Thermal limits of survival and reproduction depend on stress duration: A case study of Drosophila suzukii.

Studies of ectotherm responses to heat extremes often rely on assessing absolute critical limits for heat coma or death (CTmax), however, such single parameter metrics ignore the importance of stress exposure duration. Furthermore, population persistence may be affected at temperatures considerably below CTmax through decreased reproductive output. Here we investigate the relationship between tolerance duration and severity of heat stress across three ecologically relevant life-history traits (productivity, coma and mortality) using the global agricultural pest Drosophila suzukii. For the first time, we show that for sublethal reproductive traits, tolerance duration decreases exponentially with increasing temperature (R2 > 0.97), thereby extending the Thermal Death Time framework recently developed for mortality and coma. Using field micro-environmental temperatures, we show how thermal stress can lead to considerable reproductive loss at temperatures with limited heat mortality highlighting the importance of including limits to reproductive performance in ecological studies of heat stress vulnerability.

The impact of heat treatment on E. coli cell physiology in rich and minimal media considering oxidative secondary stress.

AIMS: This study investigates the cell physiology of thermally injured bacterial cells, with a specific focus on oxidative stress and the repair mechanisms associated with oxidative secondary stress. METHODS AND RESULTS: We explored the effect of heat treatment on the activity of two protective enzymes, levels of intracellular reactive oxygen species, and redox potential. The findings reveal that enzyme activity slightly increased after heat treatment, gradually returning to baseline levels during subculture. The response of Escherichia coli cells to heat treatment, as assessed by the level of superoxide radicals generated and redox potential, varied based on growth conditions, namely minimal and rich media. Notably, the viability of injured cells improved when antioxidants were added to agar media, even in the presence of metabolic inhibitors. CONCLUSIONS: These results suggest a complex system involved in repairing damage in heat-treated cells, particularly in rich media. While repairing membrane damage is crucial for cell regrowth and the electron transport system plays a critical role in the recovery process of injured cells under both tested conditions.

Neuromotor deficits and altered physiological responses to repeated exertional heat stroke exposures in mice.

Exertional heat stroke (EHS) is a life-threatening illness that can lead to negative health outcomes. Using a "severe" preclinical mouse model of EHS, we tested the hypotheses that one EHS exposure results in altered susceptibility to a subsequent EHS and reduced neuromotor performance. Female C57BL/6 mice underwent two protocols, 2 wk apart, either an EHS trial (EHS) or a sham exercise control trial (EXC). For EHS, mice ran in a forced running wheel at 37.5°C/40% relative humidity until loss of consciousness, followed by a slow cooling protocol (2 h recovery at 37.5°C). EXC mice exercised equally but in ∼22°C. Mice were randomized into three groups: 1) EXC-EXC (two consecutive EXC, n = 6, 2) EHS-EXC (EHS followed by EXC, n = 5), and 3) EHS-EHS (repeated EHS, n = 9). Mice underwent noninvasive neuromotor and behavioral tests during recovery and isolated soleus force measurements at the end of recovery. At the first EHS, mice reached average peak core temperatures (Tc,max) of 42.4°C, (46% mortality). On the second EHS, average Tc,max was reduced by ∼0.7°C (P < 0.05; mortality 18%). After the first EHS, both EHS-EX and EHS-EHS showed significant reductions in maximum strength (24 h and 1 wk post). After the second EHS, strength, horizontal rotation, hindlimb tone, suspended hindlimb splay, trunk curl, and provoked biting continued to decline in the EHS-EHS group. In conclusion, exposure to a second EHS after 2 wk leads to increased exercise times in the heat, symptom limitation at a lower Tc,max, and greater deficits in neuromotor and behavioral function during recovery.

Evaluation of distinct modes of oxidative secondary injury generated in heat-treated cells of Escherichia coli with solid/liquid and complex/semi-synthetic media sets.

AIMS: To characterize and evaluate oxidative secondary injury generated in heat-treated Escherichia coli cells during recovery cultivation either on agar or in a broth of a semi-synthetic enriched M9 (EM9) medium and a complex Luria broth (LB) medium with different types of antioxidants. METHODS AND RESULTS: E. coli cells grown in the EM9 and LB broth were heated at 50°C in a buffer (pH 7.0). Heated cells were recovered on the same kind of agar medium as that used for growth, with or without different antioxidants. Although these antioxidants mostly protected the cells from oxidative secondary injury on the recovery media, sodium thiosulphate and sodium pyruvate were most protective on EM9 and LB agars, respectively. Determination of viability using the most probable number and growth delay analysis methods showed significant reductions in the protective effects of antioxidants in the EM9 and LB media. CONCLUSION: Oxidative secondary injury generated in heated E. coli cells was found to be qualitatively and quantitatively diverse under cellular and environmental conditions. SIGNIFICANCE AND IMPACT OF THE STUDY: Our results suggest that different modes of oxidation should be considered in viability determination and injured cell enumeration of heat-treated cells.

Organ Histopathology and Hematological Changes Associated With Heat Exposure in Australian Desert Birds.

An inability of the body to appropriately respond to extreme temperatures will result in pathological changes to vital organs and adverse hematological changes. Mild heat exposure of a bird to a temperature above the zone of thermoneutrality can induce subclinical heat stress, which may be a precursor to illness. The ability to identify subtle changes that may be associated with subclinical heat stress can be important in early diagnosis and treatment of heat stress in birds. Pathological changes to internal body organs, post-heat exposure, were microscopically examined in 13 budgerigars (Melopsittacus undulatus), 15 zebra finches (Taeniopygia guttata), and 8 diamond doves (Geopelia cuneata) as model species for the bird orders Psittaciformes, Passeriformes, and Columbiformes, respectively. There was mild to moderate congestion of the lungs of 28/36 birds examined, including all of the budgerigars and diamond doves. In 8/15 zebra finches no significant lung congestion was noted. Interstitial and pulmonary hemorrhage was in observed in one diamond dove. The most common hepatic pathologic change identified was micro- and macro-vesicular hepatocellular vacuolation (4/15 zebra finches, 5/13 budgerigars, and 8/8 diamond doves). There was mild to moderate congestion in the kidneys of 1/15 zebra finch, 2/ 13 budgerigars, and 4/8 diamond doves, as well as in the gastrointestinal tract of 1/15 zebra finch and 7/8 budgerigars. Budgerigars showed a decrease in hematocrit and a significant change in the numbers of heterophils and lymphocytes following heat exposure. The basophil population of cells remained relatively stable in both budgerigars and diamond doves. These findings indicate avian species differences in body organ and hematological changes following exposure to similar elevations in environmental temperatures.

Heat injured stromal cells-derived exosomal EGFR enhances prostatic wound healing after thulium laser resection through EMT and NF-κB signaling.

BACKGROUND: This study investigated shallow heat injury to prostate stromal fibroblasts and epithelial cells and their interaction to regulate the wound healing and the underlying molecular events. METHODS: Prostate stromal fibroblasts and epithelial cells were cultured individually or cocultured and subjected to shallow heat injury for assessments of cell proliferation, migration, apoptosis, cell cycle distribution, and gene expression. The supernatant of heat-injured WPMY-1 cells was collected for exosome extraction and assessments. Furthermore, beagle dogs received thulium laser resection of the prostate (TmLRP) and randomly divided into Gefitinib, GW4869, and control treatment for the histological analysis, tissue re-epithelialization, and epidermal growth factor receptor (EGFR) expression on the prostatic wound surface. Immunofluorescence was to evaluate p63-positive basal progenitor cell trans-differentiation and macrophage polarization and ELISA was to detect cytokine levels in beagles' urine. RESULTS: Shallow heat injury caused these cells to enter a stressed state and enhanced their crosstalk. The prostate stromal fibroblasts produced and secreted more exosomal-EGFR and other cytokines and chemokines after shallow heat injury, resulting in increased proliferation and migration of prostate epithelial cells during wound healing. The wound healing of the canine prostatic urethra following the TmLRP procedure was slower in the Gefitinib and GW4869 treatment group than in the control group of animals. Immunofluorescence and ELISA showed that reduced EGFR expression interrupted macrophage polarization but increased the inflammatory response. CONCLUSIONS: Shallow heat injury was able to promote the interaction of prostate stromal cells with prostate epithelial cells to enhance wound healing. Stromal-derived exosomal-EGFR plays a crucial role in the balance of the macrophage polarization and prostatic wound healing.

Optimization of broth recovery for repair of heat-injured Salmonella enterica serovar Typhimurium and Escherichia coli O157:H7.

AIMS: The purpose of this research was to determine optimum conditions for broth recovery of heat-injured Salmonella Typhimurium and Escherichia coli O157:H7. METHODS AND RESULTS: Exposure to 55°C for 15 and 25 min, respectively, induced cellular injury to those pathogens. Comparison was made with the commonly used overlay method using selective medium for recovering sublethally injured cells of S. Typhimurium. For E. coli O157:H7, phenol red agar base with 1% sorbitol was used. After cell suspensions were heated at 55°C for selected time intervals, microbes were 10-fold diluted with brain heart infusion (BHI), tryptic soy broth (TSB) and TSB with 0·6% yeast extract (TSBYE) and incubated at 37°C for up to 3 h. At hourly intervals, diluents were plated onto selective medium for recovery. Simultaneously, diluents were plated onto tryptic soy agar (TSA) for recovery of sublethally injured cells. For overlays, diluents were plated onto TSA and overlaid with selective agar after a resuscitation interval. Broth recovery conditions for S. Typhimurium and E. coli O157:H7 were determined to be 1 h in any of the following broth media: BHI, TSB or TSBYE. When liquid resuscitation was applied to sublethally injured cells in food samples (milk), 1 h was also sufficient time for recovery. CONCLUSIONS: The broth recovery method is a convenient alternative to conventional recovery methods. SIGNIFICANCE AND IMPACT OF THE STUDY: Cells sublethally injured by control interventions might not grow on selective medium because they have no resistance to several selective compounds. However, injured cells can recuperate and multiply under conditions sufficient for recovery. To repair and detect heat-injured cells, the overlay method is commonly used but this method has some limitations. This study confirms the effectiveness of liquid resuscitation method on recovery of injured cells. The broth recovery can replace the overlay method due to greater convenience and timesaving.

CD8+ lineage dendritic cells determine adaptive immune responses to inflammasome activation upon sterile skin injury.

The molecular links between sterile inflammation and induction of adaptive immunity have not been fully identified. Here, we examine how damage-associated molecular patterns (DAMPs), as opposed to pathogen-associated molecules (PAMPs), regulate the immune response to non-self-antigens presented at the site of a physical injury. Heat applied briefly to the skin invokes sterile inflammation, characterized by local cell death and caspase-1 activation without demonstrably disrupting skin integrity. Co-delivery of ovalbumin (OVA) with heat injury induces OVA-specific CD8+ T-cell responses, and this is dependent on caspase-1 activation and MyD88 signalling. Using Id2flox/flox-CD11cCre+ mice, we demonstrate that CD8+ lineage DCs are required to induce OVA-specific CD8+ T-cell responses following heat injury. Consistent with this observation, intradermal administration of CD8+ lineage DCs but not CD11b+ lineage DCs restores priming of CD8+ T-cell responses in Casp-1-/- mice. Thus, we conclude that a sterile injury induces CD8+ T-cell immune responses to local antigen through caspase-1 activation and requires CD8+ lineage DCs, a finding of significance for immunotherapy and for the pathogenesis of autoimmunity.

Females exposed to 24 h of sleep deprivation do not experience greater physiological strain, but do perceive heat illness symptoms more severely, during exercise-heat stress.

There is limited and inconclusive evidence surrounding the physiological and perceptual responses to heat stress while sleep deprived, especially for females. This study aimed to quantify the effect of 24 h sleep deprivation on physiological strain and perceptual markers of heat-related illness in females. Nine females completed two 30-min heat stress tests (HST) separated by 48 h in 39°C, 41% relative humidity at a metabolic heat production of 10 W · kg-1. The non-sleep deprived HST was followed by the sleep deprivation (SDHST) trial for all participants during the follicular phase of the menstrual cycle. Physiological and perceptual measures were recorded at 5 min intervals during the HSTs. On the cessation of the HSTs, heat illness symptom index (HISI) was completed. HISI scores increased after sleep deprivation by 28 ± 16 versus 20 ± 16 (P = 0.01). Peak (39.40 ± 0.35°C vs. 39.35 ± 0.33°C) and change in rectal temperature (1.91 ± 0.21 vs. 1.93 ± 0.34°C), and whole body sweat rate (1.08 ± 0.31 vs. 1.15 ± 0.36 L · h-1) did not differ (P > 0.05) between tests. No difference was observed in peak, nor rise in: heart rate, mean skin temperature, perceived exertion or thermal sensation during the HSTs. Twenty-four hours sleep deprivation increased perceptual symptoms associated with heat-related illness; however, no thermoregulatory alterations were observed.

Astragaloside-IV Protects Against Heat-induced Apoptosis by Inhibiting Excessive Activation of Mitochondrial Ca2+ Uniporter.

BACKGROUND: Heat causes airway damage during inhalation injury because of bronchial epithelial cell damage. Accumulating evidence shows that mitochondrial uniporter (MCU) is involved in cell damage. We investigated the MCU activity after heat treatment and assessed whether Astragaloside-IV (AS-IV) suppresses heat-induced apoptosis in bronchial epithelial cells by inhibiting the activation of the mitochondrial Ca2+ uniporter (MCU), mitochondrial depolarisation and reactive oxygen species (ROS) production. METHODS: The bronchial epithelial cell line 16HBE14o- was heat treated, and cell apoptosis was induced in vitro and in vivo. AS-IV was inorganically administered to Wistar rats twice a day after thermal inhalation injury, and 16HBE140- cells were treated with AS-IV after incubation at 47°C for 5 min. Protein expression was determined using Western blotting and commercial kits, apoptosis with TUNEL staining, mitochondrial channel activity by patch clamp, reactive oxygen species by MitoSOXTM fluorescence, ATP levels and enzyme activities by commercial kits as well as mitochondrial respiration and calcium by fluorescence. RESULTS: AS-IV markedly inhibited heat-induced apoptosis, as indicated by the increased expression of the pro-apoptotic genes Bak, Bik and Bmf and increased expression of the apoptosis markers Bax, cleaved parp, cleaved caspase3 and cytochrome C. We found that MCU activation promoted mitochondrial Ca2+ overload, ATP depletion, mitochondrial ROS production and cytochrome c release and rapidly induced apoptosis. However, AS-IV treatment reduced excessive MCU activation and led to resistance against mitochondrial Ca2+ overload and excessive cytochrome C release; these effects were blocked by the MCU activator spermine. AS-IV treatment elevated ATP production and decreased ROS activity. CONCLUSIONS: MCU plays crucial roles in heat-induced mitochondrial apoptosis in 16HBE140- cells, suggesting a potential target for AS-IV treatment.

Heat stress is associated with disruption of ion balance in the migratory locust, Locusta migratoria.

Thermal tolerance is important in determining the spatial and temporal distributions of insects but the mechanisms which determine upper thermal limits remain poorly understood. In terrestrial insects heat tolerance is unlikely to be limited by oxygen supply but in some arthropods, heat stress has been shown to cause haemolymph hyperkalaemia which is known to have detrimental effects on neuromuscular excitability. It is however unresolved if heat-induced hyperkalemia is the cause or the result of cellular heat injury. To address the putative role of heat-induced hyperkalemia we quantified changes in ion and water balance in haemolymph and muscle tissue of the migratory locust during exposure to two static temperatures clustered around the CTmax (48°C and 50°C). We show that heat stress caused a loss of ion balance and severe haemolymph hyperkalaemia which coincided with the onset of heat stupor. Locusts were able to maintain their haemolymph volume throughout exposure, suggesting it is unlikely that osmoregulatory failure is responsible for haemolymph hyperkalaemia. When locusts were allowed to recover from heat stupor, they recovered ion balance quickly but were still unable to function optimally after 24h. The results therefore indicate that both the haemolymph hyperkalaemia and associated depression of muscular function (heat stupor) are secondary results of cellular heat injury and that the cause of heat stupor most be sought elsewhere.

Heat injury to the inferior vena cava by bipolar tissue sealer.

BACKGROUND: Although energy devices have brought big advantages to surgery, there are few reports about disadvantages. We conducted an animal experiment to clarify the thermal effect of the bipolar tissue sealing system, Enseal™, to adjacent vessels of the inferior vena cava. METHODS: We used an experimental miniature pig for the experiment. After laparotomy and mobilization of the intestine, the inferior vena cava was exposed. We activated the device under two different conditions: In the first group, the so-called contact group (Group C), the blade of Enseal™ touched the surface of the IVC directly. In the other group, referred to as non-contact group (Group N), the blade was held about 1 mm away from the IVC. Activation time of the generator was 5, 10, and 15 s, respectively, in both groups. RESULTS: In Group C, the mean IVC surface temperature was 47.2, 57.6, and 60.4 °C for 5, 10, and 15 s, respectively. The difference between the mean temperature of 5 and 15 s is statistically significant. In Group N, no statistical significance was achieved in all time-settings. The muscular layers of the IVC wall in Group C after 10 s of activation were broken, and cell nuclei were shrunken. CONCLUSIONS: When Enseal™ is used, contact with the adjacent vessels of the IVC should be avoided at all. It could increase the risk of heat injury to the vessel wall.

Application of iodinated starch powder using an atomizer spray gun - a new and effective tool to evaluate hypohidrosis.

BACKGROUND: Hypohidrosis is defined as diminished sweating in response to an appropriate thermal or sympathetic stimulus. When encountered in a clinical setting, it necessitates an accurate documentation of its pattern and extent to prognosticate the risk of associated heat-related illnesses. This can be achieved by thermoregulatory sweat testing which includes a starch-iodine sweat test that can be administered via various methods. OBJECTIVE: To describe and evaluate the effectiveness and safety of a novel method of using an atomizer spray gun in administering the starch-iodine test. METHODS: We describe the administration of the starch-iodine test via an atomizer spray gun (Series 700 Lab Model; Mitsuba Systems, Mumbai, India). The method was utilized for the evaluation of 30 individuals who presented with symptoms of hypohidrosis. RESULTS: Application of iodinated starch powder prepared in-house with the atomizer spray gun achieved a lightweight and homogeneous coat on our patients' skin which allowed for clear visualization of the sweating pattern in areas of anhidrosis. The sharp demarcation of the pathological regions enabled the precise calculation of the affected body surface area of impaired sweating. Unlike the starch-iodine tests using the Minor and Wada methods, neither staining of the skin nor irritation was detected in this method. CONCLUSION: We report a novel method of using an atomizer spray gun to perform the starch-iodine test in a rapid, reproducible, effective, and safe manner suitable for use in the clinical evaluation of hypohidrosis.

Seasonal heat acclimatization in wildland firefighters.

The purpose of this study was to determine changes in physiological markers of heat acclimatization across a 4-month wildland fire season. Wildland firefighters (WLFF) (n=12) and non-WLFF (n=14) were assessed pre- and post-season for body mass, percent body fat, and peak VO2. Both groups completed a 60-min heat stress trial (walking at 50% of peak VO2) in a climate controlled chamber (43.3 °C, 33% RH) pre and post-fire season (May through September). During the trials, core (Tc) and skin (Tsk) temperatures, heart rate (HR), physiological strain index (PSI), and rating of perceived exertion (RPE) were measured. There were no differences pre or post-season between the WLFF and non-WLFF groups in body mass, percent body fat, or peak V.O2. During the 73 days where the WLFF were involved in direct wildland fire suppression, daily high temperature for the WLFF was higher compared to the non-WLFF, 30.6 ± 5.4 °C and 26.9 ± 6.1 °C, respectively, p<0.05. Tc was lower at post-season compared to pre-season (p<0.05) for the WLFF at 30, 45, and 60 min (pre 30, 45, and 60: 37.9 ± 0.3, 38.3 ± 0.3 and 38.5 ± 0.3 °C, respectively; post 30, 45, and 60: 37.8 ± 0.3, 38.1 ± 0.3 and 38.2 ± 0.4 °C, respectively). For WLFF, PSI was lower (p<0.05) at 15, 30, 45, and 60 min at post-season compared to pre-season (4.2 ± 0.7, 5.6 ± 0.9, 6.5 ± 0.9, and 7.1 ± 1.1 for 15, 30, 45, and 60 min pre-season, respectively; 3.6 ± 0.8, 4.9 ± 1.0, 5.7 ± 1.2, 6.3 ± 1.3 for 15, 30, 45, and 60 min post-season, respectively). For WLFF, RPE was lower during the post-season trial at 30, 45, and 60 min (pre 30, 45, and 60: 11.7 ± 1.4, 12.3 ± 1.2, and 13.5 ± 1.4, respectively; post 30, 45, and 60: 10.7 ± 1.2, 11.3 ± 1.3, and 11.9 ± 1.5, respectively), p<0.05. There were no differences between pre and post-season for the non-WLFF for Tc and PSI, but RPE was lower at 15 min during the pre-season trial. WLFFs demonstrated significant decreases in Tc, PSI, and RPE during controlled heat stress after the season. Since an age and fitness-matched control group experienced no indication of heat acclimatization, it is suggested that the long-term occupational heat exposure accrued by the WLFFs was adequate to incur heat acclimatization.

In vitro heat insulation efficacy of 5% dextrose versus 0.9% saline during radiofrequency ablation.

PURPOSE: This study compared the efficacy of heat insulation between 5% dextrose and 0.9% saline in radiofrequency ablation (RFA). Accordingly, temperature variations and maximum temperatures were assessed at identical distances and heat field distributions. METHODS: Cubes of porcine liver tissue, measuring 10 mm across, were selected to precisely align the ablation boundary with the tissue boundary. An 18-gauge electrode with a 7-mm tip was inserted into each cube (10 per group) in a stainless-steel cup containing 40 mL of 5% dextrose or 0.9% saline. Fixed ablation was performed for 3 minutes using continuous mode at 30 W, simulating the typical thermal environment during thyroid RFA. Real-time temperature measurements were recorded by sensors positioned 0, 1, 3, and 5 mm from the cube's edge. A comparative analysis was conducted to assess the maximum temperature, temperature variation, and duration of temperatures exceeding 42℃. RESULTS: In both groups, the temperature curve declined with increasing distance from the edge of the ablated tissue. However, 0.9% saline exhibited higher maximum temperatures at 1, 3, and 5 mm compared to 5% dextrose (1 mm: 44.55°C±5.25°C vs. 34.68°C±3.07°C; 3 mm: 39.64°C±2.53°C vs. 29.22°C±2.21°C; 5 mm: 38.86°C±2.14°C vs. 28.74°C±2.51°C; all P<0.001). Considering a nerve injury threshold of 42°C, the 0.9% saline also displayed a greater proportion of samples reaching this temperature and a longer duration of temperatures exceeding it (P<0.05). CONCLUSION: The heat insulation efficacy of 5% dextrose at 1-5 mm exceeds that of 0.9% saline at identical distances and in a common thermal environment during thyroid RFA.

[Retracted] Downregulation of let­7b promotes COL1A1 and COL1A2 expression in dermis and skin fibroblasts during heat wound repair.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the western blotting data shown in Figs. 4B and 5 and the H&E immunostaining data shown in Fig 1A were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time.  Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 2683-2688, 2016; DOI: 10.3892/mmr.2016.4877].

Exertional hyponatremia among active component members of the U.S. Armed Forces, 2008-2023.

Exertional hyponatremia, or exercise-associated hyponatremia, occurs within 24 hours after physical activity due to a serum, plasma, or blood sodium concentration (Na+) below the normal reference range of 135 mEq/L. If not detected early and managed properly, hyponatremia can be fatal. From 2008 to 2023, 1,812 cases of exertional hyponatremia were diagnosed among U.S. active component service members (ACSMs), with an overall incidence rate of 8.3 cases per 100,000 person-years (p-yrs). In 2023 there were 153 cases of exertional hyponatremia diagnosed among ACSMs, resulting in a crude incidence rate of 11.7 per 100,000 p-yrs. Female service members, those older than 40, non-Hispanic Black service members, Marine Corps members, recruits, those in combat-specific occupations, and ACSMs stationed in the Northeast U.S. region had higher incidence rates of exertional hyponatremia diagnoses than their respective counterparts. During the surveillance period, annual rates of incident exertional hyponatremia diagnoses peaked in 2010 (12.8 per 100,000 p-yrs) and then decreased to a low of 5.3 cases per 100,000 p-yrs in 2013. Thereafter the incidence rate fluctuated but has increased from 6.2 per 100,000 p-yrs in 2017 to its second-highest level in 2023. Service members and their supervisors should be aware of the dangers of excessive fluid consumption and prescribed limits for consumption during prolonged physical activity including field training exercises, personal fitness training, or recreational activities, particularly in hot, humid weather.

Exertional rhabdomyolysis among active component members of the U.S. Armed Forces, 2019-2023.

A largely preventable condition, exertional rhabdomyolysis persists as an occupational hazard of military training and operations, especially in high heat environments among individuals exerting themselves to their physical endurance limits. During the 5-year surveillance period of this study, unadjusted incidence rates of exertional rhabdomyolysis per 100,000 person-years among U.S. active component service members fluctuated, reaching a low of 38.0 cases in 2020 and peaking at 40.5 cases in 2023. The rate in 2020 constituted a decline of 3.8% from the rate in 2019 (39.5 cases). Beginning in 2020, incidence rates per 100,000 person-years gradually increased, by 1.8% in 2021 (38.7 cases), 5.3% in 2022 (40.0 cases), and 6.6% in 2023 (40.5 cases). Consistent with prior reports, subgroup-specific crude rates in 2023 were highest among men, those less than 20 years old, non-Hispanic Black service members, Marine Corps or Army members, and those in combat-specific and 'other' occupations. Recruits experienced the highest rates of exertional rhabdomyolysis during each year, with incidence rates 6 to 10 times greater than all other service members.

Therapeutic effect of mitochondrial transplantation on burn injury.

As mitochondrial damage or dysfunction is commonly observed following burn injuries, we investigated whether mitochondrial transplantation (MT) can result in therapeutic benefits in the treatment of burns. Human immortalized epidermal cells (HaCaT) and Kunming mice were used to establish a heat-injured cell model and a deep partial-thickness skin burn animal model, respectively. The cell model was established by exposing HaCaT cells to 45 or 50 °C for 10 min, after which cell proliferation was assayed using fluorescent double-staining and colony formation assays, cell migration was assessed using colloidal gold migration and scratch assays, and cell cycle progression and apoptosis were measured by flow cytometry. Histopathological staining, immunohistochemistry, nick-end labeling analysis, and enzyme-linked immunosorbent assays were used to evaluate the effects of MT on inflammation, tissue recovery, apoptosis, and scar growth in a mouse model. The therapeutic effects were observed in the heat-injured HaCaT cell model. MT promoted cell viability, colony formation, proliferation, and migration; decreased G1 phase; promoted cell division; and decreased apoptosis. Wound-healing promotion, anti-inflammation (decreased mast cell aggregation, down-regulated of TNF-α, IL-1ß, IL-6, and up-regulated IL-10), acceleration of proliferation recovery (up-regulated CD34 and VEGF), apoptosis reduction, and scar formation reduction (decreased collagen I/III ratio and TGF-ß1) were observed in the MT mouse model. The MT mode of action was, however, not investigated in this study. In conclusion, our data indicate that MT exerts a therapeutic effect on burn injuries both in vitro and in vivo.

Heat exhaustion and heat stroke among active component members of the U.S. Armed Forces, 2019-2023.

The most serious types of heat illnesses, heat exhaustion and heat stroke, are occupational hazards associated with many of the military's training and operational environments. These illnesses can typically be prevented by appropriate situational awareness, risk management strategies, along with effective countermeasures. In 2023, the crude incidence of heat stroke and heat exhaustion were 31.7 and 172.7 cases per 100,000 person-years, respectively. The rates of incident heat stroke declined during the 2019 to 2023 surveillance period, but rates of incident heat exhaustion increased over the same period. In 2023, higher rates of heat stroke were observed among male service members compared to their female counterparts, and female service members experienced higher rates of heat exhaustion compared to male personnel. Heat illness rates were also higher among those younger than age 20, Marine Corps and Army service members, non-Hispanic Black service members, and recruits. Leaders, training cadres, and supporting medical and safety personnel must inform their subordinate and supported service members of heat illness risks, preventive measures, early signs and symptoms of illness, and appropriate interventions.