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Biomedical subjects

H Mizukoshi

Publications and source records attributed to H Mizukoshi.

36 records · Page 2Linked to original sources
PubMed1977

The metabolism of 17beta-estradiol-3-glucosiduronate and estrone-3-glucosiduronate in the rabbit.

[6, 7-3H]-17beta-Estradiol-3-glucosiduronate, [6, 7-3H]-estrone-3-glucosiduronate or [6, 7-3H]-estrone was administered intravenously into the rabbit, and analysis and identification of the urinary metabolites were carried out. In either case, the major urinary metabolite was found to be a diconjugate. The sequential enzymic hydrolysis indicated that this diconjugate was glucosiduronate-N-acetyglucosaminide of 17alpha-estradiol. From these results, the conversion of the estrogen glucosiduronate into a diconjugate was thought a rather universal phenomenon in the rabbit.

Animals↗
PubMed1976

Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma.

The authors describe studies performed on material aspirated from chronic subdural hematomas. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 mug/ml with an average of 2604 mug/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that if a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.

Cerebral Hemorrhage↗
PubMed1975

Further studies on the existence of a sensitizing factor to pressor agents in hypertension.

Further studies are reported on the existence of a sensitizing factor in plasma of hypertensive subjects, which increases the vascular sensitivity to pressor agents when injected iv into nephrectomized rats. Plasma samples from normotensive subjects, patients with malignant hypertension, normotensive dogs, and dogs with experimental renovascular hypertension were fractionated on Bio-Gel P-10 columns after cold acetone precipitation, and on DEAE-cellulose columns eluted with sodium chloride and pH gradients. The effect of the various fractions on the vascular sensitivity to angiotensin was tested utilizing nephrectomized rats. The sensitizing activity was found only in fractions obtained from plasma of hypertensive patients and dogs and it was concentrated primarily in three fractions. Th results suggest that the sensitizing factor is negatively charged at neutral pH and it could be a polypeptide or a small protein.

Angiotensin II↗