The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Igor B Mekjavic - One of the best experts on this subject based on the ideXlab platform.
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finger and toe temperature responses to local cooling and rewarming have limited predictive value identifying susceptibility to local Cold Injury a cohort study in military cadets
Applied Ergonomics, 2020Co-Authors: Lena Norrbrand, Igor B Mekjavic, Roger Kolegard, Michail E Keramidas, Ola EikenAbstract:Abstract The purpose was to evaluate whether a Cold-water immersion test could be used to identify individuals susceptible to local Cold injuries (LCI). Sixty-five healthy non-injured (N–I) subjects, and fifteen subjects, who were tested either prior to or after a LCI, sequentially immersed one hand and one foot, in 8 °C water for 30 min (CWI phase); this was followed by 15 min of spontaneous rewarming (RW phase). The LCI group showed a lower toe temperature during the CWI phase, and a lower maximum RW temperature of the fingers than the N–I group. However, digit temperatures during the CWI and RW phases exhibited low predictive values for LCI, e.g. results implied that to identify 80% of the LCI subjects, 34–78% of the N–I subjects would also be excluded. Thus, the results suggest that, in practice, hand or foot Cold-water immersion tests cannot be used to identify individuals at high risk of LCI.
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finger and toe temperature responses to Cold after freezing Cold Injury in elite alpinists
Wilderness & Environmental Medicine, 2015Co-Authors: Shawnda A Morrison, Jurij Gorjanc, Ola Eiken, Igor B MekjavicAbstract:Objective To assess whether previous freezing Cold injuries (FCI) would affect digit skin temperatures and rewarming rates during a follow-up Cold stress test protocol. Design Nonrandomized control trial. Methods Twenty elite alpinists participated; alpinists with previous FCI requiring digit amputations (injured, INJ: n=10 total, n=8 male) were compared with ability-matched, uninjured alpinists (control, CON: n=10, all male). Digit skin temperature was measured using infrared thermography as an index of peripheral digit perfusion after a Cold stress test, which consisted of 30 minutes of immersion in 8°C water. Results The INJ alpinists' injured toes were warmer (approximately 6%) than their uninjured toes immediately after Cold immersion (95% CI, 0.01°C to 1.00°C; P = .05); there were no differences between the rates of rewarming of injured and uninjured toes (INJ, 0.5° ± 0.1°C/min; CON, 0.7° ± 0.3°C/min; P = .16). Although the INJ alpinists had Colder injured fingers immediately after the 35°C warm bath compared with their own uninjured fingers (32.2° ± 2.0°C vs 34.5° ± 0.5°C; P = .02), there were no differences observed between the rates of rewarming of injured and uninjured fingers after Cold exposure (INJ, 1.1° ± 0.2°C/min; CON, 1.3° ± 0.5°C/min; P = .22). Conclusions Even after FCI that requires digit amputation, there is no evidence of different tissue rates of rewarming between the injured and uninjured fingers or toes of elite alpinists.
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static and dynamic evaluation of biophysical properties of footwear the jozef stefan institute sweating thermal foot manikin system
人間-生活環境系シンポジウム報告集, 2005Co-Authors: Igor B Mekjavic, Borut Lenart, Miro Vrhovec, Martin Tomsic, Naoshi Kakitsuba, Nigel A S Taylor, Howard OakleyAbstract:Abstract : Freezing and non-freezing Cold Injury occurs predominantly in the extremities, with the feet being at greatest risk. Inappropriate footwear is the main cause for Cold Injury of the feet. Ensuring that footwear meets minimal biophysical standards is therefore essential in preventing Cold Injury. The Thermal Foot Manikin System comprises a sweating thermal foot manikin, a gait simulator and a control unit. The foot manikin has 10 segments constructed of a silver-copper alloy. Each segment is heated and the temperature of each segment is monitored. Water is delivered to 6 sweat glands in each of the 10 segments, distributed over the segment surface by a thin cotton layer. Each segment is covered by a water impermeable, but water vapor permeable membrane, ensuring that only water vapor crosses the membrane. In this manner, the resistance to water vapor may be determined from each of the 10 segments. By disconnecting the sweat gland activity, the same analysis provides a value of insulation for each segment. The manikin is attached to a gait simulator, which can simulate different stride magnitudes and walking paces. The gait simulator simulates the heel-to-toe action of walking and also simulates the ground reaction forces. The manikin also allows biomechanical analysis of footwear during simulated gait. The thermal foot manikin is able to analyze the static and dynamic biophysical properties of footwear in sub-zero environments. The differences in the results obtained in the static and simulated gait mode are due to friction between the foot manikin and footwear, and due to footwear design. In the biomechanical mode, the foot manikin allows the assessment of wear, as well as how such wear affects biophysical properties. The developed thermal foot manikin gives industry the capability to develop footwear with biophysical properties specified by the customer. Such a strategy will reduce the risk of Cold Injury.
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static and dynamic evaluation of biophysical properties of footwear the jozef stefan institute sweating thermal foot manikin system
人間-生活環境系シンポジウム報告集, 2005Co-Authors: Igor B Mekjavic, Borut Lenart, Miro Vrhovec, Martin Tomsic, Naoshi Kakitsuba, Nigel A S Taylor, Howard OakleyAbstract:Abstract : Freezing and non-freezing Cold Injury occurs predominantly in the extremities, with the feet being at greatest risk. Inappropriate footwear is the main cause for Cold Injury of the feet. Ensuring that footwear meets minimal biophysical standards is therefore essential in preventing Cold Injury. The Thermal Foot Manikin System comprises a sweating thermal foot manikin, a gait simulator and a control unit. The foot manikin has 10 segments constructed of a silver-copper alloy. Each segment is heated and the temperature of each segment is monitored. Water is delivered to 6 sweat glands in each of the 10 segments, distributed over the segment surface by a thin cotton layer. Each segment is covered by a water impermeable, but water vapor permeable membrane, ensuring that only water vapor crosses the membrane. In this manner, the resistance to water vapor may be determined from each of the 10 segments. By disconnecting the sweat gland activity, the same analysis provides a value of insulation for each segment. The manikin is attached to a gait simulator, which can simulate different stride magnitudes and walking paces. The gait simulator simulates the heel-to-toe action of walking and also simulates the ground reaction forces. The manikin also allows biomechanical analysis of footwear during simulated gait. The thermal foot manikin is able to analyze the static and dynamic biophysical properties of footwear in sub-zero environments. The differences in the results obtained in the static and simulated gait mode are due to friction between the foot manikin and footwear, and due to footwear design. In the biomechanical mode, the foot manikin allows the assessment of wear, as well as how such wear affects biophysical properties. The developed thermal foot manikin gives industry the capability to develop footwear with biophysical properties specified by the customer. Such a strategy will reduce the risk of Cold Injury.
Duncan J Stewart - One of the best experts on this subject based on the ideXlab platform.
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increased caveolin 1 expression precedes decreased expression of occludin and claudin 5 during blood brain barrier breakdown
Acta Neuropathologica, 2007Co-Authors: Sukriti Nag, Roopa Venugopalan, Duncan J StewartAbstract:The significance of caveolin-1, a major constituent of caveolae, and the tight junction proteins occludin and claudin-5 in early blood–brain barrier (BBB) breakdown was assessed by sequential demonstration of the expression of these proteins over a period of 12 h to 6 days post-lesion in the rat cortical Cold Injury model. Pial and intracerebral vessels of control rats showed punctuate endothelial immunoreactivity for caveolin-1 and caveolin-2, while claudin-5 and occludin were localized as longitudinal strands in endothelium. During the early phase of BBB breakdown following Injury at 12 h and on day 2, western blot analyses detected a significant increase in caveolin-1 expression at the lesion site while immunohistochemistry showed that the caveolin-1 increase was localized to the endothelium of lesion vessels. Decreased expression of occludin occurred at the lesion site only on days 2 and 4 post-lesion while claudin-5 expression was decreased only on day 2. Dual labeling for fibronectin, a marker of BBB breakdown, and caveolin-1 or the tight junction proteins demonstrated that only lesion vessels with BBB breakdown showed a marked increase of caveolin-1, loss of occludin and reduced localization of claudin-5. The issue whether these alterations precede or follow BBB breakdown is uncertain; however, increased expression of caveolin-1 preceded the decreased expression of occludin and claudin-5. Thus caveolae and caveolin-1 have an important role in early BBB breakdown and could be potential therapeutic targets in the control of early brain edema.
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altered expression of angiopoietins during blood brain barrier breakdown and angiogenesis
Laboratory Investigation, 2003Co-Authors: Nima Nourhaghighi, Jaime Davis, Krystyna Teichertkuliszewska, Duncan J StewartAbstract:Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) belong to a novel family of endothelial growth factors that function as ligands for the endothelial-specific receptor tyrosine kinase, Tie-2. Ang-1 reduces endothelial permeability of noncerebral vessels and has a major role in vascular stabilization and maturation, whereas Ang-2 is thought to be an endogenous antagonist of the action of Ang-1 at Tie-2. Expression of these ligands at the mRNA and protein level were studied during both blood-brain barrier (BBB) breakdown and cerebral angiogenesis occurring in the rat cortical Cold-Injury model by RT-PCR analysis and immunohistochemistry respectively, during a time course of 6 hours to 6 days. In addition, immunohistochemical detection of fibronectin was used to detect BBB breakdown at the lesion site and dual labeling was used to determine whether the vessels demonstrating BBB breakdown expressed endothelial Ang-1 or Ang-2. Endothelial Ang-1 and Tie-2 proteins were present in all cerebral vessels of normal brain including those of the choroid plexuses, whereas both these proteins as well as Ang-2 were present in choroid plexus epithelium and in ependymal cells, suggesting that angiopoietins have an autocrine effect on these cell types as well. In contrast, in the early phase after Injury during the known period of BBB breakdown, increased Ang-2 mRNA and protein and decreased endothelial Ang-1 and Tie-2 proteins were observed. Two to 6 days after Injury, the progressive increase in Ang-1 mRNA and protein and the decrease in Ang-2 coincided with cerebrovascular angiogenesis. Confocal microscopy showed colocalization of both Ang-1 and Ang-2 in endothelium of lesion vessels, and our observation of colocalization of Ang-1 and Ang-2 in polymorphonuclear leukocytes and macrophages has not been reported previously. This study demonstrates that Ang-1 is an important factor in maintaining normal homeostasis in the brain. Thus Ang-1 therapy may have therapeutic potential in reducing BBB breakdown and the ensuing edema after massive brain Injury.
Richard E Lee - One of the best experts on this subject based on the ideXlab platform.
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rapid Cold hardening protects against sublethal freezing Injury in an antarctic insect
The Journal of Experimental Biology, 2019Co-Authors: Nicholas M Teets, Yuta Kawarasaki, Leslie J Potts, Benjamin N Philip, J D Gantz, David L Denlinger, Richard E LeeAbstract:ABSTRACT Rapid Cold hardening (RCH) is a type of beneficial phenotypic plasticity that occurs on extremely short time scales (minutes to hours) to enhance insects9 ability to cope with Cold snaps and diurnal temperature fluctuations. RCH has a well-established role in extending lower lethal limits, but its ability to prevent sublethal Cold Injury has received less attention. The Antarctic midge, Belgica antarctica, is Antarctica9s only endemic insect and has a well-studied RCH response that extends freeze tolerance in laboratory conditions. However, the discriminating temperatures used in previous studies of RCH are far below those ever experienced in the field. Here, we tested the hypothesis that RCH protects against non-lethal freezing Injury. Larvae of B. antarctica were exposed to control (2°C), direct freezing (−9°C for 24 h) or RCH (−5°C for 2 h followed by −9°C for 24 h). All larvae survived both freezing treatments, but RCH larvae recovered more quickly from freezing stress and had a significantly higher metabolic rate during recovery. RCH larvae also sustained less damage to fat body and midgut tissue and had lower expression of two heat shock protein transcripts (hsp60 and hsp90), which is consistent with RCH protecting against protein denaturation. The protection afforded by RCH resulted in energy savings; directly frozen larvae experienced a significant depletion in glycogen energy stores that was not observed in RCH larvae. Together, these results provide strong evidence that RCH protects against a variety of sublethal freezing injuries and allows insects to rapidly fine-tune their performance in thermally variable environments.
Pak H Chan - One of the best experts on this subject based on the ideXlab platform.
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overexpression of copper and zinc superoxide dismutase in transgenic mice prevents the induction and activation of matrix metalloproteinases after Cold Injury induced brain trauma
Journal of Cerebral Blood Flow and Metabolism, 2000Co-Authors: Yuiko Moritafujimura, Miki Fujimura, Yvan Gasche, Jean Christophe Copin, Pak H ChanAbstract:Matrix metalloproteinases (MMPs), a family of proteolytic enzymes which degrade the extracellular matrix, are implicated in blood-brain barrier disruption, which is a critical event leading to vasogenic edema. To investigate the role of reactive oxygen species (ROS) in the expression of MMPs in vasogenic edema, the authors measured gelatinase activities before and after Cold Injury (CI) using transgenic mice that overexpress superoxide dismutase-1. A marked induction of pro-gelatinase B (pro-MMP-9) was seen 2 hours after CI and was maximized at 12 hours in wild-type mice. The pro-MMP-9 level was significantly lower in transgenic mice 4 hours (P < 0.001) and 12 hours (P < 0.05) after CI compared to wild-type mice. The activated MMP-9 was detected from 6 to 24 hours after Injury. A mild induction of pro-gelatinase A (pro-MMP-2) was seen at 6 hours and was sustained until 7 days. In contrast, the activated form of MMP-2 appeared at 24 hours, was maximized at 7 days, and was absent in transgenic mice. Western blot analysis showed that the tissue inhibitors of metalloproteinases were not modified after CI. The results suggest that ROS production after CI may contribute to the induction and/or activation of MMPs and could thereby exacerbate endothelial cell Injury and the development of vasogenic edema after Injury.
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Cold Injury in mice a model to study mechanisms of brain edema and neuronal apoptosis
Progress in Neurobiology, 1999Co-Authors: Kensuke Murakami, Takeo Kondo, Guoyuan Yang, Sylvia F Chen, Yuiko Moritafujimura, Pak H ChanAbstract:Small rodents, mice in particular, have been widely used for genetic manipulation because of the extensive knowledge in development, embryology and other molecular aspects of this species. However, the use of mice for neurobiology research in the area of brain edema and neuronal Injury has not been common. Here we summarize the studies of Cold Injury-induced brain edema and neuronal apoptosis using mice. Blood-brain barrier (BBB) permeability, demonstrated by extravasation of a serum albumin tracer, Evans Blue, was increased immediately after the Injury and returned to the control level by 24 hr. Water content was maximized at 24 hr, whereas a secondary lesion gradually progressed up to 72 hr after Cold Injury. The mechanism of the development of the Cold Injury-induced edema and the secondary lesion, involving of oxygen radicals in particular, was determined using superoxide dismutase (SOD)-1 transgenic (Tg) mice with overexpressed copper, zinc-SOD. All of the parameters, BBB permeability, water content and secondary lesion, were attenuated in the Tg mice as compared to littermate non-Tg mice. This clearly demonstrates that oxygen radicals, superoxide anion in particular, mediate Cold Injury. We also studied whether apoptosis contributes to brain Injury following Cold Injury. Staining with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling showed the apoptotic cells widespread throughout the entire lesion while still remaining in the margin. DNA laddering was exhibited by gel electrophoresis. These studies indicate that oxidative mediates the development of Cold Injury-induced edema and the secondary Injury, and induces apoptotic cell death. We believe that Cold Injury in mice provides a simple animal model to study the pathogenesis of brain edema and apoptosis in genetically altered animals.
Mike Tipton - One of the best experts on this subject based on the ideXlab platform.
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peripheral thermal responses in normal and Cold sensitive individuals to sublingual glyceryl trinitrate gtn
Extreme physiology and medicine, 2015Co-Authors: Katrina Hope, Clare Eglin, Frank Golden, Mike TiptonAbstract:Non-freezing Cold Injury (NFCI) is caused by prolonged exposure of the extremities to Cold. The long-term sequelae of NFCI, include Cold-sensitivity and pain[1]. The Cold sensitivity is characterised by a reduction in basal skin blood flow and augmented vasoconstriction during Cold exposure. We tested the hypothesis that sublingual GTN would increase blood flow in the peripheral microcirculation during and after a mild Cold challenge in individuals who had not been diagnosed with NFCI, but were Cold-sensitive.
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sublingual glyceryl trinitrate and the peripheral thermal responses in normal and Cold sensitive individuals
Microvascular Research, 2014Co-Authors: Katrina Hope, Clare Eglin, Frank Golden, Mike TiptonAbstract:Non-freezing Cold Injury (NFCI) is a prevalent, but largely undiagnosed and poorly understood syndrome afflicting many who, as part of their work or leisure, expose their extremities to Cold temperatures. The long term sequelae of NFCI are hyperhidrosis, Cold-sensitivity and pain; these can last a lifetime. We tested the hypothesis that, in comparison with a placebo, sublingual glyceryl trinitrate (GTN) would increase the peripheral microcirculation during and after a mild Cold challenge of individuals who had not been diagnosed with NFCI, but were Cold-sensitive. Naive participants were categorised into two cohort groups: control (n=7) or Cold-sensitive (n=6). All participants undertook a standardised two minute Cold exposure of their right foot while toe skin temperature (Tsk; infra-red thermograms) and blood flow (toe pad laser Doppler) were measured. GTN increased the rate of rewarming and absolute Tsk of the Coldest toe after the Cold challenge in Cold-sensitive individuals. GTN also increased the blood flow in the great toe during rewarming in some Cold-sensitive individuals. We accept our hypothesis and suggest that the impairment in the vasodilatory response seen in individuals with Cold-sensitivity can be overcome by the use of GTN, an endothelial-independent NO donor, and thereby improve the rewarming of cooled peripheral tissues.
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Cold sensitivity test for individuals with non freezing Cold Injury the effect of prior exercise
Extreme physiology and medicine, 2013Co-Authors: Clare Eglin, Frank Golden, Mike TiptonAbstract:One of the chronic symptoms of non-freezing Cold Injury (NFCI) is Cold sensitivity. This study examined the effects of prior exercise on the response to a Cold sensitivity test (CST) in NFCI patients with the aim of improving diagnostic accuracy. Twenty three participants, previously diagnosed with NFCI by a Cold Injuries Clinic, undertook two CSTs. Participants either rested (air temperature 31°C) for approximately 80 min (prior rest condition (REST)) or rested for 30 min before exercising gently for 12 min (prior exercise condition (EX)). Following REST and EX, the participants placed their injured foot, covered in a plastic bag, into 15°C water for 2 min; this was followed by spontaneous rewarming in 31°C air for 10 min. The great toe skin temperature (Tsk) before immersion averaged 32.5 (3.4)°C in both conditions. Following immersion, the rate of rewarming of the great toe Tsk was faster in EX compared to REST and was higher 5 min (31.7 (3.4)°C vs. 29.8 (3.4)°C) and 10 min (33.8 (4.0)°C vs. 32.0 (4.0)°C) post-immersion. Over the first 5 min of rewarming, changes in the great toe Tsk correlated with the changes in skin blood flow (SkBF) in EX but not the REST condition. No relationship was observed between Tsk in either CST and the severity of NFCI as independently clinically assessed. Exercise prior to the CST increased the rate of the toe Tsk rewarming, and this correlated with the changes in SkBF. However, the CST cannot be used in isolation in the diagnosis of NFCI, although the EX CST may prove useful in assessing the severity of post-Injury Cold sensitivity for prognostic and medico-legal purposes.