Drug addiction is a chronic relapsing brain disease. Repeated drug exposure can cause neuroadaptations in major brain circuitries,leading to compulsive drug consumption behav-ior and relapse after abstinence.Many studies have found that intercellular signaling cascades mediated central nervous system remodeling in the rewarding circuitry and addiction associated neuroplasticity of learning and memory are important molecular mechanism of drug addiction.Studies show that extracellular sig-nal-regulated kinase (ERK)is associated with drug-mediated psychomotor activity,rewarding properties and relapse of drug seeking behaviors.Therefore,this article has reviewed the role of ERK signaling pathway in drug addiction.Research on the role of ERK signaling pathway in drug addiction will provide im-portant theoretical foundation for in-depth understanding of the molecular mechanism of drug addiction and shine a light on new molecular targets and treatment strategies for drug addiction.

In order to show the development situation and trend in plaque research, Thomson Innovation Platform-covered application of patents associated with plaque researches was quantitatively analyzed using the Thomson Data Analyzer and Thomson Innovation or other tools, which revealed the overall development situation, the main accepted countries, the main application institutions and the technological direction layout of patents associated with plaque researches.

Objective To evaluate the effect of Jian Pi Bu Shen prescription on inflammatory factors and iron metabolism in the brain of T2DM model mice.Methods A total number of 30 healthy 12-week-old male mice were used in the present study.The groups were randomly assigned to one of the following experimental groups:(1) control group:n=5,the mice were maintained on a normal diet for 4 weeks;(2) model group:n=25,the mice were maintained a high fat diet for 4 weeks.Then,the mice were deprived of food for 12 hours before a single intraperitoneal injection of streptozotocin (STZ,30 mg/kg).Then,the blood glucose levels were measured randomly 3 times within 24 hours after injection.The mice whose blood glucose was less than 16.7 mmol/l would receive another single intraperitoneal injection of STZ.Finally,we got a total number of 19 mice meeting the criteria of animal model we described above.The final 19 mice were randomized to 2 groups:diabetes group (n=10)and Jian Pi Bu Shen (JPBS) group(n=9).JPBS group received gavage administration of JPBS Prescription 7.4 g/kg/d(8weeks).Diabetes group and control group were maintained treated with saline for 8 weeks.Mice were decapitated 24 hours after the last drug treatment.The mice brain tissue slices were prepared for pathological observation.To examine the effects of JPBS prescription on neuroinflammation and iron metabolism in cerebrum and hippocampi,the relative mRNA levels of IL-6,IL-1β,DMT1,FPN1 and CP were tested by RT-PCR.Results mRNA levels of IL-6,IL-1β and DMT1 in the brains of diabetes group were higher while the levels of FPN1 and CP were lower than that of the control group (P＜0.01).Compared with diabetes group,in JPBS group,mRNA levels of IL-6,IL-1β and DMTl in cerebrum and hippocampi were decreased while the levels of FPN1 and CP were increased (P＜0.01).The brain tissue slices of diabetes group showed neuron loss and signs of neurodegeneration.But JPBS group attenuated neurodegenerative change.Conclusion JPBS prescription can protect neuron from apoptosis,suppress neuroinflammation and attenuate iron metabolism,which may be one of the mechanisms of traditional Chinese medicine in treating cognitive dysfunction.

Objective To investigate the effects of bevacizunab on the antioxidative function of human retinal pigment epithelium (RPE),in order to explore the possible mechanism of macular atrophy induced by the application of anti-vascular epithelial growth factor (VEGF) agents in age-related macular degeneration.Methods Human RPE cells were incubated in DMEM/F12 medium containing 0.25 g · L-1 bevacizumab and divided into 5 groups according to incubation period:0 hour(control),12 hours,24 hours,48 hours and 72 hours,and then the oxidative stress was induced by adding H2O2.Cell viability was measured by the CCK8 assay.MitoSox Red was used to determine mitochondrial reactive oxygen species (mtROS) production.Mitochondrial membrane potential was measured using the JC-1 assay.The expression levels of NOX4 and HO-1 were detected by RT-PCR and Western blot,respectively.Results CCK8 assay determination showed that the above treatment had no significant effect on cell viability,the cell viability of 0 hours,12 hours,24 hours,48 hours and 72 hours were (100.2 ±3.3)％,(99.2 ±2.7)％,(102.5 ±6.4)％,(103.9 ±3.7)％,(103.6 ±3.3)％,the difference was not statistically significant (P ＞ 0.05).Compared with the control group,the levels of mtROS increased at 12 hours,24 hours,48 hours and 72 hours,the difference was statistically significant (P ＜ 0.05).Mitochondrial membrane potential at 12 hours,24 hours,48 hours,72 hours were lower than the control group,the difference was significant,48 hours reached the lowest,72 hours significantly increased,but still lower than the control group.RT-PCR and western blot results demonstrated that the expression of NOX4 mRNA and protein increased at 12 hours,24 hours,48 hours and 72 hours,and reached the highest at 24 hours,then decreased significantly,but still higher than the control group,the difference was statistically significant (P ＜0.01).Compared with the control group,the expression of HO-1 mRNA decreased at 24 hours,48 hours and 72 hours,while the expression of HO-1 protein decreased at 48 hours and 72 hours,the difference was statistically significant (P ＜ 0.05).Conclusion The clinical concentration of bevacizumab can reduce the anti-oxidative function of RPE cells,which may be one of the causes of progressive macular atrophy after long-term anti-VEGF therapy.

Objective To investigate the risk factors of hepatitis B virus (HBV) reactivation after microwave ablation (MWA) and its prevention.Methods 72 patients who met the inclusion criteria were enrolled into the study.30 patients were in the control group and 42 patients in the prophylactic antivirus group.Results 8.3％ (6/72) patients developed HBV reactivation.A high HBV DNA load and no prophylactic antivirus therapy were independent risk factors of viral reactivation.Conclusion Prophylactic antivirus therapy can prevent HBV reactivation.

Objective:To investigate the change of expression of miR-7 in activated CD4+ T cells in vitro, and preliminary explore its possible significance. Methods: CD4+CD62L+T cells was purified from splenocytes of FVB mice by magnetic cell sorting system (MACS). After stimulation with anti-CD3/CD28 antibody,the relative expression of miR-7 was examined by Real-time PCR, and the expression level of CD69 molecular was analyzed by FACS. Furthermore,the relative expression of miR-7 in CD4+T cells was detected at different time points during stimulation. With the treatment of ERK inhibitor PD98059,change of miR-7 expression was de-termined by Real-time PCR. Meanwhile, the proliferation of CD4+T cells was examined by CCK-8 assay and the expression level of CD69 and CD62L molecular were analyzed by FACS. Finally,the expression of cytokines IL-6,IL-10,and IFN-γ were determined by Real-time PCR. Results:Compared with control group,the relative expression of miR-7 was increased significantly after stimulation with anti-CD3/CD28 antibody,as well as expression level of CD69 molecular was augmented(P<0. 05). In contrasted with 0 h and 24 h,the expression of miR-7 was significantly increased after 48 h and 72 h during stimulation(P<0. 05). Furthermore,the relative expression of miR-7 was significantly declined in CD4+T cells in ERK inhibitor PD98059 treatment group. Finally, the expression level of CD69 molecular,as well as cytokines IL-6, IL-10 and IFN-γ, were also decreased significantly ( P<0. 05 ) . Conclusion: The relative expression of miR-7 was significantly increased in activated CD4+T cells,closely related to ERK pathway,which provided an important foundation for successive research work on exploring the functional role of miR-7 in the CD4+T cells.

Objective To assess the effects of fenofibrate on myocardial remodeling in obese rats by echocardiography.Methods Twenty-six SD rats were fed with high fat chow to establish twenty obese rats models,which were randomly divided into two groups:obesity group (OB group,n =10) and fenofibrate group(F group,n =10).The same week-old SD rats group (n =10) was also randomly selected as normal control group.F group was given fenofibrate 60 mg · kg-1 · d-1 for 8 weeks,the other groups were given normal saline.Echocardiographic scan was performed in each group at the beginning and ending of the experiment.Twenty-four weeks later,all rats were executed and the cardiac muscle was used to histological inspect.Results After the experiment,compared with the control group,the body weight,the ventricular thickness,interventricular septal thickness and the left ventricular mass in OB group were significantly increased than those of control group(P ＜0.01),the E/A ratio was significantly decreased(P ＜0.01).Histological detection showed that myocardial structure was disordered,and that interstitial collagen was deposited in the myocardium.Compared with OB group,the parameters all above in F group were significantly improved (P ＜0.01).Left ventricular mass from echocardiography correlated well with the results from pathologic specimen (r =0.98,P ＜0.01).Conclusions Fenofibrate has beneficial effects on preventing myocardial remodeling.By general echocardiography,the effects can be assessed comprehensively and accurately.

Objective To construct the eukaryotic expression plasmid for the expression of human Connexin26 in COS-7 cells.Methods Total RNA was isolated from human peripheral blood lymphocytes and used as template for the PCR cloning of the human Connexin26 gene.The human Cx26 cDNA containing the 678 bp whole coding region of the human Connexin26 gene was amplified by PCR using specific primers and cloned into the pCI-neo vector to construct the recombinant eukaryotic expression plasmid,pCI-Cx26.The recombinant plasmid was identified by restriction endonuclease digestion,and transfected into COS-7 cells by liposome.The expression of Cx26 mRNA and the protein were analyzed by RT-PCR and SDS-PAGE,respectively.Results Restriction endonuclease digestion analysis verified successful construction of the recombinant plasmid,pCI-Cx26.The expression of Cx26 mRNA and protein in the transfected COS-7 cells were detected by RT-PCR and SDS-PAGE,respectively.Conclusion The eukaryotic expression plasmid for human Cx26 has been constructed successfully with the capability of expression in COS-7 cells.

Objective To determine attention networks impairmnet in patients with localized brain injury and to examine the characteristics of the impairment.Methods The attention network test was used to compare patients(n=59)with controls(n=53)on the efficiency of 3 anatomically defined attention networks:alerting,orienting,and executive control.Results Firstly,patients with frontal lobe injury showed a significant deficit in the executive network(frontal lobe injury,controls:(143.7±46.6),(91.6±46.4)ms,Z=-4.714,P＜0.01)and also a significant deficit in the orienting network(frontal lobe injury,controls:(71.2±35.2),(55.1±21.8)ms,Z=-2.125,P＜0.05).There was no deficit in the alerting network(Z=-0.901,P＞0.05).Secondly,the orienting network effect was significantly lower in patients with parietal lobe injury((34.9±25.2)ms)than in normal controls((55.1±21.8)ms.Z=-2.418.P＜0.05).However,there were no significant difierences between the other two networks and between the patients and the controls(Z=-1.873,-0.186.P＞0.05).Thirdly,patients with temporal lobe injury showed no deficit in the three networks(Z=-0.037,-1.224,-0.718,all P＞0.05)as well as in overall RT and accuracy(Z=-1.385,-0.699,all P＞0.05).Conclusions These results suggest that there are selective impairments of the orienting and executive networks in patients with the frontal lobe and the parietal lobe injury,while the alerting network is spared.Furthermore,the frontallobe plays a key role in the executive control.meanwhile,the orienting network is closely related with the parietal lobe.

To explore the serum miR-338-5p expression characteristics in renal transplant recipients ,and the role of regulating BAFF signal ,then investigate its biological significance.Methods:Healthy volunteers were enrolled as control group.Serum miR-338-5p was detected by real-time PCR;soluble BAFF was detected by ELISA;anti-HLA-Ⅰantibody,anti-HLA-Ⅱ antibody and anti-MICA antibody were detected by liquid chip technology.SPSS17.0 software was applied.t-test was used to compare the means of two independent samples;Paired samples t-test was used to compare the means of two paired samples;Spearman method and Pearson method were used to analyse the correlation;P<0.05 was considered to be statistically significant.Results: Compared with healthy controls,serum miR-338-5p in renal transplant recipients decreased significantly (P<0.001),while serum BAFF increased significantly (P<0.01).Serum miR-338-5p levels within 1 year post-transplantation were significantly lower than that of more than 1 year post-transplantation (P<0.01);Serum miR-338-5p levels within 3 years post-transplantation were significantly lower than that of more than 3 years post-transplantation (P<0.01);To all research objects,serum miR-338-5p was significantly negatively correlated with serum BAFF (r=-0.51,P<0.001),and serum miR-338-5p was significantly negatively correlated with anti-HLA-Ⅱ antibody(r=-0.322, P<0.05);Serum miR-338-5p within 3 years was significantly negatively correlated with anti-HLA-Ⅱantibody (r=-0.423,P<0.05), and serum miR-338-5p within 3 years was significantly negatively correlated with anti-MICA antibody(r=-0.411,P<0.05);Serum miR-338-5p more than 3 years was significantly positively correlated with anti-MICA antibody(r=0.486,P<0.05),and Serum miR-338-5p more than 3 years was significantly positively correlated with anti-HLA & MICA antibody(r=0.578,P<0.01).Conclusion:miR-338-5p may directly or indirectly target BAFF signal ,and participate antibody mediated immune response by regulating its target genes and interfere with the long-term survival of transplanted renal.