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Biomedical subjects

S Shimoda

Publications and source records attributed to S Shimoda.

At least 127 records · Page 7Linked to original sources
PubMed1982

[Effects of gamma-oryzanol on the hypothalamo-pituitary axis in the rat].

The effects of gamma oryzanol (gamma-OZ), a ferulic acid of triterpene alcohol, on the synthesis and release of the growth hormone (GH) and prolactin (PRL) in vitro and turnover rates of hypothalamic catecholamines were investigated. A single subcutaneous injection of 20 mg/kg of gamma-OZ suppressed GH synthesis and PRL release 1 hour after the injection. gamma-OZ increased medial basal hypothalamic (MBH) dopamine (DA) content, and the DA content was decreased by a treatment of alpha-methyl-p-tyrosine (alpha MpT), a tyrosine hydroxylase inhibitor, indicating increased synthesis and release of DA in MBH by gamma-OZ. gamma-OZ did not alter norepinephrine (NE) content in MBH, while the NE content was significantly decreased, indicating unchanged synthesis and increased release of NE in MBH by gamma-OZ. These results may explain the previous data concerning the changes in serum levels of GH and PRL by gamma-OZ and also suggest that gamma-OZ can affect the synthesis and/or release of at least two hypothalamic neurotransmitters, DA and NE, resulting in the alterations of anterior pituitary hormone synthesis and/or release.

Animals↗
PubMed1982

Improvement in abnormal secretion of thyrotropin and gonadotropin after restoration of serum calcium is pseudohypoparathyroidism.

A 25 yr-old woman patient was admitted because of convulsion. The diagnosis of pseudohypoparathyroidism was made on the basis of typical stigmata, lowered serum calcium, increased serum phosphorus and parathyroid hormone levels, and defective response in urinary excretion of cyclic AMP and phosphorus to exogenous parathyroid extract. Endocrine studies performed in the hypocalcemic state revealed several abnormalities of the pituitary gland such as an exaggerated response of TSH to TRH, high basal levels and exaggerated responses of LH/FSH and a blunted GH response to arginine-HCl, while there was no clinical evidence of hypothyroidism and hypogonadism. These abnormalities of anterior pituitary function were normalized after the restoration of normocalcemia by using 1 alpha-hydroxy-cholecalciferol. These results suggest that some endocrine abnormalities observed in pseudohypoparathyroidism might be functional and reversible disorders secondary to hypocalcemia rather than genetic ones.

Adult↗
PubMed1981

[Clinical evaluation of hyperglucagonemia in patients with myotonic dystrophy (author's transl)].

In order to clarify the possible participation of glucagon in glucose intolerance in myotonic dystrophy, six patients with myotonic dystrophy were examined. Three out of the six patients had an abnormal oral glucose tolerance curve. Two had frank diabetic glucose tolerance curves and the other had a high glucose value at 30 min after glucose loading, which fell beyond the normal range (Mean +/- 2 S.D.). Total insulin response to oral glucose, calculated as insulin area, was significantly exaggerated (p less than 0.01 vs control value). In addition to these results, hyperglucagonemia was observed throughout the test in two patients with myotonic dystrophy. In the arginine infusion test, insulin response was not so exaggerated but plasma glucagon was significantly higher (p less than 0.05 vs control value) at each 30, 45, 60 minutes after arginine infusion, and the mean glucagon area under the curves was significantly greater (p less than 0.05 vs control value). None of the myotonic patients showed growth hormone or cortisol excess during an arginine infusion and/or insulin tolerance test. Three patients with myotonic dystrophy who had abnormal glucose tolerance curves showed absolutely or relatively high glucagon levels and exaggerated response to arginine infusion. These findings suggested that hyperglucagonemia might contribute to the appearance of glucose intolerance in myotonic dystrophy.

Adolescent↗
PubMed1981

Quantitative studies on the polarization optical properties of living cells. I. Microphotometric birefringence detection system.

A method of polarization optical analysis is described in which phase retardation attributable to birefringence of a minute area in a microscopic object is determined. The optical system consists of a polarizing microscope with "rectified" strain-free lenses, a photoelectric detector to determine the intensity of the light passing through a minute window located at the image plane of the specimen, and a stage that moves the specimen at appropriate velocities for scanning. The error resulting from any flare of light emerging from outside of the area to be measured is minimized by limiting the illuminated area. The specimen can be observed during the measurement of light intensity by illuminating the whole microscope field at a wavelength different from that of the light used for the measurement. The retardation of the specimen is determined by comparing the specimen and background intensities as functions of the azimuth of a Brace-Köherl compensator. Alternatively, retardation is obtained directly from the light intensity at a fixed compensator angle, using the theory of polarization optics. The basal noise level for the present apparatus is approximately 0.03 nm when measuring birefringence of a 4-micron2 area in 0.1 s, using a X 40, NA 0.65 objective. The noise decreases in inverse proportion to the square root of the area times the duration of measurement.

Animals↗
PubMed1981

Quantitative studies on the polarization optical properties of living cells II. The role of microtubules in birefringence of the spindle of the sea urchin egg.

Birefringence of the mitotic apparatus (MA) and its change during mitosis in sea urchin eggs were quantitatively determined using the birefringence detection apparatus reported in the preceding paper (Hiramoto el al., 1981, J. Cell Biol. 89:115-120). The birefringence and the form of the MA are represented by five parameters: peak retardation (delta p), through retardation (delta t), interpolar distance (D1), the distance (D2) between chromosome groups moving toward poles, and the distance (D3) between two retardation peaks. Distributions of birefringence retardation and the coefficient of birefringence in the spindle were quantitatively determined in MAs isolated during metaphase and anaphase. The distribution of microtubules (MTs) contained in the spindle is attributable to the form birefringence caused by regularly arranged MTs. The distribution coincided fairly well with the distribution of MTs in isolated MAs determined by electron microscopy. Under the same assumption, the distribution of MTS in the spindle in living cells during mitosis was determined. The results show that the distribution of MTs and the total amount of polymerized tubulin (MTs) in the spindle change during mitosis, suggesting the assembly and disassembly of MTs as well as the dislocation of MTs during mitosis.

Animals↗
PubMed1980

[Dopaminergic control of aldosterone secretion in man (author's transl)].

To evaluate the dopaminergic control of aldosterone secretion, the following experiments were performed on 10 normal subjects (3 men and 7 women, aged 21 approximately 69 yrs.), 16 diabetics (8 men and 8 women, aged 20 approximately 74 yrs.) and 7 patients with untreated hyperthyroidism (2 men and 5 women aged 16 approximately 58 yrs.). Blood samples were withdrawn from an intravenous cannula indwelled in an antecubital vein at 0, 15, 30, 45, 60, 90 and 120 min after intravenous injection of 10mg metoclopramide with a volus. Plasma aldosterone levels and plasma renin activities (PRA) were measured by radioimmunoassay. In normal subjects, plasma aldosterone levels were significantly increased from basal levels of 111.8 +/- 1.3 Opg/ml (Mean +/- S.E.) to 183.4 +/- 23.3pg/ml 15 min after an intravenous injection of metoclopramide and were sustained for about 90 min. This increase induced by metoclopramide was, however, abolished by pretreatment with 2.5mg of bromocriptine. It is suggested that metoclopramide and bromocriptine are in a competitive relationship at the level of dopaminergic receptor. In diabetics, the mean plasma level of aldosterone was as low as 66.3 +/- 8.7pg/ml, which was significantly lower than that in normal subjects (p less than 0.01), and aldosterone response to metoclopramide was significantly diminished. Although this tendency was more apparent in diabetics with such complications as neuropathy or retinopathy, aldosterone response to metoclopramide implied that aldosterone secretion was under dopaminergic inhibition in this hypoaldosteronemic state. While aldosterone responded well to metoclopramide, PRA was not significantly altered in this treatment in normal subjects and diabetics. In patients with untreated hyperthyroidism, aldosterone response was similar to that in normal subjects.

Adolescent↗