Abstract Fibrillar type I and III collagens are the major constituents of the extracellular matrix, providing the tissue with tensile strength and influencing cell attachment and migration. The amount of type III collagen and the extent of its processing and cross-link maturation were studied in human atherosclerotic plaques, abdominal aortic aneurysms, colon and ovarian cancer, and finally, colon diverticulosis, using a novel radioimmunoassay for the cross-linked aminoterminal telopeptide of type III collagen. In addition, immunoassays for different structural domains of type I and type III collagens, together with immunohistochemical methods, were applied. In atherosclerotic plaques, the fully cross-linked type III collagen was the major collagen type. Type III collagen was completely processed, since the amount of type III pN-collagen was negligible. The amounts of free type I and III procollagen propeptides in the soluble fraction were small, indicating a low rate of collagen turnover. The proportion of type III collagen was lower in abdominal aortic aneurysms than in atherosclerotic aortic control samples. Furthermore, the amount of type III pN-collagen was significantly increased in aneurysms. Type I and III collagens were also maturely cross-linked in colon diverticulosis, the only difference from normal colon tissue being the increased amount of the aminoterminal propeptide of type III procollagen in the soluble tissue extract, indicating a slightly increased metabolic activity of type III collagen. In malignant ovarian tumors, the cross-linking of type I and III collagens was defective. A similar trend was also seen for type I collagen in colon cancer. Even though procollagen synthesis was increased in these malignancies, the total collagen content and the amounts of cross-linked collagens were decreased. The amount of type III pN-collagen was increased in malignant ovarian tumors, whereas no such tendency was seen in colon cancer. These findings suggest a wide variety of changes in the metabolism of type I and III collagens in diseases. Defective processing and cross-link maturation of these collagen types might result in impaired fibril formation or increased susceptibility of collagens to proteolytic attack - both of them processes with a potential role in the pathogenesis of diseases.

The biosynthesis of purine nucleotides in Ehrlich ascites carcinoma cells was investigated under different conditions. In initial studies the effect of actinomycin D was examined. The nucleotides from the acid soluble fraction of Ehrlich ascites carcinoma cells incubated with actinomycin D and ¹⁴C-formate were adsorbed on charcoal and eluted with a mixture of pyridine and ethanol. The eluted nucleotides were separated by two dimensional paper chromatography using isobutyric acid-ammonia-water in the first direction and aqueaus ammonium acetate-ethanol in the second. .The nucleotides were estimated by ultra violet spectrophotometry and the radioactivity incorporated was determined by liquid scintillation counting. As the results of these studies using small amounts of cells were inconclusive due to variations from experiment to experiment, similar studies were carried out using larger amounts of cell suspensions. The acid soluble nucleotides from these experiments were separated by ion-exchange chromatography on DEAE-cellulose and finally by paper chromatography. It was observed that there was an accumulation of acid soluble nucleotides in Ehrlich ascites carcinoma cells incubated with ¹⁴C-formate and actinomycin D. The specific activities of these nucleotides were not significantly different from those of the control experiments. The incorporation of ¹⁴C-formate into nucleic acids was inhibited by actinomycin D in these cells. From these observations it was concluded that actinomycin D did not inhibit the biosynthesis of purine nucleotides in Ehrlich ascites carcinoma cells in vitro. It is suggested that the effect of actinomycin D on nucleic acid metabolism is therefore, at a stage beyond the synthesis of nucleotides. Further studies on the effect of actinomycin D revealed that the antibiotic inhibited the respiration of Ehrlich ascites carcinoma cells in vitro slightly. The glycolysis in Ehrlich ascites carcinoma cells was unaffected by actinomycin D. In experiments where the effect of glucose on the incorporation of radioactive precursors into nucleotides and nucleic acids of Ehrlich ascites carcinoma cells was examined, contrary to the results of many, a decrease in incorporation was observed. This decrease in incorporation was independent of the presence of Ca⁺⁺ ions in the incubation medium, the buffer and of the radioactive precursors used in these incubations. It was observed that there were two factors controlling the incorporation of radioactive precursors in. vitro into the nucleotides and nucleic acids of Ehrlich ascites carcinoma cells in presence of glucose; the concentration of glucose in the medium and the concentration of cells in suspension. In dilute cell suspensions (packed cell volume less than 5%) glucose at a concentration of 5.5 mM decreased whereas in dense cell suspensions (packed cell volume above 8%) the same concentration of glucose increased the incorporation of labelled precursors into both acid soluble nucleotides and nucleic acids. 2-Deoxyglucose, an analogue of glucose at a similar concentration decreased the incorporation of ¹⁴C-formate in dilute as well as in dense cell suspension. Dinitrophenol, an uncoupler of oxidateive phosphorylation, also decreased the incorporation of ¹⁴C-formate in these cells which was more marked in dilute cell suspensions in presence of glucose. It was concluded from these observations that the main factor controlling the incorporation in vitro of radioactive precursors into nucleotides and nucleic acids of Ehrlich ascites carcinoma cells was the transient depletion and regeneration of ATP in these cells in presence of glucose. Glucose increased the incorporation of ¹⁴C-formate into the serine of the acid soluble fraction of Ehrlich ascites carcinoma cells. A marked increase in the incorporation of ¹⁴C-formate into serine was observed in presence of 2-deoxyglucose. These effects were independent of the concentration of cells in suspension. It was suggested that when the availability of the common precursor, N⁵-N¹º methylenetetrahydrofolic acid was increased particularly due to a decrease in incorporation into nucleic acids, more of the labelled precursor may be incorporated into serine. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate

Orientador: Laura Sterian Ward / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-27T08:20:48Z (GMT). No. of bitstreams: 1 Marcello_MarjoryAlana_D.pdf: 3126956 bytes, checksum: ea75ec396afc3fdc6448f9bd6ee786dc (MD5) Previous issue date: 2015 / Resumo: A incidência da obesidade, bem como do câncer diferenciado de tireoide (CDT), tem aumentado exponencialmente em todo o mundo e existem sólidos indícios de que essas duas condições se associam. Diversos estudos demonstram que adipocinas como adiponectina, leptina e resistina e também a grelina podem ser o elo entre essas doenças. O objetivo deste trabalho foi de verificar os perfis antropométrico e molecular das adipocinas: adiponectina, leptina, resistina e grelina de pacientes com diversos tipos de nódulos tireoidianos e compará-los a indivíduos saudáveis, buscando encontrar o elo entre a obesidade e o CDT, além de identificar possíveis marcadores de diagnóstico, evolução e prognóstico para o CDT. Estudamos pacientes com CDT, pacientes com nódulos tireoidianos benignos e indivíduos controle saudáveis. Todos foram entrevistados quanto a seus hábitos alimentares e rotina, além de passarem por avaliação antropométrica completa. Para investigar o perfil molecular da adiponectina, leptina, resistina e grelina, investigamos as concentrações séricas dessas citocinas através da técnica de ELISA, genotipamos os pacientes para 21 SNPs nos genes que codificam as adipocinas e tambem seus receptores através da técnica Taqman SNP Genotyping, analisamos ainda, espécimes cirúrgicos dos pacientes quanto a produção de RNAm dessas adipocinas. Demonstramos que o excesso de peso aumenta o risco de desenvolvimento de CDT em quase 4 vezes e esse risco pode aumentar ainda mais com a ingesta excessiva de calorias, associada ao consumo excessivo de carboidratos e proteínas. As concentrações séricas das adipocinas podem ser excelentes marcadores de diagnostico entre nódulos tireoidianos malignos e benignos, sendo que a acurácia do teste utilizando a leptina e resistina chegou a 100%. A herança genetica dos polimorfismos rs7799039 em LEP, rs1137101 em LEPR e rs2232165 em GHSR aumentou o risco de desenvolvimento de CDT em 4, 11 e 22 duas vezes, respectivamente. Além disso, a herança de SNPs em LEP (rs7799039, rs2167270), ADIPOQ - rs12629945, ADIPOR1 ¿ rs2232853 e rs1342387, ADIPOR2 - rs1058322 e GHSR - rs2232165 alterou as concentrações séricas de leptina, adiponectina e grelina. Demonstramos, ainda, que embora a célula tireoidiana não seja a principal produtora de adipocinas, a adiponectina e seus receptores, o receptor da leptina, e a grelina e seu receptor são produzidos por células tumorais tireoidianas, uma vez que encontramos RNAm para todas essas citocinas nos tecidos analisados, sugerindo que essas adipocinas desempenham um papel importante nesses tecidos. Concluímos que indivíduos portadores de nódulos tireoidianos, especialmente os indivíduos portadores de CDT possuem um perfil antropométrico e molecular (em relação às adipocinas) diferenciado, sendo que aqueles que estão mais fora do peso considerado adequado estão mais suscetíveis ao desenvolvimento do CDT, assim como aqueles que apresentam alterações genéticas e/ou de expressão da adiponectina, leptina, resistina e grelina. Sugerimos que é possível traçar um perfil do individuo portador de CDT em relação a sua constituição física, seus hábitos alimentares e também o seu perfil molecular a adiponectina, leptina, resistina e grelina, que foram identificadas como boas candidatas a marcadores moleculares para o CDT, além de serem potenciais links entre a obesidade, inflamação e CDT / Abstract: The incidence of obesity and of differentiated thyroid cancer (DTC) has increased exponentially over the world and there are strong indications that these two conditions are combined. Several studies have shown that adipokines such as adiponectin, resistin, leptin and ghrelin may be the link between these diseases. The objective of this investigation was to study the molecular profile of adipokines: adiponectin, leptin, resistin and ghrelin and its relationship with the anthropometric features of patients with various types of thyroid nodules in order to investigate the link between obesity and neoplasms and identify possible markers of diagnosis, evolution and prognosis for DTC. A group of patients with DTC, patients with benign thyroid nodules and healthy control subjects were interviewed about their eating habits and routine, and went through a complete anthropometric assessment. The serum concentrations of adiponectin, leptin, resistin, and ghrelin were measured by ELISA. Patients were genotyped for 21 SNPs in genes encoding adipokines and their receptors using Taqman SNP Genotyping technique. In addition, surgical specimens were investigated for mRNA of these adipokines. We demonstrated that being overweight increases the risk of developing CDT almost 4 times and this risk may increase when there is excess intake of calories associated with excessive consumption of carbohydrates and proteins. Serum concentrations of adipokines were excellent markers of nodules malignancy diagnosis, with a 100% accuracy using leptin and resistin. The genetic inheritance of polymorphisms rs7799039 in LEP rs1137101 and rs2232165 in LEPR in GHSR increased the risk of developing CDT 4, 11 and 22 times, respectively. In addition, SNPs heritage in LEP (rs7799039, rs2167270), ADIPOQ - rs12629945, ADIPOR1 - rs2232853 and rs1342387, ADIPOR2 - rs1058322 and GHSR - rs2232165 altered sérum concentrations of leptin, adiponectin and ghrelin. Also, we showed that although the thyroid cell is not the main producer of adipokines, adiponectin, leptin, and ghrelin resitina are produced by thyroid câncer cells, findng mRNA for all cytokines in the tissues analyzed, suggesting that they play an important role in tumorigenesis or thyroid tumor proliferation. We conclude that individuals with thyroid nodules, especially individuals with DTC have diferente anthropometric and molecular adipokine profiles that increases the susceptibility to DTC as well as genetic changes and / or expression of adiponectin, leptin, resistin and ghrelin. We suggest that it is possible to draw a CDT carrier Individual profile for body constitution, eating habits and molecular profile of adiponectin, leptin, resistin and ghrelin may identify individuals at risk for DTC, and are a potential link between obesity, inflammation, and DTC / Doutorado / Clinica Medica / Doutora em Clínica Médica

Ovarian carcinoma is considered to be the most deadly of the gynaecological malignancies which in its earliest stages is usually asymptomatic. The unsatisfactory survival rates of patients on conventional chemotherapy regimens, necessitates vehicles capable of carrying cytotoxic agents directly to the malignant cells. This mode of targeted delivery allows for efficient tumour cell kill whilst sparing surrounding normal tissue and substantially reducing side-effects. This project examined the possible therapeutic role of a targetable sustained drug delivery system, albumin immunomicrospheres containing the chemotherapeutic agents, cisplatin and 5-fluorouracil, for the treatment of ovarian adenocarcinoma. A rodent cell line, as a model, has proved to be similar to its human counterpart and also has shown to be transplantable from one animal to another. Such a model could therefore be useful for performing experiments relating to drug delivery targetability and therapeutic trials, as well as survival studies, in cases of ovarian adenocarcinoma. In particular, this project examines the efficacy of the immunospecific microspheres containing the drugs in a highly concentrated form, administered intraperitoneally and targeted to an ovarian adenocarcinoma, in an attempt to enhance tumour cell kill whilst largely sparing surrounding normal tissue. It is widely recognized that the effectiveness of most chemotherapeutic drugs would be enhanced if they were to act selectively where they are needed. In order to achieve a therapeutically relevant dose in tumour cells, the amount of drug required usually proves also to be highly toxic to normal tissues. It was postulated that, to overcome the above, it may be feasible to develop a sustained immunospecific drug delivery system to optimize the action of cisplatin and 5-fluorouracil at the target site. With the attainment of the above, it was further postulated that higher doses of drugs could be delivered to the target area effecting higher tumour cell kill, that less normal tissue damage should occur and that toxic side effects of the drugs should be reduced. The rationale for selecting combination therapy of cisplatin and 5-fluorouracil is that, although it has been inferred that DNA intrastrand and interstrand cross-links produced by the cisplatin often repair, this repair can be blocked by 5-fluorouracil by inhibition of thymidylate synthetase, thus preventing DNA strand repair. Albumin immunomicrospheres are relatively innocuous in terms of toxicity, non-antigenic and are capable of accommodating chemotherapeutic agents in a non-specific fashion. We showed that they were capable of a 0. 94% entrapment of 5-fluorouracil and 1.23% cisplatin. Delivery of these drugs at a target site, and at these concentrations, should effect extensive cell kill. As the microspheres are chemically stable and can be manipulated to offload the entrapped drugs satisfactorily, in vitro drug release profiles were performed employing immunospecific microspheres directed towards its target cells. Slow degradation of the drug- containing albumin immunomicrospheres showed that 0.283 μg cisplatin/ml plasma and 0. 799 μg 5-fluorouracil/ml plasma could be made available at the target site over a 14-day period. These concentrations could be maintained over at least another 14 days and effect tumour cell kill satisfactorily. In order to assess the tumour cell kill, we performed clonogenic assays, cell survival growth curves, MTT cytotoxicity assays and assessed the induction of micronuclei in the tumour cells. The synergism between 5-fluorouracil and cisplatin showed a modulation of cisplatin cytotoxicity and total tumour cell kill was achieved at concentrations of 0.5 μg/ml 5-fluorouracil and 0.1 μg/ml cisplat in at the target site. The above-mentioned evidence of effective targeting of the drugs was then investigated in female Wistar rats with ovarian adenocarcinoma to assess comparative survival times when treated with free drugs or immunospecific albumin microspheres containing the drugs. Animals given a free drug dose of 5 mg/kg cisplatin and 20mg/kg 5-fluorouracil, followed by a repeat dose at the same concentrations 7 days later showed that only 14% of the animals survived a 90-day trial period. Animals given an intraperitoneal bolus dose of immunomicrospheres at a dose of 1 O mg/kg cisplatin and 40 mg/kg 5-fluorouracil showed that 60% of the animals survived the 90-day trial period. This data indicated to us that the survival probability of animals treated with drug-containing immunomicrospheres was substantially superior to other protocols employed in this study.

Hemangiomas are defined as soft tissue lesions in the maxillofacial or oral region. Hemangiomas of salivary glands constitute 30% of the non-epithelial tumors in major salivary glands. Benign tumors in salivary glands are located 85% in parotid gland and 13% in submandibular gland. We present a case of submandibular hemangioma in an infant patient that had some complications and a challenging diagnosis. A 3-month-old female patient presented a giant hemangioma located in the submandibular, preauricular and right malar region with purplish color that during hospitalization had a cardiorespiratory arrest as a severe complication of the disease. / Revisión por pares

Mutation of the p53 gene is the most common genetic alteration in human cancers. The mutant p53 protein is more stable than the wild type and can be detected by immunohistology. The objective of the current study was to evaluate the immunohistological detection of p53 protein in prostate cancer and its utility as a prognostic indicator. We used a monoclonal anti-p53 antibody and immunostained primary prostate adenocarcinomas (stages Al to Dl) from 109 patients with a mean follow-up of 3.8 years (range, 1.3 to 9.3 years). Immunoreactivity for p53 was seen in 23 cancers (21%). There were 12 instances of progression (14%) among the p53-negative cancers versus seven (30%) among the p53-positive group. Survival analysis using three univariate statistical tests showed that p53 reactivity (P < .03), Gleason score (P < .01), and stage (P < .05) had significant effects on time to progression of prostate cancer. Multivariate analyses showed that Gleason score was significant with all three tests; p53 reactivity was significant with the Wilcoxon test but only approached significance by the log rank and Cox tests. When the analyses included only patients with Gleason scores 2 to 7 (N = 94), univariate analyses showed that p53 reactivity was strongly related to progression of prostate cancer (P < .007). Stage also was significant (P < 0.04), but Gleason score was not. Multivariate analyses showed only p53 reactivity to be significant (P < .007). In conclusion, mutation of the p53 gene may be involved in prostate cancer carcinogenesis. p53 reactivity marks an aggressive subset of prostate cancer and appears to be an independent prognostic indicator that is particularly valuable among the low to intermediate grade cancers.

A research report submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in partial fulfilment of the requirements for the degree of Master of Medicine in Diagnostic Radiology Johannesburg, 2019 / INTRODUCTION Breast cancer is one of the leading causes of cancer deaths worldwide. Triple negative breast Cancer (TNBC) is an aggressive subtype, commonly described as presenting at a younger age, in women of African descent and in low socioeconomic groups. Commonly it demonstrates benign imaging features making diagnosis a challenge. Early detection and treatment is imperative. AIM To determine the common imaging features of TNBC in South Africa. METHOD A retrospective study was conducted at a tertiary institution in South Africa. the study population included all biopsy proven TNBC patients presenting between 01/01/2012 – 30/06/2016. All the initial mammograms were re-read by three independent radiologists using a data collection sheet. Illegible or incomplete reports were excluded from the study. RESULTS In our population, TNBC commonly presented in African women with an average age of 54.2 and range 25-95 years, with 47% being pre-menopausal. Typical mammographic features were an oval (27%) or irregular (27%) shaped mass with well circumscribed margins (33%). Our lesions were much larger than those reported in the literature (1). Global asymmetry and architectural distortion were commonly associated features. On ultrasound, the lesions were mostly irregularly shaped (56%) with spiculated borders (29%) and hypoechoic (80%) with axillary adenopathy (81%). CONCLUSION The majority of our patient population presented with a clinically palpable mass, that was larger and had more aggressive features than usually described in the literature. This can be attributed to delayed presentation, due to numerous factors. In order to improving the detection rate and reduce mortality, education and screening programs play a major role. / E.K. 2019

Wang Ya-ping. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 111-120). / CONTENT / ACKNOWLEDGMENT / ABSTRACT / Chapter Chapter 1. --- Introduction / Chapter Chapter 2. --- Review of relevant literature / Chapter 2.1 --- Mammary structure and embryology / Chapter 2.2 --- Pathology of breast cancer / Chapter 2.3 --- Risk factors in breast cancer / Chapter 2.4 --- Prognostic factors in breast cancer / Chapter 2.5 --- Treatment of breast cancer / Chapter 2.6 --- Breast cancer research by flow cytometry / Chapter 2.7 --- c-erbB-2 oncogene research in breast cancer / Chapter 2.8 --- Tables and figures of chapter2 / Chapter Chapter 3. --- Materials and methods / Chapter 3.1 --- Flow cytometry assay of breast cancer tissue / Chapter 3.1.1 --- Sample collection / Chapter 3.1.2 --- Sample preparation for flow cytometric assay / Chapter 3.1.3 --- DNA content assay by flow cytometry / Chapter 3.1.4 --- Solutions for flow cytometric analysis / Chapter 3.2 --- c-erbB-2 and EGF receptor protein detection by immunohistochemical methods / Chapter 3.2.1 --- Preparation of sections / Chapter 3.2.2 --- Methods of staining / Chapter 3.2.3 --- Methods of analysis / Chapter 3.2.4 --- Confirmation of expression of c-erbB-2 protein by immunoblotting method / Chapter 3.2.5 --- Solutions for immunohistochemical and immunoblotting methods / Chapter 3.3 --- Clinical data from 346 breast cancer patients and method of analysis / Chapter 3.4 --- Tables and figures of chapter3 / Chapter Chapter 4. --- Results / Chapter 4.1 --- Results of flow cytometric analysis / Chapter 4.1.1 --- Tumour characteristics of 94 breast cancer patients / Chapter 4.1.2 --- Survival analysis by results of flow cytometry / Chapter 4.2 --- Results of immunohistochemical assay of c-erbB-2 and EGFr / Chapter 4.2.1 --- C-erbB-2 and EGFr expression in breast cancer / Chapter 4.2.2 --- The distribution of c-erbB-2 and EGFr expression in breast cancer / Chapter 4.2.3 --- Analysis of clinical outcome by c-erbB-2 and EGFr expression / Chapter 4.3 --- Clinical data of 346 patients with breast cancer / Chapter 4.3.1 --- Patients' characteristics / Chapter 4.3.2 --- Analysis of clinical data and outcome / Chapter 4.3.3 --- Analysis of clinical outcome according to histopathological characteristics of breast tumour / Chapter 4.3.4 --- Types of operation and clinical outcome / Chapter 4.3.5 --- Postoperative adjuvant therapy and clinical outcome / Chapter 4.3.6 --- Results from statistical analysis by Cox-regression / Chapter 4.4 --- Tables figures of chapter4 / Chapter Chapter 5. --- Discussion and conclusion / Chapter 5.1 --- Flow cytometric analysis of paraffin-embedded breast cancer tissue / Chapter 5.1.1 --- Evaluation of DNA flow cytometric results / Chapter 5.1.2 --- Correlation between tumor DNA aneuploidy or cell subpopulation and clinical outcome / Chapter 5.1.3 --- Correlation between S-phase fraction of breast tumour and clinical outcome / Chapter 5.1.4 --- Observation of high proportion of DNA hypoaneuploidy in this study / Chapter 5.2 --- c-erbB-2 oncogene overexpression in breast cancer / Chapter 5.2.1 --- c-erbB-2 oncoprotein expression in other studies / Chapter 5.2.2 --- Correlation between c-erbB-2 oncoprotein expression status and breast cancer pathogenesis / Chapter 5.3 --- Evaluation of EGFr expression in breast cancer / Chapter 5.4 --- Analysis of clinical data / Chapter 5.4.1 --- Clinical characteristics of patients with breast cancer / Chapter 5.4.2 --- Clinical characteristics of breast cancer and clinical outcome / Chapter 5.4.3 --- Clinical outcome by types of postoperative treatment / Chapter 5.5 --- Prognostic factors / Chapter 5.5.1 --- Our observations in comparison to other studies / Chapter 5.5.2 --- Prognostic factors for clinical application / Chapter 5.6 --- Tables and figures of chapter5 / References:

Chan Chi-keung. / Thesis (M.Sc.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 93-107). / Abstracts in English and Chinese. / List of Tables --- p.ix / List of Figures --- p.x / Chapter 1. --- Literature Review --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Oncogenic anatomy of the prostate gland --- p.1 / Chapter 1.3 --- Characteristics of prostate cancer --- p.7 / Chapter 1.4 --- Incidences of prostate cancer --- p.8 / Chapter 1.5 --- Risk factors for prostate cancer --- p.14 / Chapter 1.5.1 --- Endogenous risk factors --- p.14 / Chapter (A) --- Age --- p.14 / Chapter (B) --- Race --- p.16 / Chapter (C) --- Family history --- p.21 / Chapter (D) --- Hormonal factors --- p.24 / Chapter (I) --- Androgen --- p.24 / Chapter (II) --- Vitamin D --- p.32 / Chapter 1.5.2 --- Exogenous risk factors --- p.41 / Chapter (A) --- Dietary factors --- p.41 / Chapter (B) --- Body Mass Index & physical condition --- p.44 / Chapter (C) --- Occupation --- p.46 / Chapter (D) --- Vasectomy --- p.47 / Chapter (E) --- Others --- p.48 / Chapter 2. --- Introduction to the project --- p.49 / Chapter 3. --- Objectives --- p.50 / Chapter 4. --- Materials and Methods --- p.51 / Chapter 4.1 --- Prostate cancer cases --- p.51 / Chapter 4.2 --- Controls --- p.52 / Chapter (A) --- Benign prostatic hyperplasia --- p.52 / Chapter (B) --- Population control --- p.52 / Chapter 4.3 --- DNA extraction --- p.53 / Chapter 4.4 --- Amplification of target DNA --- p.54 / Chapter 4.5 --- Allele typing --- p.55 / Chapter 4.6 --- Statistical analysis --- p.55 / Chapter 5. --- Results --- p.60 / Chapter 5.1 --- Optimization of DNA extraction --- p.60 / Chapter 5.2 --- Optimization of PCR condition --- p.61 / Chapter 5.3 --- Allele typing --- p.65 / Chapter 5.4 --- Characteristics of subjects samples --- p.68 / Chapter 5.4.1 --- Age of subjects and tumor grading --- p.68 / Chapter 5.4.2 --- Genotype typing --- p.69 / Chapter (A) --- Bsm genotype --- p.69 / Chapter (B) --- Fok genotype --- p.69 / Chapter 6. --- Discussions --- p.73 / Chapter 6.1 --- Technical issues --- p.73 / Chapter (A) --- DNA extraction --- p.73 / Chapter (B) --- Primer design --- p.76 / Chapter (C) --- Determination of the optimal PCR condition --- p.77 / Chapter (D) --- Restriction enzyme digestion --- p.82 / Chapter 6.2 --- Age distribution of prostate cancer patients --- p.83 / Chapter 6.3 --- Genotype frequency --- p.84 / Chapter 6.4 --- Histopathological samples of case and control --- p.87 / Chapter 6.5 --- Vitamin D receptor genotypes and prostate cancer --- p.89 / Chapter 7. --- Conclusions --- p.92 / Chapter 8. --- References --- p.93

by Cheung Yuk Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 95-111). / Abstracts in English and Chinese; questionnaires in Chinese. / Acknowledgements --- p.i-ii / 摘要 --- p.iii-iv / Abstract --- p.v-vi / Table of Contents --- p.vii-viii / List of Tables --- p.ix / List of Figures --- p.x / Chapter Chapter 1. --- Introduction --- p.1 / Chapter Chapter 2. --- Literature Review / Anxiety --- p.3 / Quality of Life --- p.8 / Quality of Life for Stoma Patients --- p.19 / Progressive Muscle Relaxation in Reducing Anxiety and Promoting Quality of Life --- p.24 / The Rationale of Using PMRT in Reducing Anxiety and Promoting Quality of Life --- p.35 / Summary of Literature Review --- p.38 / Chapter Chapter 3. --- Methods / Research Design --- p.40 / Aim and Objectives --- p.41 / Hypotheses --- p.42 / Operational Definitions --- p.43 / Ethical Consideration --- p.44 / Sample --- p.45 / Intervention --- p.47 / Instruments --- p.49 / Data Collection and Randomization --- p.54 / Pilot Study --- p.56 / Method of Data Analysis --- p.57 / Chapter Chapter 4. --- Results / Internal Consistency of the Instruments --- p.59 / Subjects' Characteristics --- p.60 / "Baseline Assessment of State-Anxiety, Trait-Anxiety, QoL-Colostomy and WHO-QoL Scores " --- p.64 / Effect of PMRT on the State-Anxiety and Quality of Life --- p.65 / The Frequency of Practicing PMRT --- p.71 / Chapter Chapter 5. --- Discussion and Conclusion / Discussion --- p.75 / Limitations --- p.84 / Recommendations and Implications for Future Studies --- p.88 / Conclusion --- p.93 / References --- p.95 / Appendixes / Chapter 1 . --- Letters of Ethical Approval / Chapter 2. --- Letter of Request for Access Aapproval / Chapter 3. --- Informed Consent / Chapter 4. --- Questionnaires / Chapter 5. --- Content Validity Index of Chinese Version of QoL-Colostomy