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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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Relationship of alveolar epithelial injury and repair to the induction of pulmonary fibrosis.

TL;DR: It is suggested that severe injury and retarded repair of the alveolar epithelium disturbs normal epithelial-fibroblast interactions and is sufficient to promote the fibrotic process.
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Interleukin-6-induced protection in hyperoxic acute lung injury.

TL;DR: It is demonstrated that IL-6 markedly diminishes hyperoxic lung injury and that this protection is associated with a marked diminution in hyperoxia-induced cell death and DNA fragmentation.
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IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury

TL;DR: IL-13 has protective effects in hyperoxic acute lung injury, and it is demonstrated that IL-13, alone and in combination with 100% (2), stimulates pulmonary VEGF accumulation, that this stimulation is isoform-specific, and that the protective effects of IL- 13 are mediated, in part, by VEGf.
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Targeted lung expression of interleukin-11 enhances murine tolerance of 100% oxygen and diminishes hyperoxia-induced DNA fragmentation.

TL;DR: It is demonstrated that IL-11 markedly diminishes hyperoxic lung injury and this protection is associated with small changes in lung antioxidants, diminished hyperoxia-induced IL-1 and TNF production, and markedly suppressed hyperoxIA-induced DNA fragmentation.
Journal ArticleDOI

Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development

TL;DR: The data suggest that perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells.
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