B-type natriuretic peptide after open-water and hyperbaric chamber exposure to 10 msw.

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. METHODS: Nine healthy volunteers performed a 1-h open-sea air dive at 10 m depth (T); a few days later they were compressed in air in a hyperbaric chamber (CT) using the same dive profile. Three venous blood samples were drawn for each session: before starting the dives (T0 and CT0), immediately after exiting the water and the chamber (T1 and CT1), and 5 h later (T2 and CT2). RESULTS: A significant increase in plasma BNP was found with respect to baseline conditions after scuba diving both at T1 (median increment +32.69% [interquartile range +25.62 to +65.35%]) and at T2 (+28.03% [+23.08 to +38.92%]) while no differences were documented after the same dive in dry conditions either at CT1 (+1.34% [-17.57 to +33.55%]) or at CT2 (0.00% [17,67 to +21.62%]). DISCUSSION: These preliminary findings show that scuba diving and dry hyperbaric exposure, although at the same environmental pressure, cause different effects on ventricular loads in healthy subjects.

A role of the TRAIL-TRAIL receptor system in the pathogenesis of diabetes.

The 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. Noteworthy, depending on the type of diabetes and on the disease stage, TRAIL can have a dual role, either as immune modulator as well as a regulatory molecule of the vascular wall fitness.

Hormonal responses to a long duration exploration in a cave of 700 m depth.

We 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. Friedman two-way ANOVA test evidenced significant changes through the different time intervals for detrended (i.e., test values minus control values) growth hormone (GH) (P = 0.003), detrended cortisol (P = 0.004) and FT4 (P = 0.002), while this was not true for TSH and FT3. Successively pairwise comparisons were done both through the different time intervals and between test and control values. The rise of GH values during the performance underlines the great intensity and long duration characteristic of potholing as well as the possibility that the climbing sit harness can cause problems due to vascular hypo-perfusion. Cortisol data, peaking before entering the cave, suggest that there was a marked anticipatory stress reaction followed by less stressing phase during the performance. Finally, the rise of FT4 is likely due to the typical increase of free fatty acids that usually occurs during endurance exercise.

TNF-related apoptosis-inducing ligand (TRAIL) up-regulates cyclooxygenase (COX)-1 activity and PGE(2) production in cells of the myeloid lineage.

Tumor 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. Importantly, the ability of TRAIL to increase PGE(2) production was also observed in normal, human CD34-derived myeloid cells and in freshly isolated peripheral blood CD14(+) monocytes. Moreover, in contrast to HL-60 cells, primary, normal cells were not susceptible to TRAIL cytotoxicity. These data indicate that the ability of TRAIL to up-regulate eicosanoid production and release is not confined to malignant leukemic cells, but it may also play a role in normal hematopoiesis.