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T Tsukada

Publications and source records attributed to T Tsukada.

At least 307 records · Page 17Linked to original sources
PubMed1980

On the methods calculating mean survival time in 51Cr-platelet survival study.

The International Committee for Standardization in Hematology recommended three methods for calculating objectively the mean platelet survival time, ie, weighted mean of linear estimate and logarithmic estimate, truncated exponential model, and gamma model. For determining which method is better, data of the survival study were fitted to each of three methods, as well as the Paulus polynomial and exponential polynomial models, and the mean survival time and the mean square error were compared. Mean survival obtained by each method was always longest in healthy controls and shortest in ITP. In 3rd degree of polynomial estimate and 2nd and 3rd degrees of logarithmic estimate, several cases showed practically outlying mean survival time of more than 12 days. In healthy controls, highest mean square error was observed in 1st degree logarithmic estimate, and in cases with short mean survival time the highest one was obtained in 1st degree polynomial estimate. Mean square error in ITP pre- and postsplenectomy and in aplastic anemia was smallest in the gamma model. Among nine methods recommended by the International Committee for Standardization in Hematology and by Dr. Paulus, the gamma model so far provides the best method for calculating the mean survival time of 51Cr-platelets.

Blood Platelets↗
PubMed1980

Adenine nucleotide metabolism in Azotobacter vinelandii. Two metabolic pathways of AMP degradation.

AMP-degrading pathways in Azotobacter vinelandii cells were investigated. AMP nucleosidase (EC 3.2.2.4) was rapidly synthesized and reached a maximum at 24 h, while the activity of 5'-nucleotidase (EC 3.1.3.5) specific for AMP, which was negligible during the logarithmic phase of the growth, first appeared in 24 h-cultures, and reached a maximum after complete exhaustion of sucrose from the growth medium (70 h). Cell-free extracts of A. vinelandii of 48 h-cultures hydrolyzed AMP to ribose 5-phosphate and adenine in the presence of ATP, and adenine was deaminated to hypoxanthine. When ATP was excluded, AMP was dephosphorylated to adenosine, which was further metabolized to inosine, and finally to hypoxanthine. Hypoxanthine thus formed was reutilized for the salvage synthesis of IMP under the conditions where 5-phosphoribosyl 1-pyrophosphate was able to be supplied. These results suggest that the levels of ATP can determine the rate of AMP degradation by the AMP nucleosidase- and 5-'nucleotidase-pathways. The role of ATP in the AMP degradation was discussed in relation to the regulatory properties of AMP nucleosidase, inosine nucleosidase (EC. 3.2.2.2) and adenosine deaminase (EC 3.5.4.4).

Adenine Nucleotides↗
PubMed1980

Adenosine deaminase from Azotobacter vinelandii. Purification and properties.

Adenosine deaminase (EC 3.5.4.4) was found to occur in the extract of Azotobacter vinelandii, strain 0, and purified by heating at 65 degrees C, fractionation with ammonium sulfate, DEAE-cellulose chromatography and gel filtration on Sephadex G-150. Purified adenosine deaminase was effectively stabilized by the addition of ethylene glycol. The molecular weight of the enzyme was estimated to be 66,000 by gel filtration on Sephadex G-150. The enzyme specifically attacked adenosine and 2'-deoxyadenosine to the same extent, and formycin A to a lesser extent. The pH optimum of the enzyme was observed at pH 7.2. Double reciprocal plot of initial velocity versus adenosine concentration was concave upward, and Hill interaction coefficient was calculated to be 1.5, suggesting the allosteric binding of the substrate. ATP inhibited adenosine deaminase in an allosteric manner, whereas other nucleotides were without effect. The physiological significance of the enzyme was discussed in relation to salvage pathway of purine nucleotides.

Adenosine Deaminase↗
PubMed1980

Peripheral effects of guanfacine compared to those of clonidine in the dog.

Comparative studies of the antihypertensive agents, guanfacine and clonidine, on their peripheral effects were performed using normotensive canine preparations. On the peripheral vascular beds, both drugs constricted cerebral renal and femoral vasculatures, but there were no decreases in the renal blood flow. This vasoconstriction was blocked by phentolamine, and guanfacine was about 3 times less potent than clonidine. Both drugs contracted the canine nictitating membrane, and had no effect on the ganglionic transmission in the cervical sympathetic ganglion. Qualitatively different effects were observed in their effects on renal function. Guanfacine slightly increased the urinary volume and Na excretion, while clonidine increased the urinary volume and K excretion. All these peripheral effects do not seem to be responsible for their hypotensive effect.

Animals↗
PubMed1979

Triamterene-induced immune haemolytic anaemia with acute intravascular haemolysis and acute renal failure.

Acute intravascular haemolysis and renal failure developed while a patient was taking triamterene. A direct antiglobulin test with a polyvalent reagent was positive. Serum caused agglutination of normal red cells in the presence of triamterene and caused an increase of partial haemolysis of both trypsin-treated erythrocytes and red cells from a patient with paroxysmal nocturnal haemoglobinuria (PNH) in the presence of complement. From the results of antibody-neutralization test and treatment with 2-mercaptoethanol, the presence of IgM antibody with lambda light chain could be demonstrated. The triamterene seemed to bind strongly to the red cells in vitro but in vivo there was no detectable adsorption to red cells. Haptenic inhibition was not demonstrated. From these results, it was assumed that this antibody was found to cross-react with methotrexate which has a structure similar to that of triamterene.

Acute Kidney Injury↗
PubMed1979

Effects of 2-nicotinamidoethyl nitrate on the cardiovascular system.

Using the dog as experimental animal, effects on the cardiovascular system of a new vasodilator, 2-nicotinamidoethyl nitrate (SG-75), were studied. In the heart-lung preparation, the compound produced a dose-dependent increase in the coronary blood flow, which was associated with only a minimal increase in the myocardial oxygen consumption. There was essentially no change in the myocardial function. The myocardial redox potential was shifted to more positive values. In the isolated perfused heart preparation (Langendorff's preparation), SG-75 produced a dilatation of only the small resistive arterioles. However, it produced a dilatation of the large conductive artery in underperfused myocardium. SG-75 produced a significant increase in the cerebral venous outflow, associated with an increase in the cerebro-spinal fluid pressure. It produced a reducation of the venous return, which was especially prominent in the lower half of the body. In the isolated smooth muscle preparation of the coronary artery, high-doses of SG-75 induced calcium antagonistic effects and produced a relaxation of the lanthanum contracture.

Animals↗