Dissertations / Theses on the topic 'Respiratory investigations'
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Blaza, James Nicholas. "Spectroscopic investigations of catalysis by respiratory complex I." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708587.
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Darling, Katharine Elizabeth Anna. "Investigations of respiratory epithelial host defence against bacterial pathogens." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417941.
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Taylor, Claire Louise. "Biochemical investigations of defects of the mitochondrial respiratory chain." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281706.
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Donne, Adam. "Investigations into recurrent respiratory papillomatosis and the evaluation of current therapy." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678786.
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Villiger, Carmel G. "Investigations into transient respiratory control using the work rate of breathing and a non-linear breather." Thesis, This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-02132009-170901/.
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Lotriet, Cornelius Jacob. "Investigations on the respiratory effects of ozone in the rodent / Cornelius Jacon Lotriet." Thesis, North-West University, 2010. http://hdl.handle.net/10394/4650.
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Ozone, being an unstable molecule, is believed to be one of the strongest oxidant
agents known to man. Rapid growth in the application of ozone — both as
disinfectant and as form of alternative medicine — led to questions about the effects
of uncontrolled ozone exposure and inhalation, whether intentional or unintentional,
on the human body.
This study specifically focussed on examining, identifying and substantiating the
respiratory effect of acute exposure (10 min or less) to considerably higher ozone
concentrations than reported on before (19.5 ± 0.5 ppm). Respiratory tissue of
rodents (Duncan–Hartley guinea pigs of both sexes and Male Wistar rats) was
subjected to ozone by utilising three distinctly diverse models of ozone introduction:
(a) in vitro exposure, (b) in vivo exposure, and (c) ex vivo by employing an isolated
lung perfusion model which allows for real–time, breath–by–breath data acquisition of
ozone’s effect on respiratory mechanics. The effect of ozone on the isolated trachea
in the presence of various drugs with well–known effects, including methacholine,
isoproterenol and ascorbic acid was also examined.
The results found in this study identified two direct effects on the isolated trachea due
to ozone exposure: (1) a definite contraction of the isolated trachea immediately after
exposure to ozone, and (2) a clearly visible and significant hyper responsiveness of
the isolated trachea to irritants, e.g. methacholine. Although ozone has a negative
effect on the trachea, it was concluded that ozone has no adverse effect on
muscarinic acetylcholine receptors. An apparent EC50 value of ozone on the trachea
was established by two different methods as (2.77 ± 0.02) x 10–3 M and (2.10 ± 0.03)
x 10–3 M, respectively. Ozone furthermore displayed an attenuation of the beneficial pharmacological
response of –sympathomimetic drugs (i.e. isoproterenol), while isoproterenol itself
has a relaxing effect on the ozone–induced contraction of the isolated trachea.
Indomethacin pre–treatment of isolated tracheal tissue significantly (77%) reduced
the ozone–induced contraction of tracheal smooth muscle, suggesting that COXproducts
of arachidonic acid play a prominent role in the development of pulmonary
function decrements consequent to acute high–dose ozone exposure. Ascorbic acid
exhibited a meaningful prophylactic effect on ozone–induced contraction of both
isolated tracheal tissue and in the isolated lung perfusion model, emphasising the
major role antioxidants play in both the epithelium lining fluid (ELF) of the respiratory
system and in plasma throughout the body in protecting against the destructive
effects of ozone.
Surprisingly, pre–treatment with ascorbic acid did not prevent hyper responsiveness
of isolated tracheal preparations to methacholine after a 10 min ozone (19.5 ± 0.5
ppm) exposure. In the lung perfusion model, the presence of ascorbic acid in the
perfusion medium did, however, significantly reduce the magnitude and rate of
decline in lung compliance after ozone exposure (46% decline with ascorbic acid
versus 96% in the control study without ascorbic acid).
Examination of a lung perfusion model exposed to ozone (19.5 ± 0.5 ppm O3; 5
seconds) presented a significant decline in lung compliance (95.6% within 2 min),
tidal volume (70%) and maximum inspiratory flow (71.2%), with an ensuing reduction
in lung elasticity and severely hampered breathing pattern.
Microscopic examination after acute high–dose inhalation studies did not display any
significant cellular damage, oedema or inflammation after acute high–dose ozone
exposure. This suggests that significant cellular injury and inflammation is possibly
not the causative factor of early breathing difficulty experienced after acute high–dose
ozone inhalation, as these symptoms and particularly the result of inflammatory
precursors, is believed to probably only set in at a later stage.
Although the potential advantages of ozone in certain fields of medicine are not
disputed, ozone, depending on its concentration and cumulative dose, can be either therapeutic or toxic. Observations in this study emphasised that even short bursts of
high–dose ozone inhalation have deleterious effects on respiratory health and care
should be taken not to jump to conclusions regarding ozone’s medical application
without relevant scientific evidence. It must be stressed that high–dose inhalation of
ozone should be avoided at all cost – especially by those with existing airway
diseases.Thesis (Ph.D. (Pharmacology))--North-West University, Potchefstroom Campus, 2011.
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Patel, Nimisha Bhanuprasad. "Investigations into the neurophysiological basis of respiratory perception in humans using transient inspiratory occlusions." Thesis, Keele University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491697.
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In humans breathing is an essential behaviour for life. It is recognized that humans and animals can perceive or sense their breathing, although the actual cortical and sub cortical structures by which this occurs remains unknown. The processing of sensations presumably arise from afferent information originating from mechanoreceptors within the muscles of the upper and lower airways, lungs and chest wall. This information is integrated by the central nervous system, which leads to a perception of respiratory sensations at th~ cortex, although the specific contnbutions of these sources remain unknown. In addition, distressing respiratory sensations such as breathlessness (dyspnoea) . and hyperinflation occur in individuals exhibiting pulmonary disease, such as asthma and chronic obstructive pulmonary disease (COPD). In response to these sensations, individuals can also voluntarily or behaviourally adjust their breathing. Hence, the aim of this thesis was to investigate: (i) the modulation of respiratory related sensory activity measured from the cortex in humans, using electroencephalography in response to applications of transient inspiratory occlusions (TIas) during hyperinflation, voluntary breathing and in tracheostomy patients' who lack an upper airway and (ii) the cortical and subcortical structures mediating the response to the TIO by using functional magnetic resonance imaging (fMRI). The results of these studies show that (i) voluntary breathing modulates respiratory perception, whereas perception is unaffected in tracheostomy patients and in hyperinflated states in response to TIas; and (ii) TIas can also generate cortical and sub cortical activity specifically activating sensory - motor structures including the, primary motor cortex, primary somatosensory cortex, supplementary motor area, inferior parietal areas, thalamus and cerebellum. In conclusion, respiratory perception (i) is altered by voluntary breathing; (ii) is unaffected .in hyperinflated and tracheostomized states; and (iii) can be investigated . using fMRl through the application of TIOs.
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Heraghty, Jane Lesley. "Investigations of respiratory muscle function in children with neuromuscular disease using a novel device." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702155.
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In progressive neuromuscular diseases such as Duchenne muscular dystrophy (DMD), loss of respiratory muscle strength and endurance leads initially to nocturnal hypercapnia and then daytime respiratory failure. Non-invasive ventilation has improved quality of life and survival but requires overnight sleep assessments and there remains uncertainty about the optimal time to initiate non-invasive ventilation. The aim of this project was to develop a method to identify patients at high risk of nocturnal hypoventilation in a clinic-based setting. The main work was modifying and testing measurements made with a novel device, the respiratory muscle analyser (MicroRMA) that was developed to measure respiratory muscle endurance. The MicroRMA allowed incremental loading of the respiratory muscles after a pre determined number of breaths. The device calculated energy as a product of time, pressure and flow. Protocols were developed in healthy adults, then healthy children to produce a brief and tolerable 6-minute test of respiratory muscle endurance. Several protocols were tested and the outputs of the device compared. The main hypothesis was that children at high risk of nocturnal hypoventilation would be more likely to fail to complete a standardised test protocol or would adapt their respiration to use less cumulative energy to accomplish test completion. Children with neuromuscular weakness had a lower completion rate on some protocols but test failure was not associated with other markers of disease severity, including lower forced vital capacity or nocturnal hypercapnia. Similarly, in children completing the test protocol, no relationship between MicroRMA outputs and disease severity was detected. In addition, handgrip strength was also evaluated in DMD but lower strength was not related to worse nocturnal gas exchange. Finally, overnight oximetry was compared with oxicapnography but, using recommended threshold criteria, only identified half of the children with nocturnal hypercapnia. In conclusion, none of the tests evaluated were able to predict which children with neuromuscular weakness had nocturnal hypercapnia.
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Atkinson, Hilary A. C. "Investigations of the potential of inhaled xenobiotics to induce respiratory hypersensitivity reactions in the rat." Thesis, University of Surrey, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303227.
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Dasari, Paul Krupaker Reddy. "Characterization and Compensation of Hysteretic Cardiac Respiratory Motion in Myocardial Perfusion Studies Through MRI Investigations." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-dissertations/159.
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Respiratory motion causes artifacts and blurring of cardiac structures in reconstructed images of SPECT and PET cardiac studies. Hysteresis in respiratory motion causes the organs to move in distinct paths during inspiration and expiration. Current respiratory motion correction methods use a signal generated by tracking the motion of the abdomen during respiration to bin list- mode data as a function of the magnitude of this respiratory signal. They thereby fail to account for hysteretic motion. The goal of this research was to demonstrate the effects of hysteretic respiratory motion and the importance of its correction for different medical imaging techniques particularly SPECT and PET. This study describes a novel approach for detecting and correcting hysteresis in clinical SPECT and PET studies. From the combined use of MRI and a synchronized Visual Tracking System (VTS) in volunteers we developed hysteretic modeling using the Bouc-Wen model with inputs from measurements of both chest and abdomen respiratory motion. With the MRI determined heart motion as the truth in the volunteer studies we determined the Bouc Wen model could match the behavior over a range of hysteretic cycles. The proposed approach was validated through phantom simulations and applied to clinical SPECT studies.
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Bursby, Timothy Patrick. "Investigations of the mitochondrial #beta#-oxidation trifunctional protein and its association with complex 1 of the respiratory chain." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364807.
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Chiu, Chih-Yung. "Molecular and genomic investigations of the role of MAP3K8 in IL-1β-induced response in respiratory epithelial cells." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9854.
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Mitogen Activated Protein 3 Kinase 8 (MAP3K8) is a member of the serine/threonine protein kinase family and has been demonstrated to be involved in the mitogen activated protein kinase (MAPK) pathway. The latter pathway plays an important role in many aspects of the immune mediated inflammatory response. Inhibition of MAP3K8 in primary human cell types decreases the production of TNF-α and other pro-inflammatory mediators during inflammatory events. Pharmacologic inhibition of MAP3K8 has been shown to be an appropriate therapeutic target for rheumatoid arthritis and other human inflammatory diseases. Inhibition of MAP3K8 may therefore potentially be a new therapeutic strategy for airway inflammation. Investigation of the role of MAP3K8 in regulation of the inflammatory response was conducted using epithelial cell lines. A MAP3K8 gene knockdown experiment using small interfering RNA (siRNA) was carried out to establish the effect of MAP3K8 on the inflammatory response following IL-1β stimulation. In addition the effect of MAP3K8 gene knockdown on the therapeutic outcome of dexamethasone (Dex) was investigated. ELISAs were used to establish whether knockdown of MAP3K8 resulted in inhibition of IL-1β-induced IL-6, IL-8 and RANTES. The effect of treatment with Dex in combination with MAP3K8 gene silencing on ERK and MEK phosphorylation was determined by Western Blotting. The impact of MAP3K8 gene silencing on global gene expression was also assessed using Affymetrix Human Gene 1.1ST arrays. Differential expression and network analyses were performed on the data generated. A significant rise in MAP3K8 gene expression was found 2 hours after IL-1β stimulation in both A549 and normal human bronchial epithelial (NHBE) cells. In addition, siRNA against MAP3K8 resulted in approximately 40% inhibition of IL-6, IL-8 and RANTES expression after IL-1β stimulation. Furthermore, MAP3K8 gene silencing enhanced by approximately 40% the decrease in IL-8 and RANTES release seen at different concentrations of Dex. The combination of MAP3K8 gene silencing and Dex also resulted in a greater inhibition of phosphorylated ERK compared to that seen with Dex alone. Data from global gene expression arrays revealed that the MAP3K8 regulated inflammatory response was predominantly involved in the ERK/MAPK and SAPK/JNK pathways but not the p38 MAPK pathway. Among the genes regulated by MAP3K8, it is interesting to note that IL-6, MMP-1, MMP-3, MMP-12 and CCL20 have previously been reported to be linked with airway diseases, such as COPD and asthma. Furthermore, MAP3K8 regulated the AP-1 transcription factor up-regulation of IL-1β-induced IL-6 and MMP-1 through the ERK1/2 and JNK signaling pathways. MAP3K8 however appears to regulate NF-kB activation through IKKα/β activation independent of the MAPK pathway regulated by itself. In conclusion, MAP3K8 plays a key role in the inflammatory cytokine response post IL-1β stimulation. MAP3K8 gene silencing by siRNA not only suppresses these key inflammatory cytokines but also enhances the therapeutic effect of steroids. MAP3K8 inhibitors might therefore provide a new therapeutic strategy for airway inflammation.
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Tsao, Tzu-Hsin B. "From molecular pathways to neural populations: investigations of different levels of networks in the transverse slice respiratory neural circuitry." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/37296.
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By exploiting the concept of emergent network properties and the hierarchical nature of networks, we have constructed several levels of models facilitating the investigations of issues in the area of respiratory neural control. The first of such models is an intracellular second messenger pathway model, which has been shown to be an important contributor to intracellular calcium metabolism and mediate responses to neuromodulators such as serotonin. At the next level, we have constructed new single neuron models of respiratory-related neurons (e.g. the pre-Btzinger complex neuron and the Hypoglossal motoneuron), where the electrical activities of the neurons are linked to intracellular mechanisms responsible for chemical homeostasis. Beyond the level of individual neurons, we have constructed models of neuron populations where the effects of different component neurons, varying strengths and types of inter-neuron couplings, as well as network topology are investigated.
Our results from these simulation studies at different structural levels are in line with experiment observations. The small-world topology, as observed in previous anatomical studies, has been shown here to support rhythm generation along with a variety of other network-level phenomena. The interactions between different inter-neuron coupling types simultaneously manifesting at time-scales orders of magnitude apart suggest possible explanations for variations in the outputs measured from the XII rootlet in experiments. In addition, we have demonstrated the significance of pacemakers, along with the importance of considering neuromodulations and second-messenger pathways in an attempt to understand important physiological functions such as breathing activities.
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Dunroy, Helen Mary Agnes. "CO2 retention in respiratory disease : Investigations into potential pre-existing mechanisms in healthy yang subjects using added external dead-space." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497523.
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McNamara, Joanne. "Investigation of two respiratory monitoring systems used for 4D CT and respiratory gating." Faculty of Engineering, 2008. http://ro.uow.edu.au/theses/107.
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Respiratory gating enables breathing synchronised activation of CT image acquisition and linear accelerator radiation output. Two commercially available respiratory gating systems used for planning and treatment of thoracic and abdominal cancer are investigated. The strain gauged AZ-733V respiratory gating system (Anzai Medical Systems, Tokyo, Japan) was used concurrently with the infrared Real-time Position Management system (Varian Medical Systems, Palo Alto, CA) to measure the respiratory cycle of 15 volunteers. Correlation between systems was measured in six locations and the optimum position of the external surrogates determined based on signal amplitude, reproducibility of breathing waveforms and the coefficient of determination between Anzai and RPM signals. The mean value of R2 between the two systems was found to be 0.611, 0.788 and 0.925 when both markers were positioned at the xiphoid, midway between the xiphoid process and umbilicus, and at the umbilicus respectively. When positioned in separate locations results were varied, R2 values ranging from 0.345-0.965. Results highlighted the importance of external surrogate position to the respiratory signal obtained, and indicated that the external marker position on the chest wall needs to be reproducible between 4D CT scanning and treatment. Recommendations are made that external surrogates must always be positioned at the umbilicus for the most clinically useful scans. Image distortion and artifacts were studied using the Anzai AZ-733V respiratory gating system in combination with the Siemens Sensation Open CT scanner. A moving respiratory phantom was constructed and the volumetric accuracy of retrospectively reconstructed 4D CT images for three moving test objects, across five frequencies and four amplitudes of movement was compared. Volumetric accuracy was found to be within 10% for retrospectively reconstructed gated objects moving with a period of 4 s, amplitude 1 cm. Large deviations of 19.4-51.6% from the static volume of the objects were observed in gated images for periods of 3 s or less. Significant distortion and under sampling was observed in gated images of the objects moving with a period of 10 s. Artifacts were related to the partial projection effect and data sufficiency conditions outlined in literature (Keall 2004, Pan 2004, Dinkel 2007).
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O'Connor, Annette M. "A seroepidemiological investigation of undifferentiated bovine respiratory disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/NQ55633.pdf.
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Wood, James Lionel Norman. "An epidemiological investigation of respiratory disease in racehorses." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286919.
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Hixon, Sally J. "An investigation of the psychometric properties of a clinical simulation examination for respiratory care practitioners /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487261919111437.
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Martin, Matthew J. "Investigating the symptoms of airways disease." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/46745/.
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Background Airways diseases are increasingly recognised to be poorly defined phenomena with overlapping pathophysiology and symptoms. They are a significant and growing cause of morbidity, with increasing numbers of people affected globally and no improvement in key outcomes in the UK for the last decade despite ever increasing expenditure. The classification of airway diseases has changed little in the last 50 years, and may no longer be fit for purpose due to the growing appreciation of the complexity and heterogeneity of airways disease and the advent of molecular-based diagnostic techniques to target specific treatment. Aim To investigate whether strategies based on the measurement of selected phenotypic and biological characteristics of airways disease can help to improve the understanding of their pathogenesis and targeting of treatment. Methods Three characteristics of airways disease, namely (1) exhaled nitric oxide, (2) chronic productive cough of unknown cause and (3) the airway microbiota were described/measured in selected cohorts of patients in three clinical studies. Measurement of each of these characteristics was used to answer focused clinical questions regarding the pathogenesis and treatment of aspects of airways disease. Results (1) The baseline measurement of FENO in steroid naïve subjects with symptoms suggestive of asthma had a low diagnostic value for asthma but was an excellent predictor of inhaled steroid treatment response. (2) A cohort of subjects with chronic productive cough of unknown cause was described. These subjects tended to have radiological evidence of airway dilatation and chronic inflammatory changes but not significant bronchiectasis. Their cough responded well to treatment with azithromycin, with ongoing neutrophilic airway inflammation a particularly strong predictor of treatment response. (3) There were no significant differences in the abundance or community structure of the bacterial communities in the airways between subjects with mild (BTS 2) or severe (BTS 4) asthma or between severe (BTS 4) asthma patients taking inhaled fluticasone or budesonide. However a number of differences in relative abundance of certain species (including enrichment of Haemophilus parainfluenzae in the fluticasone group) were noted on comparison of the groups. Conclusions This thesis provides support for a new approach to the classification and treatment of airways disease. The recognition of pathologically important processes (treatable traits) which can be used to predict response to targeted treatment has the potential to revolutionise the management of airways disease and result in improved patient outcomes.
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Howse, J. N. "An investigation into respiratory disease in the racing pigeon." Thesis, University of Liverpool, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383448.
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Anderson, Maggie (Margaret). "Investigating the robustness of the Anzai respiratory gating system." Thesis, University of Canterbury. Physics, 2013. http://hdl.handle.net/10092/8796.
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This research was undertaken in order to investigate the robustness of the Anzai respiratory gating system. Tests were performed to verify the transfer of image data, to identify the method of gating and the accuracy of phase identification. It was found to have sizeable limitations which could result in either incorrectly gated images or serious artefacts. For these reasons it is recommended it be used under the guidance of a suitably qualified physicist.
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Johnson, Jo-Anne. "Investigating factors governing cell fate decisions in respiratory epithelium." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278966.
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The maintenance of the airway/respiratory epithelium during adult homeostasis and repair and its construction during embryonic development require tightly regulated cell fate decisions. This regulation takes the form of complex transcription factor and signalling cascades, much of which are unknown, particularly in human lung development. Multiciliogenesis describes the process of specification/differentiation of airway epithelial progenitors/stem cells into mature multiciliated cells (MCCs). Here, I have identified 2 novel transcription factors, Fank1 and Jazf1 which form part of the transcription factor cascade regulating multiciliogenesis in adult and embryonic mouse tracheas. Mouse tracheal epithelium is representative of epithelium lining the entire human airway and it is possible that we will also be able to extrapolate these findings to the human airway. It is not until we fully understand the regulation of multiciliogenesis that it will be possible to look at ways of pushing basal cells towards a MCC fate for purposes of cell replacement therapy, for example in patients with mucociliary disease. As well as exploring cell fate decisions in the mouse upper airway epithelium using embryonic tracheal explants and mouse tracheal epithelial cell (MTEC) cultures, I have also explored the regulation of cell fate decisions in distal human lung epithelium at the pseudoglandular stage of development. At this stage SOX9+ distal tip cells are self-renewing and multipotent and give rise to SOX2+ stalk descendents, which differentiate into airway epithelium. The regulation of SOX9+ lung tip cell multipotency and migration of SOX2+ stalk descendents during human lung development is poorly understood. I have compared human tip (SOX9+) versus stalk (SOX2+) transcriptomes using gene ontology (GO), which has highlighted some key signalling pathways enriched in tip cells which could be important in maintaining distal tip cell multipotency. These pathways have been utilised in optimising conditions for propagating self-renewing tip-derived organoids. These organoids have the potential to be differentiated into bronchiolar and alveolar fates and as such are an invaluable research tool for studying human lung epithelial development, whilst minimising the use of human embryos and its associated ethical implications. I have also performed human tip versus mouse tip transcriptome GO analysis which highlights that although there are many similarities, there are also differences between human and mouse lung epithelium development, emphasising the need for research on human tissue.
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Galvao, Ferrarini Mariana. "Metabolic Investigation of the Mycoplasmas from the Swine Respiratory Tract." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10302/document.
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L'appareil respiratoire des porcs est colonisé par plusieurs bactéries, parmi lesquelles trois espèces de mycoplasmes : Mycoplasma flocculare, Mycoplasma hyopneumoniae et Mycoplasma hyorhinis. Lors de ce doctorat, notre principal objectif était de mieux comprendre le métabolisme différentiel dans chacune des espèces à l'aide de différentes approches. Nous avons reconstruit les réseaux métaboliques complets pour toutes les souches séquencées de ces trois espèces de mycoplasmes afin d'y détecter des caractéristiques distinctes. Nous avons pu montrer que, bien que les trois espèces de mycoplasmes du porc ont des capacités métaboliques semblables, certaines différences existent qui incluent, d'une part, le catabolisme de myo-inositol et un système plus complet pour l'absorption du glycérol, et d'autre part, une large gamme de moyens d'absorption de carbohydrates chez M. hyorhinis. L'utilisation de glycérol comme source de carbone, une activité qui est absente uniquement dans M. flocculare, produit du peroxyde d'hydrogène qui est toxique, ce qui peut expliquer l'absence de pathogénicité de cette espèce. L'absorption d'un plus large éventail de sources de carbone chez M. hyorhinis peut également expliquer pourquoi cette espèce est un contaminant largement connu des cultures cellulaires. Des expériences de croissance ont montré que les milieux définis décrits pour d'autres espèces de mycoplasmes ne sont pas appropriés pour la croissance de mycoplasmes du tractues respiratoire de porcs, et que la peptone est essentielle pour le maintien de la viabilité des cellules à la fois de M. hyopneumoniae et de M. flocculare dans des milieux définis. Dans ce travail, nous proposons également de nouveaux média définis qui, in silico, sont extrêmement appropriés pour les mycoplasmes du porc. Les données de métabolomique suggèrent que même si ces espèces sont extrêmement similaires du point de vue de leurs génomes et des métabolismes, les produits et les taux de réaction diffèrent et la régulation des gènes peuvent interférer directement dans le métabolisme. Pour expliquer ces différences ainsi que d'autres décrits dans la littérature qui suggèrent que certains types de régulation de l'expression du gène existent en effet dans ces espèces, nous avons également essayé de recueillir des informations sur de nouvelles séquences promotrices. Ainsi, cette thèse servira de base pour l'étude du métabolisme différentiel et des pathologies causées par les mycoplasmes du tractus respiratoire du porc et pourra aider à proposer des façons de prévenir à l'avenir le développement des maladies associéesIn this PhD thesis, we presented three main types of analyses of metabolism, and in most cases involving symbiosis: metabolic dialogue between a trypanosomatid and its symbiont, comparative analyses of metabolic networks and exploration of metabolomics data. The respiratory tract of swines is colonized by several pathogenic bacteria, among which are three mycoplasma species: Mycoplasma flocculare, Mycoplasma hyopneumoniae, and Mycoplasma hyorhinis. In this work, we created whole-genome metabolic network reconstructions for all sequenced strains from these three Mycoplasma species. Similar to other Mycoplasma models all reconstructed networks exhibit low connectivity due to the simplicity of the biological model. We were able to show that the three swine mycoplasma species have similar metabolic capabilities. Interesting metabolic differences include the myo-inositol catabolism and a more complete system for glycerol uptake in M. hyopneumoniae and a wide range of carbohydrate uptake in M. hyorhinis. Glycerol conversion to DHAP, a missing activity only in M. flocculare, produces toxic hydrogen peroxide and may explain the lack of pathogenicity of this species. The uptake of a wider range of carbon sources in M. hyorhinis may also explain why this species is a wide-known contaminant in cell cultures. Growth experiments showed that defined media described for other Mycoplasma species are not suitable for the growth of respiratory tract swine mycoplasmas and that peptone is essential for the maintenance of cell viability of both M. hyopneumoniae and M. flocculare in defined media. Metabolomic data suggests that even though these species are extremely similar from a genomic and metabolic point of views, the products and reaction rates differ and gene regulation may interfere directly in metabolism. This, in turn, may account for many aspects still unknown that influence directly different levels of pathogenicity in each of them
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Kennedy, Ashleigh. "An investigation of the effects of fentanyl on respiratory control." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/5998/.
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Respiration is a complex rhythmic motor behaviour that metabolically supports all physiological processes in the body and is continuous throughout the life of mammals. A failure to generate a respiratory rhythm can be fatal. Understanding how the respiratory rhythm is generated by the brainstem presents a substantial challenge within the field of respiratory neurobiology. Studies utilising in vitro and in vivo rodent models have provided compelling evidence that a small bilateral region of the ventrolateral medulla, known as the preBötzinger complex (preBötC), is the site for respiratory rhythmogenesis. There is also evidence to suggest a second distinct neuronal group, the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG), plays a specialised role in respiratory rhythm generation in the neonatal rodent. During early life in rodents and humans, the respiratory system is immature and an irregular breathing pattern is generated, making this period of life potentially vulnerable to external perturbations. However a step in maturity occurs early in life after which breathing becomes regular. Currently, the underlying mechanisms involved in respiratory rhythm generation during early life are not fully understood. It is hypothesised that the RTN/pFRG functions as the dominant respiratory rhythm generating oscillator during early life when the respiratory system is immature, after which the preBötC becomes the dominant rhythm generator. However, how the preBötC and the RTN/pFRG interact in vivo to produce rhythmic breathing during postnatal development remains elusive. The first aim of this thesis was to assess postnatal maturation of breathing patterns in the mouse using non-invasive whole body plethysmography. Between postnatal day (P) 2 and P3, a critical maturation step occurred, whereby breathing transitioned from an unstable and dysrhythmic pattern to a regular and robust pattern. The second aim of the thesis was to investigate the influence of this postnatal maturation on central respiratory control. Mu (μ) opioid receptor agonists are known respiratory depressants. The activity of the preBötC is depressed by μ opioids in vitro. Furthermore, fentanyl, a potent μ opioid receptor agonist, evokes respiratory frequency depression in vivo by exclusively targeting and depressing preBötC neurons. Conversely, the RTN/pFRG is insensitive to μ opioids. Accordingly, fentanyl was utilised as a pharmacological tool to selectively perturb the preBötC in vivo throughout postnatal development and through to early adulthood. The acute respiratory depressive effects of fentanyl were measured in order to investigate the level of involvement of the preBötC in respiratory rhythm generation throughout this critical developmental time period. Based on the general hypothesis that the preBötC functions as the dominant respiratory rhythm generator when the respiratory system has matured, it was hypothesised that mice would be more susceptible to the respiratory depressive effects of fentanyl after the maturation step has occurred i.e. the respiratory sensitivity to fentanyl would be age-dependent. Initially, mice were repeatedly exposed to fentanyl throughout postnatal development. However, fentanyl failed to induce a respiratory depression at all postnatal ages, suggesting repeated exposure had induced a rapid desensitisation to fentanyl’s respiratory effects. The study design was consequently altered to allow the hypothesis to be sufficiently tested, whereby different mice were studied on each postnatal day i.e. each mouse was only exposed to fentanyl once. This study revealed a trend towards an age-dependent increase in respiratory sensitivity to fentanyl, where mice displayed a heightened respiratory frequency depression in response to fentanyl after the maturation step had occurred from P3 onwards. This data therefore lends support to the hypothesis that the preBötC functions as the dominant respiratory rhythm generator post-maturation. In the clinical setting fentanyl is widely utilised for treating chronic and acute pain. However, despite the potent respiratory depressive actions of fentanyl, the long-term respiratory consequences of repeated exposure remain unexplored both clinically and pre-clinically. Owing to the immaturity of the respiratory system and the corresponding fragile nature of breathing patterns during neonatal life in mammals, a further aim of the thesis was to determine the long-term effects of fentanyl exposure during this vulnerable respiratory time period in the mouse. To establish if the postnatal age of fentanyl-exposure influences long-term respiratory effects, fentanyl exposure during juvenile life, which is regarded as being post-respiratory maturation, was also assessed. Neonatal mice were exposed to fentanyl (0.04 mg/kg daily) from P1-P5 and juvenile mice were exposed from P9-P13. When mice reached adulthood, baseline respiratory activity and the respiratory response to a subsequent fentanyl challenge were assessed during wakefulness and under anaesthesia. When awake, neonatal-exposed mice exhibited a reduced baseline respiratory frequency and an attenuated respiratory sensitivity to fentanyl. Under anaesthesia, neonatal-exposed mice displayed a depressed baseline minute ventilation and a high frequency of spontaneous augmented breaths. In direct contrast to the wakeful state, when anaesthetised, neonatal-exposed mice exhibited a striking hypersensitivity to the acute respiratory depressive actions of fentanyl. In all neonatal-exposed mice, fentanyl evoked a respiratory failure. In juvenile-exposed mice, baseline respiratory activity remained unaltered in the wakeful state and fentanyl also failed to induce a respiratory depression. When anaesthetised, baseline minute ventilation remained unchanged and the high occurrence of augmented breaths exhibited by the neonatal-exposed mice was not observed. Unlike the wakeful state, fentanyl evoked a depression of respiratory activity in the juvenile-exposed mice when anaesthetised, however the augmented sensitivity to fentanyl and consequential respiratory arrest displayed by the neonatal-exposed was not observed. This data indicates that the anaesthetised state is more susceptible to respiratory depression. Furthermore, the data suggests that neonatal life represents a time period that is particularly vulnerable to the respiratory effects of opioid depression. The final aim of the thesis was to determine the long-term effects of neonatal fentanyl exposure on neurokinin-1 (NK1R) and μ opioid receptor expression within the ventral respiratory column (VRC), a region of the ventrolateral medulla comprising the preBötC. Neonatal-exposed mice exhibited significantly less NK1R and μ opioid receptor expressing cells in the region of the preBötC. This data suggests that repeated fentanyl exposure in neonatal life induces a long-term downregulation of these receptors. In conclusion, fentanyl’s acute respiratory effects were age-dependent, which lends supports to the hypothesis that the preBötC functions as the dominant rhythm generator post-maturation. Furthermore, this thesis highlights the vulnerabilities of neonatal life to the lasting effects of opioid respiratory depression, whilst also providing invaluable insight into state-dependent respiratory modulation and depression.
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Jones, Una. "Respiratory function in people with Huntington's disease : investigation and intervention." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/70032/.
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Huntington’s disease (HD) is an inherited neurodegenerative condition characterised by progressive motor, cognitive and psychiatric symptoms. The most frequent cause of death is respiratory failure, yet little is known about respiratory function through the progression of the disease or the underlying causes of respiratory failure. A thorough exploration of the relevant literature led to the development of a conceptual framework for respiratory failure in people with HD. Within this framework respiratory failure was characterised as type 1 hypoxaemic and type2 hypercapnic failure and further evaluated through (i) an observational study to investigate respiratory function in people with HD, and (ii) the benefit and feasibility of inspiratory muscle training in people with HD. In order to develop understanding of potential underlying causes of type 1 hypoxaemic and type 2 hypercapnic respiratory failure, the observation study aimed to investigate if there was a difference in respiratory function between healthy controls and people with HD at different stages of the disease, and to explore factors that may influence or be influenced by respiratory function. The framework was further evaluated through the intervention study which investigated the feasibility and benefit of inspiratory muscle training in people with HD as a method of increasing capacity of the respiratory system. Method In the observation study 67 people with HD and 39 healthy control participants underwent a series of measurements of respiratory function based on underlying causes of type 1 hypoxaemic respiratory failure and type 2 hypercapnic respiratory failure. These included measurement of lung volume, respiratory muscle strength and endurance. Exercise capacity, physical activity, swallow and posture as potential influencing factors were also measured in people with HD. In the intervention study 20 people with HD were randomly allocated either to inspiratory muscle training at 50% of maximal inspiratory pressure, or to training against a load suggested to have no effect, completed in the home. The training protocol was 30 breaths, twice daily for six weeks, which was preceded by a habituation period of one week. Sniff nasal inspiratory pressure, peak cough flow and 30 second sit to stand were measured before and after the intervention. The programme was supported by alternate weekly phone calls and home visits. Results All measures of respiratory function, except FEV1/FVC were significantly decreased (p <0.001) in people with manifest HD compared to healthy control participants and people with pre-manifest HD. There was no difference between healthy control participants and people with pre-manifest HD. Respiratory function demonstrated a significant linear decline with disease progression measured by the total functional capacity scale (p<0.001). In particular, peak cough flow was abnormal at the middle stage of the disease. Exercise capacity, physical activity, swallow and posture were significantly related to respiratory function in people with manifest HD (p range 0.016-0.001). In people with manifest HD, exercise capacity was 27.73% ±26.29 predicted and swallow capacity was abnormal in 84.80% of participants. In the intervention study, five participants completed the intervention arm and 7 completed the sham arm. Adherence to the inspiratory muscle training programme ranged from 37-100% across both groups, with mean adherence rates of 70.67% ±26.35 and 74.53% ±21.03 for intervention and sham groups respectively. There was no difference in inspiratory muscle strength, peak cough flow or 30 second sit to stand as a result of the intervention. Participants and their carers identified carer support as a key enabler and life events as a barrier for carrying out the exercises. Conclusion The findings from this study indicate that people with HD are susceptible to type 1 hypoxaemic respiratory failure and predisposed to type 2 hypercapnic respiratory failure due to increased elastic and resistive loads and decreased capacity of respiratory muscles. The risk of type 1 hypoxaemic respiratory failure is high due to decreased swallow capacity and concomitant decreased cough efficacy. Decreased lung volume leading to hypoventilation may be impact on both type 1 hypoxaemic respiratory failure and lead on to type 2 hypercapnic respiratory failure. The predisposition to type 2 hypercapnic respiratory failure is due to decreased respiratory muscle capacity and increased elastic and resistive load. The study also highlighted the complex relationship between respiratory function, exercise capacity and physical activity. Although inspiratory muscle strength, cough efficacy and functional activity remained unchanged in this small sample, the results of the intervention study suggest that inspiratory muscle training is feasible in people with HD. Further studies should use protocols that are directly related to the primary outcome measure e.g. a power based protocol to improve cough efficacy or an endurance based protocol to improve physical activity. A model of respiratory failure in people with HD incorporating both type 1 hypoxaemic and type 2 hypercapnic respiratory failure can be proposed based from the findings of the studies that informs future research and clinical management of people with HD.
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Chatterjee, Krishnashis. "Analytical and Experimental Investigation of Insect Respiratory System Inspired Microfluidics." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/85688.
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Microfluidics has been the focal point of research in various disciplines due to its advantages of portability and cost effectiveness, and the ability to perform complex tasks with precision. In the past two decades microfluidic technology has been used to cool integrated circuits, for exoplanetary chemical analysis, for mimicking cellular environments, and in the design of specialized organ-on-a-chip devices. While there have been considerable advances in the complexity and miniaturization of microfluidic devices, particularly with the advent of microfluidic large-scale integration (mLSI) and microfluidic very-large-scale-integration (mVLSI), in which there are hundreds of thousands of flow channels per square centimeter on a microfluidic chip, there remains an actuation overhead problem: these small, complex microfluidic devices are tethered to extensive off-chip actuation machinery that limit their portability and efficiency. Insects, in contrast, actively and efficiently handle their respiratory air flows in complex networks consisting of thousands of microscale tracheal pathways. This work analytically and experimentally investigates the viability of incorporating some of the essential kinematics and actuation strategies of insect respiratory systems in microfluidic devices. Mathematical models of simplified individual tracheal pathways were derived and analyzed, and insect-mimetic PDMS-based valveless microfluidic devices were fabricated and tested. It was found that not only are these devices are capable of pumping fluids very efficiently using insect-mimetic actuation techniques, but also that the fluid flow direction and magnitude could be controlled via the actuation frequency alone, a feature never before realized in microfluidic devices. These results suggest that insect-mimicry may be a promising direction for designing more efficient microfluidic devices.Ph. D.
Microfluidics or the study of fluids at the microscale has gained a lot of interest in the recent past due to its various applications starting from electronic chip cooling to biomedical diagnostic devices and exoplanetary chemical analysis. Though there has been a lot of advancements in the functionality and portability of microfluidic devices, little has been achieved in the improvement of the peripheral machinery needed to operate these devices. On the other hand insects can expertly manipulate fluids, in their body, at the microscale with the help of their efficient respiratory capabilities. In the present study we mimic some essential features of the insect respiratory system by incorporating them in microfluidic devices. The feasibility of practical application of these techniques have been tested, at first, analytically by mathematically modeling the fluid flow in insect respiratory tract mimetic microchannels and tubes and then by fabricating, testing and analyzing the functionality of microfluidic devices. The mathematical models, using slip boundary conditions, showed that the volumetric fluid flow through a trachea mimetic tube decreased with the increase in the amount of slip. Apart from that it also revealed a fundamental difference between shear and pressure driven flow at the microscale. The microfluidic devices exhibited some unique characteristic features never seen before in valveless microfluidic devices and have the potential in reducing the actuation overhead. These devices can be used to simplify the operating procedure and subsequently decrease the production cost of microfluidic devices for various applications.
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Taylor, Robert William. "Mitochondrial respiratory chain dysfunction in human pathology : investigation, pathogenicity and treatment." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577189.
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The work presented in this thesis comprises 100 peer-reviewed publications, mostly original research papers but some key review articles are included, which highlight my ongoing research in understanding the role of mitochondrial respiratory chain dysfunction and mitochondrial DNA (mtDNA) mutation in human pathologies over a twenty year period, and in no small part have contributed to the development of my laboratory as a national referral centre in the UK for diagnostic biochemical and molecular genetic testing, funded by the NHS Specialist Commissioners. A significant proportion (at least 50%) of all the papers which are included in this application are either first author or senior author publications. Mitochondrial respiratory chain disease exhibits marked clinical and genetic heterogeneity, often requiring the study of clinically-relevant, post-mitotic tissues to make a diagnosis which in many cases is made difficult on account of the peculiarities of mitochondrial genetics. Understanding this phenotypic diversity and elucidating the basic molecular mechanisms leading to cellular dysfunction continues to be challenging, with progress in the development of curative therapies hampered by our inability to manipulate the mitochondrial genome, and difficulties in obtaining alternative models of disease other than patients with pathogenic mtDNA mutations. . In an attempt to submit a cohesive application, the papers have been organised into relevant sections, beginning with general reviews of the clinical, biochemical and molecular features of mitochondrial genetic disease (Section A) followed by sections on the investigation and laboratory diagnosis of mitochondrial disease including epidemiology (Sections 8-0). The largest collection of papers document the molecular investigation of mitochondrial disorders, many describing novel mutations and disease mechanisms associated with both mtDNA- encoded and nuclear mitochondrial genes (Sections E-K). The next section describe studies investigating the role of somatic mtDNA abnormalities in neurodegenerative disease, cancer and ageing pathologies - including marking stem cell populations (Section L) - before a series of original research articles and invited reviews that focus on pharmacological and gene therapy strategies for the treatment of patients with mtDNA disease (Section M).
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Ferrarini, Mariana Galvão. "Metabolic investigation of the mycoplasmas from the respiratory tract of swines." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/141904.
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Hlongwana, Simangele I. "Investigating adherence of authorised prescribers to standerd treatment guidelines/essential medicine list when treating children presenting with respiratory conditions at primary health care level in the umkhanyakude health district, Kwazulu Nata." Thesis, University of Limpopo (Medunsa Campus), 2013. http://hdl.handle.net/10386/1076.
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Thesis (MSc(Med)(Pharmacy) ) -- University of Limpopo, 2013.Introduction: Primary Health Care (PHC) is regarded as the first level of contact with the National Health System with health care services provided mainly by nurses with varying competences. PHC is about interaction with people thus the quality of PHC depends extensively on the competence of the people who provide it. Therefore, the way health care personnel are trained and how capacity continues to be developed is of fundamental importance to PHC. Following the Alma-Ala Declaration, policies, such as the National Drug Policy (NDP) were developed in South Africa to guide health care services. The NDP resulted in the formulation of Standard Treatment Guidelines/Essential Medicine List (STGs/EML). Emphasis has been placed on all prescribers to strictly adhere to these guidelines when providing clinical patient care. Despite these developments reports still indicate that antibiotics are irrationally used when treating respiratory infections. It is therefore imperative that localised reasons for deviations from the STGs/EML when treating respiratory conditions are thoroughly investigated to facilitate relevant interventions. Objectives: The objectives of the study were to: (1) document the treatment prescribed to children up to 12 years of age for respiratory conditions, (2) assess adherence of the authorised prescribers to the 2008 PHC STGs/ EML and (3) determine factors impacting on deviations from the 2008 STGs/EML. Method: Twenty randomly selected PHC facilities in the district participated in the study. In each of the 20 selected PHC facilities, three prescribers were randomly selected for the structured interview and auditing of their prescription registers. Five prescriptions from each of the sampled prescription registers of the selected authorised prescribers, containing any of the children's respiratory conditions to be studied, were audited. A total of 15 prescriptions from each of the selected PHC facilities were audited. Descriptive statistics was used to xii analyse data and responses to categorical variables were summarised as frequency counts and percentages. Results were presented as tables, figures and graphs. Results: Pneumonia (39.7%) was found to be the most common respiratory condition seen at Umkhanyakude Health District followed by the common cold and influenza. Amoxicillin (52%) was the most often prescribed antibiotic for these respiratory conditions. Only 4% of prescribers showed full adherence to the 2008 PHC STGs/EML. While prescribers had a positive attitude towards the 2008 PHC STGs/EML, their sense of adherence, content understanding of these guidelines, as well as knowledge of medicine used for respiratory conditions, were exaggerated. Failure to accurately diagnose respiratory conditions and lack of implementation and monitoring strategies were also amongst the factors impacting on adherence. Conclusion: Adherence to the 2008 PHC STGs/EML for the treatment of respiratory conditions in children up to 12 years of age was found to be a challenge in Umkhanyakude PHC facilities with only four percent of prescribers adhering to these guidelines. The Umkhanyakude Health District Management team must consider employing multifaceted interventions from the recommendations of this study in order to improve adherence to the PHC STGs/EML. Recommendations: Strategies such as intensified monitoring and evaluation, improved supervision, targeted training and education together with compulsory in-service training are recommended to improve adherence to the STGs/EML in the Umkhanyakude Health District. Guideline implementation strategies with integrated approaches to guideline dissemination must also be strengthened.
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Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma /." Connect to this title, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0097.
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Braithwaite, Emma Annette. "Neural networks for medical condition prediction : an investigation of neonatal respiratory disorder." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/12658.
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This thesis investigates how various signal processing techniques can be applied to diagnose problems in the medical domain. In particular it concentrates on breathing problems often experienced by premature babies who undergo artificial respiration. Medical Decision Support is an area of increasing research interest. The neonatal intensive care unit (NICU) is a prime example. This thesis describes the investigation of techniques to be used as the core of a decision support device in Edinburgh's NICU. At present physiological signals are taken from the patient and archived, little diagnostic use is made of these signals and no investigation has taken place into their diagnostic relevance. Within the scope of the work an investigation has taken place into the application area and some of its current problems have been identified. From these a physiological problem, respiratory disorder, was identified with characteristics which made it worthy of detailed study: it was extremely common, moreover expert knowledge and data about it already existed. With the current techniques the development of respiratory disorder is often missed or diagnosed too late. Signal processing techniques were evaluated with a view to applying them to predict the onset, or classify the development of, respiratory disorder, and a multi-layer perceptron network was chosen to perform as a classifier in the decision support tool. A number of tests were run which included an investigation of the efficiency of the chosen feature extraction techniques and the diagnostic relevance (with respect to the condition under investigation) of the signals being used to assist in diagnosis. Results show that at present the signals of greatest diagnostic relevance are not always used: a decision support device can be developed using a multi-layer perceptron classifier in combination with other signal processing techniques. The thesis also identifies other techniques where there is potential for improving the decision support tool's predictive and classification ability.
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Connolly, Martin J. "The development and use of a dosimeter for the investigation of non-specific bronchial responsiveness." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241368.
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Laird, C. "Investigation of the immunogenicity of vitamin E and selenium deficiency on the pathogenicity of avian encephalomyel." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368595.
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Sabuncu, Sinan. "Investigation of enzymes from the respiratory chain by using electrochemical and spectroscopic techniques." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAF017/document.
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Le présent travail porte sur l’étude de deux protéines de la famille des oxydases à hème-fer par des techniques de spectroscopie et d’électrochimie. Le premier chapitre décrit l’étude du cytochrome bo3 oxydase issue d’E. coli. Nous nous sommes intéressés à l’étude des interactions enzyme-quinone par l’utilisation de quinones avec des longueurs chaines isoprenyl différentes. Notre but est de mieux comprendre le rôle de la longueur de la chaine des quinones sur l’activité catalytique de l’enzyme et sur les propriétés redox des cofacteurs à hème. Dans l’étape suivante, on a étudié les résidus impliqués dans le site de liaison des quinones (haute affinité, QH). Plusieurs mutations de ces résidus sont étudiées pour mieux comprendre l’importance de chacun des résidus dans cette liaison. Dans la dernière partie de ce premier chapitre, la spectroscopie SEIRAS «spectroscopie d’absorption infrarouge exaltée de surface» est introduite comme une technique alternative pour l’étude des protéines membranaires. Dans le second chapitre, la protéine membranaire cNOR issue de P. denitrificans est étudiée. Nous nous sommes focalisés sur l’effet de différents environnements (pH, présence de protéo-liposomes) sur la stabilité de la cNOR. Pour ce faire, trois valeurs de pH (6.5, 7.5 et 8.5) sont choisies et quelques échantillons de cNOR sont reconstitués dans des protéo-liposomes. Enfin, le donneur de proton terminal (au centre binucléaire) dans la protéine cNOR était étudié. De plus, nous avons étudié les ligands des ions Ca2+ puisqu’il est proposé que le donneur de proton est situé proche de cette régionThis thesis is focused on the study of two members of the heme-copper oxidase family by using spectroscopic and electrochemical techniques. In the first chapter cytochrome bo3 oxidase from E. coli was studied. We focused on the quinone-enzyme interactions by using quinones with different isoprenyl chains. Our aim was to better understand the role of isoprenyl chain on the catalytic activity of the enzyme and the redox properties of the heme cofactors. In the next step we studied the residues that are suggested to be in the high-affinity (QH) quinone binding site. Several site-directed mutants of these residues were investigated in order to better understand the position of QH binding site and the importance of each residue. In the last part of this chapter surface-enhanced infrared absorption spectroscopy (SEIRAS) was introduced as an alternative technique to study the membrane proteins. In the second chapter cytochrome c dependent nitric oxide reducates (cNOR) from P. denitrificans was studied. We focused on the effect of different environment (pH, proteoliposomes) on the stability of cNOR. For that purpose three pH values (6.5, 7.5 and 8.5) was selected and some of the cNOR samples were reconstituted in liposomes. Finally, the terminal proton donor (to the binuclear center) in cNOR was investigated. We studied the ligands of the Ca2+ site in cNOR since it was suggested that the proton donor may be close to this area
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Wu, Weining. "Investigation of the interaction between human respiratory syncytial virus and the host cell." Thesis, University of Leeds, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574626.
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Human respiratory syncytial virus (HRSV) is a leading cause of virus-induced paediatric respiratory disease. HRSV can cause severe lower respiratory tract diseases in young children and upper respiratory tract diseases in all ages. HRSV infection results in large economical and healthcare burdens every year, however, there is no approved vaccine and the antiviral therapies are generally costly and less effective due to the high mutant rate of this RNA virus and the imbalanced host immune responses in response to HRSV infection. The virus-host interactions of HRSV have not been well understood so far, which therefore limited the knowledge of HRSV pathogenesis and the development of vaccinations and antiviral drugs. This study focused on investigations of the interactions between HRSV and host NF-KB activation and host cell cycle manipulation, as well as the interactions between HRSV nonstructural proteins and host cellular proteins. In conclusion, different NF-KB activation characteristics have been found between HRSV subgroups A and B, suggesting the implication with the different pathology of HRSV subgroup A and B. HRSV infection resulted in cell cycle arrest at GO/G1 phase with different mechanism in continuous and primary cell cultures, which benefited progeny virus production. HRSV NS1 protein was found to act as a role in HRSV induced cell cycle arrest, and a potential inhibitor of RNA polymerase". All of these findings provided a better understanding of HRSV virus-host interactions and HRSV pathogenesis.
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Cole, Aidan. "Investigation of the radiobiological and dosimetric implications of respiratory motion in advanced radiotherapy." Thesis, Queen's University Belfast, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.673797.
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The primary aim of radiotherapy is to deliver sufficient dose to eradicate a tumour whilst sparing normal tissue. This balance in tumour control probability (TCP) and normal tissue complication probability (NTCP) can be influenced by a number of factors, one of which is respiratory motion. This thesis investigates the potential dosimetric and radiobiological differences as a result of respiratory motion in lung cancer radiotherapy. It demonstrates significant dosimetric improvements by using advanced motion management techniques (4DCT and respiratory gating) and modulated radiotherapy (VMAT), in regi~ns of lung tumour motion. These techniques confer improvements in NTCP and can allow for dose escalation. However, when patient characteristics and tumour characteristics are included in clinical modelling algorithms, the potential gain may not be as clinically relevant as anticipated. Many advanced techniques currently used in radiotherapy departments, have been implemented without a clear understanding of potential differences in radiobiological response compared with previous techniques. This thesis demonstrates significant differences in the radiation induced bystander effect (RISE), in the presence of respiratory motion and modulated radiotherapy. In vitro studies of respiratory gating indicate a trend towards increased survival as treatment delivery time increases. There is an increased dependence on the use of these radiotherapy techniques which introduce complex spatiotemporal dose modulation. The data presented in this thesis indicates that radiobiological consequences may not be fully explained by existing theories. These findings may be of particular relevance for modulated radiotherapy in NSCLC radiotherapy.
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Withers, Howard Keith. "A spectrophotometric investigation of the respiratory cytochromes of aerobically-grown Escherichia coli K-12." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/31032.
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The cytochrome o and cytochrome d oxidase complexes provide twin termini for the branched respiratory chain of aerobically grown Escherichia coli. Combined use of mutant strains, modulated growth conditions and high resolution analytical techniques enabled cytochromes to be resolved, identified and partially characterized. The cytochrome complement of everted membrane vesicles and detergent extracts fractionated by liquid chromatography is more complex than previously recognised.
Multiple type-b cytochromes were resolved by potentiometry and by high resolution spectrophotometry in membrane vesicles from mutant strains lacking the cytochrome d oxidase complex and grown under conditions minimising respiratory chain diversity. Cytochrome o was identified with Em = +235 mV (vs. NHE) as were low potential cytochromes associated with dehydrogenases. Spectrally distinct components of the cytochrome d complex yielded Em values of +125 mV (cytochrome 6595) and +187 mV (cytochrome d). The latter displayed atypical redox behaviour with extreme hysteresis during potentiometric titrations.
Several cytochromes b₅₅₆ displaying single, symmetrical redox α-bands at 77 K were resolved from detergent extracts of vesicles. Mutant strains identified one with Mr = 52500 (gel filtration) and Em = +20 mV as the sdhC gene product, a component of succinate dehydrogenase. DL-lactate induced another while a hydroperoxidase, Mr = 386000 (gel filtration) with twin Em values of -2mV and -121 mV and a split Soret absorption band at 77 K (λ[symbol omitted]max= 426.0 nm + 434.0 nm) was produced under limited oxygen tension.
The Triton-solubilized and purified cytochrome 0 complex exhibited Mr = 516000 (gel filtration) with five component peptides of Mr= 55000, 32000, 31000, 21000 and 16000 (SDS-PAGE). It displayed mid-point potentials of -58 mV, +127 mV and +260 mV and three a-absorption maxima at 77 K : 554.5 nm, 557.0 nm and 563.5 nm. These components were reduced equivalently during poised-potential low temperature spectrophotometric analyses. Carbon monoxide binding changed the complex's redox α-absorption spectrum minimally but shifted the high potential Em to approximately +420 mV. Quinone analogues inhibited both reduction and
reoxidation of the complex. Cytochrome o complex prepared from cloned sources contained a significantly greater proportion of the component with mid range electrochemical potential absorbing at 554.0 nm. These results are discussed in relation to possible structures of the complex, its respiratory interactions and the identity of cytochrome o itself.Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate
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Topor, Zbigniew L. "Investigation of the human respiratory control system by computer modeling and system identification techniques." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ47917.pdf.
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Whelan, Jillian Nicole. "Investigation of Respiratory Syncytial Virus Structural Determinants and Exploitation of the Host Ubiquitin System." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6431.
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Respiratory syncytial virus (RSV) is a globally circulating, non-segmented, negative sense (NNS) RNA virus that causes severe lower respiratory infections. This study explored several avenues to ultimately expand upon our understanding of RSV pathogenesis at the protein level. Evaluation of RSV intrinsic protein disorder increased the relatively limited description of the RSV structure-function relationship. Global proteomics analysis provided direction for further hypothesis-driven investigation of host pathways altered by RSV infection, specifically the interaction between the RSV NS2 protein and the host ubiquitin system. NS2 primarily acts to antagonize the innate immune system by targeting STAT2 for proteasomal degradation. The goal was to identify NS2 residues important for interaction with the host ubiquitin system, as well as describe the mechanism by which NS2 induces host protein ubiquitination. Bioinformatics analysis provided a platform for development of loss-of-ubiquitin-function NS2 mutants. Combining critical mutations as double or triple NS2 ubiquitin mutants displayed an additive effect on reducing NS2-induced ubiquitination. Recombinant RSV (rRSV) containing NS2 ubiquitin mutations maintained their effect on ubiquitin expression during infection in addition to limiting STAT2 degradation activity. NS2 ubiquitin mutants decreased rRSV growth and increased levels of innate immune responses, indicating a correlation between NS2’s ubiquitin function and antagonism of type I IFN to enhance viral replication. Finally, several proteomics strategies were employed to identify specific cellular proteins ubiquitinated by NS2 to further define host-pathogen interactions during RSV infection. This study demonstrates an effective approach for limiting viral protein function to enhance immune responses during infection.
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au, Liping@unsw edu, and Liping Wang. "An investigation of the association between herpes viruses and respiratory disease in racehorses in Western Australia." Murdoch University, 2003. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20040820.112222.
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Respiratory disease is an important cause of wastage in the Australian horse racing industry and viruses are frequently suspected as aetiological agents of respiratory disease or poor performance by clinicians and trainers but confirmation is seldom attempted. This thesis deals with the potential role of equine herpes virus types 1, 2, 4 and 5 in upper respiratory disease and poor performance in horses in Western Australia.
The methodology selected for the identification of equine herpes viruses in tissues of horses was polymerase chain reaction (PCR) and therefore individual PCR assays were developed for the detection of each herpes virus, and then a nested multiplex PCR was developed to detect all four viruses. There was good correlation between the multiplex PCR for the detection of EHV and the detection of virus by isolation in cell culture, although a combination of the 2 techniques provided greater sensitivity than either technique alone. The multiplex PCR described appeared equally sensitive as specific PCR assays using a single set of primers for each individual virus but reduced labour and reagent costs.
As latency is a well recognised phenomenon in the equine herpes viruses and the horse is subjected to a number of stresses which might induce reactivation of latent infections, it was hypothesised that there would be a background level of replication of the equine herpes viruses in clinically normal horses. Nasal swabs and peripheral blood leukocytes (PBL) were obtained from 282 clinical normal horses and examined for EHV. The results clearly demonstrated the widespread occurrence of EHV in the clinically healthy horses. The rate of detection of different types of EHV varied, as did the prevalence in young and adult horses. The most common EHV detected was EHV5: in 83.2% of 131 of horses <2 years of age; in 40% of horses >2 years of age.
A prospective clinical study was conducted whereby respiratory tract samples and PBL from adult horses with respiratory disease and/or poor performance were examined for equine herpes viruses; the aim was to determine a possible association between equine herpes virus infection and respiratory disease and/or poor performance. The relative incidence of factors identified in the history, signalment, physical and laboratory evaluation of horses in the study population was compared between horses from which EHV was identified in respiratory samples and horses negative for equine herpes virus. The results indicated that equine herpes viruses were important causes of respiratory disease in the study population, and that haematological and cytological data were a poor indicator of such equine herpes virus infection.
The occurrence of equine herpes virus in nasal swabs and PBL of weaned or unweaned foals from Thoroughbred breeding establishments was determined and provided data on the occurrence of EHV in association with respiratory disease. EHV5 was detected in nasal swabs and/or PBL at a high prevalence rate in healthy foals and yearling horses but its occurrence was not associated with clinical signs of respiratory disease. In contrast, EHV2 was detected more commonly in nasal swabs and/or PBL from foals with respiratory disease than in similar samples from healthy horses. Experimental infection of 8 horses with EHV2 was attempted and induced clinical signs of respiratory disease, but less severe than observed in the epidemiological studies. The results suggested that EHV2 is associated with mild upper respiratory tract infection in young horses.
41
Simon-Lombes, Anne. "Investigations moleculaires des maladies mitochondriales humaines." Paris 5, 1997. http://www.theses.fr/1997PA05N003.
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Steyn, Helena. "Investigation of the cytotoxic potential and anti-inflammatory properties of Euphorbia hirta alone and in combination with Selenium in vitro." Pretoria : [s.n.], 2009. http://upetd.up.ac.za/thesis/available/etd-02172010-184404/.
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Chow, Tat Ming. "Investigation into the use of a novel respiratory monitor for gated radiotherapy of lung tumours." Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526771.
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Kerr, Margaret Heather. "An investigation of the pulmonary surfactant system in children with severe respiratory syncytial virus infection." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265640.
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Brockett, Emma Grace. "An investigation of respiratory abnormalities in a male and female mouse model of Rett Syndrome." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4097/.
Full textAbstract:
Rett Syndrome (RTT) is a severe neurodevelopmental disorder affecting 1 in 10,000 girls and is often associated with respiratory abnormalities. RTT is almost exclusively caused by loss-of-function mutations in the human MECP2 gene. It remains unknown as to whether the respiratory abnormalities seen in RTT patients and MeCP2 deficient animals may be due to problems with respiratory rhythmogenesis or the result of an inappropriate chemosensitive response. The main aim of this thesis was to investigate the respiratory abnormalities presented in a male and female mouse model of RTT syndrome. In a male mouse model, the endogenous Mecp2 gene was silenced by insertion of a Lox-Stop cassette, which mimicked a number of RTT symptoms, including disordered breathing (Guy et al., 2007). The Mecp2 gene was reactivated by Tamoxifen(TM)-induced deletion of the Lox-Stop cassette. As such, the progression and development of respiratory disturbances were monitored in the early stages of MeCP2 deficiency and also assessed during and after gene reactivation. Respiratory parameters were recorded using whole body plethysmography, a non-invasive method of recording respiratory behaviour. Compared to WT, MeCP2 deficient male mice had an increased respiratory frequency and increased number of sighs prior to gene reactivation. The fact that animals were still viable suggests that neuronal development can occur in the absence of MeCP2, but signs of respiratory instability e.g. the increased number of sighs, indicate that MeCP2 may be required for neuronal maturation as the animal develops. Gene reactivation reduced respiratory frequency and the number of sighs in MeCP2 deficient mice to a level comparable with WT suggesting that TM-induced activation of Mecp2 can reverse some of the respiratory abnormalities. Since RTT syndrome is a predominantly female based disorder it was of benefit to observe the progression of the respiratory phenotype in a female model. Female mice which were heterozygous for the Mecp2-null mutation were also studied using plethysmography. It was observed that at 23 wks of age, following a period of normal development, the Mecp2+/- mice began to display an increased number of respiratory abnormalities compared to WT animals which suggested an inability of the respiratory network to maintain optimal function. Also, the respiratory response to hypoxia was significantly greater in Mecp2+/- mice compared to WT, yet the hypercapnic response of the two genotypes was comparable. This indicates that the response to hypoxia and hypercapnia are mediated by two different mechanisms and that the hypoxic response may be affected by a reduction in the level of MeCP2. Neuromodulators such as noradrenaline and serotonin are important in modulation of the respiratory pattern and the chemosensitive response. Previous research has implicated changes in bioamine content in the pathophysiology of RTT patients and MeCP2 deficient animals (Riederer et al., 1985; Ide et al., 2005; Viemari et al., 2005; Roux et al., 2010) Thus, cells expressing tyrosine hydroxylase (TH), a marker for noradrenergic cells, and cells expressing 5-HT were quantified in the brainstems of MeCP2 deficient male mice to observe how the absence and subsequent reactivation of Mecp2 may affect noradrenergic and serotonergic cell number. Compared to WT, MeCP2 deficient mice exhibited a trend towards a decrease in the number of TH and 5-HT expressing cells in various noradrenergic and serotonergic regions of the brainstem, which may account for the development of the respiratory abnormalities in the mutant mice. It was also found that reactivation of Mecp2 did not restore the number of MeCP2 expressing cells to WT level. MeCP2 was often found to be co-expressed with 5-HT and TH, yet many MeCP2 positive neurons were not found to be 5-HT or TH positive indicating that these MeCP2 expressing neurons may be co-localised with another as yet unidentified neuromodulator. Interestingly, reactivation of Mecp2 appeared to occur at a greater rate in noradrenergic TH expressing neurons than 5-HT expressing neurons. Whilst studying MeCP2 deficient male mice it was noted that some of the mutant animals began to develop rale-like rattling within the chest and also began to foam at the mouth. Much of the research in RTT syndrome focuses on the neurological aspect, whereas this phenotype indicated a problem within the lungs. Lungs of WT and MeCP2 deficient mice were removed and processed with various histological stains to highlight various aspects of the lung morphology. Comparison of WT and MeCP2 deficient tissue revealed that there was a trend towards an increase in the amount of elastin surrounding airways and an increase in the thickness of the interalveolar septum in MeCP2 deficient mice compared to WT. An increase in interalveolar septum may interfere with ventilation and may account for the increased occurrence of sighing observed in the male MeCP2 deficient mice. These morphological changes in the lung may indicate that the respiratory abnormalities of RTT may not be solely neurological. Since changes in the morphology of the lung were clearly present in the male with evidence of increased elastin deposits surrounding the airways, investigation into the presence of pulmonary arterial hypertension (PAH) was carried out in the female model. Results indicated that there was a trend towards a higher right ventricular pressure in Mecp2+/- animals compared to WT, along with a trend towards right ventricular hypertrophy, indices of the presence of PAH. In conclusion, Mecp2 has been shown in vivo to be involved in both the development and maintenance of neurons involved in the respiratory network, both neuromodulatory and chemosensitive, and the absence or reduction of MeCP2 is also proposed to have a novel role in the development of lung pathology in MeCP2 deficient mice.
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Wang, Liping. "An investigation of the association between herpesviruses and respiratory disease in racehorses in Western Australia." Thesis, Wang, Liping (2003) An investigation of the association between herpesviruses and respiratory disease in racehorses in Western Australia. PhD thesis, Murdoch University, 2003. https://researchrepository.murdoch.edu.au/id/eprint/386/.
Full textAbstract:
Respiratory disease is an important cause of wastage in the Australian horse racing industry and viruses are frequently suspected as aetiological agents of respiratory disease or poor performance by clinicians and trainers but confirmation is seldom attempted. This thesis deals with the potential role of equine herpes virus types 1, 2, 4 and 5 in upper respiratory disease and poor performance in horses in Western Australia.
The methodology selected for the identification of equine herpes viruses in tissues of horses was polymerase chain reaction (PCR) and therefore individual PCR assays were developed for the detection of each herpes virus, and then a nested multiplex PCR was developed to detect all four viruses. There was good correlation between the multiplex PCR for the detection of EHV and the detection of virus by isolation in cell culture, although a combination of the 2 techniques provided greater sensitivity than either technique alone. The multiplex PCR described appeared equally sensitive as specific PCR assays using a single set of primers for each individual virus but reduced labour and reagent costs.
As latency is a well recognised phenomenon in the equine herpes viruses and the horse is subjected to a number of stresses which might induce reactivation of latent infections, it was hypothesised that there would be a background level of replication of the equine herpes viruses in clinically normal horses. Nasal swabs and peripheral blood leukocytes (PBL) were obtained from 282 clinical normal horses and examined for EHV. The results clearly demonstrated the widespread occurrence of EHV in the clinically healthy horses. The rate of detection of different types of EHV varied, as did the prevalence in young and adult horses. The most common EHV detected was EHV5: in 83.2% of 131 of horses <2 years of age; in 40% of horses >2 years of age.
A prospective clinical study was conducted whereby respiratory tract samples and PBL from adult horses with respiratory disease and/or poor performance were examined for equine herpes viruses; the aim was to determine a possible association between equine herpes virus infection and respiratory disease and/or poor performance. The relative incidence of factors identified in the history, signalment, physical and laboratory evaluation of horses in the study population was compared between horses from which EHV was identified in respiratory samples and horses negative for equine herpes virus. The results indicated that equine herpes viruses were important causes of respiratory disease in the study population, and that haematological and cytological data were a poor indicator of such equine herpes virus infection.
The occurrence of equine herpes virus in nasal swabs and PBL of weaned or unweaned foals from Thoroughbred breeding establishments was determined and provided data on the occurrence of EHV in association with respiratory disease. EHV5 was detected in nasal swabs and/or PBL at a high prevalence rate in healthy foals and yearling horses but its occurrence was not associated with clinical signs of respiratory disease. In contrast, EHV2 was detected more commonly in nasal swabs and/or PBL from foals with respiratory disease than in similar samples from healthy horses. Experimental infection of 8 horses with EHV2 was attempted and induced clinical signs of respiratory disease, but less severe than observed in the epidemiological studies. The results suggested that EHV2 is associated with mild upper respiratory tract infection in young horses.
47
Wang, Liping. "An investigation of the association between herpesviruses and respiratory disease in racehorses in Western Australia." Wang, Liping (2003) An investigation of the association between herpesviruses and respiratory disease in racehorses in Western Australia. PhD thesis, Murdoch University, 2003. http://researchrepository.murdoch.edu.au/386/.
Full textAbstract:
Respiratory disease is an important cause of wastage in the Australian horse racing industry and viruses are frequently suspected as aetiological agents of respiratory disease or poor performance by clinicians and trainers but confirmation is seldom attempted. This thesis deals with the potential role of equine herpes virus types 1, 2, 4 and 5 in upper respiratory disease and poor performance in horses in Western Australia.
The methodology selected for the identification of equine herpes viruses in tissues of horses was polymerase chain reaction (PCR) and therefore individual PCR assays were developed for the detection of each herpes virus, and then a nested multiplex PCR was developed to detect all four viruses. There was good correlation between the multiplex PCR for the detection of EHV and the detection of virus by isolation in cell culture, although a combination of the 2 techniques provided greater sensitivity than either technique alone. The multiplex PCR described appeared equally sensitive as specific PCR assays using a single set of primers for each individual virus but reduced labour and reagent costs.
As latency is a well recognised phenomenon in the equine herpes viruses and the horse is subjected to a number of stresses which might induce reactivation of latent infections, it was hypothesised that there would be a background level of replication of the equine herpes viruses in clinically normal horses. Nasal swabs and peripheral blood leukocytes (PBL) were obtained from 282 clinical normal horses and examined for EHV. The results clearly demonstrated the widespread occurrence of EHV in the clinically healthy horses. The rate of detection of different types of EHV varied, as did the prevalence in young and adult horses. The most common EHV detected was EHV5: in 83.2% of 131 of horses <2 years of age; in 40% of horses >2 years of age.
A prospective clinical study was conducted whereby respiratory tract samples and PBL from adult horses with respiratory disease and/or poor performance were examined for equine herpes viruses; the aim was to determine a possible association between equine herpes virus infection and respiratory disease and/or poor performance. The relative incidence of factors identified in the history, signalment, physical and laboratory evaluation of horses in the study population was compared between horses from which EHV was identified in respiratory samples and horses negative for equine herpes virus. The results indicated that equine herpes viruses were important causes of respiratory disease in the study population, and that haematological and cytological data were a poor indicator of such equine herpes virus infection.
The occurrence of equine herpes virus in nasal swabs and PBL of weaned or unweaned foals from Thoroughbred breeding establishments was determined and provided data on the occurrence of EHV in association with respiratory disease. EHV5 was detected in nasal swabs and/or PBL at a high prevalence rate in healthy foals and yearling horses but its occurrence was not associated with clinical signs of respiratory disease. In contrast, EHV2 was detected more commonly in nasal swabs and/or PBL from foals with respiratory disease than in similar samples from healthy horses. Experimental infection of 8 horses with EHV2 was attempted and induced clinical signs of respiratory disease, but less severe than observed in the epidemiological studies. The results suggested that EHV2 is associated with mild upper respiratory tract infection in young horses.
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Crag, Thelma R. "Investigation into the mechanisms and treatment of acute living injury and the acute respiratory distress syndrome." Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534709.
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Dancer, Rachel Catherine Anne. "Investigation into a potential role for vitamin D in the pathogenesis of acute respiratory distress syndrome." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7859/.
Full textAbstract:
Patients undergoing oesophagectomy are at risk of developing Acute Respiratory Distress Syndrome (ARDS), an immune mediated form of severe respiratory failure. The immunomodulatory properties of Vitamin D are increasingly recognised. We hypothesised that preoperative Vitamin D supplementation would reduce levels of perioperative alveolar oedema in patients undergoing oesophagectomy. Vitamin D deficiency is common in patients with and at risk of ARDS. High dose supplementation with cholecalciferol is a safe and effective method of increasing Vitamin D levels. Supplementation reduces perioperative increases in inflammatory alveolar oedema. Circulating levels of the active form of Vitamin D relate to long term post-operative mortality. Patients who survive at least 2 years post-op have higher preoperative circulating numbers of Natural Killer cells. We did not find any evidence of an effect of Vitamin D on Natural Killer Cells. In conclusion, preoperative Vitamin D status relates to perioperative changes in inflammatory alveolar oedema and high dose Vitamin D supplementation is a safe and effective method of improving preoperative Vitamin D status. Preoperative cholecalciferol administration should be considered in patients with and at risk of vitamin D deficiency.
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Thompson, Christopher David. "An analytical and experimental investigation of respiratory dynamics using P/D control and carbon dioxide feedback." Thesis, Virginia Tech, 1988. http://hdl.handle.net/10919/43059.
Full textAbstract:
This thesis addresses the problem of defining the control law for human respiration.
Seven different drivers have been identified as possibly having an input to the
respiratory controller. These seven represent a combination of feedforward and feedback
inputs arising from neural and humoral mechanisms.
Using the assumption that carbon dioxide concentrations in the arterial blood have the
strongest effect, a control equation with proportional and derivative components based on
this driver was evaluated. The methodology for the evaluation was to create a model of
the respiratory system incorporating the P/D controller, obtain experimental data of one
test subject's respiratory response to exercise, then compare model generated output with
experimental data, and adjust the parameters in the control equation to yield optimal
model performance.
The usual practice of testing controller performance has been to apply single step loads
to a model and evaluate its response. A multi-step protocol was used here to provide a
better, more generalized test of controller performance. This thesis may represent the
first documented use of an approach of this type for evaluating respiratory controller
performance.
Application of a multi-step protocol revealed a non-linear controller was needed to keep
pace with system changes. Respiratory system operation was effectively managed using
a controller of the form:
VENTILATION = F(dCO2/dT,Q) + F(CO2,Q) + CONSTANT.Master of Science