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Biomedical subjects

O Kawanami

Publications and source records attributed to O Kawanami.

At least 55 records · Page 3Linked to original sources
PubMed1988

Primary biliary cirrhosis with fibrosing alveolitis.

A 65-year-old case diagnosed as primary biliary cirrhosis without definite signs of Sjögren's syndrome at age 62 developed interstitial lung disease, which was clinically, histologically, radiographically, and scintigraphically compatible with fibrosing alveolitis. Analysis of the cells in bronchoalveolar lavage fluid revealed, however, increased proportions of not only neutrophils but also lymphocytic cells, which were predominant. This case should focus attention on the association of primary biliary cirrhosis and fibrosing alveolitis.

Aged↗
PubMed1988

Endoscopic observation of peripheral airway lesions.

Peripheral airways of 2 mm or less in diameter were observed in 142 patients by means of an ultrathin bronchofiberscope measuring 1.8 mm in outside diameter. On the basis of the observed and photographed endoscopic findings, an endoscopic classification of peripheral airway lesions was proposed. The endoscopic findings showed changes in the bronchial wall consisting of reddening, pallor, absence of mucosal luster, edema, engorgement of blood vessels, irregular mucosal surface, and elevated mucosa. In the lumen, stenosis, obstruction, ectasis, and deformation due to pressure were recognized, in addition to excessive secretion and pigmentation as morphologic abnormalities or abnormal findings at bifurcation.

Adolescent↗
PubMed1987

The role of intraalveolar fibrosis in the process of pulmonary structural remodeling in patients with diffuse alveolar damage.

For a study of the processes and mechanisms of pulmonary structural remodeling in fibrotic lungs and metaplastic squamous epithelial cells in fibrotic alveoli, immunohistochemical, ultrastructural, and light-microscopic morphometric observations were made of the lungs in acute and proliferative stages of diffuse alveolar damage (n = 40) obtained from biopsies and autopsies. Morphometry showed that intraalveolar fibrosis developed in the early proliferative stage and was more prominent than interstitial fibrosis. In the early proliferative stage, activated myofibroblasts migrated into intraalveolar spaces through gaps in the epithelial basement membrane. They then attached to the luminal side of epithelial basement membrane and produced intraalveolar fibrosis and coalescence of alveolar walls. This intraalveolar fibrosis was the essential factor in the remodeled lungs. Albumin, fibrinogen, immunoglobulins, and surfactant apoprotein were present throughout the hyaline membrane. Fibronectin was not found in hyaline membrane of the lesions in early acute stage but was demonstrated in later stages in outer layers of hyaline membranes and in the areas of intraalveolar fibrosis. Fibronectin may be responsible for the migration and proliferation of myofibroblasts in intraalveolar spaces. Metaplastic single-layered and stratified squamous epithelial cells were keratin-positive and surfactant apoprotein-negative. These metaplastic epithelial cells were frequently found in the alveoli with minimal Type II epithelial cell proliferation and in the grossly scarred alveoli.

Cell Division↗
PubMed1985

Motheaten mice--an animal model with an inherited form of interstitial lung disease.

The motheaten gene represents a single recessive mutation that occurs in mice and is associated with systemic immune abnormalities. Although they have abnormalities in several organs, homozygote animals (me/me) die by 8 wk of age from a diffuse, noninfectious lung disease. To evaluate this genetically determined model of interstitial lung disease, the lungs of these animals were studied by light and transmission electron microscopy and by bronchoalveolar lavage. Two control groups of mice were evaluated: (1) littermate normal mice, including mice without the motheaten gene (+/+) and mice heterozygous (me/+) the motheaten gene, and (2) nonlittermate normal mice (+/+). While the lungs of both control groups were normal morphologically, the lung disease in the homozygous motheaten mice progressed through 3 stages: (1) focal intra-alveolar hemorrhage with accumulations of alveolar macrophages and neutrophils in the lower respiratory tract; (2) persistent alveolitis and hemorrhage, and reparative processes including frequent mitoses of fibroblasts and type II alveolar epithelial cells; and (3) consolidation of the alveolar structures by massive accumulation of macrophages and marked derangement and fibrosis of the alveolar walls. Consistent with the morphologic findings, evaluation of mid-stage lung disease by lavage demonstrated that the alveolitis was characterized by a marked expansion of the total number of effector cells, an accumulation of neutrophils, and a marked expansion of the total numbers of T-lymphocytes and B-lymphocytes. Thus, the motheaten mouse can be regarded as a genetically determined model of interstitial lung disease characterized by alveolar hemorrhage, derangement of parenchymal cells, fibrosis, and an alveolitis with distinctive features.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Hereditary emphysema in the tight-skin mouse. Evaluation of pathogenesis.

The tight-skin (Tsk/+) mouse is a genetically determined model characterized by alveolar enlargement and physiologic evidence of emphysema. Morphologic evaluation of the lungs of these animals demonstrated increased numbers of potential protease-secreting cells (alveolar macrophages and neutrophils) in the lower respiratory tract prior to development of the emphysematous lesions. Quantitation of the neutrophils in the lungs of these animals was carried out by bronchoalveolar lavage. In the Tsk/+ mice, neutrophils constituted 3.5 +/- 2% of all inflammatory and immune effector cells present compared with 0.4 +/- 0.1% in control (+/+) mice (p less than 0.01). The Tsk/+ animals had no evidence of infection to explain the presence of the neutrophils and had normal proportions of lung T- and B-lymphocytes, suggesting that their lungs were immunologically normal. There was no evidence that the Tsk/+ mice have an antiprotease deficit; the capacity of serum of Tsk/+ mice to inhibit neutrophil elastase was no different from that of control +/+ animals. However, the fact that these animals have a persistent low level macrophage-neutrophil alveolitis prior to the development of the emphysematous lesion implies that the lung destruction may be associated, in part, with a chronic protease-antiprotease imbalance, similar to that hypothesized for human emphysema.

Animals↗
PubMed1984

Role of pleural mesothelial cells in the production of the submesothelial connective tissue matrix of lung.

The pleura is comprised of a single layer of mesothelial cells resting on a complex layer of connective tissue. The ability of mesothelial cells to produce the components of this connective tissue was investigated using cultured rat mesothelial cells. These cells produced several components of extracellular matrix, including 6.8 +/- 0.2 X 10(5) collagen pro-alpha-chains per cell per hour, which represented 3.09 +/- 0.05% of all proteins synthesized by these cells. Chemical and immunologic criteria were used to demonstrate that these collagen chains included those of collagen types I, III, and IV. In addition, these cells produced elastin, as well as the connective tissue glycoproteins laminin and fibronectin. Moreover, electron microscopic studies revealed that lung mesothelial cells were capable of organizing these components into complex structures that resembled components of the extracellular matrix (thick collagen fibers, the amorphous component of elastic fibers, and basement membranelike structures), and restricted the formation of these structures to the basal region below the cells in culture. Thus, pleural mesothelial cells are active sources of a variety of connective tissue macromolecules found beneath mesothelial cells in situ, and can assemble these components into structures resembling the pleural extracellular matrix.

Animals↗
PubMed1984

A new bronchofiberscope for the study of diseases of very peripheral airways.

A new device, the BF-1.8T, has been designed to go through the 2.6 mm channel of the conventional fiberoptic bronchoscope (Olympus BF type ITR). It measures 1.8 mm in outer diameter; it has a visual angle of 75 degrees, a range of observation of 3 to 30 mm, an effective length of 950 mm, and a total length of 1120 mm. The tip can extend from the wedge of the outside endoscope by up to 180 mm, providing safe manipulation by the examiner. The results of four cases were briefly presented out of nearly 100 so far examined in our hospital. Selective alveolobronchography (SAB) was simultaneously performed because SAB could be done easily and the results were complementary to the direct observation which was obtained with the BF-1.8T. These data were also correlated with the results of transbronchial lung biopsies.

Adult↗