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

The role of supply vessels in offshore logistics

Oil companies are gradually becoming more focused on optimizing their upstream logistics. However, little research regarding upstream logistics has been published. We argue that more research would be beneficial and that more attention must be given to one of the largest cost elements in the upstream chain – the supply vessels. We explore the supply vessel as a means of transport and carry out a logistics analysis based on their use on the Norwegian continental shelf. Carrying capacity, sailing, loading and unloading capabilities are established as the main features of a supply vessel. Thereafter we discuss relevant logistical trade-offs within and among these features, and also in relation to the environment the vessels operate in. This elaboration clearly shows the complexity involved when searching for the ‘optimal’ supply vessel. The analysis also indicates the design and logistics system features that should be challenged in the future. We believe that the findings in this article will be of considerable value for both practitioners and academic

Therapeutic Concentrations of Mitoxantrone Elicit Energetic Imbalance in H9c2 Cells as an Earlier Event

Mitoxantrone (MTX) is a chemotherapeutic agent that emerged as an alternative to anthracycline therapy. However, MTX also causes late cardiotoxicity, being oxidative stress and mitochondrial-impaired function proposed as possible mechanisms. This work aimed to investigate the relevance of these mechanisms to the MTX toxicity in H9c2 cells, using therapeutic concentrations. The observed cytotoxicity of MTX was time and concentration dependent in both lactate dehydrogenase leakage assay and MTT reduction assay. Two therapeutic concentrations (100 nM and 1 lM) and three time points were selected (24, 48, and 96 h) for further studies. Both MTX concentrations caused a significant increase in caspase-3 activity, which was not prevented by inhibiting MTX CYP450-metabolism. Significant decreases were observed in the total and reduced glutathione levels only in MTX 100 nM at 96 h; however, neither alterations in oxidized glutathione nor increases in the malondialdehyde levels were observed at any time or concentrations tested. On the other hand, changes in the intracellular ATP levels, mitochondrial membrane potential, and intracellular calcium levels were observed in both concentrations and all time tested. Noteworthy, decreased levels of ATP-synthase expression and activity and increases in the reactive species generation were observed at 96 h in both working concentrations. However, the radical scavenger N-acetylcysteine or the mitochondrial function enhancer L-carnitine did not prevent MTX cytotoxicity. Thus, this work evidenced the early MTX-induced energetic crisis as a possible key factor in the cell injury.This work received financial support from ‘‘Fundação para a Ciência e Tecnologia (FCT),’’ Portugal (EXPL/ DTP-FTO/0290/2012) and by ‘‘Fundo Comunitário Europeu’’ (FEDER) under the frame of ‘‘Eixo I do Programa Operacional Fatores de Competitividade (POFC) do QREN’’ (COMPETE: FCOMP- 01-0124-FEDER-027749). The work was also supported by FCT within the framework of Strategic Projects for Scientific Research Units of R&D (project PEst-C/EQB/LA0006/2011). LGR and VVB thank FCT for their PhD Grant (SFRH/BD/63473/2009 and SFRH/ BD/82556/2011, respectively) and VMC thank FCT for her Post-doc Grant (SFRH/BPD/63746/2009)