Relevant bibliographies by topics / Noradrenalin in the body

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Academic literature on the topic 'Noradrenalin in the body'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Noradrenalin in the body"

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Goncharov, N. P., N. I. Verbovaya, and T. P. Krivchenko. "The state of the sympathetic-adrenal system in patients with hypothalamic syndrome of puberty." Problems of Endocrinology 43, no. 4 (August 15, 1997): 18–20. http://dx.doi.org/10.14341/probl199743418-20.

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Twenty-nine male patients with the hypothalamic syndrome of puberty and 13 healthy controls aged 15 to 23 were examined in order to elucidate the contribution of the sympathoadrenal system to the pathogenesis of arterial hypertension in this patient population. The sympathoadrenal activity was assessed from the level of dopamine, noradrenalin, and adrenalin in the blood plasma measured by high-pressure liquid chromatography using highly sensitive detectors. Adrenalin level was significantly decreased in the patients with arterial hypertension, probably because of suppression of phenylethanol methyltransferase, which may indicate that the sympathoadrenal system does not participate in the development and stabilization of arterial hypertension in patients with the hypothalamic syndrome of puberty. Noradrenalin level was reliably decreased in the patients with body weight index of more than 35.0 kg/m2, probably due to suppression of thyrosine hydroxylase, whose activity regulates corticotropin. Catecholamine level did not depend on the disease duration, standing of hypertension, or stage of obesity.
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Zakharov, A. G., L. S. Ivanov, E. V. Khmelevskii, and V. K. Bozhenko. "Arteriolar reactivity of rat skeletal muscle to noradrenalin after whole-body gamma-irradiation in a dose of 1 Gy." Bulletin of Experimental Biology and Medicine 114, no. 4 (October 1992): 1416–19. http://dx.doi.org/10.1007/bf00841580.

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Menozzi, R., M. Bondi, A. Baldini, M. G. Venneri, A. Velardo, and G. Del Rio. "Resting metabolic rate, fat-free mass and catecholamine excretion during weight loss in female obese patients." British Journal of Nutrition 84, no. 4 (October 2000): 515–20. http://dx.doi.org/10.1017/s0007114500001823.

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The reduction in resting metabolic rate (RMR) during weight loss exceeds that accounted for by changes in body composition by 15%, suggesting that factors other than fat-free mass (FFM) explain the metabolic adaptation during food restriction in obesity. Our study aimed to establish if changes in the sympathoadrenal system activity, as inferred from an integrated measure such as 24 h urinary excretion of catecholamines, may play a role in the RMR adaptation observed during dietary restriction in obese patients. Ninety-three obese female subjects consumed a low-energy diet (LED) (2930 kJ/d (700 kcal/d)) for a 3-week period. At the beginning and at the end of the study, 24 h urinary excretion of catecholamines, FFM and RMR were measured. The LED induced a significant reduction in body weight (-3·3 (SEM 0·4) KG; P < 0·01), FFM (-1·9 (sem 0·7) kg; P < 0·01) and in the fat mass (-1·2 (sem 0·5) kg; P < 0·01). Noradrenalin excretion (24 h) decreased during the LED from 264 (sem 26) during a weight-maintenance period to 171 (sem 19) nmol/24 h after consumption of the LED for 3 weeks (P < 0·001); mean 24 h adrenalin excretion did not change during the LED (22 (sem 3) during the weight-maintenance period v. 21 (sem 3) nmol/24 h after consumption of the LED for 3 weeks; NS). The LED induced a significant decrease in RMR (7300 (sem 218) v. 6831 (sem 138) kJ/24 h; P < 0·001). The only independent variable that significantly explained variations in RMR both before and after consumption of the LED for 3 weeks, was FFM (r2 0·79 and r2 0·80 respectively). Urinary noradrenalin excretion explained a further 4 % of the variability in RMR, but only before the diet, so that a role of sympathoadrenal system on RMR seems to be present in obese patients in basal conditions but not at the end of the LED.
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Jacobs, Marie-Cecile, David S. Goldstein, Jacques J. Willemsen, Paul Smits, Theo Thien, and Jacques W. M. Lenders. "Differential Effects of Low- and High-Intensity Lower Body Negative Pressure on Noradrenaline and Adrenaline Kinetics in Humans." Clinical Science 90, no. 5 (May 1, 1996): 337–43. http://dx.doi.org/10.1042/cs0900337.

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1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (−15 versus −40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during −15 and −40 mmHg of lower body negxative pressure. 3. During lower body negative pressure at −15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25–50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 ± 0.16 to 0.94 ± 0.23 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at −40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 ± 0.19 to 1.32 ± 0.36 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.
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McCance, Alastair J., and J. Colin Forfar. "Cardiac and Whole-Body [3H]Noradrenaline Kinetics during Adrenaline Infusion in Man." Clinical Science 80, no. 3 (March 1, 1991): 227–33. http://dx.doi.org/10.1042/cs0800227.

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1. To investigate the possible role of adrenaline as a modulator of noradrenaline release from the sympathetic nervous system, the responses of cardiac and whole-body noradrenaline kinetics to intravenous infusions of adrenaline (30 ng min−1 kg−1) and matching saline placebo were determined at rest and during supine bicycle exercise in 16 patients undergoing cardiac catheterization, in whom β-adrenoceptor antagonists had been discontinued for 72 h. 2. At rest and compared with placebo, infusion of adrenaline was associated with a small increase in arterial plasma noradrenaline from 211 ± 129 pg/ml to 245 ± 29 pg/ml (P < 0.05). Increases in whole-body noradrenaline spillover to arterial plasma were larger (from 282 ± 40 ng min−1 m−2 to 358 ± 41 ng min−1 m−2, P < 0.01) and there was a trend towards an increase in whole-body noradrenaline clearance. Cardiac noradrenaline clearance was modestly increased during adrenaline infusion, but cardiac noradrenaline spillover was not altered despite increases in heart rate and coronary sinus plasma flow. Adrenaline infusion was associated with symptomatic myocardial ischaemia in four of 14 patients with coronary heart disease. 3. Supine bicycle exercise was associated with significant increases in peripheral noradrenaline concentrations and in cardiac and whole-body noradrenaline spillover. The increases on exercise were not significantly different for these variables during saline and adrenaline infusions. 4. Infusion of adrenaline to produce ‘physiological’ increases in plasma adrenaline concentration was associated with an increase in total noradrenaline release, as assessed by whole-body noradrenaline spillover to plasma. This is consistent with the hypothesis that adrenaline may modulate noradrenaline release by acting upon pre-junctional β-adrenoceptors, but could also be explained by reflexogenic responses to the haemodynamic effects of adrenaline.
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Ferrier, Claudia, Helen Cox, and Murray Esler. "Elevated total body noradrenaline spillover in normotensive members of hypertensive families." Clinical Science 84, no. 2 (February 1, 1993): 225–30. http://dx.doi.org/10.1042/cs0840225.

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1. In prehypertension, abnormalities in cardiovascular control mechanisms have been described. It has been postulated that this may involve hereditary disturbances in the sympathetic regulation of blood pressure. Since the neurochemical methods used to test sympathetic nervous system activity have been rather imprecise, in the present study we have applied noradrenaline plasma kinetic methodology to evaluate sympathetic activity in normotensive subjects with a familial predisposition to essential hypertension. 2. Total body noradrenaline spillover to plasma, an index of integrated sympathetic nerve firing rates, was calculated during infusion of l-[7-3H] noradrenaline in 11 normotensive offspring of essential hypertensive parents and 11 age-, height- and weight-matched normotensive offspring of normotensive parents. 3. The resting arterial plasma noradrenaline concentration was higher in healthy subjects with a family history of essential hypertension (1.41 ± 0.15 nmol/l, mean ± SEM, P < 0.002) than in normotensive subjects with no family history of essential hypertension (0.82 ± 0.07 nmol/l). The overall rate of spillover of noradrenaline to plasma was also elevated in the normotensive offspring of hypertensive parents (4.34 ± 0.54 nmol/min) compared with subjects with a negative family history of essential hypertension (2.02 ± 0.20 nmol/min). Similarly, the arterial plasma concentration of the noradrenaline precursor 3,4-dihydroxyphenylalanine was higher in subjects with a positive family history of essential hypertension (7.55 ± 0.24 nmol/l) than in normotensive control subjects (5.97 ± 0.30 nmol/l, P < 0.001). Despite this apparent evidence of relative sympathetic nervous activation in the subjects with a positive family history of hypertension, their blood pressure and heart rate were only marginally, and non-significantly, higher. 4. Biochemical indices of sympathetic function in normotensive offspring of hypertensive parents suggest a familial disturbance in sympathetic nervous system activity, which may be a predictor for the development of hypertension in adult life.
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NESTEL, Paul J., Takeshi YAMASHITA, Takayuki SASAHARA, Jaye P. F. CHIN-DUSTING, Murray D. ESLER, Anthony M. DART, and Garry L. JENNINGS. "Control of the forearm microcirculation: interactions with measures of obesity and noradrenaline kinetics." Clinical Science 95, no. 2 (August 1, 1998): 203–12. http://dx.doi.org/10.1042/cs0950203.

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1.Obesity influences the responsiveness of the microcirculation; constriction is augmented probably reflecting heightened sympathetic nervous activity. 2.The responsiveness of the microcirculation in the forearm to constriction and dilation was therefore examined in 14 men and women with varying degrees of abdominal adiposity, to determine the potential effects of sympathetic nervous activity and adiposity on flow. Changes in basal blood flow were measured by venous occlusion plethysmography during intra-arterial infusions of noradrenaline, acetylcholine and sodium nitroprusside and after temporary ischaemia. Total body noradrenaline spillover was also measured, as an index of sympathetic neuronal activity. 3.Parameters of obesity were found to influence the responsiveness of the microcirculation. Changes in vascular resistance with noradrenaline (100 ;ng/min) were positively correlated with body weight, body mass index and waist circumference (r = 0.63, P = 0.02), whereas waist circumference was negatively correlated with post-ischaemia vasodilatation (r = -0.76, P = 0.002). Acetylcholine-induced vasodilatation was inversely related to body mass index (r = -0.53, P = 0.053). 4.Basal blood flow did not correlate with adiposity. Furthermore, vasodilatation with 800 ;ng/min sodium nitroprusside was inversely correlated with total body noradrenaline spillover (r = -0.77, P< 0.001); and changes in flows with noradrenaline (constriction) and post-ischaemia (dilation) were inversely related (r = -0.56, P = 0.035). 5.These findings, taken together, are consistent with increased local sympathetic neuronal responsiveness and diminished nitric-oxide-mediated dilation in the forearm vasculature with increasing body adiposity.
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Glazova, N. Yu, S. A. Merchieva, M. A. Volodina, E. A. Sebentsova, D. M. Manchenko, V. S. Kudrun, and N. G. Levitskaya. "Effects of Neonatal Fluvoxamine Administration on the Physical Development and Activity of the Serotoninergic System in White Rats." Acta Naturae 6, no. 3 (September 15, 2014): 98–105. http://dx.doi.org/10.32607/20758251-2014-6-3-98-105.

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Selective serotonin reuptake inhibitors (SSRIs), including fluvoxamine, are widely used to treat depressive disorders in pregnant women. These antidepressants effectively penetrate through the placental barrier, affecting the fetus during the critical phase of neurodevelopment. Some clinical studies have linked prenatal exposure to SSRIs with increased neonatal mortality, premature birth, decreased fetal growth and delay in psychomotor development. However, the effects of prenatal exposure to SSRIs remain unknown. The administration of SSRIs in rodents during the first postnatal weeks is considered as an model for studying the effects of prenatal SSRIs exposure in human. The aim of this work was to study the acute effects of chronic fluvoxamine (FA) administration in white rat pups. The study was carried out in male and female rat pups treated with FA (10 mg/kg/day, intraperitoneally) from postnatal days 1 to 14. The lethality level, body weight, age of eye opening, and motor reflex maturation were recorded. The contents of biogenic amines and their metabolites in different brain structures were also determined. It was shown that neonatal FA administration led to increased lethality level, reduced body weight, and delayed maturation of motor reflexes. Furthermore, increased noradrenalin level in hypothalamus, serotonin level in hippocampus and serotonin metabolite 5-HIAA level in frontal cortex, hypothalamus, hippocampus, and striatum were observed in drug-treated animals compared to the control group. We can conclude that the altered activity of the serotoninergic system induced by fluvoxamine administration at early developmental stages leads to a delay in physical and motor development.
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Thurlby, Peter L., and Rodney D. M. Ellis. "Differences between the effects of noradrenaline and the β-adrenoceptor agonist BRL 28410 in brown adipose tissue and hind limb of the anaesthetized rat." Canadian Journal of Physiology and Pharmacology 64, no. 8 (August 1, 1986): 1111–14. http://dx.doi.org/10.1139/y86-189.

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In mature (450–600 g) 21 °C-acclimated male rats, anaesthetized with urethane, blood flow (measured by the radioactive microsphere technique) to brown adipose tissue (BAT) was determined during the infusion of the β-adrenoceptor agonist BRL 28410 or noradrenaline bitartrate at doses chosen to give similar increases in whole body oxygen uptake. Blood flow to BAT during BRL 28410 infusion was only about one third of that found during noradrenaline infusion although increases in whole body thermogenesis were similar (55 and 77% for BRL 28410 and noradrenaline, respectively). This suggests that BAT may be less involved in the thermogenic response to BRL 28410 than to noradrenaline. In a separate experiment using slightly smaller rats (350–500 g) hind limb oxygen uptake was measured in situ using a venous bypass preparation. BRL 28410, at a dose having a maximum effect on whole body thermogenesis (53% increase), had no effect on oxygen delivery to the hind limb but significantly increased oxygen extraction by 33% (p < 0.001). In contrast, noradrenaline, also at a dose that maximally increased whole body thermogenesis, led to a 35% decrease in oxygen delivery to the hind limb and no change in oxygen extraction. For the thermogenic β-agonist BRL 28410 the hind limb, and presumably muscular tissue in general, may be contributing to thermogenesis.
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Seidelin, Peter H., Joseph G. Collier, Allan D. Struthers, and David J. Webb. "Angiotensin II augments sympathetically mediated arteriolar constriction in man." Clinical Science 81, no. 2 (August 1, 1991): 261–66. http://dx.doi.org/10.1042/cs0810261.

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1. In animal studies, angiotensin II facilitates adrenergic neurotransmission by both pre- and postsynaptic mechanisms. We have investigated whether this interaction occurs in forearm resistance vessels in man. 2. The effect of arterial infusion of angiotensin II (320 fmol/min) on sympathetic vasoconstriction produced by lower-body negative pressure (15 mmHg) was studied in six subjects, and that on the response to exogenous noradrenaline (37.5–150 pmol/min) was studied in a further eight subjects. Forearm blood flow was measured by strain-gauge plethysmography. 3. The dose of angiotensin II was chosen to produce no alteration in resting blood flow, and those of noradrenaline were selected to provide a reduction in blood flow equivalent to that produced by lower-body negative pressure. 4. Lower-body negative pressure produced no change in heart rate or diastolic blood pressure, but caused an initial 5 mmHg fall in systolic blood pressure (P < 0.01). Blood flow was reduced by 21 ± 6% in both forearms by lower-body negative pressure during saline infusion. During angiotensin II infusion, there was a marked difference in the response to lower-body negative pressure, with blood flow being reduced by 40 ± 7% in the infused arm, but only by 21 ± 4% in the control arm (P < 0.05). Angiotensin II infusion had no effect on resting blood flow or the responses to noradrenaline. 5. We conclude that angiotensin II augments sympathetic vasoconstriction in forearm resistance vessels in man at a concentration that has no direct effect on blood flow. The absence of an effect of angiotensin II on the response to noradrenaline suggests that augmentation of sympathetic vasoconstriction occurs pre-synaptically through facilitation of noradrenaline release.
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Dissertations / Theses on the topic "Noradrenalin in the body"

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Yaldizli, Natalie [Verfasser], Anna [Akademischer Betreuer] Mitchell, and Bodo [Akademischer Betreuer] Levkau. "Bedeutung der Endothelinrezeptoren für die Endothelin- und Noradrenalin- induzierte Vasokonstriktion bei Patienten mit Arteriosklerose / Natalie Yaldizli. Gutachter: Bodo Levkau. Betreuer: Anna Mitchell." Duisburg, 2012. http://d-nb.info/1022790978/34.

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Korhonen, I. (Ilkka). "Thermal, hormonal and cardiovascular responses to single and repeated nonhypothermic cold exposures in man." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289262.

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Abstract The purpose of this study was to find out and compare the physiological effects of different types of non-hypothermic cold exposure tests in man. In whole-body cold exposures lightly clothed subjects were exposed to 10°C for 2 hours (single exposure), as well as repeatidly for 2 h and 1 h on ten successive days in separate studies. For local cold exposures, cold pressor tests (immersion into ice-cold water) of both hands and both feet were used. In whole-body cold exposures, several hormonal and metabolic parameters as well as cold sensations were measured. In local cold exposures the measured parameters were blood pressure, heart rate and skin temperatures. The single 2-h whole-body cold air exposure decreased rectal and skin temperatures and body heat content, but increased the metabolic rate. At the same time the serum noradrenaline concentration increased indicating a general activation of the sympathetic nervous system. Serum free fatty acid concentration increased whereas cortisol, GH and prolactin concentrations fell. No significant changes were found in serum concentrations of adrenalin, TSH, T3, T4, testosterone or LH. Serum total proteins were enhanced apparently due to cold-induced hemoconcentration. After repeating the 2-h whole-body cold exposure for five days the increase in serum noradrenaline level was markedly lower in the cold. At the same time hemoconcentration, judged from serum protein concentrations, was attenuated and the subjects became habituated to the cold sensations. However, the results showed that the repeated 1-h cold exposure in 10°C was not sufficiently intensive to reduce the noradrenaline response. Comparison of the hand and foot cold pressor tests to whole-body cold exposure tests showed that all tests caused significant increases in systolic and diastolic blood pressures, but that heart rate increased significantly only in the cold pressor test of feet. During the 2-h cold air exposure the heart rate fell. This caused a reduction in rate pressure product (RPP, the product of heart rate and systolic blood pressure). In both cold pressor tests the rate pressure product increased, indicating the enhancement of the O2-need in the heart muscle. The results showed no significant correlation in systolic or diastolic blood pressures between whole-body and local cooling of hands or feet. The lack of the association between local and whole-body cold exposure tests may be due to differences in severity and site of the tests: whole-body cold exposure tests cause general cold discomfort while cold pressor tests cause local cold pain
Tiivistelmä Tämän tutkimuksen tarkoituksena oli selvittää ja verrata eri tyyppisten lievien kylmäaltistustestien fysiologisia vaikutuksia ihmiseen. Yksittäisessä koko kehon kylmäaltistuksessa koehenkilöt olivat kevyesti vaatetettuina kahden tunnin ajan 10°C:n lämpötilassa. Toistetussa koko kehon kylmäaltistuksessa koehenkilöt oleskelivat myös 10°C:n lämpötilassa kahden tai yhden tunnin ajan kymmenenä perättäisenä päivänä. Paikallisessa kylmäaltistuksessa käytettiin kylmävesitestiä (ns. cold pressor koe). Testi tehtiin sekä käsille että jaloille. Koko kehon kylmäaltistuksessa mitattiin useita hormonaalisia, aineenvaihdunnan ja lämpötasapainon vasteita, sekä verenpainetta ja sydämen syketiheyttä. Paikallisissa kylmäaltistuksissa mitattiin verenpainetta, sydämen syketiheyttä ja iholämpötiloja. Yksittäinen koko kehon kahden tunnin kylmäaltistus laski syvälämpötilaa, iholämpötiloja ja kehon lämpösisältöä. Samanaikaisesti kehon lämmöntuotanto kasvoi. Seerumin noradrenaliinipitoisuus lisääntyi ilmentäen sympaattisen hermoston tehostunutta aktivoitumista. Seerumin vapaiden rasvahappojen pitoisuus kasvoi, samoin kokonaisproteiinipitoisuus, mutta kasvuhormonin, kortisolin ja prolaktiinin osalta todettiin pitoisuuksien vähenemistä. Merkitseviä muutoksia ei tapahtunut seerumin adrenaliinissa, TSH:ssa, T3:ssa, T4:ssä, testosteronissa tai LH:ssa. Toistetussa kahden tunnin pituisessa kylmäaltistuksessa seerumin noradrenaliinipitoisuudessa tapahtunut kasvu oli merkitsevästi vähäisempää viiden päivän jälkeen. Samanaikaisesti seerumin proteiinipitoisuus kylmässä väheni ja kylmätuntemukset muuttuivat lievemmiksi. Sen sijaan yhden tunnin toistettu altistus 10°C:ssa ei ollut riittävän voimakas vähentämään kylmän aiheuttamaa veren noradrenaliinipitoisuuden kasvua. Verenpaineen ja sydämen syketiheyden reaktioita verrattiin samoilla koehenkilöillä yksittäisessä kahden tunnin koko kehon kylmäaltistuksessa ja kylmävesitesteissä. Kaikki nämä testit kohottivat merkitsevästi systolista ja diastolista verenpainetta. Sydämen syketiheys laski koko kehon kylmäaltistuksessa. Jalkojen kylmävesitestissä sydämen syketiheys nousi merkitsevästi, mutta käsien testissä tämä nousu ei ollut merkitsevä. Verenpaineen nousu koko kehon kylmäaltistuksessa ei korreloinut merkitsevästi paikallisissa kylmäaltistuksissa mitattuihin verenpaineen nousuihin. Selittävänä tekijänä tähän lienee näiden kylmäaltistusmuotojen erilaisuus. Lievä koko kehon kylmäaltistus aiheuttaa yleistä epämiellyttävyyttä, kun taas äkilliseen, nopean iholämpötilan laskun aiheuttamaan paikalliseen kylmäaltistukseen liittyy usein kiputuntemuksia
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Glawe, Inken. "Der Einfluss von Noradrenalin auf Gap Junction Kanäle." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-77667.

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Gap Junction Kanäle sind wesentlich für die interzelluläre Kommunikation im Herzen. Die wichtigsten kardialen Gap Junction Proteine sind Connexin 43, Connexin 40 und in frühen Entwicklungsstadien Connexin 45. Da Katecholamine eine wichtige Rolle in der kardialen Physiologie bzw. Pathophysiologie spielen, sollte geklärt werden, ob Katecholamine die Expression von Connexin 40 und Connexin 43 beeinflussen. Es wurden neonatale Rattenkardiomyozyten in Zellkultur 24 Stunden mit aufsteigenden Noradrenalinkonzentrationen (1-10000 nM) (physiologischer Agonist für α-und β-Adrenozeptoren) inkubiert. Hier zeigte sich ein signifikanter Anstieg der Connexin 43 Expression, während die Connexin 40 Expression nicht beeinflußt wurde. Um zu zeigen über welchen Adrenozeptor (α oder β) die Hochregulation von Cx 43 durch Noradrenalin erfolgt, wurden die Zellkulturen in zwei weiteren Versuchsreihen zusätzlich mit einem β-Blocker (Propranolol 100µM) bzw. einem α- Blocker (Prazosin 10 µM) über 24 Std. inkubiert. Hier zeigte sich eine deutliche Inhibierung des Noradrenalineffektes durch die Blockade der α-Rezeptoren durch Prazosin. Eine Blockade der β-Rezeptoren hatte keinen inhibitorischen Effekt auf die Hochregulation der Expression von Cx 43 durch Noradrenalin. Es kam hier sogar zu einer verstärkten Expression verglichen mit der Cx 43 Expression unter Noradrenalin ohne Rezeptorblockade. Desweiteren wurde überprüft, ob es auch unter der Behandlung von Sprague– Dawley-Ratten mit einem β-Mimetikum (Isoprenalin) bzw. einem α-Mimetikum (Phenylephrin) zu einer Veränderung der Connexinexpression kommt. Die Western Blot Analysen ergaben hierbei wieder einen α-Rezeptoren vermittelten Effekt, indem es zu einem wesentlichen Konzentrationsanstieg von Connexin 43 unter der Behandlung mit Phenylephrin kam.
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Miller, Peta, and Miller@dewr gov au petajohnmiller@bordernet com au Peta. "THE HUMAN COSTS AND BENEFITS OF WORK: JOBLOAD, SELF-PERCEIVED PERFORMANCE, AND EMPLOYEE WELLBEING." La Trobe University. School of Human Biosciences, 2004. http://www.lib.latrobe.edu.au./thesis/public/adt-LTU20070319.145144.

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The primary purpose of this project was to investigate some relationships between workload and employee wellbeing. The necessary first stage was to formulate a theoretical framework � the JobLoad Model � to support a comprehensive and detailed investigation of the main factors that contribute to a job's workload. Building on the ergonomics concept of �workload�, this Model incorporates task- and job-level factors that have been identified within the research literatures of physical and cognitive ergonomics as important; additional constructs were added to take account of additional factors shown to be relevant to employee wellbeing, drawing on evidence from occupational health and organizational psychology literatures. Using this framework, available questionnaire-based measurement instruments for assessing workload and employee wellbeing were reviewed, new items were developed as required, and the JobLoad Index (JLI) was developed. The JLI was used to collect data from public servants in two different workplaces, with participation rates of 63% and 73% respectively. Relationships were determined between major task, job and organisational environment factors, self-perceived performance adequacy, and various aspects of employee wellbeing including job satisfaction, physical discomfort and psychological fatigue, stress and arousal. For a sub-sample of participants in one of the two workplaces, levels of adrenaline, noradrenaline and cortisol were also measured from 24-hour urine collections. The factors measured by the JLI accounted for a very substantial proportion of variance in these various dimensions of work-related wellbeing. The results provide potentially very useful insights into the relative influences of a wide range of work- and job-related variables on people's perceived abilities to cope with their job demands, and on several aspects of their wellbeing. Further, the importance of measuring multiple dimensions of wellbeing, and differentiating their separate sets of work-related determinants, was well demonstrated. Finally, and perhaps most significantly, this study has identified the powerful role that self-perceived performance plays as an intervening variable between job demands and people's work-related wellbeing.
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Gessner, Kathrin. "Die Wirkung von Noradrenalin auf die Gedächtniskonsolidierung im Schlaf." Lübeck Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/1000322483/34.

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Wiege, Eva-Maria. "Der Effekt des Noradrenalin Wiederaufnahmehemmers Reboxetin auf die Gedächtniskonsolidierung im Schlaf." Lübeck Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/999436279/34.

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Moldovanova, Iryna [Verfasser]. "Einfluss weiblicher Sexualhormone auf die Kreislaufregulation unter Noradrenalin-Wiederaufnahmehemmung / Iryna Moldovanova." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023709678/34.

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Gessner, Kathrin [Verfasser]. "Die Wirkung von Noradrenalin auf die Gedächtniskonsolidierung im Schlaf / Kathrin Gessner." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/1000322483/34.

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Schröder, Christoph. "Selektive Hemmung der Noradrenalin-Wiederaufnahme als humanes Modell für orthostatische Intoleranz." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14846.

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Hintergrund. Untersuchungen bei Patienten mit funktionellen Mutationen des Noradrenalin-Transporter-Gens deuten darauf hin, dass eine verminderte Noradrenalin-Wiederaufnahme zur Pathophysiologie der idiopathischen Orthostatischen Intoleranz beitragen kann. Methoden. In einer doppeltblinden, placebokontrollierten, randomisierten Studie wurden die kardiovaskulären Effekte einer selektiven pharmakologischen Noradrenalin-Wiederaufnahmehemmung (2x 8 mg Reboxetin p.o.) bei gesunden Testpersonen untersucht. In der ersten Teilstudie (n=23) wurden autonome Funktionstests und eine Kipptischuntersuchung durchgeführt. Herzfrequenz, Blutdruck und zerebrale Blutflussgeschwindigkeit wurden dabei kontinuierlich nicht-invasiv gemessen. Herzzeitvolumen und peripherer Widerstand wurden impedanzkardiografisch bestimmt. In einer zweiten Teilstudie (n=10) wurde der Effekt akuter selektiver Noradrenalin-Wiederaufnahmehemmung auf die Sensitivität gegenüber blutdruckwirksamer Pharmaka getestet. Dafür wurden steigende intravenöse Dosen von Phenylephrin, Isoproterenol und Nitroprussid gegeben und die Änderungen von Blutdruck und Herzfrequenz in individuellen Dosis-Wirkungskurven bestimmt. Ergebnisse. Unter Noradrenalin-Wiederaufnahmehemmung waren Herzfrequenz und Blutdruck im Liegen erhöht. Während der Kipptischuntersuchung führte die Noradrenalin-Wiederaufnahmehemmung zu einer deutlich gesteigerten Herzfrequenz (120+/-3 /min vs. 83+/-3 /min unter Placebo, p
Background. Observations in patients with functional mutations of the norepinephrine transporter (NET) gene suggest that impaired norepinephrine uptake may contribute to idiopathic orthostatic intolerance. Methods. In a double-blind, placebo-controlled, and randomized crossover study we investigated the cardiovascular effects of acute selective pharmacological inhibition of the norepinephrine transporter (2x 8mg reboxetine p.o.) on healthy volunteers. Autonomic function test and a graded head-up tilt test were performed (n=23). Heart rate, blood pressure and cerebral blood flow velocity were measured non-invasively and continuously. Cardiac output and peripheral resistance were measured by impedance cardiography. In a smaller subset of volunteers (n=10) we also investigated the effects of acute inhibition of the Norepinephrine transporter on the sensitivity to pressor and depressor agents. Therefore, increasing doses of phenylephrine, isoproterenol, and nitroprusside were administered intravenously and individual dose-response-curves were plotted. Results. Norepinephrine reuptake inhibition increased both, supine heart rate and blood pressure. During head-up tilt, heart rate was profoundly increased with norepinephrine reuptake inhibition (120+/-3 /min vs. 83+/-3 /min with placebo, p
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Birkenfeld, Andreas L. "Autonome, kardiovaskuläre und metabolische Wirkungen kombinierter pharmakologischer Noradrenalin- und Serotonin-Wiederaufnahme-Hemmung." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973084871.

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Books on the topic "Noradrenalin in the body"

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Hentschel, Erwin. Occurence and function of biogenic amines (5-hydroxytryptamine, dopamine, noradrenaline, adrenaline and octopamine) in invertebrates: Bibliography = Vorkommen und Funktion biogener Amine (5-hydroxytryptamin, Dopamin, Noradrenalin, Adrenalin und Octopamin) bei wirbellosen Tieren : Bibliographie. Jena: Universitätsbibliothek, 1986.

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Kamath, Anoop. Body x body. New Delhi: Nitanjali Art Gallery, 2008.

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Brita, Granström, ed. My body, your body. New York: Franklin Watts, 1997.

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Bill, Reynolds, ed. Body flex-body magic. Chicago: Contemporary Books, 1992.

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David, Altheim, ed. Body bizarre, body beautiful. St Leonards, N.S.W: Allen & Unwin, 1999.

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Resnick, Stella. Body-to-Body Intimacy. New York, NY : Routledge, 2019.: Routledge, 2018. http://dx.doi.org/10.4324/9781315648552.

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Simon, Seymour. Body sense, body nonsense. Mineola, N.Y: Dover Publications, 2012.

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Body. New York: Poseidon Press, 1990.

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Crews, Harry. Body. New York: Poseidon Press, 1990.

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Haslam, Andrew. Body. Chicago, IL: World Book/Two-can, 1997.

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Book chapters on the topic "Noradrenalin in the body"

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Persky, Harold. "Chemical Determination of Adrenaline and Noradrenaline in Body Fluids and Tissues." In Methods of Biochemical Analysis, 57–82. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470110188.ch2.

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Heinert, G., D. J. Paterson, G. E. Bisgard, N. Xia, R. Painter, and P. C. G. Nye. "The Excitation of Carotid Body Chemoreceptors of the Cat by Potassium and Noradrenaline." In Advances in Experimental Medicine and Biology, 323–30. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1933-1_61.

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Laux, G., B. Bondy, U. Breyer-Pfaff, A. Delini-Stula, H. Berzewski, and C. Hiemke. "Noradrenalin-selektive Antdeessva(NRI)." In Neuro-Psychopharmaka Ein Therapie-Handbuch, 365–402. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-6150-0_5.

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Laux, G., A. Eckert, W. E. Müller, M. Linden, and H. Sauer. "Serotonin-Noradrenalin-selektive Antidepressiva (SNRI/NaSSA)." In Neuro-Psychopharmaka Ein Therapie-Handbuch, 403–36. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-6150-0_6.

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Gooch, Jan W. "Body." In Encyclopedic Dictionary of Polymers, 88. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_1457.

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Heffernan, Julián Jiménez. "Body." In Shakespeare's Extremes, 56–85. London: Palgrave Macmillan UK, 2015. http://dx.doi.org/10.1057/9781137523587_2.

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Weik, Martin H. "body." In Computer Science and Communications Dictionary, 137. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_1746.

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Behnke, Elizabeth A. "Body." In Contributions to Phenomenology, 66–71. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-017-5344-9_14.

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Genta, Giancarlo, Lorenzo Morello, Francesco Cavallino, and Luigi Filtri. "Body." In The Motor Car, 227–53. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-8552-6_8.

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Dauphinee, Elizabeth. "Body." In Visual Global Politics, 30–34. Abingdon, Oxon ; New York, NY : Routledge, 2018. | Series: Interventions: Routledge, 2018. http://dx.doi.org/10.4324/9781315856506-2.

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Conference papers on the topic "Noradrenalin in the body"

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Liu, Yuwei, Ruojian Wen, Huilin Yi, Xiaoqing Chen, and Dan Huang. "Propofol Mediates Ambient GABA-activated Tonic Inhibition of VLPO Noradrenalin-Excited Neurons." In 2015 Seventh International Conference on Measuring Technology and Mechatronics Automation (ICMTMA). IEEE, 2015. http://dx.doi.org/10.1109/icmtma.2015.194.

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Paulus, W., and W. Janni. "Kinderwunsch unter mütterlicher Langzeittherapie mit kombiniert-selektiven Serotonin- und Noradrenalin Wiederaufnahmehemmern (SSNRI)." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730476.

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Hesse, S., A. McLeod, M. Rullmann, GA Becker, J. Luthardt, F. Zientek, M. Patt, et al. "Association between Emotional Regulation (ER) and Prefrontal Noradrenalin Transporter (NAT) Availability in Human Obesity." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708420.

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Turbic, Kenan, Slawomir J. Ambroziak, and Luis M. Correia. "A body-shadowing model for off-body and body-to-body communications." In 2018 Baltic URSI Symposium (URSI). IEEE, 2018. http://dx.doi.org/10.23919/ursi.2018.8406703.

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Vinciarelli, Alessandro. "Body Language Without a Body." In MM '17: ACM Multimedia Conference. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3133944.3133954.

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Antonova, Natalya, Anatoly Merenkov, Anna Gurarii, and Elena Grunt. "Body Image: Body Modification Practices." In Proceedings of the 2019 International Conference on Pedagogy, Communication and Sociology (ICPCS 2019). Paris, France: Atlantis Press, 2019. http://dx.doi.org/10.2991/icpcs-19.2019.64.

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Maman, M., B. Denis, and R. D'Errico. "Research trends in wireless body area networks: From On-Body to Body-to-Body cooperation." In 2014 8th International Symposium on Medical Information and Communication Technology (ISMICT). IEEE, 2014. http://dx.doi.org/10.1109/ismict.2014.6825240.

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Yasir, Muhammad, and Ammar J. Malik. "Body to body network using ZigBee." In 2011 IEEE 3rd International Conference on Communication Software and Networks (ICCSN). IEEE, 2011. http://dx.doi.org/10.1109/iccsn.2011.6013543.

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ZLATEV, JORDAN, MERLIN DONALD, and GÖRAN SONESSON. "FROM BODY – TO MOUTH AND BODY." In Proceedings of the 8th International Conference (EVOLANG8). WORLD SCIENTIFIC, 2010. http://dx.doi.org/10.1142/9789814295222_0126.

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Kondo, Ryota, Maki Sugimoto, Masahiko Inami, and Michiteru Kitazaki. "Scrambled Body: A Method to Compare Full Body Illusion and Illusory Body Ownership of Body Parts." In 2019 IEEE Conference on Virtual Reality and 3D User Interfaces (VR). IEEE, 2019. http://dx.doi.org/10.1109/vr.2019.8798346.

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Reports on the topic "Noradrenalin in the body"

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Champion, Theresa. Studies of Charmless Two-Body, Quasi-Two-Body and Three-Body B Decays. Office of Scientific and Technical Information (OSTI), November 2000. http://dx.doi.org/10.2172/784763.

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Pritchard, Joy, H. R. Whay, and A. Brown. Body condition. Brooke, 2011. http://dx.doi.org/10.46746/gaw.2020.abi.bcs.

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Brown, Ashleigh. Firing: body areas. Brooke, April 2011. http://dx.doi.org/10.46746/gaw.2020.abi.firbdar.

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Pritchard, Joy, and H. R. Whay. Body lesions - severity. Brooke, 2011. http://dx.doi.org/10.46746/gaw.2021.abi.les.sev.

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Brown. Body lesions - size. Brooke, 2011. http://dx.doi.org/10.46746/gaw.2020.abi.les.size.

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Lewis, Sarah. Gendering the Body: Exploring the Construction of the Sexually Dimorphic Body. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.152.

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Barrera, Barbara. Measurements of Charmless Three-Body and Quasi-Two-Body B Decays. Office of Scientific and Technical Information (OSTI), August 2000. http://dx.doi.org/10.2172/764975.

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Hepner, David J., and Thomas E. Harkins. Determining Inertial Orientation of a Spinning Body With Body-Fixed Sensors. Fort Belvoir, VA: Defense Technical Information Center, January 2001. http://dx.doi.org/10.21236/ada391881.

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Krishnaprasad, P. S. Eulerian Many-Body Problems. Fort Belvoir, VA: Defense Technical Information Center, January 1989. http://dx.doi.org/10.21236/ada444546.

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Browder, Timothy D., and Deborah A. Kuhls :John. Portable Body Temperature Conditioner. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada613803.

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