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Biomedical subjects

Y Hamamoto

Publications and source records attributed to Y Hamamoto.

At least 109 records · Page 6Linked to original sources

A consideration on histopathologic variability of diffuse pleural mesothelioma based on DNA cytophotometry.

Nuclear DNA cytophotometry of the tumor cells was performed for an autopsy case of malignant diffuse pleural mesothelioma diagnosed histologically as a mixed type. The DNA distribution of these tumor cells confirmed bimodality, one being situated in the triploid and the other in the pentaploid DNA range, thus indicating two stemline cell populations. In the former, the majority were epithelial mesothelioma cells resembling the normal mesothelial cells. The latter were mesenchymal tumor cells with spindle and occasionally bizarre shaped nuclei. This cytophotometric data strongly suggests that the histologic variability in mesotheliomas results probably from the change in number and ploidy level of the stemline cell population accompanied by neoplastic development.

Adult↗

Experimental production of pulmonary granulomas: III. Plasma-cell granulomas in mice.

Endobronchial instillation of Freund's complete adjuvant (FCA) induced plasma-cell granulomas in the lungs of DD strain mice. One week after administration, plasma cells appeared in monolayered cell clusters around pulmonary arterioles running along the bronchial tree. The plasma cells increased in number with time to form granulomas consisting mainly of well developed plasma cells with an admixture of lymphocytes and macrophages. At the peak of production of granulomas (4-10 weeks), the plasma cells piled up around the arterioles and infiltrated the connective tissues surrounding the bronchioles. Germinal-centre-like foci could be demonstrated in the granulomas. The lymph nodes draining the treated lobe showed marked proliferation of plasma cells in the medullary cord, suggesting that the plasma cells passed through alveolar walls into the lung and migrated to periarteriolar connective tissue.

Animals↗

Experimental production of pulmonary granulomas. IV. Eosinophilic granuloma.

Pulmonary granulomas induced in rabbits by the endobronchial instillation of mycobacterial chemical fractions were re-examined for eosinophilic infiltration. Delayed type hypersensitivity reactions either of tuberculin type or of wax D type did not induce but rather suppressed eosinophilic infiltration in the inflamed area, although some peptidoglycans which are antigenic for the induction of immediate hypersensitivity and fatty acid fractions were weak stimulators of eosinophilic infiltration. Bacterial endotoxin, LPS, was a potent stimulator. It was found that some long chain fatty acids can cause severe eosinophilic infiltration in the induced granulomas. Arachidonic acid was the most active of those examined, so the activity of its metabolites was tested and PGE2 was found to be most active. As the eosinophilic infiltration was markedly suppressed in animals treated with a cyclooxygenase inhibitor (aspirin), the stimulators of eosinophilic infiltration were not fatty acids themselves but their metabolites, PGE2 and some others. The site of permeation of eosinophils from the circulation was found to be arteriolar in the inflamed lung. The granulomatous lesion with eosinophilic infiltration in rabbits is discussed to shed light on the aetiology of eosinophilic granuloma in the human lung.

Animals↗

Experimental production of pulmonary granulomas; II. Age dependency and immune modulation of granuloma production.

Endobronchial instillation of Freund's complete adjuvant (FCA) induced epithelioid cell granulomas in the lungs of juvenile rabbits which had been kept free from contamination with the microbiol antigens. The granulomas were named "juvenile granulomas", because, unlike FCA granulomas in adult animals, prior immunization was unnecessary for their induction. The granulomas developed in several weeks with a peak at 14 weeks of age, after which the production decreased gradually. The rate of granuloma production seemed to vary with the acquisition of skin hypersensitivity to tuberculin (OT), suggesting that granuloma production, as well as skin hypersensitivity, is in the category of T-dependent immune reactions. In fact, T-generating lymphoid organs developed in parallel with the dermal and pulmonary reactions. Thus, juvenile rabbits at about 14 weeks of age are most susceptible to the microbial antigens. This susceptibility results in the unexpected production of immune granulomas in response to depot antigens at the site of instillation. The treatment of foetal or neonatal rabbits with FCA markedly suppressed granuloma production in juveniles but not in adults and did suppress but gradually enhanced the tuberculin skin reaction. It is suggested that generation of suppressor T cells is the cause of suppression of juvenile granuloma production.

Aging↗

Arteriovenous malformation of the brain -- histological study and micrometric measurement of abnormal vessels.

An autopsy case of arteriovenous malformation (AVM) of the brain in a 29-year-old housewife was reported. Several important and characteristic findings were obtained by detailed histological examination and micrometric measurement of abnormal vessels composing the nidus of the AVM. Structural imperfectness and immaturity of their vascular wall suggested that the AVM is a histoembryogenic maldevelopment. Prominent dilatation in calibre, hypertrophy of muscular layer, hyalinization, and abnormal increasing of elastic fibers were interpreted as the result of changed cerebral hemodynamics caused by an arteriovenous fistulous communication.

Adult↗

Experimental production of pulmonary granulomas. I. Immune granulomas induced by chemically modified cell walls and their constituents.

The intrabronchial instillation of stimulants in an oily vehicle induces a solitary inflammatory focus in the rabbit lung. When heat-killed tubercle bacilli were administered to tuberculo-immune animals, a necrotizing focus with cavities was induced. Delipidation of the bacterial cells stimulated the production of a necrotizing focus. In contrast, acetylation of the mycobacterial cell walls resulted in the replacement of cavity formation with epithelioid-cell granuloma production similar to that seen after the administration of Wax D, a peptidoglycolipid fraction of the cell walls. These lesions were induced much faster than in controls, indicating that some immune mechanisms are involved. In the present study of the specific granuloma induction mechanism, the biological activities of the chemical constituents of Wax D were examined. It was concluded that specific granuloma induction is due to the long delayed hypersensitivity antigenicity of Wax D which is brought about by the conjugation of biologically inactive mycolic acid with Arthus-antigenic peptidoglycan. Wax D glycolipids with delayed-type antigenicity also take part in the induction. The intrinsic adjuvant activity of these compounds may stimulate granuloma production. The haemagglutination antigenicity and Arthus-type antigenicity of the polysaccharide or peptidoglycan moiety are not involved.

Acetylmuramyl-Alanyl-Isoglutamine↗

An extra idic(15p)(q11) chromosome in Prader-Willi syndrome.

Using a nonfluorescent AT-specific oligopeptide antibiotic, Distamycin A, on DAPI fluorescent banding of human chromosome (DA-DAPI) as described by Schweizer et al. (1978), we have detected an additional idic(15p) chromosome in a patient with typical Prader-Willi syndrome. On the basis of the evidence available in previous studies and of our own present results, we suspect that the fundamental genetic error in the syndrome is not caused by a chromosome aberration but by a gene aberration on chromosome 15.

Aneuploidy↗