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Träfflista för sökning "WFRF:(Lindqvist Niclas) srt2:(2005-2009)"

Sökning: WFRF:(Lindqvist Niclas) > (2005-2009)

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  • Lönnermark, Anders, 1968- (författare)
  • New Energy Carriers in Tunnels
  • 2010
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Environmental issues such as climate change and scarcity of resources have forced the development of new energy carriers for vehicles. This also means that there will be an increase in the number of vehicles running on these new energy carriers in tunnels and other confined spaces. New energy carriers do not necessarily mean higher risks, but they do represent a new situation and imply new risks. These risks need to be evaluated and considered. The mixture of different energy carriers (flammable liquids, gases lighter than air, gases denser than air, batteries, etc.) can also constitute a risk itself, since there are situations where different safety measures need to be taken depending on the energy carrier used and the scenario in question. In this paper some selected new energy carriers are described, in terms of trends and properties. Some countries have restrictions on the use of some energy carriers in confined spaces. These restrictions are presented. Vehicles are involved in accidents, so also vehicles running on new energy carriers. Some vehicle fires involving new energy carriers are presented and discussed in the paper. It is important to learn from these accidents. It is also important that safety issues related to the use of new energy carriers in tunnels are considered, investigated and reported. Systems, not only components, need to be tested to study different possible scenarios and to develop models for these scenarios. When the scenarios are described in a representative way, technical safety solutions, mitigations systems, and rescue service tactics can be developed. It is also important to study how the different systems (detection, ventilation, mitigation) interact and how the models should be altered depending on the scenario.
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  • Näsström, Birgit (författare)
  • Lipoprotein lipase in hemodialysis patients and healthy controls : effects of heparin
  • 2004
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Mortality from cardiovascular disease in patients on chronic hemodialysis (HD) is 10 to 20 times greater than in the general population. One major risk factor is renal dyslipidemia, characterised by an impaired catabolism of triglyceride (TG)-rich lipoproteins with accumulation of atherogenic remnant particles. A contributing factor may be derangement of the lipoprotein lipase (LPL) system, the major lipase in the catabolism of TG-rich lipoproteins. The functional pool of LPL is located at vascular surfaces, and is released by heparin into the circulating blood and extracted and degraded by the liver. Unfractionated heparin (UFH) is commonly used during dialysis to avoid clotting in the extracorporeal devices, but is increasingly replaced by various low molecular weight heparin (LMWH) preparations. Plasma LPL activity is usually lower after injection of LMWH which is therefore said to release less LPL and cause less disturbance of lipoprotein metabolism than UFH. However, animal studies have revealed that LMWH is as efficient as UFH in releasing LPL but is less efficient in retarding hepatic uptake. The aim of this study was to explore the effects of UFH and a LMWH (dalteparin) on LPL activity and TG concentrations in HD-patients compared with healthy controls, matched for age and gender. A disturbed LPL system might contribute to an impaired lipoprotein metabolism, and hence, an aggravated cardiovascular condition. An 8-hour primed infusion of UFH to controls gave rise to an initial peak of LPL activity within 30 minutes. The activity then dropped by almost 80% over the next two hours and levelled off to a plateau that corresponded to 15% of the peak level. When UFH was infused to HD-patients the curve for LPL activity resembled that for controls, but was reduced by 50% during the peak, while the plateau activities were comparable. The interpretation was that the functional pool, represented by the initial peak, was impaired in HD-patients, while the production of lipase molecules, reflected by the plateau, was only marginally reduced. During the peak of LPL activity TG decreased in both groups, but less in HD-patients, as was expected from the lower circulating lipase activity. During the plateau phase with low lipase activity, TG increased towards and beyond baseline values. When dalteparin was infused, the same pattern of plasma LPL activity was observed, although remarkably reduced. In controls the peak was only 30% and the subsequent plateau 40% compared with the activities during the UFH infusion. A bolus of UFH given when the LPL activity had levelled off to a plateau brought out about the same amount of activity, regardless of whether dalteparin or UFH had been infused. The conclusion was that both heparin preparations had reduced endothelial LPL to a similar extent, but that dalteparin less efficiently retarded the hepatic uptake of the enzyme. As a consequence to this, TG tended to reach higher levels after the dalteparin infusion. The LPL activities were further reduced in HD-patients during infusion with dalteparin, the peak was only 27% and the plateau 35% compared with the activities when UFH was infused. There was no decrease in TG, but rather a continuous increase, suggesting a profound depletion of functional LPL. In another study in HD-patients, two anticoagulation regimes based on present clinical practice were compared, and the doses were adjusted to the respective manufacturers recommendation. UFH was administered as a primed infusion, whereas dalteparin was given only as a single bolus pre-dialysis, not followed by an infusion. The results were in line with those in the experimental studies and indicate that also in the clinical setting LMWH interferes with the LPL system as least as much as an infusion of UFH does, and temporarily impairs lipolysis of TG. This interference might, in consequence, contribute to an aggravated cardiovascular condition in HD-patients.
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