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7 Department of Molecular Pathology, Institute of Gerontology Oichi Kawanami The respiratory system of man and animals is uniquely composed of a dual blood circulation, including pulmonary and bronchial arteries. The pulmonary arteries originating from the right ventricle of the heart perfuse alveolar capillaries which are located in the interface between blood and air. In contrast, the bronchial arteries derived from the aorta and/or intercostal arteries `distribute along the bronchovascular bands, lobular connective tissue and large vessels. The interactions between the two artery systems are well confirmed by the infusion technique of carbon-containing saline in rat. In the recent studied we found that the communication points of the two blood flows (bronchopulmonary anastomoses) were located at a level of small vessels situated along the bronchial trees. The function and the morphological details of endothelial cells markedly diverse, particularly according to organs and sizes of the vessels. The alveolar capillary endothelial cells of the lung express HLA-DR antigen and thrombomodulin on their cell surfaces under normal condition, but these antigens become concealed when they are embedded in fibrotic lesions. Ultrastructurally, the cytoplasm of the alveolar capillary endothelial cells spread their thin segments along the flat surface of type I alveolar epithelial cells. These capillary endothelium develop no fenestrated portions in their cytoplasm in contrast to the bronchial artery-oriented capillary endothelial cells which occasionally demonstrate fenestrations in their thin segments. We first found the fenestrated capillary endothelial cells in the alveolar regions of interstitial lung diseases of man. Such phenotypic alteration in alveolar capillary endothelial cells was well revealed in the experimentally-induced silicosis or highly fibrotic lungs of rats. In this study we indicated 3 different processes of capillary remodelings. One is due to loss of capillary beds in association with massive accumulation of collagen matix. Secondaly, we showed an active mitosis of endothelial cells in peribronchiolar small vessels which correspond to the sites of broncho-pulmonary anastomosis. New capillary formation or vascular sprouting was well demonstrated in the granulation tissue reaction which took place in peribronchiolar connective tissue. Thirdly, it was a unique result that regeneration of the alveolar capillary endothelial cells in this experiment was induced through transition processes of migration and adhesion of the endothelial cells of microvessels which were closely located to the bronchial circulation. Following maturation periods, the endothelial cells acquired their own phenotypes of fenestrated cytoplasm, a differentiated form of bronchial arteryrelated capillary endothelium. Morphologic alteration of the endothelial cells may be completed under the influences of a variety of cytokines released by inflammatory cells. The roles of endothelial growth factors such as vascular endothelial growth factor, basic fibroblast growth factor, and their corresponding receptors are vaguely understood in lung tissues despite a large number of studies in vitro and in vivo in other organs.

8 (593)99 In this connection, we are interested in the following research subjects: 1) Indentification of antigens expressed on the cell surface or in the cytoplasm of capillary endothelial cells of the pulmonary circulation and/or of the bronchial circulation in the lung. 2) Clarification in vivo reactivities of endothelial growth factors, and their corresponding receptors in the microvessels of both circulation systems. Evaluation of their characteristics under normal lung development in fetuses, maturation and aging in adults. 3) Implication of the endothelial growth factor functions under inflammation and neoplastic lesions to know how the proliferation, migration and regeneration activities of the endothelium are integrated, and how the processes of vascular sproutings or neovascularization take place in lesions of inflammation and neoplasia. 4) Appreciation of inhibitory functions to the growth factors, possibly taking place in vivo by the induction of matrix metalloproteinases and their tissue inhibitors. These evaluations should be made at two different levels : one is by localizing protein antigens with an immunohistochemical technique and by expressing messenger RNA with in situ hybridization. We wish to clarify the basic mechanisms of maintenance and repair of capillary endothelial cells and of neovascularization, which would contribute to the understanding of pathogenesis and for choices of treatment of lung diseases. Details in this subject use further described in the reviews, "The endothelium of the pulmonary microvessels" in the journal (J Nippon Med Sch '1997 ; 64(6).).

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14 1. Itoh Y, Hamada H, Imai T, Seki T, Igarashi T, Yuge K, Fukunaga Y, Yamamoto M : Antinuclear antibodies in children with chronic nonspecific complaints. Autoimmunity 1997 (in press).

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54 P-61) Chronic active gastritis in relation to Helicobacter pylori infection: Light and Electron microscopic studies Central Institute for Electron Microscopic Musashigaoka Researches Aldiyarova Malika-Liu Qiao-ling Shinryojyo Liu Ai-min-Kaoru Aihara Kodo Okuyama Objective: To evaluate the role of H. pylori in the pathogenesis of chronic active gastritis, thirty gastric endoscopic biopsies were performed and observed by light and electron microscopy. Patients and Methods : Twenty one men and nine women ranging in age from 27 to 8 years (mean age : 59.2 years), underwent diagnostic gastroendoscopy. For light microscopic observation, the biopsy specimens were processed routinely and stained with HE and Giemsa. For routine electron microscopic observation, only 15 out to 30 specimens were processed. Furthermore, we assessed the relationship between H. pylori infection and histological findings related to gastritis in accordance with the Sydney system. Results: The endoscopic diagnosis varied as follows; gastric ulcer (17/30), gastric erosion (2/30), chronic gastritis (6/30), gastric polyp (4/30) and gastric carcinoma (1/30). By light microscopy, our observations focused on the background mucosa which showed chronic active gastritis. H. pylori-positive were found in 22 cases. In 16 out of 22 cases we found severe active inflammation. The incidence of atrophy and intestinal metaplasia also showed significant relation to H Pyloriinfection. Bacteria were distributed in clusters over the luminal surface of the epithelium and in the gastric mucus layer. By electron microscopy, colonization of H. pylori was observed in 6 cases only, and the bacteria with bounded membrane and vesicular structure, were seen on the surface of epithelial cells and in the overlying mucus. Increase or decrease of intracytoplasmic mucus and immature cells are also noted in the regenerating epithelium. Conclusion : These observations demonstrated that H. pylori infection was highly presented in chronic active gastritis, suggesting that H. pylori is the most important cause of chronic active gastritis.

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57 P-72) Focal spared area in fatty liver associated with aberrant gastric venous drainage

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