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Biomedical subjects

V Riley

Publications and source records attributed to V Riley.

At least 19 recordsLinked to original sources
PubMed1991

Quantification of Candida albicans morphology in vaginal smears.

The morphology index (Mi) of Candida albicans cells was determined by microscopic image analysis in vaginal smears from 26 patients. The morphology of the cells typically showed a broad distribution of forms, but the mean Mi was greater than 2.0 in 23/26 instances, indicating a preponderance of pseudohyphal and hyphal forms. No association could be found between Mi and the clinical assessment of signs or symptoms of Candida infection. Comparison of these 26 patients with 43 others who had Candida-positive vaginal smears but with fewer than 15 fungal cells in the smear revealed significantly lower scores for vulvovaginal symptoms among the latter.

Candida albicans↗
PubMed1978

Increased tyrosine phenol-lyase activity in mice following pyridoxal phosphate administration.

A limiting factor in the depletion of plasma tyrosine following tyrosine phenol-lyase injection into normal mice was found to be the availability of an essential cofactor, pyridoxal phosphate. Because of the extremely short half-life of this cofactor, adequate elevation of circulating cofactor levels for prolonged periods by injection of a pyridoxal phosphate solution was not practical. Similarly, long-term diets enriched with pyridoxine and pyridoxal phosphate did not significantly improve the efficiency of the injected holoenzyme. A repository dosage form was devised that consisted of an s.c. implant of pyridoxal phosphate suspended in a spermaceti and peanut oil mixture. Under these conditions a sustained increase in holoenzyme activity levels and a significant resulting decrease in plasma tyrosine levels were obtained.

Animals↗
PubMed1976

Breast cancer patients: substance in blood causing acceleration of erythrocyte sedimentation rate.

The frequency distribution curve of the erythrocyte sedimentation rates obtained from a population of 3523 normal females was compared with the distribution found in 544 patients with benign breast disease and that for 385 patients with carcinoma of the breast. No significant difference was found between the normal female population and patients with benign lesions of the breast. This was in contrast to the distorted distribution curve of erythrocyte sedimentation rates exhibited by the population of patients having malignant breast lesions. An unknown substance present in the blood plasma of the cancer patients appears to be responsible for the abnormal sedimentation rate phenomenon.

Blood Sedimentation↗
PubMed1976

Antibody-producing cells: virus-induced alteration of response to antigen.

Spleen antibody-forming cells of mice yield a 3- to 10-fold increase in their response to sheep erythrocyte antigen if they are acutely infected by lactate dehydrogenase-elevating virus. This early stimulation is replaced by a long-term inhibition of the antibody-forming cells as the viremia goes into its persisting chronic stage. These contrasting immunological phenomena are examined as contributing factors responsible for the enhancement by this virus of asparaginase (EC 3.5.1.1; L-asparagine amidolydrolase) therapy against leukemia in mice, and for the alteration of the susceptibility of mice to various neoplastic processes.

Acute Disease↗
PubMed1975

Mouse mammary tumors: alteration of incidence as apparent function of stress.

Eighty to 100 percent of female mice of the C3H/He strain carrying the Bittner oncogenic virus usually develop mammary tumors within 8 to 18 months after birth when studied under the usual housing and experimental conditions. By subjecting various groups of such mice to environmental circumstances providing different degrees of chronic stress, mammary tumor incidence at 400 days was modified, with incidences ranging from 92 percent under stress to 7 percent in a protected environment. The data suggest that moderate chronic or intermittent stress may predispose such mice to an increased risk of mammary carcinoma, possibly through a resultant compromise of their immunological competence or tumor surveillance system, and that adequate protection from physiological stress may reduce mammary tumor occurrence in mice.

Animals↗