Objective To analyze the genotypic characteristics of T. violaceum, and offer evidence for molecular epidemiological study of causative agents of pediatric tinea capitis, in Xinjiang Uygur Autonomous Region. Methods The PCR-restriction fragment length polymorphisim (RFLP) of the nontranscribed spacer region of ribosomal DNA (rDNA-NTS) was assessed by using 5 restriction enzymes, including HaeⅢ, Bgl Ⅰ,MspⅠ, DdeⅠ and MboⅠ, for 30 clinical isolates of T. violaceum from children with tinea capitis in Xinjiang Uygur Autonomous Region. Nine strains of T. violaceum from Beijing and 2 strains from Taiwan served as the control.Results All the 41 strains of T. violaceum were classified into 12 genotypes with the restriction enzyme Ddel.Ten genotypes were revealed in the 30 strains from Xinjiang; among them, 17 strains showed 7 different genotypes (D, F, G, H, I, J and K) with a high intraspecies diversity in comparison with the Beijing and Taiwan isolates; the remaining 13 strains from Xinjiang showed 3 genotypes, which were shared by the Beijing and Taiwan isolates. Conclusions The T. violaceum isolates from children with tinea capitis in Xinjiang Uygur Autonomous Region have unique genotypes, but also show genetic homogeneity with the strains from Beijing and Taiwan, hinting the genetic diversity of T. violaceum.

Objective To investigate the relationship between the mutation of ERG11 gene,a target of azole antifungal drugs (fluconazole,itraconazole,voriconazole),and azole-resistance in Candida albicans isolates from patients with AIDS.Methods Ninety-three Candida albicans strains were isolated from patients with AIDS.DNA was extracted from these isolates,and ERG11 gene was amplified by PCR followed by bidirectional sequencing.DNAman software was used to compare the resultant sequence with the reference sequence of ERG11 gene (GenBank accession no.X13296).Then,different base sequences were translated into amino acid sequences to determine whether missense mutations occured.Results A total of 40 mutation sites were identified in these isolates,including 27 silent mutations and 13 missense mutations.One or no missense mutation was detected in Candida albicans strains resistant to 1 antifungal agent,while those resistant to 2 or 3 antifungal agents simultaneously harbored 2 or 3 missense mutations.Conclusion The missense mutations in ERG11 gene are probably connected with azole resistance in Candida albicans.

h Kaposi' s sarcoma in Xingjiang, which have a high homology with those strains from Africa and Europe. A5 and C7 genotypes of HHV-8 have been first isolated in China.

Objective To investigate the effects of crude Fomes officinalis polysaccharide ( FOPS ) and its purified constituent ( FOPS-a) on mitogen-activated protein kinases ( MAPK) signaling pathway and se-cretion of tumor necrosis factor-α (TNF-α) in RAW264. 7 macrophages. Methods RAW264. 7 macrophages were treated with FOPS and FOPS-a respectively at different concentrations (50, 100, 200 μg/ml) for 24 h. RT-qPCR and Western blot methods were respectively used to detect the expression at mRNA level and the phos-phorylated proteins of p38, c-Jun NH2-terminal kinase ( JNK ) and extracellular signal-regulated kinase ( ERK) . Changes in the phosphorylation of these proteins and TNF-α secretion were respectively detected by Western blot and ELISA after treating the macrophages with MAPK-specific inhibitors ( PD98059, SP600125, SB203580). Results Compared with the blank control group, different concentrations of FOPS and FOPS-a could significantly increase the expression at mRNA level and the phosphorylation of p38 and ERK (P<0. 05). Three inhibitors of MAPK could markedly decrease the phosphorylation of ERK1/2 and p38 and TNF-αsecretion that were induced by FOPS and FOPS-a (P<0. 05). Conclusions FOPS and FOPS-a might have immunomodu-latory effects on RAW264. 7 macrophages through activating ERK1/2 and p38 MAPK signal transduction pathways.

Objective To investigate prevalence of atrial fibrillation (AF) in Uygur and Han elderly populations in Xinjiang Uygur autonomous region (Xinjiang).Methods Epidemiological survey was conducted among the residents selected through stratified random cluster sampling in the southern,northern and eastern Xinjiang.Results The overall AF prevalence among Uygur and Han elderly people was 3.56％.The crude prevalence of AF was 2.91％ among Uygur elderly people and 4.13％ among Han elderly people.The sex specific prevalence of AF were 3.19％ and 2.61％ among Uygur males and females respectively,and 5.01％ and 3.31％ among Han males and females respectively.The prevalence of valvular AF among Uygur ethnic group was higher than that in Han ethnic group;the prevalence of non-valvular and isolated AF in Han ethnic group were higher than those in Uygur ethnic group.The compliance of aspirin and β-blocker medication among Han ethnic group was better than that in Uygur ethnic group.The compliance of warfarin medication was poor in both Uygur ethnic group and Han ethnic group.The prevalence of ischemic stroke were 8.82％ and 0.98％ in Uygur elderly people with or without AF.The prevalence of ischemic stroke were 6.08％ and 0.70％ in Han elderly people with or without AF.Conclusion The prevalence of AF in elderly people in Xinjiang is similar to the results from other domestic studies,the prevalence of AF in Han elderly people was higher than that in Uygur elderly peoples.

OBJECTIVETo assess the association of KCNE1 (rs1805127) and KCNE4 (rs12621643) polymorphisms with atrial fibrillation (AF) among ethnic Uygur and Han Chinese in Xinjiang.

METHODSA case-control study was carried out. The patients and controls were selected based on ethnicity, gender and age with an 1:1 ratio. DNA was extracted from peripheral blood samples. Genotypes of KCNE1 (rs1805127) and KCNE4 (rs12621643) were determined with a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay.

RESULTSMultivariate Logistic regression analysis showed KCNE1 (rs1805127) to be an independent risk factor for AF among Uygurs, while KCNE4 (rs12621643) was a risk factor for both Uygur and Han patients with AF (P < 0.05). The population attributable risk percentage (PARc%) of obstructive sleep apnea hpoventilation syndrome, obesity, hypertension, cholesterol, Hcy, hs-CRP, IL-6, KCNE1 (rs1805127) and KCNE4 (rs12621643) were 9.68%, 12.06%, 15.76%, 6.91%, 11.37%, 17.78%, 9.31%, 11.27% and 6.46% among the Uygurs, respectively. The PARc% of drinking, hypertension, cholesterol, Hcy, hs-CRP, IL-6, and KCNE4 (rs12621643) were 12.94%, 14.48%, 7.24%, 8.49%, 17.29%, 9.49% and 7.41% among Hans.

CONCLUSIONThe KCNE1 (rs1805127) appears to an independent risk factor for AF in the Uygur population. And the KCNE4 (rs12621643) was an independent risk factor for AF among both Uygurs and Hans. Management of the risk factors of AF based on testing of "risk genes" may have an impact on the prevention and treatment of AF.

Atrial Fibrillation ; etiology ; genetics ; Case-Control Studies ; China ; ethnology ; Humans ; Polymorphism, Genetic ; Potassium Channels, Voltage-Gated ; genetics ; Risk Factors

Objective To investigate the molecular mechanism of miR-126-EPC-MPs in ameliorating oxygen glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes.Methods The cardiomyocytes were used to establish the control and OGD/R injury models,and EPC-MPs and miR-126 mimic EPC-MPs treatments were administered respectively.The structural changes in cardiomyocyte organelles were assessed by transmission electron microscopy.ELISA was used to detect the expression levels of IL-6,TNF-α and HMGB-1 in cardiomyocytes.The protein and mRNA expression levels of Ang Ⅱ,caspase-6,eNOS,FOXO1,MPO,NF-κB,ERK1,LKB1,SIRT1,GRP78,GM130 and PGC-1α in cardiomyocytes after different treatments were detected by Western blot and quantitative PCR.Results The mitochondria structure in some cardiomyo-cytes of the OGD/R+miR-126 mimic EPC-MPs group was complete,the size of some mitochondria was in-creased,the surface of the endoplasmic reticulum had fewer ribosomes,and some of the Golgi vesicles gath-ered.Compared with the OGD/R+EPC-MPs group,the expression levels of IL-6,TNF-α and HMGB-1 in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated.Compared with the OGD/R+EPC-MPs group,the expression levels of Ang Ⅱ,caspase-6,p-ERK1/2 and GRP78 protein in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated,and the expression levels of p-LKB1,GM130 and PGC-1α protein in the OGD/R+miR-126 mimic EPC-MPs group were up-regulated.The quantitative PCR(qPCR) results showed that compared with the OGD/R+EPC-MPs group,the expression levels of Ang Ⅱ,MPO and GRP78 in the OGD/R+miR-126 mimic EPC-MPs group were down-regulated,and the expression levels of eNOS,GM130 and PGC-1α were up-regulated.Conclusion When OGD/R injury occurs in cardiomyocytes,miR-126 mimic EPC-MPs regulates PGC-1α/GM130 expression and inhibits Ang Ⅱ-induced stress injury response,thereby reduces the OGD/R damage in cardiomyocytes.