Objective To investigate the inhibitory effect of curcumin on the telomerase activity of HeLa cells.Methods The growth inhibition rate of HeLa cells treated with curcumin was measured with MTT method.The expression of hTERT mRNA was studied using RT-PCR.Telomerse activity was examined by TRAP-ELISA.Results The growth of HeLa cells treated with curcumin was inhibited in concentration dependent manner and the expression of hTERT mRNA and the level of telomerase activity were down-regulated significantly.Conclusion Curcumin can inhibit telomerase activity of HeLa cells.The underlying mechanism might be related to the down-regulation of hTERT transcription.

Objective To evaluate the prognosis of the decompensated liver cirrhosis by means of MELD-Na score combined with serum cholesterol and endotoxin concentration.MethodsData of 156 hospitalized patients with decompensated liver cirrhosis was retrospectively analyzed.Patients were divided into survival and death group according to follow-ups at 6 months,12 months and 24 months.MELD-Na score was made among 156 patients by detecting relevant indicators.Serum cholesterol and cholesterol levels were measured,too.The relationship between decompensated liver cirrhosis prognosis and MELD-Na score combined with serum cholesterol and endotoxin concentration was analyzed.ResultsNinteen patients died at the follow-up for 6 months.Fifty nine patients died at the followe-up for 12 months.Seventy seven patients died at the follow-up for 24 months.There was significant difference on MELD-Na score,endotoxin concentration and serum cholesterol between the survival group and the death group (t =-9.68,-9.22,11.4,-4.65,-19.60,16.20,-20.0,-18.7,17.3,respectively,P ＜0.05).The best critical value of MELD-Na score to predicate death in patients with decompensated liver cirrhosis was 32 points.The risk of death would rise if MELD-Na score increased.The best critical value of plasma endotoxin to predicate death in patients with decompensated liver cirrhosis was ≥ 12 ng/L.The best threshold value of serum cholesterol to predict death in patients with decompensated liver cirrhosis was ≤ 1.70 mmol/L.ConclusionMELD-Na score,serum cholesterol and serum endotoxin were of higher prognostic value to judge the prognosis of patients with decompensated liver cirrhosis.

Caveolin-1(Cav-1) is a scaffold protein of caveolae that acts as a tumor modulator by interacting with cell adhesion molecules and signaling receptors.Evidence from a variety of studies indicate that caveolin-1 exhibits the heterogeneity of Cav-1 expression in different tumors.Current research has clearly established a role for Cav-1 as a a novel prognostic marker,Future studies will undoubtedly offer novel exciting opportunities to develop anti-cancer therapies.

Objective: To explore sarcoplasmic reticulum ryanodine receptor2 (RyR 2) expression and calcium releasing function in chronic heart failure (CHF) rabbits and to study the impact of long term valsartan treatment in relevant animals. Methods: HF model was established by volume overloading with pressure overloading in experimental rabbits. 27 rabbits were divided into 3 groups: Sham group, HF group and HF+valsartan group. n=9 in each group and the animals were treated for 7 weeks. Left ventricular structure, hemodynamic parameters, expression and functional changes of myocardiocyte sarcoplasmic reticulum RyR 2 were observed and compared among different groups. Results: Compared with Sham group, HF group had increased left ventricular mess index (LVMI), left ventricular end diastolic pressure (LVEDP) and decreased left ventricular shortening fraction, LVEF, all P<0.05. Compared with HF group, HF+valsartan group showed decreased LVMI, LVEDP and increased left ventricular shortening fraction, LVEF, all P<0.05. Sarcoplasmic reticulum RyR 2 expression and calcium releasing function were lower in HF group than Sham group, P<0.05; while they were both higher in HF+valsartan group than HF group, P<0.05. Conclusion: Long term application of valsartan could improve the cardiac function which might be related to increased myocardial sarcoplasmic reticulum RyR 2 expression and calcium releasing function in experimental CHF rabbits.