Thyroid Hormone
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Genetics of Familial Non-Medullary Thyroid Carcinoma (FNMTC)
cancers Review Genetics of Familial Non-Medullary Thyroid Carcinoma (FNMTC) Chiara Diquigiovanni * and Elena Bonora Unit of Medical Genetics, Department of Medical and Surgical Sciences, University of Bologna, 40138 Bologna, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-051-208-8418 Simple Summary: Non-medullary thyroid carcinoma (NMTC) originates from thyroid follicular epithelial cells and is considered familial when occurs in two or more first-degree relatives of the patient, in the absence of predisposing environmental factors. Familial NMTC (FNMTC) cases show a high genetic heterogeneity, thus impairing the identification of pivotal molecular changes. In the past years, linkage-based approaches identified several susceptibility loci and variants associated with NMTC risk, however only few genes have been identified. The advent of next-generation sequencing technologies has improved the discovery of new predisposing genes. In this review we report the most significant genes where variants predispose to FNMTC, with the perspective that the integration of these new molecular findings in the clinical data of patients might allow an early detection and tailored therapy of the disease, optimizing patient management. Abstract: Non-medullary thyroid carcinoma (NMTC) is the most frequent endocrine tumor and originates from the follicular epithelial cells of the thyroid. Familial NMTC (FNMTC) has been defined in pedigrees where two or more first-degree relatives of the patient present the disease in absence of other predisposing environmental factors. Compared to sporadic cases, FNMTCs are often multifocal, recurring more frequently and showing an early age at onset with a worse outcome. FNMTC cases Citation: Diquigiovanni, C.; Bonora, E. -
Thyroid and Parathyroid Glands
HISTOLOGY Endocrine Block – 432 Histology Team Lectures 2 and 3: Thyroid and Parathyroid Glands Done by: Lama Al Tawil Bayan Al Mugheerah Reviewed by: Ammar Alyamani Color Guide: Black: Slides. Red: Important. Green: Doctor’s notes (Female). Blue: Doctor’s notes (Male). Orange: Explanation. Objectives 1. Describe the histological structure of thyroid gland. 2. Identify and correlate between the different endocrine cells in thyroid gland and their functions. 3. Describe the microscopic structure of the parathyroid gland. 4. Describe the functional structure of the parathyroid cells. Mind Map THYROID GLAND STROMA PARENCHYMA Reticlular Follicular Parafollicular Capsule Septa cells cells (C cells) fibers Parathyroid Gland Stroma Parenchyma Reticlular Capsule Septa Chief Cells Oxyphil Cells C.T Thyroid Gland THYROID GLAND STROMA PARENCHYMA OF THYROID GLAND 1- Capsule: THYROID FOLLICLES: Dense irregular collagenous C.T. Are the structural and functional units of the 2- Septa (Interlobular septa): thyroid gland. (Variable in size and spherical in shape). Dense irregular collagenous C.T because L/M: it’s part of the capsule divides the thyroid 1- Simple cuboidal epithelium: into lobules. a- Follicular cells. 3- Reticular fibers: b- Parafollicular cells. (Adjacent to a). Thin C.T., composed mostly of reticular 2- Colloid: central colloid-filled lumen. (Acidophilic without any cells and rich in iodine and fibers with rich capillary plexus thyroglobulin, and so it has the stored hormone & (fenestrated blood capillary) surrounds it’s also the place of iodination). each thyroid follicle. N.B. Each follicle is surrounded by thin basal lamina. Each follicle is single layered. a) FOLLICULAR (PRINCIPAL) CELLS L/M: E/M: - Simple cuboidal cells. -
ENDOCRINE SYSTEM the Nervous and Endocrine Systems Act Together to Coordinate Functions of All Body Systems
ENDOCRINE SYSTEM The nervous and endocrine systems act together to coordinate functions of all body systems. Recall that the nervous system acts through nerve impulses (action potentials) conducted along axons of neurons. At synapses, nerve impulses trigger the release\ of mediator (messenger) molecules called neurotransmitters The endocrine system also controls body activities by releasing mediators, called hormones, but the means of control of the two systems are very different A hormone (hormon _ to excite or get moving) is a mediator molecule that is released in one part of the body but regulates the activity of cells in other parts of the body. Most hormones enter interstitial fluid and then the bloodstream. The circulating blood delivers hormones to cells throughout the body. Both neurotransmitters and hormones exert their effects by binding to receptors on or in their ―target‖ cells. Several mediators act as both neurotransmitters and hormones. One familiar example is norepinephrine, which is released as a neurotransmitter by sympathetic postganglionic neurons and as a hormone by chromaffin cells of the adrenal medullae. The body contains two kinds of glands: exocrine glands and endocrine glands. Exocrine glands (exo- _ outside) secrete their products into ducts that carry the secretions into body cavities, into the lumen of an organ, or to the outer surface of the body. Exocrine glands include sudoriferous (sweat), sebaceous (oil), mucous, and digestive glands. Endocrine glands (endo- _ within) secrete their products (hormones) into the interstitial fluid surrounding the secretory cells rather than into ducts. From the interstitial fluid, hormones diffuse into blood capillaries and blood carries them to target cells throughout the body. -
Metabolism of Reverse Triiodothyronine by Isolated Rat Hepatocytes
Metabolism of reverse triiodothyronine by isolated rat hepatocytes. S J Rooda, … , M A van Loon, T J Visser J Clin Invest. 1987;79(6):1740-1748. https://doi.org/10.1172/JCI113014. Research Article Reverse triiodothyronine (rT3) is metabolized predominantly by outer ring deiodination to 3,3'-diiodothyronine (3,3'-T2) in the liver. Metabolism of rT3 and 3,3'-T2 by isolated rat hepatocytes was analyzed by Sephadex LH-20 chromatography, high performance liquid chromatography, and radioimmunoassay, with closely agreeing results. Deiodinase activity was inhibited with propylthiouracil (PTU) and sulfotransferase activity by sulfate depletion or addition of salicylamide or dichloronitrophenol. Normally, little 3,3'-T2 production from rT3 was observed, and 125I- was the main product of both 3, [3'-125I]T2 and [3',5'-125I]rT3. PTU inhibited rT3 metabolism but did not affect 3,3'-T2 clearance as explained by accumulation of 3,3'-T2 sulfate. Inhibition of sulfation did not affect rT3 clearance but 3,3'-T2 metabolism was greatly diminished. The decrease in I- formation from rT3 was compensated by an increased recovery of 3,3'-T2 up to 70% of rT3 metabolized. In conclusion, significant production of 3,3'-T2 from rT3 by rat hepatocytes is only observed if further sulfation is inhibited. Find the latest version: https://jci.me/113014/pdf Metabolism of Reverse Triiodothyronine by Isolated Rat Hepatocytes Sebo Jan Eelkman Rooda, Maria A. C. van Loon, and Thoo J. Vissef Department ofInternal Medicine III and Clinical Endocrinology, Erasmus University Medical School, Rotterdam, The Netherlands Abstract It deiodinates only the outer ring of substrates such as T4 and rT3 (2-4). -
United States Patent (10) Patent N0.: US 7,288,257 B2 Powell (45) Date of Patent: Oct
US007288257B2 (12) United States Patent (10) Patent N0.: US 7,288,257 B2 Powell (45) Date of Patent: Oct. 30, 2007 (54) DIAGNOSIS AND TREATMENT OF HUMAN 5,342,788 A 8/1994 Kunst et a1. .............. .. 436/500 DORMANCY SYNDROME 5,691,456 A 11/1997 AdamcZyk et al. ....... .. 530/405 6,087,090 A 7/2000 Mascarenhas ................ .. 435/4 (76) Inventor: Michael Powell, 150 Catherine Lance, 2003/0007941 A1 1/2003 Cornelius et a1, Suite 1, Grass Valley, CA (US) 95945 ( * ) Notice: Subject to any disclaimer, the term of this patent is extended or adjusted under 35 OTHER PUBLICATIONS U.S.C. 154(b) by 199 days. _ Hannah V. Carey, The American Physiological Society, Physical _ Rev 83; Mammalian Hibernation: Cellular and Molecular (21) Appl' NO" 10/444’845 Responses to Depressed Metabolism and Low Temperature, 2003, (22) Filed: May 23, 2003 PP' 1153'1181' _ _ _ Primary ExamineriRuth A Davis (65) Pnor Pubhcatlon Data (74) Attorney, Agent, or F irmiBorson LaW Group, PC; D. US 2003/0228628 A1 Dec. 11, 2003 Benjamin Borson Related US. Application Data (57) ABSTRACT (60) Provisional application No. 60/382,913, ?led on May $112002’ provlslonal apphcanon NO‘ 60/383’271’ New methods for diagnosis of human dormancy syndrome e on May 24’ 2002' are provided. Human dormancy syndrome is characterized (51) Int C1 by elevated serum ratio of rT3/iT 3 compared to a population 1462K 3'9/00 (2006 01) of normal subjects from Which subjects suffering from A 61K 38/22 (200601) ?bromyalgia, chronic fatigue, obesity, dementias including A 61K 38/27 (200601) AlZheimer’s Disease and related dormancy conditions are C1 2 Q 1/00 (200601) excluded, and the presence of one or more ?ndings related ' A / A / A to reduced activity including torpor, chronic fatigue, insulin (52) US. -
Dopamicue Somatostatin Corticosteroids
https://theses.gla.ac.uk/ Theses Digitisation: https://www.gla.ac.uk/myglasgow/research/enlighten/theses/digitisation/ This is a digitised version of the original print thesis. Copyright and moral rights for this work are retained by the author A copy can be downloaded for personal non-commercial research or study, without prior permission or charge This work cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given Enlighten: Theses https://theses.gla.ac.uk/ [email protected] Role of Bioaetive Peptides In Autoimmune Thyroid Disease Thesis Submitted To The Faculty of Medicine University of Glasgow For The Degree of Doctor of Philosophy By Gholam Reza Moshtaghi Kashanian Department of Pathological Biochemistry Gartnavel General Hospital Glasgow June 1996 ProQuest Number: 10391489 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 10391489 Published by ProQuest LLO (2017). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLO. -
Thyroid Hormone Synthesis Continues Despite Biallelic Thyroglobulin Mutation with Cell Death
Thyroid hormone synthesis continues despite biallelic thyroglobulin mutation with cell death Xiaohan Zhang, … , Viviana A. Balbi, Peter Arvan JCI Insight. 2021. https://doi.org/10.1172/jci.insight.148496. Research In-Press Preview Endocrinology Graphical abstract Find the latest version: https://jci.me/148496/pdf Thyroid hormone synthesis continues despite biallelic thyroglobulin mutation with cell death Authors: Xiaohan Zhang1, Aaron P. Kellogg1, Cintia E. Citterio1,2,3, Hao Zhang1, Dennis Larkin1, Yoshiaki Morishita1,4, Héctor M. Targovnik2,3, Viviana Balbi5, and Peter Arvan1* Affiliations: 1Division of Metabolism, Endocrinology & Diabetes, University of Michigan, Ann Arbor, MI 48105 2Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Microbiología, Inmunología, Biotecnología y Genética/Cátedra de Genética. Buenos Aires, Argentina. 3CONICET, Universidad de Buenos Aires, Instituto de Inmunología, Genética y Metabolismo (INIGEM), Buenos Aires, Argentina 4Division of Diabetes, Department of Internal Medicine, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan 5Department of Endocrinology and Growth, Hospital de Niños Sor María Ludovica, La Plata, Argentina Conflict of interest: The authors declare that no conflict of interest exists. Short Title: Thyroxine synthesis from dead cells 1 Complete absence of thyroid hormone is incompatible with life in vertebrates. Thyroxine is synthesized within thyroid follicles upon iodination of thyroglobulin conveyed from the endoplasmic reticulum (ER), via the Golgi complex, to the extracellular follicular lumen. In congenital hypothyroidism from bi-allelic thyroglobulin mutation, thyroglobulin is misfolded and cannot advance from the ER, eliminating its secretion and triggering ER stress. Nevertheless, untreated patients somehow continue to synthesize sufficient thyroxine to yield measurable serum levels that sustain life. -
Comprehensive Thyroid Plus Adrenal Report
Comprehensive Thyroid Plus Adrenal Report Jane Doe SAMPLEDate Collected: 2/13/2017 Comprehensive Thyroid Plus Adrenal Report Patient Name: Doe, Jane Batch Number: B0000 Patient DOB: 12/10/1960 Accession Number: Q00000 Gender: F Date Received: 2/14/2017 Physician Jon Doe, ND Report Date: 2/22/2017 Test Patient Results Reference Value DHEAS µg/dL 0 125 250 375 500 107 35 - 430 TSH µIU/mL 0.020 1.260 2.500 3.740 4.980+ 7.030 0.358 - 3.74 T4, Total µg/dL 0.5 4.4 8.3 12.1 16.0 7.2 4.5 - 12.5 T3, Free pg/mL 0.5 1.9 3.3 4.6 6.0 3.6 2.2 - 4.0 T4, Free ng/dL 0.10 0.83 1.55 2.28 3.00 0.87 0.76 - 1.46 Cortisol µg/dL 0.2 11.4 22.6 33.8 45.0 6.5 3.1 - 22.4 AntiTPO Ab IU/mL 10.0 20.0 30.0 40.0 50.0 + > 1000.0 0.0 - 35.0 AntiThyroglobulin Ab IU/mL 20 30 40 50 60 + 97 ND - 40 Thyroglobulin ng/mL 0 20 40 60 80 38 <= 55 Thyroxinebinding globulin, TBG µg/mL SAMPLE0 11 23 34 45 20 14 - 31 10401 Town Park Drive, Houston, Texas 77072 USA CLIA# 45D0710715 (800)227-LABS(5227) / (713)-621-3101 James W. Jacobson, Ph.D., Laboratory Director Comprehensive Thyroid Plus Adrenal Report Patient Name: Doe, Jane Batch Number: B0000 Patient DOB: 12/10/1960 Accession Number: Q00000 Gender: F Date Received: 2/14/2017 Physician Jon Doe, ND Report Date: 2/22/2017 Test Component Flag Result Reference Range DHEA-S µg/dL 107 35 - 430 TSH µIU/mL H 7.030 0.358 - 3.74 T4, Total µg/dL 7.2 4.5 - 12.5 T3, Free pg/mL 3.6 2.2 - 4.0 T4, Free ng/dL 0.87 0.76 - 1.46 Cortisol µg/dL 6.5 3.1 - 22.4 Anti-TPO Ab IU/mL H > 1000.0 0.0 - 35.0 Anti-Thyroglobulin Ab IU/mL H 97 ND - 40 Thyroglobulin ng/mL 38 <= 55 Thyroxine-binding globulin, TBGSAMPLE µg/mL 20 14 - 31 10401 Town Park Drive, Houston, Texas 77072 USA CLIA# 45D0710715 (800)227-LABS(5227) / (713)-621-3101 James W. -
Chang Et Al Thyroid
Available online at www.sciencedirect.com Toxicology 243 (2008) 330–339 Thyroid hormone status and pituitary function in adult rats given oral doses of perfluorooctanesulfonate (PFOS)ଝ Shu-Ching Chang a, Julie R. Thibodeaux b,1, Mary L. Eastvold c, David J. Ehresman a, James A. Bjork d, John W. Froehlich e,2, Christopher Lau b, Ravinder J. Singh c, Kendall B. Wallace d, John L. Butenhoff a,∗ a Medical Department, 3M Company, St. Paul, MN 55144, United States b United States Environmental Protection Agency, ORD, NHEERL, Reproductive Toxicology Division, Research Triangle Park, NC 27711, United States c Mayo Clinic and Foundation, Department of Laboratory Medicine and Pathology, Rochester, MN 55095, United States d University of Minnesota, Medical School, Department of Biochemistry and Molecular Biology, Duluth, MN 55812, United States e Pace Analytical Services, Inc., Minneapolis, MN 55414, United States Received 29 August 2007; received in revised form 18 October 2007; accepted 20 October 2007 Available online 26 October 2007 Abstract Introduction: Perfluorooctanesulfonate (PFOS) is widely distributed and persistent in humans and wildlife. Prior toxicological studies have reported decreased total and free thyroid hormones in serum without a major compensatory rise in thyrotropin (TSH) or altered thyroid gland histology. Although these animals (rats, mice and monkeys) might have maintained an euthyroid state, the basis for hypothyroxinemia remained unclear. We undertook this study to investigate the causes for the PFOS-induced reduction of serum total thyroxine (TT4) in rats. Hypotheses: We hypothesized that exposure to PFOS may increase free thyroxine (FT4) in the rat serum due to the ability of PFOS to compete with thyroxine for binding proteins. -
Ontogenesis of Iodothyronine-5'-Deiodinase
Ontogenesis of iodothyronine-5'-deiodinase. Induction of 5'- deiodinating activity by insulin, glucocorticoid, and thyroxine in cultured fetal mouse liver. K Sato, … , T Tsushima, K Shizume J Clin Invest. 1984;74(6):2254-2262. https://doi.org/10.1172/JCI111652. Research Article To elucidate the regulatory mechanism of ontogenetic development of iodothyronine-5'-deiodinase in the fetal and neonatal period, fetal mouse liver of the 19th day of gestation, in which no iodothyronine-5'-deiodinating activity was detectable, was cultured in Dulbecco-Vogt medium supplemented with 10% thyroid hormone-depleted fetal calf serum, insulin, hydrocortisone, and thyroid hormones. Iodothyronine-5'-deiodinating activity of the homogenate was assessed by the amount of iodide released from outer-ring-labeled reverse T3 and expressed as picomoles of 127I- per milligram of protein per minute. The enzyme activity was induced in a dose-dependent manner; optimal concentrations for insulin, hydrocortisone, and thyroxine were 1 microgram/ml, 0.4 microgram/ml, and 10(-6) M, respectively. Without supplementation of either hydrocortisone or thyroxine, no 5'-deiodination was detected. The enzyme activity was observed after 3 d of culture, peaked at days 14-20, and then gradually decreased. Lineweaver-Burk analysis revealed that the increase in activity was primarily due to an increase in Vmax (day 3, 0.2 pmol/mg protein per min; day 20, 2.5 pmol/mg protein per min). Half maximal thyroxine (T4) and triiodothyronine (T3) concentrations were 1 X 10(-7) M (free T4: 4 X 10(-10) M), and 2 X 10(-9) M (free T3: 5.0 X 10(-11) M), respectively, whereas reverse T3 did not elicit any activity at 10(-8)-10(-6) M. -
Review: Molecular Thyroidology
Annals of Clinical & Laboratory Science, vol. 31, no. 3, 2001 221 Review: Molecular Thyroidology William E. Winter and Maria Rita Signorino Department of Pathology, Immunology and Laboratory Medicine, University of Florida College of Medicine, Gainesville, Florida Abstract. Novel disorders involving aberrations of the hypothalamic-pituitary-thyroid gland-thyroid hormone axis have been described in the last 5 to 10 years. The following topics are addressed: molecular mutations causing central hypothyroidism (isolated autosomal recessive TRH deficiency; autosomal recessive TRH-receptor inactivating mutations; TSH beta-subunit bio-inactivating mutations; Pit-1 mutations; Prop1 mutations; high molecular weight bio-inactive TSH); defects in response to TSH (mutations in the TSH receptor: TSH receptor gain-of-function mutations; TSH receptor loss-of-function mutations); defects in thyroid gland formation: transcription factor mutations (TTF-2 and Pax8); defects in peripheral thyroid hormone metabolism (defective intrapituitary conversion of T4 to T3; hemangioma consumption of thyroid hormone); and defects in tissue response to thyroid hormone (generalized thyroid hormone resistance, selective pituitary thyroid hormone resistance). While molecular diagnosis of such conditions is rarely indicated for clinical management, knowledge of the molecular mechanisms of these diseases can greatly enhance the clinical laboratory scientist’s ability to advise clinicians about appropriate thyroid testing and to interpret the complex and sometimes confusing results of thyroid function tests. (received 17 March 2001; accepted 20 March 2001) Key words: TRH, TRH receptor, TSH, TSH receptor, thyroid hormone receptor Introduction Normal Thyroid Function The goal of this review is to introduce the clinical The hypothalamus and anterior pituitary gland laboratorian to several recent advances in molecular thyrotrophs monitor free thyroid hormone levels in thyroidology. -
Dissertation / Doctoral Thesis
DISSERTATION / DOCTORAL THESIS Titel der Dissertation /Title of the Doctoral Thesis „ The natural compound curcumin: impact of cellular uptake and metabolism on in vitro activity “ verfasst von / submitted by Qurratul Ain Jamil angestrebter akademischer Grad / in partial fulfilment of the requirements for the degree of Doktorin der Naturwissenschaften (Dr.rer.nat.) Wien, 2018 / Vienna 2018 Studienkennzahl lt. Studienblatt / A 796 610 449 degree programme code as it appears on the student record sheet: Dissertationsgebiet lt. Studienblatt / Pharmazie, Klinische Pharmazie und Diagnostik field of study as it appears on the student record sheet: Pharmacy, Clinical Pharmacy and Diagnostics Betreut von / Supervisor: Ao.Univ.Prof.Magpharm.Dr.rer.nat.WalterJӓger “Verily in the Creation of the Heavens and the Earth, and in the Alteration of Night and Day, and the Ships which Sail through the Sea with that which is of used to Mankind, and the Water (Rain) which God sends down from the Sky and makes Earth Alive there with after its Death, and the moving Creatures of all kind that he has Scattered therein, and the Veering of Winds and Clouds which are held between the Sky and the Earth, are indeed Signs for Peoples of Understanding.” Acknowledgements While writing this section, I remember the first day in my lab, having a warm welcome from my supervisor; ao. Univ.-Prof. Mag. Dr. Walter Jӓger (Division of Clinical Pharmacy and Diagnostics, University of Vienna). He was waiting for me, offered me coffee and told me how to operate the coffee machine. He showed me, my office and asked me to make a list of all stuff, I need for daily work.