Object: To explore the effects and the influent agents of early education on the healthy termed infants. Methods: 52 healthy termed infants voluntary to the exercise center as experimental group were early educated. The other 52 infants as control group were in the same elementary conditions comparing to the experimental group. The experimental group was trained the corresponding projects and examined DQ at the beginning and the 3 rd,6 th,9 th month after training. The control group was only examined DQ at the beginning and after 9 months. Results:①At the 9 th month after training, DQ of the experimental group was improved 21.9?13.6, which was much 7 times higher than that of the control group, which was improved 3?3.0 (P

90 ). ③For the experimental group at baseline, DQ of the gross movement was the highest (71.5?10.5), while that of the other four areas were similar (fine movement 56.7?10.4, adaptability 59.6?12.5, language 54.3?11.7, social 56.8?14.7).Conclusions:Early intervention had significant effects for the development of children with mental retardation, which medicine has less role.

Objective To understand the molecular mechanism by which protein kinase C? mediates multidrug resistance of human glioma cell line SHG-44.Methods SHG-44/ADM was constructed by stepwise concentration increasing method and intermittent administration method.SHG-44/WT and SHG-44/ADM were treated by PKC? reactivator PMA and PKC? inhibitor staurosporine,then the expressions of PKC? and MDR-1 were detected by Western blotting,the PKC? activity was assayed by kinase,and ADM accumulation was determined by fluorescence spectrometry.Results PMA increased PKC? activity and MDR-1 protein expression and activity.Staurosporine was able to block PKC? activity and decrease MDR-1 expression and activity.Conclusion Multidrug resistance in human glioma cells is mediated by PKC? via MDR-1 pathway.

Objective To systematically review the efficacy and safety of photodynamic therapy (PDT) and intravitreal vascular endothelial growth factor (VEGF) inhibitors in the treatment of polypoidal choroidal vasculopathy (PCV),and to investigate the primary treatment tentatively.Methods A systematic search of Pubmed,Embase,the Cochrane Library and the Wanfang Data was performed to identify all comparative studies that compared the outcomes of PDT alone,intravitreal VEGF inhibitors alone and combined intravitreal VEGF inhibitors and photodynamic therapy.Outcomes of interest included the regression and recurrence rate of polypoidal lesions,best corrected visual acuity (BCVA),central retinal thickness (CRT),therapeutic times,and the occurrence rate of adverse events.2 randomized controlled trials (RCT) and 19 non-RTCs were identified.According to treatment methods,the data extracted was classified to 3 groups,analyzed with odds ratio (OR),weighted mean difference (WMD) and 95％confidence interval (95％CI).Results Meta-analysis suggests that the regression rate of polypoidal lesions (OR=0.34,0.07;95％CI=0.13-0.88,0.02-0.36) and BCVA (WMD=0.25,0.11;95％CI=0.14-0.36,0.01-0.21) in combined therapy group were significantly better than those in PDT group and intravitreal VEGF inhibitors group (P＜0.05).The recurrence rate of polypoidal lesions in PDT group was significantly lower than intravitreal VEGF inhibitors group (OR=0.35,95％CI=0.16-0.74,P=0.006).BCVA (P=0.025) and the occurrence rate of adverse events (OR=60.36,95％CI=6.04-603.50,P=0.000 5) in intravitreal VEGF inhibitors group were significant better than PDT group.Conclusions Combined treatment appeared to be superior to PDT alone or intravitreal VEGF inhibitors alone.Combined treatment takes priority over all others in the primary treatment of PCV.

Balb/c mice were immunized by intraperitoneal iniection of group A erythrocytes. Immunized spleen cells were fused with Sp2/0 murine myeloma cells from the solid tumour. After 10～15 days of incubation at 37℃ CO_2, the supernatants were screened for the agglutinabal antibodies. Three hybridoma cell lines secreting high titer and specific monoclonal anti-A antibodies were established.These hybridoma cells have the ability of constant seceting antibodies which belong to the IgM class. The specificity monocloal anti-A sera was the same as the human anti-A sera.

Objective To study the effects of extracellular-signal regulated kinase mitogenactivated protein kinase (ERK-MAPK) signaling pathway inhibition on histone phosphorylation and the related gene expression in human colorectal cancer cells.Methods Two human colorectal cancer cell lines (SW1116 and HCT116) were cultured and treated with gradient(0,20,40/μmol/L) doses of ERK-MAPK signaling pathway inhibitor U0126.Cell viability was determined by cell counting kit 8 (CCK-8) assay.Cell cycle distribution was assessed by flow cytometry.The expression levels of histone H3 kinases including ribosomal S6 serine-threonine kinase (RSK-2) and mitogen-and stressactivated protein kinase 1 and 2 (MSK1 and MSK2),and the levels of histone H3 (Ser10) phosphorylation and c-Fos protein were detected using Western blotting.Results Treatment of these two human colorectal cancer cell lines with ERK-MAPK inhibitor resulted in a time and dose-dependent inhibition of cell proliferation significantly. Proliferation rate of HCT116 was reduced to 47% at 72 hours after 40/μmol/L U0126 treatment. Cell cycle analysis showed that the percentage of phase G0/G1 cells significantly increased (P<0. 01) and the percentage of phase S cells decreased (P<0.01) after treatment with ERK-MAPK inhibitor. The expression of MSK1 and RSK2 reduced obviously in both of human colorectal cancer cell lines treated with U0126, which resulted in a 28% and 40% reduction of levels of MSK1 and RSK2 as compared with control HCT116 cells respectively,while no detectable change in the expression of MSK2 was found. Consistent with this, the expression level of histone H3 (ser10) phosphorylation was markedly down-regulated by ERK-MAPK inhibitor, and the related protein c-Fos expression decreased accordantly. Conclusions Decreased ERK-MAPK signaling pathway may reduce histone H3 (Ser10) phosphorylation via suppression of the activity of histone H3 kinase including MSK1 and RSK2, but not MSK2, consequently decrease the expression of c-Fos protein, which results in the inhibition of colorectal cancer cells proliferation.

Cytochrome P450 (CYP450) is a key element in the Ganoderma triterpenoid biosynthetic pathway. The catalytic reaction process for CYP450 requires NADPH / NADH for electron transfer. After searching the genome dataset of Ganoderma lucidum, the unique sequence encoding CYP450 and NADPH were discovered, separately. The open reading frames of GLCYP450 and GLNADPH were cloned separately using RT-PCR strategy from G lucidum. The appropriate restriction enzyme cutting sites were introduced at the 5' and 3' ends of gene sequence. The genes of GLCYP450 and GLNADPH were recombined into the yeast expression vector pESC-URA, leading to the formation of the yeast expression plasmid pESC-GLNADPH-GLCYP450. This study provides a foundation for researching Ganoderma triterpene biosynthesis using the approach of synthetic biology.

ObjectiveTo investigate the related factors which influencing endoscopists in the accuracy of diagnosis of chronic atrophic gastritis (CAG). Methods With retrospective analysis method,from January to December in 2009,10 765 chronic gastritis cases underwent endoscopy examination in Renji Hospital,school of medicine,Shanghai Jiaotong University were collected.The influence of congestion and exudation,gastric ulcer,bile reflux,gastric polyps and H.pylori infection under endoscopy on CAG endoscopic and pathological diagnosis was analyzed.ResultsThe percentage of histopathological diagnosed CAG was 69.41％,endoscopic diagnosed CAG was 54.27％. The coincidence rate was 62.30％.2575 cases were H.pylori positive (23.92％),the coincidence rate between endoscopic and histopathological diagnosis in H.pylori positivc cascs was 90％.of that of H.pylori negative cases (β=-0.1067,P＜0.05).The coincidence was positively related to age.For each 1 year increase in age,the coincidence rate increased by 0.01 time [OR=exp(0.00855)=1.01]; For each 10-year increase in age,the coincidence rate increased by 0.09 time [OR=exp(0.0855) =1.09].The coincidence rate was negatively related to congestion and exudation.The coincidence rate of CAG between endoscopic and histopathological diagnosis in cases with congestion and exudation was 40％ of that without congestion and exudation (β=-0.1067,P＜0.01).ConclusionCAG diagnosed under endoscopy was somewhat subjective and should be combined with histopathological analysis.The patients' age,H.pylori infection,congestion and exudation may have influence on the coincidence rate between endoscopic and histopathological diagnosis of CAG.

Objective To investigate the effect of folic acid on the DNA methylation of tumorrelated genes promoters in healthy human peripheral blood mononuclear cells(PBMC). Methods Ten healthy volunteers were divided into two groups, and were randomized to receive either 5 mg folic acid (n=5)or placebo(n = 5) , one time per day for 3 months. The serum folic acid concentration was detected with chemiluminescence enzyme immunoassay kit before and after the intervention. The methylation statuses of five tumor-related genes promoter, including oncogenes c-myc, c-Ha-ras,tumor suppressor genes p16INK4A, E-cadherin and mismatch repair gene hMLH1 in PBMC were detected by bisufite sequencing. Results After folic acid intervention, the level of serum folic acid increased significantly in intervention group (t= -4. 739,P<0. 05) , however no significant difference in control group. After three-month folic acid intervention, the level of methylation of oncogene c-myc promoter increased from 4%, 3. 3%, 4. 1% before intervention, one week after intervention, one month after intervention respectively to 8%(t= -4. 079,P<0. 05), while no significant change in placebo taken group. Before and after the folic acid intervention, there was no significant difference of DNA methylation of other tumor-related genes promoter, including c-Ha-ras、E-cadherin、p16INK4Aand hMLH1. Conclusion Folic acid intervention can up-regulate DNA methylation of oncogene c-myc promoter, but can not affect the promoter methylation status of tumor suppressor genes E-cadherin,p16INK4Aand hMLH1.