INTRODUCTION: Decompression sickness (DCS) is a complex and poorly understood systemic disease caused by inadequate desaturation after a decrease of ambient pressure. Strong variability between individuals is observed for DCS occurrence. This raises questions concerning factors that may be involved in the interindividual variability of DCS occurrence. This study aimed to experimentally assess the existence of heritable factors involved in DCS occurrence by selectively breeding individuals resistant to DCS from a population stock of Wistar rats.

Background: Ocean racing has become increasingly demanding, both physically and psychologically. The aim of the study was to assess global changes after a transoceanic race. Materials and methods: Eight male sailors were evaluated pre- and post-race through anthropometric measurements (weight, skinfold, girth at different level and estimated body fat percentage), multifrequency tetrapolar bioelectrical impedance, muscular performance, visual analogic scale for perceived fatigue and Critical Flicker Fusion Frequencies for cerebral arousal.

The clinical application of Hyperbaric Oxygen Therapy (HBOT), although based on sound physiological principles as well as on a logical rationale, has often been characterized by empirical procedures, and the choice of the treatment schedules has been more fortuitous than rational. The indication for HBOT and the treatment protocol are originated by the general and often acritical assumption that a given lesion or malfunction is caused, facilitated or worsened by hypoxia. Furthermore, the increasingly common use of multiplace hyperbaric chambers, where many patients can be treated at the same time, although maximizing the cost benefit ration of HBOT and the performance of the chamber technical and nursing personnel justified the commonly adopted routine of using average treatment pressures and schedules without considering the differences between indications, patients, disease conditions and the evolving physiopathological stages of the healing process in the individual patients. As a consequence, it is quite frequent to witness the very strange paradox that a treatment based on extremely solid physiological grounds is often applied empirically and nonrationally.

Saturation divers are exposed to elevated partial pressure of oxygen (ppO2) in their hyperbaric work environment. Experimental studies indicate that oxygen transport is altered, and we have previously reported a drop in hematocrit and extensive downregulation of genes involved in blood oxygen transport capacity after decompression from professional saturation diving. Here we investigate the initial period of hematological adjustment back to normobaric air after professional saturation diving. Erythropoietin (EPO) and hemoglobin (Hb) were measured in blood from 13 divers at two time-points after saturation assignments lasting up to 4 weeks; first immediately after decompression and again 24 h later. Pre-dive levels defined baselines.

Oxygenation conditions are crucial for growth and tumor progression. Recent data suggests a decrease in cancer cell proliferation occurring after exposure to normobaric hyperoxia. Those changes are associated with fractal dimension. The purpose of this research was to study the impact of hyperoxia on apoptosis and morphology of leukemia cell lines. Two hematopoietic lymphoid cancer cell lines (a T-lymphoblastoid line, JURKAT and a B lymphoid line, CCRF-SB) were tested under conditions of normobaric hyperoxia (FiO2 > 60%, ± 18h) and compared to a standard group (FiO2 = 21%). We tested for apoptosis using a caspase-3 assay.