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不同浓度石英吸入后吞噬作用和炎症的数学模型。

Mathematical model of phagocytosis and inflammation after the inhalation of quartz at different concentrations.

作者信息

Tran C L, Jones A D, Donaldson K

机构信息

The Institute of Occupational Medicine, Edinburgh, Scotland, UK.

出版信息

Scand J Work Environ Health. 1995;21 Suppl 2:50-4.

PMID:8929690
Abstract

A mathematical model was developed with several distinctive features to represent the various processes leading to silicosis. It assures the phagocytosis of quartz by the resident alveolar macrophages. It then models the necrosis of macrophages caused by the ingestion of quartz particles and the subsequent release of these clusters onto alveolar surfaces. The inflammatory recruitment of alveolar macrophages and neutrophils in response to the cell necrosis caused by the ingestion of quartz particles is described in a functional form and is included in the model. The model also describes the pathological and other biological reactions to quartz particles in the interstitium. Specifically, once the quartz particles arrive at the interstitium, they can be phagocytozed by interstitial macrophages. The pathological interaction between quartz and interstitial macrophages may lead to quartz particles being sequestered in silicotic nodules, and also cleared to the efferent lymph nodes.

摘要

开发了一种具有若干独特特征的数学模型,以代表导致矽肺病的各种过程。它确保驻留的肺泡巨噬细胞对石英进行吞噬作用。然后,该模型模拟由石英颗粒摄取引起的巨噬细胞坏死以及这些聚集体随后释放到肺泡表面的过程。以功能形式描述了肺泡巨噬细胞和中性粒细胞对石英颗粒摄取引起的细胞坏死的炎症募集,并将其纳入模型。该模型还描述了间质中对石英颗粒的病理和其他生物学反应。具体而言,一旦石英颗粒到达间质,它们就可以被间质巨噬细胞吞噬。石英与间质巨噬细胞之间的病理相互作用可能导致石英颗粒被隔离在矽结节中,并且还会被清除到输出淋巴结。

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