published_or_final_version / abstract / Surgery / Master / Master of Surgery

The C57 BL/KsJ db/db mouse is obese, hyperglycemic, hyperinsulinemic and serves as a model for noninsulin dependent diabetes mellitus (NIDDM). This study reports a dysfunction in the pituitary-thyroid axis and apparent peripheral resistence to thyroid hormones due to a reduction in T3 receptor binding. Diabetic mice have subnormal serum T4 concentrations and supranormal T3 concentrations which are most pronounced between 8 and 10 weeks of age. Thyroid glands of diabetic animals appear hypoactive histologically. Serum TSH concentrations approximate those found in normal mice. In vitro studies show that thryroid glands from diabetic animals are responsive to TSH. Pituitary glands from the same animals hypersecrete TSH and are responsive to TRH. Ultrastructural analysis of pituitary thyrotropes from diabetic mice indicate that these cells are hypersecretory and may be under chronic stimulation by TRH. Diet restriction maintains diabetic mice at a normal total body weight but these animals still possess abnormally large fat deposits. The thyroid hormone profile of these mice appears normal as does the histological appearance of the thyroid gland. Similarly, the blockade of peripheral deiodination by daily injection of iopanoic acid returns the thyroid hormone profile to normal.

Student Number : 9600048X - MSc (Med) research report - Faculty of Health Sciences / Disorders of the thyroid gland are amongst the most common endocrine disorders. The diagnosis of thyroid disease consists of a history and clinical examination, followed by specific confirmatory investigations. These investigations are an important diagnostic component in thyroid disease and are amongst the most common investigations ordered in clinical laboratories. Although these tests are relatively inexpensive individually, they account for a disproportionately large amount of health care expenditure for diagnostic testing. Appropriate laboratory investigation is critical to establish the diagnosis and cause of thyroid disease in the most costeffective way. Discovery Health released a set of evidence-based guidelines in order to educate the clinician with regard to the selection of thyroid function tests. According to these guidelines a TSH (Thyroid Stimulating Hormone) test is the investigation of choice in suspected thyroid disease. This study is a retrospective investigation that compares the difference in ordering patterns of laboratory investigations by clinicians before and after the publication of the guidelines. Two data sets were generated from the data bank of Discovery Health. The first data set (I) was based on records compiled before March 2003 whereas the second data set (II) was based on records compiled from April 2003. Following use of the exclusion and inclusion criteria the sample size totaled 73 850 cases. An analysis was made with regard to the requesting frequency of specific tests. This study will focus solely on the appropriateness of thyroid function tests ordered. It is beyond the scope of this study to attach a specific clinical diagnosis to the results. The thyroid function tests requested before the publication of the evidence-based guidelines were often requested without careful thought and consideration on the part of the clinician. Some of the combination tests ordered (Free T3 and Free T4) are not advocated as an initial investigation in the evaluation of thyroid function and waste funds in this instance. The ordering of inappropriate thyroid function tests often leads to the depletion of funds available to a patient within the financial year. The results revealed that after publication of the guidelines there was an increase in the requesting frequency of TSH as a first line investigation, as well as Free T4 while a decrease in requests for Free T3 was noted. The publication of evidence-based guidelines as a guide to requesting the correct thyroid function tests in order to diagnose suspected thyroid disease appears to have impacted in increasing awareness amongst clinicians with regard to the tests required to diagnose and monitor thyroid disease.

Ho Wing Man. / On t.p. "gamma" appears as the Greek letter. / Thesis submitted in: December 2007. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 95-106). / Abstracts in English and Chinese. / ABSTRACT --- p.I / 摘要 --- p.III / ACKNOWLEDGMENTS --- p.V / ABBREVIATIONS --- p.VI / LIST OF FIGURES --- p.IX / LIST OF TABLES --- p.X / CONTENTS --- p.XII / Chapter CHAPTER ONÉؤ --- GENERAL INTRODUCTION --- p.1 / Chapter 1.1 --- Background --- p.2 / Chapter 1.1.1 --- Thyroid cancer --- p.2 / Chapter 1.1.2 --- Apoptosis and thyroid cancer --- p.4 / Chapter 1.2 --- Estrogen receptors and apoptosis --- p.5 / Chapter 1.2.1 --- Estrogen receptor-α (ERα) and estrogen receptor-β (ERβ) --- p.5 / Chapter 1.2.2 --- Differential roles of estrogen receptor-α(ERα) and estrogen receptor-β (ERβ) in apoptosis --- p.6 / Chapter 1.2.3 --- Bcl-2 family --- p.8 / Chapter 1.3 --- Peroxisome proliferator-activated receptor-γ (PPARγ) --- p.9 / Chapter 1.3.1 --- Molecular aspects of PPAR --- p.9 / Chapter 1.3.2 --- PPAR/RXR complex --- p.13 / Chapter 1.3.3 --- PPARγ ligands --- p.16 / Chapter 1.3.4 --- PPARγ and apoptosis in thyroid cancer --- p.19 / Chapter 1.3.5 --- PPARγ ligands-mediated apoptosis pathway --- p.21 / Chapter 1.4 --- Previous results from our laboratory --- p.25 / Chapter 1.5 --- Summary of previous studies --- p.27 / Chapter 1.6 --- Perspectives --- p.28 / Chapter 1.7 --- Objectives of this project --- p.29 / Chapter CHAPTER TWÓؤ --- GENERAL MATERIALS AND METHODS --- p.30 / Chapter 2.1 --- Materials --- p.31 / Chapter 2.1.1 --- Cell lines --- p.31 / Chapter 2.1.2 --- Plasmid vectors used in this study --- p.31 / Chapter 2.1.3 --- Antibodies --- p.32 / Chapter 2.1.4 --- Culture media and transfection reagents --- p.32 / Chapter 2.1.5 --- Materials for protein manipulation --- p.33 / Chapter 2.1.6 --- Drugs for treatment --- p.34 / Chapter 2.1.7 --- Kits --- p.35 / Chapter 2.1.8 --- Instruments --- p.35 / Chapter 2.2 --- Methods --- p.36 / Chapter 2.2.1 --- Cell culture --- p.36 / Chapter 2.2.2 --- Cell viability analysis --- p.36 / Chapter 2.2.3 --- Preparation of protein extract --- p.37 / Chapter 2.2.4 --- Determination of the concentration of target protein --- p.37 / Chapter 2.2.5 --- Gel electrophoresis and protein transfer --- p.38 / Chapter 2.2.6 --- Immunoblotting --- p.39 / Chapter 2.2.7 --- Apoptosis detected by Cell Death ELISAplus --- p.41 / Chapter 2.2.8 --- PPARγ-ligand Enzyme Immunoassay --- p.45 / Chapter 2.2.8.1 --- 15d-PGJ3 Enzyme Immunoassay --- p.45 / Chapter 2.2.8.2 --- 15(S)-HETE Enzyme Immunoassay --- p.46 / Chapter 2.2.8.3 --- 13(S)-HODE Enzyme Immunoassay --- p.46 / Chapter 2.2.9 --- Transient tranfection and luciferase activity assay --- p.47 / Chapter 2.2.10 --- Statistical Analysis --- p.52 / Chapter CHAPTER THREÉؤ --- ESTROGEN RECEPTORa (ERa) AND ESTROGEN RECEPTORP(ERP) MEDIATE THE PROLIFERATION AND APOPTOSIS OF HUMAN THYROID PAPILLARY CARCINOMA CELLS --- p.53 / Chapter 3.1 --- Introduction --- p.54 / Chapter 3.2 --- Materials and Methods --- p.56 / Chapter 3.2.1 --- Cell culture and treatment --- p.56 / Chapter 3.2.2 --- Western Blot --- p.56 / Chapter 3.2.3 --- Cell proliferation determined by MTT assay --- p.57 / Chapter 3.2.4 --- Apoptosis detected by Cell Death ELISAplus assay --- p.58 / Chapter 3.3 --- Results --- p.59 / Chapter 3.3.1 --- "The expression of ERα, ERβ and PPARγ in NPA, FRO, ARO and WRO thyroid cancer cell lines" --- p.59 / Chapter 3.2.2 --- Effects of PPT and DPN on cell viability --- p.61 / Chapter 3.3.3 --- Apoptotic cells quantification by Cell Death ELISAplus assay --- p.64 / Chapter 3.4 --- Discussion --- p.67 / Chapter CHAPTER FOUŔؤ --- THE RELATIONSHIP BETWEEN PPARγ AND ESTROGEN RECEPTOR AND THE REGULATION OF THE APOPTOSIS IN THYROID CANCER CELL LINES --- p.70 / Chapter 4.1 --- Introduction --- p.71 / Chapter 4.2 --- Material and Methods --- p.74 / Chapter 4.2.1 --- Transient transfection --- p.74 / Chapter 4.2.2 --- Luciferase assay --- p.74 / Chapter 4.2.3 --- 15d-PGJ2 ELISA assay --- p.75 / Chapter 4.2.4 --- 15S-HETE ELISA assay --- p.76 / Chapter 4.2.5 --- 13S-HODE ELISA assay --- p.77 / Chapter 4.3 --- Results --- p.78 / Chapter 4.3.1 --- "PPT, ERα-agonist, increased thyroid cancer cell proliferation and caused the decrease the level of PPARγ ligands" --- p.78 / Chapter 4.3.2 --- "DPN, ERβ-agonist, inhibited thyroid cancer cell proliferation, induced apoptosis and caused the increase the level of PPARγ ligands" --- p.83 / Chapter 4.3.3 --- PPT did not alter the transcriptional activity of PPARγ --- p.88 / Chapter 4.4 --- Discussion --- p.90 / Chapter CHAPTER FIVÉؤ --- CONCLUSIONS AND FUTURE PROSPECT --- p.92 / Chapter 5.1 --- Summary of results --- p.93 / Chapter 5.2 --- Conclusion --- p.94 / Chapter 5.3 --- Future prospects --- p.94 / REFERENCE LIST --- p.95

The thyroid gland is positioned directly below the larynx in the anterior portion of the neck (Kumrow & Dahlen, 2002). The nerves and arteries of the thyroid and larynx are intertwined thus damage to one structure could easily affect the other structure. Thyroid dysfunction may also affect the histology of the larynx thus changing vocal quality (Stemple, 2010). This study measured vocal quality of patients with thyroid disease using the Consensus Auditory Perceptual Evaluation of Voice (CAPE-V). Voice samples from 16 subjects with thyroid disease were compared to an age-matched group of 18 control subjects with no reported history of thyroid dysfunction. An experienced voice clinician rated each sample on the six parameters of the CAPE-V: overall severity, roughness, breathiness, strain, pitch and loudness. Statistical analysis of the results revealed a significant difference between the thyroid disease group and the control group for overall severity of vocal quality and vocal roughness. These results further strengthen the connection between thyroid disease and vocal dysfunction. Further research is warranted to explore the specific thyroid diagnoses that relate to vocal dysfunction, as well as to strengthen the findings on a larger population of participants. / Lori Lombard, Ph.D., CCC-SLP David Stein, Ph. D., CCC-SLP Jill Brady, Ph.D., CCC-SLP

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

Thesis (doctoral)--Universität Zürich, 1956.

Thesis (M.S.)--West Virginia University, 2000. / Title from document title page. Document formatted into pages; contains viii, 46 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-38).

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2008. / Härtill 4 uppsatser.

Thesis (doctoral)--Universität Zürich, 1956.