Objective To determine whether rs28364072 polymorphism in the low-affinity IgE receptor (FCER2)is associated with asthma risk in Chinese Han nationality asthmatics.Methods 120 cases of asthmatics and 116 healthy control subjects were enrolled in this study.DNA was purified from peripheral blood,and genotyping of rs28364072 SNP was performed by PCR and Sanger sequencing.The clinical indexes were compared between asthmatic subjects.Results A significant difference was found in the distributions of the genotyges (TT,TC,CC)and allele frequency among populations in north Indian,Saudi Arabian,Romas and Chinese Han nationality.A significant difference was also found in the distributions of the genotyges (TT,TC,CC) between asthmatic subjects and controls.Significant difference was observed in the allele (T/C) frequency between asthmatic subjects and healthy controls.The presence of C allele of GLCCI1 gene was found to be a greater risk factor in asthmaticsubjects compared with the healthy controls.The odds ratio (OR) of CC and CC+TC were 2.73 (1.19 ～ 6.23),2.05 (1.21 ～ 3.48),respectively.There was significant difference in the ACT score,EOS％ between CC and TT genotyge.Conclusion The minor alleles C of rs28364072 SNP was significantly associated with the increase of asthma risk in asthma patients of of Han Nationality of Chinese.

To explore the expression and clinical significance of molecular chaperone heat shock protein 90 (HSP90) in peripheral blood mononuclear cells (PBMC) and plasma level of interleukin-6 (IL-6) in patients with systemic lupus erythematosus (SLE), HSP90 was detected in PBMC by Western blot assay and the plasma level of IL-6 was measured by ELISA in 38 SLE patients and 20 normal controls. The correlation analysis was performed between the SLE disease activity index (SLE-DAI) and the expression of HSP90 and IL-6. The results showed that there was increased expression of HSP90 in the SLE patients. The active SLE group exhibited higher HSP90 levels (0.82+/-0.10) than the inactive SLE group (0.54+/-0.09) (P<0.01). The expression of HSP90 in normal control group (0.37+/-0.11) showed significant statistical difference as compared to both the inactive and active SLE groups (P<0.01, P<0.01, respectively). The plasma level of IL-6 exhibited a significant increase in both the inactive and active SLE groups (28.99+/-1.74 pg/mL, 44.58+/-9.15 pg/mL, respectively) compared with normal control group (P<0.01, P<0.01, respectively). The expression of HSP90 and IL-6 in SLE patients showed significant positive correlation with SLEDAI scoring (r=0.80, P<0.01: r= 0.74, P<0.01, respectively). In addition, there was a positive correlation between the level of IL-6 and HSP90 in SLE patients (r=0.86, P<0.01). The increased expression of molecular chaperone HSP90 and IL-6 may play an important role in the pathogenesis of SLE by regulating autoimmunity.

Objective To investigate the mRNA expression of a proliferation inducing ligand (APRIL) and its receptors including B cell maturation antigen (BCMA),transmembrane activator.calcium modulator and cyclophilin ligand interactor (TACI) in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SEE).Methods APRIL mRNA、BCMA mRNA and TACI mRNA in PBMCs were detected by real-time quantitative PCR in 66 SLE patients and 25 normal controls.Gene expression level was measured as 2-AACT.Results The expression levels of APRIL mRNA、BCMA mRNA and TACI-mRNA were significantly increased in both active SLE group and stable SLE group compared with those in the normal controls(P<0.01 for all).The expression levels of APRIL mRNA and TACI mRNA in active SLE group were significantly higher than those in stable SLE group(P<0.01,P<0.05,respectively).But there was no significant difierence in the expression levels of BCMA mRNA between the SLE stable and active groups-Beside,the expression levels of APRIL mRNA and TACI mRNA were significantly increased in patients with lupus nephritis (LN) compared to patients with non-LN (P<0.01 for all).Conclusion The expression levels of APRIL and its receptors are significantly elevated in SLE patients.It may suggest that APRIL and its receptors play an important role in the pathogenesis of SLE.

AIM:To investigate whether the association of connexin 43 ( Cx43 ) and L-type calcium channel involved in the pathogenesis of atrial fibrillation ( AF) .METHODS:The biochemical assays and whole-cell patch-clamp technique were used to study the expression of Cx43 in human atrial tissue.The co-localization of Cx43 and L-type calcium channel, and the regulation of L-type calcium current in atrial myocytes were investigated.RESULTS:The expression of Cx43 at mRNA and protein levels was decreased in human atrial tissues of AF patients.In cultured atrium-derived myocytes ( HL-1 cells) , knockdown of Cx43 significantly inhibited the mRNA expression of L-type calcium channelα1c subunit, as well as L-type calcium current.Co-localization of Cx43 with L-type calcium channel α1c subunit in mouse atrial myocytes was observed.CONCLUSION:The decrease in Cx43 is involved in the pathogenesis of AF, probably through reducing the L-type calcium current in atrial myoctyes by co-localization with L-type calcium channel, thus representing the potential pathogenesis in atrial fibrillation.

AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .

To explore the expression and clinical significance of molecular chaperone heat shock protein 90 (HSP90) in peripheral blood mononuclear cells (PBMC) and plasma level of interleukin-6ells (PBMC) and plasma level of interleukin-6(IL-6) in patients with systemic lupus erythematosus (SLE), HSP90 was detected in PBMC by West and the plasma level of IL-6 was measured by ELISA in 38 SLE patients and 20 normal controls. The correlation analysis was performed between the SLE disease activity index (SLEe results showed that there was increased expression of HSP90 in the SLE patients. The active SLE group exhibited higher HSP90 levels (0.82±0.10) than group (0.54±0.09) (P＜0.01). The expression of HSP90 in normal control group (0.37±0. 11) showed significant statistical difference as compared to both the inactive and active SLE The plasma level of IL-6 exhibited a significant increase in both the inactive and active SLE groups (28.99±1.74 pg/mL, 44.58±9.15 pg/mL, respectively) com0.01, P＜0.01, respectively). The expression of HSP90 and IL-6in SLE patients showed significant positive correlation with SLEDAI scoring (r=0.80, P＜0.01: r=. In addition, there was a positive correlation between the level of IL-6 and HSP90 in SLE patients (r= 0.86, P＜0.01). The increased expression of molecular chaperone HSP90thogenesis of SLE by regulating autoimmunity.

Summary: CD4+CD25+ regulatory T cells (Tregs) and the expression of their molecular markers (GITR, Foxp3) in peripheral blood of the patients with systemic lupus erythematosus (SLE) were investigated in order to reveal the pathogenesis of SLE on the cellular and molecular levels. The level of Tregs in peripheral blood was detected by flow cytometry. The expression levels of GITR and Foxp3 mRNA in peripheral blood mononuclear cells (PBMCs) were assayed by reverse transcriptasepolymerase chain reaction (RT-PCR). The level of IL-6 in the plasma was measured by ELISA.Comparisons were made among 3 groups: the active SLE group, the inactive SLE group, and normal control group. The level of Tregs in the active SLE group and the inactive SLE group was significantly lower than in the normal control group (P<0.01). The level of Tregs in the active group was lower than in the inactive group with the difference being not significant (P>0.05). The level of Tregs in SLE patients was significantly negatively correlated with the disease active index in SLE (SLEDAI) (r=--0.81, P<0.01). The expression levels of GITR mRNA in PBMCs of the active SLE group and the inactive SLE group were significantly higher than in the normal control group (P<0.05), and those of Foxp3 mRNA in SLE patients of both active and inactive SLE groups were significantly lower than in the normal control group (P<0.05). There was no significant difference in the expression of GITR and Foxp3 mRNA between the active SLE group and inactive SLE group (P>0.05). The plasma levels of IL-6 in both the inactive SLE group and active SLE group were significantly higher than in the normal control group (P<0.01). The plasma level of IL-6 in the active S LE group was significantly increased as compared with that in the inactive SLE group (P<0.05), and the plasma level of IL-6 in SLE was significantly positively correlated with SLEDAI scores (r=0.58, P<0.01) and significantly negatively correlated with the ratio of CD4+CD25+ cells/CD4+ cells (r=-0.389, P<0.05). It was concluded that the levels of Tregs and Foxp3 mRNA in peripheral blood of SLE patients were decreased and the levels of GITR mRNA and plasma IL-6 were increased. The Tregs and their molecular markers GITR, Foxp3 as well as the plasma IL-6 might play an important role in the pathogenesis of SLE.