Venous gas embolism as a predictive tool for improving CNS decompression safety

A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached

Resolution of inflammation: a new therapeutic frontier

Dysregulated inflammation is a central pathological process in diverse disease states. Traditionally, therapeutic approaches have sought to modulate the pro- or anti-inflammatory limbs of inflammation, with mixed success. However, insight into the pathways by which inflammation is resolved has highlighted novel opportunities to pharmacologically manipulate these processes — a strategy that might represent a complementary (and perhaps even superior) therapeutic approach. This Review discusses the state of the art in the biology of resolution of inflammation, highlighting the opportunities and challenges for translational research in this field

Measurement of the beam-normal single-spin asymmetry for elastic electron scattering from C12 and Al27

We report measurements of the parity-conserving beam-normal single-spin elastic scattering asymmetries $B_n$ on $^{12}$C and $^{27}$Al, obtained with an electron beam polarized transverse to its momentum direction. These measurements add an additional kinematic point to a series of previous measurements of $B_n$ on $^{12}$C and provide a first measurement on $^{27}$Al. The experiment utilized the Qweak apparatus at Jefferson Lab with a beam energy of 1.158 GeV. The average lab scattering angle for both targets was 7.7 degrees, and the average $Q^2$ for both targets was 0.02437 GeV$^2$ (Q=0.1561 GeV). The asymmetries are $B_n$ = -10.68 $\pm$ 0.90 stat) $\pm$ 0.57 (syst) ppm for $^{12}$C and $B_n$ = -12.16 $\pm$ 0.58 (stat) $\pm$ 0.62 (syst) ppm for $^{27}$Al. The results are consistent with theoretical predictions, and are compared to existing data. When scaled by Z/A, the Q-dependence of all the far-forward angle (theta < 10 degrees) data from $^{1}$H to $^{27}$Al can be described by the same slope out to $Q \approx 0.35$ GeV. Larger-angle data from other experiments in the same Q range are consistent with a slope about twice as steep