The long noncoding RNAs refers to RNA transcripts more than 200 nucleotides in length,and do not encode proteins.In the end of the 20th century,the lncRNAs were found to play crucial role in many important biological processes,including embryonic development,cell differentiation,species evolution,metabolism,and disease occurrence by the scientific community.Currently,multiple studies have indicated that long noncoding RNAs have participated in rheumatic diseases,immune response,immune cell differentiation,and dynamic balance of the immune system.Therefore,summary of the roles of lncRNAs in rheumatic diseases could be beneficial to understand the pathogenesis of autoimmune diseases.This review article attempts to highlight the recent progresses regarding IncRNAs studies and the relationship between long noncoding RNA and rheumatic diseases by taking systemic lupus erythematosus,rheumatoid arthritis,arthritis and other typical diseases as examples.

Objective To study the inner diameter and hemodynamics of ophthalmic artery(OA)and central retinal artery(CRA)in hyperuricemia by Enhance-flow(eFlow)imaging and spectral Doppler.Methods One hundred and one patients with hyperuricemia and 30 volunteers were selected,the inner diameter in eFlow imaging and the peak systolic velocities(PSV),the end diastolic velocities(EDV),the resistive index(RI)were measured,and pulsatility index(PI)of OA and CRA were measured by spectral Doppler.The 101 patients were divided into two groups according to the time of diagnosing hyperuricemia,one group had a diagnosis of hyperuricemia for more than five years and the other had such a diagnosis for less than five years.The data were compared by t-test.Then,the patients were further divided into a group of hyperuricemia combined with hypertension and the other without hypertension.The differences between the experimental group and the group of volunteers were carried out by One-way ANOVA,the comparison between two groups were analyzed with SNK.Results The RI(0.68±0.09)and PI(1.3±0.4)of OA in patients who were diagnosed as hyperuricemia for more than 5 years was higher[RI:0.63±0.09,PI:1.1±0.3(t=3.504,P=0.001 ;t=3.164,P=0.002)],the EDV[(6±3)cm/s]of OA was lower than those patients with a diagnosis of hyperuricemia for less than 5 years[(8±5)cm/s,t=1.988,P=0.049].The PSV[(11.5±3.5)cm/s]and EDV[(3.7±1.1)cm/s]of CRA in hyperuricemia combination hypertension group was lower,and the RI (0.88±1.40)was higher than hyperuricemia without hypertension group[PSV:(13.5±4.0)cm/s,EDV:(4.1±1.2)cm/s,RI:0.67±0.08].Conclusion By eFlow and spectral Doppler,we have found that hyperu-ricemia could accelerate OA and CRA atherosclerosis.The eFlow and spectral Doppler are valuable methods to study the hemodynamics in ophthalmic artery of patients with hyperuricemia.

Objective To explore the characteristics of hematological changes in patients with primary Sj(o)gren'syndrome (pSS).Methods The clinical data of 49 cases with pSS were retrospectively analyzed.Resuits The data showed that 25 patients (51%) among 49 cases had hematological changes.of which 15 cases were anaemia (31%).8(16%) were leukopenia,and 10 cases (20%) were thrombocytopenia.And 6 cases had two cell lines involved.2 cases had three cell lines involved.Twenty-three bone marrow aspirations revealed active proliferation or normal cell proliferation and the morphology of all 3 cells lines were normal.Bone marrow examination had strong positive iton stain and 15 cases with anaemia showed positive iron stain.Seven out of 10 patients with thrombocytopenia had megakaryocyte maturation defect.Conclusion Hemotologieal changes are common.and anemia is the most common findings.Cytopenia is related to autoantibodies mediated stem cell damages.but anemia iS caused by iron metabolic disturbance.while thrombocytopenia is generally due to functional impairment of megakaryocytes.

Objective To explore the role of interleukin (IL)-1β in the pathogenesis of gout.Methods Real-time quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay(ELISA) were used to measure the expression of IL-1β mRNA in peripheral blood mononuclear cells (PBMCs) and IL-1β in plasma samples from 120 acute gouty (AG) arthritis,70 chronic gouty (CG) arthritis,80 intercritical gouty (IG) arthritis patients and 96 healthy control subjects respectively.Results The expression of PBMCs IL-1β mRNA and plasma concentration of IL-1β were both much higher in gout patients than those in controls (P ＜ 0.01,respectively).And the plasma levels of IL-1β mRNA and IL-1β significantly increased in the AG group compared with CG and IG groups (P ＜ 0.01,respectively) and much higher in the CG group than those in the IG group.Positive correlations existed between plasma concentration of IL-1β and the levels of white blood cell,neutrophil,monocyte,erythrocyte sedimentation rate,blood uric acid,globulin and PBMCs IL-1β mRNA (P ＜ 0.01,respectively) while negative correlation between plasma IL-1β and plasma level of apolipoprotein in gout patients (P ＜ 0.05).Conclusion Elevated plasma level of IL-1β may be involved in the pathogenesis of acute and chronic gouty arthritis.

OBJECTIVE: To evaluate the efficacy and ADR of palipeddone sustained release tablet in the treatment of schizophrenia in outpatient. METHODS: Outpatients with schizophrenia treated with palipeddone sustained release tablet(observation group) in our hospital from Apr. to Sep. in 2009 were followed up and compared with those treated with risperidone(control group) during the same period. PANSS and TESS were applied to evaluate efficacy and ADR. RESULTS: The cure rates were 42.4% for control group and 49.6% for observation group. The effective rates were 74.8% for control group and 80.3% for observation group (P

Objective:To explore the expression and clinical significance of late autophagy in per-ipheral blood mononuclear cells (PBMCs) of patients with primary gouty arthritis (GA).Methods:Peripheral blood, clinical data, and laboratory tests were collected from 30 patients with acute gout (AG), 30 patients with intermittent gout (IG), and 50 healthy controls (HC). Quantitative polymerase chain reaction (RT-qPCR) was used to detect mRNA expression levels of autophagy-related genes (ATG5, ATG12, ATG16, ATG3, ATG7, ATG10, ATG4B, LC3-2/LC3B). Measurement data conformed to normal distribution were tested using t test or analysis of variance (ANOVA), and non-normal distribution data were tested using Mann-Whitney test or Kruskal-Wallis H test. SNK was used for pairwise comparison among the three groups. Correlation between variables was tested by Spearman correlation analysis. Results:① The expression level of ATG5 mRNA,ATG12 mRNA, ATG16 mRNA, ATG10 mRNA and LC3-2 mRNA in the AG group was lower than that of the IG group and the HC group, and the expression level of the IG group was lower than that of the HC group[9.16×10 -3(6.04×10 -3, 15.00×10 -3) vs 14.48×10 -3(9.95×10 -3, 21.38×10 -3) vs 0.08×10 -3(12.21×10 -3, 42.79×10 -3), H=19.377, P<0.001; 18.89×10 -3(13.85×10 -3, 24.92×10 -3) vs 21.13×10 -3(12.11×10 -3, 28.06×10 -3) vs 33.57×10 -3(13.11×10 -3, 49.89×10 -3), H=7.545, P=0.023; 8.72×10 -3(4.96×10 -3, 13.74×10 -3) vs 10.62×10 -3(7.48×10 -3, 24.71×10 -3) vs 20.07×10 -3(11.99×10 -3, 39.56×10 -3), H=20.962, P<0.001; 1.05×10 -3(0.73×10 -3, 1.84×10 -3) vs 1.60×10 -3(0.93×10 -3, 2.58×10 -3) vs 1.69×10 -3(1.05×10 -3, 3.54×10 -3), H=8.193, P=0.017; 2.31×10 -3(1.22×10 -3, 3.53×10 -3) vs 2.78×10 -3(1.68×10 -3, 5.96×10 -3) vs 3.68×10 -3(2.00×10 -3, 5.67×10 -3) , H=7.135, P=0.028]. The expression level of ATG4B mRNA in the AG and IG group was higher than that in HC group, and there was significant difference between IG group and AG group, IG group and HC group[9.95×10 -3(6.32×10 -3, 12.23×10 -3) vs 10.86×10 -3 (8.80×10 -3, 17.03×10 -3) vs 8.07×10 -3(5.52×10 -3, 11.63×10 -3), H=8.531, P=0.014]. There was no significant difference between the ATG3 mRNA and ATG7 mRNA groups ( H=0.539, 3.739, bothall P values >0.05). ② The results of Spearman correlation analysis suggested that in patients with acute gout, ATG3 was negatively correlated with PDW and MPV ( r=-0.499, P=0.006; r=-0.463, P=0.011); ATG4B was positively correlated with HDL-C ( r=0.408, P=0.048); ATG7 was negatively correlated with GLOB ( r=-0.554, P=0.001); ATG10 was positively correlated with ALB ( r=0.412, P=0.024) and negatively correlated with Crea and hsCRP ( r=-0.459, P=0.011; r=-0.375, P=0.045); ATG12 was negatively correlated with MO ( r=-0.434, P=0.017); ATG16 was negatively correlated with ALT and AST ( r=-0.389, P=0.034; r=-0.366, P=0.047); LC3-2 was positively correlated with UA ( r=0.381, P=0.041) and negatively correlated with MPV and PDW ( r=-0.413, P=0.026; r=-0.449, P=0.015). In patients with intermittent gout, ATG3 and ATG4B were negatively correlated with apoB100 ( r=-0.555, P=0.011; r=-0.462, P=0.040); ATG5 was negatively correlated with Crea ( r=-0.456, P=0.011); ATG10 was negatively correlated with TC, LDL-C, and apoB100 ( r=-0.526, P=0.017; r=-0.556, P=0.011; r=-0.515, P=0.020). Conclusion:Autophagy is involved in the development of gout, and is correlated with ibflammatory and metabolic indicators, suggesting that autophagy is an important feature in the pathogenesis of GA.

Objective To investigate the association of TLR4 gene polymorphisms with susceptibility to primary gouty arthritis (GA) in Chinese Han population.Methods A total of 459 patients with GA and 459 healthy control subjects were enrolled into this study.All the genotyping assays of TLR4 gene polymorphisms loci [rs4986790 (Asp299Gly),rs4986791 (Thr399Ile),rs2 1 49356T＞G] were measured using TaqMan probes that specifically target the alternate alleles.Results All the subjects were found to be homozygous for the wild-type TLR4 alleles (Asp/Asp,Thr/Thr) on TLR4 Asp299Gly and Thr399Ile genotyping.There was no significant deviation from HWE both in GA and controlsin the rs2149356 (x2=0.778,1.295; P＞0.05,respectively).Significant differences were observed between the GA and control groups with respect to genotype and allele frequencies of TLR4 gene rs2149356 (x2=16.23,17.08; P＜0.01,respectively),and TT genotype was the risk factor for gout (adjusted OR=2.09).Conclusion The TLR4 gene rs2149356 SNP may be associated with GA susceptibility,and TT genotype may be the risk factor for developing gout.

Objective To investigate the role of adiponectin (ADP) and its receptors (ADR) in pati ents with primary gouty arthritis (GA).Methods Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of plasma ADP in 88 GA and 80 healthy controls (NC).Real time quantitative polymerase chain reaction (RT-qPCR) was employed to study the expression of ADR1 and ADR2 mRNA in peripheral blood mononuclear cells (PBMCs).The biochemical indicator of TG,HDL,LDL,VLDL,apoA1,apoB100 and uric acid (UA) were detected at the same time.T test,Spearman's correlations and regression analysis were used for statistical analysis.Results The concentration of plasma ADP was significantly lower in GA than that in NC [(6±7) μg/ml,(8±6) μg/ml,t=-3.71,P＜0.01 ],the expression of ADR1 and ADR2 mRNA in GA (ADR1:0.09±0.08,ADR2:0.0122±0.0164) was significantly increased when compared to the NC (ADR1:0.05±0.03,ADR2:0.0054±0.0024) (t=2.71,2.35,P＜0.05).In the GA patients,the level of ADP was negatively correlated with the lymphocytes count (LY) and UA (r=-0.32,-0.36,P＜0.05),and it was positively correlated with ESR and LDL level (r=0.31,0.39,P＜0.05).The expression of ADR1 mRNAwas negatively correlated with TG (r=-0.43,P＜0.05 ),but positivdy correlated with ESR and CRP level (r=0.45,0.57,P＜0.05).The expression of ADR2 mRNA was negatively correlated with glucose and UA(r=-0.50,-0.59,P＜0.05).Conclusion Altered expression of ADP and its receptors may be involved in thepathogenesis of gouty inflammation.

Objective To study the expression level of NLRP3 (NLR family, pyrin domain containing3) inflammasome (NLRP3, ASC, caspase-1 ) mRNA in peripheral blood monocytes (PBMCs) from patients with gout arthritis (GA) and to explore the pathogenesis of GA. Methods NLRP3 inflammasome mRNA was measured using quantitative real-time PCR in PBMCs. The expression of NLRP3 inflammasome mRNA in PBMCs was compared between patients with GA (n=24) and healthy controls (n=24). β-actin was selected as the internal control. Students' t-test was used in two independent samples and Spearman's correlation was used to evaluate the relationship between mRNA level and inflammatory parameters. Results The expression of ASC mRNA in GA increased significantly when compared to healthy controls [(0.029±0.021 ) vs (0.009±0.007 ), P＜0.01 ], and the expression of NLRP3 and caspase-1 mRNA was significantly lower in patients with GA compared to healthy controls [(0.062±0.084) vs (0.133±0.106), P＜0.05; (0.025±0.014) vs (0.117±0.156), P＜0.01]. Moreover, the expression of ASC mRNA was found to correlate significantly with globulin (r=-0.547, P＜0.05) and very low density lipoprotein cholesterol (r=-0.540, P＜0.05) in GA patients,and caspase-1 was correlated to globulin(r= -0.773. P＜0.01) and very low density lipoprotein cholesterol (r=-0.465. P＜0.05). Furthermore, the ASC mRNA in GA patients was associated significantly with NLRP3 mRNA(r=-0.450, P＜0.05) and caspase-1 (r=0.604, P＜0.01 ). Conclusion Dysregulated expression of the NLRP3inflammasome is involved in the inflammatory response and plays a key role in the pathogenesis of GA.

Objective To determine the level of monocyte chemoattractant protein-1 (MCP-1) in patients with systemic lupus erythematosus (SLE) and to assess its relationship with disease activity and organ damage. Methods The plasma levels of MCP-I were measured by enzyme linked immunosorbent assay (ELISA) in 95 patients with SLE and 21 healthy controls. Disease activity in SLE patients was assessed using the SLE Disease Activity Index (SLEDAI). Results Plasma level of MCP-1 was significantly elevated in SLE patients than in healthy controls [(849±289) pg/ml vs (426±266) pg/ml, P<0.01]. Moreover, level of MCP-1 was significantly higher in SLE patients with lupus nephritis (LN) than in patients without LN (P<0.01), andin SLE patients with neuropsychiatric symptoms than in patients without neuropsychiatric involvement (P< 0.01). In addition, significant correlation between plasma MCP-I levels and the SLEDAI was observed (r= 0.3699, P<0.01), and this relationship was not influenced by the treatment with glucocorticoid and cyclophosphamide. Conclusion MCP-I may play an important role in the pathogenesis of SLE, including renal and neuropsychiatric involvement. MCP-I is also a serologic marker of disease activity in patients with SLE, and its measurement in SLE patients may be useful for the evaluation of disease activity.