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Biomedical subjects

S Ida

Publications and source records attributed to S Ida.

119 records · Page 7Linked to original sources
PubMed1971

Effect of antilymphocyte serum on reovirus infection of mice.

Reovirus type 3 infection in mice was investigated, with particular reference to the effect of antilymphocyte serum. With virus inoculation, a characteristic acute disease was manifested in the mice younger than 5 days old but not in mice 7 days old or older. However, a single injection of antilymphocyte serum, which was prepared in rabbits immunized with mouse thymocytes, followed by virus inoculation induced the acute disease in mice 7 days old or older. The latter result suggests that this production of the acute disease may be due to a suppression of the cellular immune mechanism sensitive to antilymphocyte serum.

Journal Article↗
PubMed1965

Permeability of Nitrobacter agilis to Organic Compounds.

Ida, S. (Cornell University, Ithaca, N.Y.), and M. Alexander. Permeability of Nitrobacter agilis to organic compounds. J. Bacteriol. 90:151-156. 1965.-None of a variety of inorganic ions or organic compounds served as a sole energy source for the growth of Nitrobacter agilis, and the test substrates were not oxidized by either intact cells or extracts of the obligate chemoautotroph. The organic substances did not serve as sole carbon sources for the bacterium in a synthetic medium, and they failed to enhance the rate of nitrite oxidation. The organism was permeable to acetate and a number of other simple carbon compounds, however, and exogenously supplied acetate was converted to a number of products. On the basis of these findings, possible reasons are examined for the inability of the chemoautotroph to use exogenous organic compounds as energy or carbon sources.

Journal Article↗
PubMedDate not supplied

Urinary coproporphyrin isomers in Rotor's syndrome: a study in eight families.

Urinary coproporphyrin isomers were measured in 17 patients with Rotor's syndrome, 65 phenotypically normal relatives of 14 patients from eight families, and 21 normal subjects. coproporphyrin I was elevated in Rotor's syndrome (p less than 0.001) and, to a lesser degree, in phenotypically normal parents (p less than 0.005), children, and siblings (p less than 0.025) as compared to normal controls. Coproporphyrin III in patients, parents, and children did not differ from that in normal controls. Genetic analysis was consistent with transmission of Rotor's syndrome as an autosomal recessive trait with respect to urinary excretion of coproporphyrin I. After i.v. injection of delta-aminolevulinic acid, urinary coproporphyrin I increased to a similar extent in Rotor's syndrome and in normal subjects; urinary coproporphyrin III excretion was less in Rotor's syndrome than in normal subjects.

Adult↗
PubMedDate not supplied

Preparation of N-alkylated 5-oxo-3-carboxamyl-1,4-thiazinanes on solid support.

A general method was developed to generate six-membered cyclic thiazinanes on solid support. Three diversity sites were introduced into this scaffold using primary amines, aldehydes, and 2-bromoalkanoic acids. The methodology to prepare individual cyclic thiazinanes as well as combinatorial libraries of these compounds is described.

Alkylation↗
PubMedDate not supplied

Acute effects of griseofulvin on the pharmacokinetics and pharmacodynamics of warfarin in rats.

It has been reported that prothrombin time (PT), which is prolonged by warfarin, is reduced when patients on warfarin also take griseofulvin repeatedly. We investigated the cause of the drug interaction and the initial effects of griseofulvin on warfarin pharmacokinetics. Total cytochrome P-450, and the activities of aminopyrine N-demethylase, aniline p-hydroxylase and 7-ethoxycoumarin O-deethylase, after repeated administration of griseofulvin (100 mg/kg orally daily for 5 days) were examined. Acute effects of single doses of griseofulvin (100 mg/kg) on coagulation activity (prothrombin time) and warfarin pharmacokinetics after administration of warfarin were also studied. Repeated administration of griseofulvin induced warfarin-metabolizing enzymes. In contrast, a single administration of griseofulvin increased prothrombin time and serum warfarin concentrations. The activity of a warfarin-metabolizing enzyme (7-ethoxycoumarin O-deethylase) was reduced when griseofulvin was added to rat liver microsomes. The results suggest that reduced warfarin action after repeated administration of griseofulvin may be due to induction of warfarin-metabolizing enzymes, but that there is also an initial increase in warfarin action.

Animals↗