Objective To observe the effect of interventional therapy of urokinase on sudden hearing loss.Methods65 patients with sudden hearing loss were divided into the treatment group (n=35) and control group (n=30). The patients of the treatment group were treated with urokinase pouring into vertebral artery accordingly into labyrinthine artery in order to improve internal ear microcirculation. Those of the control group were treated with routine drug dropping in vein. All patients of two groups were examined by pure tone test before and after treatment and the therapeutic effect of two groups was compared.ResultsIn the treatment group, the audition of 21 cases recovered, 12 cases got 15～30 dB increasing, 2 cases increased <15 dB. In the control group, the audition of 10 cases recovered, 4 cases got 15～30 dB increasing, 9 cases increased <15 dB and 7 cases had no obvious improvement. There was a significant difference between effects of two groups ( P<0.05).ConclusionThe effect of urokinase on sudden hearing loss is superior to routine drug dropping in vein.

The effects of L-arginine (L-Arg), the physiological NO precureor and NO synthetase inhibitor NG-nitro-L-arginine (L-NNA) on endogenous endothelin (ET) secretion and renal function were observed in a model of glycerol-induced acute renal failure (ARF) in rat. It was found that endogenous ET secretion was significantly increased, while serum NO was markedly decreased in ARF rats. The administration of L-NNA to the ARF rats induced significant increases in plasma ET and positive immunoreactive particles of ET in renal tubular epithelial cells(EP cells), and the impairment of renal function was exaggerated. L-Arg might effectively decrease the level of plasma ET and the positive immunoreactive particles of ET in renal tubular EP cells, suggesting the improvement of the renal function. It is suggested that the ability of NO in improving renal function may relatedto the inhibition of endogenous ET secretion in glycerol-induced ARF rats.

Objective To determinate the serum level of adiponectin,visfatin and resistin in patients with rheumatoid arthritis (RA) and to explore its role in the development of RA and its clinical significance.Methods Blood samples were collected from 67 cases of RA patients and 65 healthy controls,the serum levels of adiponectin,visfatin and resistin were tested by enzyme linked immunosorbent assay (ELISA).Adipokine levels in different groups were compared using the Mann-Whitney U test.Spearman test and multivariate analysis were used to evaluate the correlation with clinical and laboratory parameters [erythrocyte sedimentation rate (ESR),C reactive protein (CRP),blood platelet (PLT),rheumatoid factor (RF),anti-cyclic citrullinated peptide (CCP),disease activity score (DAS)28].Results The serum level of adiponectin,visfatin and resistin in RA patients were significantly higher than those in healthy controls[8.17(4.51,28.53) μg/ml vs 6.83(4.48,25.32) μg/ml,U=1 663,P=0.019];[6.56(5.34,8.40) ng/L vs 4.24 (3.01,6.65) ng/L,U=762,P=0.001];[10.65 (5.99,20.70) ng/ml vs 6.12 (4.49,9.98) ng/ml,U=1 406.5,P=0.000].The serum level of visfatin was positively correlated with RF in patients with RA (r=0.186,P=0.013),and serum levels of adiponectin,visfatin and resistin were positively correlated with DAS28 (r=0.370,0.263,0.285;P＜0.05).The level of visfatin in RA patients with high activity group was higher than that in the low and moderate activity group [4.37(2.72,7.53)ng/L vs 4.11 (3.11,6.44) ng/L,U=133.5,P=0.019].Conclusion Multivariate analysis has showm that ESR,PLT and DAS28 can significantly affect adiponectin,and CRP can significantly influence resistin.Serum level of adiponectin,visfatin and resistin are elevated and correlate with DAS28,suggesting that they may be involved in the chronic inflammation of RA.

Objective:To explore the effect of adipose derived mesenchymal stem cells to regulate the differentiation of macrophage RAW264.7.Methods:First,we used RAW264.7 cells to simulate macrophage and induced them to M 1 macrophage with lipopolysaccharide ( LPS,1 μg/ml) .Then we cultured these RAW264.7 cells in culture mediums which were previously used to culture adipose derived mesenchymal stem cells to imitate the transplantation of ADMSC .Last,the mRNA relative expression of IL-10, IGF-1,Arg-1,TNF-α,FIZZ1,SPHK-1 was detected by real-time PCR.The protein expression of IL-12 p40,IL-27 Rα,IL-10 was detected by Western blot.Results:After been cultured in ADMSCCM and induced by LPS ,M1 markers (TNF-αmRNA,IL-12 p40;P<0.05) of the RAW264.7 cells declined while M2 markers (IGF-1 mRNA,IL-10 mRNA,IL-10;P<0.05) rose.Conclusion: ADMSC can secrete soluble cytokines to induce the RAW264.7 cell,which have been induced to the M1 macrophages,to differentiate towards M2 macrophages.

Objective To determine the mRNA levels of microRNA-223 (miR-223) and NLRP3 in-flammasome components [Nod-like receptor pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1] in peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE) and to explore its clinical significance. Methods Real time polymerase chain reaction (PCR) was used to detect the mRNAlevels of miR-223 and NLRP3 inflam-masome components in PBMCs from 35 SLE patients, 30 healthy controls and 20 SLE patients after treatment, and then their correlations with clinical and laboratory parameters [anti-double-stranded deoxyribon-ucleic acid (dsDNA) antibody, anti-nucleosome antibody (AnuA), erythrocyte sedi-mentation rate (ESR)] were evaluated. Data were analyzed using t test or x2 test and Pearson test was used for correlation analysis. Results Com-pared with healthy controls, mRNA levels of miR-223 and Caspase-1 were higher in the PBMCs from SLE patients [(1.17 ±0.15) vs (0.68 ±0.14), t=2.416, P=0.0186; (1.89 ±0.13) vs (1.32 ±0.13), t=3.123, P=0.0027], but the NLRP3 and ASC mRNA expression levels were in the opposite [(0.64 ±0.05) vs (0.98 ±0.06), t=4.442, P<0.01;(0.98±0.08) vs (1.32±0.12), t=2.391, P=0.0198]. Correlation analysis results showed that there was a negative correlation of mRNA levels between the miR-223 and NLRP3 (r=-0.7849, P<0.05), but the miR-223 had no correlation with ASC and caspase-1. The mRNA levels of miR-223 was positively correlated with anti-dsDNA antibody, SLEDAI and ESR (r=0.7035, 0.6923, 0.6873, all P values<0.05), but had no correlation with AnuA. After treatment, the mRNA expression of miR-223 and caspase-1 in PBMCs from SLE patients was significantly reduced [(1.30±0.22) vs (0.79±0.11), t=2.07, P=0.0453; (2.05±0.19) vs (1.50±0.11), t=2.471, P=0.0183], while the mRNA level of NLRP3 increased [(0.69 ±0.08) vs (0.94 ±0.07); t=2.445, P=0.0193]. There was no significant difference in the expression of miR-223 mRNA in PBMCs between lupus nephritis (LN) patients and SLE patients without renal impairment. Conclusion miR-223 and caspase-1 are highly ex-pressed in the PBMCs from patients with SLE, while the mRNA of NLRP3 and ASC is in low expression. The mRNA expression of miR-223 is negatively correlated with NLRP3 and disease activity. Expression of miR-223 mRNA decreases significantly after treatment. So miR-223 may play an important role in the pathogenesis of SLE.