This study investigates the effects of exertional heat stress and acclimation status on physiological and cognitive performance. Forty male soldiers performed an exertional heat stress test (EHST) either in a cool (20 degrees C, 16 degrees C wet bulb globe temperature), or in a hot environment (40 degrees C, 29 degrees C wet bulb globe temperature), unacclimatized, or after 10 days of passive or active acclimation. Mean skin and tympanic (Tty) temperatures and heart rates (HR) measured physiological strain. A cognitive test (the computerized Cambridge Neuropsychological Test Automated Batteries attention battery) is administered before and immediately after EHST. EHST in hot conditions induced physiological heat stress (increase in Tty and HR), which caused mild deficits in attention in U group (decreased number of correct responses, and prolonged movement time). Acclimated (passive and active) soldiers suffered no detrimental effects of exertional heat stress, despite almost the same degree of heat strain, measured by Tty and HR.
The aim of this study was to assess the prognostic value of tumor necrosis factor (TNF) alpha, interleukin (IL)-8, IL-4, and IL-10 in combat casualties. Fifty-six casualties with severe trauma (blast and explosive) who developed sepsis and 20 casualties with the same severity of trauma without sepsis were enrolled in this study. Fifty-five casualties developed multiple organ dysfunction syndrome; 36 died. Blood was drawn on the first day of trauma. Concentrations of IL-8, TNF-alpha, IL-4, and IL-10 were determined in plasma using enzyme-linked immunosorbent assays. Mean values of IL-8 were 230-fold, IL-10 were 42-fold, and TNF-alpha were 17-fold higher in trauma and sepsis group (p < 0.01). Mean values of IL-8 were 60-fold, TNF-alpha were 43.5-fold, and IL-10 were 70-fold higher in the multiple organ dysfunction syndrome group (p < 0.01). Mean values of IL-8 were 2.3-fold and IL-10 were 1.4-fold higher in nonsurvivors and TNF-alpha were 2.2-fold higher in survivors (p < 0.01). IL-4 had no significance as a predictor of severity and outcome.
Acute pancreatitis is an inflammatory process which occurs in severe form in 20% of all patients, out of whom 15%-25% will die. The incidence of severe acute pancreatitis-associated lung injury (APALI) varies from 15% to 55% and its severity varies from mild hypoxemia to acute respiratory distress syndrome (ARDS). Acute lung injury (ALI) and ARDS are the most significant manifestations of extra abdominal dysfunctions in severe acute pancreatitis with mortality rate as high as 60% in the first week of the onset of illness. Different pathophysiological mechanisms of severe acute pancreatitis-associated lung injury have been described. The role of enzymes, adhesion molecules, neutrophils, fibronectin and various inflammatory mediators has been emphasized. Mechanism of the acute lung injury associated with the acute pancreatitis is very complex and has not been clear yet. There is no specific therapeutic procedure and mortality rate is very high. Therefore, further studies are necessary to address this acute and growing problem in intensive medicine.
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