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Psychoactive pharmaceuticals as environmental contaminants may disrupt highly inter-connected nodes in an Autism-associated protein-protein interaction network

机译:作为环境污染物的精神活性药物可能会破坏自闭症相关蛋白-蛋白相互作用网络中高度互连的节点

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摘要

BackgroundMost cases of idiopathic autism spectrum disorder (ASD) likely result from unknown environmental triggers in genetically susceptible individuals. These triggers may include maternal exposure of a fetus to minute concentrations of pharmaceuticals, such as carbamazepine (CBZ), venlafaxine (VNX) and fluoxetine (FLX). Unmetabolized pharmaceuticals reach drinking water through a variety of routes, including ineffectively treated sewage. Previous studies in our laboratory examined the extent to which gene sets were enriched in minnow brains treated with pharmaceuticals. Here, we tested the hypothesis that genes in fish brains and human cell cultures, significantly enriched by pharmaceuticals, would have distinct characteristics in an ASD-associated protein interaction network. We accomplished this by comparing these groups using 10 network indices.
机译:背景大多数特发性自闭症谱系障碍(ASD)病例可能是由遗传易感人群中未知的环境触发因素引起的。这些诱因可能包括孕妇暴露于微量浓度的药物,例如卡马西平(CBZ),文拉法辛(VNX)和氟西汀(FLX)。未代谢的药物通过多种途径到达饮用水,包括未经有效处理的污水。我们实验室以前的研究检查了用药物治疗的min鱼大脑中基因集的富集程度。在这里,我们测试了一种假设,即鱼脑和人类细胞培养物中的基因被药物大大丰富了,在ASD相关蛋白相互作用网络中将具有独特的特征。我们通过使用10个网络索引比较这些组来实现此目的。

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