Relevant bibliographies by topics / TSHr stimulation

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'TSHr stimulation'

Author: Grafiati
Published: 11 September 2021
Last updated: 13 February 2022

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Journal articles on the topic "TSHr stimulation"

1

Unfried, Claudia, Nariman Ansari, Shinobu Yasuo, Horst-Werner Korf, and Charlotte von Gall. "Impact of Melatonin and Molecular Clockwork Components on the Expression of Thyrotropin β-Chain (Tshb) and the Tsh Receptor in the Mouse Pars Tuberalis." Endocrinology 150, no. 10 (July 9, 2009): 4653–62. http://dx.doi.org/10.1210/en.2009-0609.

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Abstract Photoperiodic regulation of reproduction in birds and mammals involves thyrotropin β-chain (TSHb), which is secreted from the pars tuberalis (PT) and controls the expression of deiodinase type 2 and 3 in the ependymal cell layer of the infundibular recess (EC) via TSH receptors (TSHRs). To analyze the impact of melatonin and the molecular clockwork on the expression of Tshb and Tshr, we investigated melatonin-proficient C3H wild-type (WT), melatonin receptor 1-deficient (MT1-/-) or clockprotein PERIOD1-deficient (mPER1-/-) mice. Expression of Tshb and TSHb immunoreactivity in PT were low during day and high during the night in WT, high during the day and low during the night in mPER1-deficient, and equally high during the day and night in MT1-deficient mice. Melatonin injections into WT acutely suppressed Tshb expression. Transcription assays showed that the 5′ upstream region of the Tshb gene could be controlled by clockproteins. Tshr levels in PT were low during the day and high during the night in WT and mPER1-deficient mice and equally low in MT1-deficient mice. Tshr expression in the EC did not show a day/night variation. Melatonin injections into WT acutely induced Tshr expression in PT but not in EC. TSH stimulation of hypothalamic slice cultures of WT induced phosphorylated cAMP response element-binding protein in PT and EC and deiodinase type 2 in the EC. Our data suggest that Tshb expression in PT is controlled by melatonin and the molecular clockwork and that melatonin activates Tshr expression in PT but not in EC. They also confirm the functional importance of TSHR in the PT and EC.
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Tagami, Tetsuya, Kaho Hiroshima-Hamanaka, Hironobu Umakoshi, Mika Tsuiki-Naruse, Toru Kusakabe, Noriko Satoh-Asahara, Akira Shimatsu, and Kenji Moriyama. "Experimental Reproduction of Dynamic Fluctuation of TSH Receptor–Binding Antibodies Between Stimulation and Inhibition." Journal of the Endocrine Society 3, no. 12 (September 23, 2019): 2361–73. http://dx.doi.org/10.1210/js.2019-00012.

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Abstract Context Hyperthyroidism in Graves disease (GD) is caused by autoantibody stimulation of the TSH receptor (TSHR). TSHR autoantibody (TSHR-Ab) activity is measured routinely by inhibition of labeled ligand (TSH or M22) binding to the TSHR [TSH-binding inhibitory immunoglobulins (TBIIs)] or by stimulation of cAMP production in isolated cells [TSH receptor–stimulating antibodies (TSAbs)]. Usually, measurements of TSHR-Abs by TBIIs agree reasonably well with TSAb values at least in the setting of hyperthyroidism, and both measurements tend to change in parallel during treatment with some exceptions. In this study, we describe three unusual cases, which illustrate nearly pure stimulating, blocking, or neutral properties of TSHR-Abs. Objective Whether patient serum TSHR-Abs can be reproduced by mixtures of human monoclonal autoantibodies to the TSHR was studied because the sera in most patients show moderate properties having both of TBII and TSAb activities. Design We compared the TBII and TSAb activities of serum from four unusual patients in detail with mixtures of human monoclonal TSHR-Abs (mAbs) M22 (stimulating), K1-18 (stimulating), and K1-70 (blocking). Results Characteristic of a patient’s serum was similar to M22 or K1-18, another was similar to K1-70, whereas another was similar to a mixture of K1-70 and M22 (or K1-18). Additionally, some patients seemed to have neutral TSHR-Abs in their sera. Conclusions Our studies suggest that the characteristics of TSHR-Abs in the patient serum can be mimicked by mixtures of human mAbs to the TSHR, stimulating, blocking, and neutral if any.
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Neumann, Susanne, Elena Eliseeva, Joshua G. McCoy, Giorgio Napolitano, Cesidio Giuliani, Fabrizio Monaco, Wenwei Huang, and Marvin C. Gershengorn. "A New Small-Molecule Antagonist Inhibits Graves' Disease Antibody Activation of the TSH Receptor." Journal of Clinical Endocrinology & Metabolism 96, no. 2 (February 1, 2011): 548–54. http://dx.doi.org/10.1210/jc.2010-1935.

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abstract Context: Graves' disease (GD) is caused by persistent, unregulated stimulation of thyrocytes by thyroid-stimulating antibodies (TSAbs) that activate the TSH receptor (TSHR). We previously reported the first small-molecule antagonist of human TSHR and showed that it inhibited receptor signaling stimulated by sera from four patients with GD. Objective: Our objective was to develop a better TSHR antagonist and use it to determine whether inhibition of TSAb activation of TSHR is a general phenomenon. Design: We aimed to chemically modify a previously reported small-molecule TSHR ligand to develop a better antagonist and determine whether it inhibits TSHR signaling by 30 GD sera. TSHR signaling was measured in two in vitro systems: model HEK-EM293 cells stably overexpressing human TSHRs and primary cultures of human thyrocytes. TSHR signaling was measured as cAMP production and by effects on thyroid peroxidase mRNA. Results: We tested analogs of a previously reported small-molecule TSHR inverse agonist and selected the best NCGC00229600 for further study. In the model system, NCGC00229600 inhibited basal and TSH-stimulated cAMP production. NCGC00229600 inhibition of TSH signaling was competitive even though it did not compete for TSH binding; that is, NCGC00229600 is an allosteric inverse agonist. NCGC00229600 inhibited cAMP production by 39 ± 2.6% by all 30 GD sera tested. In primary cultures of human thyrocytes, NCGC00229600 inhibited TSHR-mediated basal and GD sera up-regulation of thyroperoxidase mRNA levels by 65 ± 2.0%. Conclusion: NCGC00229600, a small-molecule allosteric inverse agonist of TSHR, is a general antagonist of TSH receptor activation by TSAbs in GD patient sera.
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Krieger, Christine C., Susanne Neumann, and Marvin C. Gershengorn. "Is There Evidence for IGF1R-Stimulating Abs in Graves’ Orbitopathy Pathogenesis?" International Journal of Molecular Sciences 21, no. 18 (September 8, 2020): 6561. http://dx.doi.org/10.3390/ijms21186561.

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In this review, we summarize the evidence against direct stimulation of insulin-like growth factor 1 receptors (IGF1Rs) by autoantibodies in Graves’ orbitopathy (GO) pathogenesis. We describe a model of thyroid-stimulating hormone (TSH) receptor (TSHR)/IGF1R crosstalk and present evidence that observations indicating IGF1R’s role in GO could be explained by this mechanism. We evaluate the evidence for and against IGF1R as a direct target of stimulating IGF1R antibodies (IGF1RAbs) and conclude that GO pathogenesis does not involve directly stimulating IGF1RAbs. We further conclude that the preponderance of evidence supports TSHR as the direct and only target of stimulating autoantibodies in GO and maintain that the TSHR should remain a major target for further development of a medical therapy for GO in concert with drugs that target TSHR/IGF1R crosstalk.
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Neumann, Susanne, Christine C. Krieger, and Marvin C. Gershengorn. "Targeting TSH and IGF-1 Receptors to Treat Thyroid Eye Disease." European Thyroid Journal 9, Suppl. 1 (2020): 59–65. http://dx.doi.org/10.1159/000511538.

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Graves’ disease (GD) is an autoimmune disease caused in part by thyroid-stimulating antibodies (TSAbs) that activate the thyroid-stimulating hormone receptor (TSHR). In Graves’ hyperthyroidism (GH), TSAbs cause persistent stimulation of thyroid cells leading to continuous thyroid hormone synthesis and secretion. Thyroid eye disease (TED), also called Graves’ orbitopathy, is an orbital manifestation of GD. We review the important roles of the TSHR and the insulin-like growth factor 1 receptor (IGF-1R) in the pathogenesis of TED and discuss a model of TSHR/IGF-1R crosstalk that considers two pathways initiated by TSAb activation of TSHR in the eye, an IGF-1R-independent and an IGF-1R-dependent signaling pathway leading to hyaluronan (HA) secretion in orbital fibroblasts. We discuss current and future therapeutic approaches targeting the IGF-1R and TSHR. Teprotumumab, a human monoclonal anti-IGF-1R-blocking antibody, has been approved as an effective treatment in patients with TED. However, as the TSHR seems to be the primary target for TSAbs in patients with GD, future therapeutic interventions directly targeting the TSHR, e.g. blocking antibodies and small molecule antagonists, are being developed and have the advantage to inhibit the IGF-1R-independent as well as the IGF-1R-dependent component of TSAb-induced HA secretion. Antigen-specific immunotherapies using TSHR peptides to reduce serum TSHR antibodies are being developed also. These TSHR-targeted strategies also have the potential to treat both GH and TED with the same drug. We propose that combination therapy targeting TSHR and IGF-1R may be an effective and better tolerated treatment strategy for TED.
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Neumann, Susanne, Eshel A. Nir, Elena Eliseeva, Wenwei Huang, Juan Marugan, Jingbo Xiao, Andrés E. Dulcey, and Marvin C. Gershengorn. "A Selective TSH Receptor Antagonist Inhibits Stimulation of Thyroid Function in Female Mice." Endocrinology 155, no. 1 (January 1, 2014): 310–14. http://dx.doi.org/10.1210/en.2013-1835.

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Because the TSH receptor (TSHR) plays an important role in the pathogenesis of thyroid disease, a TSHR antagonist could be a novel treatment. We attempted to develop a small molecule, drug-like antagonist of TSHR signaling that is selective and active in vivo. We synthesized NCGC00242364 (ANTAG3) by chemical modification of a previously reported TSHR antagonist. We tested its potency, efficacy, and selectivity in a model cell system in vitro by measuring its activity to inhibit stimulation of cAMP production stimulated by TSH, LH, or FSH. We tested the in vivo activity of ANTAG3 by measuring its effects to lower serum free T4 and thyroid gene expression in female BALB/c mice continuously treated with ANTAG3 for 3 days and given low doses of TRH continuously or stimulated by a single administration of a monoclonal thyroid-stimulating antibody M22. ANTAG3 was selective for TSHR inhibition; half-maximal inhibitory doses were 2.1 μM for TSHR and greater than 30 μM for LH and FSH receptors. In mice treated with TRH, ANTAG3 lowered serum free T4 by 44% and lowered mRNAs for sodium-iodide cotransporter and thyroperoxidase by 75% and 83%, respectively. In mice given M22, ANTAG3 lowered serum free T4 by 38% and lowered mRNAs for sodium-iodide cotransporter and thyroperoxidase by 73% and 40%, respectively. In conclusion, we developed a selective TSHR antagonist that is effective in vivo in mice. This is the first report of a small-molecule TSHR antagonist active in vivo and may lead to a drug to treat Graves' disease.
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Sanders, Jane, Yasuo Oda, Sara Roberts, Angela Kiddie, Tonya Richards, Jane Bolton, Vivienne McGrath, et al. "The Interaction of TSH Receptor Autoantibodies with 125I-Labelled TSH Receptor." Journal of Clinical Endocrinology & Metabolism 84, no. 10 (October 1, 1999): 3797–802. http://dx.doi.org/10.1210/jcem.84.10.6071.

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Abstract Detergent-solubilized porcine TSH receptor (TSHR) has been labeled with 125I using a monoclonal antibody to the C-terminal domain of the receptor. The ability of sera containing TSHR autoantibody to immunoprecipitate the labeled receptor was then investigated. Sera negative for TSHR autoantibody (as judged by assays based on inhibition of labeled TSH binding to detergent-solubilized porcine TSHR) immunoprecipitated about 4% of the labeled receptor, whereas sera with high levels of receptor autoantibody immunoprecipitated more than 25% of the labeled receptor. The ability to immunoprecipitate labeled TSHR correlated well with ability of the sera to inhibit labeled TSH binding to the receptor (r = 0.92; n = 63), and this is consistent with TSHR autoantibodies in these samples being directed principally to a region of the receptor closely related to the TSH binding site. Preincubation of labeled TSHR with unlabeled TSH before reaction with test sera inhibited the immunoprecipitation reaction, providing further evidence for a close relationship between the TSHR autoantibody binding site(s) and the TSH binding site. This was the case whether the sera had TSH agonist (i.e., thyroid stimulating) or TSH antagonist (i.e., blocking) activities, thus, providing no clear evidence for different regions of the TSHR being involved in forming the binding site(s) for TSHR autoantibodies with stimulating and with blocking activities. The ability of TSHR autoantibodies to stimulate cyclic AMP production in isolated porcine thyroid cells was compared with their ability to immunoprecipitate labeled porcine TSHR. A significant correlation was observed (r = 0.58; n = 50; P < 0.001) and the correlation was improved when stimulation of cyclic AMP production was compared with inhibition of labeled TSH binding to porcine TSHR (r = 0.76). Overall, our results indicate that TSHR autoantibodies bind principally to a region on the TSHR closely related to the TSH binding site, and this seems to be the case whether the autoantibodies act as TSH agonists or antagonists.
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Bäck, Christer M., Stefanie Stohr, Eva A. M. Schäfer, Heike Biebermann, Ingrid Boekhoff, Andreas Breit, Thomas Gudermann, and Thomas R. H. Büch. "TSH induces metallothionein 1 in thyrocytes via Gq/11- and PKC-dependent signaling." Journal of Molecular Endocrinology 51, no. 1 (April 23, 2013): 79–90. http://dx.doi.org/10.1530/jme-12-0200.

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Metallothioneins (MTs) are cytoprotective proteins acting as scavengers of toxic metal ions or reactive oxygen species. MTs are upregulated in follicular thyroid carcinoma and are regarded as a marker of thyroid stress in Graves' disease. However, the mechanism of MT regulation in thyrocytes is still elusive. In other cellular systems, cAMP-, calcium-, or protein kinase C (PKC)-dependent signaling cascades have been shown to induce MT expression. Of note, all of these three pathways are activated following the stimulation of the TSH receptor (TSHR). Thus, we hypothesized that TSH represents a key regulator of MT expression in thyrocytes. In fact, TSHR stimulation induced expression of MT isoform 1X (MT1X) in human follicular carcinoma cells. In these cells, Induction of MT1X expression critically relied on intact Gq/11signaling of the TSHR and was blocked by chelation of intracellular calcium and inhibition of PKC. TSHR-independent stimulation of cAMP formation by treating cells with forskolin also led to an upregulation of MT1X, which was completely dependent on PKA. However, inhibition of PKA did not affect the regulation of MT1X by TSH. As in follicular thyroid carcinoma cells, TSH also induced MT1 protein in primary human thyrocytes, which was PKC dependent as well. In summary, these findings indicate that TSH stimulation induces MT1X expression via Gq/11and PKC, whereas cAMP–PKA signaling does not play a predominant role. To date, little has been known regarding cAMP-independent effects of TSHR signaling. Our findings extend the knowledge about the PKC-mediated functions of the TSHR.
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Krieger, Christine C., Robert F. Place, Carmine Bevilacqua, Bernice Marcus-Samuels, Brent S. Abel, Monica C. Skarulis, George J. Kahaly, Susanne Neumann, and Marvin C. Gershengorn. "TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis." Journal of Clinical Endocrinology & Metabolism 101, no. 6 (June 1, 2016): 2340–47. http://dx.doi.org/10.1210/jc.2016-1315.

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Abstract Context: The TSH receptor (TSHR) is considered the main target of stimulatory autoantibodies in the pathogenesis of Graves' ophthalmopathy (GO); however, it has been suggested that stimulatory IGF-1 receptor (IGF-1R) autoantibodies also play a role. Objective: We previously demonstrated that a monoclonal stimulatory TSHR antibody, M22, activates TSHR/IGF-1R cross talk in orbital fibroblasts/preadipocytes obtained from patients with GO (GO fibroblasts [GOFs]). We show that cross talk between TSHR and IGF-1R, not direct IGF-1R activation, is involved in the mediation of GO pathogenesis stimulated by Graves' autoantibodies. Design/Setting/Participants: Immunoglobulins were purified from the sera of 57 GO patients (GO-Igs) and tested for their ability to activate TSHR and/or IGF-1R directly and TSHR/IGF-1R cross talk in primary cultures of GOFs. Cells were treated with M22 or GO-Igs with or without IGF-1R inhibitory antibodies or linsitinib, an IGF-1R kinase inhibitor. Main Outcome Measures: Hyaluronan (hyaluronic acid [HA]) secretion was measured as a major biological response for GOF stimulation. IGF-1R autophosphorylation was used as a measure of direct IGF-1R activation. TSHR activation was determined through cAMP production. Results: A total of 42 out of 57 GO-Ig samples stimulated HA secretion. None of the GO-Ig samples exhibited evidence for IGF-1R autophosphorylation. Both anti-IGF-1R antibodies completely inhibited IGF-1 stimulation of HA secretion. By contrast, only 1 IGF-1R antibody partially blocked HA secretion stimulated by M22 or GO-Igs in a manner similar to linsitinib, whereas the other IGF-1R antibody had no effect on M22 or GO-Ig stimulation. These findings show that the IGF-1R is involved in GO-Igs stimulation of HA secretion without direct activation of IGF-1R. Conclusions: IGF-1R activation by GO-Igs occurs via TSHR/IGF-1R cross talk rather than direct binding to IGF-1R, and this cross talk is important in the pathogenesis of GO.
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McLachlan, Sandra M., Holly Aliesky, Bianca Banuelos, Jessica Magana, Robert W. Williams, and Basil Rapoport. "Immunoglobulin Heavy Chain Variable Region and Major Histocompatibility Region Genes Are Linked to Induced Graves' Disease in Females From Two Very Large Families of Recombinant Inbred Mice." Endocrinology 155, no. 10 (October 1, 2014): 4094–103. http://dx.doi.org/10.1210/en.2014-1388.

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Abstract Graves' hyperthyroidism is caused by antibodies to the TSH receptor (TSHR) that mimic thyroid stimulation by TSH. Stimulating TSHR antibodies and hyperthyroidism can be induced by immunizing mice with adenovirus expressing the human TSHR A-subunit. Prior analysis of induced Graves' disease in small families of recombinant inbred (RI) female mice demonstrated strong genetic control but did not resolve trait loci for TSHR antibodies or elevated serum T4. We investigated the genetic basis for induced Graves' disease in female mice of two large RI families and combined data with earlier findings to provide phenotypes for 178 genotypes. TSHR antibodies measured by inhibition of TSH binding to its receptor were highly significantly linked in the BXD set to the major histocompatibility region (chromosome 17), consistent with observations in 3 other RI families. In the LXS family, we detected linkage between T4 levels after TSHR-adenovirus immunization and the Ig heavy chain variable region (Igvh, chromosome 12). This observation is a key finding because components of the antigen binding region of Igs determine antibody specificity and have been previously linked to induced thyroid-stimulating antibodies. Data from the LXS family provide the first evidence in mice of a direct link between induced hyperthyroidism and Igvh genes. A role for major histocompatibility genes has now been established for genetic susceptibility to Graves' disease in both humans and mice. Future studies using arrays incorporating variation in the complex human Ig gene locus will be necessary to determine whether Igvh genes are also linked to Graves' disease in humans.
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Dissertations / Theses on the topic "TSHr stimulation"

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Johnsen, Hanna. "The Importance of the TSHR-gene in Domestic Chicken." Thesis, Linköpings universitet, Biologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-103687.

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Thyroid hormones are known to be important in several processes in chicken, such as growth, metabolism and reproductive system. In previous studies the thyroid stimulating hormone receptor (TSHR)-gene has been identified as a target for a selective sweep in commercial breeds of chicken such as broiler and White Leghorn. The evolution of domesticated species can be split into three periods. The first is the natural selection in their natural habitat, the second the beginning of the domestication process, when humans started to tame and breed the wild animals and the third is when animals were bred for commercial interests such as egg laying properties and meat production in chicken. Landraces, which are domesticated but not commercially bred races, are a great resource for identifying during which period a specific gene, which differs between wild type and commercial bred breeds, were selected. In this study Swedish landrace chickens were used in order to analyze the importance of a mutation in the TSHR-gene in the domestication process. The results of this study gave that all, except two individuals from the Bohuslän-Dals svarthöna were homozygous for the mutation known from commercial breeds. The two individuals from Bohuslän-Dals svarthöna were both heterozygous for the mutation. These results suggest that the TSHR mutation is important for the domestication process and were already more or less fixed at the commencement of commercial breeding. The mutation is thought to be dominant and to have an inhibitory impact on the TSHR activity. This might result in hypothyroidism which would make alterations in the reproductive system. This is plausible because the constant availability of food in captivity makes the seasonal reproductive system no longer critical for survival of progeny.
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Bach, Albert. "Techniques de stimulation par la tsh dans la surveillance du cancer differencie de la thyroide : comparaison de 2 methodes." Nancy 1, 1990. http://www.theses.fr/1990NAN11193.

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Lee, Kok-Onn. "The biological activity of TSH (Thyrotropin)." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335319.

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Larsen, Donald A. "Quantification and regulation of thyroid stimulating hormone (TSH) and TSH messenger RNA in salmon /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/5343.

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Svemer, Frida. "A mutation in the TSHR gene - how does it affect social and fear related behaviours in chickens?" Thesis, Linköpings universitet, Biologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-77975.

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Thyroid hormones are well known important to be in development and growth in birds and that signaling of thyrotropin (TSH) regulates the photo induced seasonal reproduction. A mutation at the thyroid stimulating hormone receptor (TSHR) gene in domestic breeds of chicken could be involved in the release of the photoperiodic regulation. Furthermore, TSH can affect a wide range of domestication related phenotypes, such as behaviour, growth rate and pigmentation. The aim of this study was to investigate the behaviours expressed in the different genotypes on the TSHR gene in chickens. Four standard tests were conducted, aerial predator, fear of human, social dominance and tonic immobility. An advanced intercross line of chickens between red junglefowl and White leghorn was used. Male domestic type chickens explored more, showed more less fear behaviours and showed least fear behaviours in the fear of human test. Increased activity and flight response has been interpreted as a lower fear response, which is in line with this study. The wild type chickens showed more social dominance than domestic type chickens which are in line with previous results. In tonic immobility there was a difference between the wild type male and heterozygous male chickens in latency until first head movement. The conclusion of this study is that there is a difference between the wild type and domestic type chickens. This indicates that the TSHR gene is involved in behavioural changes during domestication, but whether it is due to passive or active selection is the question.
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Bachmayer, Clarissa Johanna Marina. "Das Phänomen der graduellen Rekrutierung neuer sekretorischer Zellen nach TSH-Stimulation der Schilddrüse /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Axling, Johanna. "Effects of a mutation on the TSHR gene on social and fear related behaviours in chickens." Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-69120.

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It has been shown that thyroid hormones are important in development and growth in birds and further that thyrotropin (TSH) signaling regulated photoinduced seasonal reproduction. In addition to controlling the development of certain physiological traits, TSH can affect a wide range of phenotypes related to domestication such as behaviour, growth rate, more frequent reproductive cycle’s, pigmentation and also behaviour. Studies indicate that thyroid hormone physiology could potentially be responsible for differences in individual stress response as well as differences in social dominance. This project investigated behaviours expressed in the different genotypes on the Thyroid stimulating hormone receptor (TSHR) gene in chickens. Standard test such as Fear of human, Aerial predator, Tonic immobility and Social hierarchy were carried out with White leghorn (WL) as a domesticated species and Red Junglefowl (Rjf) as their wild counterpart; these were considered to be the control group. There was no significant result on genotype effect for the TSHR animals observed in those variables tested. The TSHR mutants were expected to mirror the White leghorn behavioural response and the TSHR wildtype the behaviour of Rjf. This was however not confirmed. There were a significant interaction between genotype effect and sex effect for TSHR for stand alert in the Aerial predator test which mirrored the results seen in the control groups. The male wildtype followed the male Rjf pattern however the mutant did not mirror the WL male. This study would benefit from more individuals to be tested, for stronger statistical results, plus also to have all genotypes represented to fully investigate the affect the TSHR mutation have on domesticated chickens and potentially the domestication process in a range of species.
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Hanon, Elodie. "A novel model of action for TSH (thyrotropin stimulating hormone) in the mammalian neuroendocrine system." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=53386.

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Durand, Jason AJ. "Regulation of Adipocyte Lipolysis by TSH and its Role in Macrophage Inflammation." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22694.

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Elevated Thyroid-Stimulating Hormone (TSH) is associated with an increased risk of cardiovascular disease (CVD). We hypothesized that TSH-stimulated FA release from adipocytes contributes to macrophage inflammation. 3T3-L1 and human subcutaneous differentiated adipocytes were treated with TSH for 4 hours under various conditions and lipolysis assessed via glycerol secretion. Optimal conditions were determined and protein expression of ATGL, HSL and perilipin remained stable. TSH-stimulated 3T3-L1 or human adipocyte-conditioned medium (T-ACM) was placed on murine J774 or human THP-1 macrophages, respectively, and macrophage cytokine mRNA levels (IL-1β, IL-6, MCP-1, and TNFα) were measured by real-time RT-PCR. T-ACM did not change cytokine mRNA expression in J774 macrophages or THP-1 macrophages when compared to ACM. Absence of BSA in the medium may have hindered release of FA from differentiated adipocytes into the medium, BSA may be required to permit adequate FA accumulation in the medium to then evaluate the effect of T-ACM on macrophages. Further investigation is required to determine the effect of FA on J774 and THP-1 inflammatory response.
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Lan, Ling [Verfasser]. "Adult stem cells derived from human goiters form spheres in response to intense growth stimulation and differentiate TSH-dependently into thyroid cells / Ling Lan." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1022824856/34.

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Book chapters on the topic "TSHr stimulation"

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Colao, Annamaria, and Claudia Pivonello. "Thyroid-Stimulating Hormone (TSH)." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5121-1.

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Campbell, Daniel, Corey Ray-Subramanian, Winifred Schultz-Krohn, Kristen M. Powers, Renee Watling, Christoph U. Correll, Stephanie Bendiske, et al. "Thyrotropin, Thyroid-Stimulating Hormone (TSH)." In Encyclopedia of Autism Spectrum Disorders, 3119. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_101452.

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Pickardt, C. R., C. Bernutz, and K. Horn. "Thyroidal and extrathyroidal influences on TSH before and after TRH stimulation." In Thyrotropin, edited by G. Leb, A. Passath, O. Eber, and H. Höfler, 173–84. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110867398-018.

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Vitti, P., L. Chiovato, A. Lombardi, G. Lopez, F. Santini, P. Ceccarelli, C. Mammoli, et al. "Autoantibodies Blocking the TSH-Induced Adenylate Cyclase Stimulation in Idiopathic Myxedema and Hashimoto’s Thyroiditis." In Thyroid Autoimmunity, 393–95. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0945-1_63.

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Marshall, N. J., and P. A. Ealey. "Recent Developments in the in vitro Bioassay of TSH and Thyroid-Stimulating Antibodies." In Immunology of Endocrine Diseases, 25–49. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4171-7_2.

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Schleusener, H., G. Holl, A. Stadler, P. Kotulla, U. Bogner, K. Badenhoop, R. Finke, and J. Hensen. "Clinical significance of antibodies to the TSH-receptor (stimulating and blocking thyroid function)." In Thyrotropin, edited by G. Leb, A. Passath, O. Eber, and H. Höfler, 323–36. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110867398-039.

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Filetti, Sebastiano, Giuseppe Damante, Daniela Foti, Rosaria Catalfamo, and Riccardo Vigneri. "The Effect of Thyroid Stimulating Immunoglobulins (TSI) on Thyroid Camp: Comparison with TSH Activity." In Thyroid Autoimmunity, 351–54. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0945-1_53.

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Vitti, Paolo, Luca Chiovato, Paola Ceccarelli, Mozart Novaes, Claudia Mammoli, Paolo Del Guerra, and Ginafranco Fenzi. "Effect of TSH and Thyroid-Stimulating Antibody (TSAb) on the Desensitization of the Adenylate Cyclase Activity in FRTL-5 Cells." In Frontiers in Thyroidology, 403–6. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_70.

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Marcocci, Claudio, Alberto Luini, Pilar Santisteban, and Evelyn F. Grollman. "Norepinephrine and TSH Stimulation on Iodide Efflux in FRTL-5 Thyroid Cells Involves Metabolites of Arachidonic Acid and is Associated with the Iodination of Thyroglobulin." In Frontiers in Thyroidology, 397–401. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_69.

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"TSH-Stimulation." In Springer Reference Medizin, 2376. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_313751.

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Conference papers on the topic "TSHr stimulation"

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Bacher, R., M. Dietlein, C. Kobe, M. Hohberg, M. Wild, A. Drzezga, and M. Schmidt. "Response-Bewertung nach adjuvanter Radioiodtherapie in Abhängigkeit einer endogenen TSH-Stimulation versus rhTSH-Gabe." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683580.

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Yulianti, Kartika, Aris Wibudi, and Mila Citrawati. "Relation Between Tiroid Status with Glycemic Control of Type 2 DM Patients at RSPAD Gatot Soebroto." In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.12.

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ABSTRACT Background: Diabetes Mellitus (DM) is a group of symptoms that arise due to increased blood sugar levels. Diabetes Mellitus type 2 has a higher risk of developing thyroid dysfunction. Thyroid dysfunction can affect various body metabolism and result in insulin resistance, significantly affecting glycemic control in DM patients. This study aimed to determine the relation between thyroid status as assessed by the level of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and glycemic control (HbA1c). Subjects and Method: A cross-sectional study. A sample of 38 DM patients was selected by purposive sampling. The dependent variable was glycemic control. The independent variables were TSH and FT4. Patients were classified into 4 quartiles (Q) based on their TSH and FT4 levels. Statistic test used was non parametric for category group of variables, which was Chi square test. Results: Mean of fasting blood glucose was 200,56 mg/dL (modus 137 mg/dL), mean of 2 hours post prandial blood glucose was 247 mg/dL (modus 305 mg/dL). Subjetcs with poor glycemic control dominated as much as 76%. Most subjects had TSH level at Q4 (36%), while most of the subjects had FT4 level at Q1 (34%). The results showed that 38 samples with poor glycemic control were 72% in the 4th quartile (Q4) (> 3.1750 mU / L) TSH, and 64.7% were in Q1 (≤ 11.8400) FT4. The analysis showed that there was a significant relation between TSH (p = 0.047) and FT4 (p = 0.041) with glycemic control in type 2 DM patients. Conclusion: FT4 and TSH levels relate to glycemic control in type 2 DM patients Keywords: TSH, FT4, HbA1c, Diabetes Mellitus Correspondence: Mila Citrawati. Department of Faal, Faculty of Medicine, UPN Veteran, Jakarta. Jl. RS Fatmawati, Pondok Labu, South Jakarta 12450, Telp. (021) 7656971. E-mail: milacitrawati@upnvj.ac.id. Mobile: 081282990515 DOI: https://doi.org/10.26911/the7thicph.05.12
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Mondul, Alison M., Stephanie J. Weinstein, Tracey Bosworth, Alan T. Remaley, Jarmo Virtamo, and Demetrius Albanes. "Abstract 4472: Circulating thyroxine (T4), thyroid-stimulating hormone (TSH), and hypothyroid status and the risk of prostate cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4472.

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Jia Mei Lim, Vanessa, Chin Pin Yeo, Jayme Sau Yeng Wong, Carly Yanlin Wu, Wan Li Ong, and Daisy Kwai Lin Chan. "353 Will increasing the screening cut-off thyroid stimulating hormone (TSH) level in the newborn miss cases of congenital hypothyroidism?" In RCPCH Conference Singapore. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjpo-2021-rcpch.192.

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Giassi, Karina, Renato Gorga Bandeira de Mello, Bruna Cambrussi de Lima, Gabriela Stahl, Raquel Almeida de Oliveira, and Marina Siqueira Flores. "RANDOMIZED CONTROLLED TRIAL COMPARING MORNING VERSUS NIGHT ADMINISTRATION OF LEVOTHYROXINE IN OLDER PERSONS." In XXII Congresso Brasileiro de Geriatria e Gerontologia. Zeppelini Publishers, 2021. http://dx.doi.org/10.5327/z2447-21232021res04.

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OBJECTIVE: To evaluate the effectiveness of levothyroxine administration strategies in the treatment of hypothyroidism in older persons in a tertiary outpatient clinic. METHODS: A randomized controlled trial of older persons with a diagnosis of primary hypothyroidism who had been receiving levothyroxine for at least 6 months with a stable dose in the last 3 months. Patients were randomly assigned to one of two administration strategies: morning (1 hour before breakfast) or night (1 hour after the last meal). In a period ≥ 12 weeks, patients were instructed to cross over between strategies. Laboratory tests for thyroid-stimulating hormone (TSH) and free thyroxine (FT4) were performed at visit 0 (baseline), visit 1 (period ≥ 12 weeks), and visit 2 (completion — period ≥ 24 weeks); a standardized questionnaire was also applied. Preliminary analyses of the period before crossover are presented. RESULTS: The preliminary sample consisted of 98 patients, with a mean age of 71.26 (SD 7.12) years; 83.67% were women. Fifty-three patients started with the morning strategy and 45 with the night strategy, and one patient did not return for reassessment. Median TSH levels ranged from 2.74 (IQR 1.06–4.19) at baseline to 2.77 (IQR 0.75–4.41) after a 12-week follow-up in the morning group, and from 2.36 (IQR 1.48–4.85) to 2.28 (IQR 1.69–3.56) in the night group. Mean FT4 levels ranged from 1.44 (SD 0.39) to 1.42 (SD 0.36) in the morning group, and from 1.35 (SD 0.27) to 1.37 (SD 0.32) in the night group. CONCLUSIONS: The administration of levothyroxine at night was as effective as morning administration at controlling primary hypothyroidism in older persons. Therefore, this can be considered an alternative dosage strategy for the treatment of this condition.
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Jung, W., J. Han, J. Kai, J. Y. Lim, D. Sul, and C. H. Ahn. "An innovative sample-to-answer polymer lab-on-a-chip with on-chip reservoirs for the POCT of thyroid stimulating hormone (TSH)." In 2013 IEEE 26th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2013. http://dx.doi.org/10.1109/memsys.2013.6474430.

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