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M Katikineni

Publications and source records attributed to M Katikineni.

10 recordsLinked to original sources
PubMed1982

Thyroid nodules after high-dose external radiotherapy. Fine-needle aspiration cytology in diagnosis and management.

From 1974 to 1980, we studied six patients, five treated for Hodgkin's disease and one for a hemangioma, in whom thyroid nodules developed after high-dose (2,500 to 4,000 rad) thyroid radiation. Fine-needle aspiration cytology of the thyroid in five cases showed moderate to severe cellular atypia in four (three of whom had elevated serum thyrotropin levels) and mild atypia in one (who was overtly hypothyroid). In the four with marked atypia, surgical pathology disclosed Hashimoto's thyroiditis in one, diffuse hyperplasia and epithelial atypia in two, and a sclerosing papillary carcinoma in one. Among five patients who had total thyroidectomy, three had carcinoma (microscopic papillary, papillary-follicular, or sclerosing papillary) in addition to one or more follicular adenomas or colloid nodules. Thyroid nodules and neoplasia may be more common than previously appreciated in patients exposed to high-dose radiation.

Adenocarcinoma↗
PubMed1982

Compartmentalization of luteinizing hormone pools: dynamics of gonadotropin releasing hormone action in superfused pituitary cells.

Cultured rat anterior pituitary cells were continuously perfused with medium 199, and exposed to short (5 min), intermediate (30 min), or long (6 h) pulses of a maximally effective concentration of gonadotropin-releasing hormone (GnRH). Assay of the effluent by radioimmunoassay and interstitial-cell bioassay revealed a biphasic response to GnRH, and indicated that 3 pools of luteinizing hormone (LH) are present in the gonadotroph. A rapidly releasable peak of bioactive LH comprising about 2% of the total cellular LH was mobilized within 1 min of GnRH addition, lasted for 3-4 min, and was independent of the duration of stimulation. The second, larger pool of bioactive LH varied from 15 to 50% of the total LH as the duration of exposure to GnRH was increased from 5 min to 6 h. A third LH pool comprising up to 50% of the total LH could be mobilized by 50 mM potassium but not by continuous GnRH treatment, due to refractoriness of the cells to prolonged stimulation by the decapeptide. In contrast, repeated pulses of GnRH evoked a series of biphasic LH peaks with profiles similar to that observed during a single response to GnRH, indicating that continuous exposure to GnRH is necessary for densensitization. Release of LH from the perfused cells was calcium-dependent, and the bio-immuno ratio of the first and second pools of LH was similar. The in vitro secretion profile of cultured rat cells is comparable with the early and late phases of LH release observed in GnRH-infused man, but occurs much more rapidly, and demonstrates heterogeneity of the LH release process at the level of the gonadotroph. The superfusion technique provides a powerful tool to further investigate the bioactivity of GnRH and its analogs for use in fertility control.

Animals↗
PubMed1980

Lactogenic receptor regulation in hormone-stimulated steroidogenic cells.

Receptor sites for lactogenic hormones such as prolactin (PRL), human growth hormone (HGH), and placental lactogens, are widely distributed in mammalian tissues, including mammary glands, steroid-secreting cells of the adrenal, testis, and ovary, and target cells of steroid hormone action such as liver, prostrate, and kidney. Although the biological functions of lactogen binding sites remain uncertain, a relationship between prolactin and lipoprotein metabolism is implied by the occurrence of prolactin receptors in steroidogenic cells of the gonads and adrenal, and by the ability of prolactin to increase esterified cholesterol in the testis. Recently, loss of testicular prolactin receptors has been observed following elevation of circulating luteinising hormone (LH) concentrations by the gonadotropin releasing hormone (GnRH) and its agonist analogues. The hormone dependence of lactogen receptor sites in steroid-secreting cells was further analysed in rat testis, ovary, and adrenal glands after treatment with the respective trophic hormones, gonadotropin and ACTH. In each of these tissues, rapid and transient loss of lactogen receptors was observed after trophic hormone stimulation. These findings indicate that increased turnover of lactogen receptors is an important component of the target-cell response, and suggest that prolactin receptors might be involved in the transport of lipoprotein precursors for steroid biosynthesis.

Adrenal Glands↗
PubMed1980

Direct inhibition of testicular function by gonadotropin-releasing hormone: mediation by specific gonadotropin-releasing hormone receptors in interstitial cells.

Agonist analogs of gonadotropin-releasing hormone (GnRH) have been shown to exert antigonadal effects in male and female animals. In hypophysectomized male rats treated with follicle-stimulating hormone, administration of a potent GnRH agonist caused depletion of luteinizing hormone and prolactin receptors and marked suppression of serum testosterone levels. The possibility that such direct effects of GnRH agonists on testicular function could be expressed through specific receptors located in the interstitial cells of the testis was supported by the selective concentration of a 125I-labeled GnRH agonist by the testis in vivo. Specific receptors for the releasing hormone were demonstrated in testis particles and dispersed interstitial cells by direct binding analysis with the 125I-labeled GnRH agonist. The binding affinity (Ka = G X 10(9) M-1) and peptide specificity of the testicular GnRH binding sites were similar to those of anterior pituitary and ovarian GnRH receptors. The presence of GnRH receptors in the testis indicates that these sites mediate the direct inhibitory actions of GnRH agonists upon testicular endocrine function.

Animals↗