Aim To investigate the role of fenofibrate (FF),a selective PPAR-? agonist,in cardiac hypertrophy induced by high glucose and insulin (HGI) and its mechanisms related to nitric oxided (NO) signal transduction pathway. Methods The cultured neonatal rat cardiomyocytes were used to observe the effects of FF on cardiomyocyte hypertrophy induced by HGI (glucose at 25.5 mmol?L-1 and insulin at 0.1 ?mol?L-1),and the cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area,protein content,and atrial natriuretic factor (ANF) mRNA expression. The expressions of mRNA and protein were assayed by Real-time PCR and Western blot,as well as NOS activity and NO concentration in cultured media were determined by using the spectrophotometry and nitrate reluction method.Results In cultured cardiomyocytes,FF (at 0.1,0.3 and 1 ?mol?L-1) could inhibit the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P

Aim To study the role of calcineurin signal transduction pathway in the anti-hypertrophic effect of L-arginine in vivo and in vitro.Methods The hypertrophic effects was assayed by calculating the right ventricular hypertrophy index(RVHI=right ventricle weight/left ventricle and septum weight),and atrial natriuretic peptide(ANP)mRNA expression in rat right ventricle hypertrophy model induced by monocrotaline(MCT) or by measuring the cell diameter,protein content,and ANP mRNA expression in hypertrophic cardiomyocyte induced by prostaglandin F2?(PGF2?).For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura 2/AM as a fluorescent indicator.ANP and CaN mRNA expressions,and expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blot,respectively,in vivo and in vitro.Results In MCT-hypertrophic model,prevention-and treatment-administration of L-arginine,a nitric oxide(NO) precursor,200 mg?kg-1?d-1,could obviously inhibit the elevated RVHI and ANP mRNA expression;similar to that found in vivo.Addition of L-arginine 1 mmol?L-1 could markedly inhibit the increased cell diameter,protein content and the expression of ANP mRNA in the hypertrophic cardiomyocyte induced by PGF2? 100 nmol?L-1,and it could also decrease the elevated [Ca2+]i in vitro;notably,the above dose or concentration of L-arginine could blunt the elevated expressions of calcineurin mRNA and the calcineurin-,NFAT3-,GATA4-proteins induced by MCT or by PGF2?.These effects of L-arginine were blocked by NG-nitro-L-arginine-methyl ester,a NO synthase inhibitor,in vivo and in vitro.Conclusion These results suggest that calcineurin signal transduction pathway may play an important role in the NO-induced inhibition of cardiac hypertrophy.The anti-hypertrophic effects of L-arginine may involve the decrease of [Ca2+]i,and then inhibit the activated calcineurin pathway,through the release of NO.

ObjectiveTo enhance the fund efficiency of dental research programs supported by National Natural Science Foundation (NSFC) and to reveal the achievements and progresses of the funds.MethodsThe data of programs in dental and craniofacial field supported by NSFC from 1999 to 2006 and completed between 2003 and 2009 were collected based on the final reports by the investigators.The data of personnel training,research publication,patent,awards,and academic communication at domestic and international levels were all collected and analysed. Results There were 307 grants in total,including 185 general programs,73 Young Scientists Funds,13 regional funds,3 Key Programs,1 National Science Fund for Distinguished Young Scholars and 32 others.An average of 4 postgraduate students was trained by each program.In general,the outcomes of general programs were better than those of Young Scientists Fund,and the latter was better than regional fund.There was steady increase each year in the amount of papers published in SCI journals,and about half of the investigators published SCI papers.In addition,9 patents were registered and 13 prizes were won, and the investigators participated 610 domestic and international exchanges.Conclusions The continuously increase of NSFC support in dental field has led to substantial achievement,although patent application,the quality of papers and novel ideas need to be improved.

AIM: To study the role of peroxisome proliferator-activated receptor-α (PPAR-α) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS: The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF), a selective PPAR-α agonist, on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 μmol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS: In cultured cardiomyocytes, HGI induced profound change of hypertrophic morphology, the significant increase in cell surface area, protein content and ANF mRNA expression compared to those in vehicle control (P<0.01), but the expressions of PPAR-α mRNA and protein decreased significantly (P<0.05). At the same time, the expression of cyclooxygenase 2 (COX-2), one of the PPAR-α downstream effectors was obviously elevated (P<0.05). However, FF (0.1, 0.3 and 1 μmol/L) inhibited the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P<0.01). FF at concentration of 0.3 μmol/L increased the expressions of PPAR-α in both mRNA and protein levels (P<0.05) and inhibited the expressions of COX-2 (P<0.05), which were abolished by MK 886 (0.3 μmol/L), a selective PPAR-α antagonist (P<0.05). CONCLUSION: PPAR-α signal transduction pathway and its downstream effector COX-2 might involve in the cardiomyocyte hypertrophy induced by HGI.

Aim To study the role of histone acetyla-tion and its involvement in the depression-like behav-iors of rats induced by chronic unpredictable stress (CUS ). Methods Thirty male Sprague Dawley (SD ) rats were randomly divided into control group and model group.The method of solitary condition with CUS for consecutive 28 days was used to establish the rat depression model.The open-field test (OFT)and the forced swimming test (FST)were used to evaluate the depressive behaviors of rats;the real time PCR was used to detect the change of HDAC2 mRNA, and Western blot was used to determine the protein expres-sions of H3,H4,acH3 and acH4 in the prefrontal cor-tex and hippocampus of rats.Results Model group showed obvious depression-like behaviors with decrea-sing locomotive activity in OFT (P <0.01 )and in-creasing immobility time in FST (P<0.01),up-regu-lating the mRNA and protein expression of HDAC2 (P<0.0 1 ),and down-regulating the protein expression of acH3 and acH4 (P<0.01)in the prefrontal cortex and hippocampus significantly,compared with control group.Conclusion The mechanism of depressive be-haviors of rats induced by CUS may be associated with down-regulating the level of histone acetylation modifi-cation.

AIM:To study the role of peroxisome proliferator-activated receptor-? (PPAR-?) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS:The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF),a selective PPAR-? agonist,on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 ?mol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area,protein content,and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS:In cultured cardiomyocytes,HGI induced profound change of hypertrophic morphology,the significant increase in cell surface area,protein content and ANF mRNA expression compared to those in vehicle control (P

To improving the teaching quality of the pharmacology theory teaching,we adopt questionnaire to understand the students’ request of teaching method and teaching content,thus to elevate the teaching overall level by raising their ability to teach and study.

Objective To investigate clinical efficacy of simultaneous integrate boost for glioblastoma with intensity?modulated radiotherapy ( SIB?IMRT). Methods A total of 46 patients with glioblastoma who underwents SIB?IMRT from January 2013 to August 2014,were retrospectively analyzed. Toxicity after completion of SIB?IMRT were assessed. Kaplan?Meier method was used to analyze survival and progression?free survival. Multivariate analyses were performed to determine significant prognostic factors. Results There was no patients delayed by more than grade 3 radiation toxicity. The median overall survival and 1?year survival rates was 69 weeks and 73%,respectively. The progression free survival and 1?year progression?free survival rate were 43 weeks and 39%,respectively. The pattern of failure was identical (9 Local, 7 distant and 0 marginal recurrence). Multivariate analyses show that temozolomide concurrent chemoradiotherapy were independent factors correlated to prognosis. Conclusions The preliminary results demonstrate that SIB?IMRT for glioblastoma appear to be effective and safe. With the limted number of patients in this group,SIB?IMRT could be used for treating glioblastoma with caution,which deserves further study.

Aim To investigate the effect of GW0742 on the endothelial dysfunction induced by high glucose
(glucose at 55 mmol · L -1 )in isolated rat thoracic aorta and its related mechanisms.Methods The end
othelium-dependent relaxation of acetylcholine was per-formed in the absence or presence of GW0742 at differ-ent concentrations under high glucose condition.The structure of aorta was observed by HE staining.Moreo-ver,the content of NO was also measured by nitrate re-duction method.The mRNA and protein expression were detected by quantitative real-time PCR and West-ern blot,respectively.Results Compared with the control group,acetylcholine-induced vasodilatation was impaired by high glucose.Meanwhile,the structures of endothelial cells and smooth muscle cells were also in-terrupted.Furthermore, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 ex-pression increased significantly which occurred in par-
allel with decreasing eNOS expression and NO concen-tration (P <0.01 ).GW0742 (0.01 ,0.1 ,1 μmol· L -1 )restored the relaxation of acetylcholine in a dose-dependent manner,and reversed the mRNA and pro-tein expression of PPARβ,NF-κB p65 and eNOS,as well as NO content (P <0.01 ).Conclusion GW0742 attenuates the injury of endothelial dysfunc-tion induced by high glucose,which may be,at least partly,mediated by the up-regulation of PPARβ,then the down-regulation of NF-κB,and the activation of eNOS-NO signal pathway.

Aim To investigate the relationship be-tween the depression-like behaviors of rats induced by chronically unpredictable stress( CUS) and the protein expression of tumor necrosis factor alpha( TNF-α) , in-dole-2 , 3-dioxygenase ( IDO ) and 3-hydroxyl amino acid oxygenase( HAAO) . Methods Thirty male Spra-gue Dawley( SD) rats were randomly divided into con-trol group and model group. CUS plus solitary condi-tion were used to establish the depression model. The open field test ( OFT ) and the force swimming test ( FST ) were used to evaluate the depression-like behaviors of rats ;Western blot was used to determine the protein expressions of TNF-α, IDO and HAAO in the prefrontal cortex and hippocampus of rats. Results Model group rats showed obvious depression-like be-haviors with increasing immobile time in FST ( P <0. 01) and decreasing locomotive activity in OFT( P<0. 01 ) , and up-regulating the protein expression of TNF-α, IDO and HAAO in the prefrontal cortex and hippocampus significantly ( P <0. 05 ) , compared with control group rats. Conclusion The depression-like behaviors of rats induced by CUS may be associated with the activation of IDO-HAAO pathway mediated by TNF-α.