Increase In Core Body Temperature Research Articles

Thermoregulation during Field Exercise in Horses Using Skin Temperature Monitoring.

Hyperthermia and exertional heat illness (EHI) are performance and welfare issues for all exercising horses. Monitoring the thermoregulatory response allows for early recognition of metabolic heat accumulation during exercise and the possibility of taking prompt and effective preventative measures to avoid a further increase in core body temperature (Tc) leading to hyperthermia. Skin temperature (Tsk) monitoring is most used as a non-invasive tool to assess the thermoregulatory response pre- and post-exercise, particularly employing infrared thermographic equipment. However, only a few studies have used thermography to monitor skin temperature continuously during exercise. This commentary provides an overview of studies investigating surface skin temperature mainly by infrared thermography (IRT) during exercise. The scientific evidence, including methodologies, applications, and challenges associated with (continuous) skin temperature monitoring in horses during field exercise, is discussed. The commentary highlights that, while monitoring Tsk is straightforward, continuous Tsk alone does not always reliably estimate Tc evolvement during field exercise. In addition, inter-individual differences in thermoregulation need to be recognized and accounted for to optimize individual wellbeing. With the ongoing development and application of advanced wearable monitoring technology, there may be future advances in equipment and modeling for timely intervention with horses at hyperthermic risk to improve their welfare. However, at this point, infrared thermographic assessment of Tsk should always be used in conjunction with other clinical assessments and veterinary examinations for a reliable monitoring of the welfare of the horse.

Human body heat balance equation to consider core body temperature in assessment of heatstroke risk

Increased core body temperature and dehydration are critical thermal physiological responses to heat disorders. Dehydration is preventable through adequate water intake. However, a simple heat balance equation for assessing the heatstroke risk considering the core body temperature is currently lacking. Hence, this study proposes an equation for evaluating heatstroke risk. To derive the equation, the thermal regulation of the human body and heat interactions between the body core, skin, clothing, and indoor and outdoor environments were considered. The heat flow and heat capacity were represented as water flows caused by the water head difference and cross-sectional area of the tanks, respectively. Subsequently, the importance of considering the above elements as a unified system for designing a thermally comfortable environment and preventing heatstroke is discussed. Next, a heatstroke threshold equation is presented in the form of human body heat balance equation, which considers the core body temperature. This equation enabled us to evaluate the threshold for the combination of the environmental, clothing, and activity parameters beyond which the body temperature exceeds the acceptable limit for heatstroke. The equation was validated by comparing the thresholds with the reported upper limit of the prescriptive zone. The calculated thresholds for various parameters revealed that the parameters related to evaporative heat loss, such as clothing evaporative resistance, were the dominant parameters influencing the threshold. Although the equation can evaluate the influences of various types of activity and clothing, it can be applied only to acclimatized workers in good health with sufficient water and salt intake.

The increase in core body temperature in response to exertional-heat stress can predict exercise-induced gastrointestinal syndrome

ABSTRACT Utilizing metadata from existing exertional and exertional-heat stress studies, the study aimed to determine if the exercise-associated increase in core body temperature can predict the change in exercise-induced gastrointestinal syndrome (EIGS) biomarkers and exercise-associated gastrointestinal symptoms (Ex-GIS). Endurance-trained individuals completed 2 h of running exercise in temperate (21.2-30.0°C) to hot (35.0-37.2°C) ambient conditions (n = 132 trials). Blood samples were collected pre- and post-exercise to determine the change in gastrointestinal integrity biomarkers and systemic inflammatory cytokines. Physiological and thermoregulatory strain variables were assessed every 10–15 min during exercise. The strength of the linear relationship between maximal (M-Tre) and change (Δ Tre) in rectal temperature and EIGS variables was determined via Spearman’s rank correlation coefficients. While the strength of prediction was determined via simple and multiple linear regression analyses dependent on screened EIGS and Ex-GIS confounding factors. Significant positive correlations between Tre maximum (M-Tre) and change (Δ Tre) with I-FABP (rs = 0.434, p < 0.001; and rs = 0.305, p < 0.001; respectively), sCD14 (rs = 0.358, p < 0.001; and rs = 0.362, p < 0.001), systemic inflammatory response profile (SIR-Profile) (p < 0.001), and total Ex-GIS (p < 0.05) were observed. M-Tre and Δ Tre significantly predicted (adjusted R2) magnitude of change in I-FABP (R2(2,123)=0.164, p < 0.001; and R2(2,119)=0.058, p = 0.011; respectively), sCD14 (R2(2,81)=0.249, p < 0.001; and R2(2,77)=0.214, p < 0.001), SIR-Profile (p < 0.001), and total Ex-GIS (p < 0.05). Strong to weak correlations were observed between M-Tre and Δ Tre with plasma concentrations of I-FABP, sCD14, SIR-Profile, and Ex-GIS in response to exercise. M-Tre and Δ Tre can predict the magnitude of these EIGS variables and Ex-GIS in response to exercise.

Calorie restriction partially attenuates sickness behavior induced by viral mimetic poly I:C

Calorie restriction (CR) has been shown to extend the mean and maximum lifespan in both preclinical and clinical settings. We have previously demonstrated that CR attenuates lipopolysaccharide (LPS)-induced fever and sickness behavior. CR also leads to reductions in pro-inflammatory and increases in anti-inflammatory profiles. LPS is a bacterial mimetic; however, few studies have explored this phenomenon utilizing a viral mimetic, such as polyinosinic:polycytidylic acid (poly I:C). Dose-dependently, poly I:C induced an increase in core body temperature (Tb), with the largest dose (5000 µg/kg) resulting in a 1.62 °C ( ± 0.23 °C) Tb increase at 7 h post-injection in ad libitum mice and was associated with reduced home-cage locomotor activity. We then investigated the effect of 50% CR for 28 days to attenuate fever and sickness behavior induced by a poly I:C (5000 µg/kg) viral immune challenge. CR resulted in the partial attenuation of fever and sickness behavior measures post-poly I:C. The freely fed, control mice demonstrated a 2.02 °C ( ± 0.22 °C) increase in Tb at 7 h post-injection compared to the CR poly I:C group which demonstrated an increase in Tb of 0.94 °C ( ± 0.27 °C). Locomotor patterns post-injection were different, CR mice displayed a reduction in activity during the light phase, and the control group displayed a reduction during the dark phase. CR moderately attenuated the neuroinflammatory response with a reduction in microglial density in the ventromedial nucleus of the hypothalamus. The fever and sickness behavior attenuation seen after CR may be driven by similar anti-inflammatory processes as after LPS; however, further investigation is required.

Cold-inducible lncRNA266 promotes browning and the thermogenic program in white adipose tissue.

Cold-induced nonshivering thermogenesis has contributed to the improvement of several metabolic syndromes caused by obesity. Several long noncoding RNAs (lncRNAs) have been shown to play a role in brown fat biogenesis and thermogenesis. Here we show that the lncRNA lnc266 is induced by cold exposure in inguinal white adipose tissue (iWAT). In vitro functional studies reveal that lnc266 promotes brown adipocyte differentiation and thermogenic gene expression. At room temperature, lnc266 has no effects on white fat browning and systemic energy consumption. However, in a cold environment, lnc266 promotes white fat browning and thermogenic gene expression in obese mice. Moreover, lnc266 increases core body temperature and reduces body weight gain. Mechanistically, lnc266 does not directly regulate Ucp1 expression. Instead, lnc266 sponges miR-16-1-3p and thus abolishes the repression of miR-16-1-3p on Ucp1 expression. As a result, lnc266 promotes preadipocyte differentiation toward brown-like adipocytes and stimulates thermogenic gene expression. Overall, lnc266 is a cold-inducible lncRNA in iWAT, with a key role in white fat browning and the thermogenic program.

Effect of acute heat exposure on the pressor response to a voluntary hypoxic apnea.

The pressor response induced by a voluntary hypoxic apnea is mediated largely by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Therefore, we tested the hypothesis that prior heat exposure would attenuate the pressor response induced by a voluntary hypoxic apnea. Eleven healthy adults (five women) were exposed to whole body passive heating (water-perfused suit) sufficient to increase body core temperature by 1.2°C. Voluntary hypoxic apneas were performed at baseline and in recovery when body core temperature returned to ≤ 0.3°C of baseline. Participants breathed gas mixtures of varying [Formula: see text] (21%, 16%, and 12%; randomized) for 1 min followed by a 15-s end-expiratory apnea. The change in arterial oxygen saturation during each apnea did not differ from baseline to recovery (P = 0.6 for interaction), whereas the pressor response induced by a voluntary hypoxia apnea was reduced ([Formula: see text] 21%, baseline 17 ± 7 mmHg vs. recovery 14 ± 7 mmHg; [Formula: see text] 16%, baseline 24 ± 8 mmHg vs. recovery 18 ± 7 mmHg; [Formula: see text] 12%, baseline 28 ± 11 mmHg vs. recovery 24 ± 11 mmHg; P = 0.01 for main effect of time). These data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.NEW & NOTEWORTHY The pressor response induced by a voluntary hypoxic apnea is mediated by increased sympathetic outflow. The neural control of blood pressure is altered in recovery from acute heat exposure, but its effect on the pressor response to a voluntary hypoxic apnea has never been explored. Our data suggest that prior heat exposure induces a cross-stressor effect such that the pressor response to a voluntary hypoxic apnea is attenuated.

Heat stress effects on milk yield traits and metabolites and mitigation strategies for dairy cattle breeds reared in tropical and sub-tropical countries.

Heat stress is an important problem for dairy industry in many parts of the world owing to its adverse effects on productivity and profitability. Heat stress in dairy cattle is caused by an increase in core body temperature, which affects the fat production in the mammary gland. It reduces milk yield, dry matter intake, and alters the milk composition, such as fat, protein, lactose, and solids-not-fats percentages among others. Understanding the biological mechanisms of climatic adaptation, identifying and exploring signatures of selection, genomic diversity and identification of candidate genes for heat tolerance within indicine and taurine dairy breeds is an important progression toward breeding better dairy cattle adapted to changing climatic conditions of the tropics. Identifying breeds that are heat tolerant and their use in genetic improvement programs is crucial for improving dairy cattle productivity and profitability in the tropics. Genetic improvement for heat tolerance requires availability of genetic parameters, but these genetic parameters are currently missing in many tropical countries. In this article, we reviewed the HS effects on dairy cattle with regard to (1) physiological parameters; (2) milk yield and composition traits; and (3) milk and blood metabolites for dairy cattle reared in tropical countries. In addition, mitigation strategies such as physical modification of environment, nutritional, and genetic development of heat tolerant dairy cattle to prevent the adverse effects of HS on dairy cattle are discussed. In tropical climates, a more and cost-effective strategy to overcome HS effects is to genetically select more adaptable and heat tolerant breeds, use of crossbred animals for milk production, i.e., crosses between indicine breeds such as Gir, white fulani, N'Dama, Sahiwal or Boran to taurine breeds such as Holstein-Friesian, Jersey or Brown Swiss. The results of this review will contribute to policy formulations with regard to strategies for mitigating the effects of HS on dairy cattle in tropical countries.

Impact of Phytase Supplementation on Meat Quality of Heat-Stressed Broilers.

Heat stress (HS) is one of the most challenging stressors to poultry production sustainability. The adverse effects of HS range from feed intake and growth depression to alteration of meat quality and safety. As phytase supplementation is known to improve nutrient utilization and consequently growth, we undertook the present study to evaluate the effects of dietary phytase on growth and meat quality in heat-stressed broilers. A total of 720 day-old hatch Cobb 500 chicks were assigned to 24 pens within controlled environmental chambers and fed three diets: Negative Control (NC), Positive Control (PC), and NC diet supplemented with 2000 phytase units (FTU)/kg) of quantum blue (QB). On day 29, birds were exposed to two environmental conditions: thermoneutral (TN, 25 °C) or cyclic heat stress (HS, 35 °C, 8 h/d from 9 a.m. to 5 p.m.) in a 3 × 2 factorial design. Feed intake (FI), water consumption (WI), body weight (BW), and mortality were recorded. On day 42, birds were processed, carcass parts were weighed, and meat quality was assessed. Breast tissues were collected for determining the expression of target genes by real-time quantitative PCR using the 2-ΔΔCt method. HS significantly increased core body temperature, reduced feed intake and BW, increased water intake (WI), elevated blood parameters (pH, SO2, and iCa), and decreased blood pCO2. HS reduced the incidence of woody breast (WB) and white striping (WS), significantly decreased drip loss, and increased both 4- and 24-h postmortem pH. Instrumental L* and b* values were reduced (p < 0.05) by the environmental temperature at both 4- and 24-h postmortem. QB supplementation reduced birds' core body temperature induced by HS and improved the FCR and water conversion ratio (WCR) by 1- and 0.5-point, respectively, compared to PC under HS. QB increased blood SO2 and reduced the severity of WB and WS under TN conditions, but it increased it under an HS environment. The abovementioned effects were probably mediated through the modulation of monocarboxylate transporter 1, heat shock protein 70, mitogen-activated protein kinase, and/or glutathione peroxidase 1 gene expression, however, further mechanistic studies are warranted. In summary, QB supplementation improved growth performance and reduced muscle myopathy incidence under TN conditions. Under HS conditions, however, QB improved growth performance but increased the incidence of muscle myopathies. Therefore, further QB titration studies are needed.

Body Temperature Manipulation Increases Salivary Cortisol Independent of Exercise

The vast majority of circulating cortisol in the blood is bound and inactivated by binding proteins like corticosteroid-binding globulin (CBG) and albumin. The cortisol that is free of these binding proteins is secreted via saliva and other body fluids. Ex-vivo studies have shown that CBG binding to cortisol is temperature-dependent within the physiological range of human core body temperatures. Exercise is a standard experimental paradigm for inducing cortisol responses. However, these studies rarely consider that exercise-induced changes in core body temperature might increase free cortisol independent of psychological stress or physical exertion. We tested the effect of heat exposure without exertion or other stressors on saliva cortisol. 26 Participants (18 healthy and 8 with Major Depression MDD) sat motionless in a dry infrared sauna set to 65.5 degrees C (150 F). They had their tympanic membrane temperature and salivary cortisol measured as their body temperature increased. Exposure to exogenous heat significantly increased core body temperature from 36.93 C/98.48 F (95% CI 36.79-37.07 C, 98.23-98.73 F) to 38.42 C /101.16 F (95% CI 38.24-38.6 C, 100.83-101.48 F) after 45 minutes of heat exposure, F(15,42.33)=43.509, p<0.001. Concurrently saliva cortisol also increased significantly from 4.00 nmol/l (95%CI 1.89-6.11) to 9.87 nmol/l (95% CI 5.58-14.17), F(1,33.17)=6.64, p=0.015. Elevations in core body temperature can significantly increase free cortisol levels even in the absence of exercise or overt psychological stressors.

CORE™ wearable sensor: Comparison against gastrointestinal temperature during cold water ingestion and a 5 km running time-trial

Five km running time-trials (TT) are associated with rapid and significant increases in core body temperature (TC). For such races, real-time feedback from pre-exercise and exercise TC may be helpful in the design of an optimal pacing strategy aimed at limiting the possibility of developing heat-related illnesses. This study compared measurements of TC obtained with a wearable device, the CORE™, to those of a gastrointestinal pill (GI pill), during cold water ingestion and a 5 km running TT. Twelve participants (25 ± 4 yrs) ingested 7.5 mL/kg fat-free mass of 4 °C water over the first 5 min of a 120 min sitting period, after which they completed a 5 km running TT at 30 °C, 50% relative humidity. A TC difference > ± 0.25 °C between sensors was deemed clinically unacceptable. Prior to water ingestion, the CORE-derived TC was 0.49 ± 0.25 °C lower than the GI pill. The CORE was irresponsive to the 0.26 ± 0.22 °C peak decline in TC captured with the GI pill 40 min following water ingestion. Prior to the TT, TC was 0.30 ± 0.25 °C lower with the CORE than the GI pill. During the TT, the CORE underestimated the rate of increase in TC by 0.0125 ± 0.019 °C/min compared with the GI pill, and mean absolute difference in TC between sensors was of 0.47 ± 0.34 °C. In conclusion, the CORE does not capture the cooling effect of cold water ingestion and provides a clinically relevant underestimation of TC during a 5 km running TT in the heat.

Prompted hands-free drinking improves simulated race car driving in a hot environment

ABSTRACT Race car drivers are often hypohydrated during a race. The FluidLogic drink system is a hands-free, prompted drinking system that is hypothesized to increase the likeliness of drivers’ consuming fluids and thereby mitigating hypohydration. To test the hypothesis, 20 elite professional race car drivers participated in a 2-day cross-over study in which they drove on a race simulator in an environmental chamber that was heated to regulation cockpit temperature (38°C). Drivers used either the FluidLogic drink system or a standard in-car water bottle system (Control) on one of each testing day. The results indicated that there was consistent fluid consumption with the FluidLogic system, while the Control condition elicited fluid consumption in bolus doses. The Control condition was associated with moderate (0.5%) increased core body temperature (P < 0.05) and substantial (3.3%) increased urine-specific gravity (P < 0.001) as compared to the FluidLogic condition. Driving performance metrics indicated that lap times during the Control Condition were 5.1 ± 1.4 (4.1%) seconds slower (P < 0.05) than the FluidLogic Condition, due to driving errors that occurred in the high-speed corners. Based on these results, prompted hands-free drinking can mitigate hypohydration and performance loss in automobile racing drivers.

Obstructive sleep apnea in a mouse model is associated with tissue-specific transcriptomic changes in circadian rhythmicity and mean 24-hour gene expression.

Intermittent hypoxia (IH) is a major clinical feature of obstructive sleep apnea (OSA). The mechanisms that become dysregulated after periods of exposure to IH are unclear, particularly in the early stages of disease. The circadian clock governs a wide array of biological functions and is intimately associated with stabilization of hypoxia-inducible factors (HIFs) under hypoxic conditions. In patients, IH occurs during the sleep phase of the 24-hour sleep-wake cycle, potentially affecting their circadian rhythms. Alterations in the circadian clock have the potential to accelerate pathological processes, including other comorbid conditions that can be associated with chronic, untreated OSA. We hypothesized that changes in the circadian clock would manifest differently in those organs and systems known to be impacted by OSA. Using an IH model to represent OSA, we evaluated circadian rhythmicity and mean 24-hour expression of the transcriptome in 6 different mouse tissues, including the liver, lung, kidney, muscle, heart, and cerebellum, after a 7-day exposure to IH. We found that transcriptomic changes within cardiopulmonary tissues were more affected by IH than other tissues. Also, IH exposure resulted in an overall increase in core body temperature. Our findings demonstrate a relationship between early exposure to IH and changes in specific physiological outcomes. This study provides insight into the early pathophysiological mechanisms associated with IH.

Abdominal TRPV1 channel desensitization enhances stress-induced hyperthermia during social stress in rats.

In rats, stress-induced hyperthermia caused by social interaction depends on brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction. However, the peripheral mechanisms responsible for regulating the level of hyperthermia during social stress are still unknown. The transient receptor potential vanilloid 1 (TRPV1) subfamily, expressed in sensory and visceral neurons, can serve as a thermoreceptor. Here, we tested the hypothesis that the abdominal TRPV1 is essential in regulating stress-induced hyperthermia during social stress. Male Wistar rats received an intraperitoneal injection of Resiniferatoxin (RTX) - an ultra-potent capsaicin analog, (i.e., to desensitize the TRPV1 channels) or vehicle. Seven days later, we evaluated the effects of abdominal TRPV1 channels desensitization on core body temperature (CBT), brown adipose tissue (BAT) temperature, tail skin temperature, and heart rate (HR) of rats subjected to a social stress protocol. We found abdominal TRPV1 desensitization increased CBT and BAT temperature but did not change tail skin temperature and HR during rest. However, under social stress, we found that abdominal TRPV1 desensitization heightened the increase in CBT and BAT caused by stress. Also, it abolished the increase in tail skin temperature that occurs during and after social stress. TRPV1 desensitization also delayed the HR recovery after the exposure to the social stress. These results show that abdominal TRPV1 channels desensitization heightens stress-induced hyperthermia, causing heat dissipation during and after social stress, enabling optimal thermal control during social encounters.

Uhthoff ’s Phenomenon as Presentation of COVID-19 Infection

This is the first reported case of COVID-19 associated optic neuritis (ON) presenting with classic Uhtoff’s phenomenon typically associated with multiple sclerosis (MS). Uhthoff phenomenon, also known as Uhthoff sign or syndrome, is a transient worsening of neurological function lasting less than 24 hours that can occur in multiple sclerosis patients due to increases in core body temperature. There have been some case reports of ON associated with COVID-19 infection but no reports of ON mimicking MS. The patient’s symptoms resolved very slowly and was not affected by receiving a vaccination against COVID-19.

Glucagon-Like Peptide-1 Is Involved in the Thermic Effects of Dietary Proteins in Male Rodents.

Protein intake potently increases body temperature and energy expenditure, but the underlying mechanism thereof remains incompletely understood. Simultaneously, protein intake potently stimulates glucagon-like peptide-1 (GLP-1) secretion. Here, we examined the involvement of GLP-1 in the thermic effects of dietary proteins in rodents by measuring rectal temperature and energy expenditure and modulating GLP-1 signaling. Rectal temperature of rats or mice fasted for 4 or 5 hours were measured using a thermocouple thermometer before and after an oral administration of nutrients. Oxygen consumption after oral protein administration was also measured in rats. Rectal temperature measurements in rats confirmed an increase in core body temperature after refeeding, and the thermic effect of the oral administration of protein was greater than that of a representative carbohydrate or lipid. Among the five dietary proteins examined (casein, whey, rice, egg, and soy), soy protein had the highest thermic effect. The thermic effect of soy protein was also demonstrated by increased oxygen consumption. Studies using a nonselective β-adrenergic receptor antagonist and thermal camera suggested that brown adipose tissue did not contribute to soy protein-induced increase in rectal temperature. Furthermore, the thermic effect of soy protein was completely abolished by antagonism and knockout of the GLP-1 receptor, yet potentiated via augmentation of intact GLP-1 levels through inhibition of dipeptidyl peptidase-4 activity. These results indicate that GLP-1 signaling is essential for the thermic effects of dietary proteins in rats and mice, and extend the metabolic actions of GLP-1 ensuing from nutrient ingestion to encompass the thermic response to ingested protein.

Effect of Aerobic Exercise Training on Sleep and Core Temperature in Middle-Aged Women with Chronic Insomnia: A Randomized Controlled Trial

Exercise represents a viable non-pharmacological intervention to help treating insomnia but the interaction mechanisms between sleep and physical activity still remain poorly understood. The aim of this study was to investigate the effect of a aerobic exercise training intervention on sleep and core temperature. Twenty-four adult women suffering from insomnia participated in this study. They were randomized into an exercise group and a control group. Aerobic exercise training consisted in moderate to vigorous aerobic exercise training for 12 weeks. Outcome measures included both subjective (Insomnia Severity Index, ISI) and objective (actigraphy recordings) sleep quality assessments, and core body temperature continuously recorded for a minimum 24 h. The exercise group showed a decrease in ISI (p < 0.001) and in various objective sleep parameters. The core temperature batyphase value was lowered (p = 0.037) whereas its amplitude was larger (p = 0.002). We also found a tight correlation between the evolution of insomnia and the evolution of mean night-time core temperature and batyphase values. A moderate to vigorous aerobic exercise program appears to be an effective non-drug therapy for improving sleep in women with insomnia. In addition, exercise programs should aim to increase core body temperature during practice to induce sleep-promoting adaptations and rebound.

Wavelength-Dependent Effects of Photobiomodulation for Wound Care in Diabetic Wounds.

Photobiomodulation, showing positive effects on wound healing processes, has been performed mainly with lasers in the red/infrared spectrum. Light of shorter wavelengths can significantly influence biological systems. This study aimed to evaluate and compare the therapeutic effects of pulsed LED light of different wavelengths on wound healing in a diabetic (db/db) mouse excision wound model. LED therapy by Repuls was applied at either 470 nm (blue), 540 nm (green) or 635 nm (red), at 40 mW/cm2 each. Wound size and wound perfusion were assessed and correlated to wound temperature and light absorption in the tissue. Red and trend-wise green light positively stimulated wound healing, while blue light was ineffective. Light absorption was wavelength-dependent and was associated with significantly increased wound perfusion as measured by laser Doppler imaging. Shorter wavelengths ranging from green to blue significantly increased wound surface temperature, while red light, which penetrates deeper into tissue, led to a significant increase in core body temperature. In summary, wound treatment with pulsed red or green light resulted in improved wound healing in diabetic mice. Since impeded wound healing in diabetic patients poses an ever-increasing socio-economic problem, LED therapy may be an effective, easily applied and cost-efficient supportive treatment for diabetic wound therapy.

Determinants of body core temperatures at fatigue in rats subjected to incremental-speed exercise: The prominent roles of ambient temperature, distance traveled, initial core temperature, and measurement site

Understanding the factors that underlie the physical exercise-induced increase in body core temperature (TCORE) is essential to developing strategies to counteract hyperthermic fatigue and reduce the risk of exertional heatstroke. This study analyzed the contribution of six factors to TCORE attained at fatigue in Wistar rats (n = 218) subjected to incremental-speed treadmill running: ambient temperature (TAMB), distance traveled, initial TCORE, body mass, measurement site, and heat loss index (HLI). First, we ran hierarchical multiple linear regression analyses with data from different studies conducted in our laboratory (n = 353 recordings). We observed that TAMB, distance traveled, initial TCORE, and measurement site were the variables with predictive power. Next, regression analyses were conducted with data for each of the following TCORE indices: abdominal (TABD), brain cortex (TBRAIN), or colonic (TCOL) temperature. Our findings indicated that TAMB, distance traveled (i.e., an exercise performance-related variable), initial TCORE, and HLI predicted the three TCORE indices at fatigue. Most intriguingly, HLI was inversely related to TABD and TBRAIN but positively associated with TCOL. Lastly, we compared the temperature values at fatigue among these TCORE indices, and the following descendent order was noticed - TCOL, TABD, and TBRAIN - irrespective of TAMB where experiments were conducted. In conclusion, TCORE in rats exercised to fatigue depends primarily on environmental conditions, performance, pre-exercise TCORE, and measurement site. Moreover, the influence of cutaneous heat loss on TCOL is qualitatively different from the influence on TABD and TBRAIN, and the temperature values at fatigue are not homogenous within the body core.

Roles of leptin on energy balance and thermoregulation in Eothenomys miletus.

Leptin is a hormone mainly synthesized and secreted by white adipose tissue (WAT), which regulates various physiological processes. To investigate the role of leptin in energy balance and thermoregulation in Eothenomys miletus, voles were randomly divided into leptin-injected and PBS-injected groups and placed at 25°C ± 1°C with a photoperiod of 12 L:12 D. They were housed under laboratory conditions for 28days and compared in terms of body mass, food intake, water intake, core body temperature, interscapular skin temperature, resting metabolic rate (RMR), nonshivering thermogenesis (NST), liver and brown adipose tissue (BAT) thermogenic activity, and serum hormone levels. The results showed that leptin injection decreased body mass, body fat, food intake, and water intake. But it had no significant effect on carcass protein. Leptin injection increased core body temperature, interscapular skin temperature, resting metabolic rate, non-shivering thermogenesis, mitochondrial protein content and cytochrome C oxidase (COX) activity in liver and brown adipose tissue, uncoupling protein 1 (UCP1) content and thyroxin 5'-deiodinase (T45'-DII) activity in brown adipose tissue significantly. Serum leptin, triiodothyronine (T3), thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) concentrations were also increased significantly. Correlation analysis showed that serum leptin levels were positively correlated with core body temperature, body mass loss, uncoupling protein 1 content, thyroxin 5'-deiodinase activity, nonshivering thermogenesis, and negatively correlated with food intake; thyroxin 5'-deiodinase and triiodothyronine levels were positively correlated, suggesting that thyroxin 5'-deiodinase may play an important role in leptin-induced thermogenesis in brown adipose tissue. In conclusion, our study shows that exogenous leptin is involved in the regulation of energy metabolism and thermoregulation in E. miletus, and thyroid hormone may play an important role in the process of leptin regulating energy balance in E. miletus.

SEVERE ATOPIC DERMATITIS IMPROVED WITH OMALIZUMAB TREATMENT OF CHOLINERGIC URTICARIA

<h3>Introduction</h3> Interrupting the itch-scratch cycle can be key to managing atopic dermatitis (AD). We present a patient with severe AD who improved with omalizumab treatment of coexistent cholinergic urticaria (CholU). <h3>Case Description</h3> A 17-year-old girl with longstanding AD, on dupilumab for two years, presented for recurrent hives and anaphylaxis. Patient's mother described several episodes of itching, small wheals, and "fainting" over the previous 18 months. All episodes occurred when the patient was "feeling hot" and had been engaged either in strenuous physical exertion or light exertion in heat. With one episode, she received intramuscular epinephrine and returned to baseline; others resolved after cooling. Her AD control had deteriorated since episodes began. CholU was considered in the differential. After four months of daily second-generation antihistamine, she reported worsening eczema and no change in urticaria/anaphylaxis episodes. Urticaria treatment was escalated to maximal daily doses of fexofenadine, famotidine, and montelukast, with minimal improvement. She underwent provocation skin testing with methacholine, off antihistamines. Histamine prick was positive with wheal/flare of 7/26mm. Methacholine intradermal tests were positive at two concentrations: 0.1 mg/ml (5/13mm) and 1.0 mg/ml (8/20mm). Intradermal saline control was non-reactive. CholU was definitively diagnosed. The patient stopped dupilumab and initiated omalizumab 300 mg every four weeks. Her urticaria and eczema improved dramatically, and she had no further anaphylaxis. <h3>Discussion</h3> CholU is a type of urticaria induced by increase in core body temperature. Anaphylaxis may occur in advanced cases. In patients unresponsive to antihistamines, omalizumab has proven effective.