We have experimentally elevated the triiodothyronine ("3) content of striped bass (Morone saxutilis) eggs by injecting female striped bass intramuscularly with a large dose of T3 (20 pglg body weight) shortly before the induction of spawning. The significant elevation of T3 concentrations in the eggs from the hormone-injected fish (to 180 ng per gram), compared with those of vehicleinjected controls (about 19 nglg), confirms the transfer of T3 from the maternal circulation into oocytes. There were significant differences in the development of embryos and larvae from the two groups. Within the first week after hatching, the hormone-treated cohorts showed significantly greater larval body area, length, and dry weight, despite similar patterns of yolk and oil-globule utilization. The rate of swimbladder inflation and the survival rate were also significantly enhanced in the cohorts produced by T3-treated females. There was a positive and highly significant correlation between the concentration of T3 in the unfertilized oocytes and the rate of survival within the cohort. The improvement in larval survival may be a result of the maintenance of elevated T3 levels through the first week of development: during the transition to active feeding but before the onset of larval thyroid function. Thyroid hormone supplements appear to confer a distinct advantage to larval striped bass during this early, fragile developmental stage.
The gene for the alpha polypeptide chain (alpha s) of the heterotrimeric G protein Gs can be activated to the putative oncogene gsp by specific point mutations at codons 201 and 227. Such mutations have been reported in 40% of human growth hormone-secreting pituitary adenomas and in a single autonomously functioning thyroid adenoma. We examined an archival series of 45 differentiated human thyroid tumors by polymerase chain reaction amplification and oligonucleotide hybridization to identify point mutations at each of the affected codons. Successful amplification was achieved in 38 cases, and activating mutations were identified in 5 of 13 (38%) autonomously functioning adenomas, but in none of 16 nonfunctioning adenomas, six papillary carcinomas, or three follicular carcinomas. Our results confirm that the gsp oncogene is involved in the pathogenesis of autonomously functioning tumors but do not support a role in other thyroid tumors.
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