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The hypothalamic-pituitary-adrenal (HPA) axis is a key adaptive neuroendocrine system, dysfunction of which plays an important role in the increasing incidence of stress-dependent age-related pathology. Among the environmental factors effecting increase age-related diseases, great importance is given to disturbances of the light-dark schedule, particularly with increased illumination at night. While disruption of the light-dark schedule has long been recognized as a powerful behavioral stressor, little is known regarding stress reactivity of the HPA under constant light (CL) conditions, especially with aging and depending on the features of stress behavior. The purpose of this investigation was to study the age-related and individual features of the HPA axis response to acute stress exposure (ASE) under chronic CL in nonhuman primates that are known to differ in behavioral responsiveness to stress. Young and old female rhesus monkeys (with control standard behavior or anxiety and depression-like behavior) were exposed to CL (24 h light/day, 330-400 lux for 4 to 8 weeks). Control young and old monkeys were exposed to standard lighting (SL) with natural light during the day and darkness at night. All animals were subjected to ASE (restriction of mobility for 2 hours), functional tests with corticotrophin-releasing hormone and arginine-vasopressin, and study of circadian rhythms of cortisol and pineal melatonin secretion. For the first time an inhibitory effect of CL on the reaction of the adrenal cortex to ASE was revealed in all individuals, regardless of age and preexisting behavior stress reactivity, the mechanisms of which were age-dependent: due to inhibition of the pituitary ACTH secretion in young animals and mainly not affecting the ACTH secretion in old individuals. There were no significant changes in melatonin secretion both in young and old animals. The observed CL inhibition of adrenal cortical reactivity to ASE may be useful to correct increased vulnerability to ASE observed in individuals with preexisting anxiety and depression-like stress behaviors. On the other hand, the CL induced decrease in adrenal stress reactivity of behaviorally normal animals suggests a potential risk of reducing the adaptive capacity of the organism under conditions of continuous light exposure.

EDITORIAL article Front. Endocrinol., 02 June 2023Sec. Adrenal Endocrinology Volume 14 - 2023 | https://doi.org/10.3389/fendo.2023.1222033

Since the 2003 heatwave in Europe, evidence has been rapidly increasing on the association between extreme temperature and all-cause mortality. Little is known, however, about cause-specific cardiovascular mortality, effect modification by air pollution and aircraft noise, and which population groups are the most vulnerable to extreme temperature. We conducted a time-stratified case-crossover study in Zurich, Switzerland, including all adult cardiovascular deaths between 2000 and 2015 with precise individual exposure estimates at home location. We estimated the risk of 24,884 cardiovascular deaths associated with heat and cold using distributed non-linear lag models. We investigated potential effect modification of temperature-related mortality by fine particles, nitrogen dioxide, and night-time aircraft noise and performed stratified analyses across individual and social characteristics. We found increased risk of mortality for heat (odds ratio OR = 1.28 [95% confidence interval: 1.11–1.49] for 99th percentile of daily Tmean (24 °C) versus optimum temperature at 20 °C) and cold (OR = 1.15 [0.95–1.39], 5th percentile of daily Tmean (−3 °C) versus optimum temperature at 20 °C). Heat-related mortality was particularly strong for myocardial infarctions and hypertension related deaths, and among older women (>75 years). Analysis of effect modification also indicated that older women with lower socio-economic position and education are at higher risk for heat-related mortality. PM2.5 increased the risk of heat-related mortality for heart failure, but not all-cause cardiovascular mortality. This study provides useful information for preventing cause-specific cardiovascular temperature-related mortality in moderate climate zones comparable to Switzerland.

Tuberculosis (TB) has been responsible for the greatest number of human deaths due to an infectious disease in general, and due to antimicrobial resistance (AMR) in particular. The etiological agents of human TB are a closely-related group of human-adapted bacteria that belong to the Mycobacterium tuberculosis complex (MTBC). Understanding how MTBC populations evolve within-host may allow for improved TB treatment and control strategies. In this review, we highlight recent works that have shed light on how AMR evolves in MTBC populations within individual patients. We discuss the role of heteroresistance in AMR evolution, and review the bacterial, patient and environmental factors that likely modulate the magnitude of heteroresistance within-host. We further highlight recent works on the dynamics of MTBC genetic diversity within-host, and discuss how spatial substructures in patients' lungs, spatiotemporal heterogeneity in antimicrobial concentrations and phenotypic drug tolerance likely modulates the dynamics of MTBC genetic diversity in patients during treatment. We note the general characteristics that are shared between how the MTBC and other bacterial pathogens evolve in humans, and highlight the characteristics unique to the MTBC.