Endocrine
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Activin responsiveness of the murine GnRH receptor (GnRHR) gene promoter requires two spatially distinct regulatory elements termed the GnRH receptor activating sequence or GRAS and the downstream activin regulatory element or DARE. While GRAS interacts with multiple transcription factors, DARE activity requires tandem homeodomain binding motifs (TAAT) and displays specific binding to the LIM homeodomain protein LHX3. Herein, we find that both the murine GnRHR gene promoter and DARE fused to a minimal heterologous promoter are responsive to LHX3 overexpression. ⋯ To determine if this spatial organization is functionally relevant, multiples of 5 bp were inserted or deleted between GRAS and DARE. Any insertion or deletion that resulted in a half-turn alteration in the helical positioning between the two elements reduced promoter activity. Thus, an important spatial relationship underlies functional cooperation between GRAS and DARE and the emergence of a complex activin responsive unit (ARU) within the mouse GnRHR promoter.
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Ovarian hormones can protect against brain injury, neurodegeneration, and cognitive decline. Most attention has focused on estrogens and accumulating data demonstrate that estrogen seems to specifically protect cortical and hippocampal neurons from ischemic injury and from damage due to severe seizures. Although multiple studies demonstrate protection by estrogen, in only a few instances is the issue of how the steroid confers protection known. ⋯ Analysis of neurogranin mRNA, a marker of viability of hippocampal neurons, with in situ hybridization, revealed that estrogen treatment protected the dorsal CA1 regions not only when administered before, but also when given 1 h after occlusion. Estrogen rarely is secreted alone and studies of neuroprotection have been less extensive for a second key ovarian hormone progesterone. In the second half of this review, we present data on neuroprotection by estrogen and progesterone in animal model of epilepsy followed by exploration into ovarian steroid effects on neuronal damage in models of multiple sclerosis and traumatic brain injury.
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Review Case Reports
Epinephrine-secreting cystic pheochromocytoma presenting with an incidental adrenal mass: a case report and a review of the literature.
Cystic adrenal masses are a relatively rare condition, and are usually nonfunctioning and asymptomatic. Differential diagnosis includes pheochromocytoma (PHEO) and adrenal carcinoma; 8-10% of patients with PHEO may be completely asymptomatic. Moreover, fewer than 10% of PHEOs secrete pure epinephrine. ⋯ Right adrenalectomy was performed; the surgical specimen revealed pure cystic PHEO. Postoperatively, the urine metanephrine level returned to normal range and urine epineprine level was decreased approx 60%. In conclusion, a diagnosis of E-secreting PHEO should be considered in patients with nonspecific symptoms, presenting with an incidental cystic adrenal mass, even in the absence of hypertension.
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Although surgical extirpation by transsphenoidal microsurgery is a major remedy for pituitary adenomas, adjuvant therapy also plays an important role in achieving tumor growth control and endocrine normalization in hormone-secreting tumors. Historically, the treatment options for pituitary adenomas included microsurgery, medical management, and fractionated radiotherapy, but radiosurgery has recently emerged as a practical treatment option. In this paper, we will describe the indications, radiosurgical procedure, results, histological change, and complications of gamma knife radiosurgery (GKS) for pituitary adenomas based on our experience since 1991 and a review of the literature.
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Thyrotoxic hypokalemic periodic paralysis (THPP) is a very rare complication of thyrotoxicosis in whites, but is more frequently reported in individuals of Asian descent. Hypokalemia, with associated flaccid paralysis, and signs of hyperthyroidism, are the hallmark. We have reported a case of a 28-yr-old white man with Graves' disease presenting with a 2-wk history of episodic flaccid quadriplegia. ⋯ He was treated with propranolol and, subsequently, methimazole. He had no further episodes of hypokalemic paralysis. To the best of the author's knowledge, and after a Medline search, THPP has not been described previously in a Turkish man.