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Biomedical subjects

Y Inada

Publications and source records attributed to Y Inada.

At least 397 records · Page 22Linked to original sources
PubMed1979

Fibrin membrane endowed with biological function. IV. Formation of cross-links between fibrinogen (or fibrin) and ribonuclease by transglutaminase.

Transglutaminase from guinea pig liver catalyzed the formation of cross-links between fibrinogen (or fibrin) and ribonuclease. Using transglutaminase, immoblized ribonuclease was prepared by two separate methods: (1) fibrinogen-ribonuclease conjugates formed by transglutaminase were treated with thrombin to make fibrin membrane bound covalently to the enzyme; (2) fibrin polymer formed from fibrinogen with thrombin was covalently bound to ribonuclease by transglutaminase to make fibrin-ribonuclease conjugates.

Animals↗
PubMed1979

[On the phenomena of multiple extravasations of contrast medium in cerebral angiogram of the cases of hypertensive intracerebral hematoma (author's transl)].

It is interesting to note the pathological findings that the rupture of multiple microaneurysms in the basal ganglia appears to be the cause of the hypertensive intracerebral hematoma. But there is few report that the carotid angiogram demonstrated multiple leakages of contrast medium of intracerebral hematoma in vivo than in Westberg's postmortem angiogram. The authors experienced 15 cases of hypertensive intracerebral hematoma whose cerebral angiogram showed extravasation of contrast material. It was fifty-seven per cent of which angiogram within 6 hours after the stroke showed leakage of contrast medium. However, there was remarkably decreased appearance of the extravasation after 9 hours after the stroke. Moreover, emphasis showed be placed upon the facts that eleven cases of 15 cases showed more than two adjacent spotty extravasations of contrast medium and that six cases demonstrated the simultaneous multiple leakages of contrast material from more than two lentriculostriate arteries. These angiographic findings has led us to the conclusion that there is intimate correlation between the large hematoma and multiple ruptures of the microaneurysms of lentriculostriate arteries.

Adult↗
PubMed1978

Functional consequences of tryptophan modification in human fibrinogen.

When human fibrinogen was modified with H2O2, inter- and intra-molecular cross-links of fibrinogen were formed, accompanied with oxidation of tryptophan, methionine and tyrosine residues. These cross-links may be closely associated with oxidation of tryptophan residues. The polymerization activity of fibrinogen with thrombin was decreased markedly by this modification. Modification of tryptophan residues in fibrinogen was also performed with 2-hydroxy-5-nitrobenzyl bromide. Modification of two out of a total 78 tryptophan residues in the molecule with the reagent led to the intensification (1.7 times) of the polymerization activity with thrombin and further modification of the next two residues led to complete loss of the polymerization activity. The first two tryptophan residues to be modified are in Fragment D, and the next two occur in Fragment E.

2-Hydroxy-5-nitrobenzyl Bromide↗
PubMed1978

Four states of tyrosine residues in the fibrinogen molecule.

The ionization of tyrosine residues in fibrinogen was studied by a spectrophotometric method. The total of 100 tyrosine residues in the fibrinogen molecule was classified into four states: (1) 28 tyrosine residues with pK 10.1 (m = 1.0). (2) tyrosine residues with pK 11.5 (m = 1.0), (3) 20 tyrosine residues with pK 12.2 (m = 3.0) and (4) 10 tyrosine residues non-ionizable. When fibrinogen was treated with 4 M guanidine . HCl, all of the tyrosine residues became ionizable with the ionization characteristics of pK 10.1 (m = 1.0). The ionization characteristics of tyrosine residues in plasmin-digested fibrinogen were similar to those of fibrinogen, while in CNBr-treated fibrinogen they were fairly different. The value, m, stands for the number of hydroxyl ions involved in the ionization of a tyrosine residue.

Fibrinogen↗
PubMed1978

Photooxidation of fibrinogen in the presence of methylene blue and its effect on polymerization.

Human fibrinogen was illuminated in the presence of methylene blue. The resulting photooxidized fibrinogen was devoid of polymerization activity and thrombin-induced coagulability. The initial rate of the thrombin catalysed release of fibrinopeptides from photooxidized fibrinogen was normal. It was shown that illumination of photooxidized fibrinogen and photooxidized fragment N-DSK caused the modification of histidine residues. Tryptophan residues were also modified. When fibrinogen was photooxidized immediately after the addition of thrombin, the capacity to polymerize was lost. The inhibition of polymerization was less marked when oxidation was initiated at the time when polymerization began or thereafter. Photooxidized fibrinogen acts as an inhibitor of the polymerization of fibrin monomers. Photooxidized fibrinogen has affinity for thrombin-activated fibrinogen-Sepharose and thrombin-activated fragment N-DSK-Sepharose. When the former conjugate is illuminated in the presence of methylene blue its affinity for fibrinogen is decreased. It is concluded that the fragment N-DSK domain of fibrinogen is affected by photooxidation.

Amino Acids↗
PubMed1978

Antidiuresis induced by beta1- and beta2-adrenergic agonists in ethanol-anesthetized rats.

The beta1- and beta2-components in antidiuresis and sodium retention induced by beta-adrenergic agonists were analysed in ethanol-anesthetized, water-diuretic rats. Intravenous infusions of isoprenaline, salbutamol and carbuterol did not affect insulin clearance but increased plasma renin concentration to the same same extent. Propranolol completely blocked the decreases in urine volume (V) and urinary sodium excretion (UNaV) induced by isoprenaline; practolol (beta1-blocker) inhibited only the decrease in UNaV and butaxamine (beta2-blocker) inhibited only the decrease in V. The ratios of doses of beta-agonists which decreased UNaV and by 50% (ED50 UNaV decrease/ED50 V decrease) were 0.34, 0.68, 1.56 and 2.36 for isoprenaline, tretoquinol, salbutamol and carbuterol, respectively. This increasing order of the ratios coincided with the order reported for the preponderance of the beta2- over beta1-component of these agonists. These results indicate that the decrease in UNaV induced by beta-agonists is related to beta1 stimulation, while the decrease in V is related to beta2 stimulation.

Adrenergic beta-Agonists↗