Thesis (Ph. D.)--University of Wisconsin--Madison, 1948. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1941. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 58-60).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1944. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 80-81).

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 65-75).

by Linda Shiou-mei Ooi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 95-109). / Abstract --- p.i / Acknowledgements --- p.iii / List of Figures --- p.viii / Chapter Chapter I. --- Introduction --- p.1 / Objectives --- p.4 / Chapter Chapter II. --- Literature Review --- p.5 / Chapter II. 1. --- Lipoprotein-Lipids --- p.5 / Chapter II.1.1. --- General Concept and Metabolism of Lipoprotein-lipids --- p.5 / Chapter II. 1.2. --- Factors affecting plasma lipoprotein-lipids --- p.11 / Chapter II. 1.2.1. --- Ageing --- p.11 / Chapter II. 1.2.2. --- Obesity --- p.12 / Chapter II. 1.2.3. --- Diet --- p.13 / Chapter II. 1.2.4. --- Alcohol --- p.13 / Chapter II. 1.2.5. --- Cigarette smoking --- p.14 / Chapter II. 1.2.6. --- Exercise --- p.14 / Chapter II. 1.2.7. --- Gender differences --- p.14 / Chapter II.2. --- Sex Hormones --- p.14 / Chapter II.2.1. --- General concepts of sex hormone-production and the metabolism of sex hormones --- p.15 / Chapter II.2.1.1. --- Biosynthesis of testosterone --- p.16 / Chapter II.2.1.2. --- Metabolism of testosterone --- p.17 / Chapter II.2.1.3. --- Dihydrotestosterone (DHT) --- p.18 / Chapter II.2.1.4. --- Androstenedione --- p.18 / Chapter II.2.1.5. --- Biosynthesis of estrogen in men --- p.18 / Chapter II.2.1.6. --- Metabolism of estrogen --- p.19 / Chapter II.2.2. --- Factors affecting sex hormone levels in plasma --- p.19 / Chapter II.2.2.1. --- Sex hormone binding globulin (SHBG) --- p.19 / Chapter II.2.2.2. --- Sampling time --- p.19 / Chapter II.2.2.3. --- Stress and acute or chronic non-endocrine illnesses --- p.20 / Chapter II.2.2.4. --- Ageing --- p.21 / Chapter II.2.2.5. --- Diet and nutrition --- p.21 / Chapter II.2.2.6. --- "Medication, drugs and alcohol" --- p.22 / Chapter II.2.2.7. --- Body composition and obesity --- p.22 / Chapter II.2.2.8. --- Variations in states of sleep-wake cycle --- p.23 / Chapter II.2.2.9. --- Levels of physical and sympathetic nervous system activity --- p.23 / Chapter II. 3. --- The relationship between sex hormones and lipoproteins --- p.24 / Chapter II.3.1. --- "Gender difference in sex hormones, menopause and lipoprotein-lipids" --- p.24 / Chapter II.3.2. --- "Interventional study, exogenous sex hormone and lipoprotein-lipidsin men" --- p.25 / Chapter II.3.3. --- The relationships of endogenous sex hormones and lipoprotein-lipids --- p.26 / Chapter Chapter III. --- Materials and Methods --- p.28 / Chapter III.l. --- Subjects and Sampling Methods --- p.28 / Chapter III.2. --- Quantitation of serum lipoprotein-lipids --- p.29 / Chapter III.2.1 --- Determination of cholesterol and triglyceride --- p.29 / Chapter Table III.2.1.A. --- Intra-assay variations for cholesterol and triglyceride --- p.30 / Chapter Table III.2.1.B. --- Inter -assay variations for Cholesterol and Triglyceride --- p.30 / Chapter III.2.2. --- Determination of HDL-Cholesterol and its subfractions --- p.31 / Chapter Table III.2.2. --- Intra- and inter-assay variation for HDL-cholesterol --- p.31 / Chapter III.2.3. --- Determination of VLDL-C and LDL-C --- p.32 / Chapter III.2.4. --- Quantitative determination of serum apolipoproteins and Lp(a) --- p.32 / Chapter III.2.4.1. --- Determination of Apolipoproteins A-I and B --- p.33 / Chapter III.2.4.2. --- Determination of Lipoprotein (a) --- p.33 / Chapter III. 3. --- Quantitative determination of sex hormones --- p.33 / Chapter III.3.1. --- For urinary unconjugated and serum total testosterone --- p.34 / Chapter III.3.1.1 --- Experimental Procedures --- p.35 / Determination of the optimal antibody titre --- p.35 / Establishment of a standard curve and quality controls --- p.35 / Preparation of standards --- p.35 / Purification of radioactively-labelled 3H-testosterone --- p.37 / Preparation of charcoal- stripped urine as zero calibrator (blank) --- p.37 / Preparation of spiked urine or plasma --- p.38 / Preparation of samples for RIA --- p.38 / RIA --- p.39 / Calculation --- p.40 / Chapter III.3.1.2. --- Characteristics of the radioimmunoassay for testosterone --- p.40 / Sensitivity --- p.40 / Precision studies --- p.42 / Within- and between- batch imprecisions --- p.42 / Chapter Table III.3.1.2.A. --- Within-run variation --- p.42 / Chapter Table III.3.1.2.B. --- Between-run variation --- p.42 / Recoveries --- p.43 / Chapter Table III.3.1.2.C. --- "The recoveries of known amounts of testosterone added to charcoal-stripped urine, between immunoassays" --- p.43 / Test of linearity --- p.43 / Comparison with another procedure --- p.43 / Cross reactivity of the antiserum --- p.44 / Procedure --- p.46 / Chapter Table III.3.1.2.D. --- Cross reactivity of some naturally occurring steroids with testosterone antiserum --- p.47 / Chapter III.3.2 --- For urinary total testosterone --- p.47 / Test of linearity and recovery --- p.48 / Chapter III.3.3. --- For urinary unconjugated and serum total 17β-Estradiol --- p.50 / Chapter III.3.3.1 --- Experimental procedure --- p.50 / Determination of the optimal antibody titre --- p.50 / Establishment of a standard curve and quality controls --- p.52 / Preparation of standards --- p.52 / Preparation of tracer 3H-estradiol and construction of a standard curve --- p.52 / Preparation of spiked control urine or plasma --- p.52 / Preparation of samples for RIA --- p.53 / Chapter III.3.3.2. --- Characteristics of the radioimmunoassay for E2 --- p.53 / Sensitivity --- p.54 / Precision studies --- p.54 / Within- and between- batch imprecisions --- p.54 / Chapter Table III.3.3.2.A. --- Within-run variation of known amount of E2 added to charcoal- stripped urine --- p.54 / Chapter Table III.3.3.2.B. --- Between-run variation of known amount of e2 added to charcoal- stripped urine --- p.54 / Recoveries --- p.56 / Chapter Table III.3.3.2.C. --- "The recoveries of known amount of e2 added to charcoal- stripped urine, between immunoassays" --- p.56 / Test of linearity --- p.56 / Comparison with another procedure --- p.56 / Chapter III.3.4. --- For urinary total estradiol --- p.58 / Test of linearity and recovery --- p.58 / Chapter III.4. --- Determination of serum sex hormone-binding globulin (SHBG) --- p.60 / Chapter III.5. --- Determination of urinary unconjugated Cortisol --- p.60 / Chapter III.6. --- Statistical methods --- p.62 / Chapter III.6.1. --- Biological Variations --- p.62 / Chapter III.6.2. --- Univariate and multivariate correlations --- p.62 / Chapter Chapter IV. --- Results --- p.64 / Chapter IV. 1. --- The characteristics of the experimental subjects and their lipoprotein-lipids profiles --- p.64 / Chapter Table IV. 1. A. --- The anthropometric and biochemical characteristics of the experimental male subjects --- p.64 / Chapter Table IV.1.B. --- The lipoprotein-lipids profiles in 46 healthy Hong Kong Chinese men --- p.65 / Chapter IV. 2. --- "Levels of sex hormones in serum and urine, and urinary free Cortisol" --- p.65 / Chapter Table IV.2. --- The sex hormones at serum and urinary levels and urinary free Cortisol in 46 healthy Hong Kong Chinese men --- p.66 / Chapter Table IV.2.A. --- Formula for the indirect calculation of unbound (free) testosterone levels in plasma --- p.67 / Chapter Table IV.2.B. --- Formula for the indirect calculation of unbound (free) 17β-estradiol levels in plasma --- p.68 / Chapter IV. 3. --- Biological variations --- p.69 / Chapter Table IV. 3. --- "The biological variations of serum lipoprotein-lipids, serum sex hormones and urinary sex hormones and Cortisol in 46 healthy Hong Kong Chinese men" --- p.69 / Chapter Table IV.3.A. --- Correlations of serum lipoprotein-lipids between short-term (3- week) variations --- p.70 / Chapter Table IV.3.B. --- Correlations of serum and urinary sex hormones and urinary unconjugated Cortisol between short-term (3-week) variations --- p.70 / Chapter IV. 4. --- Univariate correlation --- p.71 / Chapter Table IV.4. --- The univariate correlation table --- p.72 / Chapter IV.4.1. --- Inter-relationship among serum and urinary sex hormones --- p.73 / Chapter IV.4.2. --- Urinary free Cortisol and sex hormones and serum lipoprotein-lipids --- p.73 / Chapter IV.4.3. --- Correlation between urinary sex hormones and serum lipoprotein- lipids --- p.73 / Chapter IV.4.4. --- Correlations among serum lipoprotein-lipids --- p.74 / Chapter IV.4.5. --- Correlations between serum lipoprotein-lipids and sex hormones --- p.74 / Chapter IV.4.6. --- "Correlations between anthropometric variables, sex hormones and lipoprotein-lipids" --- p.75 / Chapter IV.4.7. --- Correlation of the ratio of HDL2 and HDL3 and other variables --- p.76 / Chapter IV. 5. --- Multiple linear stepwise regression --- p.77 / Chapter Table IV.5. --- "Stepwise multiple linear regression of lipoprotein-lipids on BMI, W/H Ratio, and Age" --- p.77 / Chapter Table IV.5. A. --- "Stepwise multiple linear regression of lipoprotein-lipids on BMI, W/H Ratio, Age, SHBG, and serum and urinary Sex Hormones" --- p.80 / Chapter Table IV.5.B. --- "Stepwise multiple linear regression of lipoprotein-lipids on BMI, W/H Ratio, Age, SHBG, Triglyceride and serum and urinary Sex Hormones" --- p.81 / Chapter Chapter V. --- Discussion --- p.82 / Chapter V. l. --- Experimental subjects and their lipoprotein-lipids profiles --- p.82 / Chapter V. 2. --- Levels of sex hormones in serum and urine --- p.84 / Chapter Table V.2. --- Values of sex steroids in 46 healthy Hong Kong Chinese men compared to others cited in literature --- p.85 / Chapter V. 3. --- "17β-Estradiol,atherogenic lipoprotein-lpids and HDL3" --- p.88 / Chapter V. 4. --- "Testosterone, and HDL-C and its subfractions" --- p.90 / Chapter Chapter VI. --- Conclusions --- p.92 / References --- p.95 / Appendices --- p.110

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 130-145).

Diss. (sammanfattning) Umeå : Univ., 2005. / Härtill 4 uppsatser.

Thesis (Ph.D. (Physiology)) -- Mahidol University, 1978.

Orientador: Luis Carlos Spolidório / Resumo: Hormônios esteroides sexuais participam de diversos eventos celulares e moleculares, e exercem influência sobre o epitélio e tecido conjuntivo do periodonto. A testosterona (T), principal hormônio androgênico, pode ser convertida em estradiol (E2) pela ação da enzima aromatase, ou em di-hidrotestosterona (DHT) pela ação da enzima 5α-redutase. Para elucidar o impacto de andrógenos sobre as células que compõem os tecidos conjuntivo e epitelial, fibroblastos e queratinócitos foram avaliados em relação aos efeitos de diferentes concentrações de T e DHT, além da exposição ao anastrozol (ANA), flutamida (FLU), fulvestranto (FUL), e às associações farmacológicas T+ANA, T+FLU e T+FUL. Os resultados do presente estudo indicaram que, de modo geral, hormônios esteroides androgênicos exercem efeitos opostos sobre eventos celulares de fibroblastos gengivais humano e células epiteliais HaCaT em cultura celular. Enquanto a T e a DHT agem promovendo o aumento da proliferação e atividade de fibroblastos, a exposição de células HaCaT a estes mesmos andrógenos resulta em inibição ou exiguidade do crescimento celular, atividade metabólica ou a capacidade de repovoamento da área de arranhão in vitro. Além disso, o tratamento farmacológico com ANA, FLU, FUL, e suas respectivas associações à T, parece influenciar eventos celulares de fibroblastos gengivais humano e células epiteliais HaCaT in vitro. / Abstract: Sex steroid hormones take part in different cellular and molecular process and exert their functions on the epithelium and connective tissue of the periodontium. Testosterone (T), the main androgenic hormone can be converted to estradiol (E2) through the aromatase enzyme action, or into dihydrotestosterone (DHT) by 5α-reductase activity. To elucidate the impact of androgens on the cells that constitute the connective and epithelial tissues, fibroblasts and keratinocytes were evaluated under the effects of different concentrations of T and DHT, besides to be both exposed to anastrozole (ANA), flutamide (FLU), fulvestrant (FUL), and the pharmacological associations T+ANA, T+FLU and T+FUL. The results of this study indicated that, in general, androgenic steroid hormones exert opposite effects on cellular events of human gingival fibroblasts and epithelial cells. While androgens act stimulating gingival fibroblasts, in HaCaT cells androgens promotes a shortage or inhibition of cell growth and activity. Furthermore, pharmacological treatment with ANA, FLU, FUL, and their associations to T, appears to influence cellular events of human gingival fibroblasts and HaCaT cells in vitro. / Mestre

Orientador: Lúcia Helena Simões da Costa Paiva / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-19T17:10:16Z (GMT). No. of bitstreams: 1 Leao_RogeriodeBarrosFerreira_M.pdf: 2600347 bytes, checksum: 3c70f4a08f6a98df16d66375a85ccd5f (MD5) Previous issue date: 2012 / Resumo: Introdução: O tamoxifeno é utilizado no tratamento do câncer de mama receptor de estrogênio positivo. Seu mecanismo de ação está na inibição do crescimento das células malignas por antagonismo competitivo com estrógenos pelos receptores estrogênicos. A ação do tamoxifeno nestes receptores é variável e, dependendo do tecido, pode ter ação antagonista ou agonista. Em mulheres menopausadas usuárias de tamoxifeno, observa-se uma maior incidência de patologias endometriais, sendo o pólipo endometrial a alteração mais frequente. Sua patogênese não está bem estabelecida, mas parece estar relacionada a fatores hormonais. Objetivos: Comparar a expressão de receptor de estrógeno (RE) e de receptor de progesterona (RP) em pólipos endometriais de usuárias de tamoxifeno com pólipos endometriais e endométrio atrófico de não usuárias na pós-menopausa. Material e métodos: Entre mulheres submetidas à histeroscopia cirúrgica no Hospital da Mulher Prof. Dr. Aristodemo Pinotti - CAISM/UNICAMP de janeiro de 1998 a dezembro de 2008, foram selecionadas 84 mulheres na pós-menopausa usuárias de tamoxifeno, com pólipo endometrial benigno. Esse grupo foi comparado a 84 amostras de endométrio atrófico e 252 pólipos benignos de mulheres na pós-menopausa não usuárias de tamoxifeno e sem antecedente de terapia hormonal. As expressões de RE e RP foram avaliadas através de imuno-histoquímica segundo a porcentagem de células coradas, intensidade da coloração nuclear e escore final. A expressão de RE e RP no epitélio glandular e no estroma dos pólipos de usuárias de tamoxifeno foi comparada com o endométrio atrófico e os pólipos de não usuárias separadamente, utilizando o Teste de Mann-Whitney, corrigido pelo método de Bonferroni, teste exato de Fisher ou Qui-quadrado. Resultados: os pólipos de usuárias de tamoxifeno apresentaram maior expressão de RE e RP no epitélio glandular e estroma, em relação ao endométrio atrófico (p<0,0001). Em relação aos pólipos de não usuárias, as usuárias apresentaram maior expressão de RP no epitélio glandular (p=0,0014) e estroma (p=0,0056), não apresentando diferença significativa em relação ao RE. A maioria dos pólipos das usuárias e não usuárias de tamoxifeno apresentavam RE/RP positivos enquanto a maioria dos endométrios atróficos era RE/RP negativos. Conclusões: Os pólipos apresentam aumento frequente de RE, independentemente do uso do tamoxifeno. Por outro lado, os altos níveis de RP parecem consistentes com os efeitos agonistas da droga / Abstract: Introduction: Tamoxifen has been used for the treatment of strogen receptor-positive breast cancer. The effect of tamoxifen in breast cancer is the it inhibition cancer cell growth by competitive antagonism with strogen for strogen receptor (ER). The mechanism of action of tamoxifen in this receptor varies among different tissues, with antagonist effect (e.g. in breast) ou agonist (e.g. in endometrium). Thus, in menopausal women who use tamoxifen, a higher incidence of endometrial alterations is observed and endometrial polyps are the most common. The pathophysiology of endometrial polyp is still not definitely established but it seems to be related to hormone influence. Objectives: To compare the expression of estrogen receptors (ER) and progesterone receptors (PR) in endometrial polyps of tamoxifen users to atrophic endometrium and endometrial polyps of postmenopausal nonusers of tamoxifen. Material and methods: Among women undergoing surgical hysteroscopy in Hospital da Mulher Prof. Dr. Aristodemo Pinotti - CAISM/UNICAMP, from January 1998 to December 2008, 84 tamoxifen users with benign endometrial polyp were selected. This group was compared to 84 samples of atrophic endometrium and 252 benign polyps of postmenopausal women who were non-users of tamoxifen and no previous history of hormone therapy use. ER/PR expression was assessed by immunohistochemistry study according to the percentage of stained cells, intensity of nuclear color and final score. The expression ER and PR in the glandular epithelium and stroma of polyp tissue from tamoxifen users was compared to atrophic endometrium and polyps from non-users separately, using the Mann-Whitney test corrected by the Bonferroni method, Fisher's exct test or Chi-square test. Results: Polyps of tamoxifen users had a higher expression of ER and PR in the glandular epithelium and stroma, in relation to the atrophic endometrium (p<0.0001). Regarding polyps of women not treated with tamoxifen, users had a higher PR expression in the epithelium (p=0.0014) and stroma (p=0.0056), without any difference in ER expression. Most of polipys expressed ER/PR positives while atrophic endometrium were ER/PR negatives. Conclusions: Polyps frequently exhibit increase in ER expression, independent of the use of tamoxifen. High levels of PR seem to be consistent with agonist effects of the drug / Mestrado / Fisiopatologia Ginecológica / Mestre em Ciências da Saúde