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Biomedical subjects

Y Fukuhara

Publications and source records attributed to Y Fukuhara.

At least 73 records · Page 4Linked to original sources

Gentamicin inhibits Na+-dependent D-glucose transport in rabbit kidney brush-border membrane vesicles.

We studied the effect of gentamicin on Na+-dependent D-glucose transport into brush-border membrane vesicles isolated from rabbit kidney outer cortex (early proximal tubule) and outer medulla (late proximal tubule) in vitro. We found the same osmotically active space and nonspecific binding between control and gentamicin-treated brush-border membrane vesicles. There was no difference in the passive permeability properties between control and gentamicin-treated brush-border membrane vesicles. Kinetic analyses of D-glucose transport into 1 mM gentamicin-treated brush-border membrane vesicles demonstrated that gentamicin decreased Vmax in the outer cortical preparation, while it did not affect Vmax in the outer medullary preparation. With regard to Km, there was no effect of gentamicin in any vesicle preparation. When brush-border membrane vesicles were incubated with higher concentrations of gentamicin, Na+-dependent D-glucose transport was inhibited dose-dependently in both outer cortical and outer medullary preparations. Dixon plots yield inhibition constant Ki = 4 mM in the outer cortical preparation and Ki = 7 mM in the outer medullary preparation. These results indicate that the Na+-dependent D-glucose transport system in early proximal tubule is more vulnerable to gentamicin toxicity than that in late proximal tubule.

Animals↗

Formation of mutagens by heating foods and model systems.

We have demonstrated that the pyrolysis products of amino acids and proteins in model systems are mutagenic. The mutagenic principles in the pyrolyzates of amino acids have been isolated and identified by Sugimura et al. We have isolated and identified amino-alpha-carbolines from pyrolyzed soybean globulin as mutagens. The yield of mutagens by the heating of food constituents is changed by the heating method. Effects of heating methods on the yield of amino-alpha-carbolines were studied in a series of experiments, and the results are shown in this paper. Additionally, it has been shown that by the heating of creatine-sugar mixtures imidazoquinoline or quinoxaline mutagens are formed.

Animals↗

[Leiomyosarcoma of the remnant stomach--a case report].

A case of leiomyosarcoma of the remnant stomach is reported. The patient was a 57-year-old woman whose chief complaint was easy fatigability. Twenty six years earlier, she had undergone gastrectomy with the diagnosis of duodenal ulcer. By X-ray examination of the stomach, a Borrmann type I gastric cancer was suspected on admission. Endoscopic study of the stomach was performed, and a diagnosis of leiomyosarcoma was made from the biopsy specimens. Total gastrectomy was performed. On the resected specimen, a Borrmann type I like tumor measuring 4.5 X 5.5 X 3.2 cm was identified in the anterior part of the body of the remnant stomach. Histologically, the lesion was confirmed as leiomyosarcoma of the stomach.

Duodenal Ulcer↗

Cation dependence of renal outer cortical brush border membrane L-glutamate transport.

The cation dependence of L-glutamate transport in renal outer cortical brush border membrane vesicles was studied. Both cis sodium and trans potassium were required for optimal L-glutamate flux. Relative to simultaneous sodium (out greater than in) and potassium (in greater than out) gradient conditions, flux was reduced 50-fold by potassium removal and more than 100-fold by sodium removal. The effect of potassium removal in this preparation was markedly larger than that observed in other renal brush border membrane preparations. No other monovalent cation tested was effective in replacing sodium. However, Rb+ and Cs+ and to a lesser degree NH+4 were found to be effective potassium substitutes. Kinetic analysis of the Na/K-dependent component of L-glutamate flux indicated a single transport system of Km = 13 microM and Vmax = 1.3 nmol X min-1 X mg protein-1. Studies of the dependence of L-glutamate flux on potassium and sodium concentrations yielded Hill coefficients of 0.9 and 1.9, respectively, consistent with involvement of one potassium ion and two or more sodium ions in the L-glutamate transport event. Efflux studies indicated that sodium and potassium act at different steps in the transport cycle, sodium to facilitate the translocation of the glutamate-carrier complex, and potassium to facilitate the return of the unloaded carrier. A model for renal Na/K-dependent L-glutamate transport is suggested on the basis of these results.

Animals↗

The mechanism of decreased Na+-dependent D-glucose transport in brush-border membrane vesicles from rabbit kidneys with experimental Fanconi syndrome.

In our previous paper (Yanase, M. et al. (1983) Biochim. Biophys. Acta 733, 95-101) we reported that the Na+-dependent D-glucose uptake into brush-border membrane vesicles is decreased in rabbits with experimental Fanconi syndrome (induced by anhydro-4-epitetracycline). In the present paper we investigate the mechanism underlying this decrease. D-Glucose is taken up into the osmotically active space in anhydro-4-epitetracycline-treated brush-border membrane vesicles and exhibits the same distribution volume and the same degree of nonspecific binding and trapping as in control brush-border membrane vesicles. The passive permeability properties of control and anhydro-4-epitetracycline-treated brush-border membrane vesicles are shown to be the same as measured by the time-dependence of L-glucose efflux from brush-border membrane vesicles. D-Glucose flux was measured by the equilibrium exchange procedure at constant external and internal Na+ concentrations and zero potential. Kinetic analyses of Na+-dependent D-glucose flux indicate that Vmax in anhydro-4-epitetracycline-treated brush-border membrane vesicles (79.3 +/- 7.6 nmol/min per mg protein) is significantly smaller than in control brush-border membrane vesicles (141.3 +/- 9.9 nmol/min per mg protein), while the Km values in the two cases are not different from each other (22.3 +/- 0.9 and 27.4 +/- 1.8 mM, respectively). These results suggest that Na+-dependent D-glucose carriers per se are affected by anhydro-4-epitetracycline, and that this disorder is an important underlying mechanism in the decreased Na+-dependent D-glucose uptake into anhydro-4-epitetracycline-treated brush-border membrane vesicles.

Animals↗

The static head method for determining the charge stoichiometry of coupled transport systems. Applications to the sodium-coupled D-glucose transporters of the renal proximal tubule.

The static head method for determining the charge stoichiometry (the number of moles of charge translocated per mole of substrate) of a coupled transport system is presented. The method involves establishing experimental conditions under which a membrane potential exactly balances the thermodynamic driving force of a known substrate gradient. The charge stoichiometry can then be calculated from thermodynamic principles. In contrast to the usual steady-state method for determining charge stoichiometry in cell suspensions and vesicle preparations, the static head method is applicable to systems which are not capable of maintaining a constant membrane potential over time. The charge stoichiometries of two renal sodium coupled D-glucose transporters previously identified in brush-border membrane vesicle preparations from the outer cortex (early proximal tubule) and outer medulla (late proximal tubule) are determined. The charge stoichiometries of these transporters are in good agreement with their sodium/glucose coupling ratios arguing against the possibility that glucose transport is coupled to ions other than sodium in these membranes.

Animals↗

[Right ventricular free wall imaging using thallium-201 exercise myocardial scintigraphy with special reference to coronary angiography].

Right ventricular wall images of ischemic heart disease were evaluated during exercise myocardial scintigraphy using thallium-201. Among 33 subjects, ten were normal controls, 11 had left coronary artery disease (LAD group), 12 had right coronary artery disease (RCA group), all of whom received exercise myocardial scintigraphy. The submaximal or symptom-related ergometer exercise test was performed by the protocol being with 25 watt (W) loading, and then increased by 25 W every 3 min, while 3 mCi thallium-201 were injected intravenously at the maximal exercise point. Early imaging was obtained 5 min after exercise; delayed imagings, 1 and 4 hours after exercise. Early imaging and delayed imaging at 4 hours after exercise were obtained in the AP, lateral, LAO 30 degrees, LAO 45 degrees, and LAO 60 degrees projections. Only the LAO 45 degrees was obtained for delayed imaging 1 hour after exercise. To assess the radioactivity in the right ventricular wall, with regions of interest (ROI) in the upper part of the right ventricle [RV (U)] lower part of the right ventricle [RV (L)] and the most radioactive region in the left ventricle [LV (P)], we calculated the count ratio of the RV(U) or RV(L) to the LV(P) and defined it as the RV uptake ratio [RV(U)/LV(P)] or [RV(L)/LV(P)]. The results obtained were as follows: There were no significant changes in the RV uptake ratio between the early and delayed images both in the control and LAD groups, but the RV uptake ratio decreased significantly in the delayed images compared with an early image in the RCA group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Mutagenicity and co-mutagenicity of catechol on Salmonella.

Catechol was not mutagenic for Salmonella typhimurium TA98, TA100 or TA1537 in the presence or absence of S9 mix. At the lower level of S9 in the Ames method, the mutagenic activity of benzo[a]pyrene decreased with the increased addition of catechol. When catechol was added to the pre-incubation mixture at a higher concentration than in the conventional Ames method, the mutagenic activity of benzo[a]pyrene increased with the increased addition of catechol. Catechol is believed to be a co-mutagen for benzo[a]pyrene in the presence of a sufficient amount of S9 in the incubation mixture.

Benzopyrenes↗

Sodium-dependent succinate transport in renal outer cortical brush border membrane vesicles.

The transport of succinate into outer cortical brush border membrane vesicles (early proximal tubule) was studied. Succinate is taken up into an osmotically active space and exhibits the same distribution volume and the same degree of nonspecific binding and trapping as D-glucose. Succinate uptake is markedly enhanced by sodium and slightly enhanced by lithium but shows no stimulation by other monovalent cations tested. Kinetic analysis of the sodium-dependent component of succinate flux indicates a single transport site obeying Michaelis-Menten kinetics (Km = 1 mM and Vmax = 50 nmol X min -1 X mg protein -1 as measured under zero trans conditions at 100 mM NaCl and 28 degrees C with delta psi = 0). Direct evidence is given that succinate transport is coupled to sodium and is rheogenic, involving the net transfer of positive charge. The sodium:succinate coupling stoichiometry is found to be 2:1 by two independent methods.

Animals↗

Effect of furosemide on mitochondrial electron transport system and oxidative phosphorylation.

The effects of furosemide on the mitochondrial electron transport system and on oxidative phosphorylation were explored. Furosemide above the concentration of 2 X 10(-3) mol/l was found to inhibit state 3 (ADP-dependent) respiration of the rat liver, renal cortex, renal medulla mitochondria. State 4 (resting) respiration was not affected by furosemide. Furosemide above the concentration of 7.5 X 10(-6) mol/l (substrate: glutamate-malate), and above 5 X 10(-6) mol/l (substrate: succinate) inhibited the respiration of rat liver mitochondria released by 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF 6847). This fact exactly indicates that furosemide inhibits the electron transport system in mitochondria. Furosemide at the concentration of 4 X 10(-3) mol/l inhibited the activities of NADH cytochrome c reductase and succinate cytochrome c reductase in sonicated mitochondrial subparticles of beef heart by 78.2% and 79.2% of control, respectively.

Animals↗