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Oxygen poisoning in mice. Ultrastructural and surfactant studies during exposure and recovery.

I Y Adamson, +2 more
- 01 Nov 1970 - 
- Vol. 90, Iss: 5, pp 463-472
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This article is published in Archives of pathology.The article was published on 1970-11-01 and is currently open access. It has received 82 citations till now. The article focuses on the topics: Pulmonary surfactant & Histocytochemistry.

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Molecular, pharmacologic, and clinical aspects of oxygen-induced lung injury.

TL;DR: It is likely that new data derived from molecular and cellular studies of O2 toxicity will continue to enrich the clinical atmosphere and allow more directed approaches to therapy of acute lung injuries, including ARDS.
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Human 8-oxoguanine DNA glycosylase increases resistance to hyperoxic cytotoxicity in lung epithelial cells and involvement with altered MAPK activity.

TL;DR: It is demonstrated, for the first time, that reduction of hyperoxic toxicity by BER proteins may be involved with MAPK activity, thereby impacting cell survival and suggesting that modulation of MAPK may be used in combination with B ER proteins to counteract hyperoxia.
Journal ArticleDOI

Early radiation dose-response in lung: An ultrastructural study

TL;DR: The capillary endothelium appeared to be the initial site of the post-irradiation pulmonary damage, and the subpheural response included diffuse septal thickening, fibrosis, edema, and reduced alveolar lumina.
Journal ArticleDOI

Hyperoxia stimulates the transdifferentiation of type II alveolar epithelial cells in newborn rats

TL;DR: Findings indicate that transdifferentiation of AECs is not suppressed but rather is increased under hyperoxic treatment by compensation; however, such repair during injury cannot offset pulmonary epithelial air exchange and barrier dysfunction caused by structural damage to A ECs.
Journal ArticleDOI

Bleomycin lung damage: The pathology and nature of the lesion

TL;DR: It is inferred that human diffuse alveolar damage develops in the same way as experimental bleomycin damage in mice where it has been shown that the changes are the result of vascular damage and type I pneumocyte necrosis.
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