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Biomedical subjects

F Numano

Publications and source records attributed to F Numano.

At least 163 records · Page 9Linked to original sources
PubMed1991

Immunocytochemical analysis of the atherosclerotic lesion.

We have performed immunocytochemical investigations on the distribution of various cell types and proliferating cells in human atherosclerotic lesions. Studies include fibrocellular tissue response following percutaneous transluminal coronary angioplasty (PTCA) or aortocoronary (A-C) bypass operation using monoclonal antibodies specific to smooth muscle cells, macrophages, endothelial cells, lymphocytes and proliferating cell nuclear antigen (PCNA). All studies were performed on methanol-Carnoy's-fixed, paraffin-embedded tissues. The cellular composition of the following three types of raised lesions were analyzed: 1) fibro-fatty lesions composed almost exclusively of macrophages; 2) fibrous lesions predominantly composed of smooth muscle cells; 3) advanced plaques characterized by complex layers of smooth muscle cells and macrophages with considerable variation from region to region. Also noted were foci of medial and even intimal vascularization subjacent to the more advanced plaques. Cells encountered within the fibrous intimal thickening in the vein graft or fibrocellular tissue response following PTCA were predominantly smooth muscle cells in origin. Some cells were PCNA-positive. These studies demonstrate the application of monoclonal antibody technology to the study of the cellular composition and cell kinetics of human atherosclerotic lesions.

Antibodies, Monoclonal↗
PubMed1990

Antiplatelet therapy for atherosclerotic disorders.

Recent studies have revealed the important roles of platelets in atherogenesis via vascular injury. Our in vivo and in vitro studies clearly demonstrate that activated platelets directly inflict injury to vascular endothelial cells, which is associated with a decrease in intracellular cyclic AMP levels in vascular tissues. Antiplatelet therapy is clinically important not only for the prevention of thrombotic episodes but also for the prevention of vascular injury and atherosclerosis. A small dose of aspirin (80 mg) induces clinically hypoaggregativeness of platelets with concomitantly decreased levels of thromboxane A2 in plasma. Our clinical study involving more than 3 years of treatment with small doses of aspirin demonstrated favorable therapeutic effects characterized by hypoaggregation of platelets and increased levels of cAMP and 6-keto PGF1 alpha in plasma which will aid in the prevention of atherosclerosis.

Animals↗
PubMed1990

Experimental studies on vein graft atherosclerosis (I). Histochemical studies using monoclonal antibodies for smooth muscle cells and macrophages.

Vein graft atherosclerosis characterized by smooth muscle cell proliferation has become the most serious cause of late graft failure. This study was designed to elucidate why marked histological differences occur in atherosclerotic changes between the vein graft and the artery. Fourteen rabbits underwent autonomous transplantation of femoral vein sections (10-12 mm in length) into femoral arteries on the same side. They were then kept on either commercial or 1% cholesterol diet. At 4, 8, 15 and 30 weeks after the operation, they were sacrificed and histochemical & immunocytochemical studies on atherosclerotic changes found in graft and arteries were carried out, using monoclonal antibodies for macrophages (RAM 11) and smooth muscle cells (HHF 35). Atherosclerotic lesions found in arteries of rabbits fed by cholesterol for more than 8 weeks were characterized with the accumulation of macrophage-derived foamy cells with fibrous caps. In contrast, the lesions found in the grafts of the same rabbits were occupied with proliferating smooth muscle cells and very few macrophages. Furthermore, in lesions of the vein grafts of rabbits fed cholesterol for 4 weeks, macrophages were rather frequently encountered in the bottom of the lesions and/or its medial layer, scattering and sometimes forming mass-lesions. These results may suggest structural differences in the vein with its thin and sparse internal elastic lamina and with its thin medial layer, allowing macrophages to pass easily through the elastic lamina and scatter into the media. This may be the reason why autonomous vein graft atherosclerosis is mainly composed of proliferated smooth muscle cells.

Animals↗
PubMed1989

In vitro study of vascular endothelial injury by activated platelets and its prevention.

We performed an in vitro study to assess injury to vascular endothelial cells by platelets. Cultured endothelial cells isolated from fetal bovine aorta were used. Addition of human platelets, activated by collagen or lysed by sonication, to the culture dish resulted in dose- and time-dependent damage to the cells as estimated by [3H]adenine release. Analysis of [3H]adenine nucleotides by thin-layer chromatography on PEI-cellulose revealed decreased intracellular ATP content in the cells treated with platelet lysate. The medium contained AMP and adenosine, the latter increasing following the treatment of the cells. Of the substances released by the activated platelets, thromboxane A2 (TxA2) and serotonin caused cell damage. Platelet-derived growth factor (PDGF), however, did not damage the endothelial cells up to a concentration of 200 ng/ml. Pretreatment of the cells with methysergide (10(-6) M) or ONO 3708 (10(-5) M), a TxA2 antagonist, only partially prevented the damage, while ZK 36374 (10(-6) M), a prostacyclin analog, and 3-isobutyl-1-methylxanthine (IBMX; 10(-3) M), a phosphodiesterase inhibitor, potently inhibited injury. We conclude that the substances released from activated platelets may injure endothelial cells in an additive or synergistic manner and that agents which produce effects that elevate cyclic AMP levels may protect the cells from damage induced by the platelets.

Adenine Nucleotides↗
PubMed1989

Hereditary factors in Takayasu disease. III. Polymorphism of human complements.

Genetic polymorphisms in C2, C4, C6, C7 and BF alleles of human complement were studied in 80 Japanese patients with Takayasu disease, and compared with those of 433 normal Japanese. Statistically significant high frequencies of C4A2 (chi 2: 27.2; p less than 0.01) and C4BQ0 allotype (chi 2: 8.7; p less than 0.01) were found in patients with Takayasu disease. Furthermore, all patients carrying C4A2 were found to be associated with C4BQ0. In addition, patients with HLA Bw52 were strongly associated with C4A2BQ0. In 5 patients homozygous C4BQ0 was found. These data suggest that some genetic factor(s) may contribute to the pathophysiological condition of Takayasu disease, which is strongly associated with the complotype of HLA Bw52-C4A2BQ0.

Adult↗
PubMed1988

Immunocytochemical investigation of atherosclerotic changes observed in aortocoronary bypass vein grafts using monoclonal antibodies.

The authors have performed immunocytochemical surveys on atherosclerotic changes observed in saphenous vein aortocoronary bypass grafts, comparing the changes occurring in coronary and aortic lesions. The two monoclonal antibodies used in this study were obtained by T. Tsukada. One of them, named HHF35, exhibited specificity to smooth muscle cells; the other, named HAM56, was specific to macrophages. These immunocytochemical studies clearly demonstrated that cells encountered within the fibrous intimal thickening in the vein graft were inevitably smooth muscle cell in origin. Macrophages were seldom seen in the grafts examined. In contrast to vein grafts, macrophages were noted within the intima of all specimens from arterial atherosclerotic lesions obtained from the same patients. These studies suggest a difference in the progression of intimal thickening between the venous graft and the arterial atherosclerotic lesions.

Antibodies, Monoclonal↗
PubMed1987

Human leucocyte antigen in variant angina.

Human leucocyte antigen analysis of 45 patients with variant angina was performed to determine the presence of causative genetic factor(s). A significantly low frequency of human leucocyte antigen DQ omega 3 was found in these patients, as compared with that in 152 normal Japanese adults. There were no differences in frequencies of antigens between patients with normal and those with atherosclerotic coronaries. These data suggest that some genetic factor(s) may contribute to the pathogenesis of coronary spasm.

Angina Pectoris, Variant↗