Xerox University Microfilms

Total Page:16

File Type:pdf, Size:1020Kb

Xerox University Microfilms THE EFFECTS OF INHIBITION OF PROSTAGLANDIN SYNTHESIS ON THYROTROPIN SECRETION Item Type text; Dissertation-Reproduction (electronic) Authors Thompson, Martha Ellen, 1947- Publisher The University of Arizona. Rights Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. Download date 05/10/2021 07:19:06 Link to Item http://hdl.handle.net/10150/289460 INFORMATION TO USERS This material was produced from a microfilm copy of the original document. While the most advanced technological means to photograph and reproduce this document- have been used, the quality is heavily dependent upon the quality of the original submitted. The following explanation of techniques is provided to help you understand markings or patterns which may appear on this reproduction. 1.The sign or "target" for pages apparently lacking from the document photographed is "Missing Page(s)". If it was possible to obtain the missing page(s) or section, they are spliced into the film along with adjacent pages. This may have necessitated cutting thru an image and duplicating adjacent pages to insure you complete continuity. 2. When an image on the film is obliterated with a large round black mark, it is an indication that the photographer suspected that the copy may have moved during exposure and thus cause a blurred image. You will find a good image of the page in the adjacent frame. 3. When a map, drawing or chart, etc., was part of the material being photographed the photographer followed a definite method in "sectioning" the material. It is customary to begin photoing at the upper left hand corner of a large sheet and to continue photoing from left to right in equal sections with a small overlap. If necessary, sectioning is continued again — beginning below the first row and continuing on until complete. 4. The majority of users indicate that the textual content is of greatest value, however, a somewhat higher quality reproduction could be made from "photographs" if essential to the understanding of the dissertation. Silver prints of "photographs" may be ordered at additional charge by writing the Order Department, giving the catalog number, title, author and specific pages you wish reproduced. 5. PLEASE NOTE: Some pages may have indistinct print. Filmed as received. Xerox University Microfilms 300 North Zeeb Road Ann Arbor, Michigan 48106 76-29,342 THOMPSON, Martha Ellen, 1947- THE EFFECTS OF INHIBITION OF PROSTAGLANDIN SYNTHESIS ON THYROTROPIN SECRETION. The University of Arizona, Ph.D., 1976 Physiology Xerox University Microfilms, Ann Arbor, Michigan 48106 THE EFFECTS OF INHIBITION OF PROSTAGLANDIN SYNTHESIS ON THYROTROPIN SECRETION by Martha Ellen Thompson A Dissertation Submitted to the Faculty of the DEPARTMENT OF PHYSIOLOGY In Partial Fulfillment of the Requirements For the Degree of DOCTOR OF PHILOSOPHY In the Graduate College THE UNIVERSITY OF ARIZONA 19 7 6 THE UNIVERSITY OF ARIZONA GRADUATE COLLEGE I hereby recommend that this dissertation prepared under my direction by Martha Til 1 e>r> Thnmpwnn entitled THE EFFECTS OF INHIBITION OF PROSTAGLANDIN SYNTHESIS ON THYROTROPIN SECRETION be accepted as fulfilling the dissertation requirement of the degree of Doctor of Philosophy /9 /May ny<, Di5.5ferta.tion Director Date After inspection of the final copy of the dissertation, the following members of the Final Examination Committee concur in its approval and recommend its acceptance:» — /9 T J//<?/-?-<£ This approval and acceptance is contingent on the candidate's adequate performance and defense of this dissertation at the final oral examination. The inclusion of this sheet bound into the library copy of the dissertation is evidence of satisfactory performance at the final examination. STATEMENT BY AUTHOR This dissertation has been submitted in partial fulfillment of requirements for an advanced degree at The University of Arizona and is deposited in the University Library to be made available to bor­ rowers under rules of the Library. Brief quotations from this dissertation are allowable without special permission, provided that accurate acknowledgment of source is made. Requests for permission for extended quotation from or re­ production of this manuscript in whole or in part may be granted by the head of the major department or the Dean of the Graduate College when in his judgment the proposed use of the material is in the in­ terests of scholarship. In all other instances, however, permission must be obtained from the author. SIGNED: ACKNOWLEDGMENTS I wish to express my sincere appreciation to Dr. George Hedge who provided guidance and encouragement in both the research investi­ gation and preparation of this dissertation# I would also like to thank Dr. Gayle Orczyk, Merck Institute for Therapeutic Research, Rail­ way, New Jersey, 1975 and Dr. Delbert Fisher, Harbor General Hospital, Torrance, California, for their personal assistance in the radio­ immunoassay procedures in 1972. I also wish to thaiik Ms. Sherri Konen, Arizona Medical Center, Tucson, Arizona, Dr. Marvin Brown, Salk Insti­ tute, La Jolla, California, and the NIAMMDD Rat Pituitary Hormone Distribution Program for their invaluable assistance in the radio­ immunoassay procedures and data analysis. Appreciation is due to Drs. Douglas Stuart, Eldon Braun and Mark Haussler for their critical review of this dissertation. I am particularly indebted to Susan Dalby, Judy Cardoni and Nancy Hernden for their excellent technical assistance. iii TABLE OF CONTENTS Page LIST OF TABLES vi LIST OF ILLUSTRATIONS vii ABSTRACT x 1. INTRODUCTION 1 Hypothalamic Control of Anterior Pituitary Secretion . 1 Corticotropin-Releasing Factor (CRF) . 6 Thyrotropin-Releasing Hormone (TRH) 8 Luteinizing Hormone-Releasing Hormone (LHRH) ... 9 Growth Hormone-Releasing Factor (GRF) and Somatostatin (GIF) 12 Prolactin Release-Inhibiting Factor (PIF) and Prolactin-Releasing Factor (PRF) 13 Specificity of Releasing Factors for the Anterior Pituitary Hormones 15 Regulation of the Pituitary-Thyroid Axis 17 Hypothalamic Regulation of TSH Secretion .. • • 18 Environmental Stimuli for TSH Secretion ..... 20 Mechanism of Action of TRH 22 Thyroid Hormone Feedback Control of TSH Secretion 25 Circadian Rhythm of TSH Secretion 27 Mechanism of Action of TSH 27 Prostaglandins and the Hypothalamic-Pituitary- Endocrine Systems 28 Structure and Synthesis 29 Metabolism 31 Mechanism of Action 32 Systemic Effects of Prostaglandins 33 Aim of Present Study 39 2. MATERIALS AND METHODS **1 Animals and Care 4l Surgical Procedures 42 Chronic Indwelling Jugular Catheters 42 Thyroidectomy Procedure ............. Stereotaxic Microinjection Procedure 44 iv V TABLE OF CONTENTS—Continued Page Acute Cold Exposure . kk Pharmacological Preparations ............. kk Radioimmunoassay of Plasma TSH, T-j and T^ .. k$ Assessment of Thyroidal Activity ........... k? T^ and T* Half-life 47 Data Analysis .. 49 3. RESULTS 50 Measurement of Pituitary and Thyroid Responses to Various Stimuli 50 Thyrotropin Response 50 Thyroid Hormone Secretion ............. 63 Effect of Inhibition of Prostaglandin Synthesis on the Hypothalamic-Pituitary-Thyroid Axis •• 73 Systemic Indomethacin in Intact Rats . 73 Indomethacin or Aspirin Treatment in Thyroidec- tomized Rats .................. 8k Stereotaxic Microinjection Studies 99 DISCUSSION 103 Comparison of Plasma TSH, T^ and T^ Levels with Previously Reported Values ... ... 103 Measurement of Pituitary and Thyroid Response to Various Stimuli 105 TSH Response 105 Thyroid Hormone Secretion 109 Effects of Inhibition of Prostaglandin Synthesis on the Hypothalamic-Pituitary-Thyroid Axis 113 Systemic Indomethacin in Intact Rats ....... Ilk Indomethacin or Aspirin Treatment in Thyroidec- tomized Rats 118 Stereotaxic Microinjection Studies 122 Specificity of Indomethacin and Aspirin 123 Comparison of Results in This Study with Previous Studies Which Used Exogenous Prostaglandins ..... 126 Conclusions 127 LIST OF REFERENCES 129 LIST OF TABLES Table Page 1. Plasma thyrotropin (TSH) levels in response to ac *. ,* cold exposure with ether or pentobarbital anesthesia .. 51 2m Effect of acute cold exposure on plasma thyrotropin (TSH) concentrations in unanesthetized rats ...... 5^ 3. The effect of acute cold exposure on plasma Tj concen­ trations with ether or pentobarbital anesthesia .... 65 4. The effect of acute cold exposure on plasma Tif. concen­ trations with ether or pentobarbital anesthesia .... 66 5. Plasma levels in response to TRH with ether or pentobarbital anesthesia 69 6. Plasma T^ concentrations in response to thyrotropin (TSH) with ether or pentobarbital anesthesia ...*•• 72 7. Time schedule of the administration of drugs and sub­ sequent blood sampling for experiments in which intact rats were used 75 125 124 8. Disappearance rates for I-Tjj. and I-T^ following indomethacin treatment 82 9. Time schedules for surgery, drug (or vehicle) injec­ tions, T/j. replacement, and collection of blood samples for experiments in which TRH or thyroidectomy were used as stimuli to TSH secretion 85 10. Plasma TSH, T^, and T^ concentrations following TRH and aspirin (^5 mg/injection; Asp) or gelatin (Gel) treat­ ment in thyroidectomized rats receiving T^ replacement (3-0 /ig/100 g BW/day) 9^ vi LIST OF ILLUSTRATIONS Figure Page 1. Plasma thyrotropin (TSH) levels in response to acute cold exposure
Recommended publications
  • Te2, Part Iii
    TERMINOLOGIA EMBRYOLOGICA Second Edition International Embryological Terminology FIPAT The Federative International Programme for Anatomical Terminology A programme of the International Federation of Associations of Anatomists (IFAA) TE2, PART III Contents Caput V: Organogenesis Chapter 5: Organogenesis (continued) Systema respiratorium Respiratory system Systema urinarium Urinary system Systemata genitalia Genital systems Coeloma Coelom Glandulae endocrinae Endocrine glands Systema cardiovasculare Cardiovascular system Systema lymphoideum Lymphoid system Bibliographic Reference Citation: FIPAT. Terminologia Embryologica. 2nd ed. FIPAT.library.dal.ca. Federative International Programme for Anatomical Terminology, February 2017 Published pending approval by the General Assembly at the next Congress of IFAA (2019) Creative Commons License: The publication of Terminologia Embryologica is under a Creative Commons Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0) license The individual terms in this terminology are within the public domain. Statements about terms being part of this international standard terminology should use the above bibliographic reference to cite this terminology. The unaltered PDF files of this terminology may be freely copied and distributed by users. IFAA member societies are authorized to publish translations of this terminology. Authors of other works that might be considered derivative should write to the Chair of FIPAT for permission to publish a derivative work. Caput V: ORGANOGENESIS Chapter 5: ORGANOGENESIS
    [Show full text]
  • Hypothyroidism Mauricio Alvarez Andrade and Oscar Rosero Olarte
    Chapter Hypothyroidism Mauricio Alvarez Andrade and Oscar Rosero Olarte Abstract Hypothyroidism is a condition that results from thyroid hormone deficiency that can range from an asymptomatic condition to a life-threatening disease. The prevalence of hypothyroidism varies according to the population, from up to 3 to 4% in some populations and in the case of subclinical hypothyroidism up to 5–10%. Clinical symptoms of hypothyroidism are diverse, broad, and non-specific and can be related to many systems, reflecting the systemic effects of thyroid hormones. The severity of the symptoms is usually related to the severity of the thyroid hor- mone deficit. The most common form of hypothyroidism, primary hypothyroid- ism, is diagnosed when there is elevation of TSH and decrease in the level of free T4 and Subclinical hypothyroidism is diagnosed when there is an elevation of TSH with normal levels of free T4. The most frequent cause of primary hypothyroid- ism in populations without iodine deficiency is Hashimoto’s thyroiditis or chronic lymphocytic thyroiditis. Iodine deficiency is the main cause of hypothyroidism in populations with deficiency of iodine intake. The treatment of choice for hypothy- roidism is thyroxine (T4), which has shown efficacy in multiple studies to restore the euthyroid state and improve the symptoms of hypothyroidism. In subclinical hypothyroidism, the treatment depends on the age, functionality, and comorbidi- ties of the patients. The total replacement dose of levothyroxine in adults is approxi- mately 1.6 mcg/kg; however in elderly patients with heart disease or coronary heart disease, the starting dose should be from 0.3 to 0.4 mcg/kg/day with progressive increase of 10% of the dose monthly.
    [Show full text]
  • Hipotiroidismo Congénito Central: Correlaciones Clínico-Genéticas E Investigación De Sus Mecanismos Moleculares
    Universidad Autónoma de Madrid. Departamento de Bioquímica. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Marta García González Madrid, 2017 Departamento de Bioquímica. Facultad de Medicina. Universidad Autónoma de Madrid. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Doctoranda: Marta GARCÍA GONZÁLEZ. Licenciada en Ciencias Biológicas. Universidad Complutense de Madrid. Director: Dr. José Carlos Moreno Navarro. Laboratorio Molecular de Tiroides. Instituto de Genética Médica y Molecular (INGEMM). Hospital Universitario La Paz (Madrid). José Carlos Moreno Navarro, Doctor en Medicina y Director del Laboratorio Molecular de Tiroides en el Instituto de Genética Médica y Molecular (INGEMM) del Hospital Universitario La Paz, Madrid. CERTIFICA: Que Marta García González, Licenciada en Biología y Máster en Bioquímica, Biología Molecular y Biomedicina por la Universidad Complutense de Madrid, ha realizado bajo su dirección el trabajo de investigación titulado: Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares El que suscribe considera el trabajo realizado satisfactorio y apto para ser presentado como Tesis Doctoral en el Departamento de Bioquímica de la Facultad de Medicina de la Universidad Autónoma de Madrid. Y para que conste donde proceda expiden el presente certificado en Madrid a 19 de Junio de 2017. Fdo. José Carlos Moreno Navarro Marta García González.
    [Show full text]
  • Abnormality of the Middle Phalanx of the 4Th Toe Abnormality of The
    Glucocortocoid-insensitive primary hyperaldosteronism Absence of alpha granules Dexamethasone-suppresible primary hyperaldosteronism Abnormal number of alpha granules Primary hyperaldosteronism Nasogastric tube feeding in infancy Abnormal alpha granule content Poor suck Nasal regurgitation Gastrostomy tube feeding in infancy Abnormal alpha granule distribution Lumbar interpedicular narrowing Secondary hyperaldosteronism Abnormal number of dense granules Abnormal denseAbnormal granule content alpha granules Feeding difficulties in infancy Primary hypercorticolismSecondary hypercorticolism Hypoplastic L5 vertebral pedicle Caudal interpedicular narrowing Hyperaldosteronism Projectile vomiting Abnormal dense granules Episodic vomiting Lower thoracicThoracolumbar interpediculate interpediculate narrowness narrowness Hypercortisolism Chronic diarrhea Intermittent diarrhea Delayed self-feeding during toddler Hypoplastic vertebral pedicle years Intractable diarrhea Corticotropin-releasing hormone Protracted diarrhea Enlarged vertebral pedicles Vomiting Secretory diarrhea (CRH) deficient Adrenocorticotropinadrenal insufficiency (ACTH) Semantic dementia receptor (ACTHR) defect Hypoaldosteronism Narrow vertebral interpedicular Adrenocorticotropin (ACTH) distance Hypocortisolemia deficient adrenal insufficiency Crohn's disease Abnormal platelet granules Ulcerative colitis Patchy atrophy of the retinal pigment epithelium Corticotropin-releasing hormone Chronic tubulointerstitial nephritis Single isolated congenital Nausea Diarrhea Hyperactive bowel
    [Show full text]
  • Nomina Histologica Veterinaria, First Edition
    NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria.
    [Show full text]
  • Nomenclatore Per L'anatomia Patologica Italiana Arrigo Bondi
    NAP Nomenclatore per l’Anatomia Patologica Italiana Versione 1.9 Arrigo Bondi Bologna, 2016 NAP v. 1.9, pag 2 Arrigo Bondi * NAP - Nomenclatore per l’Anatomia Patologica Italiana Versione 1.9 * Componente Direttivo Nazionale SIAPEC-IAP Società Italiana di Anatomia Patologica e Citodiagnostica International Academy of Pathology, Italian Division NAP – Depositato presso S.I.A.E. Registrazione n. 2012001925 Distribuito da Palermo, 1 Marzo 2016 NAP v. 1.9, pag 3 Sommario Le novità della versione 1.9 ............................................................................................................... 4 Cosa è cambiato rispetto alla versione 1.8 ........................................................................................... 4 I Nomenclatori della Medicina. ........................................................................................................ 5 ICD, SNOMED ed altri sistemi per la codifica delle diagnosi. ........................................................... 5 Codifica medica ........................................................................................................................... 5 Storia della codifica in medicina .................................................................................................. 5 Lo SNOMED ............................................................................................................................... 6 Un Nomenclatore per l’Anatomia Patologica Italiana ................................................................. 6 Il NAP .................................................................................................................................................
    [Show full text]
  • BGD B Lecture Notes Docx
    BGD B Lecture notes Lecture 1: GIT Development Mark Hill Trilaminar contributions • Overview: o A simple tube is converted into a complex muscular, glandular and duct network that is associated with many organs • Contributions: o Endoderm – epithelium of the tract, glands, organs such as the liver/pancreas/lungs o Mesoderm (splanchnic) – muscular wall, connective tissue o Ectoderm (neural crest – muscular wall neural plexus Gastrulation • Process of cell migration from the epiblast through the primitive streak o Primitive streak forms on the bilaminar disk o Primitive streak contains the primitive groove, the primitive pit and the primitive node o Primitive streak defines the body axis, the rostral caudal ends, and left and right sides Thus forms the trilaminar embryo – ectoderm, mesoderm, endoderm • Germ cell layers: o ectoderm – forms the nervous system and the epidermis epithelia 2 main parts • midline neural plate – columnar epithelium • lateral surface ectoderm – cuboidal, containing sensory placodes and skin/hair/glands/enamel/anterior pituitary epidermis o mesoderm – forms the muscle, skeleton, and connective tissue cells migrate second migrate laterally, caudally, rostrally until week 4 o endoderm – forms the gastrointestinal tract epithelia, the respiratory tract and the endocrine system cells migrate first and overtake the hypoblast layer line the primary yolk sac to form the secondary yolk sac • Membranes: o Rostrocaudal axis Ectoderm and endoderm form ends of the gut tube, no mesoderm At each end, form the buccopharyngeal
    [Show full text]
  • |||GET||| Pancreatic Islet Biology 1St Edition
    PANCREATIC ISLET BIOLOGY 1ST EDITION DOWNLOAD FREE Anandwardhan A Hardikar | 9783319453057 | | | | | The Evolution of Pancreatic Islets Advanced search. The field of regenerative medicine is rapidly evolving and offers great hope for the nearest future. Easily read eBooks on Pancreatic Islet Biology 1st edition phones, computers, or any eBook readers, including Kindle. Help Learn to edit Community portal Recent changes Upload file. Pancreatic Islet Biologypart of the Stem Cell Biology and Regenerative Medicine series, is essential reading for researchers and clinicians in stem cells or endocrinology, especially those focusing on diabetes. Because the beta cells in the pancreatic islets Pancreatic Islet Biology 1st edition selectively destroyed by an autoimmune process in type 1 diabetesclinicians and researchers are actively pursuing islet transplantation as a means of restoring physiological beta cell function, which would offer an alternative to a complete pancreas transplant or artificial pancreas. Strategies to improve islet yield from chronic pancreatitis pancreases intended for islet auto-transplantation 6. About this book This comprehensive volume discusses in vitro laboratory development of insulin-producing cells. Junghyo Jo, Deborah A. Show all. Comparative Analysis of Islet Development. Leibson A. However, type 1 diabetes is the result of the autoimmune destruction of beta cells in the pancreas. Islets can influence each other through paracrine and autocrine communication, and beta cells are coupled electrically to six to seven other beta cells but not to other cell types. Pancreatic Islet Biologypart of the Stem Cell Biology and Regenerative Medicine Pancreatic Islet Biology 1st edition, is essential reading for researchers and clinicians in stem cells or endocrinology, especially those focusing on diabetes.
    [Show full text]
  • Morphometric Studies on the Development of the Human Thyroid Gland
    Hislol Hislopalhol (1997) 12: 79-84 Histology and 001: 10.14670/HH-12.79 Histopathology http://www.hh.um.es From Cell Biology to Tissue Engineering Morphometric studies on the development of the human thyroid gland. II. The late fetal life J. Bocian-Sobkowskal, W. Wozniak1 and L.K. Malendowicz2 1Department of Anatomy and 2Department of Histology and Embryology, University School of Medical Sciences, Poznan, Poland Summary. Histological and morphometric studies were upon the presence of hypothalamus (Hatakeyama, 1969). performed on 27 thyroid glands obtained from normal The placenta is permeable to thyrotropin-releasing fetuses ranging between 23 to 40 weeks of intra-uterine hormone (TRH); however, TRH plays little or no part in life. the fetal thyroid function (for review see Roti, 1988). It In the thyroids the volume of gland, colloid, and remains to be established whether the maternal TRH stroma were calculated by means of differential point­ influences thyrotropic cell differentiation in an­ counting method and the height of the thyroid follicular encephalic fetuses. cells was measured. Moreover, the epithelium/colloid In pituitary thyrotropic cells TSH-immunoreactivity ratio in the thyroid gland, a very sensitive parameter of is observed as early as 13-15 weeks of intra-uterine stimulation of the glands by TSH, was calculated. development , while by RIA the presence of TSH­ Regarding the values of this ratio in human fetal thyroid immunoreactivity in fetal pituitary gland was gland, the intra-uterine development of the gland may be demonstrated 3 weeks earlier (Fukuchi et aI., 1970; divided into three distinct stages. The first one, between Fisher et aI.
    [Show full text]
  • The Peripheral Conversion of Thyroxine (T4) Into Triiodothyronine
    The Peripheral Conversion of Thyroxine (T4) into i • Triiodothyronine (T3) and Reverse triiodothyronine (rT3) 3 The Peripheral Conversion of Thyroxine (T4) into Triiodothyronine (T3) sts- a», and Reverse triiodothyronine (rT3) ACADEMISCH PROEFSCHRIFT ter verkrijging van de graad van doctor in de Geneeskunde aan de Universiteit van Amsterdam, ?••!• op gezag van de Rector Magnificus dr. J.Bruyn, hoogleraar in de Faculteit der Letteren, in het openbaar te verdedigen in de aula der Universiteit (tijdelijk in de Lutherse Kerk, ingang Singel 411, hoek Spui), op donderdag 15 november 1979 om 16.00 uur precies door WILLEM MAARTEN WIERSINGA geboren te Leiden AMSTERDAM 1979 I; Promoter : Dr. J.L. Touber g Coreferent : Prof. dr. A. Querido 'l Copromotor : Prof. dr. M. Koster Dit proefschrift is bewerkt op de afdeling endocrinologie (Dr. J.L. Touber) van de kliniek voor inwendige ziekten (Prof.Dr. M. Koster en Prof.Dr. J. Vreeken) van het Wilhelmina Gasthuis, Academisch Ziekenhuis bij de Universiteit van Amsterdam. Het verschijnen van dit proefschrift werd mede mogeiijk gemaakt door steun van de Nederlandse Hartstichting en van ICI Holland B.V. I i*' Ii: VOORWOORD I Dit proefschrift is niet opgedragen aan iemand in het bijzonder, daar het tv, verrichte onderzoek in eerste instantie mijn eigen nieuwsgierigheid heeft 1} bevredigd en ik de indruk heb dat het meer mijn eigen genoegen heeft r ' gediend dan dat van anderen. Een woord van dank aan de velen die in de : afgelopen jaren bijgedragen hebben tot deze studies, is wel op zijn plaats, '. daar het onderzoek zonder hun steun niet mogelijk zou zijn geweest, en ; vooral ook omdat ik met plezier terugdenk aan de onderlinge , samenwerking.
    [Show full text]
  • 26 April 2010 TE Prepublication Page 1 Nomina Generalia General Terms
    26 April 2010 TE PrePublication Page 1 Nomina generalia General terms E1.0.0.0.0.0.1 Modus reproductionis Reproductive mode E1.0.0.0.0.0.2 Reproductio sexualis Sexual reproduction E1.0.0.0.0.0.3 Viviparitas Viviparity E1.0.0.0.0.0.4 Heterogamia Heterogamy E1.0.0.0.0.0.5 Endogamia Endogamy E1.0.0.0.0.0.6 Sequentia reproductionis Reproductive sequence E1.0.0.0.0.0.7 Ovulatio Ovulation E1.0.0.0.0.0.8 Erectio Erection E1.0.0.0.0.0.9 Coitus Coitus; Sexual intercourse E1.0.0.0.0.0.10 Ejaculatio1 Ejaculation E1.0.0.0.0.0.11 Emissio Emission E1.0.0.0.0.0.12 Ejaculatio vera Ejaculation proper E1.0.0.0.0.0.13 Semen Semen; Ejaculate E1.0.0.0.0.0.14 Inseminatio Insemination E1.0.0.0.0.0.15 Fertilisatio Fertilization E1.0.0.0.0.0.16 Fecundatio Fecundation; Impregnation E1.0.0.0.0.0.17 Superfecundatio Superfecundation E1.0.0.0.0.0.18 Superimpregnatio Superimpregnation E1.0.0.0.0.0.19 Superfetatio Superfetation E1.0.0.0.0.0.20 Ontogenesis Ontogeny E1.0.0.0.0.0.21 Ontogenesis praenatalis Prenatal ontogeny E1.0.0.0.0.0.22 Tempus praenatale; Tempus gestationis Prenatal period; Gestation period E1.0.0.0.0.0.23 Vita praenatalis Prenatal life E1.0.0.0.0.0.24 Vita intrauterina Intra-uterine life E1.0.0.0.0.0.25 Embryogenesis2 Embryogenesis; Embryogeny E1.0.0.0.0.0.26 Fetogenesis3 Fetogenesis E1.0.0.0.0.0.27 Tempus natale Birth period E1.0.0.0.0.0.28 Ontogenesis postnatalis Postnatal ontogeny E1.0.0.0.0.0.29 Vita postnatalis Postnatal life E1.0.1.0.0.0.1 Mensurae embryonicae et fetales4 Embryonic and fetal measurements E1.0.1.0.0.0.2 Aetas a fecundatione5 Fertilization
    [Show full text]
  • And Plurihormonal Thyrotropic Pituitary Adenomas: Pathological, Hormonal and Clinical Studies in 12 Patients
    European Journal of Endocrinology (1999) 140 519–527 ISSN 0804-4643 Mono- and plurihormonal thyrotropic pituitary adenomas: pathological, hormonal and clinical studies in 12 patients M Bertholon-Gre´goire1, J Trouillas2, M P Guigard2, B Loras3 and J Tourniaire1 1Clinique Endocrinologique. Hoˆpital de l’Antiquaille, 69321 Lyon cedex 5, France, 2Laboratoire d’Histologie et Embryologie Mole´culaires, INSERM U369, Faculte´ de Me´decine Lyon-RTH Laennec, 69372 Lyon cedex 8, France and 3Laboratoire de Biochimie B. INSERM U407, Centre Hospitalier Lyon-sud 69310 Pierre-Be´nite, France (Correspondence should be addressed to M Bertholon-Gre´goire) Abstract In a series of 12 patients (eight women and four men, aged between 20 and 62 years), operated on for a pituitary adenoma shown to be thyrotropic by immunocytochemistry, we performed a retrospective and comparative analysis of clinical and biological data, tumor studies including immunocyto- chemistry with double labeling, and proliferation marker (proliferative cell nuclear antigen (PCNA) and Ki-67) detection, electron microscopy and culture. Our study leads us to confirm that thyrotropic tumors are rare (12 of 1174 pituitary adenomas: 1%). The main points arising were that: (1) high or normal plasma TSH associated with an increase in plasma a-subunit and high thyroid hormone levels is the best criterion for diagnosis; (2) the failure of TSH to respond to TRH or Werner’s test is not a reliable criterion for diagnosis; (3) thyrotropic adenomas may be ‘silent’, without clinical signs of hyperthyroidism and with only slight increase in TSH, tri-iodothyronine and thyroxine concentrations; (4) mitoses and nuclear atypies are frequently detected in large tumors, which are invasive in more than 50% of cases – the first analysis of two proliferation markers (PCNA and Ki-67) bears out the relative aggressiveness of thyrotropic adenomas; (5) thyrotropic adenomas are frequently plurihor- monal.
    [Show full text]