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Artykuły w czasopismach na temat „Thyrotropin releasing hormone”

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Data publikacji: 4 czerwca 2021

Data aktualizacji: 7 lutego 2022

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1

GURLL, NELSON J., JOHN W. HOLADAY, DAVID G. REYNOLDS i ERIC GANES. "Thyrotropin releasing hormone". Critical Care Medicine 15, nr 6 (czerwiec 1987): 574–81. http://dx.doi.org/10.1097/00003246-198706000-00006.

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2

O'Leary, Rhonda, i Brendan O'Connor. "Thyrotropin-Releasing Hormone". Journal of Neurochemistry 65, nr 3 (23.11.2002): 953–63. http://dx.doi.org/10.1046/j.1471-4159.1995.65030953.x.

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3

ROBERTSON, ROBERT G., JULIE A. KELLY i EWAN GRIFFITHS. "Thyrotrophin-releasing hormone analogue binding to central thyrotropin-releasing hormone receptors". Biochemical Society Transactions 14, nr 6 (1.12.1986): 1245–46. http://dx.doi.org/10.1042/bst0141245.

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4

Villalobos, Carlos, Lucía Núñez i Javier García-Sancho. "Anterior pituitary thyrotropes are multifunctional cells". American Journal of Physiology-Endocrinology and Metabolism 287, nr 6 (grudzień 2004): E1166—E1170. http://dx.doi.org/10.1152/ajpendo.00194.2004.

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Anterior pituitary (AP) contains some unorthodox multifunctional cells that store and secrete two different AP hormones (polyhormonal cells) and/or respond to several hypothalamic-releasing hormones (HRHs; multiresponsive cells). Multifunctional cells may be involved in paradoxical secretion (secretion of a given AP hormone evoked by a noncorresponding HRH) and transdifferentiation (phenotypic switch between different mature cell types without cell division). Here we combine calcium imaging (to assess responses to the four HRHs) and multiple sequential immunoassay of the six AP hormones to perform a single-cell phenotypic study of thyrotropes in normal male and female mice. Surprisingly, most of the thyrotropes were polyhormonal, containing, in addition to thyrotropin (TSH), luteinizing hormone (40–42%) and prolactin (19–21%). Thyrotropes costoring growth hormone and/or ACTH were found only in females (24% of each type). These results suggest that costorage of the different hormones does not happen at random and that gender favors certain hormone combinations. Our results indicate that thyrotropes are a mosaic of cell phenotypes rather than a single cell type. The striking promiscuity of TSH storage should originate considerable mix-up of AP hormone secretions on stimulation of thyrotropes. However, response to thyrotropin-releasing hormone was much weaker in the polyhormonal thyrotropes than in the monohormonal ones. This would limit the appearance of paradoxical secretion under physiological conditions and suggests that timing of hormone and HRH receptor expression during the transdifferentiation process is finely and differentially regulated.

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5

Takeuchi, Yoshihiro. "Thyrotropin-Releasing Hormone (Protirelin)". CNS Drugs 6, nr 5 (listopad 1996): 341–50. http://dx.doi.org/10.2165/00023210-199606050-00001.

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6

Colson, A., i M. Gershengorn. "Thyrotropin-Releasing Hormone Analogs". Mini-Reviews in Medicinal Chemistry 6, nr 2 (1.02.2006): 221–26. http://dx.doi.org/10.2174/138955706775476019.

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7

Le Dafniet, Michèle, Anne-Marie Brandi, Michèle Kujas, Philippe Chanson i Françoise Peillon. "Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas". European Journal of Endocrinology 130, nr 6 (czerwiec 1994): 559–64. http://dx.doi.org/10.1530/eje.0.1300559.

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Le Dafniet M, Brandi A-M, Kujas M, Chanson P, Peillon F. Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas. Eur J Endocrinol 1994:130:559–64. ISSN 0804–4643 In order to see whether, in thyrotropic adenomas with thyrotoxicosis, plasma thyroid hormones regulate the thyrotropin-releasing hormone (TRH) binding sites and the thyrotropin (TSH) response to TRH, we investigated: the presence of TRH binding sites in two cases of thyrotropic adenomas associated with hyperthyroidism and in one case of thyrotropic adenoma secondary to thyroid failure; and the in vitro effect, in a perifusion system, of triiodothyronine (T3) on the response of TSH to TRH in three cases of TSH-secreting adenomas associated with hyperthyroidism. The TRH binding sites were absent in the adenomas associated with high levels of circulating thyroid hormones, whereas they were present in the adenoma secondary to primary thyroid failure (K4 =47 nmol/l, Bmax = 40 nmol/ kg membrane proteins). In vitro, the three adenomas spontaneously released TSH in the perifusion medium (1.49 ±0.06 (mean ± sem), 7.25±0.12 and 16.73±0.36 mIU·−1·106 cells−1·2 min−1) and exhibited an ample TSH response to 10−7 mol/l TRH pulses. In two cases, tumoral secretion of fragments was compared with those of fragments maintained since the time of surgical removal in the presence of 10−8 mol/l T3. The TSH responses to TRH were abolished in the presence of T3 in these two cases. We conclude that thyrotropic adenomas associated with hyperthyroidism are still controlled in vivo by T3. In particular, T3 regulates the TSH response to TRH, probably via a down-regulation of the TRH binding sites. Michèle Le Dafniet, Unité INSERM 223, Faculté de Médecine, Pitié-Salpêtrière, 105 Boulevard de l'Hôpital, 75013 Paris, France

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8

Oturai, Peter S., Lars Friberg, Ian Sam i Hans Perrild. "Effects of thyrotropin-releasing hormone on regional cerebral blood flow in man". Acta Endocrinologica 126, nr 3 (marzec 1992): 243–46. http://dx.doi.org/10.1530/acta.0.1260243.

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To assess the regional changes in cerebral blood flow, 10 healthy volunteers were given 400 μg thyrotropin-releasing hormone iv in a double-blind, randomized, cross-over study. Regional cerebral blood flow was determined simultaneously in two slices of the brain, using a single photon emission computerized tomograph and inhalation of 133Xe. Thyrotropin-releasing hormone caused a significant mean increase of 3.7% (range −8.8–22.7) in blood flow in a region consistent with the left thalamus compared to placebo (3.2% decrease). In 25 other regions no significant change was detected. The thalamic region has previously been shown to be a region especially affected by thyrotropin-releasing hormone in animal studies. The thyrotropin-releasing hormone injection was followed by a minor rise in systemic blood pressure, but not a rise that could affect the cerebral blood flow. The effect of thyrotropin-releasing hormone on the regional cerebral blood flow in the thalamic region was much lower compared to changes found in sedated animals given a hundredfold higher dose of thyrotropin-releasing hormone.

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9

Bulatov, A. A., E. E. Makarovskaya, N. B. Smirnova, V. G. Shlykova i S. Yu Kasumova. "Multigormonal secretory activity of cells of clinically non-functioning pituitary tumors in vitro and the effect of tyroliberin on it". Problems of Endocrinology 45, nr 1 (6.10.2019): 40–43. http://dx.doi.org/10.14341/probl11705.

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Experiments on cell cultures demonstrated that isolated cells of clinically inert pituitary tumors release several hormones in small amounts into the medium: luteinizing and follicle-stimulating hormones, alpha-subunit of glycoprotein hormones, prolactin, and growth hormone. Multihormonal secretion of these cells indicates their poor morphofunctional differentiation. In contrast to normal pituitary cells, cells of clinically inert pituitary tumors respond nonspeciflcally to hypothalamic thyrotropin releasing hormone: by increased secretion of prolactin, gonadotropins, glycoprotein hormone alpha-subunit, and growth hormone. This capacity of tumor cells detected in vitro agrees with the probability of increased levels of gonadotropins and glycoprotein hormone alpha-subunit in the serum of patients with clinically inert pituitary tumors during pharmacodynamic thyrotropin releasing hormone test.

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10

BROOKE, MICHAEL H. "Thyrotropin-Releasing Hormone in ALS." Annals of the New York Academy of Sciences 553, nr 1 Thyrotropin-R (marzec 1989): 422–30. http://dx.doi.org/10.1111/j.1749-6632.1989.tb46663.x.

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11

Horita, A., M. A. Carino i H. Lai. "Pharmacology of Thyrotropin-Releasing Hormone". Annual Review of Pharmacology and Toxicology 26, nr 1 (kwiecień 1986): 311–32. http://dx.doi.org/10.1146/annurev.pa.26.040186.001523.

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12

Wilber, John F., Pei Feng, Qiao-Ling Li i Zhan Xiang Shi. "The thyrotropin-releasing hormone gene". Trends in Endocrinology & Metabolism 7, nr 3 (kwiecień 1996): 93–100. http://dx.doi.org/10.1016/1043-2760(96)00022-7.

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13

Holsboer, F., A. Gerken, U. von Bardeleben, W. Grimm, H. Beyer, O. A. Müller i G. K. Stalla. "Human corticotropin-releasing hormone in depression—correlation with thyrotropin secretion following thyrotropin-releasing hormone". Biological Psychiatry 21, nr 7 (czerwiec 1986): 601–11. http://dx.doi.org/10.1016/0006-3223(86)90121-6.

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14

PERSANI, LUCA. "Hypothalamic Thyrotropin-Releasing Hormone and Thyrotropin Biological Activity". Thyroid 8, nr 10 (październik 1998): 941–46. http://dx.doi.org/10.1089/thy.1998.8.941.

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15

Jackson, I. M. "Thyrotropin-releasing hormone and corticotropin-releasing hormone--what's the message?" Endocrinology 136, nr 7 (lipiec 1995): 2793–94. http://dx.doi.org/10.1210/endo.136.7.7789303.

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16

Lehnert, H., M. Nink, K. Mann, J. Röschke i Dirk H. Hellhammer. "Extrapituitary Effects of Corticotropin Releasing Hormone and Thyrotropin Releasing Hormone". Neuropsychobiology 28, nr 1-2 (1993): 54–61. http://dx.doi.org/10.1159/000119000.

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17

Caldwell, G., S. M. Gow, V. M. Sweeting, G. J. Beckett, J. Seth i A. D. Toft. "Value and limitations of a highly sensitive immunoradiometric assay for thyrotropin in the study of thyrotroph function." Clinical Chemistry 33, nr 2 (1.02.1987): 303–5. http://dx.doi.org/10.1093/clinchem/33.2.303.

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Abstract Using a highly sensitive and specific immunoradiometric assay for thyrotropin, we studied thyrotroph function in 232 new patients referred to a thyroid clinic and in 13 patients after treatment for hyperthyroidism. Significant thyrotroph responsiveness to thyroliberin (thyrotropin-releasing hormone, TRH) was found in all patients with values for basal thyrotropin greater than 0.1 milli-int unit/L. In no overtly hyperthyroid patient was any increment in thyrotropin recorded at 20 min after thyroliberin administration. In seven patients, four subclinically hyperthyroid and three who had received treatment, increments in thyrotropin from undetectable basal values were recorded, consistent with incomplete thyrotroph suppression. By use of assays with even higher sensitivity, one may be able to distinguish these patients from overtly hyperthyroid patients.

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18

Lesch, K. P., U. Müller, R. Rupprecht, K. Kruse i H. M. Schulte. "Endocrine responses to growth hormone-releasing hormone, thyrotropin-releasing hormone and corticotropin-releasing hormone in depression". Acta Psychiatrica Scandinavica 79, nr 6 (czerwiec 1989): 597–602. http://dx.doi.org/10.1111/j.1600-0447.1989.tb10308.x.

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19

Banki, Csaba M., Lajos Karmacsi, Garth Bissette i Charles B. Nemeroff. "CSF corticotropin releasing hormone, somatostatin, and thyrotropin releasing hormone in schizophrenia". Psychiatry Research 43, nr 1 (lipiec 1992): 13–21. http://dx.doi.org/10.1016/0165-1781(92)90137-r.

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20

Piccini, Paola, Angelo Nuti, Anna Maria Paoletti, Alessandro Napolitano, Gian Benedetto Melis i Ubaldo Bonuccelli. "Possible Involvement of Dopaminergic Mechanisms in the Antimigraine Action of Flunarizine". Cephalalgia 10, nr 1 (luty 1990): 3–8. http://dx.doi.org/10.1046/j.1468-2982.1990.1001003.x.

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Flunarizine, a calcium antagonist widely used in the prophylactic treatment of migraine, may interfere with dopaminergic systems. Flunarizine therapy can in fact induce extrapyramidal side effects and can increase basal as well as stimulated prolactin levels. To better define the mechanism of flunarizine action in migraine, we studied prolactin and growth hormone responses to thyrotropin releasing hormone and sulpiride in 13 female migraineurs before and after 60 days of flunarizine therapy. The treatment did not modify basal prolactin and growth hormone levels, but prolactin response to thyrotropin releasing hormone was enhanced. A paradoxical increase of growth hormone to thyrotropin releasing hormone observed before therapy was blunted after flunarizine treatment. These data indicate a modulatory action of flunarizine on dopaminergic systems which might to some extent explain the antimigraine action of this drug.

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21

Millichap, J. Gordon. "Thyrotropin-Releasing Hormone for Cerebellar Ataxia". Pediatric Neurology Briefs 3, nr 3 (1.03.1989): 21. http://dx.doi.org/10.15844/pedneurbriefs-3-3-6.

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22

García, Silvia I., i Carlos J. Pirola. "Thyrotropin-releasing hormone in cardiovascular pathophysiology". Regulatory Peptides 128, nr 3 (czerwiec 2005): 239–46. http://dx.doi.org/10.1016/j.regpep.2005.01.002.

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23

Sevarino, K. A., R. H. Goodman, J. Spiess, I. M. Jackson i P. Wu. "Thyrotropin-releasing hormone (TRH) precursor processing". Journal of Biological Chemistry 264, nr 36 (grudzień 1989): 21529–35. http://dx.doi.org/10.1016/s0021-9258(20)88217-9.

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24

KARYDIS, IOANNIS, i GEORGE TOLIS. "Orexis, Anorexia, and Thyrotropin-Releasing Hormone". Thyroid 8, nr 10 (październik 1998): 947–50. http://dx.doi.org/10.1089/thy.1998.8.947.

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Frye, Mark A., Keith A. Gary, Lauren B. Marangell, Mark S. George, Ann M. Callahan, John T. Little, Teresa Huggins i in. "CSF Thyrotropin-Releasing Hormone Gender Difference". Journal of Neuropsychiatry and Clinical Neurosciences 11, nr 3 (sierpień 1999): 349–53. http://dx.doi.org/10.1176/jnp.11.3.349.

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Munsat, T. L., J. Taft i I. M. D. Jackson. "Pharrnacokinetics of intrathecal thyrotropin-releasing hormone". Neurology 37, nr 4 (1.04.1987): 597. http://dx.doi.org/10.1212/wnl.37.4.597.

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Van den Berghe, Greet, Francis de Zegher, Dirk Vlasselaers, Miet Schetz, Charles Verwaest, Patrick Ferdinande i Peter Lauwers. "Thyrotropin-releasing hormone in critical illness". Critical Care Medicine 24, nr 4 (kwiecień 1996): 590–95. http://dx.doi.org/10.1097/00003246-199604000-00007.

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Sirén, Anna-Leena. "Cardiovascular pharmacology of thyrotropin releasing hormone". Peptides 9 (styczeń 1988): 69–73. http://dx.doi.org/10.1016/0196-9781(88)90226-4.

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Angelucci, L., S. Scaccianoce, F. R. Patacchioli i R. Nicolai. "Pharmacological aspects of thyrotropin-releasing hormone". Pharmacological Research 22 (wrzesień 1990): 16. http://dx.doi.org/10.1016/1043-6618(90)90052-f.

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Negrev, Negrin, Yuri Nyagolov, Margarita Stefanova i Emiliya Stancheva. "Thyroid hormonal axis regulates protein C anticoagulation pathway in rats". Open Life Sciences 6, nr 4 (1.08.2011): 518–23. http://dx.doi.org/10.2478/s11535-011-0031-y.

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AbstractEffects of the hormones of the hypothalamic-pituitary-thyroid axis on some basic parameters of the activity of protein C anticoagulation pathway in rats are studied. Thyrotropin-releasing hormone (0.06 mg/kg body mass), thyrotropin (1 IU/kg), triiodothyronine (T3) (0.08 mg/kg), thyroxine (T4) (0.08 mg/kg), administered subcutaneously for three consecutive days on four different groups of rats increased significantly activated protein C, free protein S and protein S activity, and reduced the soluble endothelial protein C receptor. Protein C antigen and total protein S were significantly elevated only by thyrotropin-releasing hormone and thyroid-stimulating hormone, but they were not affected by T3 and T4 treatment. The data indicate the hypothalamic-pituitary-thyroid axis is involved in the regulation of the protein C anticoagulation pathway in rats by activation of this system, suggesting a tendency of hypocoagulability.

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31

de Greef, Wim J., Jan MM Rondeel, Rogier Heide, Wim Klootwijk i Theo J. Visser. "Is thyrotropin-releasing hormone immunoreactivity in peripheral blood an estimate for hypothalamic thyrotropin-releasing hormone release?" Acta Endocrinologica 126, nr 3 (marzec 1992): 276–81. http://dx.doi.org/10.1530/acta.0.1260276.

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The significance of TRH for pituitary function is still unresolved mainly due to limitations in determining in vivo hypothalamic TRH release. We therefore examined whether TRH immunoreactivity (TRH-IR) in peripheral blood is an index for hypothalamic TRH release. Peripheral TRH-IR varied between 10 and 55 pmol/l and was similar in euthyroid and hypothyroid rats, but lower in hyperthyroid rats. Destruction of the hypothalamic paraventricular area reduced peripheral TRH-IR, while stimulation of this area increased it. Clearance of TRH during continuous TRH infusion was 1.9±0.2, 3.5±0.3 and 5.9±0.8 ml/min in hypothyroid, euthyroid and hyperthyroid rats, respectively. These and previous data on TRH in hypophysial portal blood indicate that 5–25 pmol TRH/I peripheral blood is of hypothalamic origin. Chromatography revealed that TRH-IR from hypothalamus and portal blood co-eluted with TRH, but in peripheral blood two peaks were found, one of which was authentic TRH. Thus, peripheral TRH-IR alters in experimental conditions and part of it seems to be of hypothalamic origin. However, the presence of TRH-like material in peripheral blood not identical to TRH and the fact that experimental conditions alter TRH clearance indicate that peripheral TRH-IR is not an index for hypothalamic TRH release.

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32

HEUER, HEIKE, MARTIN K. H. SCHÄFER i KARL BAUER. "The Thyrotropin-Releasing Hormone-Degrading Ectoenzyme: The Third Element of the Thyrotropin-Releasing Hormone-Signaling System". Thyroid 8, nr 10 (październik 1998): 915–20. http://dx.doi.org/10.1089/thy.1998.8.915.

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Sumita, S., Y. Ujike, H. Iwasaki, M. Kawamata, Y. Schichinohe, H. Watanabe i A. Namiki. "Plasma Somatostatin Correlates with Blunted Thyrotropin Secretion after Stimulation by Thyrotropin-Releasing Hormone in Critical Illness". Anaesthesia and Intensive Care 25, nr 3 (czerwiec 1997): 267–71. http://dx.doi.org/10.1177/0310057x9702500311.

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To clarify whether plasma somatostatin affects thyrotropin secretion in critical illness, plasma somatostatin and thyrotropin responses to thyrotropin-releasing hormone were studied in forty-three critically ill patients. High somatostatin levels were associated with blunted thyrotropin secretion in critically ill patients. There was an inverse correlation between plasma somatostatin levels and the maximum increment of thyrotropin after stimulation by thyrotropin-releasing hormone. Decreased somatostatin and increased thyrotropin secretion before discharge from the intensive care unit were demonstrated in survivors. On the other hand, non-survivors maintained high somatostatin levels and had blunted thyrotropin secretion during their intensive care admission. These results suggest that high plasma somatostatin levels may play a role in the blunted thyrotropin secretion observed in critical illness.

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34

AMARANT, Tanchum, Mati FRIDKIN i Yitzhak KOCH. "Luteinizing Hormone-Releasing Hormone and Thyrotropin-Releasing Hormone in Human and Bovine Milk". European Journal of Biochemistry 127, nr 3 (3.03.2005): 647–50. http://dx.doi.org/10.1111/j.1432-1033.1982.tb06921.x.

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YU, RUN, RACHEL ASHWORTH i PATRICIA M. HINKLE. "Receptors for Thyrotropin-Releasing Hormone on Rat Lactotropes and Thyrotropes". Thyroid 8, nr 10 (październik 1998): 887–94. http://dx.doi.org/10.1089/thy.1998.8.887.

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Stevenin, Boris, i Stephanie L. Lee. "Hormonal Regulation of the Thyrotropin Releasing Hormone (TRH) Gene". Endocrinologist 5, nr 4 (lipiec 1995): 286–96. http://dx.doi.org/10.1097/00019616-199507000-00008.

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Thakore, J. H., i T. G. Dinan. "Serum thyrotropin responses to thyrotropin-releasing hormone in Korsakoff's syndrome". Acta Psychiatrica Scandinavica 88, nr 3 (wrzesień 1993): 218–20. http://dx.doi.org/10.1111/j.1600-0447.1993.tb03442.x.

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Wahby, Victor S., Guirguis A. Ibrahim, Earl L. Giller, John W. Mason, Fouad W. Saddik, John R. Adams, Richard P. Martin i Emad R. Milad. "Thyrotropin response to thyrotropin-releasing hormone in RDC schizodepressed men". Journal of Affective Disorders 15, nr 1 (lipiec 1988): 81–85. http://dx.doi.org/10.1016/0165-0327(88)90012-2.

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Tükel, Raşit, Kaan Kora, Nezih Hekim, Harika Oğuz i Faruk Alagöl. "Thyrotropin stimulating hormone response to thyrotropin releasing hormone in patients with panic disorder". Psychoneuroendocrinology 24, nr 2 (luty 1999): 155–60. http://dx.doi.org/10.1016/s0306-4530(98)00067-5.

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Chiamolera, Maria Izabel, i Fredric E. Wondisford. "Thyrotropin-Releasing Hormone and the Thyroid Hormone Feedback Mechanism". Endocrinology 150, nr 3 (29.01.2009): 1091–96. http://dx.doi.org/10.1210/en.2008-1795.

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Thyroid hormone (TH) plays a critical role in development, growth, and cellular metabolism. TH production is controlled by a complex mechanism of positive and negative regulation. Hypothalamic TSH-releasing hormone (TRH) stimulates TSH secretion from the anterior pituitary. TSH then initiates TH synthesis and release from the thyroid gland. The synthesis of TRH and TSH subunit genes is inhibited at the transcriptional level by TH, which also inhibits posttranslational modification and release of TSH. Although opposing TRH and TH inputs regulate the hypothalamic-pituitary-thyroid axis, TH negative feedback at the pituitary was thought to be the primary regulator of serum TSH levels. However, study of transgenic animals showed an unexpected, dominant role for TRH in regulating the hypothalamic-pituitary-thyroid axis and an unanticipated involvement of the thyroid hormone receptor ligand-dependent activation function (AF-2) domain in TH negative regulation. These results are summarized in the review. The thyrotropin-releasing hormone neuron is well-positioned to integrate information about the environment as well as circulating TH levels and ultimately affect metabolism in response to these physiological changes.

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41

Pierpaoli, Walter. "Aging-Reversing Properties of Thyrotropin-Releasing Hormone". Current Aging Science 6, nr 1 (1.07.2013): 92–98. http://dx.doi.org/10.2174/1874609811306010012.

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42

Banki, C. M., L. Karmacsi, G. Bissette i C. B. Nemeroff. "CSF THYROTROPIN-RELEASING HORMONE IN PSYCHIATRIC DISORDERS". Clinical Neuropharmacology 15 (1992): 31B. http://dx.doi.org/10.1097/00002826-199202001-00058.

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Bladon, Christine M. "Synthesis of heteroaromatic thyrotropin-releasing hormone analogues". Journal of the Chemical Society, Perkin Transactions 1, nr 4 (1990): 1151. http://dx.doi.org/10.1039/p19900001151.

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TAKEYAMA, Masaharu, Akira OTAKA i Nobutaka FUJII. "Enzyme Immunoassay of Thyrotropin Releasing Hormone(TRH)." CHEMICAL & PHARMACEUTICAL BULLETIN 40, nr 8 (1992): 2199–201. http://dx.doi.org/10.1248/cpb.40.2199.

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Knutsen, Havar, Lars Oystein Dolva, Sverre Skrede, Roald Bjorklund i Jorg Morland. "Thyrotropin-releasing Hormone Antagonism of Ethanol Inebriation". Alcoholism: Clinical and Experimental Research 13, nr 3 (czerwiec 1989): 365–70. http://dx.doi.org/10.1111/j.1530-0277.1989.tb00337.x.

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