Biomedical subjects

T H Kennedy

Publications and source records attributed to T H Kennedy.

13 recordsLinked to original sources

PubMed1976

Carcinogenicity of dimethylnitramine in NZR rats in NZO mice.

Lifetime tests were done in NZR inbred rats of dimethylnitramine (DMNO) by addition to the drinking water (average dose 1.83 g/kg body weight) and in NZO mice by repeated subcutaneous injection from birth to 7 months of age followed by administration in drinking water (total average dose 4.72 g/kg body weight). Rats developed hepatocellular carcinomas (85%), some of which metastasized. Mice developed hepatocellular carcinomas (81%) and renal adenocarcinomas (48%). Statistically significant increases of other tumor types also occurred in mice. The main targets for DMNO carcinogenesis appeared to be the liver cell epithelium and, at higher dose rates, renal tubular epithelium.

Adenocarcinoma↗

PubMed1976

Evidence that mouse thyroid stimulator does not stimulate the human thyroid gland.

Thyroid 131I uptake and human thyroid stimulator (HTS) level were measured in 20 untreated thyrotoxic patients who also showed mouse thyroid stimulator (MTS) ACtivity. The correlation between thyroid uptake and HTS level was highly significant (P less than 0-005), the coefficient, r, being 0-66, comparable with the value 0-68 obtained in a previous study of patients not showing MTS. Thus, the presence of widely varying amounts of MTS does not impair the close correlation existing between HTS level and thyroid 131I uptake in thyrotoxic people. There was no correlation between MTS level and thyroid 131I uptake (r = 0-11, n.s.). It is concluded that MTS, a potent stimulator of the thyroid glands of mice, guinea pigs and monkeys, does not stimulate the human thyroid gland.

Animals↗

PubMed1975

Hyperthyroidism in Tasmania following iodide supplementation: measurements of thyroid-stimulating autoantibodies and thyrotropin.

Serum thyroid-stimulating autoantibodies (LATS and LATS protector) and thyrotropin (TSH) concentrations were measured in the serum of 30 patients with hyperthyroidism living in Tasmania who developed their disease following correction of iodine deficiency by addition of iodate to the bread. Patients were grouped according to thyroid scan results. None of 8 patients with autonomous thyroid nodules had thyroid-stimulating autoantibodies. These were present in both of the patients with uniform thyroid scans and 14 of 20 patients (70%) with irregular scans without demonstrated localized autonomy. Serum TSH, measured by immunoassay of concentrated serum extracts, was 0.15 muU/ml or less in all patients, below the range of 0.35 to 2.60 muU/ml found in normal subjects. Only 6 (20%) of the 30 patients failed to show either localized autonomy or thyroid-stimulating autoantibodies. In most regards these patients resembled those with antonomous nodules. The findings support the conclusion that the increased incidence of phyerthyroidism in Tasmania was due to an increased supply of iodine to patients with latent hyperthyroidism whose thyroid glands, due to the presence of toxid nodule(s) or thyroid-stimulating autoantibodies, were unresponsive to control by TSH deprivation. There was no evidence for additional pathogenic mechanisms

Adult↗

PubMed1974

Correlation between long-acting thyroid stimulator protector level and thyroid 131-I uptake in thyrotoxicosis.

Out of 50 consecutive untreated patients with diffuse toxic goitre 15 showed long-acting thyroid stimulator (LATS), 30 showed LATS protector only, and five showed neither. LATS protector was present in all the patients with LATS. Infiltrative ophthalmopathy was less common in patients with LATS protector only (40%) than in patients with LATS also (67%), but the difference was not significant. There was a correlation between LATS protector level and thyroid (131)I uptake rate factor (k(1)), the coefficient (r) being 0.68 (P < 0.001). LATS level showed no such correlation. The results support the hypothesis that LATS protector is a pathogenic thyroid stimulator in patients with diffuse toxic goitre.

Animals↗

PubMed1974