Diss. (sammanfattning) Stockholm : Karolinska institutet, 2001. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 5 uppsatser.

The frequency of chromosome breaks was increased in replicate cultures from each of ten individuals when lysergic acid diethylamide at a concentration of 1 ug/ml of culture was added 24 hours prior to the harvest of the cells. The differences between the control and treated cultures ranged from +3.00 to +7.93 with a mean of +4.63, indicating no variation in response between individuals. The breaks were randomly distributed among the seven groups of chromosomes of the complement. No significant difference in either the number of cells with aberrations, or the number of breakage events was observed between cells cultured from a patient with Fanconi's anaemia before and 24 hours after treatment with 250 ug. of growth hormone. Both were significantly increased over the control. After treatment with growth hormone, the number of breaks per aberrant cell was decreased, and the distribution of frequencies of specific types of aberrations was changed. Non-homologous exchange figures were the only two break events observed in cultures from the patient. None were observed in control cells. The distribution of breaks among the seven groups of chromosomes was random. The frequency of chromosome aberrations was increased in cultures from a single individual when treated with 1 ug/ml of mitomycin-C for one hour at the beginning of the culture period. In the treated cultures, 181 breaks were observed in 64 of the 100 cells examined, whereas only 5 breaks were observed in three of the 100 cells scored in the control samples. Forty-seven exchange configurations were observed in the treated cultures, 42.56% of these being non-homologous exchanges. No marker or dicentric chromosomes were observed. Breaks were randomly distributed among the seven groups of chromosomes of the complement. / Medicine, Faculty of / Medical Genetics, Department of / Graduate

The aim of the study was to investigate whether non-thermal levels of radiofrequency (RF) fields, characteristic of some mobile phones, might be directly genotoxic when applied in vitro to unstimulated G0 or stimulated human lymphocytes. Also, the study aimed to investigate the possibility that RF fields might act epipigenetically when combined with x-rays, by modifying their effect when applied in vitro to G0 lymphocytes. In addition, the possibility of RF fields inducing apoptosis in murine neuroblastoma (N2a) cells was also examined. G0 lymphocytes from 4 donors were exposed for a total of 24 h to a continuous or an intermittent RF signal. The signals were 935 MHz GSM (Global System for Mobile Communication) Basic, 1800 MHz GSM Basic, 935 MHz continuous wave (CW) carrier frequency, and 935 MHz GSM Talk. Stimulated lymphocytes were exposed for a total of 48 h to intermittent 1800 MHz RF signals that were GSM Basic or the carrier frequency only. The RF fields used for the 24 h exposure of N2a cells were all at 935 MHz and consisted of GSM Basic, GSM Talk and a CW signal. The chosen Specific energy Absorption values of the signals were either 1 or 2 W/kg. These values are near the upper limit of actual energy absorbed in localised tissue by a person from some mobile phones. The field was applied to G0 human lymphocytes either alone or combined with an exposure to 1 Gy x-rays given immediately before or after the RF field. A dose of 4 Gy x-rays was used as a positive control for apoptosis induction in N2a cells and in the study with stimulated lymphocytes no x-rays were used. The lymphocytes were assayed by several standard methods to demonstrate genotoxicity. Unstable chromosome aberrations (stimulated lymphocytes and those exposed in G0), sister chromatid exchanges (SCE) and cytokinesis blocked micronuclei (MN) (lymphocytes exposed in G0). In addition the SCE and MN assays allowed nuclear division indices (NDI) to be calculated as NDI defines the cell cycle progression of lymphocytes after PHA stimulation and how this might be affected by RF exposure. N2a cells were assessed by fluorescence microscopy for levels of apoptosis at a number of time points post RF field or x-ray exposure, between 0 and 48 h. Three independent assays that detect different stages of the apoptotic pathway were used, the Annexin V binding, caspase activation and in situ end labelling. By comparison with appropriate sham exposed samples no effect of RF fields alone could be found in G0 or PHA stimulated lymphocytes exposed in vitro. Also, RF fields did not modify any measured effects of x-rays either given before or after RF exposure. No statistically significant difference in apoptosis levels were observed between RF exposed and sham exposed N2a cells in either a proliferating or differentiated state for any assay at any time point post exposure.

by Jenney Yin-mei Tse. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 122-146). / 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.

Bik-Yu Hui. / "July 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 187-203). / 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.

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by Wang Wei. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references (leaves 154-168). / ACKNOWLEDGMENTS --- p.v / SUMMARY --- p.vi / PUBLICATIONS --- p.viii / STATEMENT OF ORIGINALITY --- p.ix / LIST OF ABBREVIATIONS --- p.x / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.5 / Chapter 2.1 --- Chromosome --- p.6 / Chapter 2.2 --- Chromosome and Human Disease --- p.9 / Chapter 2.3 --- Chromosome and Tumour --- p.12 / Chapter 2.4 --- Chromosome in Gynaecologic Tumours --- p.17 / Chapter 2.4.1 --- Cervical tumour --- p.17 / Chapter 2.4.2 --- Uterine corpus tumour --- p.20 / Chapter 2.4.3 --- Ovarian tumour --- p.23 / Chapter 2.5 --- Methodology in cytogenetics --- p.26 / Chapter 2.5.1 --- Materials --- p.27 / Chapter 2.5.2 --- Methods of chromosome preparation --- p.28 / Chapter 2.5.3 --- Karyotype analysis --- p.34 / Chapter 2.6 --- Problems of cytogenetic analysis in solid tumour --- p.42 / Chapter CHAPTER 3 --- MATERIALS AND METHODS --- p.47 / Chapter 3.1 --- Chemicals and Solutions --- p.48 / Chapter 3.2 --- Chromosome preparation from solid gynaecologic tumours --- p.50 / Chapter 3.2.1 --- Solid tumour specimens --- p.50 / Chapter 3.2.2 --- Chromosome preparation --- p.54 / Chapter 3.3 --- Chromosome preparation from an established ovarian carcinoma cell line --- p.61 / Chapter 3.3.1 --- Origin of OCC1 cell line --- p.61 / Chapter 3.3.2 --- Characteristics of OCC1 cell line --- p.61 / Chapter 3.3.3 --- Maintaining of OCC1 cell line --- p.62 / Chapter 3.3.4 --- Chromosome preparation --- p.62 / Chapter 3.4 --- Karyotype analysis --- p.65 / Chapter CHAPTER 4 --- RESULTS --- p.66 / Chapter 4.1 --- Cytogenetic features of gynaecologic solid tumour --- p.67 / Chapter 4.1.1 --- Cervical cancer --- p.67 / Chapter 4.1.2 --- Uterine corpus cancer --- p.94 / Chapter 4.1.3 --- Ovarian cancer --- p.104 / Chapter 4.2 --- Cytogenetic features of OCC1 ovarian carcinoma cell line --- p.114 / Chapter CHAPTER 5 --- DISCUSSION --- p.123 / Chapter 5.1 --- Methodology of chromosome preparation in solid tumour --- p.124 / Chapter 5.2 --- Chromosome changes in gynaecologic solid tumour --- p.126 / Chapter 5.2.1 --- Cervical cancer --- p.126 / Chapter 5.2.2 --- Uterine corpus cancer --- p.132 / Chapter 5.2.3 --- Ovarian cancer --- p.138 / Chapter 5.2.4 --- In summary --- p.141 / Chapter 5.3 --- Chromosome changes in an OCC1 ovarian carcinoma cell line --- p.143 / Chapter CHAPTER 6 --- CONCLUSION --- p.148 / REFERENCES --- p.154

Thesis--Copenhagen. / Summary in Danish. Bibliography: p. [88]-97.

Thesis--Copenhagen. / Summary in Danish. Bibliography: p. [88]-97.