Objective : To explore the relationship between single nucleotide polymorphisms ( SNPs) in D-loop region of mitochondrial DNA ( mtDNA) and mtDNA copy number and the risk of dermatomyositis ( DM) ，and its in- fluencing factors． Methods : 74 patients with DM and 92 healthy controls were included in the study． Genomic DNA was extracted from peripheral blood and the target fragment of mtDNA D-loop region was amplified by PCR technique，and the products were subsequently sequenced．Serum levels of ROS were assessed using a high-sensi- tivity reactive oxygen species detection kit．The expression levels of cytokines，interleukin ( IL) -5，IL-13，inter- feron-γ ( IFN-γ) ，IL-2，IL-6，IL-10，tumor necrosis factor-α ( TNF-α) and IL-4 were measured using Flow Fluo- rescence Immunmicrobeads Assay．Wilcoxon rank-sum test was used to assess the potential correlation between cy- tokines and SNPs associated with DM risk．The relative copy number of mtDNA was measured using quantitative re- al-time polymerase chain reaction ( qPCR) analysis． Results : Two SNPs ( 16304T / C，16519T / C) were found to be associated with the risk of developing DM，and alleles 16304C ( χ2 = 4. 937，P = 0. 026) and 16519C ( χ2 = 4. 405，P = 0. 036) in the mitochondrial D-loop region were confirmed to be associated with DM development risk． The DM risk-associated allele 16304C was significantly associated with lower IL-4 expression ( P = 0. 016) ．The mtDNA copy number was significantly higher in DM patients than in controls ( P ＜0. 001) ． Conclusion Mitochondrial D-loop SNPs can be potential biomarkers for DM risk，and SNPs may be involved in DM by influencing cytokines．DM shows high expression of mtDNA copy number，and the increase in mtDNA copy number may lead to mitochondrial dysfunction，which triggers the pathogenesis of DM．

Objective To explore the role and mechanism of tumor necrosis factor ligand -related molecule 1A (TL1A) in chronic experimental colitis associated intestinal fibrosis .Methods The model of chronic experimental colitis-associated intestinal fibrosis was induced by dextran sodium sulfate (DSS).The mice with high TL1A (L-Tg) expression in lymphoid cells and wild -type mice with the same genetic background were divided into wild type control group, wild type DSS group, transgenic control group and transgenic DSS group.The changes of body mass, length of colon, disease activity index (DAI) and colonic pathological score were compared among different groups .The degree of colonic inflammation was evaluated by Hematoxylin -Eosin (H-E) staining.The degree of intestinal fibrosis was assessed by Masson staining and Sirius red staining .The expression of vimentin, αsmooth muscle actin ( α-SMA), type Ⅰ collagen, Ⅲ collagen and transforming growth factor-β1 ( TGF-β1 ) /Smad3 in colon tissue was examined by immunohistochemistry .T test was performed for statistical analysis.Results The body mass of the transgenic DSS group decreased by (9.6 ± 1.8)％, which was more than wild-type DSS group (6.2 ±1.3)％, the difference was statistically significant (t =3.751, P <0.01).The DAI score and colonic pathological score of transgenic DSS group were both higher than those of wild-type DSS group (7.33 ±0.58 vs.6.00 ±1.00, and 14.00 ±1.05 vs.11.75 ±0.50, respectively), and the differences were statistically significant (t =2.818 and 4.739, both P <0.05).The results of Masson staining and Sirius red staining showed aggravation of intestinal fibrosis .The results of immunohistochemical staining showed that the cumulative positive absorbance values of vimentin , α-SMA, TGF-β1 and Smad3 of wild-type DSS group were lower than those of transgenic DSS group (0.650 ±0.050 vs. 0.800 ±0.020, 0.390 ±0.040 vs.0.600 ±0.040, 0.550 ±0.040 vs.0.730 ±0.040, 0.590 ±0.020 vs. 0.830 ±0.040), and the differences were statistically significant (t =6.823, 9.093, 7.794 and 10.390, all P <0.01).Conclusion TL1A may promote the proliferation and activation of fibroblasts through TGF -β1 /Smad3 pathway, leading to the genesis and development of experimental colitis associated intestinal fibrosis .

Objective To investigate the correlation between dyslipidemia and important organ damage in patients with active systemic lupus erythematosus (SLE) without treatment. Methods Serum sam-ples from 71 active SLE patients and 30 healthy controls were obtained to measure lipid profiles including total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), apolipoproteinA1 (apoA1), apolipoproteinB100 (apoB) and lipoprotein a (LPa). Clinical parameters were recorded. Results The levels of serum TC, TG, LDL, apoB in active SLE patients were higher than those in healthy controls, in contrast,the levels of HDL,apoA1 were much lower (P<0.05 or P<0.01). Patients with important organ damages had longer disease course and elevated levels of serum TC, TG, LDL and apoB concentrations than those without organ damage (P<0.05 or P<0.01), especially in patients with cadiovascular diseases (CVD) (P<0.01). Moreover, these changes in lipid metabolism were positively correl-ated with disease course and negatively with C3 level (P<0.05 or P<0.01). The elevated serum TC and LDL concentrations were negatively correlated with C4 level (P<0.05). Conclusion Severe dyslipidemia is present in active SLE patients.It is correlated with disease course and disease activity. Increased serum TC, TG, LDL and apoB concentrations play key roles in patients with important organ damages.