scholarly journals The Human Penguin Project: Climate, Social Integration, and Core Body Temperature

2018 ◽  
Vol 4 (1) ◽  
Author(s):  
Hans IJzerman ◽  
Siegwart Lindenberg ◽  
İlker Dalğar ◽  
Sophia S. C. Weissgerber ◽  
Rodrigo C. Vergara ◽  
...  

Social thermoregulation theory posits that modern human relationships are pleisiomorphically organized around body temperature regulation. In two studies (N = 1755) designed to test the principles from this theory, we used supervised machine learning to identify social and non-social factors that relate to core body temperature. This data-driven analysis found that complex social integration (CSI), defined as the number of high-contact roles one engages in, is a critical predictor of core body temperature. We further used a cross-validation approach to show that colder climates relate to higher levels of CSI, which in turn relates to higher CBT (when climates get colder). These results suggest that despite modern affordances for regulating body temperature, people still rely on social warmth to buffer their bodies against the cold.

2016 ◽  
Author(s):  
Hans IJzerman ◽  
Siegwart Lindenberg ◽  
İlker Dalğar ◽  
Sophia Christin Weissgerber ◽  
Rodrigo Clemente Vergara ◽  
...  

Social thermoregulation theory posits that modern human relationships are pleisiomorphically organized around body temperature regulation. In two studies (N=1755) designed to test the principles from this theory, we used supervised machine learning to identify social and non-social factors that relate to core body temperature. This data-driven analysis found that complex social integration (CSI), defined as the number of high contact roles one engages in, is a critical predictor of core body temperature. We further used a cross-validation approach to show that colder climates relate to higher levels of CSI, which in turn relates to higher CBT (when climates get colder). These results suggest that despite modern affordances for regulating body temperature, people still rely on social warmth to buffer their bodies against the cold.


2019 ◽  
Author(s):  
Elizabeth A. Proctor ◽  
Shauna M. Dineen ◽  
Stephen C. Van Nostrand ◽  
Madison K. Kuhn ◽  
Christopher D. Barrett ◽  
...  

AbstractHeat stroke is a life-threatening condition characterized by loss of thermoregulation and severe elevation of core body temperature, which can cause organ failure and damage to the central nervous system. While no definitive test exists to measure heat stroke severity, immune challenge is known to increase heat stroke risk, although the mechanism of this increased risk is unclear. In this study, we used a mouse model of classic heat stroke to test the effect of immune challenge on pathology. Employing multivariate supervised machine learning to identify patterns of molecular and cellular markers associated with heat stroke, we found that prior viral infection simulated with poly I:C injection resulted in heat stroke presenting with high levels of factors indicating coagulopathy. Despite a decreased number of platelets in the blood, platelets are large and non-uniform in size, suggesting younger, more active platelets. Levels of D-dimer and soluble thrombomodulin were increased in more severe heat stroke, and in cases presenting with the highest level of organ damage markers D-dimer levels dropped, indicating potential fibrinolysis-resistant thrombosis. Genes corresponding to immune response, coagulation, hypoxia, and vessel repair were up-regulated in kidneys of heat-challenged animals, and these increases correlated with both viral treatment and distal organ damage while appearing before discernible tissue damage to the kidney itself. We conclude that heat stroke-induced coagulopathy may be a driving mechanistic force in heat stroke pathology, especially when exacerbated by prior infection, and that coagulation markers may serve as an accessible biomarker for heat stroke severity and therapeutic strategies.Key pointsA signature of pro-coagulation markers predicts circadian core body temperature and levels of organ damage in heat strokeChanges in coagulopathy-related gene expression are evidenced before histopathological organ damage


2012 ◽  
Vol 26 (2) ◽  
Author(s):  
Joanna Pawlak ◽  
Paweł Zalewski ◽  
Jacek J. Klawe ◽  
Monika Zawadka ◽  
Anna Bitner ◽  
...  

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2316
Author(s):  
Daniel Mota-Rojas ◽  
Dehua Wang ◽  
Cristiane Gonçalves Titto ◽  
Jocelyn Gómez-Prado ◽  
Verónica Carvajal-de la Fuente ◽  
...  

Body-temperature elevations are multifactorial in origin and classified as hyperthermia as a rise in temperature due to alterations in the thermoregulation mechanism; the body loses the ability to control or regulate body temperature. In contrast, fever is a controlled state, since the body adjusts its stable temperature range to increase body temperature without losing the thermoregulation capacity. Fever refers to an acute phase response that confers a survival benefit on the body, raising core body temperature during infection or systemic inflammation processes to reduce the survival and proliferation of infectious pathogens by altering temperature, restriction of essential nutrients, and the activation of an immune reaction. However, once the infection resolves, the febrile response must be tightly regulated to avoid excessive tissue damage. During fever, neurological, endocrine, immunological, and metabolic changes occur that cause an increase in the stable temperature range, which allows the core body temperature to be considerably increased to stop the invasion of the offending agent and restrict the damage to the organism. There are different metabolic mechanisms of thermoregulation in the febrile response at the central and peripheral levels and cellular events. In response to cold or heat, the brain triggers thermoregulatory responses to coping with changes in body temperature, including autonomic effectors, such as thermogenesis, vasodilation, sweating, and behavioral mechanisms, that trigger flexible, goal-oriented actions, such as seeking heat or cold, nest building, and postural extension. Infrared thermography (IRT) has proven to be a reliable method for the early detection of pathologies affecting animal health and welfare that represent economic losses for farmers. However, the standardization of protocols for IRT use is still needed. Together with the complete understanding of the physiological and behavioral responses involved in the febrile process, it is possible to have timely solutions to serious problem situations. For this reason, the present review aims to analyze the new findings in pathophysiological mechanisms of the febrile process, the heat-loss mechanisms in an animal with fever, thermoregulation, the adverse effects of fever, and recent scientific findings related to different pathologies in farm animals through the use of IRT.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Keisuke Suzuki ◽  
Hirokazu Ohtaki ◽  
Motoyasu Nakamura ◽  
Hiroki Yamaga ◽  
...  

Abstract Background Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure. Methods Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS. Results The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage. Conclusions We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.


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