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Objective To explore the association of CD40 gene single nucleotide polymorphisms (SNPs) and haplotypes with the susceptibility to systemic lupus erythematosus (SLE),as well as the association of serum levels and genotypes of CD40 with the occurrence of SLE.Methods A multiplex PCR single-base extension assay (PCR-SBE) and DNA sequencing were performed to analyze 4 SNPs of the CD40 gene,including rs1883832 C/T,rs13040307 C/T,rs752118 C/T and rs3765459 G/A,in 205 patients with SLE (SLE group) and 220 healthy human controls (control group).Enzyme-linked immunosorbent assay (ELISA) was conducted to measure serum levels of CD40 in these subjects.Results Compared with the control group,the SLE group showed significantly increased serum levels of CD40 (P ＜ 0.05).There were significant differences in genotype and allele frequencies of the SNP rs1883832 C/T in the CD40 gene between the SLE group and control group (all P＜ 0.01).Relative risk analysis showed that the risk of developing SLE in rs1883832 T allele carriers was 1.517 times that in rs1883832 C allele carriers (OR =1.517,95％ CI:1.157-1.990,P=0.003).Moreover,serum levels of CD40 were significantly higher in rs1883832 T allele carriers than in rs1883832 C allele carriers (P ＜ 0.01).The risk of developing SLE was significantly increased in TCCA haplotype carriers compared with the healthy controls (OR =2.322,95％ CI:1.181-4.564,P=0.012).Conclusion The CD40 gene rs1883832 C/T polymorphism and its TCCA haplotype were both associated with the occurrence of SLE,and the rs1883832 T allele may be a gene predisposing to SLE.
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Objectives To evaluate the inhibitory effect of low dose glucocorticoid on progression of radiological damage in rheumatoid arthritis by systematic review.MethodsA search of MEDLINE (from 1966 to April 2010),Embase(from 1966 to April 2010),Cochrane Library(2 Issue,2010),CBM disc,CNKI,WANFANG and VIP Database was undertaken to collect randomized controlled trials published before April 2010 based on the Cochrane Collaboration recommendations.Additional reports were identified from the reference lists.Statistical analysis was performed with RevMan 5.0 software.ResultsEleven studies that met the inclusion criteria,in which 1395 patients,were included.Meta-analysis showed that the standardised mean difference in progression was 0.40 (95％CI 0.27～0.54 ) in favour of glucocorticoids over the first year.In studies that lasted for 2 years,the standardised mean difference in progression in favour of glucocorticoids at 1 year was -0.39[95％CI(-0.50～-0.27)] and was -0.73[95％CI(-1.29～-0.16)] at 2 years.All studies except one showed benefit of glucocorticoids treatment.ConclusionsThe results of this study has shown that low dose glucocorticoids can substantially reduce the progression rate of erosion in rheumatoid arthritis.
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Objective To investigate the association between the single nucleotide polymorphisms of interleukin-27 (IL-27) gene and susceptibility to systematic lupus erythematosus (SLE) in Guangxi Zhuang population. Methods In total, 135 patients with SLE and 150 age- and sex-matched human controls of Zhuang nationality were recruited in this study. PCR-restriction fragment length polymorphism (RFLP) analysis and DNA sequencing were performed to analyze the IL-27 gene -964 A/G and -2905 T/G polymorphisms.Results Significant differences were observed in the distribution of IL-27 gene -964 A/G polymorphism (x2 =9.88, P ＜ 0.01 ). The relative risk for SLE in carriers of G allele at position 964 of IL-27 gene was 1.725 times that in carriers of A allele at this position (OR = 1.725,95% CI: 1.227 - 2.425). A significant increase was observed in the frequency of 964G/2905G alleles of IL-27 gene in patients with SLE compared with the controls (10.7% vs. 5.3%, P ＜ 0.01 ), and the 964G/2905G alleles were associated with a significantly increased risk for SLE (OR = 2.351, 95% CI: 1.228 - 4.501 ). Conclusions The IL-27 gene -964 A/G polymorphism is associated with the development of SLE, and the -964 G allele may increase the genetic susceptibility to SLE.
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<p><b>OBJECTIVE</b>To study the role of connexin gene (Cx43) in the suppression of C6 glioma.</p><p><b>METHODS</b>Cx43 gene depleted parental C6 rats (control group) and C6 cells transfected with Cx43 cDNA (transfection group) were implanted into the right caudate nucleus of SD rats. Rats bearing cerebral C6 gliomas were treated with Cx43 cDNA (treatment group) with another group treated with empty vector (empty vector group) serving as control. The general manifestation, survival time, MRI dynamic scanning and histopathological changes in all rats were observed. Cx43 mRNA and its protein were examined by in situ hybridization and immunohistochemistry. Proliferation activity was monitored by the average number of AgNOR stain. Cell apoptosis was examined by the Tolt-mediated x-duTP nick end labeling (TUNEL) method.</p><p><b>RESULTS</b>All rats in the control and empty vector groups died of cerebral glioma within 3 weeks after implantation of C6 cells. Six in the transfection group and 8 in the treatment group were alive beyond 120 days with complete disappearance of the tumor foci, except one in this group having some residue of tumor. In the glioma of transfection and treatment groups, Cx43 gene expression was up-regulated, proliferation activity reduced while the apoptotic cells did not increase.</p><p><b>CONCLUSION</b>The development of glioma is greatly suppressed by the transfection of Cx43 gene, which has great effectiveness in rats bearing cerebral malignant gliomas. This could become a target of choice in the gene treatment of malignant gliomas.</p>