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Biomedical subjects

S Ando

Publications and source records attributed to S Ando.

At least 451 records · Page 25Linked to original sources
PubMed1981

Participation of the lower brain stem in induction of preovulatory gonadotropin surges in female rats.

The role of the lower brain stem in controlling preovulatory gonadotropin surges was investigated in female rats under acute experimental conditions. Electrolytic lesions or diethyldithiocarbamate implantations in the ventrolateral part of the medulla oblongata (VLMO), which were carried out at 1100-1330 h on the day of proestrus, resulted in a blockade of the preovulatory surges of LH, FSH and PRL as well as subsequent ovulation. Such treatments in the dorsomedial part of the medulla oblongata did not affect gonadotropin surges or ovulation. By means of electrolytic lesions in the VLMO, norepinephrine concentrations were significantly reduced in the preoptic-anterior hypothalamic area at 1700-1800 h on proestrus, though they did not change in the mid-posterior hypothalamus. Electrochemical stimulations of the suprachiasmatic part of the preoptic area or norepinephrine injections into the third ventricle at 1400-1500 h on proestrus in animals with VLMO lesions succeeded in induce gonadotropin surges and ovulation. These results suggest that the lower brain stem is involved in the induction of preovulatory gonadotropin surges and that the process may be mediated by the ascending noradrenergic system which originates in the VLMO.

Animals↗
PubMed1981

Urinary sialyloligosaccharides in adult type sialidosis: occurrence of two positional isomers.

Two positional isomers of sialyloligosaccharides were isolated from the urine of a patient with adult type sialidosis with partial deficiency of beta-galactosidase. From structural studies including sugar analysis, enzyme degradation and methylation analysis, the following structures are deduced; 1. alpha-AcNeu-(2 leads to 3)-beta-Gal-(1 leads to 4)-beta-GlcNAc-(1 leads to 2)-alpha-Man-(1 leads to 3)-beta-Man-(1 leads to 4)-GlcNAc 2. alpha-AcNeu-(2 leads to 3)-beta-Gal-(1 leads to 4)-beta-GlcNAc-(1 leads to 2)-alpha-Man-(1 leads to 6)-beta-Man-(1 leads to 4)-GlcNAc The sialyloligosaccharide 1 has previously been reported to be present in liver and urine of patients with mucolipidosis I, II and variant forms. The sialyloligosaccharide 2 was first demonstrated in human urine.

Chemical Phenomena↗
PubMed1980

Gangliosides and neutral glycolipids of human adrenal medulla.

Glycolipids were isolated from human adrenal medulla by DEAE-Sephadex A-25 and Iatrobeads column chromatography. The lipid-bound sialic acid was about 234 microgram/g fresh tissue. The glanglioside fraction contained two major gangliosides which accounted for 93% of the total lipid-bound sialic acid. They were identified as GM3, N-acetylneuraminylgalactosylglucosylceramide and GD3, N-acetylneuraminyl N-acetylneuraminylgalactosylglucosylceramide on the basis of cochromatography with authentic standards, sugar composition analysis, and neuraminidase digestion. GM3, N-acetylneuraminylgalactosylglucosylceramide and GD3, N-acetylneuraminyl N-acetylneuraminylgalactosylglucosylceramide occurred in a ratio of approximately 3 : 2, and the ratio seemed to be rather constant irrelevant of age and sex differences. The neutral glycolipid fraction consisted of GL1a, glucosylceramide (18%), GL1b, galactosylceramide (23%), GL2a, lactosylceramide (27%), GL3, digalactosylglucosylceramide (20%), and GL4, globoside (12%). The major fatty acids of all these glycolipids were 16 : 0, 18 : 0, 22 : 0, 24 : 0 and 24 :1.

Adrenal Medulla↗
PubMed1980

Structures of some new complex gangliosides of fish brain.

Three novel trisialogangliosides of fish brain, GT3, GT2 and GT1c, have been isolated in their intact forms and their structures characterized. The discovery of these ganglioside species provides essential links for a new possible biosynthetic pathway leading to the major tetrasialoganglioside, GQ1c, of the fish brain.

Animals↗
PubMed1980

Characterization of hyperlipidemia in Nagase analbuminemia rat (NAR).

The mutant analbuminemia rat (NAR) was recently reported by Nagase (1) to spontaneously develop hypercholesterolemia. A detailed lipid analysis was carried out to characterize the hyperlipidemia. The concentrations of major phospholipids as well as cholesterol were increased in plasma, whereas the triacylglycerol level remained unchanged. Free fatty acid and lysophosphatidylcholine levels, on the contrary, declined. The liver lipids were not accumulated, but appeared to be depleted.

Animals↗
PubMed1980

Experimental carbon monoxide leucoencephalopathy in the cat.

After left common carotid artery ligation, cats were exposed to different CO gas concentrations for different periods, and the cerebral lesions were examined by light and electron microscopy at different intervals after exposure. Exposure to the higher concentration produced severe cardiopulmonary disturbances, and swelling of astrocytes in the white matter on the ligated side. This change was maximal at 1 to 3 days after exposure and subsided within one week. In cats exposed longer, necrotic or cystic lesions were observed on the ligated side. Prolonged exposure to the lower concentrations resulted in edema and reactive and degenerative axonal changes, followed by disintegration and phagocytosis of myelin sheaths, patches of demyelination, such as are seen in Grinker's leucoencephalopathy, were observed on the ligated and, to a lesser degree, on the non-ligated side. These lesions in the cerebral white matter may be related to the degree and duration of anoxic or histotoxic anoxia, or both, induced secondarily by the effects of the CO gas on cardiopulmonary function, and to the survival intervals after exposure. We postulate that the pathological change in experimental Grinker's leucoencephalopathy may be due to Wallerian degeneration or a dying-back process, rather than to true demyelination.

Animals↗
PubMed1980

Effects of rapid stimulation on the transmembrane action potentials of rabbit sinus node pacemaker cells.

We studied the mechanism of post-overdrive suppression in superfused rabbit sinus node pacemaker cells. Small specimens of sinus node tissue isolated from rabbit hearts were driven at a fast rate (overdrive) for 10-120 seconds using single sucrose gap methods. During the control perfusion (35 degrees C Tyrode's solution), overdrive caused a progressive decrease in maximum diastolic potential (MDP), overshoot (OS), and maximum rate of depolarization at phase 0 [dV/dt)max]. After cessation of the overdrive, the rate of diastolic depolarization decreased, and the spontaneous activity was suppressed temporarily (post-overdrive suppression). MDP, OS, (dV/dt)max, and the spontaneous activity returned within a few seconds to the level observed before overdrive. Atropine (2 x 10(-6) g/ml) did not influence the effects of overdrive. After ouabain administration (3 x 10(-7) g/ml) or in low temperature perfusate (25 degrees C), the effects of overdrive were accentuated, and a marked suppression of spontaneous activity with a long pause of over several seconds was seen following the overdrive. These results suggest that the post-overdrive suppression of sinus node is attributable, at least in part, to ionic shifts following overdrive, and may be potentiated by metabolic dysfunction of pacemaker cells.

Action Potentials↗
PubMed1979

Isolation and characterization of two isomers of brain tetrasialogangliosides.

Two isomers of tetrasialogangliosides were isolated and purified to homogeneity from human, bovine, chicken, and cod fish brains by employing DEAE-Sephadex and Iatrobeads column chromatographies. The tetrasialogangliosides of human, bovine, and chicken brains appeared to be identical because they had identical mobilities on thin layer plates developed with six different solvent systems. The tetrasialoganglioside of cod fish brain moved slower on thin layer plates than the tetrasialoganglioside from the other species. The ganglioside preparations were subjected to mild acid hydrolysis, neuraminidase treatment, and periodate oxidation followed by borohydride reduction. The structures of the two isomers were differentiated from each other by controlled mild acid hydrolysis in both aqueous and organic solvents. The structure IV3(NeuAc)2,II3(NeuAc)2-GgOse4ceramide is assigned to the tetrasialoganglioside of human, bovine, and chicken brains; and the structure IV3NeuAc,II2(NeuAc)3-GgOse4ceramide is assigned to that of cod fish brain. The possible pathways for the synthesis of the two tetrasialogangliosides are discussed.

Animals↗
PubMed1979

Electrophysiological studies on the neural networks among estrogen and progesterone effective brain areas on lordosis behavior of the rat.

The present study was performed in an attempt to elucidate the possible neural networks and their functional modification by progesterone among estrogen and progesterone effective brain areas for lordosis behavior of the rat. Single and multiple unit activities were recorded in the medial preoptic area (MPO), dorsomedial thalamic nucleus (MD), interpeduncular nucleus (IP) and ventral part of midbrain reticular formation (MRF), and single or train pulse stimulation was applied to the MPI, MD, IP, MRF, caudate-putamen (CP), habenular nucleus (HB), dorsal hippocampus (HPC), medial and lateral septum (m- and 1-SEPT) and lateral amygdala (1-AMYG). Unit activity was recorded under urethane anesthesia in ovariectomized rats pretreated with estrogen or with estrogen and progesterone. MPO units showed facilitatory responses to stimulation in the MRF, HB and 1-SEPT, and inhibitory responses to stimulation in the MD, HPC, m-SEPT and 1-AMYG in ovariectomized estrogen-primed rats. CP stimulation inhibited the MD unit activity. Stimulation in the IP had no effect on the MPO or MD units, while the IP units were affected by stimulation in the MPO, MD, CP and HB. MRF unit was accelerated by the MD and CP and inhibited by the MPO stimulation. In the ovariectomized, estrogen and progesterone-treated rat, the MPO unit responses to the MRF and MD stimulation, and the MD unit responses to the MRF and CP stimulation were different from those in the rat with only estrogen treatment. In addition, in the ovariectomized estrogen-primed rat, local application of progesterone to the MD prevented the inhibitory effect of the MD on the MPO unit. Progesterone, when given to the stimulated brain area, accelerated the MPO unit which was activated by the MRF stimulation, and inhibited the MD neuron which was inhibited by the CP stimulation. Multiple unit recordings showed similar results. Moreover, multi-unit activity in the HB and IP was elevated following a systemic progesterone application. On the basis of these results, the possible neural networks in the brain which participate in the lordosis control mechanisms are discussed.

Animals↗
PubMed1979

Conversion of deoxycorticosterone to 3-keto-4-etienic acid, catalyzed by a partially purified preparation from bovine adrenocortical mitochondria.

Bovine adrenocortical mitochondria were sonicated and subjected to extraction with sodium cholate. The extract contained not only cytochrome P-450 activities, but also an activity which catalyzed the conversion of deoxycorticosterone to an unknown steroid (designated X). The latter activity was concentrated by (NH4)2SO4 fractionation in the presence of sodium cholate, and separated from P-450 by taking advantage of their different solubilities in phosphate buffer without sodium cholate. The specific activity of the partially purified enzyme fraction was 70 times higher than that of sonicated mitochondria. The conversion of deoxycorticosterone to steroid X required NAD or NADP. The conversion rate was dependent on the concentration of deoxycorticosterone. The major product, steroid X, was isolated from the reaction mixture by means of silicic acid and Iatrobeads column chromatography. The steroid was characterized as 3-keto-4-etienic acid (3-oxoandrost-4-ene-17beta-carboxylic acid). This result suggests that an enzyme system for the conversion of deoxycorticosterone to 3-keto-4-etienic acid exists in adrenocortical mitochondria.

Adrenal Cortex↗
PubMed1979

Adult type neuronal storage disease with neuraminidase deficiency.

We describe a patient with adult-onset neuronal storage disease characterized by myoclonus, cerebellar ataxia, convulsive seizures, cherry-red spots, skeletal dysplasia, mild gargoyle features, inguinal hernia, and angiokeratoma. Cytoplasmic inclusions consistent with lysosomal storage disease were demonstrated in neurons of the autonomic nervous system. Accumulation of GM3 and GM2 gangliosides was found in sympathetic ganglia but a catabolic disturbance of these gangliosides was ruled out by normal levels of GM3 ganglioside sialidase and N-acetyl-beta-hexosaminidase A activities. beta-Galactosidase activity was decreased in leukocytes and fibroblasts, but not in serum. GM1 gangliosidosis was ruled out by lipid analyses, and mucopolysaccharidosis by normal excretion of mucopolysaccharide in urine. Sialyl oligosaccharides were increased in urine and alpha-neuraminidase was deficient in fibroblasts. This disorder is considered to be an inherited metabolic disorder of sialyl glycoproteins and oligosaccharides due to deficiency of an alpha-neuraminidase.

Galactosidases↗