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Stress and wound healing.

机译:压力和伤口愈合。

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摘要

There are substantial data to suggest that stress-induced disruption of neuroendocrine immune equilibrium is detrimental to health, with the strongest evidence to date in wound healing. Murine and human studies demonstrated that the down-regulation of the early inflammatory response by an increase in cortisol levels results in delayed wound repair and identified several potential cellular mechanisms linking stress and wound healing. The impact of stress on wound healing has been studied almost exclusively in acute experimentally induced wounds. Because chronic wounds are different entities from acute wounds, the cellular/molecular mechanisms by which stress affects acute wound healing may not necessarily be applied to chronic wounds, hence, the need for studies in stress and chronic wound (eg, diabetic foot ulcer) healing.
机译:有大量数据表明,应激诱导的神经内分泌免疫平衡破坏对健康有害,迄今为止,在伤口愈合中有最强有力的证据。鼠科动物和人体研究表明,皮质醇水平升高可导致早期炎症反应下调,从而导致伤口修复延迟,并确定了几种可能的细胞机制将压力与伤口愈合联系起来。几乎仅在急性实验诱导的伤口中研究了应力对伤口愈合的影响。由于慢性伤口与急性伤口是不同的实体,因此应力影响急性伤口愈合的细胞/分子机制可能不一定适用于慢性伤口,因此,需要研究压力和慢性伤口(例如糖尿病足溃疡)的愈合。

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