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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Cancer staging for differentiated thyroid carcinoma

Lang, Brian., 梁熊顯. January 2006 (has links)
published_or_final_version / abstract / Surgery / Master / Master of Surgery
2

Pathology and molecular biology of malignant thyroid tumours

Lam, King-yin, Alfred., 林敬賢. January 2004 (has links)
published_or_final_version / abstract / toc / Medicine / Master / Doctor of Medicine
3

Differentiated thyroid cancer in Hong Kong

Chow, Sin-ming., 周倩明. January 2007 (has links)
published_or_final_version / Medicine / Master / Doctor of Medicine
4

Thyroid transcription factor 1 gene(TITF1): apotential heritable determinant of papillary thyroid carcinoma(PTC)

Liu, Tingting, 劉婷婷 January 2007 (has links)
published_or_final_version / Surgery / Master / Master of Philosophy
5

The role of p16 tumor suppressor gene in the diagnosis of thyroid disease

Leung, Pui-ling, Pauline., 梁培玲. January 2006 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
6

Clinicopathological roles of transforming growth factor alpha (TGFα) in papillary thyroid carcinoma

劉國培, Lau, Kwok-pui. January 2007 (has links)
published_or_final_version / abstract / Surgery / Master / Master of Philosophy
7

Regulation of proliferation and apoptosis by peroxisome proliferator-activated receptor gamma (PPAR[gamma]) in human thyroid cancer cells.

January 2008 (has links)
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
8

Ultrasonographic screening of asymptomatic thyroid cancer in Hong KongChinese

Yuen, Po-wing., 袁寶榮. January 2010 (has links)
published_or_final_version / Medicine / Master / Doctor of Medicine
9

A study of BRAF and RAS genes in papillary thyroid carcinoma

Lo, Chi-chuen, Evans., 盧致泉. January 2004 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
10

Gene expression analysis of microarray data : a case study of papilllary thyroid carcinoma data

Begum, Mst. Ferdouse January 2007 (has links)
Microarray technology allows researchers to monitor the mRNA transcription levels of thousands of genes in parallel which opens the door for more advanced cancer research. This thesis focuses on a case study of papillary thyroid carcinoma data. Fourteen publicly available Affymetrix microarray data sets were used where seven samples were collected from normal thyroid tissue and the remaining seven were collected from papillary thyroid carcinoma tissue. The present study compared the results obtained from three different normalization processes: MAS5.0, RMA and GCRMA in detecting differentially expressed genes under two conditions. Internal consistencies within the methods as well as the results across three methods were compared. Statistical packages 82.5.1 and Bioconductor 2.08 are used to perform the data analysis. Each step of normalization with MAS5.0 and RMA is described. Statistical package Limma is used to fit a linear model. Finally an empirical Bayes method is used to detect the significantly differentially expressed genes. First, considering all genes a comparison is made among the three normalization methods where RMA and GCRMA showed the maximum agreement in detecting differentially expressed genes. Then using unspecified filtering process a set of genes was selected and the whole process was replicated where the top fifty differentially expressed genes did not show any overlap with each other. / Department of Mathematical Sciences

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