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The Undersea and Hyperbaric Medical Society. A report on the annual scientific meeting 2012, Phoenix, AZ, USA June 21–23

DOI: 10.1186/2046-7648-1-14

Keywords: Diving, Hyperbaric oxygenation, Carbon monoxide poisoning, Traumatic brain injury

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The UHMS annual scientific meeting remains the premier forum for the presentation of both basic science and clinical work in the related fields of diving and hyperbaric medicine. The diving medicine and physiology stream has strong representation from the navies of the world, most notably the US Navy, while the physiology and medicine of hyperbaric oxygen (O2) exposure draws contributors from a wide range of academic institutions around the globe.The mechanisms by which bubbles produce the clinical syndrome of decompression illness (DCI) continue to receive attention. Building on previously published work from the lab of Steven Thom (Institute for Environmental Medicine, PA, USA), a number of groups presented a work further defining the role of endothelial and neutrophil activation, and the interaction of a range of immune mediators. The protective effect of hyperbaric oxygen preconditioning prior to decompression stress via heat shock proteins, as demonstrated in a rat model by Wang Xu (Faculty of Naval Medicine, Shanghai, China), further confirms the ability of hyperbaric oxygen exposure to induce anti-oxidant and anti-apoptotic effects. Thom demonstrated the production of pro-inflammatory micro particles (MPs) in the plasma of human volunteers, having previously demonstrated that the injection of such particles into naive mice reproduced the vascular injury associated with DCI. Interestingly, Thom was unable to show a positive correlation between the number of MPs and bubble numbers in the human volunteers, although there was such a correlation with β-2 integrin expression (an indication of platelet-neutrophil interactions), previously used as an index of decompression stress.Fang and Bao (Institute of Naval Medical Research, Shanghai, China) similarly demonstrated elevated levels of circulating inflammatory cytokines after a provocative decompression, including IFN-γ, TNF-α and IL-6. These changes were associated with the activation of mitogen-activated protein


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