查询词典 bronchiolar

TNF α protein and mRNA strongly expressed in the area of bronchiolar epithelium and the inflammatory cells in the lymph follicle near the bronchia and the alveolus cavity and pulmonary interstise in the model group.

此外，慢支大鼠TNFα蛋白及其mRNA在支气管周围的淋巴滤泡中的炎性细胞和肺泡间质浸润的炎性细胞中有强阳性表达，而经艾麻口服液治疗后，其表达减弱。

The percentage of Clara cells in the bronchiolar epithelium and PMN was determined in the broncho alveolar lavage fluid.

目的 探讨机械通气对大鼠肺组织中CC10蛋白表达的影响及CC10对肺炎症反应的影响。

Although migration of alveolar type II and bronchiolar ciliated epithelial cells has been examined, the migratory response of Clara cells has received little attention.

尽管人们研究了肺泡II型上皮细胞和支气管纤毛上皮细胞，但Clara细胞的迁移应答还未得到广泛关注。

Thus, Clara cells resemble alveolar type II and bronchiolar ciliated epithelial cells by showing integrin mediated pro-migratory changes to extracellular matrix components that are present in tissues after injury.

Clara细胞与肺泡II型上皮细胞和支气管纤毛上皮细胞类似，其组织损伤后向胞外基质的促迁移改变依赖于整合素的调节。

However, there have been few studies on the in vivo dynamics of cytokine gene expression in bronchiolar epithelial cells in response to CS.

但很少研究关注体内细支气管上皮细胞对于CS的细胞因子基因表达的动力学。

As the CS exposure was extended to 4, 12, 18 and 24 weeks,the bronchiolar KC and MIP-2 expression and their levels in BAL fluid were relatively dampened compared to those at 10 days.

分别暴露CS4，12，18和24周，细支气管中的KC和MIP-2表达以及在BALF中的表达变化尚不明显。

The results showed:(1) Chronic cigarette smoking down-regulated the protein synthesis and mRNA expression of BKca and Kv1.5 in bronchial and bronchiolar smooth muscles.

结果显示：(1)慢性吸烟可降低大鼠大气道和小气道BKca和Kv1.5蛋白和mRNA表达。

A common manifestation of bronchiolar edema and stiff lungs due to heart failure is a dry cough, which must be differentiated from that occurring in 5% of patients treated with ACE inhibitors.

心力衰竭引起的细支气管水肿和硬肺常表现为干咳，必须与发生率为5%的ACE抑制剂使用病人的干咳相鉴别。

These findings indicate variable patterns of bronchiolar epithelial cytokine expression depending on the duration of CS exposure, and that complex mechanisms govern bronchiolar molecular dynamics in vivo.

此研究表明CS不同暴露时间导致细支气管上皮细胞因子表达的差异。这种复杂的机制支配着体内细支气管分子动力学。

Inflammation per se may be responsible for mild airflow limitation.7 8 9 Indeed, it has been suggested that inflammation may lead to functional bronchiolar constriction by releasing mediators that may act directly on bronchiolar smooth muscle.10 The chronicity of inflammation would, in turn, produce other changes such as airways fibrosis, and may increase the smooth muscle mass either directly as a result of inflammation or indirectly as a result of chronically increased muscle tone.

炎症本身导致了气流限速轻微下降。而事实上它提示了由于释放的介质直接作用于细支气管平滑肌上，炎症引起了功能性细支气管的缢痕。慢性炎症反多来又会产生气道纤维化等其他改变，这样无论是炎症反应的直接影响结果，还是慢性肌紧张增高的直接影响结果，都会增加平滑肌质量。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。