Gotowe bibliografie tematyczne / Thyrotropin releasing hormone

Gotowa bibliografia na temat „Thyrotropin releasing hormone”

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Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 lutego 2022

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Artykuły w czasopismach na temat "Thyrotropin releasing hormone"

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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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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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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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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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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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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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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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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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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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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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Rozprawy doktorskie na temat "Thyrotropin releasing hormone"

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Kaur, Baljit. "The conformational analysis of thyrotropin releasing hormone and its analogues". Thesis, Manchester Metropolitan University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284878.

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Ouafik, L'Houcine. "Etude sur la biosynthèse de la Thyrotropin-Releasing Hormone (TRH) pancréatique". Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37608585w.

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Ouafik, L'Houcine. "Etude sur la biosynthèse de la thyrotropin-releasing hormone (TRH) pancréatique". Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX22004.

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Xiang, Shi Zhan. "Central control of the rat thyroid axis". Thesis, Brunel University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320216.

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Ebiou, Jean-Claude. "Le rôle biologique de la thyrotropin-releasing hormone (TRH) dans le pancréas endocrine". Paris 7, 1992. http://www.theses.fr/1992PA077056.

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L'objectif de ce travail est la recherche du rôle biologique de la TRH pancréatique. La TRH a été initialement isolée de l'hypothalamus et caractérisée comme pGlu-His-ProNH₂. Elle a ensuite été détectée dans le pancréas endocrine désigne comme deuxième site de synthèse du peptide. La TRH est synthétisée à partir d'un précurseur de haut poids moléculaire. La maturation complète de celui-ci génèrerait 5 molécules de TRH, et 7 peptides de connexion. Nous avons montré que la TRH secrétée par le pancréas a les mêmes caractéristiques chromatographiques que le peptide synthétique. La sécrétion de la TRH pendant le développement est stimulé par le glucose et l'arginine, tandis que ces mêmes secretagogues inhibent la sécrétion chez l'adulte. Fait intéressant, la sécrétion de la TRH augmente avec l’âge, en dépit de la chute des contenus pancréatiques. Nous avons caractérise deux peptides de connexion de la prepro-TRH: prepro-TRH160-169 et prepro-TRH178-199, dans des ilots de Langerhans, et le prepro-TRH178-199 dans le milieu de sécrétion. Concernant le rôle biologique de la TRH pancréatique, nous avons montré que: la TRH exogène stimule la sécrétion basale du glucagon; l'immunoneutralisation de la TRH endogène secrétée par l'anticorps anti-TRH inhibe significativement la sécrétion du glucagon induite par l'arginine, la sécrétion de somatostatine est légèrement inhibée. Sur une fistule pancréatique, la TRH inhibe la sécrétion exocrine des protéines, bicarbonates, et du sodium. Les résultats préliminaires sur les cellules acinaires indiquent une absence d'effet TRH. L'effet TRH, observe in vivo, serait medié par le système nerveux central. Au cours du développement, la TRH n'a pas d'effet sur les secrétions d'insuline et glucagon. Nous pensons qu'elle agirait sur le processus de prolifération des cellules insulaires. La TRH stimule la sécrétion du glucagon des cellules alpha. Il serait intéressant de rechercher l'action biologique des deux peptides de connexion. La détermination du mécanisme d'action de la TRH pancréatique implique la caractérisation des sites de liaison spécifiques. Ce travail a été publié dans: Endocrinology 1992, 130(3):1371-1379; Endocrinology 1992, 131(2) (à paraitre en aout); prostate tumeurs 1991, (7):9-10 et 1992(9):6-7.
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Hart, G. R. "Mechanism of control of growth hormone release from the anterior pituitary : A role for thyrotropin-releasing hormone". Thesis, University of Sussex, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305765.

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Nguyen, Kim Thoa Thi [Verfasser]. "Thyrotropin releasing hormone (TRH) selectively stimulates human hair follicle pigmentation / Kim Thoa Thi Nguyen". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2017. http://d-nb.info/114120309X/34.

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Carter, Rebecca Ann. "Thyroid Status in Exercising Horses and Laminitic Ponies". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/35454.

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The objective of these studies was to contribute to the understanding and assessment of thyroid function in horses. The first study evaluated methods of assessing thyroid function in horses, including validation of an enzyme immunoassay (EIA) for measuring equine thyroid hormones and development and assessment of a thyrotropin releasing hormone (TRH) response test. Our data indicated that EIA is an acceptable method for the measurement of total (T) and free (F) thyroxine (T4) and triiodothyronine (T3) in equine plasma. Its measurements are not equivalent to values obtained by radioimmunoassay (RIA), but they can be calibrated to predict corresponding RIA values. A protocol was developed for TRH response tests involving administration of 1 mg TRH intravenously, with blood sample collection immediately before, 2.5, 5.0, and 24 h after administration. Analysis of plasma TT4, FT4, TT3, and FT3 revealed that the magnitude of hormone response was best approximated by the area under the curve of hormone plotted against time and by the absolute change in thyroid hormone concentration. Baseline concentrations, peak concentrations, and percent of baseline values were not as well able to predict the magnitude of hormone response. The second study assessed the effects of exercise and feed composition on thyroid status. Thirteen mature Arabian geldings, adapted to either a high sugar and starch (SS) or high fat and fiber (FF) feed, underwent 15 wk of exercise training followed by a treadmill exercise test. The TRH response tests performed before training, after training, and the morning after the exercise test revealed that the exercise test decreased the TT4 and FT4 response, whereas feeding of high levels of sugars and starches increased the response of TT3 and FT3. During the first four weeks of training, increased TT4 and FT4 concentrations occurred simultaneously with increased nonesterified fatty acid concentrations, decreased triglyceride concentrations, and increased insulin sensitivity. The increase in TT4 and FT4 may have provided the cellular signaling necessary for increased lipolysis and insulin sensitivity. These metabolic changes facilitate the increases in lipid and carbohydrate metabolism that are needed to fulfill the additional energy requirements of regular exercise. The third study assessed thyroid status in ponies with different laminitic histories. Total T4, FT4, TT3, and FT3 were measured during March and May 2004 in 126 ponies that were categorized as either previously laminitic (PL; n = 54) or never laminitic (NL; n = 72) and evaluated for current laminitis in May (CL; n = 13). Decreased concentrations of TT4 and FT4 were found in PL ponies when compared to NL ponies in March (P = 0.018, 0.020) and May (P = 0.018, 0.001). However, TT4 and FT4 concentrations in CL ponies were not different than concentrations in NL ponies in May (P = 0.82, 0.72), and when retrospectively separated out in March, were not different than NL ponies (P = 0.90, 0.84). Therefore, basal thyroid hormone concentrations are not useful as a predictor or hormonal characteristic of pasture-associated laminitis. The decreased TT4 and FT4 in PL ponies may be an indication of a response or compensation to laminitis and may facilitate the metabolic changes necessary to cope with the disease.
Master of Science
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Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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Sun, Yuh-Man. "Cloning and charaterisation of the Thyrotrophin-releasing hormone receptor and Gonadotrophin-relasing hormone receptor from chicken pituitary gland". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26973.

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The hypothalamic hormones, thyrotrophin-releasing hormone (TRH) and gonadotrophin-releasing hormone (GnRH), play pivotal roles in the growth and sexual maturation of chickens. In chickens, TRH regulates the release and synthesis of thyrotrophin (TSH) and also acts as a growth hormone-releasing factor. GnRH stimulates the release and synthesis of gonadotrophins (LH and FSH). TRH and GnRH are released and stored in the median eminence, and both hormones are transported into the pituitary gland via the hypophysial portal circulation. TRH and GnRH exert their physiological functions by binding to their specific receptors (TRH receptor and GnRH receptor, respectively) on the surface of cells in the pituitary gland. The activated receptors couple to guanine nucleotide-binding regulatory proteins (G proteins), Gq and/or G11, which in turn triggers the secondary messenger [1,2- diacylglycerol (DAG) and inositoltrisphosphate (IP3)] signalling cascade. The signalling generates the physiological effects of the hormones. The TRH-R and GnRH-R are members of G-protein coupled receptor (GPCR) family. The objective of this thesis was to clone and characterise the chicken TRH and GnRH receptors as useful tools for investigating the regulatory roles of TRH and GnRH receptors in the growth and sexual maturation of chickens. In addition, sequence information of the receptors would potentially assist in elucidating the binding sites and the molecular nature of the processes involved in receptor activation.
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Książki na temat "Thyrotropin releasing hormone"

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Deshpande, Shripad B. Thyrotropin releasing hormone on spinal reflexes. Varanasi: Ganga Kaveri Pub. House, 1997.

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International Symposium on Protirelin Tartrate (TRH-T) (1988 Taormina, Italy). Protirelin tartrate (TRH-T): Pharmacological and clinical studies : recent advances and perspectives. London: Libbey, 1988.

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Geoffrey, Metcalf, Jackson Ivor M. D i New York Academy of Sciences., red. Thyrotropin-releasing hormone: Biomedical significance. New York, N.Y: New York Academy of Sciences, 1989.

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Metcalf, Geoffrey. Thyrotropin-Releasing Hormone: Biomedical Significance (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1989.

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Jackson, Darrell Anthony. A comparison of the effects of serotonin and thyrotropin releasing hormone on neuronal excitability in the lumbar spinal cord of the rat. 1990.

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1921-, Sobue Itsuro, red. TRH and spinocerebellar degeneration. Amsterdam: Elsevier, 1986.

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Hasey, Gary Marcel. A comparison of the thyrotropin releasing hormone stimulation test and the dexamethasone suppression test in depressed and healthy subjects. 1985.

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Części książek na temat "Thyrotropin releasing hormone"

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Goodman, R. H., i G. Mandel. "Biosynthesis of Thyrotropin releasing hormone". W Thyrotropin, redaktorzy G. Leb, A. Passath, O. Eber i H. Höfler, 3–6. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110867398-002.

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Prasad, Chandan. "Thyrotropin-Releasing Hormone". W Neurochemical Systems, 175–200. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-7018-5_8.

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Kannan, C. R. "Thyrotropin and Thyrotropin-Releasing Hormone". W The Pituitary Gland, 145–69. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1849-1_5.

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Garbutt, James C., Susan G. Silva i George A. Mason. "Thyrotropin-Releasing Hormone (TRH)". W Alcohol and Hormones, 127–45. Totowa, NJ: Humana Press, 1995. http://dx.doi.org/10.1007/978-1-4612-0243-1_6.

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Colao, Annamaria, i Claudia Pivonello. "Thyrotropin Releasing Hormone (TRH)". W Encyclopedia of Pathology, 1. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-28845-1_5122-1.

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Bambini, Giovanni, Enio Martino, Sebastiano Grasso, Giuseppe Pardo i Fabrizio Aghini-Lombardi. "Ontogeny of Human Pancreatic Thyrotropin-Releasing Hormone". W Frontiers in Thyroidology, 299–301. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_50.

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Mancini, Antonio, Domenico Valle, Gianluigi Conte, Michele Perrelli, Edoardo Menini, Vittorio Mignani, Paolo Carducci, Francesco Della Corte i Laura De Marinis. "Growth Hormone (GH) Releasing Hormone- and Thyrotropin Releasing Hormone-Induced GH Release in the Acute Phase of Trauma". W Growth Hormone Secretagogues, 335–45. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2396-2_21.

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Amir, Shimon, i Robin Pollock. "Counterregulation of Stress-Induced Hyperglycemia by Thyrotropin-Releasing Hormone". W Psychobiology of Stress, 143–49. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1990-7_12.

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Gershengorn, Marvin C. "Thyrotropin-Releasing Hormone Action in Thyrotropic Cells: Mechanism of Stimulation of Thyroid-Stimulating Hormone Secretion". W Frontiers in Thyroidology, 1–4. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_1.

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Goodman, R. H., M. R. Montminy, M. J. Low, T. Tsukada, S. Fink, R. M. Lechan, P. Wu, I. M. D. Jackson i G. Mandel. "Biosynthesis of Somatostatin, Vasoactive Intestinal Polypeptide, and Thyrotropin Releasing Hormone". W Neuroendocrine Molecular Biology, 159–73. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5131-3_15.

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Streszczenia konferencji na temat "Thyrotropin releasing hormone"

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Fekete, Csaba, i Ronald M. Lechan. "Regulation of hypophysiotropic thyrotropin- and corticotrophin-releasing hormone neurons by feeding-related signals". W Xth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2007. http://dx.doi.org/10.1135/css200709043.

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