Objective To study the clinical features of the patients with systemic lupus erythematosus (SLE) with Raynaud′ s phenomenon. Methods The clinical manifestations and laboratory findings of 42 SLE patients with Raynaud′ s phenomenon were analyzed and compared with those of 116 SLE patients without Raynaud′ s phenomenon. Results As compared with SLE patients without Raynaud′ s phenomenon, the SLE patients with Raynaud′ s phenomenon were more likely to have myalgia/myopathy(9.48％ vs 23.81％ , P

Objective To observe the clinic features and serology of systemic lupus erythematosus(SLE) in elderly patients. Methods The clinic features and serology of 27 patients with late-onset SLE in our hospital from 1994 to 2003 were analyzed and compared with non-lateonset SLE. Results The average duration from disease onset to diagnosis in late-onset SLE was 56.1 months, which was significently longer than in non-lateonset SLE (mean 10.5 months, P

Objective This study is to investigate cytokine pathway,Jak-Stat signal pathway,neuroactive ligand-receptor pathway gene expression pattern of peripheral blood mononuclear cell(PBMC) of primary sjgren syndrome patients.Methods The PBMC sample of 3 patients with sjgren syndrome and 3 healthy volunteers with consistent age were collected.The total RNAs was extracted from the PBMC samples,and reverse transcripted in vitro transcription(IVT),labeled with Cy5/Cy3 and hybridized on the gene chips.After scanning and data extraction with LuxScan 3.0,differentially expressed genes were analyzed with SAM method.The online tool of molecule analysis system(MAS) was used for biological knowledge mining.Results Statistical difference was calculated between the patient and control group in the following three pathways: cytokine pathway,Jak-Stat signal pathway,neuroactive ligand-receptor pathway.Among these,genes of IL-2RA,IL-10 were up-regulated and genes of PF4,GZMA were down-regulated.Conclusion Understanding of differently expressed genes should help us disclose the potential molecular mechanism underlying the development process of pathogenesis of primary Sjgren′s syndrome.And the research may provide new target therapy for SS.

Objective To investigate the effects of 5-Aza-CdR( methylation transferase inhibitor) on the expression levels of leptin gene in chondrocytes and methylation states of leptin promoter region between osteoarthritis (OA) group and control. Methods The chondrocytes in osteoarthritis group were treated with 5-Aza-CdR with different doses and time-points, and the expression level of leptin was detected by real-time polymerase chain reaction for picking up the optimum dose and time-point. Next, the chondrocytes in 5 osteoarthritis patients and 5 control patients (amputation due to severe trauma) were treated with 5-Aza-CdR. Lastly, leptin mRNA expression levels in the four groups osteoarthritis and control chondrocytes treated with/without 5-Aza-CdR were measured by real-time PCR and the methylation state of promoter region ( - 280- + 79) was detected by epityper quantitative DNA methylation analysis. Results ( 1 ) After treating the chondrocytes in OA groups with 10 μmol/L 5-Aza-CdR for 72 h, the mRNA expression levels of leptin were increased significantly. ( 2 ) The mRNA expression levels of leptin were significantly different among the four groups ( P ＜ 0. 05 ), and the chondrocytes in osteoarthritis groups treated with 5-Aza-CdR showed a marked induction of leptin mRNA expression. (3) Analysis of quantitative methylation data using an unsupervised hierarchical clustering algorithm, showed that methylation patterns of leptin promoter was different between control and osteoarthritis chondrocyte treated with/without 5-Aza-CdR. Conclusion Demethylation of leptin promoter might up-regulate leptin gene expression level and it might contribute to osteoarthritis.

Objective To investigate the effects of 5-Aza-CdR (methylation transferase inhibitor) on gene expression levels of interleukin-1β (IL-1β),transforming growth factor-β (TGF-β) and nitric oxide synthase (NOS) in chondrocytes.Methods Chondrocytes from patients with osteoarthritis (OA) (n=22),rheumatoid arthritis (RA) (n=3) or trauma without rheumatic diseases (n=10) were collected and cultured.The mRNA expression levels of IL-1β,TGF-β and NOS were detected by real-time polymerase chain reaction (RT-PCR).Chondrocytes in trauma group were treated with 5-Aza-CdR(10μmol/L) for 72 h,and the mRNA and protein expression levels of IL-1β,TGF-β and NOS were detected by RT-PCR and ELISA,respectively.Results The mRNA expression levels of IL-1β,TGF-β and NOS were increased in OA and RA group as compared with trauma group (P＜0.05),while they had no differences between OA and RA groups.After treated with 5-Aza-CdR,the mRNA and protein expression levels of IL-1β,TGF-β and NOS in chondrocytes rised in trauma group as compared with pretreatment (all P＜0.05).Conclusions The mRNA expression levels of IL-1β,TGF-β and NOS in chondroytes are higher in OA and RA patients.5-Aza-CdR could increase the mRNA and protein expression levels of IL-1β,TGF-β and NOS by inducing relative gene methylation,which suggests demethylation might play a role in OA pathogenesis by influncing the inflammatory signal pathway or cell apoptosis.

Objective To investigate the expression of interleukin-35 (IL-35) in serum of mice with pulmonary interstitial fibrosis.Methods Thirty-six C57BL/6 mice were divided into three groups (twelve mice in each group):control group,model group of mice with bleomycin-induced pulmonary fibrosis,glucocorticoid treatment group of mice with bleomycin-induced pulmonary fibrosis.The mice were sacrificed at day 7,day 14 and day 28 respectively,and the serum concentration of IL-35 was assayed.Statistical product and service solutions (SPSS) 17.0 statistical software was used for single factor analysis of variance and LSD-t comparison and Pearson correlation analysis was used for the comparison between each two groups.Results The serum IL-35 concentrations between groups and within groups at the time of day 7,day 14 and day 28 were compared respectively.The serum IL-35 concentration of the model group was significantly lower than the control group and the glucocorticoid treatment group at the time of day 7 (F=24.56,P＜0.05).The serum IL-35 concentration of glucocorticoid treatment group was significantly lower than the control group at the time of day 14 (F=8.85,P＜0.05),and which of glucocorticoid treatment group was significantly lower than the control group and the model group at the time of day 28 (F=36.64,P＜0.05).There was no significant difference between days 28 and day 7 within control group (t=1.03,P＞0.05).The serum IL-35 concentration of the model group at the time of day 28 was significantly higher than those of day 7 [(9.36±0.95) ng/ml vs (6.51±0.58) ng/ml,t=5.14,P＜0.05],and which of glucocorticoid treatment group was significantly lower than those of day 7 [(5.27±1.01) ng/ml vs (9.42±0.84) ng/ml,t=6.32,P＜0.05].From day 7 to day 28 the serum IL-35 concentration change of the model group and glucocorticoid treatment group showed significantly negative correlation (r =-0.743,P＜0.05).Conclusion Serum IL-35 concentration has shown an trend of increase during bleomycin-induced pulmonary fibrosis with mice model,and early glucocorticoid treatment can decrease the serum IL-35 in the model mice.

Objective To explore the effect of different concentrations of iguratimod (IGU) on mouse model of bleomycin-induced pulmonary fibrosis.Methods A total of 108 female C57BL/6 mice were randomly divided into the control group,the model group,the low dose IGU group,the moderate dose IGU group,high dose with group and the methylprednisolone (MP) group (n=18 in each group).The mice in the control group were injected with 0.2 ml normal saline endotracheally,and others were injected with 0.2 ml bleomycin (5 mg/kg) from endotracheally to induce pulmonary fibrosis model.The next day,the mice in both control group and the model group were fed with 0.2 ml normal saline every day;The mice in the IGU groups and methylprednisolone group were fed with 0.2 ml iguratimod liquid the IGU (10,30,90 mg/kg) and 0.2 ml methylprednisolone (10 mg/kg) every dayrespectively.Finally the mice were sacrificed at day 7,day 14,day 28 respectively,and the lung tissue was examined by HE staining and Masson staining to evaluate the degree of alveolitis and fibrosis.Repeated measurement of variance analysis was used to compare the differences for time and group,and multi-factor analysis of variance LSD test was used for the comparison between groups.Results ① The body mass of mice in bleomycin-induced groups were decreased compared to the control group.② The pathological alveolitis scores in the high dose IGU group and methylprednisolone group were significantly decreased compared to those of the model IGU group at day 7 and day 14 (P＜0.05),and the pathological fibrosis scores were decreased dramatically compared with the model group at day 14 and day 28 (P＜0.05).Conclusion High concentration of IGU and methylprednisolone can reduce and inhibit lung inflammation and fibrosis of bleomycin-induced pulmonary fibrosis in mice.

Objective To investigate the inhibitory effect of methylprednisolone (MP) on the development of coronary arteritis in a murine model of Kawasaki disease (KD) induced with a candida albicaus watersoluble fraction (CAWS).Methods Forty-five C57BIL/6mice were evenly divided into three groups (the control group,the CAWS group and the MP group).Mice in the CAWS group were intraperitoneally injected phosphate buffer saline (PBS) for 5 days.MP or PBS was administered to the different group.The animals were sacrificed at day 3,day 10 and day 28,and the status of vasculitis in the coronary arteries and the aortic root was investigated histologically.One-way analysis of variance (ANOVA) was used to compare the differences among three groups,and t-test for two independent groups.Results The mice in CAWS group and MP group,which induced by CAWS,showed that the body weight and heart weight decreased significantly,and the spleen weight was increased at day 10 and day 28 (P＜0.05).Vasculitis was induced in the mice of those two groups,and the severity score was the highest at day 10 (12.7±0.5).In addition,the severity of the inflammation of the aortic root and the coronary arteries were reduced in MP group (t=6.35,5.55,2.8,P＜0.05).Elastic fiber staining showed that the layers of vascular walls were in disorder and elastic fibers were broken in the CAWS group.However,there was no disruption or breakage in the MP group.Conclusion MP can suppress the progression of coronary arteritis in this CAWS-induced murine vasculitis model,which indicates the efficacy of MP in KD patients with coronary artery lesions.

Objective To investigate the association of the expression level of anti-apoptosis protein p-AKT and gastric mucasal injury induced by indomethacin in mice.Methods The cytotoxicity induced by indomethacin was measured by LDH assay.The p-AKT expression levels were measured in the gastric mucosal tissues from C57BL/6 mice and rat gastric mucosal (RGM-1) cell lines treated with indomethacin lay western blotting.Results The cytotoxicity induced by indomethacin was in a dose dependent manner.Compared with the control,a typical histological appearance of gastric ulcer was observed in the gastric mucosa of in domethacin-administered mice;p-AKT protein expression in the gastric mucosa of mice and RGM-1 cell lines was decreased after treated with indomethacin.Conclusion The reduction of Anfi-apoptesis protein p-AKT expression may be a new mechanism for the gastric mucosal injury induced by indomethacin.