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Biomedical subjects

T Matsuda

Publications and source records attributed to T Matsuda.

At least 1,531 records · Page 85Linked to original sources
PubMed1983

Surface topography of granulosa cells accompanied by fragmented oocytes.

Scanning electron microscopy of granulosa cells (GC) and granulosa cell-like structures (GCLS) revealed that both had lacy foldings, or plicae, on the surface and were identical. The plicae did not always cover the entire surface of GC or GCLS. Both structures were interconnected by multivalent processes.

Animals↗
PubMed1983

Immunocytochemical demonstration of GABAergic synapses on identified rubrospinal neurons.

GABAergic synapses on rubrospinal neurons were demonstrated with immunocytochemistry combined with intracellular injection of horseradish peroxidase. Sections containing red nucleus neurons were processed for glutamic acid decarboxylase (GAD) immunohistochemistry. GAD-immunoreactive synaptic endings formed synaptic contacts with somata and dendrites of red nucleus neurons and identified rubrospinal neurons. Our observation provides further evidence that GABA acts as an inhibitory transmitter mediating cortically evoked inhibitory postsynaptic potentials in red nucleus neurons.

Animals↗
PubMed1983

Inhibition of neuronal sodium and potassium ion activated adenosinetriphosphatase by pyrithiamin.

Since one of the electrophysiological effects of pyrithiamin, an antimetabolite of thiamin, suggested an interference with sodium pump mechanisms, the effect of pyrithiamin on Na+,K+-ATPase was investigated. We found that whereas preincubation of the antimetabolite with nonneuronal preparations of Na+,K+-ATPase produced only minimal inhibition, the enzyme derived from brain preparations was markedly inhibited. This inhibition could be prevented by thiamin but not reversed. The kinetic study showed that pyrithiamin acts in a noncompetitive manner with respect to the activation of the enzyme by ATP, Na+, and K+. Pyrithiamin inhibited Na+-dependent phosphorylation and K+-stimulated phosphatase as well as ouabain binding, and these inhibitions were parallel with that of the overall Na+,K+-ATPase reaction. In addition, the antimetabolite caused a significant change in the turbidity of the enzyme suspension. The results suggest that pyrithiamin may induce a structural change of the enzyme complex.

Animals↗
PubMed1983

Ovomucoid and ovoinhibitor isolated from chicken egg white are immunologically cross-reactive.

Ovomucoid and ovoinhibitor were isolated from chicken egg white. Enzyme-linked immunosorbent assay (ELISA) and affinity chromatography of ovoinhibitor-coupled Sepharose 4B showed that about 25% of rabbit anti-ovomucoid antibody reacted with ovoinhibitor. Ovoinhibitor required about 1000 times the concentration of ovomucoid to give 50% inhibition of anti-ovomucoid antibody binding to ovoinhibitor in the plate-binding ELISA. These results suggested that ovoinhibitor possesses antigenic determinants which are conformationally homologous with those of ovomucoid and cross-react with anti-ovomucoid antibodies.

Animals↗
PubMed1983

Blocking effect of trypsin associated with ovomucoid on the antibody binding to ovomucoid.

Ovomucoid-trypsin association complex was prepared by incubating chicken egg white ovomucoid with bovine trypsin. The reactivity of ovomucoid-trypsin complex was investigated by immunodiffusion, quantitative precipitation and enzyme-linked immunosorbent assay (ELISA). It was demonstrated that the association of trypsin with ovomucoid hindered the binding of the specific antibody at some antigenic sites of ovomucoid by lowering the antibody-binding affinity of these sites. The anti-ovomucoid antiserum was absorbed with ovomucoid-trypsin complex, and non-absorbed antibody was collected by immunoaffinity chromatography of ovomucoid-coupled Sepharose 4B. The antibody blocked the trypsin-inhibitory activity of ovomucoid in a molar ratio (antibody/ovomucoid) of about 1.2:1. The findings suggested that at least one antigenic site is located near the reactive site of trypsin inhibition (Arg89 decreases Ala90) of ovomucoid.

Animals↗
PubMed1983

Noncardiac pulmonary edema precipitated by tracheal intubation in patients with inhalation injury.

Ten patients with body surface burn and clinical evidence of inhalation injury developed transient, reversible pulmonary edema within 5 min after endotracheal intubation. Hemodynamic studies within 1 hr after intubation revealed normal cardiac output and pulmonary artery wedge pressure (WP). Additionally, in the latter 4 patients, protein concentration of edema fluid (EF) aspirated from the trachea was 58-104% of plasma (P) total protein. These findings suggest that altered capillary permeability was responsible for this transient pulmonary edema. It is postulated that glottic generated expiratory retard may increase alveolar pressure, thus preventing pulmonary edema. Bypass of glottis by tracheal intubation may render alveolar pressure atmospheric and facilitate edema formation.

Adolescent↗