Drug addiction is a chronic,relapsing brain disorder,which develops,in part,because of aberrant learning and memory. Accumulative studies during recent decades demonstrated that addictive drug hijacks the normal memory circuit in the brain to form a long-lasting drug reward memory,which determines relapse to addictive drug. In this review,we will describe what has been learned about drug reward memory,especially focused on one of the associative drug reward memory models,drug-induced conditioned place preference. Drug reward memory is a dynamic process,which consists of several stages,including acquisition,consolidation,maintenance,retrieval,reconsolidation and extinction. Interventions with pharmacological in these memory processes will differentially regulate drug reward memory. Furthermore , the recently developed novel pure behavioral procedure according to the hypothesis of memory processes,e.g. post-retrieval extinction,could erase drug reward memory,which shows more advantages than the pharmacological medications that used in memory studies. Finally, we discussed two major methodological issues in drug reward memory,procedure and timing,which should be carefully considered when designing the related studies and interpreting the results from related studies. So far,it is not sure whether it is feasible to develop a pharmacological medication that only erases drug reward memory without impairing normal memories,we propose that inhibition of drug reward memory would be a good strategy to limit the risk of relapse to addictive drug. Although current findings on drug reward memory benefits little for treatment of drug addiction,the ongoing studies on drug reward memory will provide a promising strategy for reducing the risk of relapse to addictive drug.

Vitexin, a natural flavonoid compound, has extensive pharmacological activity. In recent years, many studies have re-vealed that vitexin has significant protective effects on central nervous system and peripheral nervous system, including anti-memory impairment, anti-epilepsy, anti-ischemic hypoxic brain damage, anti-depression, analgesia, etc. Vitexin exerts neuro-protective effects through the mechanisms of multiple pathways and multi-targets, such as reducing free radical level, inhibiting neuronal apoptosis, modulating inflammatory factors and related pathways, and regulating neurotransmitters and related recep-tors. This review mainly discusses the neuroprotective effects of vitexin and its underlying mechanisms.

This review summarized some hot research fields in pharmacological effects of sinomenine such as anti-inflammatory, immunosuppressive, and anti-tumor effects. In addition to our exploration of its antinociceptive effect, we summarized above-mentioned pharmacological effects of sinomenine and its underly-ing mechanism, in order to provide an evidence for its clinical use.

It is traditionally thought that interleukins are produced by immunocytes. However, abundant evidence indicates that neuron and neuroglia also produce and excrete interleukins. Brain derived interleukins have reciprocal action with multiple neurotransmitters, and influence animal's behavior, learning and memory. Moreover, brain derived interleukins are involved in Alzheimers disease, depression and so on. Further investigation on brain derived interleukins may improve in understanding the pathophysiology of some related diseases.

Aim To investigate metabolomic profiles of acute myocardial ischemia (AMI) in rat plasma and explore the intervention effects and its mechanism of leonurine using a metabolomics approach based on nuclear magnetic resonance (NMR).Methods The plasma metabolomic characteristics in rats of sham group,AMI model group,and leonurine-treated group were detected by 1H NMR,and the different metabolites between AMI group and sham group or leonurine-treated group were analyzed by pattern recognition and multivariate data analysis.Results Orthogonal partial least squares discriminant analysis (OPLS-DA) demonstrated that six metabolites related to AMI were screened out,including alanine,lysine,glycine,creatine,N-acetyl glycoprotein,and O-acetyl glycoprotein and all their levels were elevated in AMI group compared to sham group.Treatment of leonurine decreased the levels of alanine,lysine,and glycine,and increased the levels of choline,phosphocholine,and scyllo-inositol compared with the model group.Conclusions Leonurine can improve amino acid metabolism disorder under AMI conditions and enhance the function of choline and inositol pathway,which may explain its cardioprotective effect.The developed metabolomics approach in this study is a powerful tool for the investigation of the cardioprotective effect of leonurine and provide a new insight to understand its pharmacological mechanism.

Here we reported a research project based on Black-board to integrate medical curriculum .The key points of this research is application of clinical cases as teaching data and facilitate learning of knowledge following the principle of learning by doing and , input the concept of precision medicine and informatics in learning process with an individually designed framework of learning .The learning outcome is evaluated with big data tech-nology and thus creates a student-centered pathway of medical education .

[ ABSTRACT] AIM:To determine the role of transcription factor Bach1 in the functions of human microvascular en-dothelial cells ( HMVECs ) .METHODS: Bach1 siRNA was transfected into HMVECs to knock down the expression of Bach1.In vitro endothelial cell tube formation assay in Matrigel culture was used as a surrogate assay for angiogenic poten-tial.Migration of HMVECs was determined by using Transwell chambers.Cell proliferation was measured by CCK-8 assay. Real-time PCR, Western blotting, and ELISA were employed to determine mRNA expression and protein level.Reporter as-say was performed to determine vascular endothelial growth factor ( VEGF) transcriptional activity.RESULTS:Knockdown of Bach1 expression in HMVECs led to an increase in the tube formation and increased endothelial cell migration ability, whereas it has little effect on cell proliferation.Bach1 silencing increased the mRNA and protein expression of heme oxygen-ase-1 (HO-1), and enhanced VEGF transcriptional activation, and mRNA and protein expression.CONCLUSION:Bach1 silencing increases HO-1 and VEGF expression, thus promoting the cell migration and tube formation of HMVECs, indicating that Bach1 is a repressor for angiogenesis.

Objective To evaluate the performance of serum small dense low-density lipoprotein cholesterol(sdLDL-C) kit using enzymic method and investigate the clinical value in coronary heart disease (CHD).Methods According to the standard of Clinical and Laboratory Standards Institute (CLSI),evaluae the precision,linearity ranges,reportable range and accuracy of sdLDL-C kit.The 683 patients with coronary heart disease (CHD,423 men and 260 women,age 35-79 years) who were diagnosed at the people's hospital of Peking university from October 2015 to October 2016 were divided into two groups.The treated group include 571 patients(CHD1,342 men and 229 women,age 40-79 years) which taking lipidlowering drugs and the other include 112 cases (CHD2,81 men and 31 women,age 35-70 years)without Lipid-lowing treatment.Besides,the Control group contains 472 healthy persons (274 men and 198 women,age 41-75 years),were collected from the people's hospital of Peking university between April and August 2016.The liver function,renal function,blood glucose and blood lipid in CHD group(CHD1,CHD2) and healthy control group were detected.The new enzyme assay kit was used for the determination of sdLDL-C.The data of normal distribution were compared by independent t test between the two groups.The Mann-Whitney U nonparametric test was used for comparison between two groups.Results The precision of sdLDL-C kit examination was in compliance with manufacturer'statement.The linearity was good in 0.11-2.42 mmol/L(Y =1.008 9X + 0.024 8,R2 =0.998 2),the scope of the report is 0.11-4.84 mmol/L.The level of sdLDL-C in CHD group was significantly higher than that in healthy control group,it has a statistical significance[0.824 (0.443) mmol/L,0.609 (0.361) mmol/L;Z =-5.603,P ＜ 0.001].The level of sdLDL-C in (CHD 1) was lower than (CHD 2) [0.761 (0.479) mmol/L,0.888(0.426) mmol/L;Z=-2.304,P＜ 0.021].After additional adjustment for various tradition cardiovascular risk factor,including ages,sex,CHO,TG,Hs-CRP,Lp(a),and GLU,the highest quartile of sdLDL-C comparison to the bottom quartile,the OR was 3.02,(95％ CI,1.15-9.05) for CHD.Conclusions Experiment data demonstrated that sdLDL-C kit using enzymic method has good performance in the precision,linearity ranges,reportable range and accuracy,sdLDL-C serum level was significantly higher in CHD group.

Objective: To investigate the effects of Wilms’tumor 1-associating protein (WTAP) on proliferation, migration and invasion of human lung adenocarcinoma A549 cells. Methods: Human lung adenocarcinoma cell line A549 and HEK293T cells were chosen for this study. Two sets of shWTAP interference sequences were designed to construct lentiviral vector plasmid. Human lung adenocarcinomaA549 cells were infected after packaging lentivirus in HEK293T cells, and the control group was transfected with 277 empty vector plasmid. The mRNAand protein expression levels of WTAPinA549 cells were detected by qPCR and WB. Changes in proliferation, migration and invasion of A549 cells were detected by BrdU assay, cell scratch healing assay and Transwell assay, respectively. Results: Two plasmids, shWTAP-1 and shWTAP-2, were successfully constructed. Compared with the control group, the mRNA and protein expression levels of WTAP were significantly down-regulated inA549 cells with WTAP knockdown (both P<0.05), and the proliferation, migration and invasion ability of cells were significantly decreased (all P<0.05). Conclusion: Knockdown of WTAP significantly inhibited the proliferation, migration and invasion of human lung adenocarcinoma A549 cells. The expression of WTAP gene is associated with the occurrence and development of lung adenocarcinoma. WTAP may be a potential target for the diagnosis and treatment of lung adenocarcinoma.