.Methods Twenty-four healthy male Sprague-Dawley rats,aged 8-10 weeks,weighing 220-250 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S);orthotopic liver transplantation group (group O);propofol group (group P).After the rats were anesthetized with chloral hydrate,the model of orthotopic liver transplantation was established according to the method described by Nozato et al.in O and P groups.In group P,30 min infusion of propofol was started at a rate of 20 mg · kg-1 · h-1 via the right femoral vein immediately after onset of reperfusion.At 6 h of reperfusion,blood samples were collected from the infrahepatic vena cava,and then the rats were sacrificed.The hippocampi were harvested for determination of malondialdehyde (MDA)and nitric oxide (NO) contents and superoxide dismutase (SOD) activity.The serum levels of S100β protein and neuron-specific enolase (NSE) were determined by enzyme-linked immunosorbent assay.The expression of JAK2,STAT3 and inducible nitric oxide synthase (iNOS) mRNA was detected by quantitative real-time polymerase chain reaction.The pathological changes of hippocampal tissues were examined under the light microscope,and the cell apoptosis was measured using TUNEL.The apoptotic index was calculated.Results Compared with group S,the serum levels of S100β protein and NSE were significantly increased,the contents of MDA and NO were significantly increased,the activity of SOD was significantly decreased,the expression of JAK2,STAT3 and iNOS mRNA was significantly up-regulated,the apoptotic index was significantly increased (P＜0.05),and the pathological changes of hippocampal tissues were significantly aggravated in the other groups.Compared with group O,the serum levels of S100β protein and NSE were significantly decreased,the contents of MDA and NO were significantly decreased,the activity of SOD was significantly increased,the expression of JAK2,STAT3 and iNOS mRNA was significantly downregulated,the apoptotic index was significantly decreased (P＜0.05),and the pathological changes of hippocampal tissues were significantly reduced in P group.Conclusion Propofol reduces injury to the hippocampus through blocking JAK2/STAT3 signaling pathway in the rats undergoing orthotopic liver transplantation.

Objective To evaluate the effect of dexmedetomidine on kidney injury induced by liver ischemia-reperfusion (I/R) in rats.Methods Twenty-four healthy male Sprague-Dawley rats,weighing 220-250 g,aged 8-10 weeks,were randomly divided into 3 groups (n=8 each) using a random number table:sham operation group (group S);liver I/R group (group I/R);dexmedetomidine group (group D).In group I/R,liver I/R model was established by clamping the portal vein,hepatic artery,supra-and infra-hepatic vena cava for 40 min,followed by 6 h of reperfusion in anesthetized rats.In group D,dexmedetomidine 100 μg/kg was injected intraperitoneally at 30 min before skin incision.The equal volume of normal saline was given instead of dexmedetomidine in S and I/R groups.At 6 h of reperfusion,blood samples were collected from the infra-hepatic vena cava for determination of blood urea nitrogen (BUN) and creatinine (Cr) concentrations (by automatic biochemical analyzer) and tumor necrosis factor-alpha (TNFα) and interleukin-10 (IL-10) concentrations in serum (by enzyme-linked immunosorbent assay).After blood sampling,the rats were sacrificed,and kidneys were harvested for examination of histopathological changes (with light microscope) and for determination of malondialdehyde (MDA) content (using thiobarbituric acid method) and superoxide dismutase (SOD) activity (by xanthine oxidase method),expression of activated caspase-3 (by immuno-histochemistry),and apoptotic cells (using TUNEL).Apoptotic rate was calculated.Results Compared with group S,the serum BUN,Cr and TNF-α concentrations were significantly increased,the concentration of serum IL-10 was decreased,the MDA content and apoptotic rate were increased,the SOD activity was decreased,and the expression of activated caspase-3 was up-regulated in I/R and D groups (P＜0.05).Compared with group I/R,the serum BUN,Cr and TNF-α concentrations were significantly decreased,the concentration of serum IL-10 was increased,MDA content and apoptotic rate were increased,the SOD activity was decreased,the expression of activated caspase-3 was down-regulated (P＜0.05),and the histopathological changes of renal tissues were attenuated in group D.Conclusion Dexmedetomidine can reduce kidney injury induced by liver I/R in rats,and the mechanism is probably related to inhibition of inflammatory responses,lipid peroxidation and cell apoptosis.

Objective To investigate the role of Janus kinase and signal transducer and activator of transcription (JAK/STAT)signaling pathway in dexmedetomidine’s renoprotection after autologous orthotopic liver transplantation in rats.Methods Fifty SD rats were randomly divided into five groups (n =10 each)using a random number table:sham operation group (group S);autologous orthotopic liver transplantation model group (group M);dexmedetomidine group (group D);JAK2 kinase inhibitor AG490 group (group A);dexmedetomidine+atipamezole group (group T).In group D,rats received dexmedetomidine 50 μg/kg 30 min before establishing model;In group A,rats re-ceived AG490 10 mg/kg 30 min before establishing model;In group T,rats received atipamezole (250 μg/kg)30 min prior to dexmedetomidine treatment.Other groups were given the equal volume of normal saline in the same time points.At 6 h after reperfusion,rats were sacrificed,blood samples were harvested for detecting the serum concentration of creatinine (Cr),blood urea nitrogen (BUN), interleukin-6 (IL-6)and tumor necrosis factor-alpha (TNF-α).kidneys were removed for determina-tion of the pathologic changes which were scored;Cell apoptosis was assessed by TUNEL,and apop-tosis index(AI)was calculated.The expression of phosphorylations of JAK2,STAT1 and STAT3 were assessed by Western blot.Results Compared with group S,the levels of Cr,BUN,IL-6,TNF-α,AI and renal tubular damage score were significantly increased,and the expression of p-JAK2,P-STAT1 and P-STAT3 was up-regulated in other groups (P <0.05 );Compared with group M,the levels of Cr,BUN,IL-6,TNF-α,AI and renal tubular damage score were significantly decreased,and the expression of p-JAK2,P-STAT1 and P-STAT3 was down-regulated in groups D and A (P <0.05);Compared with group D,atipamezole have abolished dexmedetomidine’s renoprotection,the levels of Cr,BUN,IL-6,TNF-α,AI and renal tubular damage score were significantly increased,and the expression of p-JAK2,P-STAT1 and P-STAT3 was up-regulated in group T (P < 0.05 ). Conclusion Dexmedetomidine can attenuate kidney injury after autologous orthotopic liver transplan-tation,and the mechanism is associated with inhibiting the JAK/STAT pathway activation, alleviating inflammation reaction and cell apoptosis.

Objective To evaluate the effect of dexmedetomidine pretreatment on activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway during intestinal injury in rats undergoing liver transplantation.Methods Thirty-two pathogen-free healthy adult male Sprague-Dawley rats,weighing 220-250 g,aged 8-10 weeks,were divided into 4 groups (n =8 each) using a random number table:sham operation group (S group),liver transplantation group (LT group),dexmedetomidine pretreatment group (D group) and dexmedetomidine plus atipamezole (specific α2-adrenergic receptor antagonist) group (D+A group).The model of liver transplantation was established in LT,D and D+A groups except group S.In group D,dexmedetomidine 50 μg/kg was injected intraperitoneally at 30 min before skin incision.In group D+A,atipamzole 250 μg/kg was injected intraperitoneally at 5 min before administration of dexmedetomidine.At 6 h of reperfusion,blood samples were collected from the inferior vena cava for determination of serum concentrations of intestinal fatty acid binding protein (iFABP),lipopolysaccharide (LPS),tumor necrosis factor-alpha (TNF-ct) and high-mobility group box 1 protein (HMGB1).Intestinal specimens were then obtained for examination of the pathological changes of intestinal tissues (under light microscope) and for determination of the expression of activated caspase-3,phosphorylated JAK2 (p-JAK2),phosphorylated STAT1 (p-STAT1) and phosphorylated STAT3 (p-STAT3).Intestinal damage was assessed and scored.Wet/dry weight ratio (W/D ratio) was calculated.Results Compared with group S,the concentrations of iFABP,LPS,TNF-α and HMGB1 in serum,intestinal damage scores and W/D ratio were significantly increased,and the expression of activated caspase-3,p-JAK2,pSTATI and p-STAT3 in intestinal tissues was up-regulated in LT and D groups (P＜0.05).Compared with group LT,the concentrations of iFABP,LPS,TNF-cα and HMGB1 in serum,intestinal damage scores and W/D ratio were significantly decreased,and the expression of activated caspase-3,p-JAK2,p-STAT1 and p-STAT3 in intestinal tissues was down-regulated in group D (P＜0.05).Compared with group D,the concentrations of iFABP,LPS,TNF-cα and HMGB1 in serum,intestinal damage scores and W/D ratio were significantly increased,and the expression of activated caspase-3,p-JAK2,p-STAT1 and p-STAT3 in intestinal tissues was up-regulated in group D+A (P＜0.05).The pathological changes of intestinal tissues were significantly attenuated in group D as compared with group LT.Conclusion The mechanism by which dexmedetomidine pretreatment reduces intestinal injury may be related to inhibition of JAK/STAT signaling pathway activation in rats undergoing liver transplantation.

近年来,随着肝移植术的飞速发展,人们逐步意识到移植术中肝缺血/再灌注损伤过程严重影响移植患者的生存预后.研究表明,缺血/再灌注过程不仅损伤肝细胞本身,还可以产生广泛的影响,包括对肺、肾、脑、心肌等远隔脏器的损伤[1].与此同时,某个远隔脏器的病理生理改变又有可能引起多器官功能障碍综合征,导致机体的恶性循环.因此,明确肝缺血/再灌注后导致远隔脏器损伤的发生机制,并对其实施有效的保护措施对改善患者预后具有重要意义.

Objective To explore the changes of the inflammatory mediators and myocardial injury during the hepato-reperfusion in patients undergoing liver transplantation.Methods A total number of24 recipients who underwent liver transplantation received general anesthesia. Blood samples were collected from central vein before skin incision(T0 baseline), at1 min of hepato-reperfusion(T1),2 h of neohepatic stage(T2), the end of surgery(T3) and four hours after surgery(T4),24 h after operation(T5). Concentration of TNF-α, IL-6, cardiac troponin I(cTnI), creatine kinase MB(CK-MB) and lactate dehydrogenase(LDH) activity were detected in blood serum.Results All patients completed surgery successfully. Hemodynamic changed obviously during the anhepatic phase and hepato-reperfusion. The serum TNF-α, IL-6, cTnI and CK-MB concentrations and LDH activity at T2-T5 increased significantly compared with the baseline at T0〔TNF-α(ng/L):182±29、89±22、71±26、28±13 vs. 21±8,IL-6(ng/L):1751±255、1420±251、947±219、417±97 vs. 70±18,cTnI(μg/L):0.126±0.045、0.215±0.065、0.252±0.055、0.198±0.045 vs. 0.042±0.018,CK-MB(μg/L):5.1±1.7、10.3±2.2、15.2±2.5、10.3±2.2 vs. 1.6±0.5,LDH(U/L):547±216、620±251、751±255、417±97 vs. 170±58,P < 0.05 or P<0.01)〕.Conclusion To some degree, myocardial injury could be found during the neohepatic stage in patients undergoing liver transplantation, which may be associated with a great deal of inflammatory mediators releasing.

It was essential to rapidly reactivate and restore the function of the inhibited acetylcholinesterase(AChE) in the treatment of nerve agents poisoning. However, the blood-brain barrier(BBB) restricts the rapid transport of reactivators from the blood into the brain in therapeutically relevant concentrations. In this study, human serum albumin nanoparticles(HSA NPs) were prepared via desolvent method; HI-6, the known reactivator with higher reactivating efficiency were bound to HSA NPs through electrostatic interaction; at last, on zebrafish BBB model and soman-intoxicated mice, the permeability on BBB and the reactivation on inhibited brain AChE of nanoparticulate oxime formulations were evaluated. All characterization data revealed that HSA NPs loaded with HI-6 had met the basic demand for nanodrug therapy. Compared with free HI-6, HSA NPs loaded HI-6 could cross the BBB and improve the reactivating rates two times, suggesting HSA NPs could carry HI-6 into CNS successfully. In brief, we improved and established a method to prepare the brain-targeted nanoparticles with small-size, low-toxicity and high-efficiency, the targeted drug based on this method could efficiently release and rapidly antagonize the nerve agents poisoning.

Objective:To clarify whether miR-146b-5p can modulate the expression of MMP-16 and to observe its effects on migration, invasion,proliferation,and apoptosis of the glioblastoma cell line.Methods:TJ905 cells were transfected with the expression plasmid of the nonsense scrambled sequence(Group 1 ) or that of miR-146b-5p(Group 2 ).The expression levels of miR-146b-5p, MMP16 mRNA,and MMP16 protein were measured by quantitative real-time polymerase chain reaction(qRT-PCR ) and Western blot assay.Migratory and invasive abilities and cell cycle distribution and apoptosis in the two groups were assessed by in vitro migration assays and by invasion and flow cytometry.Results:Compared with Group 1,the expression levels of MMP16 mRNA and MMP16 protein significantly decreased in Group 2.MMP16 mRNA and MMP16 protein expression levels positively correlated with each other, whereas they negatively correlated with the expression level of miR-146b-5p.The number of migrated and invaded cells was significantly lower in Group 2 than in Group 1,which was positively correlated with the expression level of MMP16.The apoptotic level was significantly higher in Group 2 than in Group 1 and was positively correlated with the miR-146b-5p expression level in Group 2.However, the two groups shared a similar pattern on cell cycle distribution.Conclusion:MiR-146b-5p is a tumor-suppressive mRNA against glioma.Exogenous miR-146b-5p can effectively promote apoptosis of the glioma cells and can inhibit invasive and migratory abilities by down-regulating the expression level of MMP16.Our results suggest a potential value of miR-146b-5p in the gene therapy of malignant gliomas.

Objective:To investigate the stimulatory effects of miR-218 on the differentiation of glioblastoma cells.Methods: The SNB-19 glioblastoma subcell line overexpressing miR-218(SNB19-miR218 ) and the control subcell line overexpressing a nonsense scrambled sequence(SNB19-scr ) were established via plasmid transfection and G418 screening.The expression levels of miR-218,CD133,and nestin were detected via quantitative reverse transcription polymerase chain reaction and western blot analysis, whereas the differentiation status was assessed via glial fibrillary acidic protein(GFAP ) immunocytochemistry.Using low-copy plasmid transfected cells,the distribution of CD 133-and nestin-positive cells was detected via immunofluorescence against an enhanced green fluorescent protein(EGFP ) reporter.Results:The expression levels of miR-218,CD133,and nestin in the cells transfected with SNB19-miR218 were 26.23-fold,17.9%,and 54.2%of those of SNB19-scr.The GFAP labeling index of SNB19-miR218(96.0%±3.81%) was significantly higher than that of SNB19-scr(49.6%±5.13%,t = 16.24,P < 0.0001 ).Immunofluorescence showed that the constituent ratios of the CD 133-and nestin-positive cells in the EGFP(+ ) and(-) subpopulations were significantly uneven(χ~2 = 586.38 and 658.53,respectively,P < 0.0001 ),confirming that the CD133 and nestin were downregulated specifically in the tumor cells successfully transfected with the miR-218 expression plasmid.Conclusion:miR-218 promotes glioma stem cell differentiation, and therefore downregulates CD133 and nestin expression.This effect may be an important mechanism for inhibiting the proliferation of glioma cells.

老年人癫痫是指60岁以后发病的癫痫,其发病率较高,且其病因、临床表现有其特异性,不同于其他年龄组.老年人癫痫多为继发性,病因中以脑血管疾病最常见,如高血压动脉硬化性脑血栓形成、脑出血、蛛网膜下腔出血、脑栓塞等,其次为脑肿瘤、脑萎缩、颅内感染、脑外伤、代谢性疾病等.因老年人的记忆力和认知功能减退、自诉能力差,所以老年人癫痫的表现多不典型.尤其空巢独居老人,其癫痫常难以被发现而延误诊治.老年人癫痫发作临床类型各家报告不一,有人认为老年人癫痫以部分性癫痫占优势,尤其是复杂部分性癫痫随年龄而明显增加.

Purpose To study the effects of rTMS on the expression of BDNF, NMDAR1 and SYN in hippocampal CA1 area of rats model with VaD, and to further explore the molecular mechanism of the rTMS treatment on vascular dementia. Methods Rats were randomly divided into four groups. Low-frequency stimulation group rats were accepted 0.5Hz rTMS for six weeks. High-frequency stimulation group rats were accepted 5Hz rTMS for six weeks. The expression of BDNF, NMDAR1 and SYN in hippocampal CA1 area were detected by immunohistochemistry. Results The expressions of BDNF, NMDAR1 and SYN protein in the stimulation groups were higher than that in the dementia model group (P<0.05). Conclusion rTMS had a role in the restoration treatment of vascular dementia, which may be related to the mechanism that rTMS can increase the expressions of BDNF, NMDAR1 and SYN, and affect the synaptic plasticity in hippocampal CA1 area of the VaD rats.

With the continuous deepening of the research on risk factors for vascular dementia, the gene studies associated with risk factors have also attracted great attention. This has provided a new clue for revealing the causes and pathogenesis of vascular dementia from the point view of molecular genetics, and also provided a new approach for individualized prophylaxis and treatment, This article reviews the advances in research on gene associated with risk factors for vascular dementia. Key words: vascular dementia;  risk factor;  gene polymorphism