系统性红斑狼疮的肺胸膜损害

分析了系统性红斑狼疮并肺、胸膜损害30例,胸膜改变占首位,共19例,(63.3％),其中胸膜积液16例,合并心包积液3例。其次为SLE肺炎5例(16.7％),尿毒症肺水肿3例(10％),弥漫性肺间质纤维化2例(6.7％),肺不张1例(3.35％)。对临床表现、诊断、治疗和预后进行了讨论。     

磁共振成像对胸膜外脂肪显示的研究

目的：研究MRI对正常及异常胸膜外脂肪显示的价值。材料和方法：对21例健康志愿者进行了MRI化学位移同相位成像、反相位成像、T1WI、T2WI及STIR序列扫描，并对胸膜外脂肪的绝对信号强度及信号强度比进行比较分析，同时还对20例累及胸膜外脂肪的病人进行检查。结果：在MRI各序列中，化学位移反相位成像显示胸膜外脂肪最佳，各序列绝对信号强度没有差别，而信号强度比存在差异。异常的胸膜外脂肪可以表现为移位、受压、中断、增厚及信号改变。结论：MRI可以作为观察正常及异常胸膜外脂肪的有效检查方法。     

'Pleural' and pulmonary carcinosarcomas.

The histological distinction between carcinosarcoma and mesothelioma has received little attention. The object of this study was to describe the histology and immunohistochemistry of two carcinosarcomas presenting as pleural tumours. These were compared with 12 carcinosarcomas from sites within the lung, and with the established features of mesothelioma. Histologically and immunohistochemically, these 'pleural' carcinosarcomas are similar to conventional pulmonary carcinosarcomas but accurate recognition is hindered by their gross appearance and biphasic histology which closely mimic mesothelioma. They may exhibit features such as neutral mucin, expression of carcinoembryonic antigen, squamous differentiation, and neuroendocrine differentiation which, when present, are evidence against mesothelioma. These tumours are rare and have passed unnoticed until now.     

恶性胸膜间皮瘤：3例尸解病例的组织化学和免疫组织化学研究

本文报告8例恶性胸膜间皮瘤尸解病例,上皮型2例,1例纤维型大体改变为巨大结节,并推挤膈肌至脐平面。对此3例进行了PAS、D-PAS,CM、AB、H-AB、CI、H-CI和CEA、Keratin、Vimentin等组化和免疫组化研究,并结合文献复习对人体胸膜间皮的组化和免疫组化特征进行了讨论,提出了人体胸膜间皮瘤的临床病理诊断与鉴别诊断意见。本组3例均合并DIC,推测本病有产生DIC的倾向性,临床对此病应警惕DIC发生的危险。     

Post-capillary venules in the “milky spots” of the greater omentum are the major site of plasma protein and leukocyte extravasation in rodent models of peritonitis

Intraperitoneal injection of inflammatory agents in the mouse and rat causes plasma protein and leukocyte extravasation into the peritoneal cavity. Following an intraperitoneal injection of zymosan A, the milky spots of the omentum were the only abdominal sites detected where intravenously administered Monastral Blue labeled interendothelial cell gaps responsible for plasma extravasation. In addition, when colored microspheres were intraventricularly administered to quantify blood flow, the omentum was the only abdominal organ which showed an increase in blood flow during zymosan A peritonitis. A combination of light and electron microscopy, plus measurement of myeloperoxidase activity (a marker of neutrophil accumulation) demonstrated that the omental milky spots are the major route through which leukocytes migrate into the peritoneal cavity. Identical structures in the pleura likewise are the sites of protein leakage into the pleural cavity. In contrast, selective sites of protein and cellular extravasation could not be detected in the synovial lining of the inflamed knee joint.     

Relative motion of lung and chest wall promotes uniform pleural space thickness

The pleural space is modeled in two dimensions as a thin layer of fluid separating a deformable membrane and a rigid surface containing a bump. We computed the steady-state membrane configuration and fluid pressure distribution during relative sliding of the two surfaces. For physiologically relevant values of membrane tension, shear flow-induced pressures near the bump and far-field pressure gradients are similar to those measured in vivo within the pleural space (e.g. Lai-Fook et al.) [J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 56 (1984) 1633-1639]. Deformation of the membrane over the bump suggests that the pressure field generated by the sliding motion promotes an even layer of fluid in the pleural space, preventing asperities from touching. Results also suggest a possible mechanism for pleural fluid redistribution during breathing, whereby irreversible fluid motion is associated with the deformability of the membrane.     

Elastohydrodynamic separation of pleural surfaces during breathing

To examine effects of lung motion on the separation of pleural surfaces during breathing, we modeled the pleural space in two dimensions as a thin layer of fluid separating a stationary elastic solid and a sliding flat solid surface. The undeformed elastic solid contained a series of bumps, to represent tissue surface features, introducing unevenness in fluid layer thickness. We computed the extent of deformation of the solid as a function of sliding velocity, solid elastic modulus, and bump geometry (wavelength and amplitude). For physiological values of the parameters, significant deformation occurs (i.e. bumps are 'flattened') promoting less variation in fluid thickness and decreased fluid shear stress. In addition, deformation is persistent; bumps of sufficient wavelength, once deformed, require a recovery time longer than a typical breath-to-breath interval to return near their undeformed configuration. These results suggest that in the pleural space during normal breathing, separation of pleural surfaces is promoted by the reciprocating sliding of lung and chest wall.     

Respiratory mechanics and pleural remodelling in pleurodesis induced by barium sulphate

The aim of this study was to determine whether an intrapleural injection of barium sulphate would produce pleurodesis in rats. Additionally, respiratory mechanics and pleural remodelling were analysed. Single intrapleural injection of barium sulphate (100%) or saline was given to Wistar rats. Respiratory system, lung, and chest wall elastic, resistive and viscoelastic/inhomogeneous pressures were measured by the end-inflation occlusion method at 2 and 30 days after injection. The pleura were examined for gross and histopathological evidence of pleural inflammation and fibrosis, and the underlying lungs were also studied by morphometry. All pulmonary mechanical parameters increased at day 2, but were not different from control at 30 days after injection. Chest wall mechanical parameters did not change. Macroscopic evaluation demonstrated pleural adherence without haemothorax. Histopathologic analysis showed pleural inflammation and fibrosis. There was no alveolar inflammation or fibrosis in both groups. In conclusion, barium sulphate induced pleurodesis with either no changes in respiratory mechanics or lung lesion at day 30.     

肺内炎性肿块的CT分析

目的探讨在职业病防治中肺内炎性肿块的CT诊断及鉴别诊断。方法对15例经螺旋CT扫描并经病理证实的肺内炎性肿块进行回顾性分析。结果肺内炎性肿块的CT表现为病灶位于肺的外围，呈三角形、方形、楔形、类圆形；病变与胸膜广基底相连，临近胸膜反应性增生；肺内及纵隔无明显淋巴结肿大。经抗炎治疗后多明显吸收缩小、消失，形成炎性假瘤，可无变化。结论结合临床病史分析肿块的CT表现，肺内炎性肿块的CT表现有一定的特点，可以与结核球、尘肺大阴影及周围型肺癌鉴别。     

Monoclonal antibodies anti-TGFβ1 and anti-VEGF inhibit the experimental pleurodesis induced by silver nitrate

Background. The mechanisms underlying pleural inflammation and pleurodesis are poorly understood. We hypothesized that the cytokines transforming growth factor β (TGFβ1) and vascular endothelial growth factor (VEGF) play a major role in pleurodesis after intrapleural silver nitrate (SN) injection. Method. Forty rabbits received intrapleurally 0.5% SN alone or 0.5% SN + anti-TGFβ1, anti-IL-8, or anti-VEGF. After 28 days, the animals were euthanized and macroscopic pleural adhesions, microscopic pleural fibrosis, and collagen deposition were analyzed for characterization of the degree of pleurodesis (scores 0–4). Results. Scores of pleural adhesions, pleural fibrosis, total collagen, and thin collagen fibers deposition after 28 days were significantly lower for 0.5% SN + anti-TGFβ1 and 0.5% SN + anti-VEGF. Significant correlations were found between macroscopic adhesion and microscopic pleural fibrosis with total collagen and thin collagen fibers. Conclusions. We conclude that both TGFβ1 and VEGF, but not IL-8, mediate the pleural inflammatory response and pleurodesis induced by SN.