胸膜

Chemical pleurodesis is a technique in which a sclerosing agent is used to abrade the pleural surfaces producing an adhesion between the parietal and visceral pleurae.

化工pleurodesis 是一个硬化代理被使用磨蚀胸膜表面引起黏附力在头顶骨和发自内心的肋膜之间的技术。

Results: The most common locations of PIP were at the margin of both lower lobes and associated with local pleural thickening and adhesion. The density of nodule in which CT attenuation value was 15~60 HU (26.9±13.5HU) was lower than that of PLC. Most of them were round/round-like and irregular in shape. The interior density of lesion was inhomogeneous. The presence of calcification or multiple cavitations, straight margin sign, hole sign and without hilar and mediastinal adenopathy were of great significance in the diagnosis of such kind of disease.

结果：炎性假瘤多位于两肺下叶，邻近胸膜增厚、粘连，病灶密度偏低（平扫CT值15~60HU，平均26.9±13.5HU），与周围型肺癌比较有统计学差异，其形态以圆形／类圆形和不规则形多见，病灶内密度多不均匀，可见钙化及多发空洞，边缘呈平直状、周围见毛玻璃样改变及肺门纵隔无淋巴结肿大等征象对本病的CT诊断有意义。

Rational and active antituberculous chemotherapy and aspiration of effusion are essential to the prevention of pleural thickening.

积极合理的抗结核化疗及胸穿抽液是预防胸膜肥厚的重要措施。

During the active stage antituberculous treatment combined with unlimit...

在积极抗结核治疗的同时采用不限量缓慢抽液及胸腔内注药治疗，治愈48例(占55.81%)，胸膜增厚38例(占44.19%)，其预后与诊治的时机有密切关系。

Similar to asbestosis and other forms of asbestos-related diseases, pleural disease is a latent disease.

类似石棉和其他形式的石棉相关疾病，胸膜疾病，是一种潜在的疾病。

Results: The lesions wryer usually located at the periphery, the base of the lesion were extensively adhesive to pleural with localized pleural thickening, most of them were round or round-like mass, margin was smooth, density was homogeneous, diameter was around 2cm-5cm; the edge of lesion presented long and thick speculations, or shallow lobulation, and mediastinal lymphadenectasis.

结果：病灶多位于肺胸膜下，广基地与胸膜相连；多呈圆形或类圆形，边缘光滑，直径2-5 cm ，密度均匀；边缘可见粗长毛刺，棘状突起或浅分叶；可有淋巴结肿大。

Over time, the fibers cause chronic inflammation, the development of pleural fibroses (a thickening of the pleural surfaces) and pleural effusions (buildup of fluid in the pleural spaces) and in many people, cancerous cell development.

随着时间的推移，这些纤维导致慢性炎症，使得胸膜纤维化和胸膜腔积液，并在大部分人中，癌细胞开始生长。

The results showed that the sheep had fibrinous pneumonia and lymphocyte interstitial pneumonia, which were typical pathologic changes of this disease. Remarkable changes were observed in the lung: fibrinous exudates, infiltration of inflammatory cells, pleura thickening, interstitial edema, hemorrhage and formation of thrombiand lymph clot. The heart, liver and kidney had different degeneration degree. Reactive hyperplasia presented in bronchales lymphonodi.

结果发现该病例具有胸膜肺炎的典型病理变化，呈现纤维素性肺炎和淋巴细胞性间质肺炎，纤维素性物质的渗出和炎性细胞的浸润很明显，肺胸膜增厚，同时在肺间质还可见水肿、出血、血栓和淋巴栓的形成；另外心、肝、肾也均有不同程度的变性，淋巴结呈反应性增生。

Spicules,protrusion,bronchovascular convergence,pleural adhesion and pleural indentation also can be found in brim of mass.

胸膜粘连多见于肿块较大的肺癌，胸膜凹陷征多见于肿块较小的肺癌。

The apxⅢA gene of Actinobacillus pleuropneumonie was amplified by PCR. The amplified DNA fragment 3 466bp was cloned into pMD18-T. After R.E. analysis and sequencing, the apxⅢA gene in pMD18-T was ligated into pBluescripⅡSK, the recombinant expression plasmid pET-28b/apxⅢA was constructed and analysed with R.E., the protein of apxⅢA gene expressed in E.coli BL21 was detected by Western blotting.

因胸膜肺炎放线杆菌的致病性主要是由毒素决定的，故参照猪胸膜肺炎放线杆血清2型菌株的序列(GenBankL1 2 1 4 5)设计了一对特异性引物，用PCR的方法扩增apxⅢA基因并得到了长 3 466bp的片段，然后将其克隆到pMD 1 8T中，经酶切鉴定和序列分析表明克隆是成功的；再将apxⅢA插入到原核表达载体pET 2 8b后，转化BL2 1 (DE3)，在IPTG诱导下获得高效表达，经Westernblotting检测证实表达产物有活性。

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。