Energy cost of bimanual cranking; difference between two motion patterns.
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Adult↗
Biomedical subjects
K Hashizume
Publications and source records attributed to K Hashizume.
Extra-adrenal pheochromocytoma manifesting renovascular hypertension.
A case with extra-adrenal pheochromocytoma, which was found by chance in the course of renovascular hypertension, is reported. The tumor was on the stenotic portion of the right renal artery. The results of examinations for pheochromocytoma were not conclusive, that is, inconsistent elevation of plasma catecholamines and urinary catecholamine excretion, equivocal results of pharmacological tests for pheochromocytoma, and negative results in [131I]metaiodobenzylguanidine scintigraphy. The stenosis of the right renal artery disappeared, the blood pressure was normalized by surgical resection of the tumor, and the extra-adrenal pheochromocytoma was finally diagnosed by pathohistological findings. Renovascular hypertension appeared to be the primary cause of this hypertension, judging from the significant decrease in blood pressure induced by an angiotensin II analog and a renal vein renin ratio of 7.3. Even in the case of obvious renovascular hypertension, the possibility of this unusual coexistence with pheochromocytoma should be considered.
Adult↗
Effect of insulin on glucagon binding to isolated rat epididymal adipocytes.
Effect of insulin on glucagon binding to rat epididymal adipocytes was studied in vitro. [125I]iodoglucagon binding to isolated adipocytes was increased by preincubation of the cells with insulin. Maximal increase was observed with 7 X 10(-10) M insulin. In Scatchard analysis, [125I]iodoglucagon competition data generated one binding site with a single affinity for glucagon binding in the cells pretreated with buffer alone. Pretreatment of the cells with insulin increased the affinity without changes in the number of binding sites. [125I]iodoglucagon binding to isolated adipocytes was not affected by pretreatment of the cells with luteinizing hormone, follicle-stimulating hormone, growth hormone, or with prolactin. These results suggest that insulin stimulates glucagon binding to adipocytes.
Adipose Tissue↗
Significant increase in plasma immunoreactive atrial natriuretic polypeptide concentration during head-out water immersion.
To investigate the physiological regulatory mechanism of human atrial natriuretic polypeptide (hANP) secretion, plasma hANP was measured by a direct radioimmunoassay during head-out total body water immersion (WI) in normal men. Five healthy men were immersed in water for 1 hr. Urine volume and Na excretion were significantly increased during WI. Plasma hANP increased significantly during WI peaking at 30 min. and returned toward the baseline after WI. Plasma renin activity and norepinephrine were suppressed occasionally during WI. Plasma ADH did not change throughout the study period. Maximal increments in plasma hANP correllated with that in urine output or urinary Na excretion during WI. These data suggest that acute central hypervolemia caused by WI increases hANP secretion and that this increase may participate in the diuretic response to WI.
Adrenal Cortex Hormones↗
The effects of aging on physiological properties of fast and slow twitch motor units in the rat gastrocnemius.
The mechanical properties of individual motor units were studied in the medial gastrocnemius of old (26-30 months) rats anesthetized with urethane and chloralose. The data were compared with results from motor units in the same muscle of middle-aged (11-14 months) rats. In the old rats there was a significant increase in mean tetanic tension for type S (slow twitch) units, whereas there was a slight decrease for type F (fast twitch) units. Twitch contraction time after maximum post-tetanic potentiation was shortened in type F units, but not in type S units. Conduction velocity of motor axons decreased in both unit types, but more marked change was found in type F units. These findings suggest the differential effects of aging on type F and type S motoneurons.
Aging↗
Experimental studies of photo radiation therapy on neuroblastoma.
A combination of Photo Radiation Therapy (PRT) using Argon-Dye Laser with hematoporphyrin derivatives (HpD) was used experimentally on a cytogenetically highly malignant neuroblastoma xenograft, which exhibited a homogeneously staining region and caused DNA amplifications in chromosomes. The tumor tissue was treated with 500 joules/cm2 of laser. The dosage of HpD was 50 mg per kg body weight. Necrosis of over 50% of the tumor was observed in half the specimens. Swollen cytoplasmic organelles and ruptured cell and nuclear membranes were observed by electron microscopy after PRT. PRT may be used with other treatment modalities for the removal of residual and metastatic tumors.
Animals↗
Glucagon alters insulin binding to isolated rat epididymal adipocytes: possible role of adenosine 3',5'-monophosphate in modification of insulin action.
Effects of glucagon on insulin action in rat epididymal adipocytes were studied in vitro. [125I]iodoinsulin binding to isolated adipocytes was inhibited by preincubation of the cells with isoproterenol, epinephrine, or glucagon. Fifty percent inhibition was observed with 2 X 10(-8) M glucagon, 10(-6) M isoproterenol, and 10(-7) M epinephrine. Maximal (90%) inhibition induced by glucagon was observed at 10(-6) M. In Scatchard analysis, [125I]iodoinsulin competition data generated curvilinear plots in buffer- and glucagon-treated cells. Pretreatment of the cells with (Bu)2cAMP reduced insulin binding activity. However, the simultaneous addition of (Bu)2cAMP with [125I]iodoinsulin did not produce the inhibition of the binding when the cells were not pretreated with the agent. cAMP level in the cells was increased by incubation with glucagon. 3-O-[Methyl-3H]methylglucose uptake by isolated adipocytes was inhibited by pretreatment of the cells with glucagon. These results suggest that glucagon regulates insulin action through decrease in insulin receptor activity, and that it is possible that the inhibition is mediated by cAMP production in adipocytes.
3-O-Methylglucose↗
Active and inactive forms of 3,5,3'-triiodo-L-thyronine (T3)-binding protein in rat kidney cytosol: possible role of nicotinamide adenine dinucleotide phosphate in activation of T3 binding.
Extraction of rat kidney cytosol with 10% charcoal at 4 C inactivated specific T3 binding. The decreased T3 binding in extracted cytosol could be restored by addition of boiled kidney cytosol. Three different factors (a, b, and c) which could increase T3 binding were identified by Sephadex G-50 column chromatography of boiled cytosol. Two factors (b and c) were eluted as relatively small molecules. Factor a was present in small amounts. Factor c was neutralized by incubation with EDTA, but factor b was not. Factor b was not destroyed by trypsin, protease, DNase, or RNase, but was destroyed by alkaline phosphatase. Factor b was destroyed by incubation with nicotinamide adenine dinucleotide phosphate (NADPH)-dependent glutathione reductase in the presence of oxidized glutathione. Although T3 binding to charcoal-extracted cytosol protein was not influenced by reduced glutathione or dithiothreitol, it was markedly increased by NADPH. Maximal activation induced by 50 microM NADPH was not further increased by further addition of endogenous factor b. The elution position of NADPH in gel chromatography corresponded to the elution position of factor b. Factor b or NADPH increased maximal binding capacity without changes in affinity constant. These observations suggest that T3-binding protein in cytosol is present in inactive and active forms and that the active form is generated by NADPH, which is present as one of the activators in cytosol. The effect of these cytosolic T3-binding proteins on nuclear T3 binding in vitro was also studied. In the absence of cytosolic T3-binding protein, [125I]T3 binding to nuclear receptor was decreased by unlabeled T3 in a concentration-dependent manner. In the presence of inactive form of cytosolic T3-binding protein, nuclear [125I]T3 binding was slightly diminished. In the presence of NADPH and cytosolic T3-binding protein, however, the amount of [125I]T3 bound to nuclei markedly decreased, which was associated with an increase of cytosolic [125I]T3 binding. NADPH alone did not influence nuclear T3 binding. These results suggest that T3 binding to nuclear receptor is regulated by an active form of cytosolic T3-binding protein in vitro.
Alkaline Phosphatase↗
Dependence of the mitochondrial uptake of triiodothyronine (T3) in rat kidney on cytosolic T3-binding protein.
The effect of cytosolic T3-binding protein (CTBP) on mitochondrial T3 uptake was investigated by using rat kidney tissue in vitro. [125I]T3 uptake into mitochondria was time dependent in the absence of CTBP. Addition of CTBP to the incubation medium significantly increased mitochondrial [125I]T3 uptake. When mitochondria were incubated with a [125I]T3-CTBP complex, [125I]T3 uptake into mitochondria continued to be time dependent, but the amount of [125I]T3 incorporated was greater than in mitochondria incubated with free [125I]T3. Although [125I]T3 uptake was not significantly inhibited by an excess of unlabeled T3, it was markedly inhibited by an excess of unlabeled T3-CTBP complex. The degree of inhibition was related to the concentration of T3-CTBP complex. However, [125I]T3 uptake produced by incubation of mitochondria with [125I]T3-CTBP complex was not inhibited by unsaturated CTBP. [125I]T3 binding to outer mitochondrial membranes was observed when the membranes were incubated with free [125I]T3 or [125I]T3-CTBP complex; the amount of [125I]T3 bound was greater in the membranes incubated with [125I]T3-CTBP complex. [125I]T3 binding to the membranes incubated with [125I]T3-CTBP complex was displaced by the addition of unlabeled T3-CTBP complex. These results suggest that mitochondrial T3 uptake is mediated by previous binding of T3 to CTBP, and that the uptake is possibly regulated by T3-CTBP complex binding to its receptor in the outer mitochondrial membrane.
Animals↗
Effect of thyroxine-binding globulin (TBG) on thyroxine (T4) uptake by human peripheral mononuclear cells: evidence of TBG-dependent uptake of T4.
The effect of sialylated TBG and desialylated TBG on thyroxine (T4) uptake by human peripheral mononuclear cells was investigated in vitro. [125I]-T4 uptake was observed when the cells were incubated with free [125I]-T4. The uptake was inhibited in a concentration dependent manner when TBG was added. During the incubation, [125I]-T4 binding to TBG was observed. [125I]-T4 incorporation into cells was also observed when the cells were incubated with [125I]-T4-sialylated TBG or with [125I]-T4-desialylated TBG complex. The uptake was related to the temperature and length of time of the incubation. The amount of [125I]-T4 incorporated into the cells incubated with [125I]-T4-sialylated TBG was greater than that into the cells incubated with [125I]-T4-desialylated TBG during the early 0-20 min. incubation, whereas the amount of [125I]-T4 incorporated into the cells incubated with [125I]-T4-desialylated TBG became greater than that into the cells incubated with [125I]-T4-sialylated TBG after 20 min. of incubation. Pretreatment of the cells with methylamine blocked [125I]-T4 uptake in both cases, i.e. incubated with [125I]-T4-sialylated TBG and incubated with [125I]-T4-desialylated TBG. The results suggest that TBG plays a role not only as a carrier protein for T4 in circulation but also as a protein which can transport T4 from the extracellular into the intracellular space, so that the mechanism of T4 transport mediated by desialylated TBG is different from that mediated by sialylated TBG, and that the T4 transport system in both cases, mediated by sialylated TBG and by desialylated TBG, may be related to the internalization of T4-TBG-TBG receptor complex or of T4-T4 receptor complex if TBG receptors are present in the outer surface of the cell membrane.
Cell Membrane Permeability↗
Characterization of regulation of thyrotropin (TSH) receptor function in thyroid plasma membrane: interaction between TSH receptor function and activation of adenosine 3',5'-monophosphate-dependent protein kinase.
The changes in the characteristics of thyrotropin (TSH) binding to thyroid plasma membranes during the activation of cyclic AMP-dependent protein kinase in the membranes were studied. Preincubation of thyroid plasma membranes with TSH or cyclic AMP reduced the maximal binding capacity but increased the association rate for TSH binding. In double reciprocal analysis, a marked reduction of the total number of binding sites and association constant was observed in the membranes treated with cyclic AMP. These reductions were also observed in the membranes preincubated with buffer alone. The degree of these reductions, however, was greater in the membranes pretreated with cyclic AMP. During incubation of the membranes with buffer alone, cyclic AMP formation (activation of adenylate cyclase) was observed though the degree of the formation was lower than that induced by TSH. The results suggested that not only TSH receptor release from thyroid plasma membrane but also the modification of TSH binding activity in the membrane is produced by cyclic AMP-dependent protein kinase.
Adenylyl Cyclases↗
[Age-related changes in stability in standing posture].
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Adult↗
Studies on lipoxygenase inhibitors. II. KF8940 (2-n-heptyl-4-hydroxyquinoline-N-oxide), a potent and selective inhibitor of 5-lipoxygenase, produced by Pseudomonas methanica.
Pseudomonas methanica KY4634 was found to produce 5-lipoxygenase inhibitor designated KF8940, MY12-62a and MY12-62c. The inhibitors were purified by solvent extraction, silica gel column chromatography, reversed-phase low pressure liquid chromatography and crystallization. The chemical structures of KF8940, MY12-62a and MY12-62c were determined to be 2-n-heptyl-4-hydroxyquinoline-N-oxide, 2-n-heptyl-4-hydroxyquinoline and 3-n-heptyl-3-hydroxy-1,2,3,4-tetrahydroquinoline-2,4-dione, respectively, on the basis of their physico-chemical properties. Among them, KF8940 was the most potent inhibitor. The compound inhibited 5-lipoxygenase of rat basophilic leukemia cells in a dose-dependent manner and the half maximal inhibitory concentration (IC50) was 1.5 X 10(-7) M. At this concentration, KF8940 did not inhibit bovine platelet 12-lipoxygenase and cyclooxygenase, and the IC50 values for these enzyme were 3.5 X 10(-5) M and 1.7 X 10(-4) M, respectively. The results indicated that KF8940 is a potent and selective inhibitor of 5-lipoxygenase. The IC50 value of MY12-62c for 5-lipoxygenase was 1.9 X 10(-5) M and that of MY12-62a was 1.9 X 10(-5) M.
Arachidonate Lipoxygenases↗
MY336-a, a novel beta-adrenergic receptor antagonist produced by Streptomyces gabonae.
Streptomyces gabonae KY2234 was found to produce a new compound, MY336-a, which bound to beta-adrenergic receptor. The compound was isolated from the fermentation broth of KY2234. MY336-a showed a high affinity for the beta-receptor, labeled with [3H]dihydroalprenolol in the membrane fractions of rat heart (beta 1-adrenergic receptor) or lung (beta 2-adrenergic receptor), whereas the compound bound very weakly to alpha-adrenergic receptor, labeled with [3H]dihydroergokryptine in rat brain. the inhibition constants (Ki) of the compound were 0.73 and 0.14 microM for the beta-receptors of heart and lung, respectively. 5'-Guanylylimidodiphosphate (Gpp(NH)p) did not alter the affinity of the beta-receptors for MY336-a. In isolated guinea-pig atria, MY336-a produced an inhibition of the positive chronotropic and inotropic effects of isoproterenol. MY336-a also antagonized the relaxation of tone induced by isoproterenol in isolated guinea-pig trachea. No partial agonistic activity was detected in MY336-a in the isolated atria and trachea. In anaesthetized dogs, MY336-a (1 mg/kg, iv) exerted negative inotropic action (left ventricular dp/dt max, -32.6%).
Adrenergic beta-Antagonists↗
[Wermer's syndrome (multiple endocrine neoplasia, type I)].
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Diagnosis, Differential↗
Radioimmunoassay of metanephrine and normetanephrine for diagnosis of pheochromocytoma.
Sensitive and specific radioimmunoassays of metanephrine and normetanephrine were developed by use of 125I-labeled synephrine and specific metanephrine antibody, and 125I-labeled octopamine and specific normetanephrine antibody. Specific antibody for both metanephrine and normetanephrine was raised in rabbits by immunization with bovine serum albumin conjugated with the corresponding hapten, prepared by the method of Grota and Brown (Endocrinology 1976;98:615). The detection limits of the metanephrine and the normetanephrine radioimmunoassays were 2 and 6 pg/tube, respectively. Mean plasma metanephrine and normetanephrine values for 24 normal subjects were 62 (SD 14) and 100 (SD 40) ng/L, respectively. Mean urinary metanephrine and normetanephrine values for 22 normal subjects were 154 (SD 74) and 217 (SD 109) micrograms/day. For 14 pheochromocytoma patients, plasma metanephrine and normetanephrine values ranged from 29 to 683 and from 28 to 7850 ng/L, and urinary metanephrine and normetanephrine values were 606 to 6630 and 296 to 4800 micrograms/day, respectively. The present methods are simple and suitable for routine tests or for mass screening for pheochromocytoma.
Adrenal Gland Neoplasms↗
Hypotensive effect of long-term oral calcium supplementation in elderly patients with essential hypertension.
Calcium gluconate (22.4 g/day; 2 g/day as Ca) was administered orally for 8 weeks to eight hospitalized elderly patients with essential hypertension in order to confirm the hypotensive effect of oral calcium supplementation and to clarify its hypotensive mechanism by analyzing changes in hormonal factors. After 2 weeks of calcium supplementation, both systolic and diastolic pressures decreased significantly and remained decreased for the duration of the study. An elevation of plasma PGE2 correlated with blood pressure reduction was observed at 2 weeks. Plasma norepinephrine decreased significantly from 4 weeks. Plasma parathyroid hormone decreased significantly from 4 weeks, and 1,25-dihydroxyvitamin D (1,25-[OH]2D) decreased significantly at 8 weeks. The reduction of plasma 1,25-(OH)2D correlated with blood pressure decrease at 8 weeks. The present study indicates that the mechanism of its hypotensive effect is multifactorial and may be different during different phases of calcium supplementation. The suppression of plasma 1,25-(OH)2D following reduction of parathyroid hormone may be involved in the hypotensive effect in the chronic phase of calcium supplementation. Enhancement of PGE2 production in the early phase and suppression of sympathetic nervous activity in the chronic phase may also be factors in blood pressure reduction.
Administration, Oral↗
[Hemostatic derangement in bone marrow transplantation].
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Adolescent↗