Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Anaerobic threshold speed (VTAM) was determined for 20 male university students using a continuous treadmill protocol. The onset of anaerobiosis was determined by analyzing excess CO₂ elimination. The following week, all subjects ran at the VTAM median speed of 7.25 miles per hour for 10 minutes. Recovery oxygen consumption was monitored after this run. Application of double exponential equations by computer and subsequent integration, calculated Total, Alactic, and Lactic Oxygen Debts. Subjects who ran above their VTAM (group L-VTAM) had significantly (p < .05) higher total, lactic and alactic debts than those subjects who ran below their VTAM (group H-VTAM). The total debt showed a significant (p < .05) negative correlation (r=-.77) to in; group L-VTAM. This appears to be due to the increasing lactic debt, that was also significantly (p < .05) negatively correlated (r=-.73) to VTAM. Group H-VTAM did not exhibit this characteristic. This study demonstrates that VTAM is a critical factor in determining oxygen debt and therefore, work above this point results in the onset of metabolic acidosis, which may limit the optimal running speed for a given distance. / Education, Faculty of / Kinesiology, School of / Graduate

An investigation of the concentration of the heavy isotope of oxygen, O18, in various samples of water was carried out. Natural variations as high as 2.9% were found - glacier water being 2.3% light and Dead Sea water 2.0% heavy, as compared to Lake Ontario water as standard. Other values - water from tank oxygen + 2.9%, atmospheric water vapor -0.9%, Atlantic Ocean water +0.4%, Pacific Ocean water - 0.8% , and atmospheric carbon dioxide - 0.5%. The water samples were equilibrated with tank carbon dioxide, which was then analyzed using the mass spectrometer. Some work was also done on photosynthesis. The free water, water of crystallization, and tissue oxygen (as water) , in a normal leaf which had bean photosynthesizing for 8 hours, were analyzed by equilibration with carbon dioxide as above. It was found that all of these were more enriched in oxygen 18 than the water with which they were fed . The free water averaged about 1.3% heavy, water of crystallization as high as 8.7% heavy, and tissue oxygen varied from 0.5% light to 5.5% heavy. This work only just touches the edges of this field - many more interesting experiments remain to be carried out later. / Thesis / Master of Science (MS)

Thesis (M.S.)--University of Michigan, 1981.

Ge, Tianfang. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 87-93). / Abstract also in Chinese. / EXAMINATION COMMITTEE LIST --- p.ii / DECLARATION --- p.iii / ACKNOWLEDGEMENTS --- p.iv / ABSTRACT --- p.v / ABSTRACT IN CHINESE --- p.vii / ABBREVIATIONS --- p.ix / TABLE OF CONTENTS --- p.xiii / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Erythropoiesis --- p.2 / Chapter 1.2 --- The TF-1 model --- p.3 / Chapter 1.3 --- The erythroid marker glycophorin A (GPA) --- p.4 / Chapter 1.4 --- Reactive oxygen species (ROS) --- p.4 / Chapter 1.5 --- Oxidative stress in human erythrocytes --- p.6 / Chapter 1.6 --- Antioxidant defense systems --- p.6 / Chapter 1.7 --- Glucose provides the majority of reducing equivalents in human erythrocytes --- p.9 / Chapter 1.8 --- Glucose transporter type 1 (Glut l) transports glucose and vitamin C into human erythrocytes --- p.10 / Chapter 1.9 --- Hypothesis and objectives --- p.11 / Chapter 1.10 --- Long-term significance --- p.12 / Figure 1.1 Stages of mammalian erythropoiesis. Adapted from (Koury et al.，2002) --- p.13 / "Figure 1.2 Conversion of major ROS. Adapted from (Ghaffari," --- p.14 / Figure 1.3 Major oxidative defense in human erythrocytes --- p.15 / "Figure 1.4 Peroxide scavenging systems. Adapted from (Day," --- p.16 / Chapter 2 --- MATERIALS AND METHODS --- p.17 / Chapter 2.1 --- Cell culture --- p.18 / Chapter 2.1.1 --- Culture media --- p.18 / Chapter 2.1.2 --- Cell maintenance --- p.19 / Chapter 2.1.3 --- Cell cryopreservation --- p.19 / Chapter 2.1.4 --- Cell differentiation --- p.20 / Chapter 2.1.5 --- Cell treatments --- p.20 / Chapter 2.1.5.1 --- Antioxidant treatments --- p.21 / Chapter 2.1.5.2 --- H2O2 challenging --- p.22 / Chapter 2.1.5.3 --- Antibiotic treatment --- p.22 / Chapter 2.2 --- Flow cytometry --- p.23 / Chapter 2.2.1 --- Flow cytometers --- p.23 / Chapter 2.2.2 --- Analysis of erythroid differentiation --- p.23 / Chapter 2.2.3 --- Analysis of cell lineage --- p.24 / Chapter 2.2.4 --- Analysis of intracellular ROS --- p.24 / Chapter 2.2.5 --- Analysis of mitochondrial transmembrane potential (Δψm) --- p.25 / Chapter 2.2.6 --- Analysis of mitochondrial mass --- p.25 / Chapter 2.2.7 --- Analysis of cell death --- p.26 / Chapter 2.2.8 --- Analysis of caspase-3 activity --- p.27 / Chapter 2.2.9 --- FACS cell sorting --- p.27 / Chapter 2.2.10 --- Two-variant flow cytometric experiments --- p.28 / Chapter 2.2.11 --- Analysis of flow cytometry data --- p.28 / Chapter 2.2.12 --- Compensation --- p.29 / Chapter 2.2.12.1 --- Compensation matrix for Annexin V-PI double-staining --- p.29 / Chapter 2.2.12.2 --- Compensation matrix for Annexin V-TMRM double-staining --- p.30 / Chapter 2.2.12.3 --- Compensation matrix for CFSE- GPA double-staining --- p.31 / Chapter 2.2.12.4 --- Compensation matrix for CFSE- TMRM double-staining --- p.31 / Chapter 2.2.12.5 --- Compensation matrix for CM- H2DCFDA-GPA double-staining --- p.32 / Chapter 2.2.12.6 --- Compensation matrix for GPA- TMRM double-staining --- p.33 / Chapter 2.3 --- Western blot --- p.35 / Chapter 2.4 --- Statistical analysis --- p.37 / Chapter 3 --- RESULTS AND DISCUSSION --- p.38 / Chapter 3.1 --- The cells with high GPA staining were younger in cell lineage --- p.39 / Chapter 3.2 --- ROS was produced during TF-1 erythropoiesis --- p.40 / Chapter 3.3 --- ROS production was not essential for TF-1 erythropoiesis --- p.41 / Chapter 3.4 --- ROS production was not the cause of cell proliferation during TF-1 erythropoiesis --- p.41 / Chapter 3.5 --- ROS production was not the cause of sub-lethal mitochondrial depolarization in TF-1 erythropoiesis --- p.42 / Chapter 3.6 --- The cells showing mitochondrial depolarization were mother cells that gave rise to differentiating cells --- p.44 / Chapter 3.7 --- ROS production was not the cause of cell death in TF-1 erythropoiesis --- p.45 / Chapter 3.8 --- ROS production confers oxidative defense during TF-1 erythropoiesis --- p.47 / Chapter 3.8.1 --- Glut l inhibition partially blocked TF-1 erythropoiesis without affecting cell viability --- p.47 / Chapter 3.8.2 --- Antioxidant defense systems were established during TF-1 erythropoiesis --- p.48 / Chapter 3.8.3 --- Antioxidant treatments blocked the establishment of antioxidant defense systems during TF-1 erythropoiesis --- p.51 / Chapter 3.9 --- Conclusion --- p.55 / Chapter 3.10 --- Future work --- p.56 / Figure 3.1 Cell lineage versus erythroid marker during erythropoiesis under vitamin E treatment --- p.59 / Figure 3.2 ROS production during erythropoiesis --- p.60 / Figure 3.3 ROS production versus erythroid marker during erythropoiesis under vitamin E treatment --- p.61 / Figure 3.4 Percentage of ROS+ cells in vitamin E-treated TF-1 erythropoiesis as compared to control --- p.63 / Figure 3.5 Percentage of GPA+ cells in vitamin E-treated TF-1 erythropoiesis as compared to control --- p.64 / Figure 3.6 Cell death versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.65 / Figure 3.7 Erythroid marker versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.67 / Figure 3.8 Cell lineage versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.69 / Figure 3.9 Change of mitochondrial mass during erythropoiesis --- p.71 / Figure 3.10 ROS production versus erythroid marker during erythropoiesis under levofloxacin treatment --- p.72 / Figure 3.11 Percentage of GPA+ cells in levofloxacin-treated TF-1 erythropoiesis as compared to control --- p.73 / Figure 3.12 Cell death versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under levofloxac in treatment --- p.74 / Figure 3.13 Expression level of antioxidant enzymes during erythropoiesis --- p.75 / Figure 3.14 Expression level of Glut l during erythropoiesis --- p.76 / Figure 3.15 Expression level of Glut l in GPA positive and GPA negative populations --- p.77 / Figure 3.16 Cell death under oxidative stress challenging during erythropoiesis --- p.78 / Figure 3.17 Expression level of antioxidant enzymes and Glutl during erythropoiesis under EUK-134 treatment --- p.79 / Figure 3.18 Expression level of antioxidant enzymes and Glutl during erythropoiesis under vitamin E treatment --- p.80 / Figure 3.19 Cell death under oxidative stress challenging during erythropoiesis under vitamin E treatment --- p.82 / Figure 3.20 Expression level of antioxidant enzymes during erythropoiesis under vitamin C treatment --- p.83 / Figure 3.21 Cell death under oxidative stress challenging during erythropoiesis under vitamin C treatment --- p.84 / Figure 3.22 Cell death under oxidative stress challenging during erythropoiesis under NAC treatment --- p.85 / Figure 3.23 Summary of oxidative stress challenging during erythropoiesis --- p.86 / REFERENCES --- p.87

Thesis (M.S.)--University of Wisconsin -- La Crosse, 2001. / Includes bibliographical references.

Thesis (M.S.)--University of British Columbia, 2004. / Includes bibliographical references (leaves 113-121). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (M.S.)--University of British Columbia, 2004. / Includes bibliographical references (leaves 113-121).

No description available.

The quality of healthcare in low-resource countries is often limited by the environment, lack of funds, staff availability, electricity availability, and more. In the words of a Malawian physician, medicine can feel like improvisation, wherein one must make due with available resources rather than desired resources. One prevalent problem among low-resource hospitals is the functionality and longevity of medical equipment. A large percentage of all medical equipment in Malawian hospitals is donated, resulting in a wide spectrum of models, necessary spare parts, and functionality. These machines can break quickly due to heavy use prior to donation, missing user and maintenance manuals, and a lack of replacement parts. Thus, finding necessary life-saving equipment in Malawian hospital wards can be a challenge. One such piece of equipment is the oxygen concentrator, necessary for treatment of respiratory disease, use with CPAP machines, and in the administration of surgical anesthesia. This device fills many roles in low-resource hospitals, but in many Malawian hospitals it is the most frequently malfunctioning piece of equipment. A survey administered to medical personnel and maintenance personnel in hospitals in Malawi’s Central and Southern Regions isolated some common causes of oxygen concentrator malfunction. Prominent among these were poor oxygen concentrator ventilation and the lack of consumable replacement parts such as the intake bacterial filter. A stand made from locally-sourced materials was developed to encourage better oxygen concentrator exhaust and raise the device out of dust and cleaning fluids on ward floors. Intake bacterial filter alternatives were researched, designed, constructed, and tested, manufactured from housing materials and filter media available in Malawi or continental Africa. A primary source of difficulty for low-resource hospitals is lack of autonomy, requiring aid from affluent nations to supply equipment and consumable materials. This work suggests that sustainable innovations, such as allowing consumables to be produced in-country, can replace aid with development and create more accessible materials to hospital maintenance personnel. Collaboration with material suppliers and engineers in Malawi can provide sustainable designs and systems to help hospitals access the supplies they need to service oxygen concentrators and other equipment. / Master of Science / The quality of healthcare in low-resource countries is often limited by the environment, lack of funds, staff availability, electricity availability, and more. In the words of a Malawian physician, medicine can feel like improvisation, wherein one must make due with available resources rather than desired resources. One prevalent problem among low-resource hospitals is the functionality and longevity of medical equipment. A large percentage of all medical equipment in Malawian hospitals is donated, resulting in a wide spectrum of models, necessary spare parts, and functionality. These machines can break quickly due to heavy use prior to donation, missing user and maintenance manuals, and a lack of replacement parts. Thus, finding necessary life-saving equipment in Malawian hospital wards can be a challenge. One such piece of equipment is the oxygen concentrator. This device fills many roles in low-resource hospitals, but in many Malawian hospitals it is the most frequently malfunctioning piece of equipment. A survey was used in hospitals in Malawi’s Central and Southern Regions to collect information on why oxygen concentrators malfunction. Common reported causes of malfunction were oxygen concentrators overheating due to clogged exhaust vents, and the unavailability of necessary disposable filters. A stand made from locally-available materials was developed to improve oxygen concentrator ventilation. Replaceable filter alternatives were researched, designed, constructed, and tested, made from housing materials and filter materials available in Malawi or continental Africa. A primary source of difficulty for low-resource hospitals is dependence on more developed nations for supplies and aid. This work suggests that designing materials from locally-available materials can lessen this dependency and make necessary medical materials more accessible. Collaboration with material suppliers and engineers in Malawi can provide sustainable designs and systems to help hospitals access the supplies they need to service oxygen concentrators and other equipment.