Change and its clinical significance of T-lymphocyte subset in patients with hepatitis B virus-associated liver cancer / 国际检验医学杂志

Objective To assess the expression of T cell subset in patients with hepatitis B virus-associated primary liver cancer (HBV-PLC) and its influence on the clinical outcome.Methods 136 cases with PLC were selected, and divided into HBV-PLC group (78 cases) and non-HBV-PLC group (58 cases) according to HBV infection.The percentage of CD4+T cells, CD8+T cells and Treg cells in serum was tested by flow cytometry.After 6 months of follow-up, HBV-PLC patients were divided into death group and survival group.Binary logistic regression analysis was performed to explore the factor and degree affecting clinical outcome of HBVPLC patients.Results As compared with non-HBV-PLC group, dysregualted T cell subset was observed in the HBV-PLC group, percentage of CD4+T cells and Treg cells in HBV-PLC patients was higher (P＜0.05), while CD8+T cell percentage was decreased (P＜0.05).The percentage of CD4+T cells and Treg cells was higher in death group than survival group (P＜0.05), but CD8+T cell percentage was lower than that of survival group (P＜0.05).T-lymphocyte subset (CD4+T cells and Treg cells) was a strong risk factor for adverse clinical outcome of HBV-PLC (OR values were 3.765 and 2.238, respectively, P＜0.05), but CD8+T cell was a protective factor (OR value was-3.537, P＜0.05).Conclusion Obvious dysfunction of T cellular immune function exists in HBV-PLC patients, and T cell subset may be a predictive factor for clinical outcome of HBV-PLC patients.

Assessment of the quality of randomized controlled trials of delirium prevention of elderly in China / 中国实用护理杂志

Objective To assess the quality of randomized controlled trials (RCTs) of delirium prevention of elderly published in China.Methods The literatures from China National Knowledge Infrastructure(CNKI),WANFANG Data and VIP Database for Chinese Technical Periodicals were evaluated according to Cochrane collaboration's tool for assessing risk of bias and Jadad scale.Results A total of 53 RCTs were included,14 (26.4％,14/53) described radom number table used to generate the random allocation sequence,4 (7.5％,4/53) conducted experiments in a blinded manner,7 (13.2％,7/53) did not use intentionto-treat to analyse those who did not complete the study,9 (17.0％,9/53) had high risk of other bias,none described allocation concealment mechanism and blinding to participants and intercention implementers.Based on Jadad scales,the score was 1-4,average score was (2.3±0.8),19 (35.8％,19/53) were high-quality literatures.Conclusions The quality of present published literatures is not high,the further domestic studies should be designed high-quality to better improve clinical practice.

Blockade of angiotensin II receptors reduces the expression of receptors for advanced glycation end products in human endothelial cells.

OBJECTIVE: Receptors for advanced glycation end products (RAGEs) play crucial roles in atherogenesis. Because tumor necrosis factor alpha (TNFalpha) is expressed and upregulates RAGE expression in atherosclerotic lesions, the TNFalpha-RAGE interaction might be involved in the inflammatory process of atherogenesis. On the other hand, an angiotensin II type-1 receptor blocker (ARB), widely used as an antihypertensive drug, has been reported to have also antiatherosclerotic effects. Thus we investigated whether an ARB exerts antiatherosclerotic effects via inhibiting the TNFalpha-RAGE interaction. METHODS AND RESULTS: Stimulation of human endothelial cells with candesartan as well as olmesartan decreased TNFalpha-induced RAGE expression in both mRNA and protein levels along with the decrease in the activity of nuclear factor kappaB and the expression of inflammatory mediators such as vascular cell adhesion molecule (VCAM)-1. Both candesartan and olmesartan inhibited the binding of nuclear factor kappaB to the RAGE gene promoter. Furthermore, gene silencing of RAGE by RNA interference decreased the expression of TNFalpha-induced VCAM-1 in both mRNA and protein levels. CONCLUSIONS: RAGE contributes at least partially to the TNFalpha-induced VCAM-1 expression in both mRNA and protein levels. Blockade of angiotensin II receptors might exert antiatherosclerotic effects via reducing TNFalpha-RAGE interaction.

The antagonism of aldosterone receptor prevents the development of hypertensive heart failure induced by chronic inhibition of nitric oxide synthesis in rats.

Aldosterone promotes cardiovascular inflammation and remodeling, both of which are characteristic changes in hypertensive and failing hearts. Since chronic inhibition of nitric oxide (NO) synthase with N(omega)-nitro-L-arginine methyl ester (L-NAME) induces systemic hypertension associated with cardiovascular inflammation and remodeling, we examined the potential role of aldosterone in this process using eplerenone, a selective aldosterone receptor antagonist. Ten-week-old male Wistar-Kyoto rats were randomly divided into 3 groups: the control group (no treatment), the L-NAME group (received L-NAME 1 g/L in drinking water), and the L-NAME+Eplerenone group (L-NAME plus eplerenone at 100 mg/kg/day). After 8 weeks of the treatment, the L-NAME group showed significantly higher systolic blood pressure than the control group (198 +/- 7 vs. 141 +/- 3 mmHg, P < 0.05). Eplerenone did not affect the increase in blood pressure caused by L-NAME (189 +/- 12 mmHg). Chronic inhibition of NO synthesis increased the plasma aldosterone concentration and CYP11B2 mRNA in adrenal glands. Cardiac inflammation and fibrosis were detected in the L-NAME group, while both changes were completely prevented by eplerenone. Cardiac hypertrophy was induced in L-NAME group, but was partially prevented by eplerenone. In the L-NAME group, left ventricular fractional shortening (LVFS: 27 +/- 2 vs. 38 +/- 1%) and E/A ratio (1.7 +/- 0.1 vs. 2.1 +/- 0.1) were significantly lower and LV end-diastolic pressure (LVEDP) was higher (4.9 +/- 0.6 vs. 13.9 +/- 0.5 mmHg) without LV enlargement, compared with those in the control group (P < 0.05). Eplerenone completely normalized LVFS (36 +/- 2%), E/A ratio (2.2 +/- 0.1), and LVEDP (6.2 +/- 0.7 mmHg). These results suggest that chronic inhibition of NO synthesis induces cardiac inflammation and dysfunction via an aldosterone receptor-dependent mechanism.