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Biomedical subjects

T Hayasaka

Publications and source records attributed to T Hayasaka.

At least 37 records · Page 2Linked to original sources
PubMed1983

Mechanism of resistance to some cephalosporins in Staphylococcus aureus.

The mechanism of resistance to some cephalosporins in Staphylococcus aureus strains was investigated with high-pressure liquid chromatography and nuclear magnetic resonance spectrometry. Drug inactivation by penicillinase was found to be the main mechanism of resistance to cefazolin, cephaloridine, and cephalothin in S. aureus.

Cephalosporins↗
PubMed1982

[C-type murine leukemia virus and the pathogenesis of necrotizing arteritis and glomerulonephritis in MRL/1 mice].

A comparative immunopathological and electron microscopic study of vasculitis and glomerulonephritis in autoimmune mice (B/W F1, SL/Ni, MRL/1) was performed. The pathogenesis of vasculitis in B/W F1 mice is due to the deposition of circulating murine leukemia virus (MuLV) gp70-immune complexes in the subendothelial space of vascular walls. Whereas, the vasculitis in SL/Ni mice is mediated by the budding of MuLV particles from vascular smooth muscle cells and the humoral immune response (Gross natural antibody) to virions and MuLV related cell surface antigens of vascular smooth muscle cells. The vasculitis in MRL/1 mice seems to be mediated mainly by the deposition of gp 70-immune complexes in vascular walls. However, the perivascular infiltration of thy1 . 2 antigen positive T-lymphocytes in an early stage of vasculitis suggests that the cellular immune response is, at least in part, important for the initiation of vasculitis in MRL/1 mice. The collective evidence suggests that several immunologic mechanisms are at works in the production of naturally occurring vasculitides in B/W F1, SL/Ni, and MRL/1 mice. The common pathogenesis of glomerulonephritis in B/W F1, SL/Ni and MRL/1 mice is the deposition of circulating gp70-immune complexes in the glomeruli. In addition, in the case of SL/Ni mice, glomerulonephritis is in some part initiated by local formations of the immune complex in the mesangium. The occurrence of vasculitis in MRL/1 mice is markedly accelerated by the treatment of methoxamine hydrochloride (Mexan), as was shown previously in SL/Ni mice.

Animals↗
PubMed1981

Comparative immunopathologic studies of thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome and disseminated intravascular coagulation.

The vascular lesion of thrombotic thrombocytopenic purpura was characterized by two distinct types of changes in the arteriole of the heart and brain: (1) multiple incomplete vascular occlusions due to the subendothelial deposits composed of a homogeneous fibrin fibrinogen-like substance and platelets without the formation of polymerized fibrin; (2) vascular wall thickening due to the intramural granular deposits of IGM and beta 1C. A patient with hemolytic-uremic syndrome 9 days after the onset of the disease, exhibited (1) the formation of fibrin-thrombi in the glomerular capillary lumens, and (2) the granular deposits of IgM and beta 1C along the glomerular capillary walls and in the mesangium. In contrast, the case in which the symptoms subsided five weeks after the onset exhibited neither fibrin-thrombus formation nor the deposits of IgM and beta 1C in the glomeruli. The vascular lesions of disseminated intravascular coagulation accompanied by pancreas carcinoma was located mainly in the capillaries, and were characterized by the formation of numerous fibrin-thrombi. Although the glomeruli contained numerous thrombi, there was neither endocapillary proliferation nor deposits of immunoglobulins and complement components.

Adult↗