Song Hong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves ). / Abstracts in English and Chinese; questionnaire in Chinese. / Abstract (English) --- p.i / Abstract (Chinese) --- p.iv / Acknowledgments --- p.vi / Table of Contents --- p.vii / List of tables --- p.x / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Printing industry and organic solvents exposure --- p.1 / Chapter 1.2 --- Risk of low level exposures to organic solvents --- p.2 / Chapter 1.3 --- Using neurobehavioral methods to study the subclinical effects --- p.3 / Chapter Chapter 2 --- Literature review --- p.4 / Chapter 2.1 --- Organic solvents and neurobehavioral impairment --- p.4 / Chapter 2.2 --- Methodology of Neurobehavioral Test --- p.6 / Chapter 2.2.1 --- Criteria for selecting test battery --- p.7 / Chapter 2.2.2 --- Standardization of neurobehavioral test battery --- p.8 / Chapter 2.2.3 --- Reliability and validity --- p.9 / Chapter 2.2.4 --- Confounding factors of neurobehavioral test --- p.10 / Chapter 2.3 --- Neurobehavioral effects of different levels of solvent exposures --- p.12 / Chapter 2.3.1 --- Positive results in field studies --- p.12 / Chapter 2.3.2 --- Negative results in field studies --- p.17 / Chapter 2.3.3 --- Dose-response relationship in the field studies --- p.18 / Chapter 2.3.4 --- To separate acute and chronic effects --- p.20 / Chapter 2.3.5 --- The long-term effects of solvent exposure --- p.21 / Chapter 2.4 --- Limitations of these studies --- p.23 / Chapter 2.5 --- Summary --- p.26 / Chapter Chapter 3 --- Aims and Objectives --- p.31 / Chapter 3.1 --- Aims of the present research --- p.31 / Chapter 3.2 --- Position of this study cm this research domain --- p.32 / Chapter Chapter 4 --- Subjects and Method --- p.33 / Chapter 4.1 --- Study design --- p.33 / Chapter 4.2 --- Study population and sampling --- p.33 / Chapter 4.2.1 --- Participation --- p.33 / Chapter 4.2.2 --- Exposed group --- p.34 / Chapter 4.2.3 --- Reference group --- p.34 / Chapter 4.2.4 --- Sample size estimation --- p.34 / Chapter 4.3 --- Data collection --- p.36 / Chapter 4.3.1 --- Exposure assessment --- p.36 / Chapter 4.3.1.1 --- Air sample measurements --- p.36 / Chapter 4.3.1.2 --- Biological monitoring --- p.38 / Chapter 4.3.2. --- Medical assessment --- p.38 / Chapter 4.3.2.1 --- Pre-test questionnaire --- p.39 / Chapter 4.3.2.2 --- Neurobehavioral assessment --- p.39 / Chapter 4.4 --- Data Analysis --- p.43 / Chapter 4.4.1 --- Data Processing --- p.43 / Chapter 4.4.2 --- Statistical analysis --- p.44 / Chapter 4.4.2.1 --- Descriptive analysis --- p.44 / Chapter 4.4.2.2 --- Identifying the main confounding factories --- p.44 / Chapter 4.4.2.3 --- Comparing the tests score adjusted for confounding --- p.45 / Chapter 4.4.2.4 --- Dose-response analysis --- p.45 / Chapter Chapter 5 --- Results --- p.47 / Chapter 5.1 --- Demographic characteristics of the subjects --- p.47 / Chapter 5.2 --- Comparison of the basic characteristics between the exposed group and the reference group --- p.48 / Chapter 5.3 --- Comparison of the symptoms between the exposed group and the reference group --- p.49 / Chapter 5.4 --- Comparison of the scores of neurobehavioral tests between the exposed group and the reference group --- p.51 / Chapter 5.5 --- Identifying potential confounding of neurobehavioral test --- p.51 / Chapter 5.5.1 --- Main confounding factors of NCTB test on performance tests --- p.51 / Chapter 5.5.2 --- Main confounding factors of Profile of Mood States --- p.54 / Chapter 5.6 --- Groups comparison of the neurobehavioral effects --- p.57 / Chapter 5.6.1 --- Comparison of the adjusted mean scores between the exposed group and the reference group --- p.57 / Chapter 5.6.2 --- Groups comparison of the adjusted tests score in Factories C and G respectively --- p.58 / Chapter 5.7 --- Exposure assessment --- p.61 / Chapter 5.7.1 --- Air sampling results of the printing factories --- p.62 / Chapter 5.7.2 --- Relationship between results of active and passive sampling systems --- p.63 / Chapter 5.7.3 --- Biological monitoring --- p.63 / Chapter 5.8 --- Dose-response relationship --- p.65 / Chapter Chapter 6 --- Discussion --- p.69 / Chapter 6.1 --- Findings of this study --- p.69 / Chapter 6.1.1 --- Subjective symptoms --- p.69 / Chapter 6.1.2 --- Neurobehavioral effects --- p.70 / Chapter 6.1.3 --- Exposure intensity --- p.72 / Chapter 6.1.4. --- Dose-response relationship --- p.75 / Chapter 6.2 --- Applications of the study results --- p.76 / Chapter 6.2.1 --- The need for prevention measures --- p.77 / Chapter 6.2.2 --- Contributing to re-setting of OELs --- p.77 / Chapter 6.2.3. --- The evidence on neurotoxicology --- p.78 / Chapter 6.3 --- Limitations of the study --- p.79 / Chapter 6.3.1. --- Possibility of bias --- p.79 / Chapter 6.3.2. --- Lack of historical hygiene measurement data --- p.80 / Chapter 6.3.3. --- Influence of workshift --- p.81 / Chapter 6.3.4. --- Combined exposures to noise and organic solvents --- p.82 / Chapter 6.4 --- Conclusion --- p.83 / Appendices --- p.84 / Appendix 1 --- p.84 / Appendix 2 --- p.97 / Appendix 3 --- p.102 / Appendix 4 --- p.103 / Appendix 5 The Administration of The WHO-NCTB Tests --- p.114 / Test 1 Profile of Mood States Test --- p.115 / Test 2. Simple Reaction Time Test --- p.116 / Test 3. Digit Span Test Test --- p.119 / Test 4. Santa Ana Test --- p.120 / Test 5. Digit Symbol Test --- p.122 / Test 6. Benton Visual Retention Test --- p.123 / Test 7. Pursuit Aiming Test --- p.125 / Appendix 6 --- p.126 / Reference List --- p.127

Although the association between high maternal alcohol consumption and adverse reproductive outcomes is well established, the effect of lower levels of consumption during pregnancy is unclear; few studies have investigated this exposure. A hospital-based case-control study of small-for-gestational age (SGA) newborns (birth weight below the 10th percentile, according national standards for gestational age and sex) was conducted in Montreal between 1998 and 2000. Controls were born at the same hospital and during the same period with birth weight at or above the 10th percentile. This analysis aims at investigating the effect of low alcohol consumption (0.25 to 3 alcoholic drinks weekly) during pregnancy on the risk of small-for-gestational-age (SGA) birth. Independent effects of wine, beer and spirits and of paternal alcohol consumption before conception were also assessed. The logistic regression analysis showed no significant effect of light maternal drinking during pregnancy on the risk of SGA birth. The association was also studied separately for consumption of wine, beer and spirits, and likewise for paternal alcohol consumption, with similarly negative results.

Made available in DSpace on 2015-07-22T20:50:31Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-07-30. Added 1 bitstream(s) on 2015-08-11T03:25:42Z : No. of bitstreams: 1 Publico-10756.pdf: 198016 bytes, checksum: b1b248dd88de1aeab5859b81fa05e4c2 (MD5) / INTRODUÇÃO: Os antagonistas 5HT-3 e corticosteróides são drogas importantes no controle da emese induzida por quimioterapia Apresentam controle de 50-80% da emese aguda porém controlam menos de 50% da emese tardia induzida por quimioterapia. Em estudo prévio realizado em nossa instituição, observou-se que o controle da emese tardia poderia ser melhorado com a omissão do segundo dia dos antagonistas 5HT-3. Reportamos aqui os resultados de um estudo fase III confirmando os achados prévios PACIENTES E MÉTODOS: Estudo fase III randomizado e duplo-cego foi realizado na FMABC Santo André/Brasil. Pacientes submetidos a esquemas quimioterápicos alta e moderadamente emetogênicos pela 1ª vez receberam Ondasetron 16mg e Dexametasona 20 mg IV antes da quimioterapia no Dia 1. Foram então randomizados em dois grupos. Grupo A recebeu metoclopramida VO 10mg 8/8hs, Granisetron VO 0,5mg/dia,e dexametasona VO 8mg /dia por 2 dias, a partir do dia 2 (dias 2 e 3). Metoclopramida VO 10 mg 8/8 hs foi continuada no dia 4. Grupo B recebeu placebo no dia 2 e o mesmo esquema de drogas dia 3 e dia 4. Pacientes foram entrevistados no dia 1 e dia 6. RESULTADOS: 73 pacientes foram incluídos no estudo. Os grupos foram bem balanceados em relação as suas características clinicas com exceção ao melhor controle da emese aguda no grupo A (p=0,04). Proteção completa de náuse a e vômito tardios (do dia 2 ao 5 ), foi semelhante em ambos os grupos (30% vs. 32%; p=0.5). Em análise multivariada, tanto a proteção completa da emese aguda (p=0.001) quanto grupo de estudo (p=0.06) estavam independentemente relacionados à proteção completa da náusea e vômito tardios. Selecionando apenas os pacientes que obtiveram controle completo da emese na fase aguda, pacientes do grupo B obtiveram maior proteção da emese tardia (85% vs 50% ,p=0,02). CONCLUSÃO: A omissão da medicação antiemética no dia 2 representa uma estratégia para redução do custo da profilaxia da emese tardia induzida pela quimioterapia. / BACKGROUND: Nausea and vomiting are important symptoms observed in cancer patients. In a previous study we showed that delayed chemotherapyinduced nausea and vomiting (CINV) control could be potentially improved by skipping the administration of a 5HT3-antagonist on day 2. We report here a trial confirming our previous findings. PATIENTS/METHODS: A phase-IIIrandomized- placebo-controlled trial was conducted in which patients received (IV) ondansetron 16mg, dexamethasone 20mg and ranitidine 50mg before highly/moderately emetogenic chemotherapy (day 1).Starting on day 2, all patients received metoclopramide 10mg PO q8 hours (days 2,3 and 4, Dexamethasone 8mg QD (days 2 and 3) and Ranitidine 150mg q12 hours (days 2 and 3). Patients were randomized to receive either Granisetron 0.5mg PO (days 2 and 3) (Group A) or Placebo instead for Granisetron on day 2 and Granisetron 0.5mg on day 3 and 4 (Group B) RESULTS: 73 patients were enrolled. Groups were similar regarding clinical characteristics, despite better control during the acute phase of CINV in group A (p=0.04). Complete delayed protection from nausea/vomiting (DCPNV) from day 2 to 5 was similar in both groups. (30% vs. 32%; p=0.5). Analyzing DCPNV by logistic regression multivariate analyses, acute complete protection from nausea/vomiting (ACPNV) (p=0.001) and study group (p=0.06) were independently associated with DCPNV. Selecting patients who achieved ACPNV, we observed that group B had a superior DCPNV (85% vs 50%, p=0.02). CONCLUSION: DCPNV can be improved just by skipping day 2 of 5HT3- antagonists. Future studies should compare this inexpensive strategy with NK1- antagonists or second generation 5HT3-antagonists. Key words: delayed chemotherapy-induced nausea and vomiting, tachyphylaxis, cost- saving regimen, antiemetics, Granisetron/administration and dosage. / TEDE / BV UNIFESP: Teses e dissertações

It is increasingly being recognised that agrichemical exposure may have adverse chronic health effects in humans, particularly on central nervous system function. However, much of this evidence sterns from studies relating to the effects of acute intoxications (i.e. short-term high dose exposures) and little data exist on the chronic effects of long-term low-dose exposures to agrichemicals in the absence of acute poisoning. Such a finding would have substantial public health implications for prevention and control of chronic morbidity and mortality. This is particularly important in South Africa, where a sizeable portion of the rural population are employed in agricultural work, often under extremely unhealthy living and working conditions, and where occupational agrichemical exposures appear to be substantial. To address this question, this study investigated the prevalence of neurological and neurobehavioural abnormalities amongst 247 fruit farm workers in the Kouebokkeveld in the Western Cape, of whom 163 were current agrichemical applicators. Outcomes measured included neurological symptoms, peripheral vibration sense, motor tremor, as well as performance on the World Health Organisation Neurobehavioural Core Test Battery (WHO NCTB) and a set of neurobehavioural tests based on the Information Processing model of cognitive psychology. These latter tests have been developed in South Africa for subjects of low educational levels and aim to by-pass the powerful effects of culture that complicate traditional neuropsychological testing, which may mask the smaller effects due to occupational chemical exposures. Cumulative, and average lifetime intensity of exposure to organophosphates were estimated using a job- exposure matrix based on a combination of secondary industry data, interview reports and farmer records. Confounders measured included age, education, smoking and alcohol habits, non-occupational exposure to agrichemicals and other potential neurotoxins, past medical history and usage of personal protective equipment. The study results confirmed low levels of education and high alcohol consumption amongst the sample of farm workers. Multiple logistic and linear regression were used to identify exposure-effect relationships and to control for confounding. Neurological symptoms were significantly associated with a history of previous pesticide poisoning, although this may have arisen as a result of reporting bias. Vibration sense and the neurobehavioural tests exhibited associations with established covariates, and regression modelling of the WHO NCTB tests was remarkably similar to findings in another study of solvent-exposed factory workers in South Africa. None of the vibration sense, tremor or neurobehavioural outcomes were associated with past agrichemical poisoning in the sample, and only two tests showed significant relationships with long-term occupational exposure. These included the Pursuit Aiming subtest of the WHO NCTB and one of the tests of long-term semantic memory in the Information Processing tests. However, the strength of these the associations were small (partial r²s less than 2%) and these findings may have occurred due to chance arising from multiple comparisons. The neurobehavioural tests based on the Information Processing model appeared to offer little improvement on the WHO NCTB in terms of being less sensitive to cultural effects, although some evidence was present that tests of semantic access were able to detect occupational effects and were less sensitive to education. The absence of a demonstrable and consistent long-term agrichemical exposure-effect relationship appears to suggest that long-term agrichemical exposure is not associated with adverse chronic nervous system effects, although the lack of organophosphate specificity in construction of exposure indices in the job-exposure matrix may partly contribute to this finding. Recommendations to improve the characterisation of agrichemical exposures at farming work place are made, as well as suggestions concerning the role of biological monitoring for agrichemicals, improving working and living conditions on South African farms, and methods of neurological and neurobehavioural assessment in occupational health.

No description available.

Made available in DSpace on 2016-08-10T10:55:21Z (GMT). No. of bitstreams: 1 ANNELISE CARRILHO CORREA DE CASTRO.pdf: 753705 bytes, checksum: 5d1101ab7100c09cec08b3f615f42a08 (MD5) Previous issue date: 2007-11-21 / Nifedipine is a diidropirine widely used for the control of arterial hypertension, wich because of its vessel dilating, in particular for the blockade by the entry of calcium. However, the chronic use of this calcium channel blocker is associated with the gingival overgrowth, resulting in the esthetic, phonetic and mastication problems. Data from the literature aren t unanimous in suggesting that cells density alterations of gingival tissues might be caused by nifedipine. The aim of this study was to analyze the variations in mast cells densities and associated with collagen and vasculature degrees of the gingival tissues by effect of nifedipine. In order to do so, fourteen samples of gingival tissue of patients undergoing chronic treatment with nifedipine were obtained. For comparative purposes, fifteen samples of gingival tissues of healthy patients who did not use drugs associated with gingival overgrowth were used. The samples were analysed in the department of oral pathology, Federal University of Goiás. The histochemical analysis of the collagen degree was made using picrosirius staining. To evaluate mast cells and blood vessels density, the samples were processed by standard immunoperoxidase immunohistochemical technique using mast cell tryptase and CD31 antibodies. The results showed that the number of tryptase-positive mast cells in nifedipine group was significantly higher than the number of tryptasepositive mast cells in the control group (Mann-Whitney test, P=0,02). However, there wasn t relationship between mast cells density and the degree of angiogenesis (Pearson test, P=0,3). The number of tryptase-positive mast cells was not correlated with collagen degree (Spearman test, P=0,6). Also there wasn t relationship between mast cells density and dose or duration of the nifedipine therapy (Pearson test, P=0,2 and P=0,7). Microscopic alterations observed in the connective tissue of nifedipine users suggest that this drug might be associated to alterations observed in tryptase-positive mast cells density. / A nifedipina é uma diidropiridina amplamente utilizada no tratamento antihipertensivo devido à sua ação vasodilatadora, especialmente, por bloquear o influxo de cálcio. Entretanto, o uso crônico deste bloqueador dos canais de cálcio está associado ao aumento da mucosa gengival, gerando problemas estéticos, fonéticos e mastigatórios. Os dados da literatura não são unânimes em sugerir que a nifedipina possa resultar na alteração da densidade celular do tecido gengival. O presente trabalho teve como objetivo avaliar a densidade de mastócitos e sua relação com os processos de colagenização e vascularização no tecido gengival sob efeito da nifedipina. Para este fim, foram utilizadas 14 amostras de tecido gengival de pacientes usuários de nifedipina. Para fins comparativos, foram utilizadas 15 amostras de tecido gengival de indivíduos saudáveis. As amostras foram avaliadas no departamento de Patologia Bucal da Universidade Federal de Goiás. A análise histoquímica do grau de colagenização foi realizada por meio da coloração de picrosirius. Para a avaliação da densidade de mastócitos, foi realizado um estudo quantitativo destas células a partir da técnica imunoistoquímica com marcação pelo anticorpo anti-triptase. A mensuração da densidade de vasos sangüíneos foi avaliada através de técnica imunoistoquímica com marcação pelo anticorpo anti-CD 31. Os resultados revelaram que os pacientes usuários de nifedipina apresentavam um aumento estatisticamente significante do número de MCs-triptase+, quando comparados ao grupo controle (Mann-Whitney, P=0,02). No entanto, não houve correlação entre a densidade de vasos e a densidade de mastócitos (Teste de Pearson, P=0,3), assim como não houve correlação entre o grau de colagenização e a densidade de mastócitos (Teste de Spearman, P=0,6). Também não foi observada correlação entre a densidade de MCs e a dose e/ou duração da terapia com nifedipina (Teste de Pearson, P=0,2 e P=0,7, respectivamente). As alterações microscópicas observadas no tecido conjuntivo de pacientes usuários de nifedipina sugerem que esta medicação está relacionada às alterações na densidade dos MCs-triptase+.

Sam Sze Wing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 156-184). / Abstracts in English and Chinese. / Publications based on work in this thesis --- p.ii / Abstract --- p.iii / Acknowledgements --- p.vii / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Corticosteroids --- p.2 / Chapter 1.1.1 --- Chemical Structure of Steroids --- p.3 / Chapter 1.1.2 --- Biosynthesis of Endogenous Corticosteroids --- p.3 / Chapter 1.1.2.1 --- Regulation of Cortisol synthesis and negative feedback system --- p.4 / Chapter 1.1.3 --- Biological Significance of Corticosteroids --- p.5 / Chapter 1.1.3.1 --- Involvement of corticosteroids as anti-inflammatory drugs --- p.6 / Chapter 1.1.3.2 --- Eicosanoid biosynthesis --- p.7 / Chapter 1.1.3.3 --- Lipoxygenase pathway --- p.9 / Chapter 1.1.3.4 --- Side-effects of prolonged use of corticosteroids --- p.9 / Chapter 1.2 --- Organisation of the Emetic Reflex --- p.11 / Chapter 1.2.1 --- Motor Pathway of Emetic Reflex --- p.12 / Chapter 1.2.1.1 --- Retching and vomiting --- p.12 / Chapter 1.2.1.2 --- Nausea --- p.13 / Chapter 1.2.2 --- Components of the Emetic Reflex --- p.14 / Chapter 1.2.2.1 --- The vomiting centre (VC) --- p.15 / Chapter 1.2.2.2 --- Area postrema (AP) / Chemoreceptor trigger zone (CTZ) --- p.15 / Chapter 1.2.2.3 --- The nucleus tractus solitarius (NTS) --- p.17 / Chapter 1.2.2.4 --- Gastrointestinal tract and vagus nerves --- p.17 / Chapter 1.2.2.5 --- Neurotransmitter receptors --- p.18 / Chapter 1.3 --- Chemotherapy-Induced Emesis --- p.19 / Chapter 1.3.1 --- Cancer as a cause of mortality in Man --- p.20 / Chapter 1.3.2 --- Chemotherapeutic Agents --- p.20 / Chapter 1.3.2.1 --- Different classes --- p.20 / Chapter 1.3.2.2 --- Emetogenic potential --- p.21 / Chapter 1.3.3 --- Cisplatin-Induced Emesis --- p.23 / Chapter 1.3.3.1 --- Unfavourable effects associated with chemotherapy-induced nausea and emesis --- p.24 / Chapter 1.3.3.2 --- Anticipatory nausea and vomiting --- p.24 / Chapter 1.3.3.3 --- Profile of cisplatin-induced emesis --- p.25 / Chapter 1.3.4 --- Animal Models of Cisplatin-Induced Acute and Delayed Emesis --- p.26 / Chapter 1.3.5 --- Mechanisms and Pathways Involves in Chemotherapy-Induced Emesis --- p.28 / Chapter 1.3.6 --- Anti-Emetic Drugs for the Treatment of Chemotherapy-Induced Emesis --- p.31 / Chapter 1.3.6.1 --- 5-HT3 receptor antagonists --- p.31 / Chapter 1.3.6.2 --- Dopamine receptor antagonists --- p.33 / Chapter 1.3.6.3 --- Benzodiazepines --- p.35 / Chapter 1.3.6.4 --- Cannabinoids --- p.35 / Chapter 1.3.6.5 --- Antihistamines and anticholinergics --- p.35 / Chapter 1.3.6.6 --- NK1 receptor antagonists --- p.37 / Chapter 1.3.6.7 --- Corticosteroids --- p.38 / Chapter 1.3.6.8 --- Multi-agent anti-emetic regimens --- p.39 / Chapter 1.4 --- Motion-Induced Emesis --- p.41 / Chapter 1.4.1 --- Incidence --- p.42 / Chapter 1.4.2 --- Mechanisms and Pathways Involved in Motion Sickness --- p.43 / Chapter 1.4.2.1 --- Importance of the vestibular apparatus --- p.44 / Chapter 1.4.2.2 --- Importance of the area postrema --- p.45 / Chapter 1.4.2.3 --- The nucleus tractus solitarius --- p.46 / Chapter 1.4.2.4 --- Hormone and neurotransmitters --- p.46 / Chapter 1.4.3 --- Animal models in Motion-Induced Emesis --- p.47 / Chapter 1.4.4 --- Anti-Emetic Drugs for the Treatment of Motion Sickness --- p.48 / Chapter 1.4.4.1 --- Anticholinergics --- p.49 / Chapter 1.4.4.2 --- Antihistamines --- p.49 / Chapter 1.4.4.3 --- Non-selective muscarinic and histamine receptor antagonists --- p.51 / Chapter 1.4.4.4 --- Sympathomimetics --- p.51 / Chapter 1.4.4.5 --- NK1i receptor antagonists --- p.51 / Chapter 1.4.4.6 --- 5-HT1A agonists --- p.52 / Chapter 1.4.4.7 --- 5-HT2 receptor agonist --- p.52 / Chapter 1.4.4.8 --- Arginine vasopressin (AVP) antagonists --- p.53 / Chapter 1.4.4.9 --- Opioid receptor agonists --- p.53 / Chapter 1.4.4.10 --- Dexamethasone and hormone levels --- p.54 / Chapter 1.4.4.11 --- Other anti-emetic drugs --- p.55 / Chapter 1.5 --- Aims of the Studies --- p.56 / Chapter 2 --- Methods --- p.59 / Chapter 2.1 --- Cisplatin-Induced Emesis Studies --- p.60 / Chapter 2.1.1 --- Animals --- p.60 / Chapter 2.1.2 --- Induction and Measurement of Emesis --- p.60 / Chapter 2.1.3 --- The Effects of Corticosteroids on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.4 --- "The Effects of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.63 / Chapter 2.1.5 --- The Effects of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.63 / Chapter 2.1.6 --- The Effects of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.7 --- The Effects of Indomethacin on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.64 / Chapter 2.1.8 --- "The Effects of DFU and L-745,337 Administered as an Intervention Treatments on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.64 / Chapter 2.1.9 --- "The Effects of MK-886 (L-663,536) on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.65 / Chapter 2.1.10 --- The Effects of a Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.65 / Chapter 2.1.11 --- Statistical Analysis --- p.66 / Chapter 2.2 --- Motion-Induced Emesis Studies --- p.67 / Chapter 2.2.1 --- Animals --- p.67 / Chapter 2.2.2 --- Measurement of Emesis --- p.67 / Chapter 2.2.3 --- Induction of Emesis in Motion-Naive Suncus murinus: Effects of Glucocorticoids --- p.68 / Chapter 2.2.4 --- Induction of Emesis in Motion-Sensitive Suncus murinus: Effects of Dexamethasone --- p.70 / Chapter 2.2.5 --- Preparation of Serum --- p.72 / Chapter 2.2.6 --- Measurement of Serum Cortisol by Enzyme-Linked Immunoassay (ELISA) --- p.72 / Chapter 2.2.6.1 --- Immunoassay kit --- p.72 / Chapter 2.2.6.2 --- Assay procedures --- p.73 / Chapter 2.2.7 --- Measurement of Serum Adrenocorticotrophin (ACTH) by Radioimmunoassay (RIA) --- p.75 / Chapter 2.2.7.1 --- Immunoassay kit --- p.75 / Chapter 2.2.7.2 --- Assay procedures --- p.76 / Chapter 2.2.8 --- Statistical Analysis --- p.79 / Chapter 3 --- Results --- p.81 / Chapter 3.1 --- Cisplatin-Induced Emesis --- p.82 / Chapter 3.1.1 --- General Profile of Emesis Induced by Cisplatin --- p.82 / Chapter 3.1.2 --- Antagonism of Cisplatin-Induced Emesis by Corticosteroids --- p.82 / Chapter 3.1.3 --- "The Effect of Dexamethasone (1 mg/kg, i.p.) Administered as an Intervention Treatment on an Established Delayed Retching and Vomiting Response Induced by Cisplatin" --- p.84 / Chapter 3.1.4 --- The Effect of Cortrosyn Depot (Tetracosactrin) on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.5 --- The Effect of Metyrapone on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.85 / Chapter 3.1.6 --- "The Effect of Indomethacin, DFU and L-745,337 on Cisplatin-Induced Acute and Delayed Retching and Vomiting" --- p.86 / Chapter 3.1.7 --- The Effect of MK-886 on Cisplatin-Induced Acute and Delayed Retching and Vomiting --- p.88 / Chapter 3.1.8 --- The Effect of Combination of Indomethacin and MK-886 on Cisplatin- Induced Acute and Delayed Retching and Vomiting --- p.89 / Chapter 3.2 --- Motion-Induced Emesis --- p.91 / Chapter 3.2.1 --- General Effect of Motion on Serum Cortisol and ACTH Levelsin Motion Naive Suncus murinus --- p.91 / Chapter 3.2.2 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Naive Male Suncus murinus --- p.92 / Chapter 3.2.2.1 --- Effect of dexamethasone --- p.92 / Chapter 3.2.2.2 --- Effect of betamethasone --- p.93 / Chapter 3.2.2.3 --- Effect of methylprednisolone --- p.93 / Chapter 3.2.3 --- The Effect of Glucocorticoids on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion Naive Female Suncus murinus --- p.94 / Chapter 3.2.3.1 --- Effect of dexamethasone --- p.94 / Chapter 3.2.3.2 --- Effect of betamethasone --- p.95 / Chapter 3.2.3.3 --- Effect of methylprednisolone --- p.95 / Chapter 3.2.4 --- The Effect of Dexamethasone on Motion-Induced Emesis and Cortisol and ACTH Levels in Motion-Sensitive Suncus murinus --- p.96 / Chapter 3.2.4.1 --- Effect of dexamethasone on male motion-sensitive animals --- p.97 / Chapter 3.2.4.2 --- Effect of dexamethasone on female motion-sensitive animals --- p.97 / Chapter 4 --- Discussion --- p.131 / Chapter 4.1 --- "Cisplatin (5 mg/kg, i.p.)-Induced Emesis in Control Animals" --- p.132 / Chapter 4.2 --- Anti-Emetic Action of Corticosteroids in the Ferret --- p.133 / Chapter 4.3 --- Metyrapone Study --- p.138 / Chapter 4.4 --- Cortrosyn Depot Study --- p.139 / Chapter 4.5 --- Role of Cycloxygenase --- p.141 / Chapter 4.6 --- Role of 5-Lipoxygenase --- p.143 / Chapter 4.7 --- Duel Inhibition of Cycloxygenase and 5-Lipoxygenase --- p.144 / Chapter 4.8 --- Anti-Emetic Potential of Glucocorticoids in Suncus murinus --- p.145 / Chapter 4.9 --- General Summary --- p.149 / Appendix I --- p.152 / Appendix II --- p.154 / References --- p.156

Tingan Chen. / "March 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 100-142). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Yuen Mong Ting. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 155-169). / Abstracts in English and Chinese. / Acknowledgements --- p.i / Abstract (English) --- p.ii / Abstract (Chinese) --- p.v / Contents --- p.vi / Chapter Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Developmental biology of the prostate --- p.1 / Chapter 1.1.1 --- Development of the prostate gland in humans and rodents --- p.1 / Chapter 1.1.2 --- Mesenchymal-epithelial interaction --- p.2 / Chapter 1.2 --- Overview of the endocrinology of prostate --- p.3 / Chapter 1.3 --- Estrogen in male and prostate gland --- p.4 / Chapter 1.3.1 --- Stimulating effect of estrogen on prostate gland --- p.4 / Chapter 1.3.2 --- Inhibitory effect of estrogen on prostate gland --- p.5 / Chapter 1.4 --- Study of the role of estrogen receptors in prostate gland with the use of estrogen receptor knockout mice --- p.6 / Chapter 1.4.1 --- The two isoforms of estrogen receptors (ER): ERα and ERβ --- p.6 / Chapter 1.4.2 --- The use of estrogen receptor knockout mice for the study of ER --- p.7 / Chapter 1.5 --- Estrogen as a carcinogen --- p.8 / Chapter 1.5.1 --- Formation of DNA adducts --- p.8 / Chapter 1.5.2 --- Formation of oxidants --- p.9 / Chapter 1.5.3 --- Estrogen as a microtubule-disrupting agent --- p.10 / Chapter 1.6 --- Estrogen carcinogenicity in animal models --- p.11 / Chapter 1.6.1 --- Syrian golden hamster model --- p.11 / Chapter 1.6.2 --- Rat model --- p.12 / Chapter 1.7 --- Animal models of prostate cancer by hormonal induction --- p.12 / Chapter 1.7.1 --- Canine model --- p.13 / Chapter 1.7.2 --- Noble rat model --- p.13 / Chapter 1.7.3 --- Sprague-Dawley rat model --- p.15 / Chapter 1.7.4 --- Wistar and F344 rat model --- p.15 / Chapter 1.8 --- Perinatal estrogen exposure and prostate development --- p.16 / Chapter 1.8.1 --- Prenatal estrogen exposure --- p.15 / Chapter 1.8.2 --- Neonatal estrogen exposure --- p.17 / Chapter 1.9 --- Therapeutic use of synthetic estrogen --- p.18 / Chapter 1.9.1 --- Use of diethylstilbestrol in treating prostate cancer --- p.18 / Chapter 1.9.2 --- Use of diethylstilbestrol during pregnancy --- p.19 / Chapter 1.10 --- Estrogen contamination in food --- p.20 / Chapter 1.10.1 --- Estrogen in milk and dairy products --- p.20 / Chapter 1.10.2 --- Estrogen in meat --- p.21 / Figure 1.1 --- p.23 / Chapter Chapter 2. --- Materials and methods --- p.25 / Chapter 2.1 --- In vitro study of estrogen carcninogenicity in normal prostatic cell line --- p.25 / Chapter 2.1.1 --- NRP-152 cell line --- p.25 / Chapter 2.1.2 --- In vitro estrogen treatment on NRP-152 cells --- p.25 / Chapter 2.1.3 --- Colony formation by soft agar assay --- p.27 / Chapter 2.1.4 --- Determination of growth parameters of estrogen-treated and untreated NRP-152 cells --- p.29 / Chapter 2.1.5 --- Gene expression profiling in estrogen-transformed and untreated parental NRP-152 cells by cDNA microarray --- p.30 / Chapter 2.1.6 --- Immunohistochemistry of cultured cells --- p.34 / Chapter 2.1.7 --- Immunofluorescence on cultured cells --- p.36 / Chapter 2.1.8 --- Electron microscopy of the estrogen-transformed and untreated parental NRP-152 cells --- p.37 / Chapter 2.1.9 --- Tumorigenicity in nude mice --- p.38 / Chapter 2.1.10 --- Protein expressions and Western blottings in estrogen-transformed and untreated parental NRP-152 cells --- p.39 / Chapter 2.2 --- In vivo study of estrorgen carcinogenicity in rat protstate gland --- p.41 / Chapter 2.2.1 --- Origin and supply of Noble rats --- p.41 / Chapter 2.2.2 --- Perinatal estrogen imprinting on male Noble rats with diethylstilbestrol --- p.42 / Chapter 2.2.3 --- Long-term hormonal treatment with sex steroids on male Noble rats at adulthood --- p.43 / Chapter 2.2.4 --- Morphological study of Noble rat prostates --- p.44 / Chapter 2.2.5 --- Protein expressions by immunohistochemistry in estrogen-primed and hormone-treated Noble rat prostates --- p.45 / Tables 2.1 -2.2 --- p.48 / Chapter Chapter 3. --- Results --- p.50 / Chapter 3.1 --- In vitro study --- p.50 / Chapter 3.1.1 --- Dose selection for estrogen treatment of NRP-152 cells from cell proliferation assay --- p.50 / Chapter 3.1.2 --- Colony formation in soft agar --- p.50 / Chapter 3.1.3 --- Morphology of NRP-152 cells and the estrogen-transformed clones --- p.51 / Chapter 3.1.4 --- Study of growth parameters --- p.52 / Chapter 3.1.5 --- CDNA array analysis of differentia] gene pattern --- p.53 / Chapter 3.1.6 --- Immunohistochemistry of untreated parental and estrogen- transformed NRP-152 cells --- p.55 / Chapter 3.1.7 --- Electron microscopy --- p.58 / Chapter 3.1.8 --- Tumorigenicity of NRP-152 cells and the estrogen-transformed clones --- p.59 / Chapter 3.1.9 --- Western blottings --- p.59 / Chapter 3.2 --- In vivo study --- p.52 / Chapter 3.2.1 --- Survival of male Nobel rats during perinatal and long-term hormone treatment --- p.62 / Chapter 3.2.2 --- Histological studies of Noble rat prostates --- p.63 / Chapter 3.2.3 --- Immunohistochemistry of the hormone-treated and control Noble rat prostates --- p.65 / Figure 3.1.1 -3.1.44 --- p.73 / Figure 3.2.1 - 3.2.50 --- p.97 / Table 3.1 -3.4 --- p.117 / Chapter Chapter 4. --- Discussions --- p.121 / Chapter 4.1 --- The study on the transformation of cells and soft agar assay --- p.121 / Chapter 4.2 --- Growth patterns of the estrogen-transformed clones --- p.123 / Chapter 4.3 --- Altered differential gene expression --- p.124 / Chapter 4.3.1 --- TUBA --- p.124 / Chapter 4.3.2 --- PTEN --- p.125 / Chapter 4.3.3 --- RAP 1A --- p.126 / Chapter 4.3.4 --- BRCA2 --- p.126 / Chapter 4.4 --- Ultrastructural study in the estrogen-transformed and untreated parental NRP-152 cells --- p.127 / Chapter 4.5 --- Neoplastic lesions induced in prostates of estrogen-imprinted and long-term combined hormone treated Noble rats --- p.129 / Chapter 4.6 --- Altered protein expressions in estrogen-transformed NRP-152 cells and estrogen-imprinted and hormone-treated Noble rat prostates --- p.132 / Chapter 4.6.1 --- Alteration in steroid hormone receptors --- p.132 / Chapter 4.6.2 --- Alternation in cytoskeleton (tubulin-α) --- p.138 / Chapter 4.6.3 --- Alternation in PTEN --- p.141 / Chapter 4.6.4 --- Alternation in Rap1 --- p.143 / Chapter 4.6.5 --- Alternation in BRCA2 --- p.145 / Chapter 4.6.6 --- "Altered in scavenger enzyme (Superoxide dismutase, SOD-1)" --- p.147 / Chapter Chapter 5. --- Summary --- p.150 / Reference --- p.155

Cheung Shu Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 124-137). / Abstracts in English and Chinese. / Abstract (English) --- p.i / Abstract (Chinese) --- p.iii / Acknowledgements --- p.iv / Contents --- p.v / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Epidemiology of Breast Cancer --- p.1 / Chapter 1.1.1 --- Epidemiology of Breast Cancer in Females --- p.1 / Chapter 1.1.2 --- Incidence and Morality of Female Breast Cancer in Hong Kong --- p.2 / Chapter 1.1.3 --- Epidemiology of Breast Cancer in Males --- p.3 / Chapter 1.2 --- Risk Factors for Female Breast Cancer --- p.4 / Chapter 1.2.1 --- Genetic Risk Factors --- p.4 / Chapter 1.2.2 --- Hormonal Risk Factors --- p.6 / Chapter 1.2.2.1 --- Endogenous Hormonal Risk Factors --- p.7 / Chapter 1.2.2.2 --- Exogenous Hormonal Risk Factors --- p.8 / Chapter 1.2.3 --- Other Environmental Risk Factors --- p.9 / Chapter 1.3 --- Oncogenetic Basis of Female Breast Cancer --- p.10 / Chapter 1.4 --- Hormonal Basis of Female Breast Cancer --- p.12 / Chapter 1.4.1 --- Mechanisms of Hormone Action --- p.12 / Chapter 1.4.1.1 --- Estrogen and Progesterone --- p.12 / Chapter 1.4.1.2 --- Prolactin --- p.14 / Chapter 1.4.2 --- Hormonal Regulation of Normal Breast Development --- p.15 / Chapter 1.4.3 --- Hormonal Regulation of Breast Carcinogensis and Its Subsequent Progression --- p.17 / Chapter 1.4.3.1 --- Androgen --- p.17 / Chapter 1.4.3.2 --- Estrogen --- p.18 / Chapter 1.4.3.3 --- Progesterone --- p.20 / Chapter 1.4.3.4 --- Prolactin --- p.22 / Chapter 1.5 --- Animal Models for Breast Cancer --- p.23 / Chapter 1.5.1 --- Mouse Models --- p.24 / Chapter 1.5.2 --- Rat Models --- p.25 / Chapter 1.5.2.1 --- Carcinogen Induced Rat Models --- p.26 / Chapter 1.5.2.2 --- Hormone Induced Rat Models --- p.28 / Chapter 1.5.2.3 --- Spontaneously Developed Rat Models --- p.31 / Chapter 1.6 --- Aims of Study --- p.34 / Tables and Figures --- p.35 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Origin and Supply of Noble Rats --- p.37 / Chapter 2.2 --- Supply of Materials --- p.37 / Chapter 2.3 --- Induction of Mammary Tumors by Singe Dose of Chemical Carcinogens in Female Rats --- p.38 / Chapter 2.3.1 --- Induction by 7，12-Dimethylbenz[a]anthracene in Female Noble Rats --- p.38 / Chapter 2.3.2 --- Induction by N-Methyl-N-Nitrosourea in Female Sprague- Dawley Rats --- p.38 / Chapter 2.4 --- Induction of Mammary Tumors by Long-Term Treatments with Steroid Hormone --- p.39 / Chapter 2.4.1 --- Preparation of Steroid Hormone-filled Silastic® Tubings --- p.39 / Chapter 2.4.2 --- Surgical Implantation of Silastic® Tubings --- p.40 / Chapter 2.4.3 --- Protocols of Hormonal Treatments --- p.40 / Chapter 2.5 --- Collection of Spontaneously Developed Mammary Tumors in Noble Rats --- p.41 / Chapter 2.6 --- Transplantation of Spontaneously Developed Mammary Tumors into Noble Rats --- p.41 / Chapter 2.7 --- Bilateral Ovariectomy of Female Noble Rats bearing Spontaneously Developed Mammary Tumors --- p.42 / Chapter 2.8 --- Measurement of Mammary Tumor Growth --- p.43 / Chapter 2.9 --- Whole Mount Preparation of the Hormone-Treated Mammary Glands in Noble Rats --- p.44 / Chapter 2.10 --- Histological Examination of Mammary Gland and Tumors in Noble Rats --- p.45 / Chapter 2.11 --- Detection of Protein Expression of Hormone Receptors in Normal Mammary Glands and Mammary Tumors of Noble Rats --- p.45 / Chapter 2.11.1 --- Antibodies --- p.45 / Chapter 2.11.2 --- Immunohistochemistry --- p.47 / Chapter 2.11.3 --- "Protein extraction, SDS-PAGE and western blotting analysis" --- p.48 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Gross Appearance of Mammary Tumors --- p.51 / Chapter 3.2 --- Incidence Rate of Mammary Tumors --- p.53 / Chapter 3.2.1 --- Spontaneously Developed Mammary Tumors in Noble Rats --- p.53 / Chapter 3.2.2 --- Hormone Induced Mammary Tumors in Female Noble Rats --- p.53 / Chapter 3.2.3 --- DMBA Induced Mammary Tumors in Female Noble Rats --- p.54 / Chapter 3.2.4 --- NMU Induced Mammary Tumors in Female SD Rats --- p.54 / Chapter 3.3 --- Histology of Normal and Lactating Mammary Glands in Female Noble Rats --- p.54 / Chapter 3.4 --- Histopathology of Mammary Tumors --- p.55 / Chapter 3.4.1 --- Histopathology of Spontaneously Developed Mammary Tumors in Noble Rats --- p.55 / Chapter 3.4.2 --- Histopathology of Hormone Induced Mammary Tumors in Female Noble Rats --- p.59 / Chapter 3.4.3 --- Histopathology of DMBA Induced Mammary Tumors in Female Noble Rats --- p.60 / Chapter 3.4.4 --- Histopathology of NMU Induced Mammary Tumors in Female SD Rat --- p.60 / Chapter 3.5 --- Whole Mount Preparation of Mammary Glands under Hormonal Treatments --- p.61 / Chapter 3.6 --- Effects of Bilateral Ovariectomy on the Growth of Spontaneously Developed Mammary Tumors --- p.61 / Chapter 3.7 --- Transplanability of the Spontaneously Developed Mammary Tumors in Noble Rats --- p.62 / Chapter 3.8 --- Examination of the Malignancy of Mammary Tumors by Immunohistochemical analysis of Epithelial Keratin Expression --- p.62 / Chapter 3.9 --- Immunohistochemical Analysis of Expression and Localization of Hormone Receptor Protein in Normal and Neoplastic Mammary Tissues of Female Noble Rats --- p.63 / Chapter 3.9.1 --- Expression and Localization of Hormone Receptors in Control Tissue --- p.63 / Chapter 3.9.2 --- Expression and Localization of Estrogen Receptor α --- p.64 / Chapter 3.9.3 --- Expression and Localization of Estrogen Receptor β --- p.65 / Chapter 3.9.4 --- Expression and Localization of Progesterone Receptor --- p.65 / Chapter 3.9.5 --- Expression and Localization of Androgen Receptor --- p.66 / Chapter 3.9.6 --- Expression and Localization of Prolactin Receptor --- p.66 / Chapter 3.10 --- Western Blot Analysis of Expression of Hormone Receptor Proteins in Normal and Neoplastic Mammary Tissues of Female Noble Rats - --- p.67 / Chapter 3.10.1 --- Expression of Estrogen Receptor α --- p.67 / Chapter 3.10.2 --- Expression of Estrogen Receptorβ --- p.68 / Chapter 3.10.3 --- Expression of Progesterone Receptor --- p.68 / Chapter 3.10.4 --- Expression of Androgen Receptor --- p.69 / Chapter 3.10.5 --- Expression of Prolactin Receptor --- p.69 / Figures and Tables --- p.71 / Chapter Chapter 4 --- Discussions / Chapter 4.1 --- Comparison of the Incidence Rate of Spontaneously developed Mammary Tumors in Noble Rats with the Previously Reported Incidence Rate --- p.102 / Chapter 4.2 --- Comparison of the Incidence rate of Spontaneously Developed Mammary Tumors in Noble Rats with the Incidence Rate in Other Rat Strains --- p.103 / Chapter 4.3 --- Crucial Factors Influencing the Incidence Rate of Spontaneously Developed Mammary Tumors in Noble Rats --- p.104 / Chapter 4.4 --- Comparison of the T+E2 Induced Mammary Tumors with the T+DES Induced Mammary Tumors in Female Noble Rats --- p.105 / Chapter 4.5 --- Comparison of the Incidence Rate & Latency Period of the Hormone Induced Mammary Tumors in Noble Rats with the Previously Reported Data --- p.106 / Chapter 4.6 --- Comparison of the Phenotypic Behaviors in Spontaneously Developed Mammary Tumors with the Hormone Induced Mammary Tumors in Female Noble Rats --- p.107 / Chapter 4.7 --- Comparison of the Behaviors of Carcinogen Induced Mammary Tumors with Spontaneously Developed & Hormone Induced Mammary Tumors in Female Noble Rats --- p.109 / Chapter 4.8 --- "Comparison of Expression Patterns of Hormone Receptor Proteins in Spontaneously Developed, Hormone Induced & Carcinogen Induced Mammary Tumors in Female Noble Rats" --- p.111 / Chapter 4.9 --- "Expressions of ERα & ERβ Proteins in Spontaneously Developed, Hormone Induced and Carcinogen Induced Mammary Tumors in Female Noble Rats" --- p.112 / Chapter 4.10 --- "Expressions of PR Proteins in Spontaneously Developed, Hormone Induced and Carcinogen Induced Mammary Tumors in Female Noble Rats" --- p.115 / Chapter 4.11 --- "Expressions of AR Proteins in Spontaneously Developed, Hormone Induced and Carcinogen Induced Mammary Tumors in Female Noble Rats" --- p.116 / Chapter 4.12 --- "Expressions of PRLR Proteins in Spontaneously Developed, Hormone Induced and Carcinogen Induced Mammary Tumors in Female Noble Rats" --- p.120 / Chapter Chapter 5 --- Conclusions --- p.123 / References --- p.124