by Lam Kai Yi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 156-165). / Abstract also in Chinese. / Chapter Chapter One: --- Introduction --- p.1 / Chapter 1.1 --- Tumor Necrosis Factor-α in Cancer Treatment --- p.1 / Chapter 1.1.1 --- Historical Background --- p.1 / Chapter 1.1.2 --- Mechanisms of Action --- p.2 / Chapter 1.1.2.1 --- Production of Reactive oxidative Species / Chapter 1.1.2.2 --- Increase of Intracellular Free Calcium Concentration / Chapter 1.1.2.3 --- Activation of Ca2+/Mg2+-dependent Endonuclease / Chapter 1.1.2.4 --- Decrease of glucose uptake and Protein Synthesis / Chapter 1.1.2.5 --- Formation of Ion-permeable Channel / Chapter 1.1.2.6 --- Activation of Phospholipase / Chapter 1.1.2.7 --- Increase of S-phase Cells / Chapter 1.1.2.8 --- Immunomodulatory Effects / Chapter 1.1.3 --- Resistance of Cells to TNF-α --- p.7 / Chapter 1.1.4 --- Clinical Studies --- p.11 / Chapter 1.1.5 --- Side Effects --- p.12 / Chapter 1.2 --- Hyperthermia and Cancer Treatment --- p.14 / Chapter 1.2.1 --- Hyperthermic Agents --- p.15 / Chapter 1.2.2 --- Intrinsic Heat Sensitivity --- p.15 / Chapter 1.2.3 --- Mechanisms of Action --- p.17 / Chapter 1.2.3.1 --- Depolarization of Membrane Potential / Chapter 1.2.3.2 --- "Reduction of glucose transport and DNA, mRNA and Protein Synthesis" / Chapter 1.2.3.3 --- Decrease of Intracellular pH / Chapter 1.2.3.4 --- Calcium Imbalance / Chapter 1.2.3.5 --- Effect on Nucleolar Protein / Chapter 1.2.3.6 --- Apoptosis / Chapter 1.2.3.7 --- Induction of Autologous Tumor Killing / Chapter 1.2.3.8 --- "Blood Flow, Tumor Oxygenation and Vascular Damage" / Chapter 1.2.4 --- Clinical Studies --- p.20 / Chapter 1.3 --- Combined Treatment --- p.21 / Chapter 1.3.1 --- Combined Treatment with TNF-α and Fixed-temperature Hyperthermia --- p.22 / Chapter 1.3.2 --- Combined Treatment with TNF + Step-down Hyperthermia --- p.22 / Chapter 1.3.3 --- In Vivo Study --- p.23 / Chapter 1.3.4 --- Sequence of Treatment --- p.24 / Chapter 1.3.5 --- Proposed Mechanism of Synergism --- p.24 / Chapter 1.4 --- Objective of Study --- p.26 / Chapter 1.4.1 --- Sequence of Treatments --- p.26 / Chapter 1.4.2 --- Comparison of Treatments' Effectiveness --- p.27 / Chapter 1.4.3 --- Effect on Normal Cell --- p.27 / Chapter 1.4.4 --- Effect on Distribution of Cells in Cell Cycle Phases --- p.28 / Chapter 1.4.5 --- In Vivo Study --- p.28 / Chapter Chapter Two: --- Materials and Methods --- p.30 / Chapter 2.1. --- Materials --- p.30 / Chapter 2.1.1 --- For Cell Culture --- p.30 / Chapter 2.1.2 --- In vitro Treatments --- p.31 / Chapter 2.1.3 --- DNA Electrophoresis --- p.31 / Chapter 2.1.4 --- Flow Cytometry --- p.32 / Chapter 2.2. --- Reagent Preparation --- p.33 / Chapter 2.2.1 --- Culture Media --- p.33 / Chapter 2.2.2 --- Human Recombinant Tumor Necrosis Factor alpha (rhTNF-α) --- p.33 / Chapter 2.2.3 --- Phosphate Buffered Saline (PBS) --- p.33 / Chapter 2.2.4 --- Lysis Buffer --- p.34 / Chapter 2.2.5 --- TE Buffer --- p.34 / Chapter 2.2.6 --- Proteinase K and Ribonuclease A (RNase A) --- p.34 / Chapter 2.2.7 --- 100 Base-Pair DNA Marker --- p.34 / Chapter 2.2.8 --- Propidium Iodide (PI) --- p.35 / Chapter 2.3 --- Methods --- p.35 / Chapter 2.3.1 --- Cell Culture --- p.35 / Chapter 2.3.1.1 --- Ehrlich Ascitic Tumor (EAT) and Human Leukemia (HL-60) / Chapter 2.3.1.2 --- Human Coronary Artery Endothelial Cells (HCAEC) / Chapter 2.3.2 --- In vitro Experiments --- p.36 / Chapter 2.3.3 --- Tumor Necrosis Factor Treatment --- p.37 / Chapter 2.3.4 --- Hyperthermia Treatments --- p.37 / Chapter 2.3.5 --- Cell Counting --- p.38 / Chapter 2.3.5.1 --- Trypan Blue Exclusion Assay / Chapter 2.3.5.2 --- Neutral Red Assay / Chapter 2.3.6 --- Determination of Additive or Synergistic Effect --- p.39 / Chapter 2.3.7 --- DNA Electrophoresis --- p.40 / Chapter 2.3.8 --- Flow Cytometry --- p.42 / Chapter 2.3.7.1 --- Preparation of Samples / Chapter 2.3.7.2 --- Flow Cytometry Acquisition / Chapter 2.3.7.3 --- Analysis / Chapter 2.3.9 --- In vivo Experiments --- p.44 / Chapter 2.3.8.1 --- Animal Strain / Chapter 2.3.8.2 --- Cell Line / Chapter 2.3.8.3 --- Tumor Necrosis Factor Treatment / Chapter 2.3.8.4 --- Hyperthermia Treatments / Chapter 2.3.8.5 --- Test of Body Temperature / Chapter 2.3.8.6 --- Cell Harvesting / Chapter Chapter Three: --- Result --- p.50 / Chapter 3.1 --- Optimal Sequence of Treatments --- p.50 / Chapter 3.1.1 --- Optimal Sequence of Treatments on Murine Ehrlich Ascitic Tumor (EAT) cells --- p.50 / Chapter 3.1.1.1 --- TNF + Fixed-temperature Hyperthermia / Chapter 3.1.1.2 --- TNF + Step-down Hyperthermia2 / Chapter 3.1.1.3 --- TNF + Step-down Hyperthermia3 / Chapter 3.1.2 --- Optimal Sequence of Treatments on Human Leukemia cells HL-60 --- p.60 / Chapter 3.1.2.1 --- TNF + Fixed-temperature Hyperthermia / Chapter 3.1.2.2 --- TNF + Step-Down Hyperthermia2 / Chapter 3.1.2.3 --- TNF + Step-Down Hyperthermia3 / Chapter 3.2 --- Comparison of Effectiveness of Treatments --- p.72 / Chapter 3.2.1 --- Effectiveness of Various treatments on EAT cells --- p.72 / Chapter 3.2.2 --- Synergistic Effect between rhTNF-α and Hyperthermia on EAT cells --- p.74 / Chapter 3.2.3 --- Decrease of Relative Growth and Viability of EAT with Time --- p.79 / Chapter 3.2.3.1 --- TNF + Fixed-temperature Hyperthermia / Chapter 3.2.3.2 --- TNF + Step-down Hyperthermia2 / Chapter 3.2.3.3 --- TNF + Step-down Hyperthermia3 / Chapter 3.2.4 --- Comparison of Effectiveness of Various Treatments on HL-60 cells --- p.82 / Chapter 3.2.5 --- Synergistic Effect between rhTNF-α and Hyperthermia on HL-60 cells --- p.87 / Chapter 3.2.6 --- Change of Relative Growth and Viability of HL-60 with Time --- p.90 / Chapter 3.2.6.1 --- TNF + Fixed-temperature Hyperthermia / Chapter 3.2.6.2 --- TNF + Step-down Hyperthermia2 / Chapter 3.2.6.3 --- TNF + Step-down hyperthermia3 / Chapter 3.3 --- Cell Death Pathway --- p.96 / Chapter 3.3.1 --- Experiments on Ehrlich Ascitic Tumor (EAT) Cells --- p.96 / Chapter 3.3.2 --- Experiments on Human Leukemia (HL-60) Cells --- p.100 / Chapter 3.4 --- Experiment on Normal Cell --- p.104 / Chapter 3.5 --- Effect of TNF + Fixed-temperature Hyperthermia on the Cell Cycle Progression --- p.107 / Chapter 3.5.1 --- Different Times of TNF Administration and Distribution of EAT cells in Cell cycle --- p.107 / Chapter 3.5.2 --- Different Times of TNF Administration and Distribution of HL-60 cells in Cell Cycle --- p.114 / Chapter 3.5.3 --- Shift of Cells Cycle after TNF Treatment --- p.120 / Chapter 3.5.3.1 --- Response of Ehrlich Ascitic Tumor Cells / Chapter 3.5.3.2 --- Response of Human leukemia Cells / Chapter 3.6 --- Effectiveness of Treatments in vivo: --- p.129 / Chapter 3.6.1 --- Dose-dependent Response --- p.129 / Chapter 3.6.2 --- Change of Body Temperature During Hyperthermia --- p.131 / Chapter 3.6.3 --- Comparison of Effectiveness of Various Treatments in vivo --- p.133 / Chapter 3.6.4 --- Synergistic Effect Between rhTNF-α and Hyperthermia in vivo --- p.135 / Chapter Chapter Four: --- Discussion --- p.138 / Chapter 4.1 --- Optimal Sequence of Treatments --- p.139 / Chapter 4.2 --- Comparison of Various Treatments --- p.143 / Chapter 4.3 --- Distribution of Cells in Cell Cycle Phases --- p.149 / Chapter 4.4 --- In vivo Study --- p.153 / Chapter Chapter Five: --- References --- p.156

by Cheung Tak Chi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 117-123). / Abstract also in Chinese. / Acknowledgeements --- p.i / Abbreviations --- p.ii / Abstract --- p.v / List of Figures --- p.viii / List of Tables --- p.xiv / Contents --- p.xv / Contents / Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Epidemiological Risk Factors --- p.1 / Chapter 1.1.1 --- Age --- p.1 / Chapter 1.1.2 --- Race --- p.2 / Chapter 1.1.3 --- Environmental or Migratory Factor --- p.2 / Chapter 1.1.4 --- Diet --- p.2 / Chapter 1.1.5 --- Genetics --- p.3 / Chapter 1.2 --- Regulation of Normal Prostate Development and Function --- p.4 / Chapter 1.3 --- Biochemistry and Development of Prostate Cancer --- p.6 / Chapter 1.3.1 --- Androgen-Dependent Prostate Cancer --- p.6 / Chapter 1.3.2 --- Androgen-Independent Prostate Cancer --- p.8 / Chapter 1.4 --- Classification of Prostate Cancer --- p.9 / Chapter 1.4.1 --- Stage A Prostate Cancer --- p.10 / Chapter 1.4.2 --- Stage B Prostate Cancer --- p.10 / Chapter 1.4.3 --- Stage C Prostate Cancer --- p.11 / Chapter 1.4.4 --- Stage D Prostate Cancer --- p.11 / Chapter 1.5 --- Methods for Early Detection of Prostate Cancer --- p.12 / Chapter 1.6 --- Clinical Treatment of Prostate Cancer --- p.12 / Chapter 1.6.1 --- Surgery --- p.12 / Chapter 1.6.2 --- Radiotherapy --- p.13 / Chapter 1.6.3 --- Chemotherapy --- p.13 / Chapter 1.6.4 --- Hormonal Therapy --- p.13 / Chapter 1.7 --- Objective --- p.14 / Chapter 1.8 --- Estrogen and Its Related Compounds --- p.16 / Chapter 1.8.1 --- 17β-Estradiol --- p.16 / Chapter 1.8.2 --- Tamoxifen --- p.18 / Chapter 1.8.3 --- Aromatase Inhibitor --- p.20 / Chapter 1.9 --- Anticancer Drugs --- p.23 / Chapter 1.9.1 --- Doxorubicin --- p.23 / Chapter 1.9.2 --- cis-Platinum --- p.24 / Chapter 1.10 --- Apoptotic Pathways --- p.25 / Chapter 1.10.1 --- BCL-2 /BAD Pathway --- p.26 / Chapter 1.10.2 --- FADD Pathway --- p.27 / Chapter 1.10.3 --- CAS Pathway --- p.27 / Chapter 2. --- Materials and Methods --- p.28 / Chapter 2.1 --- Materials --- p.28 / Chapter 2.2 --- Cell Lines --- p.32 / Chapter 2.3 --- Preparation of Drugs --- p.32 / Chapter 2.4 --- Drug Sensitivity Assay --- p.33 / Chapter 2.5 --- Cell Cycle Analysis --- p.35 / Chapter 2.6 --- DNA Fragmentation Assay --- p.36 / Chapter 2.7 --- Annexin Binding Assay --- p.37 / Chapter 2.8 --- Western Blot Analysis --- p.38 / Chapter 2.9 --- Data Analysis --- p.41 / Chapter 3. --- Results --- p.42 / Chapter 3.1 --- Response of Human Androgen-Independent Prostate Cancer Cells to Doxorubicin and cis-Platinum --- p.42 / Chapter 3.2 --- The Effect of 17p-Estradiol on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.45 / Chapter 3.2.1 --- 17β-Estradiol on Cell Growth --- p.45 / Chapter 3.2.2 --- 17β-Estradiol on Anticancer Drug Sensitivity --- p.45 / Chapter 3.2.3 --- 17β-Estradiol and Doxorubicin on Cell Cycle Progression --- p.51 / Chapter 3.2.4 --- 17β-Estradiol and Doxorubicin Induced DNA Fragmentation --- p.57 / Chapter 3.2.5 --- 17β-Estradiol and Doxorubicin on Annexin Staining --- p.59 / Chapter 3.2.6 --- 17β-Estradiol and Doxorubicin on Apoptotic Protein Expression --- p.62 / Chapter 3.3 --- The Effect of Tamoxifen on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.64 / Chapter 3.3.1 --- Tamoxifen on Cell Growth of Human --- p.65 / Chapter 3.3.2 --- Tamoxifen on Anticancer Drug Sensitivity --- p.65 / Chapter 3.3.3 --- Tamoxifen and Doxorubicin on Cell Cycle Progression --- p.71 / Chapter 3.3.4 --- Tamoxifen and Doxorubicin Induced DNA Fragmentation --- p.76 / Chapter 3.3.5 --- Tamoxifen and Doxorubicin on Annexin Staining --- p.78 / Chapter 3.3.6 --- Tamoxifen and Doxorubicin on Apoptotic Protein Expression --- p.79 / Chapter 3.4 --- The Effect of Aromatase Inhibtiors on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.81 / Chapter 3.4.1 --- Aromatase Inhibitors on Cell Growth --- p.81 / Chapter 3.4.2 --- Aromatase Inhibitors on Anticancer Drug Sensitivity --- p.83 / Chapter 3.4.3 --- 4-AcA and Doxorubicin on Cell Cycle Progression --- p.93 / Chapter 3.4.4 --- 4-AcA and Doxorubicin Induced DNA Fragmentation --- p.99 / Chapter 3.4.5 --- 4-AcA and Doxorubicin on Annexin Staining --- p.100 / Chapter 3.4.6 --- 4-AcA and Doxorubicin on Apoptotic Protein Expression --- p.102 / Chapter 4. --- Discussion --- p.105 / Chapter 4.1 --- 17 β-Estradiol and Anticancer Drug Sensitivity --- p.106 / Chapter 4.2 --- Tamoxifen and Anticancer Drug Sensitivity --- p.109 / Chapter 4.3 --- Aromatase Inhibitors and Anticancer Drug Sensitivity --- p.112 / Chapter 4.4 --- DU145 Cells vs PC3 Cells --- p.115 / Chapter 5. --- Conclusion and Perspectives --- p.116 / Chapter 6. --- References --- p.117

Thesis--University of Oklahoma. / Includes bibliographical references (leaves 51-55).

Radiobiological irradiation can be performed using appropriately collimated sealed source radioisotope machines such as Co-60 units, as well with X-ray tubes and linear accelerators. The increasing research interest in delivering organ-specific or whole body animal external irradiation has led to the introduction of dedicated X-ray units for research purposes. In this work, the proprieties of a kilovoltage X-ray biological irradiator, the Faxitron cabinet X-ray system model CP160, are investigated and dosimetrically characterized. Calculation formalisms for everyday use of the radiobiological irradiator in laboratory conditions, specifically for cell cultures and small animals total body irradiation, were developed following the AAPM TG-61 protocol. The quality of the X-ray beams generated by this irradiator was found to range between HVL 0.7 mm Cu for a 160 kVp 0.5 mm Cu filtered beam, and HVL 0.07 mm Al for a 20 kVp non-filtered beam. Our calculation formalisms for cell cultures and small animal irradiations were found to be valid within +/-5%.

Thesis (Ph.D. in Immunology) -- University of Colorado at Denver and Health Sciences Center, 2006. / Typescript. Includes bibliographical references (leaves 129-141). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

Diss. (sammanfattning) Linköping : Univ., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2002. / Härtill 5 uppsatser.

Thesis (Ph.D. in Cell Biology, Stem Cells, and Development) -- University of Colorado Denver, 2008. / Typescript. Includes bibliographical references (leaves 102-114). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

Thesis (Ph. D.)--University of Oklahoma. / Bibliography: leaves 234-253.

Thesis (M.S.)--University of Michigan, 1968.