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Thermal injury induces very early production of interleukin-1 alpha in the rat by mechanisms other than endotoxemia.

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TLDR
The data indicate that thermal or mechanical injury induce very early and organ-specific association of IL-1 alpha in vivo by mechanisms other than endotoxemia.
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This article is published in Surgery.The article was published on 1994-05-01 and is currently open access. It has received 56 citations till now. The article focuses on the topics: Alpha (ethology) & Thermal injury.

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The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill

TL;DR: A classification of different ICUAW forms (CIM, CIP, sepsis-induced, steroid-denervation myopathy) and pathophysiological mechanisms from clinical and animal model data are proposed and highlighted, allowing separation of risk factors that may trigger distinct mechanisms contributing to weakness.
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Impaired cognitive function and mental performance in mild dehydration

TL;DR: This article showed that mild dehydration is a reliable predictor of impaired cognitive status in older adults, and suggested that cognitive impairment may not be completely reversible, and that intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.
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Metabolic response to severe injury

TL;DR: An understanding of these phenomena is vital to the practising surgeon because of the plethora of new metabolic modulators threatening to become part of clinical practice.
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Cytokines in patients with polytrauma.

TL;DR: There is great promise in the study of cytokines through basic science research and clinical trials, and certain cytokine levels, such as the interleukins, can be used in predictive ways to correlate organ failure in multiply injured patients.
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Nitric oxide production is intensely and persistently increased in tissue by thermal injury

TL;DR: It is suggested that the hyperdynamic cardiovascular and hypermetabolic responses seen to continue weeks after thermal injury could be a result of the autocrine and paracrine effects of NO generated locally within the tissues in addition to that generated by inflammatory cells.
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