Formation of Adenomata in Hypophyses of Rats Subjected to Both Subtotal Thyroidectomy and Administration Of'311,And Its Preventi

Total Page:16

File Type:pdf, Size:1020Kb

Formation of Adenomata in Hypophyses of Rats Subjected to Both Subtotal Thyroidectomy and Administration Of'311,And Its Preventi Formation of Adenomata in Hypophyses of Rats Subjected to both Subtotal Thyroidectomy and Administration of'311, and its Prevention by Feeding of Desiccated Thyroid1 w. E. GRIESBACH,2 J@ L. CHAIKOFF, C. W. NICHOLS, JR., AND ROBERT C. GOLDBERG@ Department of Physiology, University of California, Berkeley, California SUMMARY The tumorigenic effect of subtotal thyroidectomy on the pituitary was studied in 212 Long-Evans female rats. Of the 133 pituitaries that contained adenomata after 2 years, 76 % were of the thyrotropic cell type. This finding confirms earlier work on the effect of long-term thyroxine deficiency. The feeding of desiccated thyroid reduced the @)ercentages of thyrotropic cell adeno mata from a mean of 60 to a mean of 33. Thyroid feeding reduced the percentages of all adenomata from a mean of 72 to a mean of 53. A single administration of 1 @ecof 1311did not increase the number of, or tendency towards, anaplastic changes in @)ituitary adenomata of subtotally thyroidectomized rats fed a stock diet. The same dose of 1311did not increase the incidence of pituitary adenomata iii unoperated animals fed either the stock diet or the stock diet supple mented with desiccated thyroid. Two rats that developed malignant thyroid car cinomata after receiving 1 @.icof131Jdid not show cell changes or adenomat.a in the pi tuitary. The absence of cytologic signs of thyroxine deficiency in the pituitary cells of these rats supports the view that irradiation per se might well have been the cause of the neoplasms found in their thyroid glands. The pituitary adenomata found in 124 unoperated rats, treated in the same way as the subtotally thyroidectomized groups with respect to ‘@‘Idosageand thyroid feed ing, closely resembled those found in the normal control group in number as well as in cell type. It has been knowii for almost 2 decades that hyperpla.sia study of the TSH-producing cells in the pituitary, lend as well as benign and nialignant neopla.sms develop ill support to this interpretation. The literature dealing thyroid glands of Irlice and rats in which, for prolonged with this subject has been reviewed by Bielschowsky (2) periods, a state of thyroxine deficiency has been estab and Bielschowsky and Horning (3). lished by any one of the following means : the feeding of a A matter of some interest as well as practical importance low-iodine diet (1, 2) ; the administration of anti-thyroid arose in the case of experiments in which irradiation was substances (5, 15, 25) ; irradiation of the gland by 131J, applied to the rodents' thyroid gland, either alone or in astatine (211At), or X-rays (7, 12, 14, 19) ; and subtotal combination with chemical or surgical means, for inducing thyroidectomy (6, 14). There is good evidence for the the thyroxine deficiency. In most cases, especially in the belief that the neopla.st.ic changes should be attributed to early work with large doses of 131J(up to 875 j@c),the irra the hyperplasia of thyrotropic hormone (TSH4)-producing diation had been sufficiently strong to destroy much or all cells in the anterior pituitary glands of the animals suffer of the thyroid tissue (11, 12). In later experiments the ing from long-terni thyroxine deficiency. Assays of TSH 131J was given in a considerably reduced dose (25—40 Mc). contetits of the hypophysis and blood, as well as cytologic It was shown that hereby the number of experimentally induced malignant thyroid neoplasms was definitely higher 1 This work was supported by a contract from the United States Atomic Energy Commission (UCB-34P11-3). (22). It could further be seen that hyperplasia of the 2 Department of Endocrinology, Medical Research Council, thyroid epithelium surrounding the neoplasms was a con Dunedin, New Zealand. stant feature of these glands. It was assumed that this 3 Department of Medicine, Permanente Medical Group and was significant for the strong and permanent action of Kaiser Foundation Hospital, Oakland, California. thyrotropic hormone. No signs of radiation damage were 4 The following abbreviations are used: TSH, thyrotropic hormone; PAS, periodic acid-Schiff; PTA, phosphotungstic acid; found. The question whether ilradiation per se can induce AF, aldehyde fuchsin. thyroid tumors was discussed in another study in which Received for publication March 4, 1965; revised June 7, 1965. either both lobes or a single lobe of the thyroid gland had 1804 Downloaded from cancerres.aacrjournals.org on September 29, 2021. © 1965 American Association for Cancer Research. GRIESBACH et al.—Hypophyseal Adenoma after Thyroidectomy and 131J 1805 TABLE 1 ADENOMATA IN PITUITARIES OF INTACT FEMALE RATS PvruITARIEsGROUPTREATMENTNo. ADRNOMATATotal CLASSIFICATIONOP OF RATS ADENOMATACYTOLOGIC EXAMINED (76%)INoneVI1 47WITH 21% 45Thyrotrophs3 (14%)Gonadotrophs2Chromophobes16 (60%)VIIDesiccated@c‘@‘Iinjected3410293 (30%)16 (70%)VIII1 thyroid in diet5723403 (13%)416 (82%)Total17171429@c1311plus desiccated thyroid in diet3317510314 (13%)10 (14%)52 (73%) TABLE 2 ADENOMATA IN PITUITARIES OF SUBTOTALLY THYROIDECTOMIZED FEMALE RATS PITUITARIES WITH CYTOLOGIC CLASSIFICATION OF ADENOMATA No. OF RATS ADENOMATA No. or Gaow' TREATMENT ADENOMATA r'ANAPLASTIC EXAMINED CHANGES IN: CLASSIFIED Total % Thyrotrophs Gonadotrophs Chromophobes II Subtotal thyroidectomy only 67 42 63 36 (86%) 3 6 (14%) 45 8 (18%) III Subtotal thyroidectomy plus 49 40 82 33 (83%) 4 5 (13%) 42 10 (24%) 1 pc 1311injected IV Subtotal thyroidectomy, 1 @IC 60 32 53 22 (69%) 3 8 (25%) 33 5 (15%) 1311 injected plus desiccated thyroid fed V Subtotal thyroidectomy plus 36 19 53 10 (53%) 2 7 (37%) 19 2 (10%) desiccated thyroid fed Total 212 133 63 101 (76%) 12 (9%) 26 (20%) 139 been irradiated (21). There, most of the carcinomata 1 and 2) received by i.p. injection 1 j@tCofcarrier-free 131J were found in rats in which both lobes had been irradiated, in 0.1 ml of normal saline. Twenty-four hr later the but 2 carcinomata also appeared in singly-irradiated lobes isthmus contained about 2 % of the radioactivity. and 1 in an opposite, shielded lobe. Hence, it could not One week after either the subtotal thyroidectomy or be decided whether thyroid carcinogenesis resulted from 1311 injection, feeding of the thyroid-supplemented diet prolonged TSH stimulation or was a direct consequence of was begun. The diet was prepared by adding desiccated the irradiation. In a more recent paper, Goldberg et al. thyroid powder (Lilly Thyroid, U.S.P., No. 58) to the (14) reported finding a papillary and a follicular carcinoma stock diet to yield a concentration of 250 nig/kg. It was in intact thyroid glands of rats that received but a single shown in a separate experiment that the uptake of ‘@‘Iby /hc of 131J The present report deals with the 383 pitui the thyroid glands of the rats fed this diet was almost com taries excised from the rats whose thyroids had been de pletely suppressed. scribed in this latter study (14). In these pituitaries, The rats were maintained for 2 years, and the survivors many adenomata were found; they are described in detail, were killed with ether. Those that failed to survive for particularly with regard to the hormonal conditions that the 2 years usually died of chronic respiratory disease, may have influenced their development. and autopsies were not performed on all of these animals. The thyroid glands of the rats of Groups I and VI-Vill MATERIALS AND METHODS were excised and weighed. In all other rats, the tracheas A total of 876 female, Long-Evans rats were randomly along with the paratracheal tissues were removed en bloc selected at 5-6 weeks of age, divided into 8 groups, and and fixed in 10 % neutral formalin. The pituitary glands treated as shown in Tables 1 and 2. After weaning, all were removed and fixed in sublimate-formol (9 : 1, v/v). rats were maintained on a nutritionally adequate diet These glands were sectioned at 2.5 and 5 @,and sections (Diablo Double-Check Labration) containing 3 @sgof from each were mounted on 4 slides, with equal distribution iodine/gm5 (20). onto each slide of the material cut at various depths of the Subtotal thyroidectomy was performed under light block. They were treated as follows : Slides 1 and 2 with ether anesthesia. Both lateral lobes of the thyroid were periodic acid-Schiff (PAS) stain and PAS stain in combi removed, leaving only the isthmus, which weighed about nation with Orange G-phosphotungstic acid (PTA), re 0. 1 mg. One week later, each rat of certain groups (Tables spectively ; Slide 3 with aldehyde fuchsin (AF) usually 5 We are indebted to Dr. G. La Roche for this determination. followed by Orange G-PTA, without previous oxidation Downloaded from cancerres.aacrjournals.org on September 29, 2021. © 1965 American Association for Cancer Research. 1806 Cancer Research Vol. 25, November 1965 TABLE 3 SUMMARY OF CYTOLOGIC FINDINGS IN THE PITUITARIES OF RATS WITH THYROID CARCINOMA GroupTreatmentpituitaryIISubtotal of ratsTyreoftlurroidType of pituitary neoplasmClassification of cells in thyroidectomyPapillaryNone3 cysts in chromophobic areas; few TSIF' foundIISubtotal and LH cells; acidophils not thyroidectomyPapillary(a) Large adenoma; (b) small TSH and “T―-granulated cells; few anaplastic adenoma(a) acidophils; (b) atypical cells, probably basophilsIVSubtotal thyroidectomy + 1 pc cells; LH cells and groups of presentVIInjection1311 injection + addition of acidophils desiccated thyroid to dietPapillaryNone“T―-granulated @ of 1 1311FollicularNoneTSH cells, LII cells, acidophils present in quantitiesVIIIInjection normal of 1 sc 13h1+ addition cells, LH cells present; acidophils in of desiccated thyroid to dietPapillaryNoneTSH creased in numbers a TSH, thyrotropic hormone; LH, luteinizing hormone. with permanganate ; and Slide 4 with the rapid Mallory The number of gonadotroph adenomata was not changed stain of Churg and Prado (4). The last is well suited for by thyroid feeding, but that of chromophobe adenomata counterstaining AF-stained tissues.
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]