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K Takeda

Publications and source records attributed to K Takeda.

At least 1,045 records · Page 58Linked to original sources
PubMed1988

Functional activity of oligosaccharide-deficient (Na,K)ATPase expressed in Xenopus oocytes.

(Na,K)ATPase from Torpedo californica was expressed in Xenopus laevis oocytes in the presence of tunicamycin by injecting mRNAs for the alpha- and beta-subunits derived from the cloned cDNAs into the oocytes. The oligosaccharide-deficient ATPase thus synthesized was transported to the oocyte plasma membrane, where it exhibited virtually the same ATPase activity, ouabain-binding capacity and 86Rb+ transport activity as the fully glycosylated enzyme. We conclude that the oligosaccharide chains on the beta-subunit has no effect on the catalytic activities of (Na,K)ATPase.

Animals↗
PubMed1988

Effect of fibroblast-derived differentiation inducing factor on the differentiation of human monocytoid and myeloid leukemia cell lines.

A fibroblast-derived differentiation inducing factor (F-DIF) purified from medium conditioned by a human fibroblast cell line (WI-26VA4) induced differentiation of human monocytic leukemia cell lines (U-937, THP-1) into cells with macrophage characteristics. F-DIF alone induced the differentiation of ML-1 cells only marginally, but it synergistically increased the differentiation when combined with TNF. Interferon-gamma, tumor necrosis factor, GM-CSF, interleukin-1 and interlukin-4 synergistically enhanced the differentiation of U-937 cells when combined with F-DIF.

Cell Differentiation↗
PubMed1988

Fast protein liquid chromatography of lymphocyte blastogenesis inhibitory factor produced by the human macrophage-like cell line U937.

The human macrophage-like cell line U937 constitutively produces a lymphocyte blastogenesis inhibitory factor (LBIF). Using fast protein liquid chromatography (FPLC)-chromatofocusing, FPLC-anion-exchange chromatography and high-performance liquid chromatography-gel permeation chromatography, LBIF has been purified to homogeneity. It is a single polypeptide chain and has a molecular weight of 57,000 daltons according to sodium dodecyl sulphate polyacrylamide gel electrophoresis under reducing conditions. LBIF shows pI 4.28-4.56 upon chromatofocusing on Mono P.

Animals↗
PubMed1988

Chemical modification of sodium channel inactivation: separate sites for the action of grayanotoxin and tetramethrin.

The gating mechanisms of the sodium channel are known to be modified by grayanotoxin and the pyrethroid tetramethrin. Voltage clamp experiments with internally perfused squid giant axons were performed to determine whether or not these two chemicals shared a common site of action in exerting their effects. An additive effect of the two drugs in prolonging sodium currents was observed. Additionally, the characteristic tetramethrin-induced sodium tail current and the grayanotoxin-induced hyperpolarizing shift in the voltage that activated the sodium current were observed simultaneously and independently of the order of drug introduction. Inactive stereoisomers of tetramethrin, which are known to prevent the active tetramethrin stereoisomers from exerting their effect, had no effect on the development of the grayanotoxin-induced modifications of sodium current. It was concluded that tetramethrin and grayanotoxin act at separate sites of action in modifying the sodium channel gating mechanisms in the squid axon membrane.

Animals↗
PubMed1988

Oxidation of NADH by vanadate plus phenylmethanesulfonyl fluoride (PMSF).

Phenylmethanesulfonyl fluoride (PMSF) enabled vanadate to catalyze the oxidation of NADH. Superoxide dismutase and manganese inhibited the oxidation, suggesting that superoxide anion played a crucial role. Since PMSF is widely used to protect enzymes from proteolytic cleavage when they are purified, attention should be paid when the toxicity of vanadate on the enzyme, whose activities are monitored by the oxidation of NADH, is evaluated or when vanadate dependent NADH oxidase is purified and assayed.

NAD↗
PubMed1988

[Serum thyrotropin concentrations in patients with Sheehan's syndrome: reevaluation of the usefulness in the diagnosis].

Serum concentrations of thyroid-stimulating hormone (TSH) were determined, using a highly sensitive immunoradiometric assay (IRMA), in 10 patients with Sheehan's syndrome. Serum TSH levels in these patients were from 2.3 to 9.0 microU/ml, with the mean of 6.4 +/- 2.3(SD) microU/ml, and the data were similar to those measured by a conventional RIA method. The levels of serum TSH in these patients were normal or even higher than those of healthy women (1.8 +/- 1.3 microU/ml). After supplement therapy by cortisol, serum TSH levels decreased, but remained within the detectable range that was greater than 0.15 microU/ml. After supplement therapy by 1-thyroxine (T4), serum TSH levels moderately decreased in all patients, and excessive 1-T4 administration resulted in a fall of serum TSH levels to lower than the detectable limit. Thyroidal 123 I uptake was low in 3 out of 6 patients examined, which supports a recent hypothesis of reduced biological activity of the patient's TSH. While, the remaining 3 patients had normal thyroidal 123 I uptake, and administration of perchlorate had no effects on thyroidal radioactivity. Thus, it may be possible that in the former group of patients the TSH has a reduced biological activity, and in the latter group of patients, iodine trapping is intact but further synthesis and secretion of thyroid hormone from the gland are impaired. When the response of serum TSH to TRH was examined, the peak serum TSH levels increased in all patients. The peak TSH levels were 4.8 to 10.2 microU/ml with the mean of 7.5 microU/ml, but the data overlapped with those of normal subjects (peak level ranging 5.9 approximately 27.7 microU/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Detection of muscular ventricular septal defect by the phase image.

A case of muscular ventricular septal defect shown by the phase image derived from Fourier analysis of gated equilibrium radionuclide angiocardiography is presented. The diagnostic feature of the defect on the phase image was a marked phase delay localized mainly in the trabecular portion of the right ventricle. This characteristic finding seemed to be caused by the left to right shunt flow through the defect located in the muscular portion of the interventricular septum.

Heart Septal Defects, Ventricular↗
PubMed1988

Characteristics of a nitrogen-fixing methanotroph, Methylocystis T-1.

A methane-oxidizing bacterium capable of nitrogen fixation was isolated from soil taken from an area which leaked methane gas. Strain T-1 was a catalase and oxidase-positive, gram-negative straight rod-shaped strictly aerobic bacterium which formed lipid cysts and type II intracytoplasmic membranes. The organism was a microaerophilic nitrogen-fixing methanotroph. Strain T-1 is considered to be classified into Methylocystis. The organism evolved hydrogen gas when grown in the nitrogen-free medium of atmospheric oxygen concentrations of 1.5% or more. Below this level, however, hydrogen gas was not evolved. In addition to methanol, formaldehyde and formate, ethanol, acetate and hydrogen gas served as oxidizable substrates for the acetylene reduction test. H2-stimulated nitrogenase activity was limited in a very narrow range of oxygen concentration and not detected at 2% O2. With acetate as the substrate, however, about an 80% of the maximum acetylene reduction activity was detected at 2% O2. These results suggest that strain T-1 is capable of recycling the hydrogen gas evolved during nitrogen fixation under low partial pressures of O2.

Hydrogen↗
PubMed1988

Pancreatic function and rehabilitation after pancreaticoduodenectomy.

Postoperative pancreatic function and rehabilitation were monitored in 149 patients who had had reconstruction of the digestive tract by Child's method, out of a total 151 patients who had undergone pancreaticoduodenectomy. The occurrence of peptic ulcer following Child's method may be prevented by the resection of a wider area of the stomach. Because the source of gut hormone secretion is removed by the pancreaticoduodenectomy, the secretion of this hormone is subsequently reduced and thus metabolic abnormalities also occur. If careful attention however, is paid to the maintenance of residual pancreatic function most patients who undergo pancreaticoduodenectomy can be expected to lead reasonably normal lives.

Duodenum↗
PubMed1988

Protein kinase C activation aggravates hypoxic myocardial injury by stimulating Na+/H+ exchange.

The physiological and pathophysiological roles of protein kinase C activation were investigated in cultured mouse myocardial cells. First, effects of 12-O-tetra-decanoyl-phorbol-13-acetate (TPA), a potent activator of protein kinase C, on the intracellular pH (pHi) and cytosolic free Ca2+ level [( Ca2+]i) were studied, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) and quin-2, respectively. In the presence of the Ca ionophore A23187, TPA induced a rise in pHi by activating amiloride-sensitive Na+/H+ exchange and also produced a rise in [Ca2+]i above that seen with A23187 alone. These effects were totally inhibited by amiloride. Second, the effect of TPA on hypoxia-induced myocardial cell injury was evaluated. The addition of TPA to the culture medium enhanced creatine kinase release from hypoxic myocardial cells (95% N2 + 5% CO2). This effect was markedly suppressed by the addition of amiloride. These data suggests that protein kinase C activation aggravates hypoxic myocardial injury, presumably by inducing Ca2+ overload. This event is secondary to activation of Na+/Ca2+ exchange through accelerated influx of Na+ into the cells as a result of Na+/H+ exchange stimulation by protein kinase C.

Animals↗
PubMed1988

Ouabain inhibits intracellular pH recovery from acidosis in cultured mouse heart cells.

Myocardial ischaemia induces cytosolic acidification, which promotes cardiac damage, dysfunction or arrhythmia. In this study, we investigated the effect of ouabain on the intracellular pH (pHi) in cultured mouse ventricular cells, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The average resting pHi in myocytes was 7.19. After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange. Ouabain inhibited this pHi recovery dose-dependently with half-maximal inhibition at 3 X 10(-5) M, but did not suppress the ionophore monensin-induced pHi elevation. The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump. Above results demonstrate the possibility that digitalis promotes intracellular acidosis or inhibits the pHi recovery from acidosis in ischaemic myocardium.

Acidosis↗
PubMed1988

Central attenuation of baroreflex by angiotensin II in normotensive and spontaneously hypertensive rats.

To determine whether angiotensin II (A II) can modify baroreflex centrally and contribute to the central resetting of baroreflex in spontaneously hypertensive rats (SHRs), the aortic depressor nerve (ADN) was electrically stimulated following intracerebroventricular (ICV) administration of A II and/or A II analog in urethane-anesthetized normotensive Wistar rats (WKYs) and SHRs. Electric stimulation of the ADN elicited frequency-dependent depressor, bradycardic, and sympatho-inhibitory responses. Angiotensin II, administered ICV, dose-dependently attenuated these responses induced by ADN stimulation in normotensive rats. We found, however, these attenuations could be abolished by ICV pretreatment with A II analog. Vasopressin (ICV) did not change any responses to ADN stimulation. The vasopressor and sympatho-inhibitory responses to ADN stimulation were significantly less in SHRs when compared with those in WKYs: In SHRs, A II analog completely cancelled the A II-attenuated responses to ADN stimulation. These findings suggest that A II can centrally attenuate baroreflex, which might be independent from vasopressin, and in the brain A II can contribute to the central resetting of baroreflex in SHRs.

Angiotensin II↗
PubMed1988

Central attenuation of baroreflex precedes the development of hypertension in DOCA-salt-treated rats.

To determine whether baroreflex is changed centrally before the development of hypertension in DOCA-salt treated rats, aortic depressor nerve was stimulated electrically 5 days after DOCA-salt treatment in urethane-anesthetized rats: compared with those of sham-operated control rats, blood pressure was not elevated in either awake or anesthetized rats. Aortic depressor nerve (ADN) stimulation elicited frequency-dependent vasodepressor, bradycardiac, and sympatho-inhibitory responses in both DOCA-salt-treated and control rats. However, the responses to ADN stimulation were significantly smaller in DOCA-salt-treated rats. These findings suggest that baroreflex is attenuated centrally before the development of hypertension and this attenuation may contribute to the pathogenesis of DOCA-salt hypertension.

Animals↗
PubMed1988

Increased extracellular concentration of norepinephrine in the hypothalamus by sinoaortic denervation.

To determine whether baroreflex can affect the norepinephrine system in the hypothalamus, the extracellular concentration of norepinephrine were measured by the brain dialysis technique in sinoaortic denervated rats (SAD). Twenty-four hours after sinoaortic denervation, systolic blood pressure and heart rate were significantly elevated, and norepinephrine concentration in perfusate of the posterior hypothalamus was significantly higher in SAD rats than in sham-operated rats. These results suggest that baroreflex could modify the activity of noradrenergic neuron projecting to the posterior hypothalamus.

Animals↗
PubMed1988

Retardation of the development of hypertension in DOCA salt rats by taurine supplement.

To study the antihypertensive effect of orally administered taurine in DOCA salt hypertension, urinary excretion of catecholamines, electrolytes, and arg-vasopressin was measured over four weeks in 20 taurine treated DOCA rats (group 1), 20 taurine untreated DOCA rats (group 2), and seven taurine untreated sham operated rats (group 3). Additional experiments were performed to determine whether or not the pressor and sympathetic responses to hypothalamic stimulation were altered after taurine treatment in DOCA rats. Systolic blood pressure decreased significantly in group 1 after the first week compared with that in group 2, and the differences became progressively more evident thereafter. At the fifth week the mean blood pressure was significantly lower in group 1 than in group 2, as was the heart rate. Although urinary excretion of adrenaline decreased significantly in group 1 at the first and fourth weeks, the difference in urinary excretion of noradrenaline between groups 1 and 2 was not significant. Urinary excretion of adrenaline and noradrenaline in group 3 was significantly lower than that in both hypertensive groups (groups 1 and 2). Urinary sodium excretion increased significantly in group 1 at the first and second week compared with group 2. With graded electrical stimulation of the ventromedial hypothalamus, resulting pressor and sympathetic responses were significantly smaller in group 1 than in group 2. These results suggest that the hypotensive effects of orally administered taurine in DOCA hypertensive rats are caused by suppression of the peripheral sympathetic nervous activity and by the resulting natriuresis.

Animals↗
PubMed1988

Attenuated cardiovascular and sympathetic nerve responses to aortic nerve stimulation in DOCA-salt hypertensive rats.

In order to verify, whether baroreflex sensitivity is changed centrally in DOCA-salt hypertension, the left aortic depressor nerve (ADN) was electrically stimulated in DOCA-salt hypertensive rats. After 3 weeks, tail-cuff systolic pressure was significantly higher in DOCA-salt treated rats than in untreated rats (169 +/- 4 versus 130 +/- 4 mmHg, respectively; P less than 0.001). After cutting both ADN and the carotid sinus nerves, the central cut end of the left ADN was electrically stimulated and frequency dependent depressor, bradycardic and sympatho-inhibitory responses were elicited in both control and DOCA-salt hypertensive rats. However, these responses were significantly smaller in DOCA-salt hypertensive rats than in normotensive controls. Bradycardic and sympatho-inhibitory responses to i.v. injection of norepinephrine were also blunted in DOCA-salt hypertensive rats. These findings suggest that baroreflexes were centrally attenuated in DOCA-salt hypertensive rats and possibly contribute to overall baroreflex attenuation.

Animals↗
PubMed1988

Salt increases blood pressure with biphasic changes in hypothalamic responsiveness in rats.

Tail-cuff systolic pressures became elevated in male Wistar rats fed chow containing 8% NaCl for 4 weeks. After 4 weeks of salt loading, pressor and sympathetic responses to ventromedial hypothalamic stimulation were larger in salt-loaded rats. When similar experiments were done following sinoaortic denervation, all of the effects previously induced by dietary salt loading persisted. By contrast, after only 1 week of salt loading, pressor and sympathetic responses to hypothalamic stimulation were reduced, instead of being increased. Since circulating plasma volume was increased in week 1, it was considered possible that reduced hypothalamic responsiveness was due to enhanced cardiopulmonary baroreflexes. Supporting this interpretation, bilateral vagotomy reversed the hypothalamic inhibition occurring in week 1. Although neither the site nor mechanism causing sympathetic hyperactivity has been determined, our results indicate that chronic dietary salt loading has biphasic effects on the ventromedial hypothalamus: an initial inhibition in the first week followed by stimulation thereafter. These results could mean that dietary salt loading eventually increases sympathetic activity and thereby induces hypertension by stimulating the ventromedial hypothalamus.

Animals↗