Objective To explore the clinical characteristic,level of plasma renin angiotensin (PRA),plas-ma angiotensin Ⅱ(Ang Ⅱ)and plasma aldosterone(Aldo)in the sleep apnea hypopnea syndrome (SAHS)patients, and to investigate the association between SAHS and hypertension.Methods The patients were selected for the study who were monitored with polysomnography.They were divided into SAHS group and non-SAHS group according to apea-hypopnea index(AHI),and there were 180 patients in the SAHS group,175 patients in the non-SAHS group. The systolic blood pressure(SBP),diastolic blood pressure(DBP)and the level of PRA,plasma Ang II and plasma Aldo were compared by variance analysis.Results The gender composition was different between the two groups,and had statistically significant difference(χ2 =16.30,P <0.01).The data of age,body mass index,neck circumference, waistline,DBP,SBP in SAHS group were significantly higher than those in non-SAHS group,and the differences were statistically significant(t =6.84,8.19,9.84,6.63,7.08,5.45,all P <0.01 ).The prevalence of hypertension in SAHS group was 46.58%,which was higher than 18.20% in non-SAHS group,and the difference had statistically significant(χ2 =46.71,P <0.01).The AHI had positive correlation with SBP,DBP,and they had statistically signifi-cant differences (rs =0.162,0.228,all P <0.01).The levels of PRA and plasma Ang Ⅱ were lower in SAHS group than those in non-SAHS group,while the level of plasma Aldo was higher in SAHS group than that in non-SAHS group,and had statistically significant differences(F =15.41,14.21,17.67,all P <0.01).In the SAHS group,the levels of PRA and plasma Ang Ⅱ were lower in hypertension group than those in non-hypertension group,while the level of plasma Aldo was higher in hypertension group than that in non-hypertension group,and had statistically signif-icant differences (F =15.41,14.21,17.67,all P <0.01).Also,the levels of PRA and plasma Ang Ⅱ were lower in SAHS group with hypertension than those in non-SAHS group with hypertension,while the level of plasma Aldo was higher in SAHS group with hypertension than that in non-SAHS group with hypertension,and the differences were sta-tistically significant(F =15.41,14.21,17.67,all P <0.01).Conclusion The occurrence of SAHS is correlated with the gender composition,age,body mass index,neck circumference,waistline,DBP and SBP.In SAHS complica-tions in each system,the highest incidence is hypertension.And the AHI has positive correlation with SBP,DBP,and the difference is significant.In the SAHS group,if the AHI is higher,the risk of hypertension is greater.In the SAHS patients with hypertension,the level of plasma Aldo is significantly elevated,while the levels of PRA and plasma AngⅡ are decreased significantly.

Objective To explore the mechanism by which the anti-human P185erbB2 scFv-Fc-IL-2(HFI)modulates tumor surface molecules and activates immune effector cells in vitro. MethodsMTT assay was used to test the proliferation and the LAK-like cytotoxicity. Flow cytometry assay was used to test the expression of ICAM-1, Fas and erbB2 receptors in tumor cells and the expression levels of CD molecules FasL and LFA-1 in human PBMC. Antibody-dependent cell-mediated cytotoxicity(ADCC)mediated by HFI against SKOV3, MCF-7 and SGC-7901 tumor cells was explored hv LDH release assay. Results The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI were upregulated, from 24.85％ and 0.53％ to 85.36％ and 59.19％ respectively, while the expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI were downregulated, from 98.48％, 42.60％ and 36.66％ to 94.01％,30.95％ and 12.36％ respectively. HFI could significantly enhance the proliferation activity of human PBMC, and CD3+ CD8+ T cells and CD3- CD16+ CD56+ NK cells were elevated, from 24.37％ and 6.90％ to 38.80％ and 13.45％ respectively. The expression levels of CD25, LFA-1 and FasL were significantly enhanced from 3.99％, 86.52％ and 5.02％ to 12.96％, 99.06％ and 16.19％. The LAK-like cytotoxicity of human PBMC treated with HFI against SKOV3, MCF-7,SGC-7901 tumor cells was significantly improved:HFI was effective in mediating ADCC against SKOV3,MCF-7 and SGC-7901 tumor cells which expressed high,medium and low levels of erbB2,respectively,and HFI-induced ADCC was correlated with the degrees of erbB2 expression on the tumor cells. Conclusion The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI are significantly upregulated. The expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI are downregulated. HFI can significantly enhance the proliferation activity of human PBMC. The LAK-like eytotoxicity of human PBMC treated with HFI against tumor cells is significantly enhanced. HFI iS effective in mediating ADCC and the activity of HFI-induced ADCC is correlated with the degrees of erbB2 expression on the tumor cells.

Objective:To study the effects of ICA on HepG2.2.15 cell proliferation, their sensitivity to the lysis by CD3AK effector cell, to investigate the reversal action of ICA on hepatocarcinoma cells from immune escape through Fas/FasL pathway.To provide the theoretical and experimental bases for ICA development.Methods:MTT assay was used to detect cell proliferation and CD3AK cells cytotoxicity activity;flow cytometry assay was used to examine expression of surface molecules and apoptosis rate of HepG2.2.15 cells.Results:When HepG2.2.15 cells line was treated with 50 ?g/ml ICA,a significant reduction of the rate of cell proliferation was observed. Inhibition rate at 48h was 22.04%,and 29.68% at 72h.Kinetic study showed that inhibition of cell proliferation was time dependent (P0.05).ICA could inhibit apoptosis of Jurkat cells induced by HepG2.2.15 cells. In the co-culture system of HepG2.2.15 cell and Jurkat T cell, apoptosis ratio of Jurkat cell was reduced from 46.66% to 18.20% by ICA (P

Objective To investigate the effects of transient receptor potential cation channel 6 (TRPC6) on the expression of nephrin, desmin and caspase 9 and on the apoptosis of podocytes in a mouse model of podocyte injury induced by TGF-β1.Methods Conditionally immortalized mouse podocytes were cultured in vitro and divided into four groups: control, TGF-β1 treatment, TGF-β1+PGPU6/GFP/Neo-TRPC6-mus-581 (TRPC6 knockdown) and TGF-β1+PGPU6/GFP/Neo-NC (negative control).Real-time RT-PCR and Western blot analysis were performed to detect the expression of nephrin, desmin and caspase 9 at mRNA and protein levels, respectively.Flow cytometry was used to analyze the apoptotic rate of podocytes.DAPI fluorescent staining was used to observe the morphological changes of apoptotic podocytes.Results Green fluorescent protein (GFP)-expressing podocytes at 48 hours after transfection were significantly more than those at 24 hours after transfection.The level of TRPC6 in mouse podocytes transfected with PGPU6/GFP/Neo-TRPC6-mus-581 was significantly decreased as compared with that of the control group (P<0.05).No significant difference in the expression of TRPC6 was observed between the negative control group and the control group.Compared with the control group, the TGF-β1 treatment group showed increased expression of desmin and caspase 9 at both mRNA and protein levels (P<0.01), but decreased expression of nephrin at mRNA and protein levels at 48 hours after TGF-β1 intervention (P<0.05).The up-regulated desmin and caspase 9 and the down-regulated nephrin induced by TGF-β1 could be inhibited by the means of TRPC6 knockdown.The apoptosis rate of podocytes in TGF-β1 treatment group was (14.0±2.1)%, while that in TRPC6 knockdown was (10.90±0.56)% (P<0.05).The apoptosis rate of podocytes in negative control group was higher than that in TGF-β1 treatment group (P>0.05).More apoptotic cells with typical morphological features of apoptosis were observed after exposure to TGF-β1 for 48 hours.Conclusion TGF-β1 could induce the apoptosis of podocytes, inhibit the expression of nephrin and enhance the expression of caspase 9 and desmin, the possible mechanisms of which may be related to TRPC6 signal pathway.These changes in TGF-β1-treated podocytes could be alleviated by inhibiting the expression of TRPC6, which might have a protective effect on podocyte injury.