Methods and Results: Fifty-four consecutive patients (mean age 58.3 years,

83% males) recovering from acute MI were included in the study protocol. All patients underwent Doppler-echocardiography, cardiopulmonary exercise, and HMGB-1 assay. HMGB-1 levels in acute MI patients were significantly higher compared with age- and body mass index-matched controls (14.8 +/- 6.8 vs. 2.3 +/- 1.0 ng/mL, P < .0001, respectively). Postinfarction patients showed oxygen consumption at peak exercise (VO(2peak)) = 14.4 CX-6258 inhibitor +/- 4.2 mL.kg.min and a slope of increase in ventilation over carbon dioxide output (VE/VCO(2slope)) = 32.1 +/- 6.2, whereas Doppler-echocardiography values were: left ventricular end-diastolic volume (LVEDV) = 53.4 +/- 8.2 mL/m(2); left ventricular ejection fraction (LVEF) = 41.7 +/- 7.0%. Multiple linear regression analysis (stepwise method) showed that VO(2peak) (beta = -0.276, P = .012), VE/VCO(2slope) (beta = 0.244, P = .005), LVEDV (beta = 0.267, P =

.018), peak creatine kmase-MB (beta = 0.339, P = .004), peak Troponin I (beta = 0.244, P = .002), and LVEF (beta = -0.312, P = .021) were significantly associated with HMGB-1 levels.

Conclusions: The present study demonstrated that in postinfarction patients, HMGB-1 levels were significantly higher compared with controls, and significantly correlated with cardiopulmonary and Doppler-echocardiography parameters. (J Cardiac Fail 2009;15:362-367)”
“beta-Amyloid (A)-induced neurotoxicity is a major pathological mechanism of Alzheimer’s disease (AD). Xanthoceraside,

a triterpene extracted from the husk of Xanthoceras find more sorbifolia Bunge, has been shown to have therapeutic effects on learning and memory impairment induced by A intracerebroventricular infusion in mice. In this study, we investigated the effect of xanthoceraside on the neurotoxicity of A(25-35) in SH-SY5Y cells. Cell viability was measured by MTT (3-(3,4-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide) assay. Cell apoptosis, reactive oxygen species (ROS) generation, and mitochondrion membrane potential (MMP) were measured using Annexin V/propidium iodide, selleck compound 2,7-dichlorofluorescein diacetate, and rhodamine 123 with flow cytometry, respectively. Intracellular calcium level was determined with Fura-2/AM. Caspase-3 activity in cell lysates was measured using the spectrophotometric method. Results indicated that pretreatment with xanthoceraside (0.01 and 0.1M) obviously increased the viability of SH-SY5Y cells injured by A(25-35) in a dose-dependent manner. A(25-35)-induced early apoptosis, ROS overproduction, MMP dissipation, intracellular calcium overload, and increase in caspase-3 activity were markedly reversed by xanthoceraside. These findings suggested that xanthoceraside might be useful in the prevention and treatment of AD.”
“Glomerular hyperfiltration (>140 ml/min per 1.