Increased heat risk in wet climate induced by urban humid heat.

Cities are generally warmer than their adjacent rural land, a phenomenon known as the urban heat island (UHI). Often accompanying the UHI effect is another phenomenon called the urban dry island (UDI), whereby the humidity of urban land is lower than that of the surrounding rural land1-3. The UHI exacerbates heat stress on urban residents4,5, whereas the UDI may instead provide relief because the human body can cope with hot conditions better at lower humidity through perspiration6,7. The relative balance between the UHI and the UDI-as measured by changes in the wet-bulb temperature (Tw)-is a key yet largely unknown determinant of human heat stress in urban climates. Here we show that Tw is reduced in cities in dry and moderately wet climates, where the UDI more than offsets the UHI, but increased in wet climates (summer precipitation of more than 570 millimetres). Our results arise from analysis of urban and rural weather station data across the world and calculations with an urban climate model. In wet climates, the urban daytime Tw is 0.17 ± 0.14 degrees Celsius (mean ± 1 standard deviation) higher than rural Tw in the summer, primarily because of a weaker dynamic mixing in urban air. This Tw increment is small, but because of the high background Tw in wet climates, it is enough to cause two to six extra dangerous heat-stress days per summer for urban residents under current climate conditions. The risk of extreme humid heat is projected to increase in the future, and these urban effects may further amplify the risk.

Proteome plasticity in response to persistent environmental change.

Temperature is a variable component of the environment, and all organisms must deal with or adapt to temperature change. Acute temperature change activates cellular stress responses, resulting in refolding or removal of damaged proteins. However, how organisms adapt to long-term temperature change remains largely unexplored. Here we report that budding yeast responds to long-term high temperature challenge by switching from chaperone induction to reduction of temperature-sensitive proteins and re-localizing a portion of its proteome. Surprisingly, we also find that many proteins adopt an alternative conformation. Using Fet3p as an example, we find that the temperature-dependent conformational difference is accompanied by distinct thermostability, subcellular localization, and, importantly, cellular functions. We postulate that, in addition to the known mechanisms of adaptation, conformational plasticity allows some polypeptides to acquire new biophysical properties and functions when environmental change endures.

Extreme escalation of heat failure rates in ectotherms with global warming.

Temperature affects the rate of all biochemical processes in ectotherms1,2 and is therefore critical for determining their current and future distribution under global climate change3-5. Here we show that the rate of biological processes maintaining growth, homeostasis and ageing in the permissive temperature range increases by 7% per degree Celsius (median activation energy Ea = 0.48 eV from 1,351 rates across 314 species). By contrast, the processes underlying heat failure rate within the stressful temperature range are extremely temperature sensitive, such that heat failure increases by more than 100% per degree Celsius across a broad range of taxa (median Ea = 6.13 eV from 123 rates across 112 species). The extreme thermal sensitivity of heat failure rates implies that the projected increase in the frequency and intensity of heatwaves can exacerbate heat mortality for many ectothermic species with severe and disproportionate consequences. Combining the extreme thermal sensitivities with projected increases in maximum temperatures globally6, we predict that moderate warming scenarios can increase heat failure rates by 774% (terrestrial) and 180% (aquatic) by 2100. This finding suggests that we are likely to underestimate the potential impact of even a modest global warming scenario.

Heat and Cardiovascular Mortality: An Epidemiological Perspective.

As global temperatures rise, extreme heat events are projected to become more frequent and intense. Extreme heat causes a wide range of health effects, including an overall increase in morbidity and mortality. It is important to note that while there is sufficient epidemiological evidence for heat-related increases in all-cause mortality, evidence on the association between heat and cause-specific deaths such as cardiovascular disease (CVD) mortality (and its more specific causes) is limited, with inconsistent findings. Existing systematic reviews and meta-analyses of epidemiological studies on heat and CVD mortality have summarized the available evidence. However, the target audience of such reviews is mainly limited to the specific field of environmental epidemiology. This overarching perspective aims to provide health professionals with a comprehensive overview of recent epidemiological evidence of how extreme heat is associated with CVD mortality. The rationale behind this broad perspective is that a better understanding of the effect of extreme heat on CVD mortality will help CVD health professionals optimize their plans to adapt to the changes brought about by climate change and heat events. To policymakers, this perspective would help formulate targeted mitigation, strengthen early warning systems, and develop better adaptation strategies. Despite the heterogeneity in evidence worldwide, due in part to different climatic conditions and population dynamics, there is a clear link between heat and CVD mortality. The risk has often been found to be higher in vulnerable subgroups, including older people, people with preexisting conditions, and the socioeconomically deprived. This perspective also highlights the lack of evidence from low- and middle-income countries and focuses on cause-specific CVD deaths. In addition, the perspective highlights the temporal changes in heat-related CVD deaths as well as the interactive effect of heat with other environmental factors and the potential biological pathways. Importantly, these various aspects of epidemiological studies have never been fully investigated and, therefore, the true extent of the impact of heat on CVD deaths remains largely unknown. Furthermore, this perspective also highlights the research gaps in epidemiological studies and the potential solutions to generate more robust evidence on the future consequences of heat on CVD deaths.

Global warming impairs stock-recruitment dynamics of corals.

Changes in disturbance regimes due to climate change are increasingly challenging the capacity of ecosystems to absorb recurrent shocks and reassemble afterwards, escalating the risk of widespread ecological collapse of current ecosystems and the emergence of novel assemblages1-3. In marine systems, the production of larvae and recruitment of functionally important species are fundamental processes for rebuilding depleted adult populations, maintaining resilience and avoiding regime shifts in the face of rising environmental pressures4,5. Here we document a regional-scale shift in stock-recruitment relationships of corals along the Great Barrier Reef-the world's largest coral reef system-following unprecedented back-to-back mass bleaching events caused by global warming. As a consequence of mass mortality of adult brood stock in 2016 and 2017 owing to heat stress6, the amount of larval recruitment declined in 2018 by 89% compared to historical levels. For the first time, brooding pocilloporids replaced spawning acroporids as the dominant taxon in the depleted recruitment pool. The collapse in stock-recruitment relationships indicates that the low resistance of adult brood stocks to repeated episodes of coral bleaching is inexorably tied to an impaired capacity for recovery, which highlights the multifaceted processes that underlie the global decline of coral reefs. The extent to which the Great Barrier Reef will be able to recover from the collapse in stock-recruitment relationships remains uncertain, given the projected increased frequency of extreme climate events over the next two decades7.

The Effect of Heat Exposure on Myocardial Blood Flow and Cardiovascular Function.

BACKGROUND: Heat extremes are associated with greater risk for cardiovascular death. The pathophysiologic mechanisms mediating this association are unknown. OBJECTIVE: To quantify the myocardial blood flow (MBF) requirements of heat exposure. DESIGN: Experimental study. (ClinicalTrials.gov: NCT04549974). SETTING: Laboratory-based. PARTICIPANTS: 61 participants, comprising 20 healthy young adults (mean age, 28 years), 21 healthy older adults (mean age, 67 years), and 20 older adults with coronary artery disease (CAD) (mean age, 70 years). INTERVENTION: Participants were heated until their core temperature increased 1.5 °C; MBF was measured before heat exposure and at every increase of 0.5 °C in core temperature. MEASUREMENTS: The primary outcome was MBF measured by positron emission tomography-computed tomography. Secondary outcomes included heart rate, blood pressure, and body weight change. RESULTS: At a core temperature increase of 1.5 °C, MBF increased in healthy young adults (change, 0.8 mL/min/g [95% CI, 0.5 to 1.0 mL/min/g]), healthy older adults (change, 0.7 mL/min/g [CI, 0.5 to 0.9 mL/min/g]), and older adults with CAD (change, 0.6 mL/min/g [CI, 0.3 to 0.8 mL/min/g]). This represented a 2.08-fold (CI, 1.75- to 2.41-fold), 1.79-fold (CI, 1.59- to 1.98-fold), and 1.64-fold (CI, 1.41- to 1.87-fold) change, respectively, from preexposure values. Imaging evidence of asymptomatic heat-induced myocardial ischemia was seen in 7 adults with CAD (35%) in post hoc analyses. LIMITATIONS: In this laboratory-based study, heating was limited to about 100 minutes and participants were restricted in movement and fluid intake. Participants refrained from strenuous exercise and smoking; stopped alcohol and caffeine intake; and withheld ß-blockers, calcium-channel blockers, and nitroglycerin before heating. CONCLUSION: Heat exposure that increases core temperature by 1.5 °C nearly doubles MBF. Changes in MBF did not differ by age or presence of CAD, but some older adults with CAD may experience asymptomatic myocardial ischemia. PRIMARY FUNDING SOURCE: Canadian Institutes of Health Research.

Nocturnal heat exposure and stroke risk.

BACKGROUND AND AIMS: In recent decades, nighttime temperatures have increased faster than daytime temperatures. The increasing prevalence of nocturnal heat exposure may pose a significant risk to cardiovascular health. This study investigated the association between nighttime heat exposure and stroke risk in the region of Augsburg, Germany, and examined its temporal variations over 15 years. METHODS: Hourly meteorological parameters, including mean temperature, relative humidity, and barometric pressure, were acquired from a local meteorological station. A data set was obtained consisting of 11 037 clinical stroke cases diagnosed during warmer months (May to October) between the years 2006 and 2020. The average age of cases was 71.3 years. Among these cases, 642 were identified as haemorrhagic strokes, 7430 were classified as ischaemic strokes, and 2947 were transient ischaemic attacks. A time-stratified case-crossover analysis with a distributed lag non-linear model was used to estimate the stroke risk associated with extreme nighttime heat, as measured by the hot night excess (HNE) index after controlling for the potential confounding effects of daily maximum temperature and other climatic variables. Subgroup analyses by age group, sex, stroke subtype, and stroke severity were performed to identify variations in susceptibility to nighttime heat. RESULTS: Results suggested a significant increase in stroke risk on days with extreme nighttime heat (97.5% percentile of HNE) (odds ratio 1.07, 95% confidence interval 1.01-1.15) during the full study period. When comparing the results for 2013-20 with the results for 2006-12, there was a significant increase (P < .05) in HNE-related risk for all strokes and specifically for ischaemic strokes during the more recent period. Furthermore, older individuals, females, and patients with mild stroke symptoms exhibited a significantly increased vulnerability to nighttime heat. CONCLUSIONS: This study found nocturnal heat exposure to be related to elevated stroke risk after controlling for maximum daytime temperature, with increasing susceptibility between 2006 and 2020. These results underscore the importance of considering nocturnal heat as a critical trigger of stroke events in a warming climate.

Extreme Temperatures and Stroke Mortality: Evidence From a Multi-Country Analysis.

BACKGROUND: Extreme temperatures contribute significantly to global mortality. While previous studies on temperature and stroke-specific outcomes presented conflicting results, these studies were predominantly limited to single-city or single-country analyses. Their findings are difficult to synthesize due to variations in methodologies and exposure definitions. METHODS: Within the Multi-Country Multi-City Network, we built a new mortality database for ischemic and hemorrhagic stroke. Applying a unified analysis protocol, we conducted a multinational case-crossover study on the relationship between extreme temperatures and stroke. In the first stage, we fitted a conditional quasi-Poisson regression for daily mortality counts with distributed lag nonlinear models for temperature exposure separately for each city. In the second stage, the cumulative risk from each city was pooled using mixed-effect meta-analyses, accounting for clustering of cities with similar features. We compared temperature-stroke associations across country-level gross domestic product per capita. We computed excess deaths in each city that are attributable to the 2.5% hottest and coldest of days based on each city's temperature distribution. RESULTS: We collected data for a total of 3 443 969 ischemic strokes and 2 454 267 hemorrhagic stroke deaths from 522 cities in 25 countries. For every 1000 ischemic stroke deaths, we found that extreme cold and hot days contributed 9.1 (95% empirical CI, 8.6-9.4) and 2.2 (95% empirical CI, 1.9-2.4) excess deaths, respectively. For every 1000 hemorrhagic stroke deaths, extreme cold and hot days contributed 11.2 (95% empirical CI, 10.9-11.4) and 0.7 (95% empirical CI, 0.5-0.8) excess deaths, respectively. We found that countries with low gross domestic product per capita were at higher risk of heat-related hemorrhagic stroke mortality than countries with high gross domestic product per capita (P=0.02). CONCLUSIONS: Both extreme cold and hot temperatures are associated with an increased risk of dying from ischemic and hemorrhagic strokes. As climate change continues to exacerbate these extreme temperatures, interventional strategies are needed to mitigate impacts on stroke mortality, particularly in low-income countries.

Global, regional, and national burden of heatwave-related mortality from 1990 to 2019: A three-stage modelling study.

BACKGROUND: The regional disparity of heatwave-related mortality over a long period has not been sufficiently assessed across the globe, impeding the localisation of adaptation planning and risk management towards climate change. We quantified the global mortality burden associated with heatwaves at a spatial resolution of 0.5°×0.5° and the temporal change from 1990 to 2019. METHODS AND FINDINGS: We collected data on daily deaths and temperature from 750 locations of 43 countries or regions, and 5 meta-predictors in 0.5°×0.5° resolution across the world. Heatwaves were defined as location-specific daily mean temperature ≥95th percentiles of year-round temperature range with duration ≥2 days. We first estimated the location-specific heatwave-mortality association. Secondly, a multivariate meta-regression was fitted between location-specific associations and 5 meta-predictors, which was in the third stage used with grid cell-specific meta-predictors to predict grid cell-specific association. Heatwave-related excess deaths were calculated for each grid and aggregated. During 1990 to 2019, 0.94% (95% CI: 0.68-1.19) of deaths [i.e., 153,078 cases (95% eCI: 109,950-194,227)] per warm season were estimated to be from heatwaves, accounting for 236 (95% eCI: 170-300) deaths per 10 million residents. The ratio between heatwave-related excess deaths and all premature deaths per warm season remained relatively unchanged over the 30 years, while the number of heatwave-related excess deaths per 10 million residents per warm season declined by 7.2% per decade in comparison to the 30-year average. Locations with the highest heatwave-related death ratio and rate were in Southern and Eastern Europe or areas had polar and alpine climates, and/or their residents had high incomes. The temporal change of heatwave-related mortality burden showed geographic disparities, such that locations with tropical climate or low incomes were observed with the greatest decline. The main limitation of this study was the lack of data from certain regions, e.g., Arabian Peninsula and South Asia. CONCLUSIONS: Heatwaves were associated with substantial mortality burden that varied spatiotemporally over the globe in the past 30 years. The findings indicate the potential benefit of governmental actions to enhance health sector adaptation and resilience, accounting for inequalities across communities.

Application of the thermal death time model in predicting thermal damage accumulation in plants.

The thermal death time (TDT) model suggests that the duration for which an organism can tolerate thermal stress decreases exponentially as the intensity of the temperature becomes more extreme. This model has been used to predict damage accumulation in ectothermic animals and plants under fluctuating thermal conditions. However, the critical assumption of the TDT model, which is additive damage accumulation, remains unverified for plants. We assessed thermal damage in Thymus vulgaris under different heat and cold treatments, and used TDT models to predict time to thermal failure of PSII. Additionally, thermal tolerance estimates from previous studies were used to create TDT models to assess the applicability of this framework in plants. We show that thermal damage is additive between 44 °C and 47 °C and between -6.5 °C and -8 °C, and that the TDT model can predict damage accumulation at both temperature extremes. Data from previous studies indicate a broad applicability of this approach across plant species and traits. The TDT framework reveals a thermal tolerance landscape describing the relationship between exposure duration, stress intensity, and percentage damage accumulation. The extreme thermal sensitivity of plants emphasizes that even a 1 °C increase in future extreme temperatures could impact their mortality and distribution.

Timing determines zooplankton community responses to multiple stressors.

Human activities and climate change cause abiotic factors to fluctuate through time, sometimes passing thresholds for organismal reproduction and survival. Multiple stressors can independently or interactively impact organisms; however, few studies have examined how they interact when they overlap spatially but occur asynchronously. Fluctuations in salinity have been found in freshwater habitats worldwide. Meanwhile, heatwaves have become more frequent and extreme. High salinity pulses and heatwaves are often decoupled in time but can still collectively impact freshwater zooplankton. The time intervals between them, during which population growth and community recovery could happen, can influence combined effects, but no one has examined these effects. We conducted a mesocosm experiment to examine how different recovery times (0-, 3-, 6-week) between salt treatment and heatwave exposure influence their combined effects. We hypothesized that antagonistic effects would appear when having short recovery time, because previous study found that similar species were affected by the two stressors, but effects would become additive with longer recovery time since fully recovered communities would respond to heatwave similar to undisturbed communities. Our findings showed that, when combined, the two-stressor joint impacts changed from antagonistic to additive with increased recovery time between stressors. Surprisingly, full compositional recovery was not achieved despite a recovery period that was long enough for population growth, suggesting legacy effects from earlier treatment. The recovery was mainly driven by small organisms, such as rotifers and small cladocerans. As a result, communities recovering from previous salt exposure responded differently to heatwaves than undisturbed communities, leading to similar zooplankton communities regardless of the recovery time between stressors. Our research bolsters the understanding and management of multiple-stressor issues by revealing that prior exposure to one stressor has long-lasting impacts on community recovery that can lead to unexpected joint effects of multiple stressors.

Large potential impacts of marine heatwaves on ecosystem functioning.

Ocean warming is driving significant changes in the structure and functioning of marine ecosystems, shifting species' biogeography and phenology, changing body size and biomass and altering the trophodynamics of the system. Particularly, extreme temperature events such as marine heatwaves (MHWs) have been increasing in intensity, duration and frequency. MHWs are causing large-scale impacts on marine ecosystems, such as coral bleaching, mass mortality of seagrass meadows and declines in fish stocks and other marine organisms in recent decades. In this study, we developed and applied a dynamic version of the EcoTroph trophodynamic modelling approach to study the cascading effects of individual MHW on marine ecosystem functioning. We simulated theoretical user-controlled ecosystems and explored the consequences of various assumptions of marine species mortality along the food web, associated with different MHW intensities. We show that an MHW can lead to a significant biomass reduction of all consumers, with the severity of the declines being dependent on species trophic levels (TLs) and biomes, in addition to the characteristics of MHWs. Biomass of higher TLs declines more than lower TLs under an MHW, leading to changes in ecosystem structure. While tropical ecosystems are projected to be sensitive to low-intensity MHWs, polar and temperate ecosystems are expected to be impacted by more intense MHWs. The estimated time to recover from MHW impacts is twice as long for polar ecosystems and one-third longer for temperate biomes compared with tropical biomes. This study highlights the importance of considering extreme weather events in assessing the effects of climate change on the structures and functions of marine ecosystems.

Hot and scared: how do heatwaves and predation risk impact resource acquisition and allocation?

Heatwaves are increasingly prevalent and can constrain investment into important life-history traits. In addition to heatwaves, animals regularly encounter threats from other organisms in their environments, such as predators. The combination of these two environmental factors introduces a decision-making conflict-heat exposure requires more food intake to fuel investment into fitness-related traits, but foraging in the presence of predators increases the threat of mortality. Thus, we used female variable field crickets (Gryllus lineaticeps) to investigate the effects of heatwaves in conjunction with predation risk (exposed food and water sources, and exposure to scent from black widow spiders, Latrodectus hesperus) on resource acquisition (food intake) and allocation (investment into ovarian and somatic tissues). A simulated heatwave increased food intake and the allocation of resources to reproductive investment. Crickets exposed to high predation risk reduced food intake, but they were able to maintain reproductive investment at an expense to investment into somatic tissue. Thus, heatwaves and predation risk deprioritized investment into self-maintenance, which may impair key physiological processes. This study is an important step towards understanding the ecology of fear in a warming world.

The combination of high temperature and Vibrio infection worsens summer mortality in the clam Meretrix petechialis by increasing apoptosis and oxidative stress.

The interaction between environmental factors and Vibrio in bivalves is not well understood, despite the widely held belief that pathogen infection and seawater temperature significantly impact summer mortality. In the present study, we conducted simulated experiments to explore the effects of high temperature and Vibrio infection on the clam Meretrix petechialis. The survival curve analysis revealed that the combined challenge of high temperature and Vibrio infection (31°C-vibrio) led to significantly higher clam mortality compared to the groups exposed solely to Vibrio (27°C-vibrio), high temperature (31°C-control), and the control condition (27°C-control). Furthermore, PCoA analysis of 11 immune genes indicated that Vibrio infection predominated during the incubation period, with a gradual equilibrium between these factors emerging during the course of the infection. Additionally, our investigations into apoptosis and autophagy processes exhibited significant induction of mTOR and Bcl2 of the 31°C-vibrio group in the early challenge stage, followed by inhibition in the later stage. Oxidative stress analysis demonstrated a substantial additive effect on malondialdehyde (MDA) and glutathione (GSH) content in the combined challenge group compared to the control group. Comparative transcriptome analysis revealed a significant increase in differentially expressed genes related to immunity, such as complement C1q-like protein, C-type lectin, big defensin, and lysozyme, in the 31°C-vibrio group, suggesting that the synergistic effect of high temperature and Vibrio infection triggers more robust antibacterial immune responses. These findings provide critical insights for understanding the infection process and uncovering the causes of summer mortality.

Protective effects of butyric acid during heat stress on the survival, immune response, histopathology, and gene expression in the hepatopancreas of juvenile pacific shrimp (L. Vannamei).

This study looked at the effects of adding butyric acid (BA) to the diets of juvenile Pacific shrimp and how it affected their response to survival, immunity, histopathological, and gene expression profiles under heat stress. The shrimp were divided into groups: a control group with no BA supplementation and groups with BA inclusion levels of 0.5 %, 1 %, 1.5 %, 2 %, and 2.5 %. Following the 8-week feeding trial period, the shrimp endured a heat stress test lasting 1 h at a temperature of 38 °C. The results showed that the control group had a lower survival rate than those given BA. Interestingly, no mortality was observed in the group receiving 1.5 % BA supplementation. Heat stress had a negative impact on the activities of alkaline phosphatase (AKP) and acid phosphatase (ACP) in the control group. Still, these activities were increased in shrimp fed the BA diet. Similar variations were observed in AST and ALT fluctuations among the different groups. The levels of triglycerides (TG) and cholesterol (CHO) increased with high temperatures but were reduced in shrimp-supplemented BA. The activity of an antioxidant enzyme superoxide dismutase (SOD) increased with higher BA levels (P < 0.05). Moreover, the groups supplemented with 1.5 % BA exhibited a significant reduction in malondialdehyde (MDA) content (P < 0.05), suggesting the potential antioxidant properties of BA. The histology of the shrimp's hepatopancreas showed improvements in the groups given BA. Conversely, the BA significantly down-regulated the HSPs and up-regulated MnSOD transcript level in response to heat stress. The measured parameters determine the essential dietary requirement of BA for shrimp. Based on the results, the optimal level of BA for survival, antioxidant function, and immunity for shrimp under heat stress is 1.5 %.

Global warming transforms coral reef assemblages.

Global warming is rapidly emerging as a universal threat to ecological integrity and function, highlighting the urgent need for a better understanding of the impact of heat exposure on the resilience of ecosystems and the people who depend on them 1 . Here we show that in the aftermath of the record-breaking marine heatwave on the Great Barrier Reef in 2016 2 , corals began to die immediately on reefs where the accumulated heat exposure exceeded a critical threshold of degree heating weeks, which was 3-4 °C-weeks. After eight months, an exposure of 6 °C-weeks or more drove an unprecedented, regional-scale shift in the composition of coral assemblages, reflecting markedly divergent responses to heat stress by different taxa. Fast-growing staghorn and tabular corals suffered a catastrophic die-off, transforming the three-dimensionality and ecological functioning of 29% of the 3,863 reefs comprising the world's largest coral reef system. Our study bridges the gap between the theory and practice of assessing the risk of ecosystem collapse, under the emerging framework for the International Union for Conservation of Nature (IUCN) Red List of Ecosystems 3 , by rigorously defining both the initial and collapsed states, identifying the major driver of change, and establishing quantitative collapse thresholds. The increasing prevalence of post-bleaching mass mortality of corals represents a radical shift in the disturbance regimes of tropical reefs, both adding to and far exceeding the influence of recurrent cyclones and other local pulse events, presenting a fundamental challenge to the long-term future of these iconic ecosystems.

A TRP channel trio mediates acute noxious heat sensing.

Acute pain represents a crucial alarm signal to protect us from injury. Whereas the nociceptive neurons that convey pain signals were described more than a century ago, the molecular sensors that detect noxious thermal or mechanical insults have yet to be fully identified. Here we show that acute noxious heat sensing in mice depends on a triad of transient receptor potential (TRP) ion channels: TRPM3, TRPV1, and TRPA1. We found that robust somatosensory heat responsiveness at the cellular and behavioural levels is observed only if at least one of these TRP channels is functional. However, combined genetic or pharmacological elimination of all three channels largely and selectively prevents heat responses in both isolated sensory neurons and rapidly firing C and Aδ sensory nerve fibres that innervate the skin. Strikingly, Trpv1-/-Trpm3-/-Trpa1-/- triple knockout (TKO) mice lack the acute withdrawal response to noxious heat that is necessary to avoid burn injury, while showing normal nociceptive responses to cold or mechanical stimuli and a preserved preference for moderate temperatures. These findings indicate that the initiation of the acute heat-evoked pain response in sensory nerve endings relies on three functionally redundant TRP channels, representing a fault-tolerant mechanism to avoid burn injury.

Adherence with statins and all-cause mortality in days with high temperature.

PURPOSE: It has been suggested that statins may exert thermo-protective effects that can reduce mortality on hot days. We aimed to examine the relationship between statin adherence and mortality in days with high temperature. METHODS: Utilizing data from a prior historical new-user cohort study, we analyzed a cohort of 229 918 individuals within a state-mandated health provider in Israel who initiated statin therapy between 1998 and 2006. Adherence to statins was assessed through the mean proportion of days covered (PDC) with statins during the follow-up period. The study's primary outcome was all-cause mortality during hot days. RESULTS: During the study follow-up period, a total of 13 165 individuals (5.7%) died. In a multivariable model, a 10% increase in PDC with statins was associated with an HR of (0.85; 95% CI: 0.72-1.00) for deaths (n = 16) in extremely hot days (≥39°C). This association was numerically stronger compared to HR = 0.94 (0.93-0.94) in cooler days and displayed a significant difference between sexes. In males, the fully-adjusted HR for a 10% increase in PDC with statins was 0.66 (0.45-0.95), while in women, it was 0.98 (0.78-1.23). In contrast, no such effect modification was observed for death in cooler days. CONCLUSIONS: These findings align with earlier research, supporting the notion that adherence with statin treatment may be associated with a reduced risk of death during extremely hot days, particularly among men.

Human adaptation to heat in the context of climate change: A conceptual framework.

Climate change is causing serious damage to natural and social systems, as well as having an impact on human health. Among the direct effects of climate change is the rise in global surface temperatures and the increase in the frequency, duration, intensity and severity of heat waves. In addition, understanding of the adaptation process of the exposed population remains limited, posing a challenge in accurately estimating heat-related morbidity and mortality. In this context, this study seeks to establish a conceptual framework that would make it easier to understand and organise knowledge about human adaptation to heat and the factors that may influence this process. An inductive approach based on grounded theory was used, through the analysis of case studies connecting concepts. The proposed conceptual framework is made up of five components (climate change, vulnerability, health risks of heat, axes of inequality and health outcomes), three heat-adaptation domains (physiological, cultural and political), two levels (individual and social), and the pre-existing before a heat event. The application of this conceptual framework facilitates the assistance of decision-makers in planning and implementing effective adaptation measures. Recognizing the importance of addressing heat adaptation as a health problem that calls for political solutions and social changes. Accordingly, this requires a multidisciplinary approach that would foster the participation and collaboration of multiple actors for the purpose of proposing effective measures to address the health impact of the rise in temperature.