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Biomedical subjects

Y Umeda

Publications and source records attributed to Y Umeda.

At least 145 records · Page 8Linked to original sources

Adrenal epinephrine in hyperuricemia induced by hypothalamic stimulation of the rat.

Peripheral neurological mechanisms involved in hyperuricemia following ventromedial hypothalamic electrical stimulation was studied in the conscious rat. The intensity of 0.2 mA was near the maximum intensity of stimulation current producing a linear increase in plasma uric acid throughout the 15-min period of stimulation, as well as a subsequent rise and fall of plasma allantoin. Bilateral adrenal demedullation abolished the stimulation-induced hyperuricemia and markedly impaired the accompanying rise of allantoin. Prior treatment of the animal with hexamethonium significantly inhibited the uric acid increase, but did not reduce the allantoin elevation so markedly. Moreover, propranolol eliminated both responses of these plasma purine metabolites, whereas phentolamine greatly increased the response. It is concluded therefore that the hypothalamic stimulation-induced rise of plasma uric acid is the result of acceleration of epinephrine release from the adrenal medulla and that, whereas some unknown extra-adrenal mechanism may be partially involved, the primary part of the accompanying allantoin elevation is explained by the combined effects of the increased uric acid and the hepatic uricase.

Adrenal Medulla↗

Cerebrovascular accidents among users of oral contraceptives. An analysis of Japanese cases.

The authors investigated 5 Japanese cases of cerebrovascular accidents among users of oral contraceptives; 4 previously reported and 1 of their own. It is estimated that 200,000 women in this country use oral contraceptives, but, as of the present, only 5 cases of resultant cerebrovascular accidents have been reported. Of particular interest is the fact that 3 of the women had undergone multiple artificial abortions. The appearance of the side effects was dose independent and the symptoms were aggravated for 2 weeks after the cessation of medication.

Abortion, Induced↗

Plasma ADH levels during heart surgery.

1) Plasma ADH levels measured by bioassay in the group with extracorporeal circulation were 2.3 +/- 0.6 muu/ml before surgery and 6.6 +/- 1.8 muu/ml during anesthesia. They increased to 196.5 +/- 62.3 muu/ml or about 100 times greater than before surgery during cardiopulmonary bypass. 2) In the group without extracorporeal circulation, plasma ADH levels were 1.5 +/- 0.9 muu/ml before surgery and increased to 44.1 +/- 15.2 muu/ml during operation. 3) After operation decrease in plasma ADH level was relatively rapid in both groups. It became three times that of the control level in the morning of the next day. 4) Marked increase in plasma ADH level during cardiopulmonary bypass was much the same as it was during hemorrhagic shock in dog experiments. 5) Fall in mean arterial blood pressure and loss of pulsatile blood flow will play main roles in this marked increase in ADH during cardiopulmonary bypass through stimulation of arterial baroreceptors and probably chemoreceptors. 6) In two cases with mitral stenosis, increase in plasma ADH during cardiopulmonary bypass was lesser than the other heart diseases.

Adult↗

Evaluation of a solid-phase enzyme immunoassay for insulin in human serum.

We describe a "sandwich-type" enzyme immunoassay for insulin in serum, in which antibody Fab'-beta-D-galactosidase conjugate and an antibody-immobilized silicone rubber solid-phase are used. The interference by serum factors with the solid-phase enzyme immunoassay can now be removed by using a buffer containing gelatin. Serum samples of 50 microL can be analyzed by the enzyme immunoassay, which is as sensitive as radioimmunoassay for human insulin. Our results correlate well with those for radioimmunoassay (r = 0.97, slope = 0.92, y-intercept = 4.6 milli-int. units /L for 181 samples). Between-assay and within-assay coefficients of variation are less than 15% over the useful ranges of the assay (5--160 milli-int. units/L).

Evaluation Studies as Topic↗

Studies on delayed hypersensitivity to protein antigen. Induction of delayed hypersensitivity by chemically modified antigen.

it was shown in our previous paper that mice primed with chemically modified bacterial alpha-amylase (BaA), which was neither cross-reactive with anti-BaA antibody nor able to induce a humoral anti-BaA response, developed enhanced responses to a subsequent challenge with native BaA and that the magnitude of the immunological memory was closely related to the priming dose of modified BaA. This paper describes the experimental conditions for induction of delayed hypersensitivity (DH) by modified BaA in relation to the development of immunological memory for antibody response to native BaA. Mice primed with either an intraperitoneal (i.p.) or subcutaneous (s.c.) injection of modified BaA in complete Freunds adjuvant (CFA) developed enhanced anti-BaA as the immunogen and modified BaA as the eliciting antigen, the relationship of anti-BaA responses to a subsequent challenge with BaA. In contrast, when mice were immunized with an s.c. injection of the modified BaA only, a significant level of DH to native BaA could be induced, as measured by the footpad reaction (FPR). The highest degree of DH was observed in mice given 50 micrograms of modified BaA. DH was detectable within 5 days and persisted for 25 days after immunization. In the reciprocal combination of native BaA as the immunogen and modified BaA as the eliciting antigen, the relationship of anti-BaA responses to DH was examined. The primary anti-BaA responses induced by an i.p. injection of large doses of BaA was markedly higher than those induced by an s.c. injection, while DH was exhibited only in mice given s.c. injection of BaA in CFA. With respect to DH to native BaA induced by the modified BaA, it was shown that C3H/He mice were high and C57BL/6 mice were low responders.

Amylases↗

Adrenergic regulation of the plasma levels of purine metabolites in the rat.

The effects of i.v. infusions of catecholamines on the plasma levels of uric acid and allantoin were investigated in the conscious rat. Isoproterenol and epinephrine, in this decreasing order of potency, remarkably elevated both uric and allantoin levels. Norepinephrine did not affect these purine metabolite levels. These effects of isoproterenol and epinephrine were completely abolished by propranolol. Phentolamine, on the contrary, slightly potentiated the effects of epinephrine. In contrast to i.v. fusion, s.c. injection of epinephrine had no effect, but, after prior treatment of animals with phentolamine, elicited striking increases in the plasma purine metabolite levels. Catecholamines thus caused hyperuricemia with a rise in plasma allantoin, both effects being mediated via beta-adrenoceptors and alpha-adrenergic mechanism sometimes functions in such a manner as to mask or inhibit this beta-mediated response.

Allantoin↗

The enzymatic spectrofluorimetric determination of uric acid in microsamples of plasma by using p-hydroxyphenylacetic acid as a fluorophor.

A sensitive spectrofluorimetric micromethod for the determination of uric acid is presented together with its application to human and rat plasma. The method is based on the reactions or uricase and peroxidase coupled with p-hydroxyphenylacetic acid as a fluorophor. There is a very wide range of proportionality between the concentration of uric acid and the increase of fluorescence intensity. 10 ng of uric acid is still determinable. At most 25 mul of human or 50 mul of rat plasma is sufficient to obtain the accurate valve of endogenous plasma uric acid concentration. The uric acid levels of normal human and rat plasma measured by present method were within the ranges of concentrations previously reported. A comparative study of this method with a standard assay method is also presented.

Animals↗