Objective To investigate the feasibility of serum cardiac troponin T(cTnT) as a marker of cardiovascular events and hemodialysis (HD) adequacy in maintainence hemodialysis (MHD) patients.Methods Forty-seven cases of MHD patients were randomly divided into two groups (group A and group B).Group A received intermittent HD 4 h thrice one week,and group B received intermittent HD 4 h twice one week plus high-flux hemodiafiltration(HDF) 4 h once one week.Serum examination for blood biochemical indicator,cTnT and echocardiogram was performed every three months and at the time of recruitment.All the patients were followed up until the occurrence of death or cardiovascular events.Results After 3 months treatment,serum cTnT deceased significantly in group B compared with group A,and maintained the lower levels throughout the follow-up.E/A and LVEF had been reduced since 3 months treatment in group A,but stable in group B,E/A was lower in group A after 18 months treatment than that in group B,LVEF was lower in group A after 12 months treatment than that in group B.There were positive correlations between cTnT and E/A or LVEF in 42 cases who accomplished the follow-up of 12 months (r =0.54,0.66,P ＜0.05).Kaplan-Meier survival curve showed that the occurrence of cardiovascular events in patients with cTnT≥0.1μ g/L was higher than that with cTnT ＜0.1 μg/L in (28.5 ± 9.7) months' follow- up (Log-rank test: P =0.02).Both survival analysis and Cox analysis indicated that serum cTnT was a predictor of cardiovascular events in MHD patients.Conclusions Serum level of cTnT can be used as a marker of HD adequacy,and it is a predictor of cardiac events in MHD patients.Regular high-flux HDF increases the adequacy of HD treatment and improves the quality of life in MHD patients.

AIM: We sought to evaluate the expression of apoptosis related genes, p53 and bcl-2, in cultured vascular smooth muscle cells (VSMCs) in which apoptosis was induced by the ligands of PPAR?-ox-LDL,ciglitazone and 15-deoxy-△ 12,14-PGJ 2,and then influenced by PGF 2?,an antagonist of PPAR?. To clarify whether PPAR? is involved in the regulations of p53 and bcl-2.METHODS: Rat aorta smooth muscle cells were isolated and cultured in DMEM containing 10%FBS. ox-LDL,ciglitazone and 15 d-PGJ 2 were added into the medium for 24 h, respectively. Using PGF 2? to inhibit PPAR? activation via activation of MAP kinase. We employed the flow cytometry analysis to quantitatively analyze the apoptosis of VSMCs. Also, we measured and analyzed the discrepancies of the expression of p53 and bcl-2 between every groups. RESULTS: During the process of apoptosis induced by PPAR?,the expression of P53 protein increased (P

Aim To investage the regulatory effect of alizarin on renal interlobar arterial smooth muscle cells. Method The effect of alizarin on BKCa channels was observed by whole-cell patch clamp recording tech-nique. Results Selective BKCa channel blocker ibTX inhibited alizarin-induced outward current(P<0. 05);single smooth muscle cells were incubated in extracel-lular fluid with no Ca2+ 30 minutes, selective L-Ca2+channel blocker nimodipine, selective calcium ion che-lating agent BAPTA-AM and ryanodine inhibited the a-lizarin-induced BKCa channels current, too ( P <0. 05 ) . Conclusion Alizarin relaxes renales interlobar arterial smooth muscle via activation of L-Ca2+ channel firstly, which lead to Ca2+ flowed into cytoplam, and rising of Ca2+ in cytoplam ryanodine receptor indirect-ly, and BKCa is activated at last.

Objective: To explore the effect of LBP X on apoptosis of human leukemia HL 60 cells. Methods: The inhibitory effect of LBP X on growth of HL 60 cells was assayed by MTT method. The membrance fludity was determined with DPH fluorigenic labeling technique. HL 60 cells were stained with Hoechst 33 258 for nuclear morphology analysis. Agarose gel electrophoresis and flow cytometry were used to analyze apoptosis qualitatively and quantitatively. Results: 20-1 000mg/L LBP X inhibited the growth of HL 60 cells in dose dependent manner and the membrance fludity decreased. The nuclei of HL 60 cells treated with LBP X for 48 h shrinked, condensed and cleaved. Agarose gel electrophoresis of DNA from cells treated with LBP X revealed "DNA ladder". HL 60 cells exposed to LBP X showed apoptotic peaks. Conclusion: LBP X can induce apoptosis in human leukemia HL 60 cells.

AIM To explore the antagonistic effect of scutellarin on the liver toxicity of upper limit intake (UL) of Se. METHODS Chemical luminescence was used to determine the scavenging effect of scutellarin on reactive oxygen species (ROS) induced by Na 2SeO 3 in vitro . MDA content, the activities of SOD, CAT, GSH Px and histopathological sections were measured to investigate the effects of scutellarin on Se toxicity in rats. RESULTS In vitro experiment showed the ability of scutellarin to inhibit the generation of ROS effectively. MDA content was significantly decreased, the activities of SOD, CAT and GSH Px were significantly increased and liver injury was alleviated obviously in the UL Se plus scutellarin group as compared to the only UL Se group. CONCLUSION Scutellarin markedly antagonized the liver toxicity of UL Se through scavenging ROS induced by excess Se.

AIM To study the effects of Scutellarin on glutathione peroxidase and thioredoxin reductase gene expression and activities in liver, kidney and testis tissues of rats supplemented with upper limit intake (UL) of Se. METHODS RT PCR and enzyme activities were used to determine GSH Px and TR mRNA levels and activities. RESULTS GSH Px and TR mRNA levels and activities were remarkably decreased in livers of rats supplemented with UL Se. Scutellarin significantly increased GSH Px and TR mRNA levels and activities in livers of rats supplemented with UL Se. No significant effects were found in rats treated with only Scutellarin as compared with the control. There were also no significant effects of UL Se on GSH Px and TR mRNA levels and activities in rat kidney and testis. CONCLUSION Scutellarin effectively antagonized the decrease of GSH Px and TR mRNA levels and activities in rat livers due to supplementation with UL. The effect of UL on GSH Px and TR mRNA levels shows tissue specificity.

Objective: To study the effects of sodium selenite at large doses on selenoenzyme gene expression and activity in rat livers. Methods: Rats were injected intra-peritoneally (ip) with 0, 20, 40, and 80 ?g /(kg?d) Se of sodium selenite dissolved in 0.9% physiological saline for 15 days. Livers were sampled and partly used for histological study. The rests were homogenized for reverse transcription-polymerase chain reaction to semi-quantitatively detect differential gene expressions of glutathione peroxidase (GSH-Px) and thioredoxin reductase (TR) in livers. Meanwhile, selenoenzyme activities, Se contents and MDA levels were also measured. Results: Compared with the control group, the mRNA levels and enzyme activities of both GSH-Px and TR increased in rats supplemented with 20 ?g/(kg?d) selenite. However, the mRNA levels and activities of both selenoenzymes decreased significantly in rats injected with selenite at doses of 40 and 80 ?g /(kg?d) respectively (P

Objective:To investigate effects of miR-503 on cisplatin sensitivity in BEL-7402 cells by targeting of bcl-2.Methods:MiR-503 and bcl-2 mRNA expression levels in hepatocellular carcinoma cells were measured by real-time quantitative (qRT)-PCR;Bcl-protein level was detected by Western blot;miR-503 mimics were transiently transfected to the BEL-7402 cells by liposome transfection;potential target genes of miR-503 were predicted by Bioinformatics software;miR-503 potential targets were validated by dual luciferase activity;and the cell viability was measured by MTT assay.Results:MiR-503 level was down-regulated and Bcl-2 protein expression level was up-regulated in BEL-7402 cells compared with HL-7702 cells.MiR-503 could interact with bcl-2 and inhibit its expression.Cell vitality with miR-503 transfection was significantly reduced compared to that in the negative control.Conclusion:MiR-503 may enhance the sensitivity of BEL-7402 cells to cisplatin and inhibit the cell proliferation by targeting bcl-2.

Objective To investigate the apoptosis of T lymphocytes,the expression of Bcl-2, Fas on the peripheral blood T lymphocytes in end stage renal disease patients;and to explore the characteristics of Th1 /Th2 profile and the influence of dialysis membranes with different permeability on the apoptosis of T lymphocytes of maintenance hemodialysis patients.Methods The study included 10 non-dialyszed (ND)patients,45 maintenance hemodialysis patients with cellulose acetate (CA) membranes(13),low-flux polusulfone(PS-LF) membranes(16),high-flux polusulfone (PS-HF) membranes (16) and 8 healthy volunteers (C).The apoptosis of T lymphocytes,expression of Bcl-2,Fas on peripheral blood T lymphocytes cultured with phytohemagglutinin (PHA) stimulation for 24 hours were measured by flow cytometry and immunohistochemical.ELISA was performed for detecting the levels of IFN-?and IL-4 in culture supematants.Results In ESRD patients,the apoptosis of T lymphocytes was greater than that of group C.Group CA was greater than group PS-HF and group PS-LF (P＜0.05).The expression of Bcl-2 on T lymphocytes in ESRD patients was lower than that of group C (P＜0.05).There was negative correlation between the T lymphocytes apoptosis and Bcl-2. The expression of Fas on T lymphocytes in ESRD patients was greater than that of group C (P＜0.05), and it was positive correlated with T lymphocytes apoptosis.The level of IFN-?of ESRD patients was decreased significantly compared with that in group C (P＜0.05),and there was negative correlation between T lymphocytes apoptosis and IFN-?.IL-4 was increased in ESRD patients (P＜0.05) and it was positive correlated with T lymphocytes apoptosis.Conclusions The accelerated apoptosis of T lymphocytes in ESRD patients may be related to the expression of Bcl-2 and Fas of T lymphocytes.ESRD patients show a suppressed secretion of IFN-?and an increased secretion of IL-4. T lymphocytes apoptosis of maintenance hemodialysis patients is influenced not only by the biocompatibility but also by the permeability of the dialysis membrane.

Gene Expression Profiling ; Humans ; Killer Cells, Natural ; pathology ; Lymphoma, T-Cell ; genetics ; metabolism ; pathology ; Nose Neoplasms ; genetics ; metabolism ; pathology ; Oligonucleotide Array Sequence Analysis ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics