Objective To investigate the effect of exercise on calcium modulin in myocardial sarcoplasmic re-ticulum of animal type 1 diabetes model in rat. Methods A total of 40 Spragne-Dawley rats were randomly dividedinto 4 groups : a normal control group, an exercise training group, a diabetes group and a diabetes plus exercise-traininggroup. At the end of 4- week-exercise training after the establishment of the diabetes model by intraperitoncal injectionof sterptozotocin, the animals were sacrificed and the level of blood glucose, insulin, blood fat and glycosylated serumprotein were tested. The gene expression of calcium modulin proteins was measured by reverse transcription-polymerasechain reaction, and the Western blotting technique was used to measure the protein of sarcoplasmic endoplasmic reticu-lure Ca<'2+> -ATPase (SERCA2) and phaspholamban (PLB). Results The level of biochemical indicator of exercisegroup is not affected when comparing with that of the control group, but significantly changed in diabetic group ( P <0. 01 ) ; The level of blood glucose, insulin, blood fat and glycosylated serum protein were ameliorated in diabetic rats inthe exercise training group. No significant changes in mRNA level of SERCA2, PLB and ryanodine receptor type 2(RYR2) were observed between control and diabetic group, the same to protein expression of SERCA2 and PLB. Butexpression of calcium modulin mRNA was significantly increased in exercise group and diabetic rats in the exercisetraining group comparing with that of the control and diabetic groups ( P < 0.01 ), the same to protein expression ofSERCA2 and PLB. Conclusion Exercise exerted good protective effects on the myocardial injury with 1 type diabetesrat, which might attribute to the upregnlated expression of SERCA2, PLB and RYR2 in diabetic rat heart.

Objective To investigate the association of single nucleotide polymorphism (SNP) in micro RNA-122 (miRNA-122) with genetic predisposition and early recurrence after resection for hepatocellular carcinoma(HCC).Methods This is a case-control study involving 173 HCC patients.DNA were exacted from cancer tissues embedded in paraffin and were amplified by PCR.The study aimed to explore SNP in gene sequence of miRNA-122 (357 base pair including extron.The outcomes of genetic predisposition were analyzed with early recurrence after resection for HCC.Results Only rs17669 was found in miRNA-122.The genetype frequence of C/C,T/T and C/T at rs17669 gene locus were 7(4.0％),110(63.6％)and 56(32.4％),respectively.When compared to T/T genetype,C/C genetype was a protective factor of risk of HCC (OR =0.213,95％ CI:0.062-0.732).Genetypes had no relationship with early recurrence after resection.Conclusion For HCC recurrence,rs17669 may be associated with genetic predisposition of HCC in Hans in Jiangxi infected with HBV.

Aim To observe the dysfunction of myocardial nuclear calcium transport in rat myocardial injury and effects of taurine on it . Methods The model of myocardial damage was induced by subcutaneous injection of isoproterenol (ISO,5 mg?kg-1?d-1). Myocardial nuclei were purified with Sucrose density centrifugation and identified zymologically. The activity of Ca2+_ATPase was measured zymologically and calcium uptake was assayed with 45Ca2+ isotope.Results Compared with the control, the Ca2+_ATPase activity of myocardial nuclear in ischemia group was decreased by 18.1%(P

AIM: To investigate the expression of microRNA-375 (miR-375) in hepatocellular carcinoma (HCC) and to analyze the target genes and signaling pathways regulated by miR-375.METHODS: The expression of miR-375 was examined at tissue microarray of HCC by in situ hybridization.The whole human genome chip and bioinforma-tics analysis were applied to screen out the differential expression genes and signaling pathways in 4 HCC cell lines trans-fected with miR-375 mimic.RESULTS:In situ hybridization showed the expression of miR-375 in HCC tissues were obvi-ously higher than that in tumor-adjacent tissues (P<0.05).There were 20 co-upregulated genes and 17 co-downregulated genes in all 4 cell lines.Bioinformatic analysis showed that there were 54 signaling pathways related to up-regulated genes and 48 signaling pathways related to down-regulated genes in all 4 cell lines.CONCLUSION: miR-375 may play a key role in the pathological process of HCC.The bioinformatic analysis is able to screen the target genes and signaling pathways regulated by miR-375 and to provide an explicit direction for further mechanism research on HCC.

Traditional research ideas of miRNA-target gene-biological function have ignored the contact between the target genes and signaling pathways involved , making the integrity and relevance of miRNA regulatory mechanisms not be fully elucidated .Integrated with systematic and relevant way of thinking , summarization and analysis for the luciferase reporter assay validated miR-205 target genes and their related signaling pathways will pave the way for new research area for miR-205 , and , it will be helpful for breaking through the status quo and exploring the novel research areas for miRNA .

Objective To approach on the expression pattern of MMP-2 and E-Cadherin in the effects of gastrin on gastric canc-er cells ,so as to investigate their role in the metastasis and invasion of gastric cancer .Methods Genomic DNA modified by sodium bisulfite was used as a template .RQ-MSP detect the methylation status of the gene promoter .The relative amount of Methylation status was performed with comparative threshold cycle (2- △ t ) method .Results MMP-2 and E-Cadherin genes in gastric cancer cells were at hemimethylated status in gastrin before and after the intervention .Gastrin can reduce the methylation levels of MMP-2 gene(P<0 .05) ,but the could be effected by proglumide receptor antagonist to some certain extent (P>0 .05) .Gastrin can pro-mote the methylation levels of MMP-2 gene ,but proglumide decrease that effect (P<0 .05) .Conclusion Gastrin plays a certain role in the biological behavior of gastric cancer impact by changeing on the expression pattern of MMP-2 and E-Cadherin in the effects of gastrin on gastric cancer cells .