Rise-time requirements for high-intensity discharge headlights

This study had two objectives. The first, more general objective was to provide background information about the maximum rise time that should be allowed for highintensity discharge headlamps. The second, more specific objective was to evaluate whether SAE’s current, rather stringent, recommendations should be relaxed or retained. To achieve these objectives, we considered several scenarios in which having early illumination is potentially of consequence. The scenarios included turning on the headlamps when starting to drive, turning on the headlamps when entering a dark tunnel, and switching between beams. New empirical data collected for this study included actual delays between turning on headlamps at night and starting to drive, and rise and falloff functions of tungsten-halogen low beams and high beams. We concluded that rise-time requirements should be more stringent for systems with noncontinuous low beam than for systems with continuous low beam, as is the case in the current SAE recommendations. Furthermore, we concluded that the current SAErecommendations for systems with noncontinuous low beam are justifiable. On the other hand, we concluded that the SAE recommendations for systems with continuous low beams could be relaxed by eliminating all minimum light-output requirements for delays of less than one second.Michigan University, Ann Arbor, Industry Affiliation Program for Human Factors in Transportation Safetyhttp://deepblue.lib.umich.edu/bitstream/2027.42/49445/1/UMTRI-2001-14.pd

The effect of fog on detection of driving hazards after dark

The presence of fog leads to an increase in road traffic accidents. An experiment was carried out using a scale model to investigate how the detection of hazards in peripheral vision was affected by changes in luminance (0.1 cd/m2 and 1.0 cd/m2 road surface luminance), scotopic/photopic (S/P) ratio (0.65 and 1.40) and fog density (none, thin and thick). Two hazards were used, a road surface obstacle and lane change of another vehicle. Increasing luminance, and reducing from thick to thin fog, led to significant increase in detection rate and a reduction in reaction time, for both types of hazard. The effect of a change in S/P ratio was significant only when measuring detection of the surface obstacle using reaction times, under the thick fog, with an increase in S/P ratio leading to a shorter reaction time

Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice

Background: Brain edema as a result of secondary injury following traumatic brain injury (TBI) is a major clinical concern. Neutrophils are known to cause increased vascular permeability leading to edema formation in peripheral tissue, but their role in the pathology following TBI remains unclear. Methods: In this study we used controlled cortical impact (CCI) as a model for TBI and investigated the role of neutrophils in the response to injury. The outcome of mice that were depleted of neutrophils using an anti-Gr-1 antibody was compared to that in mice with intact neutrophil count. The effect of neutrophil depletion on blood-brain barrier function was assessed by Evan's blue dye extravasation, and analysis of brain water content was used as a measurement of brain edema formation (24 and 48 hours after CCI). Lesion volume was measured 7 and 14 days after CCI. Immunohistochemistry was used to assess cell death, using a marker for cleaved caspase-3 at 24 hours after injury, and microglial/macrophage activation 7 days after CCI. Data were analyzed using Mann-Whitney test for non-parametric data. Results: Neutrophil depletion did not significantly affect Evan's blue extravasation at any time-point after CCI. However, neutrophil-depleted mice exhibited a decreased water content both at 24 and 48 hours after CCI indicating reduced edema formation. Furthermore, brain tissue loss was attenuated in neutropenic mice at 7 and 14 days after injury. Additionally, these mice had a significantly reduced number of activated microglia/macrophages 7 days after CCI, and of cleaved caspase-3 positive cells 24 h after injury. Conclusion: Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice

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