PubMed · 6893732
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H E Zellmann. 1980. Thyroid physiology and functional tests.. https://pubmed.ncbi.nlm.nih.gov/6893732/
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Mutations in the ret proto-oncogene constitute the germ line defect in patients with inherited forms of medullary thyroid carcinoma (MTC) and are also present in tumor DNA from a subset of patients with sporadic forms of MTC. We now show that the TT cell line of human MTC can be induced within 48 h to resemble mature C cell differentiation by activation of the raf-1 signal transduction pathway. Within this time period, expression of both the mutant and wild-type ret gene alleles, present in these cells, are silenced at the mRNA and protein levels. This definition of a signal transduction pathway that can regulate ret gene expression, and of the position of ret gene expression in endocrine differentiation, should help clarify the precise role of this gene in normal neuroendocrine development and in the formation of MTC.
The thyroid glands of 107 SIDS victims (sudden infant death syndrome) have been studied. Controls consisted of 20 thyroid glands from infants who died of other causes (accidents, pneumonia etc.). The thyroid glands were investigated histologically, immunohistologically and morphometrically. Immunohistochemistry (S-100 protein and calcitonin) and morphometry showed no significant results. Histologically, hyperemia (severe: 34 cases = 31.8%; mild: 23 cases = 21.5%), and fibrosis (45 cases = 42.1%; mild: 26 cases = 24.3%) were found. A large number of cases showed depleted follicles (87 cases = 81.3%), little colloid (little: 37 cases = 34.6%; none: 9 cases = 8.4%) and desquamation (severe: 21 cases = 19.6%; abundant: 20 cases = 18.7%). Only fibrosis and depleted follicles were found more often in SIDS than in the controls (conditional logistic regression: rise of incidence for SIDS 2.9 times, P = 0.028, and 1.2 times, P = 0.051, respectively), a commoner occurrence of hyperemia in SIDS was of limited significance (P = 0.105). The alterations found can be taken as stress reactions to current or recurrent hypoxemia and the mild fibrosis indicates recurrent hypoxemia. All alterations indicate that the victims had previously suffered near death episodes. Even though the glands were handled with care, artefacts and autolysis must be taken into consideration. Neither the histological, immunohistological nor morphometrical studies of the thyroid gland gave an explanation as to the cause of death or showed any changes providing explicit help in diagnosing SIDS.
The effect of calcium channel blockers on calcium homeostasis in postmenopausal osteoporotic women with arterial hypertension has not to date been defined. In the submitted study, the influence of nifedipine on serum parathyroid hormone (PTH), calcitonin and osteocalcin is followed in 11 patients. After one month of treatment, serum PTH markedly declined in all women and osteocalcin decreased in 10 patients. In contrast, serum calcitonin increased in five patients, whilst in another five the effect was just the opposite. In one woman this indicator was not affected. There are no mutual correlations between the mentioned indices. In conclusion, the calcitonin secretory process is not sensitive to calcium channel blockade within the present study. In spite of the fact that nifedipine inhibits PTH secretion in postmenopausal osteoporotic women, the direct effect of the drug on osteoblasts (not mediated by PTH) cannot be excluded.