The localization of a platelet GpIIb-IIIa-related protein in endothelial cell adhesion structures

Previous studies have shown that human endothelial cells (ECs) adhere to fibrinogen (fg) and fibronectin (fn) and organize their cytoskeleton on these substrata. However, the mechanism governing this chain of events is poorly known. In ECs glycoproteins immunologically and biochemically similar to the platelet membrane GpIIb-IIIa complex have been described. The functional role of this complex in ECs remains to be established. In this study we show that the antigens recognized by polyclonal antibodies raised against human platelet GpIIb-IIIa and crossreacting with the EC form have a discrete and well-organized distribution at cell adhesion structures. Indeed these antigens are located at vinculin-rich focal contacts found at the membrane insertion of microfilament bundles of the stress fiber type. They are also found at cell-to-cell contacts and, with a diffuse pattern, at the dorsal surface of ECs. GpIIb-IIIa antibodies, added to EC suspensions prior to plating, inhibit EC spreading on fg and vitronectin (vn) substrata in a concentration-dependent way. In contrast, the antibodies are very poorly active when the cells are seeded on fn-coated glass. The same antibodies, added to adherent cells, disrupt cell-to-cell contacts and cause their rounding and detachment. Overall these results indicate that EC GpIIb-IIIa complex is involved in controlling the adhesion mechanism of these cells to extracellular matrix proteins.     

Granulocyte macrophage colony-stimulating activity production by cultured human thymic nonlymphoid cells is regulated by endogenous interleukin-1

Supernatants of cultured human thymic nonlymphoid cells were assayed for granulopoietic factors using cultures of low density bone marrow mononuclear cells (LD-BMMC). Thymic nonlymphoid cell-conditioned medium (TNLC-CM) supported vigorous myeloid colony growth of LD-BMMC, and of LD-BMMC depleted of T lymphocytes and/or monocytes. Colony stimulating activity (CSA) in TNLC-CM was abrogated by a highly specific neutralizing antiserum against recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF). TNLC-CM also enhanced colony growth in LD-BMMC stimulated by colony stimulating activity from a giant cell tumor culture (GCT). The enhancing activity of TNLC-CM, unlike its CSA activity, required the presence of adherent cells in the marrow cell culture. The addition of anti-interleukin-1 (anti-IL-1) antibody to TNLC-CM inhibited the GCT-enhancing activity, but not the CSA. When the anti-IL-1 immunoglobulin was added directly to cultures of thymic nonlymphoid cells, GM-CSF production was completely inhibited, and the GCT enhancing activity was neutralized. We conclude that an intercellular regulatory network exists in cultured thymic explants in which GM-CSF expression is induced by IL-1. In this system, the granulopoietic effect of IL-1 derives not from a direct effect on myeloid progenitors, but from its ability to recruit CSA production by other cells.     

小切口开胸39例体会

1 临床资料小切口开胸39(男24,女15)例,年龄16～75(平均50.5)岁. 肺癌12,其中中央型肺癌3例,周围型肺癌9例;肺结核瘤2例;恶性胸水8例;自发性气胸肺大疱10例;食管裂孔疝3例,贲门失弛缓症4例. 术前准备同常规开胸手术. 采用单腔或双腔管气管内插管、全身静脉复合麻醉. 采用标准开胸的健侧卧位. 切口自锁骨中线至肩胛下线之间的范围沿肋间走行,长约8～12 cm,以病变的部位选择锁骨中线至腋中线或腋前线至腋后线或腋中线至肩胛线的相应肋间,依次切开皮肤、皮下组织,将背阔肌及胸大肌游离而不切断,沿欲切开之肋间将前锯肌纤维钝性分开,紧贴下位肋骨上缘切断肋间肌及壁层胸膜,用两副开胸器交叉撑开即可暴露术野进行操作. 关胸时,用10号丝线绕切口上下肋骨间隙缝合3针,关闭胸腔,逐层缝合切口各层组织,其中皮肤层以可吸收线行皮内连续缝合. 应用小切口进行肺叶切除11例;取活检1例;肺楔形切除2例;胸膜固定术8例;肺大疱切除10例;食管裂孔疝修补3例,贲门失弛缓症贲门胃底肌层切开膈肌瓣成形术4例. 开胸时间8～12(平均10)min. 关胸时间15～20(平均17.5)min. 开胸过程中出血量10～20 mL. 术后胸腔引流量70～200(平均130)mL/d. 术后伤口疼痛较标准开胸切口者明显减轻,均不用止痛剂. 术后术侧上肢活动无明显受限,肩关节活动在1 wk内均恢复正常,可耐受大范围的活动. 本组病例中,患者切口7～9 d拆线,全部I期愈合.     

Migration and lymphatic spread of calcified paraffinomas after breast augmentation

A 62 year old Chinese woman presented 25 years after having both breasts augmented with paraffin injections. Development of paraffinomas and multiple episodes of paraffin-related mastitis eventually resulted in bilateral mastectomies. The unusual distribution of migrated calcified paraffinomas in the thoracic wall and its lymphatic system is documented on computed tomography.