Burn injuries constitute a significant health concern, requiring immediate first aid to mitigate further tissue damage and complications. Most countries worldwide recommend application of 20 min of cool running water (20CRW) within 3 hours of the burn as the cornerstone in burn first aid management. Despite its widespread acceptance and proven benefits in reducing the severity of burns and subsequent interventions, concerns regarding the risk of hypothermia following this intervention persist, representing at least a perceived barrier to the delivery of 20CRW. When it does occur, hypothermia in patients with burns has been associated with higher mortality rates, even after controlling for burn injury severity. Developing an understanding of the incidence of post-burn hypothermia following 20CRW, with a specific focus on potential predictive and/or causative factors, is quintessential.

Survival during infection depends on both pathogen clearance and the ability to tolerate infection-induced physiological changes. Metabolic adaptations are a central component of this tolerance, but the mechanisms underlying these responses remain incompletely defined. Here, we identify white adipose tissue (WAT) lipolysis as a central regulator of metabolic tolerance to infection. In patients with sepsis, higher circulating non-esterified fatty acid (NEFA) levels were associated with reduced mortality. In mouse models of polymicrobial sepsis, infection induced robust adipose lipolysis and increased circulating NEFAs. Genetic ablation of adipose triglyceride lipase (ATGL) in adipose tissue impaired lipolysis, leading to hypothermia, bradycardia, and increased mortality without altering immune cell populations or pathogen burden, consistent with a defect in tolerance rather than resistance. Mechanistically, lipolysis-derived NEFAs, but not glycerol, were required for protection, as restoring circulating NEFAs rescued autonomic stability and survival in adipose tissue ATGL-deficient mice. Infection-induced lipolysis was redundantly regulated and did not depend on any single upstream signaling pathway. Both pharmacologic activation of lipolysis using a β3-adrenergic agonist and exogenous fatty acid supplementation increased circulating NEFAs, improved survival, and promoted tolerance in mice. Consistent with these findings, analysis of real-world electronic health record data demonstrated that septic patients receiving FDA-approved β3-adrenergic agonists had reduced mortality or hospice discharge in a propensity-matched cohort. Together, these results identify WAT lipolysis and circulating fatty acids as key mediators of tolerance to infection and support a therapeutic strategy based on repurposing clinically available β3-adrenergic agonists to improve outcomes in sepsis.

It's been reported that illicit drug supplies increasingly contain the α 2 -adrenergic agonist, xylazine, alongside fentanyl, yet the pharmacological basis for the greater lethality of this combination remains unclear. Prior research has shown that μ-opioid (Oprm1) receptors, on which fentanyl acts, and α 2 -adrenergic (Adra2a) receptors, on which xylazine acts, are both expressed within brainstem circuits that govern autonomic control, especially the parabrachial (PB) and Kölliker-Fuse (KF) nuclei that regulate respiration. Thus, we propose that co-activation of these inhibitory receptors and their respective pathways could potentiate or additively suppress respiratory and thermoregulatory function.

Severe accidental hypothermia represents a unique and potentially reversible cause of cardiac arrest in which prolonged resuscitation may still result in favorable neurological recovery. Unlike normothermic cardiac arrest, hypothermic cardiac arrest (HCA) is characterized by profound metabolic suppression and temperature-mediated myocardial instability, requiring a fundamentally different therapeutic paradigm. Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) provides not only circulatory support but also controlled reperfusion and rewarming, positioning it as the cornerstone of modern management. Recent international guidelines have clarified indications for extracorporeal life support (ECLS) in HCA and have contributed to improved standardization of care. Building upon these recommendations, this narrative review focuses on physiological principles underlying extracorporeal rewarming and their implications for bedside management. We examine mechanisms of ischemia-reperfusion injury, rewarming-associated hemodynamic instability and myocardial stunning, discuss dynamic risk assessment beyond statistical thresholds such as the HOPE score and summarize practical considerations regarding cannulation strategies, differential hypoxia, left ventricular unloading and neurologic evaluation. By integrating current evidence with pathophysiological insight and organizational considerations, this review proposes a clinically oriented framework to support decision-making in hypothermic cardiac arrest and to optimize meaningful neurological recovery.

Brain temperature, a fundamental modulator of neural function, remains dramatically understudied despite its critical role in health and disease. This review synthesizes current understanding of brain thermoregulation and its disruption in neurological conditions, addressing a significant knowledge gap in neuroscience. We examined the physiological mechanisms maintaining brain temperature homeostasis, including the interplay between cerebral blood flow, metabolism, and cerebrospinal fluid dynamics. Analysis of publication trends reveals brain temperature research is underrepresented by 7- to 37-fold compared to other brain physiological parameters, despite comparable clinical relevance. We evaluated current non-invasive measurement techniques, particularly magnetic resonance-based thermometry, highlighting advances and limitations for clinical application. The review presents evidence for distinct temperature dysregulation patterns in neurological diseases. In Alzheimer's disease, we propose a theoretical framework of early-stage hyperthermia driven by neuroinflammation and hypermetabolism, transitioning to late-stage hypothermia with metabolic decline. Brain tumors exhibit contrasting thermal profiles: glioblastomas frequently present as hypothermic due to necrotic cores acting as metabolic voids, while melanoma metastases show hyperthermia from sustained metabolic activity. These temperature alterations may influence disease progression through effects on protein aggregation, cellular metabolism, and neuron-glial interactions. Looking forward, brain temperature monitoring could provide biomarkers for disease staging and treatment response. Additionally, understanding thermal limits becomes urgent as climate change exposes vulnerable populations with compromised thermoregulation to extreme heat. This review establishes brain temperature as an overlooked but essential axis in neurophysiology, calling for increased research attention to address fundamental questions about thermal regulation in health and disease.

The famous serum run of 1925 has focused upon Balto, Togo, and the Norwegian mushers Gunnar Kaasen and Leonard Seppala. The mushers who ran most of the legs were actually descended from Alaskan Natives, including George and Edgar Nollner and Charlie Evans. Thanks to the Fairbanks Library archivists who sent me the interview with Charlie Evans and Edgar Nollner. This short fiction won one of the inaugural McGovern Center Writing Awards.

PurposeThis study was designed to evaluate the process of controlling body temperature in patients who were diagnosed with infection and followed up with the diagnosis of "hyperthermia" according to the NANDA-I nursing diagnosis classification according to the outcome criterion "NOC (0800) Thermoregulation Assessment."MethodThis methodological and descriptive study was conducted with 102 inpatients followed up with the nursing diagnosis of "hyperthermia" in the Department of Infectious Diseases and Clinical Microbiology of a training and research hospital between June 2024 and June 2025. The data were collected using the "Patient Information Form" and the "NOC (0800) Thermoregulation Assessment Scale." Statistical analyses specific to groups that were normally distributed (t-test) or not (Mann-Whitney U, Kruskal-Wallis, and Spearman correlation analysis) were done to analyze the data. For validity and reliability, the Davis Technique, Cronbach's α coefficient, Standardized Root Mean Square Residual fit indices, and item-total correlation statistical analyses were done.FindingsThe content validity index of the NOC scale was calculated as 0.97. When the mean scores of the patients on the NOC (0800) Thermoregulation Assessment Scale were analyzed, a statistically significant difference was observed for repeated assessments (p < 0.01). The indicators "dropped skin temperature", "hypothermia", "heat cramps", "heat stroke", and "cold-related tissue damage" were "not applicable" in the study population. No statistically significant difference was found between the NOC scale mean scores of the patients according to their gender, marital status, educational level, occupation, and presence of chronic diseases (p > 0.05).ConclusionsThe Turkish version of the NOC (0800) Thermoregulation Assessment Scale was a valid tool that could be used during the process of controlling body temperature in patients with infection.Implications of nursing practiceThe use of the NOC (0800) Thermoregulation Assessment Scale would create a common language for delivering nursing care while assessing the process of controlling body temperature.