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Biomedical subjects

G Ito

Publications and source records attributed to G Ito.

At least 73 records · Page 4Linked to original sources
PubMed1981

Identification of N-monoacetylcystine in uraemic plasma.

1. An unidentified ninhydrin-positive substance of an acidic nature was detected in the plasma of uraemic patients. This substance was isolated from haemodialysate by ion-exchange chromatography and gel filtration, and identified as a sulphur-containing amino acid: N-monoacetylcystine. 2. The quantitative determination of sulphur amino acids in plasma revealed that the plasma levels of cysteic acid, homocysteic acid, taurine, cystine and cystathionine as well as N-monoacetylcystine in uraemic patients were markedly higher than in normal subjects (P less than 0.001 for each). However, the plasma levels of methionine in uraemic patients were within normal limits.

Amino Acids, Sulfur↗
PubMed1980

Comparative heart rate effects of oral administration of bitolterol, terbutaline and trimetoquinol in unanesthetized dogs.

Effect of a clinical dose of bitolterol, a new oral bronchodilator via adrenergic beta-receptor, on heart rate was compared with those of terbutaline and trimetoquinol in unanesthetized dogs. Oral administration of bitolterol, terbutaline and trimetoquinol increased the heart rate. The heart rate effect of bitolterol was significantly weaker than those of terbutaline and trimetoquinol.

Adrenergic beta-Agonists↗
PubMed1978

Identification of beta-aspartylglycine in uremic serum and its toxicity.

An unidentified ninhydrin-positive substance of acidic nature was found in the serum of uremic patients. This substance was isolated from hemodialysate by the methods of ion-exchange chromatography, gel-filtration and paper electrophoresis, and identified as beta-aspartylglycine by amino acid analysis, N-terminal amino acid determination and comparison with authentic sample synthesized in this laboratory. The quantitative determination of beta-aspartylglycine in serum revealed that the serum concentrations of beta-aspartyl-glycine in uremic patients increased much higher than those in normal subjects. The toxicity of beta-aspartylglycine in mice with acute renal failure induced by uranyl acetate was investigated. The mice given more than 1,0 g/kg body weight of beta-aspartylglycine showed behavioral alterations: low response to the stimuli and low activity, and some mice died by the injection of 4.0 g/kg body weight of the peptide. These results suggested that beta-aspartyl-glycine might be a possible factor which influences the development of uremic toxaemia.

Acute Kidney Injury↗