No description available.

A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg for the degree of Master of Science in Medicine. / A study was undertaken to ascertain whether a low intensity, long term home walking exercise programme could produce physiological changes in patients with chronic obstructive pulmonary disease (COPD). Subjective psychological effects of such a programme were also evaluated. (Abbreviation abstract) / AC2017

Yeung Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 125-138). / Abstracts in English and Chinese; questionnaires also in Chinese. / Acknowledgement --- p.iii / Declaration --- p.iv / List of Tables --- p.v / List of Figures --- p.viii / Abstract --- p.ix / Abbreviation --- p.xiv / Chapter Chapter One --- Introduction / Background --- p.1 / Chapter 1.1 --- Definition / Chapter 1.2 --- Disease Prevalence / Chapter 1.3 --- Associated Disability / Chapter 1.4 --- Treatment-effectiveness / Chapter 1.5 --- Rehabilitation / Chapter Chapter Two --- Hong Kong Situation --- p.56 / Chapter 2.1 --- What is known --- Hong Kong elderly population database / Chapter 2.2 --- Service provision for the elderly in Hong Kong / Chapter Chapter Three --- Methodology --- p.68 / Chapter 3.1 --- Aims / Chapter 3.2 --- Subject and methodology / Chapter Chapter Four --- Results --- p.93 / Chapter 4.1 --- Results at baseline / Chapter 4.2 --- "Trend with time (0,12,48 weeks) between the exercise group and the control group" / Chapter 4.3 --- Results at first follow up (12 weeks) / Chapter 4.4 --- Results at second follow up (48 weeks) / Chapter 4.5 --- Results from baseline to second follow up within the exercise group or within the control group / Chapter Chapter Five --- Discussion --- p.113 / Chapter 5.1 --- Short-term efficacy of pulmonary program / Chapter 5.2 --- Long-term efficacy of pulmonary program / Chapter 5.3 --- The characteristics of pulmonary program / Chapter Chapter Six --- Conclusion --- p.124 / Reference --- p.125 / Appendix The Questionnaire Used in Interviews --- p.139

Thesis (M.Sc. (Nursing))--Mahidol University, 1979.

Thesis (M.S.)--University of Wisconsin-Madison, 1980. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 61-68).

Proefschrift--Groningen. / With a summary in English.

Acute respiratory distress syndrome (ARDS) is associated with high mortality rates . The aim of treatment and ventilation is to improve oxygenation. Prone positioning improves oxygenation in patients with ARDS by shifting blood flow to undamaged or better ventilated regions of the lung. Critical care nurses follow the current guidelines with respect to prone positioning, which are mostly based on the medical aspects of the treatment. Prone positioning challenges nursing care of these patients. The research question that emerges is: Which nursing interventions during prone positioning will benefit the patient and reduce or eliminate complications? The purpose of this research is to do a systematic review in order to: Explore the evidence in support of the beneficial nursing interventions during prone positioning of ventilated patients and to develop evidence-based nursing guidelines with regard to the nursing process. The research design can be described as an exploratory, descriptive and retrospective systematic review. The population consisted of experimental study designs, as well as comparative, non-randomised and observational studies on nursing interventions during the prone positioning process. Selected studies included a population of adult or paediatric subjects who were ventilated and turned into the prone position, and the search strategy was restricted to articles published or translated into English. Studies that included animals or neonates were excluded from this review. The data collection process involved the systematic extraction of relevant data onto standardised data abstraction forms and the assessment of the methodological quality of each study. Data were summarised into evidence tables and data from randomised controlled trials were used for meta-analysis. There were thirteen randomised controlled trials, of which only seven could be included for quantitative analysis. Forty five clinical trials involving prone positioning were identified, with a total population of 2 148 patients. Outcomes that were measured, included oxygenation outcomes, responder and non-responder groups, haemodynamic outcomes, complications in the prone position, mortality, the length of sta y in the intensive care units and the total number of ventilated days. Prone positioning showed significant increases in the PaO2 and PaO2 / FiO2 ratio. The effect of the outcomes compared against the different ventilation, sedation, nutrition and positioning protocols had inconclusive results. Haemodynamic variables had insignificant increases in the prone position. Pulmonary artery wedge pressure (PAWP) however, did show a significant increase in the prone position. Complications related to prone positioning were insignificantly less than expected. Patients treated in the prone position were ventilated for an insignificantly shorter period of time, but had a longer ICU stay, although the results were also insignificant. The mortality of patients in the selected trials was 33.5%. Evidence gained from the selected studies could be used to develop nursing guidelines, despite inconclusive results related to some of the measured outcomes. / Dr. Elzabé Nel

The generation of oxygen free radicals by the cytosolic enzyme, xanthine oxidase (XO), has been implicated in post-ischemic or reperfusion damage in several organs. XO catalyzes the conversion of hypoxanthine to urate with the concomitant production of superoxide anion free radical (0₂̅˙) and hydrogen peroxide (H₂O₂). Oxygen free radical-mediated injury has also been demonstrated in inflammatory lung disease. The possible involvement of XO in oxidative injury in the lung has not yet been studied. Therefore, this research project was designed to determine whether XO is present in the lung and to investigate its characteristics in porcine, bovine, rat and human lung and other tissues. Immunochemical analysis of xanthine oxidase in the tissues employed on polyclonal antibody raised to bovine milk XO. Proteins were separated by SDS-polyacrylamide gel electrophoresis of tissue homogenates. Proteins were transfered from the gels to nitrocellulose filters by Western blotting. After incubating the filters with a antisera containing the antibody to the purified bovine XO. XO on the filter was detected by its reaction with an enzyme-conjugated second antibody. XO was immunologically detectable in bovine lung and milk. Rat lung, kidney and liver all showed XO reactivity. XO was detectable in porcine liver but not detectable in porcine lung or kidney. Thus, the antibody to bovine XO was cross-reactive with porcine and rat XO. XO protein was not immunologically detectable in human lung possibly because the antibody was not cross reactive with the bovine antibody. In vivo, xanthine oxidase exists predominantly as a dehydrogenase rather than an oxidase. In this form as xanthine dehydrogenase (XDH) the enxyme does not produce either 0₂̅˙ or H₂O₂. The activity of both XDH and XO was measured in several tissues using a fluorometric assay which uses an artifical substrate, pterin which is catalytically converted to the fluorescent product isoxanthopterin (IXP). XO activity in porcine liver was of 1.1 x 10⁻³ µg IXP/mg protein/min although XO activity was not detectable in porcine lung and kidney, in rat lung of 1.7 x 10⁻² µg IXP/mg protein/min, rat kidney of 1.5 x 10⁻² µg IXP/mg protein/min, and rat liver of 2.2 x 10⁻² µg IXP/mg protein/min. Seven human lung biopsy samples were obtained after lung resection and initially tested for viability by determination of NADH oxidase activity and then assayed for XO-XDH. Three of these samples showed NADH oxidase activity indicating tissue viability, but only one of these three showed measurable XO activity of 5.35 x 10⁻⁶ µg IXP/mg protein/min. Irreversible conversion of XDH to XO is thought to be the result of limited proteolysis by a Ca²⁺/calmodulin activated protease, whereas reversible conversion of the enzyme occurs by oxidation of critical thiol groups. Studies on the rate and nature of fluorescence assay to detect catalytic activities of both enzyme forms. Incubation of lung homogenates with trypsin for 60 min caused irreverisble conversion of 90% of the XDH to XO. In contrast, incubation of homogenates at 15°C for 10 hours caused conversion of 100% of the XDH to XO. This conversion was reversible to the extent of 80% by reduction of thiol groups with dithiothreitol (DTT). The effects of free Ca²⁺ on the conversion of XDH to X0 was examined by using EDTA, a chelator of Ca²⁺ and other divalent cations; and EGTA, a more specific chelator of Ca²⁺. The presence of these chelating agents during homogenization of either normoxic or ischemic rat lung tissue did not inhibit reversible enzyme conversion. Increased XO activity was reversible by DTT. In the normoxic rat lung, homogenates prepared with EDTA and EGTA showed a similar conversion of 95% of XDH to XO which was reversible to 70% with DTT. In the ischemic rat lung, samples prepared with EDTA and EGTA showed a'conversion of 80% and 95% XDH to XO which was similar to control samples. The extent of reversibility to XDH was 75% with DTT incubation. In addition, perfusion of rat lungs with EDTA and DTT via a pulmonary artery cannula prior to 60 min of ischemia and homogenization did not affect the extent of XDH to XO conversion. These results indicate that irreversible Ca²⁺-mediated proteolytic conversion of XDH to XO does not occur to a great extent in the rat lung during either normoxia or ischemia. However, reversible conversion of XDH to XO does occur, suggesting that reversible thiol dependent conversion may play a role in the lung under both physiological and pathophysiological states. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

Lung biopsy is neither widely known nor practiced and it was only in 1949 that i first came across a paper on this subject. The title was: "Cellular analysis of the aspiration lung biopsy from normal and some pathological conditions by Z. Godlowski" (1949). The very term "lung biopsy" conjures up the picture of a needle being introduced into an air filled, very vascular structure where the bleeding of an injured vessel cannot readily be stopped, where the stage is set for air embolisms and where tension pneumothorax may occur. it was with great surprise but also an apparently innocuous procedure. Unfortunately, at that time, there was no opportunity to use the method. In 1950 I became the University Assistant at the New Somerset Hospital in Cape Town. Many of the cases admitted to the wards presented with chest pathology. Patients with pneumococcal lobar pneumonia were not infrequent and occasional cases did not resolve as expected but went on to become so-called chronic pneumonia. What happened when an acute lobar pneumonia went on to the chronic stage and why did this occur? it was suggested that investigae this problem.

In vitro studies indicate that the inflammatory response to zymosan, a fungal wall preparation, is dependent on Toll-like receptor (TLR) 2, and that this response is enhanced by the dectin-1 receptor. Complement may also play an important role in this inflammatory response. However, the relevance of these molecules within the in vivo pulmonary environment remains unknown. To examine pulmonary in vivo inflammatory responses of the lung to zymosan, zymosan was administered by intratracheal aerosolization to C57BL/6, TLR2- TLR4-, MyD88-, and complement-deficient mice. Outcomes included bronchoalveolar fluid cell counts. We next examined effects of dectin-1 inhibition on response to zymosan in alveolar macrophages in vitro and in lungs of C57BL/6, TLR2-, and complement-deficient mice. Finally, the effect of alveolar macrophage depletion on in vivo pulmonary responses was assessed. Marked zymosan-induced neutrophil responses were unaltered in TLR2-deficient mice despite a TLR2-dependent response seen with synthetic TLR2 agonists. TLR4, MyD88, and complement activation were not required for the inflammatory response to zymosan. Although dectin-1 receptor inhibition blocked the inflammatory response of alveolar macrophages to zymosan in vitro, in vivo pulmonary leukocyte recruitment was not altered even in the absence of TLR2 or complement. Depletion of alveolar macrophages did not affect the response to zymosan. Neither complement, macrophages, nor TLR2, TLR4, MyD88, and/or dectin-1 receptors were involved in the pulmonary in vivo inflammatory response to zymosan.