The pathogenesis of metabolic diseases such as obesity and type 2 diabetes are characterized by a progressive dysregulation in energy partitioning, often leading to end-organ complications. One emerging approach proposed to target this metabolic dysregulation is the application of mild cold exposure. In healthy individuals, cold exposure can increase energy expenditure and whole body glucose and fatty acid utilization. Repeated exposures can lower fasting glucose and insulin levels and improve dietary fatty acid handling, even in healthy individuals. Despite its apparent therapeutic potential, little is known regarding the effects of cold exposure in populations for which this stimulation could benefit the most. The few studies available have shown that both acute and repeated exposures to the cold can improve insulin sensitivity and reduce fasting glycemia in individuals with type 2 diabetes. However, critical gaps remain in understanding the prolonged effects of repeated cold exposures on glucose regulation and whole body insulin sensitivity in individuals with metabolic syndrome. Much of the metabolic benefits appear to be attributable to the recruitment of shivering skeletal muscles. However, further work is required to determine whether the broader recruitment of skeletal muscles observed during cold exposure can confer metabolic benefits that surpass what has been historically observed from endurance exercise. In addition, although cold exposure offers unique cardiovascular responses for a physiological stimulus that increases energy expenditure, further work is required to determine how acute and repeated cold exposure can impact cardiovascular responses and myocardial function across a broader scope of individuals.Plasma gelsolin (pGSN) levels fall in association with diverse inflammatory conditions. We hypothesized that pGSN would decrease due to the stresses imposed by high pressure and subsequent decompression, and repletion would ameliorate injuries in a murine decompression sickness (DCS) model. Research subjects were found to exhibit a modest decrease in pGSN level while at high pressure and a profound decrease after decompression. Changes occurred concurrent with elevations of circulating microparticles (MPs) carrying interleukin (IL)-1β. Mice exhibited a comparable decrease in pGSN after decompression along with elevations of MPs carrying IL-1β. Infusion of recombinant human (rhu)-pGSN into mice before or after pressure exposure abrogated these changes and prevented capillary leak in brain and skeletal muscle. Human and murine MPs generated under high pressure exhibited surface filamentous actin (F-actin) to which pGSN binds, leading to particle lysis. In addition, human neutrophils exposed to high air pressure exhibit an increase in surface F-actin that is diminished by rhu-pGSN resulting in inhibition of MP production. Administration of rhu-pGSN may have benefit as prophylaxis or treatment for DCS.NEW & NOTEWORTHY Inflammatory microparticles released in response to high pressure and decompression express surface filamentous actin. Infusion of recombinant human plasma gelsolin lyses these particles in decompressed mice and ameliorates particle-associated vascular damage. Human neutrophils also respond to high pressure with an increase in surface filamentous actin and microparticle production, and these events are inhibited by plasma gelsolin. Gelsolin infusion may have benefit as prophylaxis or treatment for decompression sickness.Non-Hispanic black individuals suffer from an elevated prevalence of hypertension and cardiovascular disease (CVD) relative to other populations. This elevated disease risk is, in large part, related to impaired vascular function, secondary to reduced nitric oxide (NO) bioavailability. Emerging evidence suggests that dietary nitrate supplementation improves several cardiovascular parameters, including vascular function, in part by increased NO bioavailability. However, whether these findings extend to a population of black individuals is unknown. This study tested the hypothesis that forearm blood flow responses in young, non-Hispanic, black (BL) men during a mental stress challenge would be blunted relative to young, non-Hispanic, white (WH) men.  https://www.selleckchem.com/peptide/avexitide.html  We further hypothesized that acute dietary nitrate supplementation would improve this response in BL men. This study comprised two parts (phase 1 and phase 2). Phase 1 investigated the difference in blood flow responses between young, BL, and WH men. In contrast, ph forearm hyperemic response to mental stress, which would be augmented following acute nitrate supplementation. The increase in forearm blood flow during mental stress was attenuated in BL men and was not impacted by nitrate supplementation. This supports findings of altered vascular function in this population. This is especially important as BL experience a higher prevalence of stress, which contributes to CVD risk.Survivors from COVID-19 pneumonia can present with persisting multisystem involvement (lung, pulmonary vessels, heart, muscle, red blood cells) that may negatively affect exercise capacity. We sought to determine the extent and the determinants of exercise limitation in patients with COVID-19 at the time of hospital discharge. Eighteen consecutive patients with COVID-19 and 11 age-, sex-, and body mass index-matched controls underwent spirometry, echocardiography, cardiopulmonary exercise test and exercise echocardiography for the study of pulmonary circulation. Arterial blood was sampled at rest and during exercise in patients with COVID-19. Patients with COVID-19 lie roughly on the same oxygen consumption isophlets than controls both at rest and during submaximal exercise, thanks to supernormal cardiac output (P less then 0.05). Oxygen consumption at peak exercise was reduced by 30% in COVID-19 (P less then 0.001), due to a peripheral extraction limit. In addition, within COVID-19 patients, hemoglobin cn. Peripheral factors, namely reduced oxygen extraction (myopathy) and anemia, which are not fully compensated by a supernormal cardiac output response, account for exercise limitation before exhaustion of the respiratory reserve. Enhanced chemoreflex sensitivity, rather increased dead space, mainly accounts for exercise hyperventilation. The pulmonary vascular response to exercise circulation of survived patients with COVID-19 does not present major pathological changes.