慢性排斥反应有肺泡上皮细胞增生、纤维结统组织增生。
The chronic rejection manifested epithelioid cells of lung alveoli and interstitial fibrous tissue proliferation.
TB主要位于癌组织中增生的肺泡上皮细胞、巨噬细胞胞浆内。
TB were found mainly in plasma of alveoli epithelial cells and alveolar macrophages with-in lung can cer tissues.
型肺泡上皮细胞形态完整，数目增多，板层小体结构趋于正常。
The structure of type I, IIalveolar cells and pulmonary alveolar capillary endothelial were maintained normal.
蛋白的跨肺泡上皮屏障转运在肺水肿液的清除中发挥着重要作用。
Transport of protein across the alveolar epithelial barrier is a critical process in recovery from pulmonary edema.
LPS致ALI的机制主要是直接损伤肺泡上皮和血管内皮细胞。
Main mechanism of ALI induced by LPS is that it directly damaged pulmonary alveolar epithelium and vascular endothelium.
结论在不吸烟的健康成年人，肺泡上皮通透性随年龄的增长而变化。
Conclusions LEP changes with age in healthy non-smokers and increases in aged people.
KGF不仅是上皮细胞的丝裂原也是促进肺泡上皮细胞的钠水转运和再生的因子。
KGF is not only the mitogen of epithelial cells, but also the cytokine, which can enhance regeneration and sodium-water transport of alveolar epithelial cells.
结论：在肺纤维化形成过程中，内源性NO的增多，有诱导肺泡上皮细胞凋亡的作用。
CONCLUSION: the apoptosis of alveolar epithelial cell is induced by high level of endogenous no in the development of pulmonary fibrosis.
目的：探讨多原发性肺癌与支气管上皮异型增生及肺泡上皮不典型腺瘤性增生之间的关系。
Objective: to investigate the correlation of multiple primary lung cancer with bronchial epithelial dysplasia and atypical adenomatous hyperplasia of bronchiolo-alveolar epithelium.
目的：研究大鼠肺纤维化形成过程中异常增多的肺内源性一氧化氮对肺泡上皮细胞凋亡的影响。
AIM: to study the role of high level of endogenous nitric oxide (no) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats.
并对肺泡上皮细胞、气血屏障造成严重的损伤 ，使细胞器出现空泡、肿胀或呈碎裂状改变 ；
The type I and type II alveolar cells appeared swollen, vacuolated and broken with the blood air barrier severely damaged and surfactants significantly decreased.
肺泡毛细血管内皮细胞基板与I型肺泡上皮细胞基板融合部及毛细血管内皮细胞基板均增厚（P<0.01）。
The fused basal lamina of the alveolar capillary endothelium and type I epithelial basal lamina, the alveolar capillary endothelium basal lamina were thickened (P<0.01).
RAS抑制可以通过多种分子机制抑制肺泡上皮细胞和血管内皮细胞的凋亡，抑制炎症级联反应和细胞外基质沉积，而使肺纤维化病变减轻。
RAS inhibition can reduce cell apoptosis of alveolar epithelial cells and endothelial cells, interfere with the inflammation cascade, and decrease fibroblast activity during tissue repair process.
RAS抑制可以通过多种分子机制抑制肺泡上皮细胞和血管内皮细胞的凋亡，抑制炎症级联反应和细胞外基质沉积，而使肺纤维化病变减轻。
RAS inhibition can reduce cell apoptosis of alveolar epithelial cells and endothelial cells, interfere with the inflammation cascade, and decrease fibroblast activity during tissue repair process.
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