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Biomedical subjects

Y Tamura

Publications and source records attributed to Y Tamura.

At least 721 records · Page 40Linked to original sources
PubMed1979

A rapid and precise method for the determination of vitamin D3 in rat skin by high-performance liquid chromatography.

In order to develop the investigations into photobiogenesis of vitamin D3, a rapid and precise method for the determination of the vitamin in rat skin was established by using high-performance liquid chromatography (HPLC). The proposed method included saponification of small pieces of rat skin, extraction of the unsaponifiable matter and application to HPLC using "Zorbax SIL" (straight-phase) as an adsorbent and 0.5% isopropanol in n-hexane as a mobile phase. The applicable lower limit of the method was 2ng of vitamin D3/cm2 of subcutaneous tissue-removed skin and it was possible to assay a concentration higher than 2 ng/cm2. The proposed method was applied to determine the content of vitamin D3 in rat skin obtained from in vivo and in vitro irradiation experiments. In the in vitro experiment, the yield of vitamin D3 increased in proportion to the irradiation time. On the other hand, the yield in the in vivo experiment showed a proportional increase similar to the in vitro experiment until 60 min irradiation, while a nearly constant value was obtained by irradiation for longer than 60 min. When the rat skin obtained from the in vitro experiment was irradiated with monochromatic UV rays in the range s60-350 nm, the most effective wavelength for the formation of vitamin D3 was confirmed to be 303 nm, which differs from the result obtained from the experiment in a test tube (295 nm). Moreover, the yield of vitamin D3 by irradiation with UV rays below 288 nm was extremely low, which again differed from the results of a test tube experiment. These differences were thought to be due to the filter effect of the malpighian layer in the epidermis of rat skin.

Animals↗
PubMed1979

Effects of glycyrrhetinic acid and its derivatives on delta 4-5 alpha- and 5 beta-reductase in rat liver.

The effect of glycyrrhetinic acid (GA) and its derivatives on delta 4-5 alpha- and 5 beta-reduction of cortisol, aldosterone and testosterone was investigated on rat liver preparations. In vitro studies demonstrated that GA and its derivatives inhibited 5 beta-reduction to a much greater extent than 5 alpha-reduction. When GA or glycyrrhizin (GL) were administered, 5 beta-reductase activity was significantly suppressed. On the contrary, 5 alpha-reductase was markedly increased though its meachnism remains to be clarified. In human beings 5 beta-reductase is quantitatively the major enzyme and plays an important role in the regulation of cortisol and aldosterone metabolism. Thus from the studies presented here, it can be presumed that the suppression of 5 beta-reductase activity by GA or GL administration may delay the clearance of corticosteroids and prolong the biological half-life of cortisol resulting in the synergism of these steroids and GA or GL.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

A method using fibrin-fixed Blue Dextran for determining the plasmin and plasmin inhibitor activities in human plasma.

The fibrinolytic activity of plasmin was determined by incubating with fibrin-fixed Blue Dextran as a substrate, the Blue Dextran released being proportional to the plasmin activity. The applicability of this method for rapid and accurate evaluation of fibrinolytic activity was demonstrated by dose-response curves with purified plasmin, plasmin generated by urokinase in human plasma and euglobulin. The method can also be used to determined plasmin inhibitors in plasma.

Coloring Agents↗
PubMed1978

An electron microscopic study of the surface structures and hemadsorption on chick embryo cells infected with rabies virus.

Characteristic alterations at the surface of chick embryo cells infected with the HF-TC strain of rabies virus and the binding sites of hemadsorption were studied employing both scanning and transmission electron microscopes. The initial alteration of the cell surface structure revealed by scanning electron microscopy was an appearance of elongated and reticulated microvilli on the 2nd day after virus inoculation. On the 3rd day, numerous bullet-shaped virions could be seen budding as single, tetrapod-like structures and as radial projections both from the perikarya and microvilli. Thereafter, elongation of microvilli, formation of numerous blebs in various sizes, disappearance of filopodia, and rounding up of infected cells were observed as characteristic cytopathic effects by rabies virus infection. The attachments of goose erythrocytes to the infected cells occured in two forms. The one was adsorption of erythrocytes to the cell surface involving microvilli and filopodia in the absence of detectable virus, and the other was adsorptio n of erythrocytes to the virus particles budding from cell surface. The former could be seen from the early stage of infection through the end of observation period, while the latter was observed only on and after the 3rd day after virus inoculation. These findings were also confirmed with transmission electron microscopy.

Cell Membrane↗
PubMed1978

Adrenal steroidogenesis and hepatic corticosteroid metabolism in hypertensive rats.

In vitro metabolism of progesterone and cholesterol by the adrenal glands and hepatic delta 4-reductase activity of SHR and ARH were investigated to clarify the possible hyperactivity of the pituitary-adrenal axis and abnormal steroid metabolism in SHR. The increased conversion rate of progesterone to 11 beta-hydroxyprogesterone, corticosterone and 18-hydroxy-deoxycorticosterone and the increased biosynthesis of pregnenolone from cholesterol were noted in ARH, which were similar to those seen with chronic ACTH administration. On the other hand, adrenal steroidogenesis in SHR showed no difference from that of control. Therefore the apparently normal adrenal steroidogenesis in SHR may suggest that the adrenal gland is not involved in the spontaneous hypertension of rats. The markedly decreased hepatic delta 4-reductase activity in ARH and SHR was observed in this investigation.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

Quantitative and qualitative estimation of urinary kallikrein in a patient with Bartter's syndrome.

Urinary kallikrein in a patient with Bartter's syndrome was remarkably higher than normal. Indomethacin treatments increased serum potassium concentration and urinary Na/K ratio, and improved the response of blood pressure to angiotensin II infusion, while it decreased plasma renin activity, plasma aldosterone and urinary kallikrein. The purified urinary kallikrein had one component of the iso-electric point 4.3 by isoelectric focusing using Ampholine system, and its molecular weight was 4.2 x 10(4), which was greater than those of three components of normal human urinary kallikreins (normal HUK). Also Km values with TAME and BAME of urinary kallikrein in our patient with Bartter's syndrome did not correspond to those of normal HUK. Thus it can be said that urinary kallikrein in our patient with Bartter's syndrome was qualitatively different from normal HUK. The present observation might be a reflection of renal tubular dysfunction in this patient with Bartter's syndrome.

Angiotensin II↗
PubMed1978

Inhibition of 7,12-dimethylbenz[alpha]anthracene-induced mammary tumorigenesis in rats by a synthetic protease inhibitor, N,N-dimethylamino-(p-(p'-guanidinobenzoyloxy)) benzilcarbonyloxyglycolate.

Oral administration of N,N-dimethylamino-(p(p'-guanidinobenzoyloxy))-benzilcarbonyloxy glycolate depressed induction of breast tumors in rats by a single intravenous injection of 7,12-dimethylbenz[alpha]anthracene. The latent period was delayed in the group fed on a diet supplemented with N,N-dimethylamino-(p(p'-guanidinobenzoyloxy))benzilcarbonyloxy glycolate. Administration of this compound for 40 days after 7,12-dimethylbenz[alpha]anthracene also significantly reduced the average weight of tumors per rat. These findings suggest that protease may play an important role in the process of mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗