The Forgotten Effects of Thyrotropin-Releasing Hormone Metabolic Functions and Medical Applications
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Hyperthyroidism with an FSH- and TSH-Secreting Pituitary Adenoma
• Hyperthyroidism with an FSH- and TSH-secreting pituitary adenoma JOHN BERMINGHAM, DO LOUIS C. HAENEL, DO A 34-year-old man was found noma is rare. The combined secretion of follicle- to have elevated thyroxine (T 4 ), triiodothy- stimulating hormone (FSH) and TSH by a pi- ronine (T3 ), calculated free T4 , thyroid- tuitary adenoma is rarer. But with current stimulating hormone (TSH), follicle-stimu- widespread use of TSH assays, plus the future lating hormone (FSH), and alpha subunits clinical availability of more sensitive TSH as- of TSH and FSH. A computed tomography says as well as TSH bioactivity testing, more scan of the head showed a 16-mm mac- patients will have pituitary-induced hyperthy- roadenoma of the pituitary gland. There roidism correctly diagnosed, and the disorder was no evidence of loss or excess secre- will be better understood. tion of other pituitary hormones. The large As illustrated in the following case study, chromophobe adenoma was removed via making the correct diagnosis of primary ver- a transphenoidal approach. The patient sus secondary hyperthyroidism is imperative has been taken off all medication. Thyroid because the treatment and potential conse- function has returned to normal and there quences of each of these diseases are totally has been no loss of pituitary secretory ca- different. pacity of other pituitary hormones. The oc- currence of a combined TSH- and FSH- Report of case secreting pituitary adenoma is rare; to the In August 1985, a 34-year-old man was seen with authors knowledge, only one case has complaints that were initially vague and nonspe- been documented in the literature. -
Laboratory Procedure Manual
Laboratory Procedure Manual Analyte: Thyroid Stimulating Hormone Matrix: Serum Method: Microparticle Enzyme Immunoassay (MEIA) Method No.: Revised: as performed by: Coulston Foundation Alamogordo, New Mexico Contact: Ms. Love Julian 1-505-434-1725 Important Information for Users Coulston periodically refines these laboratory methods. It is the responsibility of the user to contact the person listed on the title page of each write-up before using the analytical method to find out whether any changes have been made and what revisions, if any, have been incorporated. Thyroid Stimulating Hormone NHANES 2001–2002 Public Release Data Set Information This document details the Lab Protocol for NHANES 2001-2002 data. Two laboratories performed this testing during 2001-2002. In order to maintain confidentiality of the participants the quality control summary statistics and graphs were combined to mask the individual analysis dates from the two laboratories. Methods for both labs are included in this release. The method for Lab18 analyte is included in this file. The method for Lab40 is described in a separate file. A tabular list of the released analytes follows: Lab Number Analyte SAS Label lab18 LBXTSH Thyroid Stimulating Hormone Page 2 of 11 Thyroid Stimulating Hormone NHANES 2001-2002 1. Summary of Test Principle and Clinical Relevance IMx Ultrasensitive hTSH II is a Microparticle Enzyme Immunoassay (MEIA) for the quantitative determination of human thyroid stimulating hormone (hTSH) in serum or plasma on the IMx analyzer. The IMx Ultrasensitive hTSH II assay is based on the MEIA technology. The IMx Ultrasensitive hTSH II reagents and sample are added to the reaction cell in the following sequence: The probe/electrode assembly delivers the sample and anti-hTSH coated microparticles to the incubation well of the reaction cell. -
The National Drugs List
^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ. -
A Comparative Survey of the RF-Amide Peptide Superfamily
EDITORIAL published: 10 August 2015 doi: 10.3389/fendo.2015.00120 Editorial: A comparative survey of the RF-amide peptide superfamily Karine Rousseau 1*, Sylvie Dufour 1 and Hubert Vaudry 2 1 Laboratory of Biology of Aquatic Organisms and Ecosystems (BOREA), Muséum National d’Histoire Naturelle, CNRS 7208, IRD 207, Université Pierre and Marie Curie, UCBN, Paris, France, 2 Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, INSERM U982, International Associated Laboratory Samuel de Champlain, Institute for Research and Innovation in Biomedicine (IRIB), University of Rouen, Mont-Saint-Aignan, France Keywords: RF-amide peptides, receptors, evolution, functions, deuterostomes, protostomes The first member of the RF-amide peptide superfamily to be characterized, in 1977, was the cardioexcitatory peptide, FMRFamide, isolated from the ganglia of the clam Macrocallista nimbosa (1). Since then, a large number of such peptides, designated after their C-terminal arginine (R) and amidated phenylalanine (F) residues, have been identified in representative species of all major phyla. The discovery, 12 years ago, that the RF-amide peptide kisspeptin, acting via GPR54, was essential for the onset of puberty and reproduction, has been a major breakthrough in reproductive physiology (2–4). It has also put in front of the spotlights RF-amide peptides and has invigo- rated research on this superfamily of regulatory neuropeptides. The present Research Topic aims at illustrating major advances achieved, through comparative studies in (mammalian and non- mammalian) vertebrates and invertebrates, in the knowledge of RF-amide peptides in terms of evolutionary history and physiological significance. Since 2006, by means of phylogenetic analyses, the superfamily of RFamide peptides has been divided into five families/groups in vertebrates (5, 6): kisspeptin, 26RFa/QRFP, GnIH (including LPXRFa and RFRP), NPFF, and PrRP. -
Somatostatin in the Periventricular Nucleus of the Female Rat: Age Specific Effects of Estrogen and Onset of Reproductive Aging
4 Somatostatin in the Periventricular Nucleus of the Female Rat: Age Specific Effects of Estrogen and Onset of Reproductive Aging Eline M. Van der Beek, Harmke H. Van Vugt, Annelieke N. Schepens-Franke and Bert J.M. Van de Heijning Human and Animal Physiology Group, Dept. Animal Sciences, Wageningen University & Research Centre The Netherlands 1. Introduction The functioning of the growth hormone (GH) and reproductive axis is known to be closely related: both GH overexpression and GH-deficiency are associated with dramatic decreases in fertility (Bartke, 1999; Bartke et al, 1999; 2002; Naar et al, 1991). Also, aging results in significant changes in functionality of both axes within a similar time frame. In the rat, GH secretion patterns are clearly sexually dimorphic (Clark et al, 1987; Eden et al, 1979; Gatford et al, 1998). This has been suggested to result mainly from differences in somatostatin (SOM) release patterns from the median eminence (ME) (Gillies, 1997; Muller et al, 1999; Tannenbaum et al, 1990). SOM is synthesized in the periventricular nucleus of the hypothalamus (PeVN) and controls in concert with GH-releasing hormone (GHRH) the GH release from the pituitary (Gillies, 1987; Tannenbaum et al, 1990; Terry and Martin, 1981; Zeitler et al, 1991). An altered GH status is reflected in changes in the hypothalamic SOM system. For instance, the number of SOM cells (Sasaki et al, 1997) and pre-pro SOM mRNA levels (Hurley and Phelps, 1992) in the PeVN were elevated in animals overexpressing GH. Several observations suggest that SOM may also affect reproductive function directly at the level of the hypothalamus. -
1. Two Components, Two Sets of Lecturers
Conditions 1. Two components, two sets of lecturers. 2. Lectures 1-5 Prof. F. Hudecz Lectures 6-9 Dr. Gy. Domány Lectures 10-12 Dr. P. Buzder-Lantos 3. Examination: two parts determined by the lecturers and one mark. - option A: written test - option B: presentation based on literature - option C: oral examination 4. Participation at lectures > 70 % [email protected] Some Approved Peptide Pharmaceuticals and their Methods of Manufacture First generatioin Second generation New generation Oxytocin (L) Carbetocin (S) Abarelix (GnRH) (L) ACTH (1-24) & (1-39) (L,S) Terlipressin (L,S) Cetrorelix (GnRH) (L) Vasopressin (L,S) Felypressin (L,S) Ganirelix (GnRH) (L) Insulin (E,SS, R) Buserelin (L,S) Eptifibatide Glucagon (E,S,R) Deslorelin (L,S) Bivalirudin (L) Calcitonins (L,S,R) Goserelin (L) Copaxone (L) TRH (L) Histrelin (L) Techtide P-289(S) Gonadorelin (L,S) Leuprolide (L,S) Cubicin (F) Somatostatin (L,S) Nafarelin (S) Fuzeon (antiHIV (H) GHRH (1-29) & (1-44) (S) Tryptorelin (L,S) Ziconotide (pain) (S) CRF (Human & Ovine) (S) Lecirelin (S) Pramlintide (diabetes) (S) Cyclosporin (F) Lanreotide (S) Exenatide (diabetes) (S) Thymopentin (L) Octreotide (L,S) Icatibant (brady-rec) Thymosin Alpha-1 (S) Atosiban (L) Romiplostim (hormon) Secretins (Human & Porcine) (E,S) Desmopressin (L,S) Degarelix (GnRH) Parathyroid Hormone (1-34) & (1-84)(S) Lypressin (L) Mifamurtide (rák, adj.) Vasoactive Intestinal Polypeptide (S) Ornipressin Ecallantide (ödéma) Brain Natriuretic Peptide (R) Pitressin (L) Liraglutide (diabetes) Cholecystokinin (L) ACE Inhibitors (Enalapril, Lisinopril) (L) Tesamorelin Tetragastrin (L) HIV Protease Inhibitors (L) Surfaxin Pentagastrin (L) Peginesatide Eledoisin (L) Carfilzomib Linaclotide (enz.inh) L = in solution; S = on solid phase; E = extraction; F = fermentation; H = hybrid synthesis; R = recombinant; SS = semi-synthesis. -
Regulation of the Neuroendocrine Reproductive Axis by Kisspeptin-GPR54 Signaling
REPRODUCTIONREVIEW Regulation of the neuroendocrine reproductive axis by kisspeptin-GPR54 signaling Jeremy T Smith1, Donald K Clifton2 and Robert A Steiner1,2 Departments of 1Physiology and Biophysics and 2Obstetrics and Gynecology, University of Washington, Seattle, Washington 98195-7290, USA Correspondence should be addressed to R A Steiner at Department of Physiology and Biophysics, Health Sciences Building, G-424, School of Medicine, University of Washington, Box no. 357290, Seattle, WA 98195-7290, USA; Email: [email protected] Abstract The Kiss1 gene codes for a family of peptides that act as endogenous ligands for the G protein-coupled receptor GPR54. Spontaneous mutations or targeted deletions of GPR54 in man and mice produce hypogonadotropic hypogonadism and infer- tility. Centrally administered kisspeptins stimulate gonadotropin secretion by acting directly on GnRH neurons. Sex steroids regulate the expression of KiSS-1 mRNA in the brain through direct action on KiSS-1 neurons. In the arcuate nucleus (Arc), sex steroids inhibit the expression of KiSS-1, suggesting that these neurons serve as a conduit for the negative feedback regulation of gonadotropin secretion. In the anteroventral periventricular nucleus (AVPV), sex steroids induce the expression of KiSS-1, implying that KiSS-1 neurons in this region may have a role in the preovulatory LH surge (in the female) or sexual behavior (in the male). Reproduction (2006) 131 623–630 Discovery essential to initiate gonadotropin secretion at puberty and support reproductive function in the adult. GPR54 is a G protein-coupled receptor, which was orig- inally identified as an ‘orphan’ receptor in the rat (Lee et al. 1999). Although GPR54 shares a modest sequence How Kiss1 got its name homology with the known galanin receptors, galanin Investigators at the Pennsylvania State College of Medi- apparently does not bind specifically to this receptor (Lee cine in Hershey, Pennsylvania, discovered the Kiss1 gene. -
Gastric Secretory and Plasma Hormonal Responses to Sham-Feeding of Varying Duration in Patients with Duodenal Ulcer
Gut: first published as 10.1136/gut.22.12.1003 on 1 December 1981. Downloaded from Gut, 1981, 22,1003-1010 Gastric secretory and plasma hormonal responses to sham-feeding of varying duration in patients with duodenal ulcer S J KONTUREK,* J SWIERCZEK, N KWIECIEN, W OBTUTOWICZ, M DOBRZANSKA, B KOPP, AND J OLEKSY From the Institute ofPhysiology, Medica, Academy, Krakow, and District Hospital, Krakow, Poland SUMMARY Gastric acid and serum gastrin, pancreatic polypeptide, and insulin responses to cephalic vagal stimulation were studied in eight patients with duodenal ulcer using modified sham- feeding for periods varying from four to 30 minutes. In addition, the maximal acid response to sham-feeding was compared with that induced by pentagastrin in 10 healthy subjects and 14 patients with duodenal ulcer. It was found that the gastric acid response to modified sham-feeding reached the maximal value after 15 minutes of sham-feeding and amounted to about 68% of the pentagastrin maximum. The serum pancreatic polypeptide response was also increased after modified sham-feeding and depended on the duration of this procedure, whereas gastrin and insulin responses were not significantly affected by modified sham-feeding. When the peak acid output induced by modified sham-feeding was normalised as percentage of the peak response to pentagastrin, it was similar in healthy subjects and in patients with duodenal ulcer; this indicates that the increased peak acid response to modified sham-feeding observed in patients with duodenal ulcer corresponded with -
Classification Decisions Taken by the Harmonized System Committee from the 47Th to 60Th Sessions (2011
CLASSIFICATION DECISIONS TAKEN BY THE HARMONIZED SYSTEM COMMITTEE FROM THE 47TH TO 60TH SESSIONS (2011 - 2018) WORLD CUSTOMS ORGANIZATION Rue du Marché 30 B-1210 Brussels Belgium November 2011 Copyright © 2011 World Customs Organization. All rights reserved. Requests and inquiries concerning translation, reproduction and adaptation rights should be addressed to [email protected]. D/2011/0448/25 The following list contains the classification decisions (other than those subject to a reservation) taken by the Harmonized System Committee ( 47th Session – March 2011) on specific products, together with their related Harmonized System code numbers and, in certain cases, the classification rationale. Advice Parties seeking to import or export merchandise covered by a decision are advised to verify the implementation of the decision by the importing or exporting country, as the case may be. HS codes Classification No Product description Classification considered rationale 1. Preparation, in the form of a powder, consisting of 92 % sugar, 6 % 2106.90 GRIs 1 and 6 black currant powder, anticaking agent, citric acid and black currant flavouring, put up for retail sale in 32-gram sachets, intended to be consumed as a beverage after mixing with hot water. 2. Vanutide cridificar (INN List 100). 3002.20 3. Certain INN products. Chapters 28, 29 (See “INN List 101” at the end of this publication.) and 30 4. Certain INN products. Chapters 13, 29 (See “INN List 102” at the end of this publication.) and 30 5. Certain INN products. Chapters 28, 29, (See “INN List 103” at the end of this publication.) 30, 35 and 39 6. Re-classification of INN products. -
Using T3 for Treatment of Hypothyroidism - What the Evidence Say?
Journal of Endocrinology and Thyroid Research ISSN: 2573-2188 Review Article J Endocrinol Thyroid Res Volume 2 Issue 2- June 2017 Copyright © All rights are reserved by Vismay Naik, DOI: 10.19080/JETR.2017.02.555584 Using T3 For Treatment of Hypothyroidism - What the Evidence Say? Vismay Naik* Ashirvad Heart and Diabetes Centre, India Submission: March 01, 2017; Published: June 27, 2017 *Corresponding author: Vismay Naik, MD, MRCP (London), Ashirvad Heart and Diabetes Centre, Botad, Gujarat, India, Email: Introduction Hypothyroidism is due to the primary disease of the thyroid Treatment Strategies of Hypothyroidism or secondary to hypothalamic- pituitary disease [1]. Primary The objectives of management of hypothyroidism are to hypothyroidism is the most common endocrine disorder reverse clinical progression, correct metabolic abnormalities, throughout the world. Traditionally we have been using [3] and reduction of goiter size in patients with autoimmune levothyroxine in the treatment of hypothyroidism. However, there Hashimoto’s thyroiditis [4]. This can be achieved by 3 different have been reports of persisting symptoms of hypothyroidism strategies: in 5-10% of levothyroxine treated hypothyroid patients a. Standard treatment with a daily dose levothyroxine (T4) in order to reach an age adjusted TSH target [5]. The with normal serum thyrotrophin (TSH) [2]. Physiologically dose has to be titrated periodically [3]. levothyronine is the active form, so treating the patient with the active form has been considered optimum treatment. This study b. Triiodothyronine (T3) monotherapy is the biological is aimed at reviewing the literature on using T3 in treatment of hypothyroidism either alone or in combination with T4. By the its short half-life [6] end of this study we hope to answer the question, if the use of T3 active form. -
A Case of Cushing Syndrome with Both Secondary Hypothyroidism and Hypercalcemia Due to Postoperative Adrenal Insufficiency
Endocrine Journal 2004, 51 (1), 105–113 NOTE A Case of Cushing Syndrome with Both Secondary Hypothyroidism and Hypercalcemia Due to Postoperative Adrenal Insufficiency MASAHITO KATAHIRA, TSUTOMU YAMADA* AND MASAHIKO KAWAI* Department of Internal Medicine, Kyoritsu General Hospital, Nagoya 456-8611, Japan *Division of Endocrinology, Department of Internal Medicine, Okazaki City Hospital, Okazaki 444-8553, Japan Abstract. A 48-year-old woman was referred to our hospital because of secondary hypothyroidism. Upon admission a left adrenal tumor was also detected using computed tomography. Laboratory data and adrenal scintigraphy were compatible with Cushing syndrome due to the left adrenocortical adenoma, although she showed no response to the TRH stimulation test. Hypercortisolism resulting in secondary hypothyroidism was diagnosed. After a left adrenalectomy, hydrocortisone administration was begun and the dose was reduced gradually. After discharge on the 23rd postoperative day, she began to suffer from anorexia. ACTH level remained low, and serum cortisol, free thyroxine and TSH levels were within the normal range. Since her condition became worse, she was re-admitted on the 107th postoperative day at which time serum calcium level was high (15.6 mg/dl). Both ACTH response to the CRH stimulation test and TSH response to the TRH stimulation test were restored to almost normal levels, but there was no response of cortisol to CRH stimulation test. We diagnosed that the hypercalcemia was due to adrenal insufficiency. Although the serum calcium level decreased to normal after hydrocortisone was increased (35 mg/day), secondary hypothyroidism recurred. It was suggested that sufficient glucocorticoids suppressed TSH secretion mainly at the pituitary level, which resulted in secondary (corticogenic) hypothyroidism. -
Title 16. Crimes and Offenses Chapter 13. Controlled Substances Article 1
TITLE 16. CRIMES AND OFFENSES CHAPTER 13. CONTROLLED SUBSTANCES ARTICLE 1. GENERAL PROVISIONS § 16-13-1. Drug related objects (a) As used in this Code section, the term: (1) "Controlled substance" shall have the same meaning as defined in Article 2 of this chapter, relating to controlled substances. For the purposes of this Code section, the term "controlled substance" shall include marijuana as defined by paragraph (16) of Code Section 16-13-21. (2) "Dangerous drug" shall have the same meaning as defined in Article 3 of this chapter, relating to dangerous drugs. (3) "Drug related object" means any machine, instrument, tool, equipment, contrivance, or device which an average person would reasonably conclude is intended to be used for one or more of the following purposes: (A) To introduce into the human body any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (B) To enhance the effect on the human body of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; (C) To conceal any quantity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state; or (D) To test the strength, effectiveness, or purity of any dangerous drug or controlled substance under circumstances in violation of the laws of this state. (4) "Knowingly" means having general knowledge that a machine, instrument, tool, item of equipment, contrivance, or device is a drug related object or having reasonable grounds to believe that any such object is or may, to an average person, appear to be a drug related object.