Introduction: Hyperbaric environment exposure in humans has cardiovascular effects mainly characterized by an increase in afterload and a decrease in cardiac output. In a previous study we did not find B-type natriuretic peptide (BNP) changes in healthy volunteers exposed to hyperbaric oxygen while other authors documented a significant increase in N-terminal pro-BNP after scuba diving. On the basis of these data we hypothesized that dry hyperbaric exposure and scuba diving could have different effects on BNP secretion.
View Article and Find Full Text PDFThe TNF-alpha super-family of cytokines comprises structurally related proteins that play pivotal roles in regulating cell death, immune response and inflammation. A new member of the family namely Tumor necrosis factor alpha-Related Apoptosis-Inducing Ligand (TRAIL) is involved not only in apoptosis and immune regulation, but also it has a provocative role in vascular biology as reported recently. In this report we provide evidence that this new function of TRAIL may have a significance in the pathogenesis of diabetes and in particular in the vascular alterations that occur late during the natural history of the illness.
View Article and Find Full Text PDFWe studied the hypothalamus-pituitary adrenocortical, hypothalamus-pituitary and hypothalamus-pituitary thyroid system responses to a long duration activity (about 20 h) practiced in a demanding environment, characterized by darkness, low temperature and high humidity, namely alpine potholing. We performed four blood drawings in five elite potholers: (1) the morning before the performance, (2) at the bottom of the cave (-700 m), (3) at the end of the ascent, and (4) after 24 h of recovery. Two blood drawings as controls were performed on the same potholers, at the same resting time and with the same experimental procedures as the previous ones.
View Article and Find Full Text PDFTumor necrosis factor-related apoptosis-inducing ligand (TRAIL) up-regulated the expression of constitutive cyclooxygenase (COX)-1 protein in HL-60 cells without affecting COX-2. The TRAIL-mediated COX-1 up-regulation was accompanied by a significant increase of the PGE(2) synthesis and release, which was suppressed by the COX-1 inhibitor valeryl salicylate but not by the COX-2 inhibitor NS-398. Experiments carried out by adding exogenous PGE(2) to HL-60 cells indicated that PGE(2) was not involved in TRAIL cytotoxicity and rather showed a dose-dependent protection against TRAIL-induced apoptosis.
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