Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

MSc., Faculty of Science, University of the Witwatersrand, 2011 / Wild animals are captured for management, health, translocation and research purposes. Capture is an unnaturally stressful event, which may result in morbidity or mortality. An attributing cause of the morbidity and mortality is capture-induced hyperthermia; the larger the magnitude and the longer the duration of this captured-induced hyperthermia, the greater the likely risk to the animal. The most common practice currently used in the field to lower body temperature is to douse hyperthermic animals with water. However, the water used is often at ambient temperatures and its efficacy is not known. We investigated whether this method and alternative methods are effective at lowering the body temperature of hyperthermic animals. To achieve these aims we implanted 19 blesbok with miniature temperature-sensitive data loggers in their abdomens and into their subcutaneous layers (at the sites of the flank, groin, lower neck and upper neck). The loggers continuously recorded core body temperatures of the blesbok throughout the study period at an interval of six minutes. We successfully retrieved complete data sets from 12 blesbok. The animals were captured on six separate occasions using a technique which elicited hyperthermia. Five animals were cooled by dousing with water of different temperatures (4°C, 17°C, 28°C) and fanning after dousing with 28°C water, in random order. Seven animals were cooled by ice packs, spraying a fine mist spray, intravenous (IV) infusion of one litre of 4°C water and 28°C water-dousing. Through the use of our continuous logging of body temperature we established the normal body temperature of the blesbok, which displayed a regular 24 hour body temperature pattern. The average daily body temperature of the blesbok was 38.8°C ± 0.4°C, with a minimum body temperature of 37.9°C ± 0.1°C and a maximum body temperature of 39.4°C ± 0.1°C. The body temperature after capture was as high as 41°C-42°C, which was significantly higher than the normal body temperature (Student’s t-test, P < 0.05). The animals were cooled once they were immobilised and the start of cooling was denoted as time zero. In the control (no active cooling) intervention the body temperature decreased to only about 40°C. Dousing animals with water, irrespective of its temperature, resulted in significant cooling (P < 0.05) of the animals, as indicated by their minimum body temperature reached, change in body temperature and rate of cooling. The water-dousing interventions decreased the body temperature to about 38°C after an hour, which was significantly lower than the control (RM-ANOVA, P < 0.05) but there was no significant difference in the minimum body temperature reached between the different water temperatures or by the addition of fanning (RM-ANOVA, P > 0.05). The water-dousing interventions cooled the animals more quickly than did the control (RM-ANOVA, P < 0.05), and the coldest water (4°) cooled the animals quicker than did the 28°C water-dousing (RM-ANOVA, P < 0.05). The core body temperature minus the subcutaneous temperature was calculated, and revealed a peak difference of about 3.5°C after the 4°C water-dousing. Ice-packs also resulted in significant cooling (P < 0.05) of the animals, as depicted by their minimum body temperature reached, change in body temperature and rate of cooling. The ice-packs lowered the body temperature to a minimum of about 38°C, which was significantly lower than the control (RM-ANOVA, P < 0.05). The ice-packs also cooled the animals significantly faster than did the control, intravenous infusion and mist spray (RM-ANOVA, P < 0.05) but cooled as quickly as the 28°C water-dousing (RM-ANOVA, P > 0.05). The core body temperature minus the subcutaneous temperature for the ice-packs peaked at a difference of about 3°C. The IV infusion and mist spray were ineffective cooling methods and did not significantly (P > 0.05) alter the minimum body temperature or rate of cooling. Even though the IV infusion caused a significant reduction in body temperature by 1°C, the cooling effect from the IV infusion was short-lived because the minimum body temperature reached after the intravenous infusion and mist spray was ultimately similar to the body temperature seen in animals receiving the control (RM-ANOVA P > 0.05). Also, the intravenous infusion and mist-spray cooled as slowly as did the control (RM-ANOVA P > 0.05). Therefore, water-dousing in this study was the most effective and practical method to cool hyperthermic blesbok. Although all the water temperatures (4°C, 17°C and 28°C) that we tested were effective, the coldest water (4°C) cooled the animals quickest. The addition of fanning to the 28°C water-dousing did not increase cooling. Ice-packs were also effective but may be not as easy to use as the water-dousing method as ice-packs are large and need to be kept frozen, and therefore are cumbersome for use in the field.

by Lui Chi Pang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 265-281). / Acknowledgements --- p.i / Abbreviations --- p.ii / Abstract --- p.iii / Table of contents --- p.vii / Introduction / Review of Literature --- p.2 / Chapter I. --- Cellular response of hyperthermia --- p.3 / Chapter A) --- Effects on macromolecules synthesis --- p.3 / Chapter B) --- Effects on glycolysis and respiration --- p.5 / Chapter C) --- "Effects on plasma membrane, intracellular ionic level and intracellular pH" --- p.6 / Chapter II. --- Physical aspects --- p.11 / Chapter A) --- Survival curves --- p.11 / Chapter B) --- Concept of thermal dose --- p.13 / Chapter III. --- Clinical thermal theraphy --- p.21 / Chapter A) --- Hyperthermia in vivo --- p.21 / Chapter B) --- Combination of hyperthermia and radiotheraphy --- p.29 / Chapter C) --- Combination of hyperthermia and chemotherapy --- p.37 / Chapter IV. --- Thermotolerance --- p.48 / Scope of study --- p.54 / Materials and Methods / Chapter I. --- Cytotoxicity tests of cells in vitro --- p.59 / Chapter II. --- Whole body hyperthermia on Ehrlich ascite tumour (EAT)-bearing mice --- p.63 / Chapter III. --- Combination of hyperthermia and drugs --- p.66 / Chapter IV. --- Measurement of intracellular pH --- p.68 / Chapter V. --- Assay for sialic acids in the plasma membrane --- p.72 / Chapter VI. --- Assays of nucleolar proteins --- p.76 / Chapter VII. --- Acetylation of nuclear proteins --- p.80 / Chapter VIII. --- Detection of 72-kD heat shock protein --- p.93 / Results and Discussion / Chapter I. --- Cytotoxicity of hyperthermia in vitro --- p.102 / Chapter II. --- Hyperthermia on EAT cells in vivo --- p.131 / Chapter III. --- Cytotoxicity of combination of hyperthermia and drugs --- p.148 / Chapter IV. --- Intracellular pH changes during hyperthermia --- p.162 / Chapter V. --- Modification of sialic acid level in plasma membrane --- p.180 / Chapter VI. --- Conformational changes of nucleolar proteins --- p.193 / Chapter VII. --- Hyperthermic effect on acetylation of nuclear proteins --- p.209 / Chapter VIII. --- Induction of 72-kD heat shock protein --- p.223 / General Discussion / Chapter A. --- Hyperthermic cytotoxicity --- p.249 / Chapter B. --- Effects on plasma membrane and control of intracellular pH --- p.253 / Chapter C. --- Effects on the nuclear proteins --- p.256 / Chapter D. --- Conclusion --- p.263 / Bibliography --- p.264

Thesis (M.S.)--University of Toledo, 2008. / "In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 153-155.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1939. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 100-109).

Thesis--Lund Institute of Technology, 1994.

Thesis--Lund Institute of Technology, 1994.

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 Li Jian Yi. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 157-181). / 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.