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T Hato

Publications and source records attributed to T Hato.

44 records · Page 3Linked to original sources
PubMed1987

Phenotypic and genotypic analysis of chronic myelogenous leukaemia with T lymphoblastic and megakaryoblastic mixed crisis.

A case of blast crisis in chronic myelogeneous leukaemia (CML) in which two distinct cell lineages were involved is presented. The phenotype of blasts in lymph nodes was T11 (CD2)+, Ia+, TdT+, suggesting T cell lineage. On the other hand, blasts in bone marrow and peripheral blood expressed platelet glycoprotein IIb/IIIa complex on their surface, suggesting megakaryocyte lineage. Cytogenetic analysis of lymph node and bone marrow cells revealed the abnormalities, inv(7) (p15q34) and t(1;3) (q23;q21), respectively, as well as the presence of the Ph1 chromosome in both cell types. Rearrangement of the T cell receptor beta-chain gene was detected in lymph node blasts, although blast cells in peripheral blood showed a germ line configuration. The involvement of T cell and megakaryocyte lineages in the blast crisis phase of CML was confirmed in our phenotypic and genotypic analysis, and the pathogenic association between blast crisis lineages and the additional chromosome abnormalities present is discussed.

Blast Crisis↗
PubMed1984

Platelet cyclo-oxygenase deficiency in a Japanese.

A case of platelet cyclo-oxygenase deficiency in a Japanese was investigated. There was a marked decrease of aggregation with collagen and absence of aggregation with epinephrine and arachidonic acid. The platelet response to a labile aggregation stimulating substance (LASS) was normal. There was no biosynthesis of prostaglandin endoperoxides from arachidonate. The platelets, including granular volume, showed no ultrastructural abnormalities. The responses to various inducers of platelet aggregation, except for arachidonate, were different from the cases described by others. It is concluded that the defective platelet function, due to a deficiency of platelet cyclo-oxygenase, is heterogeneous.

Adult↗
PubMedDate not supplied

Discrepancy between antiplatelet antibody activities detected by immunoblot procedure and platelet counts in idiopathic thrombocytopenic purpura.

By immunoblot procedure it is possible to identify the pathogenic autoantibody responsible for platelet destruction in idiopathic thrombocytopenic purpura (ITP). We assessed the relationship between antiplatelet antibody activities detected by this technique and clinical thrombocytopenia in a patient with ITP whose antiplatelet autoantibody was directed toward an 85-kDa antigen. In this patient, over a 2-year-period, the platelet counts were not correlated with the levels of antiplatelet autoantibody detected by immunoblotting. The present observations suggest that IgG autoantibody directed toward a specific antigen is not necessarily a critical determinant of the degree of thrombocytopenia, and that factors other than IgG-Fc-receptor-mediated platelet destruction are also important in the determination of the disease activity in ITP.

Adult↗