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H Tsuchimochi

Publications and source records attributed to H Tsuchimochi.

40 records · Page 3Linked to original sources
PubMed1984

Distribution of myosin isozymes in human atrial and ventricular myocardium: comparison in normal and overloaded heart.

We have prepared monoclonal antibodies specific for either atrial or ventricular myosin and defined the isomyosin composition of myocardium in normal and overloaded human hearts. In the atrial myocardium, normal isozymic pattern was V1 dominant which converted to being V3 dominant in an overloaded condition. In contrast, normal isomyosin pattern of the ventricular myocardium was exclusively V3 dominant, and only a small change in the proportion of isomyosin was observed in an overloaded condition. From this, we conclude that isozymic changes in cardiac myosin could occur in the human heart to meet increased work induced by cardiac overload. However, the physiological importance of these isomyosin redistributions in human myocardium seems to be much greater in the atrium than in the ventricle, since larger amounts of V1 isomyosin which could be transformed to V3 isomyosin were present in the atrial myocardium.

Adenosine Triphosphatases↗
PubMed1984

Isozymic changes in myosin of human atrial myocardium induced by overload. Immunohistochemical study using monoclonal antibodies.

An immunohistochemical study using monoclonal antibodies specific for the heavy chains of either human atrial (HC alpha) or ventricular (HC beta) myosin was performed to clarify the distribution of each isozyme in normal as well as pressure-overloaded human hearts. In normal human ventricles, all muscle fibers were stained by a monoclonal antibody (HMC14) specific for HC beta, whereas a small number of fibers reacted with a monoclonal antibody (CMA19) specific for HC alpha. In contrast, in normal human atria, almost all muscle fibers were stained by CMA19, and a relatively larger number of muscle fibers also reacted with HMC14. Furthermore, in pressure-overloaded atria, muscle fibers reactive with HMC14 were strikingly increased while those reactive with CMA19 showed a corresponding decrease. The extent of this isozymic redistribution was in good correlation with atrial pressure. These results not only confirmed the existence of isoforms of myosin heavy chain in human hearts, but also demonstrated that redistribution of iso-myosins could occur as an adaptation to pressure overload.

Animals↗
PubMedDate not supplied

Treatment of infective endocarditis with granulocyte colony-stimulating factor.

Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein hormone which stimulates the proliferation and differentiation of a subset of granulocyte precursors and enhances some functional activities of mature neutrophils. We tested the effects of G-CSF on a patient with intractable infective endocarditis. The white blood cell count was increased 3-fold and the inflammatory reactions such as C-reactive protein and erythrocyte sedimentation rate were completely normalized without any side effects. This is the first report describing the use of G-CSF for infective endocarditis. Administration of G-CSF might be suitable for treating intractable infections which cannot be controlled by antibiotics alone.

Aged↗