Eestablishing a scientific supervision system is essential to achieve a better environment for teaching and learning and improve teaching quality in medical college.We took undergraduate education evaluation as an important supervising subject and made a scientific evaluation program for teaching,learning,and testing,based on specific features of medical college.The practice of the program proves to be successful.We present the main contents in this article.

Objective:To prepare poly-L-lactic acid(PLLA)electrospun nanofibers carrying icariin(ICA)(ICA /PLLA)and to evaluate the effects of the ICA /PLLA on MC3T3-E1 cells.Methods:ICA solution was dispersed into PLLA solution,and electrospun fibers were fabricated by W/O emulsion method.The morphology of ICA /PLLA was observed by SEM.The in vitro release kinetics of ICA /PLLA was examined.The attachment of MC3T3-E1 cells on ICA /PLLA was examined by propidiumiodide(PI)labling and ob-served under fluorescent microscope.The proliferation of the cells was measured by MTT assay.The differentiation of the cells was ob-served by alkaline phosphatase (ALP)assay.Results:In vitro,ICA was effectively released from ICA /PLLA for 22 days,cells were attached well on the surface in all groups,ICA did not affect the proliferation of MC3T3-E1 cells(P >0.05),but increased the ALP activity(P <0.05)of the cells.Conclusion:ICA /PLLA can effectively control the release of ICA and promote the differentiation of MC3T3-E1 cells.

Objective To investigate the antitumor activity of the procaspase-3 activator SM-1 in BGC-823 cells in vivo and in vitro and the mechanisms.Methods The inhibitory effects of SM-1 on proliferation of BGC-823 cells were evaluated using MTT method, the cell apoptosis rate was detected by flow cytometry, and the expression of caspase-3 protein and procaspase-3 mRNA was detected by Western blotting and RT-PCR, respectively.SM-1 Antitumor activity was evaluated using the xenograft of BGC-823 cells in nude mice.Results SM-1 effectively inhibited the proliferation in vitro and in-duced apoptosis of BGC-823 cells in a dose-dependent manner.After treatment with SM-1 for 48 h, the protein expression levels of caspase-3 and mRNA expression levels of procaspase-3 were increased.SM-1 significantly inhibited growth of BGC-823 xenograft tumor at the 300 mg/kg dose and the inhibition rate was 56.3%(P<0.05).Conclusion SM-1 can significantly inhibit the tumor growth of BGC-823 cells in vivo and in vitro.The mechanism is possibly related to the activation of procaspase-3 and induced apoptosis of tumor cells.

Objective To describe different types of chromosomal abnormalities on male infertility.Methods From May 2006 to May 2012,2034 infertile males with genetic counseling underwent chromosome karyotype analysis,semen routine examination and reproductive hormones levels detection.The data from them were analyzed.Results 267 cases of chromosomal abnormalities were detected in 2034 cases (13.13％).258 cases underwent semen routine examination in 267 cases with chromosomal abnormalities,of which 190 cases of azoospermia,58 cases of oligozoospermia,10 cases of semen normal.In 267 cases of chromosomal abnormalities,including 169 cases (63.30％) of number abnormalities,mainly with azoospermia,157 cases of Klinefelter syndrome (KS) (58.80％),7 cases of 47,XYY (2.62％),4 cases of Turner syndrome (1.50％),1 case of marker chromosome (0.37％) ; 49 cases (18.35％) of structural abnormalities mainly with oligozoospermia,including 32 cases of chromosomal translocations (11.99％),17 cases of inversion (6.37％) ; 4 cases of sex reversal (1.50％) with azoospermia; 45 cases of chromosome polymorphism (16.85％) mainly with oligozoospermia.Non-mosaicism KS patients' age,testicular volume,semen volume,and serum reproductive hormones levels were compared between different groups of semen results,and there were no significant difference except age.Conclusions Chromosome abnormalities were the most important genetic causes of abnormal semen quality and male infertility.It is necessary to be performed chromosome karyotype analysis for infertile males.

Objective To study the relationship between small Y and azoospermia factor (AZF)microdeletions and the effect on male infertility.Methods Data of 379 infertile males of chromosomal karyotype analysis from May 2010 to October 2011 were investigated.Patients with small Y chromosome were also performed C banding and AZF microdeletions,and their fathers and brothers were offered the same examinations.Results Eight patients were small Y chromosome,and their fathers or brothers' chromosome karyotypes were consistent with the probands.Among the 8 cases,there were 3 patients with AZF microdeletions,while their fathers and brothers didn't have microdeletions.Another 5 cases of small Y and their fathers did not exist AZF microdeletions.Conclusions The small Y karyotype is not the key factors that cause male infertility.The reason for infertile patients with small Y and AZF microdeletions was maybe the microdeletions.However,patients with small Y but without AZF microdeletions are not important to male infertility.

Objective To study the relationship between Y chromosome abnormalities and AZF microdeletions in males with reproductive failure.Methods A case-control study was conducted in 2694 reproductive failure men with age ranges from 23 to 49 years old from the Institute of Reproductive Medicine of Jilin Province.Patients were divided into three groups:spermatogenic failure group (n =1332),disadvantage pregnancy outcomes group (n =994) and adverse birth outcomes group.All patients underwent chromosomal karyotype analysis (G-banding).AZF microdeletions were further investigated in patients with Y chromosomal abnormalities by PCR.The Chi-square test was used to compare the frequency of Y chromosome abnormalities in three groups.Results Of the 51 cases of Y chromosome abnormalities (1.89％,51/2694),32 were (2.40％,32/1332) in the spermatogenic failure group,15 were (1.51％,15/994) in disadvantage pregnancy outcomes group and 4 were (1.09％,4/368) in adverse birth outcomes group.There was no significant difference in Y chromosome abnormalities among different groups (x2 =3.895,P ＞0.05).AZF microdeletions were detected in 10 cases (19.61％,10/51) of Y chromosome abnormalities patients with spermatogenic failure.Conclusions The incidence of Y chromosomal abnormalities in three reproductive failure groups is similar.Chromosome karyotype analysis and AZF microdeletions examination could identify the genetics etiology in males with reproductive failure.

Objective To identify the RNA interference action of recombined pSUPER-NRF2 vectors for the expression of NRF2 gene in colon cancer cells.Methods Two sequences targeting at the ORF of NRF2 were cloned into RNA polymerase III based expression vector pSUPER.These recombinants were transfected into Caco-2 cells.Fluorescence microscopy and flow cytometry were performed after transfection with pEGFP-N1 plasmids to observe the lipfectin transfection efficiency.The stable cells were selected in medium(48 h) after co-transfected pEGFP-N1 with G418. The expression of NRF2 was assayed by RT-PCR and Western blot.Results The construction of the recombinant expression vector pSUPER-NRF2-A1、B1 and its control vector pSUPER-NRF2-A2、B2 were successfully confirmed by the results of enzyme digestion,electrophoresis and sequencing. The transfection efficiency was 45.6%,74.3%,53.0% and 46.5% respectively in 24,48,72 and(96 h).We compared the ability of these vectors to inhibit NRF2 in a transient and stable expression experiment.Importantly,pSUPER-NRF2-B1 was able to knockdown NRF2 expression.pSUPER-NRF2-A1 only had a moderate activity,whereas pSUPER-NRF2-A2、(B2 were) inactive in this assay.Conclusion The constructed pSUPER-NRF2-A1、B1 showed an interfering effecton the expression of NRF2 and product the stable cells with low NRF2 expression.Therefore,the pSUPER vector constitutes a new and powerful system to analyze NRF2 gene function in colon cancer.

[Objective] To investigate the possible effect of microRNA-374 (miR-374) expression on tumor cells' proliferation and invasion and particular mechanism.[Methods] MiR-374 overexpression lentiviral vector (Lv-miR-374) and a control lentiviral empty vector (LEV) were stably transfected into human glioma U251 and U87 cells,to evaluate the effect of miR-374 on cell proliferation and invasion ability.Target relationship between miR-374 and PTTG were researched by dual luciferase report gene assay.Expression level of correlative signaling pathways of the downstream gene protein was analyzed by Western blot.[Results] We revealed that the overexpression of miR-374 dramatically suppressed glioma cell growth and invasion in vitro.Target relationship between miR-374 and PTTG was confirmed by dual luciferase report gene assay.And decreased protein expression of PTTG,bFGF,AKT,MMP2,and p70S6K was consistent with the effect of miR-374 overexpression.[Conclusion] Decreased miRNA-374 is an unfavorable prognosis marker and promotes glioma cell growth and invasion via direct targeting PTTG.Our findings provide new insights into the role of miR-374 in the development of gliomas,and implicate the potential application of miR-374 in cancer therapy.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, with complicated etiology and pathogenesis. As a heredity-environment-metabolism-stress disease, the genetic factors play an important role in the pathogenesis of NAFLD. In order to identify the role of genetic factors in the pathogenesis of NAFLD and to find out new clinical therapeutic targets, the present review summarizes the susceptibility genes of NAFLD, especially those identified by genome-wide association study, including the genes of patatin-like phospholipase domain-containing 3, leptin receptor, adiponectin, and tumor necrosis factor-ɑ.

Aim To explore the protective effects of lithium chloride ( LiCl ) on neurous injuries and phos-phorylation of tau protein at serine262 induced by okada-ic acid( OA) . Methods The neuroblastoma SK-N-SH cells were differentiated by all-trans-retinoic acid ( AT-RA) . The differentiated SK-N-SH cells were treated with OA to establish the Alzheimer′s disease cellular model. SK-N-SH cells′ viability and proliferation were measured by SRB test. Giemsa staining was used to observe cell morphology. The neurite length of SK-N-SH cells was measured by Image-Proplus software. Syn-aptophysin and phosphorylated tau protein at serine262 expression levels were tested by Western blot. Results The SK-N-SH cells which were treated with 10 μmol ·L-1 ATRA for 7 days displayed mature neuronal fea-tures. The synaptic length of SK-N-SH cells became longer. And the levels of serine262 phospho-tau was sig-nificantly elevated. 20~100 nmol·L-1 OA effectively inhibited the viability of differentiated SK-N-SH cells in a concentration-dependent manner and in a time-de-pendent manner. The OA treatment induced obvious synaptic atrophy in differentiated SK-N-SH cells. And the phosphorylation level of tau protein serine262 also greatly increased. The pretreatment with 10 mmol · L-1 LiCl significantly ameliorated the synaptic atrophy, the decrease of synaptophysin expression and the in-crease of tau phosphorylation at serine262 induced by OA in differentiated SK-N-SH cells. Conclusion LiCl could effectively inhibit OA-induced synaptic atro-phy in differentiated SK-N-SH cells, and it could also result in the increase of synaptophysin expression and the decrease of the phosphorylation of tau protein at serine262 .