细支气管

Panacinar emphysema occurs with loss of all portions of the acinus from the respiratory bronchiole to the alveoli.

全腺泡型肺气肿发生时则出现从呼吸性细支气管到肺泡的腺泡所有部分全部扩张。

Centrilobular emphysema occurs with loss of the respiratory bronchioles in the proximal portion of the acinus , with sparing of distal alveoli.

腺泡中央型肺气肿的发生是腺泡中央的呼吸性细支气管呈囊性扩张，而肺泡管、肺泡囊扩张不明显。

The respiratory portion begins when an air sac first arise which appears as an outpocketing of the bronchiole.

呼吸性细支气管：壁上有散在的肺泡开口，上皮为单层立方上皮，在肺泡开口处，移行为单层扁平上皮。

The result showed that there was no expression in the normal control group and an apparent expression of ERK1/2 and Elk in the asthma group. A rather dense expressing of ERK1/2 was at bronchiole and mucous membrane, sub mucous membrane, smooth muscle, cytoplasm and nuclei of the out layer of the smooth muscle cell and an expression of positive fiber at submucous membrane.

结果发现正常肺内没有发现ERK1/2和Elk的表达，而哮喘时肺内有明显的ERK1/2和Elk表达，ERK1/2较密集表达在小支气管和细支气管的粘膜层、粘膜下层、平滑肌层和平滑肌外层细胞的胞浆和胞核中，也可见粘膜下层有阳性纤维表达。

Pathologic results: The bronchioles showed obvious chronic inflammatory process of bronchioles including thickened wall, narrowed lumen, goblet cell proliferation, emphraxis in bronchiole, interstitial fibrosis and developed emphysema in stable model of COPD.

病理结果示：稳定模型组各级支气管慢性炎症明显，管壁增厚、管腔狭窄、杯状细胞增生，细支气管管腔闭塞较多，肺间质纤维化明显，肺气肿形成，小动脉管壁增厚明显。

Jq Ez6_{0An outbreak of highly pathogenic avian influenza caused by H5N1 virus occurred in Vietnam, Japan and Korea, commencing in December, 2003. By February, 2004, it has been distributed widely in Asia and brought heavy losses. H5N1 are ball-like RNA viruses, birds can shed them via respiratory system, ocular secretions and feces, sometimes transferred to human and cause lethal infection. H5N1 patients have prominent features of reactive hemophagocytic syndrome,bronchiolar inflammation, necrosis of bronchial epithelium and organizing,diffuse alveolar damage with interstitial fibrosis.

2003年12月，H5N1型禽流感病毒在越南、日本和韩国爆发，到2004年2月，该病毒已在亚洲广泛蔓延并带来了巨大损失。H5N1是球型RNA病毒，禽类间可通过呼吸系统、眼分泌物和粪便传播，也可传染人类甚至导致死亡。H5N1感染者的特征是反应性噬血细胞综合征、细支气管炎症、支气管上皮坏死和机化、弥漫性肺泡病变和间质纤维化。

Bronchi and bronchioli may contain leukocytes and cellular debris.

支气管和细支气管可能存在白细胞和细胞碎片。

Acute and chronic bronchiolitis and peribronchiolitis are the essential pathological changes in COPD, and also are the key link of the structural remodeling of the pulmonary tissue and vessels.

急、慢性细支气管炎和细支气管周围炎是COPD的重要肺部病变，也是导致肺组织和血管构形重建的重要环节。

PaO2/FiO2 of both patients was less than 225 mm Hg.In both patients, high-resolution computed tomography scans at the exacerbation showed typical signs of IPF including peripheral predominant, basal predominant reticular abnormality, with honeycombing and traction bronchiectasis and bronchiolectasis,and newly developing alveolar opacity.

呼吸困难分别在1周和半月内加重；2例患者氧合指数均小于225 mm Hg；急性加重时2例患者HRCT表现为两下肺分布的网状影、蜂窝影、牵拉性细支气管扩张和支气管扩张等典型的IPF表现，并出现新的磨玻璃影。

Results:The clinical symptom in part case of senile pulmonary infection is not typical,The clinical medical imaging manifestion is varied-among 130 cases,bronchopneumonia account for 44.6%,interstitial pneumonia was 25.4%, bronchiolitis obliterans organizing pneumonia was 1.5%,lobar pneumonia was 23.1%,spheropneumonia was 1.5%,pulmonary abscess was 3.8%.

结果 ：130例患者中，部分临床症状不甚典型，其临床医学影像表现形式多种多样。其中，表现为支气管肺炎者占 44 。6 %，间质性肺炎 2 5 。4%，闭塞性细支气管炎性机化性肺炎 1.5 %，大叶性肺炎 2 3.1%，球形肺炎 1.5 %，肺脓肿 3.8%。

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。