Search PubMed⌕ Search

Biomedical subjects

J F Wilber

Publications and source records attributed to J F Wilber.

At least 91 records · Page 5Linked to original sources

Thyrotropin-releasing hormone activity in the human placenta.

TRH immunological and biological activities were found in extracts of human placentas. Eight term placentas delivered by cesarean section were extracted with 2 N acetic acid, followed by glacial acetic acid. Lyophilized samples were resuspended in phosphate-buffered saline. TRH activity, identified in each placental extract by specific RIA, averaged 19.8 +/- 3.3 pg/mg protein. TRH in the placental extracts was similar to synthetic TRH by four criteria. 1) Serial dilutions of placental extracts defined an immunoassay inhibition curve with a slope (-1.93) identical to synthetic TRH (-1.88). 2) When placental extract or synthetic TRH was chromatographed on Sephadex G-10, TRH immunoreactivity was found in similar fractions of the eluate. 3) Both placental extract and synthetic TRH stimulated TSH release from rat pituitaries in vitro. 4) Human serum degraded placental extract and synthetic TRH in a qualitatively similar manner. Placental minces did not accumulate exogenous [3H]TRH, suggesting that the placental TRH may originate endogenously.

Animals↗

Endogenous thyrotropin-releasing hormone in the anterior pituitary: sites of activity as identified by immunocytochemical staining.

Thyrotropin-releasing hormone (TRH) immunoreactivity was localized in the rat anterior pituitary with rabbit anti-TRH sera and the unlabeled antibody peroxidase-antiperoxidase complex (PAP) technique. Stain was present in secretory granules of cells possessing morphological characteristics of thyrotropes, gonadotropes and lactotropes. Antibody absorption studies with anti-TRH sera absorbed with TRH, 3 diastereoisomeric analogues of TRH, gonadotropin-releasing hormone (GnRH), bovine serum albumin, thyrotropin, prolactin, adrenocorticotropin, luteinizing hormone, follicle stimulating hormone were performed to determine the specificity of the staining reaction. Only absorption with TRH resulted in a significant reduction in staining intensity. In vitro experiments were then begun with hemipituitaries to ascertain if intrapituitary TRH might originate by sequestration of exogenous, plasma membrane bound TRH or by de novo synthesis. The results suggest that anterior pituitary TRH is of endogenous origin.

Animals↗

Cushing's syndrome associated with galactorrhea, amenorrhea, and hypothyroidism: a primary hypothalamic disorder.

A 19-year-old woman presented with a unique constellation of endocrinopathies, including Cushing's disease, post-partum galactorrhea, hypothalamic hypothyroidism and hypothalamic amenorrhea. There was no evidence of granulomatous or neoplastic disease in pituitary or hypothalamus. The potential role of excess glucocorticoids and disturbances in normal hypothalamic regulation of anterior pituitary function in the pathophysiology of this syndrome is discussed.

Adrenalectomy↗

Thyrotropin-releasing hormone secretory physiology: studies by radioimmunoassay and affinity chromatography.

Thyrotropin-releasing hormone (TRH) in rat blood and mathanol extracts of hypothalami has been quantified by a specific TRH radioimmunoassay, in conjunction with TRH affinity chromatography. Blood TRH was found to be elevated dramatically after 1 h by the physiologic stimulus, ambient cold (4 C), which was also attended by a 2-fold rise in serum thyrotropin (TSH). The acute administration of parenteral triodothyronine (T3) over a period of 48 h prior to identical cold exposure completely abolished the rise in serum TSH. Blood TRH however, rose in a fashion qualitatively similar to that seen in euthyroid animals. Similarly, chronic induction (32 days) of experimental euthyroidism, hypothyroidism, and hyperthyroidism, which altered metabolic states were corroborated by measurement of serum thyroxine (T4) and TSH, did not result in any significant changes in either the hypothalamic content or blood concentration of TRH. These data provide direct documentation that the regulatory control of pituitary TSH secretion by T4 and/or T3 is not mediated by inhibiting the hypothalamic secretion of TRH, but presumably by inhibiting the actions of TRH at the level of the pituitary thyrotroph cell.

Animals↗

Thyrotropin-releasing hormone (TRH): Measurements in human spinal fluid.

Levels of thyrotropin-releasing hormone (TRH) were quantitated in human lumbar spinal fluid (CSF) utilizing a sensitive and specific TRH radioimmunoassay. Endogenous TRH was sufficiently stable in CSF to permit 85% recovery of intact TRH after 48 h storage at 4 C. TRH levels in AM or PM samples obtained from 15 women and 12 men were easily detected in all CSF specimens. No significant difference between the TRH concentration in CSF of men and women was observed (44.2+/-6.8 and 38.1+/-6.5 pg/ml (mean+/-SE) respectively). TRH concentrations were 40.2+/-6.9 pg/ml (mean+/-SEM) in AM and 41.4+/-8.0 pg/ml in PM samples. By contrast, CSF cortisol levels obtained concurrently were twofold higher in AM than PM (0.68+/-0.08 vs 0.38+/-0.02 mug/100 ml (mean+/-SEM) respectively, P less than 0.001). These data are consistent with the possibility that a portion of the TRH in CSF can be derived from the central nervous system (CNS) and unrelated to the hypo-physiotropic control of thyrotropin (TSH) synthesis and secretion.

Circadian Rhythm↗