The sleep architecture of Australian volunteer firefighters during a multi-day simulated wildfire suppression: Impact of sleep restriction and temperature

Ferguson, SA ORCiD: 0000-0002-9682-7971; Jay, SM ORCiD: 0000-0002-1447-7008; Smith, BP ORCiD: 0000-0002-0873-3917; Vincent, GE ORCiD: 0000-0002-7036-7823Wildland firefighting exposes personnel to combinations of occupational and environmental stressors that include physical activity, heat and sleep restriction. However, the effects of these stressors on sleep have rarely been studied in the laboratory, and direct comparisons to field scenarios remain problematic. The aim of this study was to examine firefighters' sleep during a three-day, four-night simulated wildfire suppression that included sleep restriction and physical activity circuits representative of firefighting wildfire suppression tasks in varied temperatures. Sixty-one volunteer firefighters (37.5. ±. 14.5 years of age, mean. ±. SD) were assigned to one of three conditions: control (n=25; 8. h sleep opportunities and 18-20. °C), awake (n=25; 4. h sleep opportunities and 18-20. °C) or awake/hot (n=11; 4. h sleep opportunities and 33-35. °C during the day and 23-25. °C during the night). Results demonstrated that amounts of N1, N2 and R sleep, TST, SOL and WASO declined, whilst sleep efficiency increased significantly in the awake and awake/hot conditions compared to the control condition. Results also demonstrated that SWS sleep remained relatively stable in the awake and awake/hot conditions compared to control values. Most importantly, no significant differences were found for any of the sleep measures between the awake and awake/hot conditions. Thus, working in hot daytime temperatures in combination with sleep restriction during the night did not affect patterns of sleep compared to working in temperate conditions in combination with sleep restriction during the night. However, the effects on sleep of high (>25. °C) night-time temperatures with sleep restriction in addition to physical activity remains to be studied. © 2015 Elsevier Ltd

Asthma is associated with enhanced thrombin formation and impaired fibrinolysis

Background There is evidence that altered blood coagulation and fibrinolysis are involved in the pathogenesis of asthma. Increased thromboembolic risk has been reported in asthmatics. Objective To investigate whether enhanced thrombin generation and impaired fibrinolysis occur in asthmatics. Methods Plasma thrombin generation profile together with a computational assessment of thrombin dynamics and fibrinolytic capacity expressed as clot lysis time (CLT) were determined in 164 consecutive patients with stable asthma and 72 controls matched for age, gender, weight and smoking. Results Asthma patients had 20.2% increased endogenous thrombin potential (ETP), 41.4% higher peak thrombin concentration, 61% higher maximal prothrombin conversion rate, 15.5% faster rate of thrombin formation (all, P < 0.0001) and 10% lower thrombin decay capacity (P = 0.0004) compared with controls. Asthmatics had also 14.4% longer CLT (P = 0.001) associated with 21.3% higher plasminogen activator inhibitor‐1 (PAI‐1) (P < 0.0001), and 13% higher plasma α2‐macroglobulin (P = 0.0002). Using ETP and CLT above 75th percentile of the control values as the cut‐off levels, we found increased risks of enhanced thrombin generation and hypofibrinolysis in asthmatics, also after correction for potential confounders. ETP and CLT were associated inversely with forced expiratory volume in 1 s/vital capacity (FEV1/VC) index, after adjustment for age and body mass index. Non‐allergic asthma (n = 70, 42.6%) was characterized by 17.5% longer CLT (P = 0.02), which positively associated with PAI‐1. Thrombin generation profile was not affected by allergy. Conclusion and Clinical Relevance Asthma is associated with enhanced thrombin generation and impaired fibrinolysis, which might contribute to thromboembolic events in this disease

Complement in age-related macular degeneration: a focus on function

Age-related macular degeneration (AMD) is an inflammatory disease, which causes visual impairment and blindness in older people. The proteins of the complement system are central to the development of this disease. Local and systemic inflammation in AMD are mediated by the deregulated action of the alternative pathway of the complement system. Variants in complement system genes alter an individual's risk of developing AMD. Recent studies have shown how some risk-associated genetic variants alter the function of the complement system. In this review, we describe the evolution of the complement system and bring together recent research to form a picture of how changes in complement system genes and proteins affect the function of the complement cascade, and how this affects the development of AMD. We discuss the application of this knowledge to prevention and possible future treatments of AMD