Our understanding of decompression physiopathology has slowly improved during this last decade and some uncertainties have disappeared. A better understanding of anatomy and functional aspects of patent foramen ovale (PFO) have slowly resulted in a more liberal approach toward the medical fitness to dive for those bearing a PFO. Circulating vascular gas emboli (VGE) are considered the key actors in development of decompression sickness and can be considered as markers of decompression stress indicating induction of pathophysiological processes not necessarily leading to occurrence of disease symptoms.

The article describes a dataset of doppler ultrasound audio tracks taken on a sample of 30 divers according to the acquisition protocol defined by the Divers Alert Network. The audio tracks are accompanied by a medical evaluation for the decompression sickness risk according to the Spencer's scale levels. During the acquisition campaign, each diver in the post-dive phase was subjected to a double doppler ultrasound examination of approximately 45 seconds each one in the precordial area using a Huntleigh FD1 Fetal doppler probe. The two measurements were separated by a time of 8-10 seconds necessary for carrying out specific physical exercises designed to free the bubbles trapped in the tissues.

Background: A large yet heterogeneous body of literature exists suggesting that endothelial dysfunction appears early in type 1 diabetes, due to hyperglycemia-induced oxidative stress. The latter may also affect vascular smooth muscles (VSM) function, a layer albeit less frequently considered in that pathology. This meta-analysis aims at evaluating the extent, and the contributing risk factors, of early endothelial dysfunction, and of the possible concomitant VSM dysfunction, in type 1 diabetes. Methods: PubMed, Web of Sciences, Cochrane Library databases were screened from their respective inceptions until October 2019. We included studies comparing vasodilatory capacity depending or not on endothelium (i.e., endothelial function or VSM function, respectively) in patients with uncomplicated type 1 diabetes and healthy controls.

Dr Sherlock asks for clarification on the approach adopted by the European Committee on Hyperbaric Medicine (ECHM) to assessing evidence for establishing indications for hyperbaric oxygen treatment (HBOT). Firstly, regardless of the strict process of editing and proof-reading of tables included in the above-mentioned publication, we received comments from some readers that identified imperfect layout of Table 1 and incorrect layout of Table 2 which significantly changed the conclusions to be drawn from them. This concerned both the details of the methodology used and description of the ECHM recommendations and associated levels of evidence. Therefore, those tables are republished in their correct forms in this issue, hoping that this will explain at least some of the doubts and misunderstandings.

PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) microvascular function (laser Doppler flowmetry), as well as endothelial-dependent (flow-mediated dilation) and endothelial-independent (nitroglycerin-mediated dilation) function. Bubble grades were monitored with Doppler according to the Spencer grade.