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Edwin H Kolodny - One of the best experts on this subject based on the ideXlab platform.
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lower limb Cold Exposure induces pain and prolonged small fiber dysfunction in fabry patients
Pain, 2000Co-Authors: M J Hilz, Brigitte Stemper, Edwin H KolodnyAbstract:In Fabry disease, an X-linked α-galactosidase A deficiency, painful crises and limb paresthesias are possibly linked to thermal Exposure. Small nerve fiber function has not yet been tested after Cold challenge. In two Fabry patients (15 and 17 years old), their heterozygote mother, their healthy sister, and eight controls, we determined warm and Cold perception thresholds at the dorsal foot and the lower medial calf (method of limits, Somedic-Thermotest™), before and 1, 5, 10 and 15 min after 30 s immersion of one leg into 5°C water. Discomfort was rated from 0 to 10. At baseline, thermal thresholds of all participants were normal. In contrast to controls, the patients tolerated 30 s Cold stimulation only with interruptions. The mother aborted stimulation after 6 s because of pain. The patients and their mother reported intense burning pain and numbness during and after stimulation. After Cold Exposure, thermal sensation was highly abnormal for 20 min in one and 80 min in the other brother. In controls, thermal thresholds were somewhat elevated after stimulation but normalized within 10.0±4.6 min. Discomfort during Cold Exposure was rated 8–10 by the patients and their mother, but 3–5 by the healthy persons. We assume that glycolipid accumulation in cutaneous and vasa nervorum vessels as well as small nerve axons accounts for skin and small fiber malperfusion during Cold induced vasoconstriction. Transitory ischemia initiated burning pain and prolonged small fiber dysfunction.
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lower limb Cold Exposure induces pain and prolonged small fiber dysfunction in fabry patients
Pain, 2000Co-Authors: M J Hilz, Brigitte Stemper, Edwin H KolodnyAbstract:In Fabry disease, an X-linked alpha-galactosidase A deficiency, painful crises and limb paresthesias are possibly linked to thermal Exposure. Small nerve fiber function has not yet been tested after Cold challenge. In two Fabry patients (15 and 17 years old), their heterozygote mother, their healthy sister, and eight controls, we determined warm and Cold perception thresholds at the dorsal foot and the lower medial calf (method of limits, Somedic-Thermotest), before and 1, 5, 10 and 15 min after 30 s immersion of one leg into 5 degrees C water. Discomfort was rated from 0 to 10. At baseline, thermal thresholds of all participants were normal. In contrast to controls, the patients tolerated 30 s Cold stimulation only with interruptions. The mother aborted stimulation after 6 s because of pain. The patients and their mother reported intense burning pain and numbness during and after stimulation. After Cold Exposure, thermal sensation was highly abnormal for 20 min in one and 80 min in the other brother. In controls, thermal thresholds were somewhat elevated after stimulation but normalized within 10.0+/-4.6 min. Discomfort during Cold Exposure was rated 8-10 by the patients and their mother, but 3-5 by the healthy persons. We assume that glycolipid accumulation in cutaneous and vasa nervorum vessels as well as small nerve axons accounts for skin and small fiber malperfusion during Cold induced vasoconstriction. Transitory ischemia initiated burning pain and prolonged small fiber dysfunction.
Mario Perello - One of the best experts on this subject based on the ideXlab platform.
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short term Cold Exposure activates trh neurons exclusively in the hypothalamic paraventricular nucleus and raphe pallidus
Neuroscience Letters, 2012Co-Authors: Agustina Cabral, Spring Valdivia, Mirta Reynaldo, Nicole E Cyr, Eduardo A Nillni, Mario PerelloAbstract:The neuropeptide thyrotropin releasing hormone (TRH) is necessary for adequate Cold-induced thermogenesis. TRH increases body temperature via both neuroendocrine and autonomic mechanisms. TRH neurons of the hypothalamic paraventricular nucleus (PVN) regulate thermogenesis through the activation of the hypothalamic-pituitary-thyroid axis during Cold Exposure. However, little is known about the role that TRH neurons play in mediating the sympathetic response to Cold Exposure. Here, we examined the response of TRH neurons of rats to Cold Exposure in hypothalamic regions including the PVN, the dorsomedial nucleus and the lateral hypothalamus along with areas of the ventral medulla including raphe obscurus, raphe pallidus (RPa) and parapyramidal regions. Our results using a double immunohistochemistry protocol to identify TRH and c-Fos (as a marker of cellular activity) followed by analysis of preproTRH gene expression demonstrate that only TRH neurons located in the PVN and the RPa are activated in animals exposed to short-term Cold conditions.
M J Hilz - One of the best experts on this subject based on the ideXlab platform.
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lower limb Cold Exposure induces pain and prolonged small fiber dysfunction in fabry patients
Pain, 2000Co-Authors: M J Hilz, Brigitte Stemper, Edwin H KolodnyAbstract:In Fabry disease, an X-linked α-galactosidase A deficiency, painful crises and limb paresthesias are possibly linked to thermal Exposure. Small nerve fiber function has not yet been tested after Cold challenge. In two Fabry patients (15 and 17 years old), their heterozygote mother, their healthy sister, and eight controls, we determined warm and Cold perception thresholds at the dorsal foot and the lower medial calf (method of limits, Somedic-Thermotest™), before and 1, 5, 10 and 15 min after 30 s immersion of one leg into 5°C water. Discomfort was rated from 0 to 10. At baseline, thermal thresholds of all participants were normal. In contrast to controls, the patients tolerated 30 s Cold stimulation only with interruptions. The mother aborted stimulation after 6 s because of pain. The patients and their mother reported intense burning pain and numbness during and after stimulation. After Cold Exposure, thermal sensation was highly abnormal for 20 min in one and 80 min in the other brother. In controls, thermal thresholds were somewhat elevated after stimulation but normalized within 10.0±4.6 min. Discomfort during Cold Exposure was rated 8–10 by the patients and their mother, but 3–5 by the healthy persons. We assume that glycolipid accumulation in cutaneous and vasa nervorum vessels as well as small nerve axons accounts for skin and small fiber malperfusion during Cold induced vasoconstriction. Transitory ischemia initiated burning pain and prolonged small fiber dysfunction.
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lower limb Cold Exposure induces pain and prolonged small fiber dysfunction in fabry patients
Pain, 2000Co-Authors: M J Hilz, Brigitte Stemper, Edwin H KolodnyAbstract:In Fabry disease, an X-linked alpha-galactosidase A deficiency, painful crises and limb paresthesias are possibly linked to thermal Exposure. Small nerve fiber function has not yet been tested after Cold challenge. In two Fabry patients (15 and 17 years old), their heterozygote mother, their healthy sister, and eight controls, we determined warm and Cold perception thresholds at the dorsal foot and the lower medial calf (method of limits, Somedic-Thermotest), before and 1, 5, 10 and 15 min after 30 s immersion of one leg into 5 degrees C water. Discomfort was rated from 0 to 10. At baseline, thermal thresholds of all participants were normal. In contrast to controls, the patients tolerated 30 s Cold stimulation only with interruptions. The mother aborted stimulation after 6 s because of pain. The patients and their mother reported intense burning pain and numbness during and after stimulation. After Cold Exposure, thermal sensation was highly abnormal for 20 min in one and 80 min in the other brother. In controls, thermal thresholds were somewhat elevated after stimulation but normalized within 10.0+/-4.6 min. Discomfort during Cold Exposure was rated 8-10 by the patients and their mother, but 3-5 by the healthy persons. We assume that glycolipid accumulation in cutaneous and vasa nervorum vessels as well as small nerve axons accounts for skin and small fiber malperfusion during Cold induced vasoconstriction. Transitory ischemia initiated burning pain and prolonged small fiber dysfunction.
John R Speakman - One of the best experts on this subject based on the ideXlab platform.
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limits to sustained energy intake v effect of Cold Exposure during lactation in mus musculus
The Journal of Experimental Biology, 2001Co-Authors: Maria S Johnson, John R SpeakmanAbstract:We have previously observed that female MF1 mice appeared to reach a limit in their food intake and milk production during late lactation, reaching a plateau between days 13 and 16 of lactation and between litter sizes of 9 and 15. These mice did not increase their food intake when forced to raise more offspring or when manipulated to be concurrently pregnant during late lactation, yet they did eat significantly more food at the peak of their second sequential lactation or when challenged with food of reduced energy content. These data suggest that apparent limits on sustained energy intake in this strain may not reflect central limitations but rather peripheral constraints at the mammary glands. In this study, we aimed to determine whether these were indeed limits by increasing the demands on the females during late lactation by Cold-Exposure (8 degrees C). Females responded to this manipulation by significantly increasing their food intake (F1,73=77.53, P<0.001) above that of lactating females kept in warmer conditions (21 degrees C). In addition, there was a significant reduction in the number of pups raised in the Cold (t=2.36, d.f.=18, P=0.03), with the majority of the mortality occurring within the first 2 days of Cold-Exposure. The mean mass of the pups raised in the Cold was significantly lower (F1,74=13.8, P<0.001) than that of those raised in the warm. Despite the Cold-Exposure and the increased food intake, there was no difference in the resting metabolic rates of the two groups of mothers or in the lengths of their small intestine. The greater food intake of lactating mice during Cold-Exposure supported our previous observations that they were capable of eating more food than the previously suggested limit of 23.1 g x day(-1). However, the milk energy output of females in the Cold was also significantly higher than in the warm (F1,15=11.99, P=0.003), indicating that the asymptotic food intake of females in the warm was not mediated by limitations in their milk production. Sustained energy intake in these mice does not appear to be centrally or peripherally limited. Rather, the mice may restrain their use of energy during their first lactation because of life-history consequences for future reproductive attempts.
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limits to sustained energy intake v effect of Cold Exposure during lactation in mus musculus
The Journal of Experimental Biology, 2001Co-Authors: Maria S Johnson, John R SpeakmanAbstract:SUMMARY We have previously observed that female MF1 mice appeared to reach a limit in their food intake and milk production during late lactation, reaching a plateau between days 13 and 16 of lactation and between litter sizes of 9 and 15. These mice did not increase their food intake when forced to raise more offspring or when manipulated to be concurrently pregnant during late lactation, yet they did eat significantly more food at the peak of their second sequential lactation or when challenged with food of reduced energy content. These data suggest that apparent limits on sustained energy intake in this strain may not reflect central limitations but rather peripheral constraints at the mammary glands. In this study, we aimed to determine whether these were indeed limits by increasing the demands on the females during late lactation by Cold-Exposure (8°C). Females responded to this manipulation by significantly increasing their food intake ( F 1,73 =77.53, P t =2.36, d.f.=18, P =0.03), with the majority of the mortality occurring within the first 2 days of Cold-Exposure. The mean mass of the pups raised in the Cold was significantly lower ( F 1,74 =13.8, P −1 . However, the milk energy output of females in the Cold was also significantly higher than in the warm ( F 1,15 =11.99, P =0.003), indicating that the asymptotic food intake of females in the warm was not mediated by limitations in their milk production. Sustained energy intake in these mice does not appear to be centrally or peripherally limited. Rather, the mice may restrain their use of energy during their first lactation because of life-history consequences for future reproductive attempts.
H A M Daanen - One of the best experts on this subject based on the ideXlab platform.
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relation between finger Cold induced vasodilation and rewarming speed after Cold Exposure
European Journal of Applied Physiology, 2019Co-Authors: C F Kingma, I I Hofman, H A M DaanenAbstract:The risk for local Cold injuries has been linked to poor Cold-induced vasodilation (CIVD) during Cold Exposure and to poor rewarming after Cold Exposure. The purpose of this study is to establish the relation between CIVD and rewarming speed. Twelve participants immersed one hand in ice water for 30 min to evoke CIVD and the other hand in ice water for 10 min to investigate the rewarming profile. The ring, middle and index fingertip temperatures were monitored during hand immersion and the resistance index of frostbite (RIF) was calculated. RIF depends on minimal (Tmin) and mean (Tmean) finger skin temperature and onset time. Rewarming was quantified using an infrared imaging system and the rewarming speed over 19 min was determined. Tmin (5.8 ± 3.0 °C) and Tmean (10.4 ± 3.0 °C) caused non-distinctive contributions to the total RIF-scores so that onset time (12.7 ± 3.1 min) became the dominant factor. A significant negative correlation between RIF and rewarming speed was found (rs = − 0.60, p = 0.041). The negative relation between RIF and rewarming speed may be explained by the common observation that onset time relates to the temperature of fingertip tissue, while Tmin, Tmean and rewarming speed relates to body thermal status. The rewarming test is to be preferred over the CIVD test in terms of ease of use, but the predictive value of the rewarming test for Cold injuries is limited, cannot replace the RIF since onset time of finger vasodilation is not included and should be further investigated.
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dynamic adaptation of the peripheral circulation to Cold Exposure
Microcirculation, 2012Co-Authors: Stephen S Cheung, H A M DaanenAbstract:Humans residing or working in Cold environments exhibit a stronger Cold-induced vasodilation (CIVD) reaction in the peripheral microvasculature than those living in warm regions of the world, leading to a general assumption that thermal responses to local Cold Exposure can be systematically improved by natural acclimatization or specific acclimation. However, it remains unclear whether this improved tolerance is actually due to systematic acclimatization, or alternately due to the genetic predisposition or self-selection for such occupations. Longitudinal studies of repeated extremity Exposure to Cold demonstrate only ambiguous adaptive responses. In field studies, general Cold acclimation may lead to increased sympathetic activity that results in reduced finger blood flow. Laboratory studies offer more control over confounding parameters, but in most studies, no consistent changes in peripheral blood flow occur even after repeated Exposure for several weeks. Most studies are performed on a limited amount of subjects only, and the variability of the CIVD response demands more subjects to obtain significant results. This review systematically surveys the trainability of CIVD, concluding that repeated local Cold Exposure does not alter circulatory dynamics in the peripheries, and that humans remain at risk of Cold injuries even after extended stays in Cold environments.