Tesis: "Airway (Medicine)"

1

Svensson, Holm Ann-Charlotte B. "Platelets and airway remodeling : Mechanisms involved in platelet-induced fibroblast and airway smooth muscle cell proliferation in vitro". Doctoral thesis, Linköpings universitet, Farmakologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-61623.

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Airway remodeling is a contributing cause to the pathological structural changes, such as increased cell proliferation, observed in asthma. Platelets have been found in autopsy lungmaterial obtained from asthmatic patients and are well known to induce proliferation in vitro of a variety of cells. However, the role of platelets in airway remodeling is far from understood. This thesis aims to clarify the involvement of platelets in fibroblast and airway smooth muscle cell (ASMC) proliferation in vitro and to elucidate the importance of HA, FAK, eicosanoid and ROS dependent signaling. The results demonstrate that platelets induce ASMC proliferation through NADPH-oxidase and 5-LOX dependent mechanisms. In addition, platelets also induce a 5-LOX dependent fibroblast proliferation. Furthermore, morphological analysis demonstrates that platelets bind to the extracellular matrix component HA through its receptor CD44 and thereby induce a FAK dependent ASMC proliferation. Taken together, the results obtained in this thesis suggest that platelet/HA interaction mediated through CD44 is of importance for platelets ability to induce cell proliferation. Moreover, the results propose that platelet-induced fibroblast proliferation is 5-LOX dependent and that platelets induce a HA, CD44, FAK, 5-LOX, and ROSdependent ASMC proliferation. This action of platelets represents a potential important and novel mechanism that may have an impact on the remodeling process and in the development of new pharmacological strategies in the treatment of inflammatory respiratory disease such as asthma.

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2

Noble, Peter Beresford. "Regulation of airway narrowing by dynamic and static mechanical loads". University of Western Australia. School of Biomedical and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0050.

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[Truncated abstract] The extent to which an airway narrows is strongly influenced by mechanical loads on airway smooth muscle (ASM). This thesis considers both dynamic and static mechanical loads. Dynamic load describes the time varying load on airways produced by oscillatory breathing movements. Static load is that present at a fixed lung volume ie. without breathing. In the intact lung static load principally comprises the pressure across the airway wall, that is transmural pressure (Ptm), and elastic after-load arising from distortion of airway and lung tissue by the narrowing airway. The experiments performed in this thesis were designed to answer several outstanding questions relating to how dynamic and static loads regulate airway narrowing. Dynamic load from breathing movements cyclically stretches ASM, which produces a number of physiological and cellular effects. For example in ASM strips a period of cyclical stretch reduces subsequent ASM contraction. However the response of the whole airway to dynamic load may differ from isolated ASM where non-muscle tissue also contributes. The first aim of this thesis was to characterise the response of the whole airway to dynamic load and determine whether the airway wall modifies the effects produced by ASM length cycling. Static after-loads restrict ASM shortening providing a limit to airway narrowing. Two primary sources of airway wall load include cartilage and the mucosal membrane which contribute to airway compliance. The relative importance of cartilage and mucosa to airway wall compliance and airway narrowing is unclear. ... Results demonstrate that airway narrowing is restricted by Ptm but not by parenchymal elastic after-load. The major findings of this thesis are: (1) dynamic loads produced by breathing movements regulate airway responsiveness through cyclical airway expansion and elongation; (2) the reported effects of cyclical stretch on ASM contraction differs in situ 8 possibly due to modification by one or more biomechanical or physiological properties of the airway wall; (3) parenchymal elastic after-loads, previously thought to be important during bronchoconstriction, do not restrict airway narrowing. Given the absence of an effect of parenchymal elastic after-load on airway narrowing, the static mechanical load on ASM therefore comprises Ptm and airway wall stiffness, with important contributions from cartilage and mucosa depending on lung volume.

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3

Lau, Justine Y. "Novel genes associated with airway smooth muscle proliferation in asthma". Connect to full text, 2008. http://hdl.handle.net/2123/5134.

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Thesis (Ph. D.)--University of Sydney, 2009.
Title from title screen (viewed Aug. 11, 2009) Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Pharmacology, Faculty of Medicine. Degree awarded 2009; thesis submitted 2008. Includes bibliographical references. Also available in print form.

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4

Mohammadi, Hamed. "Cephalometric airway measurements in anterior open bite deformity". Thesis, [Hong Kong : Faculty of Dentistry], The University of Hong Kong, 1997. http://sunzi.lib.hku.hk/HKUTO/record/B3862820X.

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5

Grainge, Christopher. "Determinants of airway remodelling in asthma". Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/384164/.

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6

Fitch, Patrick Stephen. "A study of airway inflammation in childhood asthma". Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326411.

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7

Pandya, Hitesh Champaklal. "Investigations of fetal human airway smooth muscle : potential mechanisms of abnormal airway wall modelling in chronic lung disease of preterm infants". Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248390.

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8

Ip, Sau-man Mary. "A pathophysiologic study of airway inflammation in bronchiectasis". [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13793895.

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9

Tang, Shu-sum. "Cephalometric airway measurements in class III skeletal deformity". Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/HKUTO/record/B38628065.

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10

葉秀文 y Sau-man Mary Ip. "A pathophysiologic study of airway inflammation in bronchiectasis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31981434.

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11

McKay, Anne. "The role of immune mediators in airway inflammation". Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4828/.

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Asthma is a chronic inflammatory condition of the airways characterised by reversible airflow obstruction, airway hyper-responsiveness and inflammatory infiltrates in the airway walls containing eosinophils, T lymphocytes and mast cells. T helper (Th) lymphocyte subsets, defined by the cytokines they secrete, are thought to play a key role in the in the initiation and perpetuation of chronic airway inflammation. Th2 cells, producing interleukin (IL)-4, IL-5, IL-9 and IL-13, are thought to be of particular importance. In contrast, Thl cells producing interferon (IFN)-y may counteract the development of Th2 responses and so down-regulate the asthmatic response. The prevalence of asthma is increasing but the reasons for this are not fully understood. In addition, some patients do not respond adequately to treatment with corticosteroids, currently the most effective anti-inflammatory agents used routinely in human asthma. There is therefore continual interest in developing new therapeutic agents for asthma. A greater understanding of the regulation of inflammatory responses in asthma will assist in the identification of potential targets for therapeutic intervention. The aims of this thesis were (i) to assess the role of the cytokine IL-18 in allergic airway inflammation by determining IL-18 levels in induced sputum in asthmatic subjects in comparison to normal subjects, and by studies in a murine model of allergic asthma using IL-18 gene deficient mice and (ii) to assess the potential antiinflammatory actions of simvastatin and thymosin beta 4 sulfoxide in the murine asthma model. IL-18 is a pro-inflammatory cytokine which can promote IFN-y secretion and, in association with IL-12, enhance the development of Thl responses. However, in some circumstances it may also stimulate Th2 responses. IL-18 therefore has the potential to suppress or exacerbate allergic airway inflammation. The role of IL-18 in both clinical and experimental asthma remains unclear. Statins are inhibitors of the rate-limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, in cholesterol biosynthesis. As such they have been widely used as cholesterol lowering agents in clinical practice. They have previously been shown to have anti-inflammatory properties independent of their cholesterol-lowering ability in clinical studies of atherosclerotic disease and in animal models of Thlmediated inflammation. Thymosin beta 4 sulfoxide (T~4S0) is a 5 kDa peptide. Intracellularly its principal activity is to regulate actin polymerization. Corticosteroid treatment of monocytes in vitro induces the release of T~4S0 extracellularly, where it can inhibit neutrophil chemotaxis. Exogenous administration of T~4S0 has been shown to reduce neutrophilic inflammation in animal models. In this study it is shown that IL-18 is detectable in induced sputum fluid and IL-18 mRNA is expressed in induced sputum cells from asthmatic and nOlmal subjects. IL- 18 protein levels in induced sputum, and IL-18 mRNA expression in induced sputum cells were not significantly different between these groups. IL-18 production was localised to sputum macrophages. However, cigarette smoking significantly reduced IL-18 levels in induced sputum fluid in both asthmatic and normal subjects. In asthmatics, but not normal subjects, the reduction in IL-18 levels in sputum fluid was associated with reduced IL-18 mRNA expression in induced sputum cells. A murine model of allergic asthma, using BALB/C mice sensitised and challenged with ovalbumin (OVA), was used to examine the role of IL-18 in allergic responses in vivo. IL-18 gene knockout (ko) had significantly reduced bronchoalveolar lavage (BAL) total cell count and eosinophilia compared to wild-type (WT) mice. IL-18 ko mice had reduced IL-4 expression in thoracic lymph nodes, as assessed by quantitative peR, and significantly reduced OVA-specific IL-4 secretion from thoracic lymph node cultures assessed by ELISA. Serum OVA-specific IgG 1, IgG2a and IgE and total IgE levels were not significantly different between IL-18 ko and WT mice. The murine model of allergic asthma was also used to examine the anti-inflammatory activities of simvastatin and T~4S0 in a Th2-mediated, eosinophilic condition. Simvastatin treatment, either orally or intraperitoneally, and T~4S0 intraperitoneally reduced the total inflammatory cell infiltrate and eosinophilia in BAL fluid in response to inhaled OV A challenge. At higher doses of simvastatin intraperitoneally, a histological reduction in inflammatory infiltrates in the lungs was observed. Treatment with simvastatin intraperitoneally, but not orally, and T~4S0 were also associated with a reduction in IL-4 and IL-5 levels in BAL fluid. OVA-induced IL-4 and IL-5 secretion was reduced in thoracic lymph node cultures from both simvastatin-treated and T~4S0-treated mice. Neither simvastatin nor T~4S0 treatment altered serum total IgE or OVA-specific IgG 1 and IgG2a levels. The results described show that IL-18 can be detected in the induced sputum fluid of asthmatic and normal subjects and that cigarette smoking significantly reduces its levels. Studies in a murine model of allergic asthma suggest that IL-18 has a proinflammatory role in allergic airway inflammation, at least in part through its ability to induce IL-4 secretion. Both simvastatin and thymosin beta 4 sulfoxide had convincing anti-inflammatory properties in the murine model of asthma used, and these agents, or related compounds, may have therapeutic potential in human asthma.

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12

Wong, Fung-ping y 黃鳳屏. "A retrospective study of tracheal morphometry in Chinese adults by computed tomography". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48273685.

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Objective: To determine the upper airway morphometry of Chinese adults by computed tomography. Study Design: This anatomical study consisted of radiological examination of Chinese adults’ upper airway and trachea using computed tomography and image analysis with the help of post-data capture processing software. Materials and Methods: A retrospective review of sixty-five Chinese adults who underwent computed tomography of head and neck region at a regional hospital in Hong Kong was conducted. Computed tomography performed by a Philips Gemini 16? PET/CTPhilips Gemini GXL 16 PET/CT Scanner. Post-data capture processing was performed on GE Advantage Window 4.3 workstation. Measurements were made on standard or oblique reformatted orthogonal planes. Results: 65 consecutive computed tomography scans of the head and neck region of Chinese adults werereviewed. The distance between lower incisor and vocal cords was 144.0mm (±12.1 SD) in men and 124.8mm (±10.4 SD) in women. The distance between the vocal cord and cricoid ring was 21.5mm (±5.8SD) in men and 16.1mm (±6.3SD) in women. The distance between the lower incisor and cricoid ring was 165.5mm (±10.7SD) in men and 140.9 mm (±11.1SD) in women. The distance between the vocal cord and carina was 142.4mm (±12.1SD) in men and 130.4mm (±12.6SD) in women. The distance between the cricoid ring and carina was 121.0mm (±12.7SD) in men and 114.3mm (±10.2SD) in women. All these measurements showed statistically significant gender difference. In men, the anteroposterior diameter of cricoid ring was 21.8mm (±1.4SD) and the transverse diameter was 17.0mm (±1.7SD). In women the anteroposterior diameter of cricoid ring was 17.4mm (±1.9SD) and the transverse diameter was 13.4mm (±1.8SD). Both were statistically different among men and women. The anteroposterior diameter of trachea of men was 21.1mm (±2.9 SD) and the transverse diameter was 17.8mm (±2.7 SD). While the corresponding anteroposterior diameter was 16.1mm (±2.2 SD) and the transverse diameter was 15.9mm (±1.6 SD) in women with statistically significant difference. Using the Pearson correlation, body height but not age of subjects was statistically correlated with all the airway measurements Conclusion: This study reports the tracheal morphometry and dimensions in a Chinese population and their correlation with body height. Details of these measurements will aid airway management and other upper airway procedures in this population. Conclusion: This study reports the tracheal morphometry and dimensions in a Chinese population and their correlation with body height. Details of these measurements will aid airway management and other upper airway procedures in this population. Conclusion: This study reports the tracheal morphometry and dimensions in a Chinese population and their correlation with body height. Details of these measurements will aid airway management and other upper airway procedures in this population.
published_or_final_version
Anatomy
Master
Master of Medical Sciences

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13

Wilkinson, Thomas Michael Alan. "The role of airway infection in chronic obstructive pulmonary disease". Thesis, Queen Mary, University of London, 2006. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1897.

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This. thesis examines the role of respiratory bacterial and viral infection in the natural history of Chronic Obstructive Pulmonary Disease. The rationale for this study is basedu pon previous data demonstratingt hat airway bacterial colonisationi s common in stable COPD and that bacterial and viral pathogens are commonly detected at exacerbations. The methodsu sed have involved the careful characterisationa nd clinical follow up of a cohort of patients with moderate to severe COPD in the stable state and at exacerbation. Sampling of airway and systemic compartments enabled the detection of respiratory pathogens and quantification of inflammation. Comparisons between clinical indices and evidence of infection were performed to determine the relationships between bacterial and viral infections and disease outcomes including lung function decline and exacerbation severity. The findings confirmed that lower airway bacterial colonisation is common in stable COPD and is associated with airway inflammation. They demonstrated for the first time a relationship between the degree of bacterial carriage and the rate of disease progression. This study has also described novel evidence for persistence of respiratorys yncytial virus in the lower airway and associationsw ith inflammation and lung function decline and impaired anti-viral immune responsesT. he combined role of human rhinoviral and bacterial infection at exacerbation has been studied and factors influencing responsesto exacerbationt herapy determinedw ith the importance of early initiation of treatment identified. The findings in this thesis indicate that both viral and bacterial pathogens may play an important role in the natural history of COPD and are therefore targets for potentially novel interventions. This work suggests that viral and bacterial infections and their interactions play an important role in modulating airway inflammation in stable disease and at exacerbation thus impacting on both disease progression and exacerbation severity. This work has provided a rationale for future investigation into the mechanisms underlying susceptibility to infection in this important disease.

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14

Neumann, Peter. "Airway pressure release ventilation : a systematic experimental approach /". Uppsala, Sweden : Uppsala University : Distributed by Uppsala University Library, 2000. http://w3.ub.uu.se/diss/eng/abstract.cfm?ISBN=91-554-4723-6.

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15

Ratnawati, Ratnawati Prince of Wale Hospital Clinical School UNSW. "Exhaled nitric oxide in asthmatic airway inflammation". Awarded by:University of New South Wales. Prince of Wale Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/25729.

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Measuring the level of exhaled NO (eNO) in the breath is a new method to monitor airway inflammation in asthma and may have a role in the management of asthma. The hypotheses were that eNO will reflect the degree of inflammation in chronic asthma, and will indicate how anti- inflammatory therapy should be altered to improve asthma control. Three studies were performed to test the hypotheses. A cross sectional study was performed to define the normal range of eNO and to compare this range with those who have asthma or atopy. The second study was observational, to compare the level of eNO during and after an exacerbation of asthma. The third study was an interventional study to evaluate eNO in management of paediatric asthma. In this latter study the level of eNO was measured to monitor airway inflammation in asthmatic children with the intention of adjusting antiinflammatory drugs (inhaled glucocorticosteroids) according to the level of eNO. These studies have shown that the mean level of eNO was significantly higher in asthmatic compared with normal subjects, but not significantly different when compared with atopic non-asthmatic subjects. eNO was correlated with the number of positive skin prick tests in atopic subjects whether asthmatic or nonasthmatic. The eNO level was increased during acute exacerbations of asthma and decreased after two weeks with therapy of GCS. In a pilot study eNO appeared to be superior to FEV1 in adjusting the dose of iGCS to control asthmatic children, but this needs to be confirmed with a larger sample size. Another non-invasive method to detect inflammatory markers is the technique of exhaled breath condensate (EBC). Although NO is degraded to NOx, it was found that eNO had no significant correlation with EBC NOx but had a significant correlation with pH. Hypertonic saline challenge, an artificial model of an asthmatic exacerbation was associated with an increase in EBC volume and the release of histamine, implicating mast cell activation. These novel findings suggest that non-invasive markers can be used both for clinical and mechanistic proposes.

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16

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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17

Wang, Dong. "Regulation of anion secretion in human airway epithelial cells /". View abstract or full-text, 2009. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202009%20WANG.

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18

鄧樹森 y Shu-sum Tang. "Cephalometric airway measurements in class III skeletal deformity". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B38628065.

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19

Au, Pui Ming. "Vibration of branched circular cylindrical shells as applied to airway walls a thesis submitted to Auckland University of Technology in fulfilment of the requirement for the degree of Doctor of Philosophy, March 2005". Full thesis. Abstract, 2005.

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20

Menon, Anilkumar S. "Flow dynamics in a model of the large airways". Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72009.

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Oscillatory velocity profiles and the pressure-flow relationship were measured in a 3:1 scale rigid model of the human central airways. A reciprocating pump provided flows with frequencies of 0.25, 1, 2 and 4 Hz and tidal volumes of 300, 500 and 1500 mL giving tracheal Womersley numbers up to 31 and peak tracheal Reynolds numbers up to 17000. A hot wire anemometer was used to measure velocities along two perpendicular diameters (one in the plane of the model and the other in the plane perpendicular to the model) at 10 stations distributed through the model. Velocities were also measured with and without a model larynx and with tracheal intubation in steady inspiratory flows. The flow distribution to the five lobar bronchi was identical in all experiments.
Oscillatory velocity profiles were compared with the steady velocity profiles at nearly identical Reynolds numbers. The flow in a branch was quasi-steady below a critical Strouhal number in agreement with an order of magnitude analysis. For quasi-steady oscillatory flows the velocity profile developed from an initially flat shape to the profiles characteristic of steady flow in branching tubes. Flows that were not quasi-steady exhibited relatively flat profiles over the entire respiratory cycle. The effects of tidal volume, frequency and the geometry of the airways on the velocity profiles were determined.
While the larynx produced a significant jet within the trachea it had no effect on the velocity profiles beyond the carina. The presence of a concentric endotracheal tube located halfway between the glottis and the carina had little effect on the velocity profiles in the main stem and the lobar bronchi. Inserting the tube further into the trachea altered the velocity profiles in the right upper lobar bronchus.
In oscillating flow the pressure was essentially uniform around the periphery of a branch in strong contrast to the results for steady flow. The pressure drop in oscillating flow was much larger than the pressure drop in steady flow at an equivalent flow rate. The functional form of the relationship between the pressure drop across the different branches of the model and the tracheal Reynolds number was similar to that suggested by earlier researchers, however the coefficients were very sensitive to the geometry of the model.

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21

Izci, Bilgay. "Breathing during sleep : studies related to upper airway calibre in pregnancy". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1971.

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Snoring is common in pregnancy, and has been associated with an increased incidence of both maternal hypertension and preeclampsia, as well as an increased incidence of low birth weight infants and significantly poorer Apgar scores at birth. Patients with pre-eclampsia have episodes of partial upper airway (UA) obstruction during sleep. These repeated episodes are associated with further increases in blood pressure (BP). Preliminary evidence indicates that preventing episodes of airflow obstruction with continuous positive airway pressure (CPAP) therapy may reduce BP in pre-eclampsia. Snoring and apnoea-hypopnoea index (AHI) subside within a few months of delivery. However, there have been no studies measuring the effect of pregnancy or the postpartum period on UA dimension. The present study aimed to compare UA dimensions in pregnant and nonpregnant women and in patients with pre-eclampsia with a follow-up of the pregnant women post partum. Apart from snoring, excessive daytime sleepiness (EDS) is the most common complaint among pregnant women. A majority of the pregnant women including preeclamptic women have experienced EDS during pregnancy, but it is not clear whether EDS is associated with snoring. Thus, this thesis also examines whether snoring and sleepiness are linked in pregnancy and pre-eclampsia. In a cross-sectional study with a 3 way comparison, 50 pregnant, 37 pregnant women with pre-eclampsia in the third trimester of pregnancy, and 50 nonpregnant women were consecutively recruited. Control subjects were matched with pregnant women (both healthy pregnant and pre-eclamptic women) for age and pre-pregnancy BMI. UA dimensions were measured using acoustic reflection. Habitual snoring was reported by 15% of nonpregnant women, 28% of pregnant women, and 48% of pre-eclamptic women (p < 0.001). Pre-eclamptic women had narrower UAs compared to non-pregnant or healthy pregnant women in seated position (p < 0.02). Supine oropharyngeal junction area was also less in the women with pre-eclampsia than in the nonpregnant women (p = 0.01) but similar in women with pre-eclampsia and pregnant women (p > 0.3). When seated, pregnant women had wider UAs than nonpregnant women (p < 0.02). There was a non-significant trend for pregnant women to have narrower airways than non-pregnant women when supine. The data suggest that there may be pregnancy related changes in UA dimension, but this was not clear from this cross-sectional study of 3 groups, non-pregnant, pregnant and pre-eclamptic women. In a cross sectional study (with a 2 way comparison) with follow up of the pregnant women at least three months after their delivery, 100 women in the third trimester of pregnancy and 100 nonpregnant women, matched for age and BMI, were recruited. Fifty women agreed to be restudied 3 months after delivery. UA dimensions were measured using acoustic reflection. Snoring was less common in nonpregnant (17%) than pregnant women (41%) and returned to nonpregnant levels after delivery (18%). Pregnant women had significantly smaller UAs than nonpregnant women at the oropharyngeal junction when seated and smaller mean pharyngeal areas in the seated, supine and lateral postures compared with the nonpregnant females (p< 0.05). Pregnant women had smaller mean pharyngeal areas compared with post-partum in the seated, supine and lateral postures (p< 0.03). This study confirmed increased snoring and showed narrower UAs during the third trimester of pregnancy. One-hundred sixty-seven healthy and 82 pre-eclamptic women in the third trimester of pregnancy and 160 non-pregnant women completed a sleep questionnaire in a prospective questionnaire-based study. Age and height did not differ significantly between groups (P>0.2), but pre-eclamptic women were heavier than pregnant and non-pregnant women and had higher BMI than pregnant women before pregnancy (all P<0.05). Seventeen percent of control, 35% of pregnant and 59% of pre-eclamptic women snored (P<0.001), but pre-pregnancy snoring rates (both 10%) were similar to those in non-pregnant women (17%) (p>0.1). Sleepiness was reported by 12% of non-pregnant, 23% of pregnant and 15% of pre-eclamptic women (p<0.04), but non-pregnant women had lower mean Epworth Sleepiness scores than both pregnant and pre-eclamptic groups (P<0.001). Snoring was correlated with (p=0.002), but explained only <2% of the variance in sleepiness. The studies presented in this thesis indicate that UA narrowing occurs in the third trimester of pregnancy, probably due to pregnancy-related changes. It is likely that reduced UA calibre may contribute to the increased rate of snoring, breathing pauses and sleepiness in the third trimester of pregnancy, especially in patients with pre-eclampsia. However, sleepiness in pregnancy is largely due to factors other than snoring or breathing pauses.

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22

Mackawan, Surussawadi. "The relationship between added lung sounds and airway dimensions". Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/354119/.

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The aim of this study was to explore potential relationships between added lung sound characteristics measured by Computer Aided Lung Sound Analysis (CALSA) and airway dimensions measured by High resolution Computed Tomography (HRCT). CALSA has been proposed as a new objective measurement to record and analyse lung sounds. However, there is still a lack of evidence as to whether and how added lung sounds relate to the geometry of airways. HRCT is considered to have the highest sensitivity of imaging measurements and is capable of generating three dimensional pictures of airways from which the dimensions may be measured. Twenty-six participants (9 healthy non-smokers, 9 healthy smokers and 8 patients with COPD) were recruited. Lung sound data were recorded using a digital stethoscope. HRCT scans were conducted using a Siemens Sensation 64 CT scanner and the resulting data were analysed using the Pulmonary Workstation 2 software to give airway dimensions. Lungs sounds were characterised in terms of Crackle 2-cycle durations (crackle 2CD), the number of crackles per breathing cycle (NCpB) and lung geometry were characterised in terms of airway diameter, length, branching angle, internal perimeter, wall thickness and percentage of wall area. The analysis showed that there was a significant positive correlation between crackle 2CD and airway wall thickness at generations 3 and 5. Crackle 2CD also significantly correlated with the branching angles at the main bronchus and at generation 3. There was also a significant negative correlation between NCpB and percentage of wall area at generation 2 and airway wall thickness at generation 5. Moreover, NCpB recorded at anterior right region of chest wall was found to predict the percentage of wall area at the right upper bronchus. These initial results suggest NCpB might be useful to predict changes in percentage of wall area caused by the chronic inflammation of the main bronchi, though a larger sample size would be needed to confirm it. This suggests that crackles could potentially be used as a biomarker of COPD.

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23

Behndig, Annelie. "Airway antioxidant responses to oxidative air pollution and vitamin supplementation". Doctoral thesis, Umeå universitet, Folkhälsa och klinisk medicin, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-742.

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Air pollutants, such as ozone (O3) and diesel exhaust particles, elicit oxidative stress in the lung. Antioxidants within the respiratory tract lining fluid (RTLF) protect the underlying tissue from oxidative injury. Supplementation with vitamins has been shown to modulate the acute ozone-induced effects, but the mechanisms behind this have not been fully clarified. The aim of this thesis was to investigate the airway responses to diesel exhaust and ozone exposure in healthy humans, with the emphasis on inflammatory and antioxidant responses. Furthermore, to study whether oral supplementation with vitamin C could increase ascorbate concentration in the RTLF and whether vitamin supplementation could modulate the negative effects induced by ozone exposure. Diesel exhaust (100 µg/m3 PM10 for 2h), evaluated 18 hours post exposure (PE), induced a neutrophilic airway inflammation and an increase in bronchoalveolar (BAL) urate and reduced glutathione. During O3 exposure (0.2 ppm for 2h), significant losses of nasal RTLF urate and ascorbate concentrations were observed. Six hours PE, a neutrophilic inflammation was evident in the bronchial wash (BW), together with enhanced concentrations of urate and total glutathione. In the bronchoalveolar lavage (BAL), where vitamin C, urate and glutathione concentrations were augmented, no inflammatory response was seen. In alveolar lavage leukocytes, there was a significant loss of glutathione and cysteine, whereas an increase in ascorbate was found in bronchial tissue samples. Following supplementation with increasing doses of vitamin C (60-1,000 mg/day, for 14 days), evaluated 24 hours after the last dose, ascorbate concentrations were unchanged in the nasal RTLF, despite elevated concentrations in plasma and urine. In contrast, following a single dose of 1g of vitamin C, vitamin C concentrations increased significantly in both plasma and nasal lavage two hours post supplementation, before returning to baseline levels at 24 hours. Notably, dehydroascorbate (DHA) accounted for the largest part of RTLF vitamin C and a number of control experiments were performed to ensure the authenticity of this finding. Healthy O3 responders were exposed to O3 (0.2 ppm for 2 h) and air, following seven days of supplementation with vitamin C and E or placebo. No protective effect on lung function or airway inflammation was observed following supplementation. BW and BAL-DHA were enhanced after O3, with further increases following supplementation. In conclusion, oxidative air pollutants induce airway inflammation, as well as a broad spectrum of antioxidant adaptations, which could ultimately limit the airway inflammatory responses. Oral vitamin supplementation was shown to augment RTLF-vitamin C concentrations, but it did not provide protection from the ozone-induced airway responses following a single insult of ozone. The finding of high concentrations of DHA in the RTLF could indicate that DHA represents an important transport form of vitamin C onto the surface of the lung.

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24

Whicker, Susan D. "Pharmacological studies of [beta]-adrenoceptors in airway smooth muscle". Thesis, The University of Sydney, 1990. https://hdl.handle.net/2123/26279.

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Airway smooth muscle receptor-mediated responsiveness and receptor characteristics for airway tissue from non-asthmatic and asthmatic patients, and guinea pigs with airway responsiveness, were investigated for airway preparations using drug concentration-response relationships and radiolabelled ligand binding studies. Between—patient variability was approximately SSO-fold greater than within-patient variability for B-adrenoceptor-mediated responsiveness of human airway tissue. Alteration in B-adrenoceptor characteristics (Kd and Bmax) could not account for the marked between-patient variability demonstrated for B-adrenoceptor mediated responsiveness. Exposure of human airway tissue in vivo with preoperative Bz-adrenoceptor agonist medication did not inﬂuence B-adrenoceptor-mediated responsiveness, however in vitro exposure of airway tissue to B-adrenoceptor agonist did reduce G-adrenoceptor-mediated responsiveness. This suggests, that in vivo concentrations reached for Bz-adrenoceptor agonist medication were not great enough to induce an alteration in B-adrenoceptor-mediated function. Chronic administration of B-adrenoceptor antagonist medication of patients and rats reduced B-adrenoceptor-mediated responsiveness of airway tissue in vivo. The B-adrenoceptor-mediated responsiveness of peripheral airway tissue from spontaneously hypertensive rats was similar to that for tissue from normotensive animals. Evidence suggests therefore that the reduced 8--adrenoceptor-mediated responsiveness is not due to the hypertension but to the accumulation of the 13--adrenoceptor antagonist in the peripheral airway tissue. Airway smooth muscle from asthmatic patients demonstrated similar relaxation responsiveness to tissue from non-asthmatics and reduced responsiveness to contractile agonists. These results suggest that airway hyperresponsiveness in vivo is regulated by factors other than smooth muscle characteristics. Relaxation responsiveness of airway smooth muscle from asthmatic patients was similar to that in non-asthmatic patients, however contractile responsiveness was reduced. Alteration of muscarinic cholinoceptor responsiveness, suggesting that alteration in muscarinic-mediated responsiveness is distal to the muscarinic cholinoceptors. B-Adrenoceptor characteristics remained unchanged. It is concluded that airway hyperresponsiveness in vivo is not represented by parallel changes in receptor-mediated tissue responsiveness, suggesting that neural and/or humoral inﬂuences may influence airway control.

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25

Kelly, Clive Anthony. "The use of bronchoalveolar lavage in the investigation of the pathophysiology of airway hyperresponsiveness". Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329175.

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26

Armstrong, Julian. "Anatomical optical coherence tomography in the human upper airway /". Connect to this title, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0022.

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27

Ramos-Barbón, David. "The role of CD4+T cells in airway remodeling in experimental asthma /". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85640.

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The aim of this work was to investigate the role of CD4 + T cells, central to airway inflammation in asthma, in airway remodeling. Structural changes that occur in asthmatic airways in association with inflammation include an increase in airway smooth muscle mass, which participates in causing airway hyperresponsiveness. We aimed to gain further insights into the mechanisms that may link inflammation with remodeling using a rat model of experimental asthma. We hypothesized that CD4+ T cells drive airway smooth muscle remodeling. Adoptive transfer of CD4+ T cells from ovalbumin-sensitized rats induced increased proliferation and inhibition of apoptosis of airway myocytes in naive recipients upon repeated antigen challenge, which resulted in an increase in airway smooth muscle mass. CD4+ T cells genetically modified to express green fluorescent protein were localized by confocal microscopy in juxtaposition to airway smooth muscle cells, suggesting that CD4 + T cells may modulate smooth muscle cell function through direct cell-cell interaction in vivo. We subsequently co-cultured antigen-stimulated CD4+ T cells with cell cycle-arrested airway smooth muscle cells and demonstrated by flow cytometry that CD4+ T cells induce myocyte proliferation, dependent on T cell activation and direct T cell/myocyte contact. Reciprocally, direct cell contact prevented activation-induced T cell apoptosis as well as spontaneous apoptosis of resting T cells, suggesting T cell/myocyte cross-talk. Our data demonstrate that CD4+ T cells drive airway smooth muscle remodeling in experimental asthma, and suggest that a mechanism involving a direct "synapse" participates in CD4+ T cell regulation of myocyte turnover and induction of remodeling. The goal of genetically modifying CD4+ T cells involved technical challenges relevant to the field of gene therapy and are dealt with in detail in this thesis. Retroviral gene transduction coupled with antigenic stimulation was

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28

Sobuwa, Simpiwe. "Prehospital airway management in severe closed traumatic brain injury an analysis of its impact on outcome". Master's thesis, University of Cape Town, 2012. http://hdl.handle.net/11427/2873.

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Includes abstract.
Includes bibliographical references.
The purpose of this study was to describe the outcomes of patients with severe traumatic brain injury managed by emergency care providers in the Cape Town Metropole.

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29

Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation". Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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30

Li, Min. "Tobramycin Disposition in the Lung Following Airway Administration". VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3275.

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Tobramycin disposition following airway administration was evaluated by meta-analysis of human data in the literature and, experimentally, using a realistic ex vivo model, the isolated perfused rat lung preparation (IPRL). Pulmonary bioavailability of inhaled tobramycin in published studies was re-evaluated separately for CF and healthy adults, with the drug’s intrinsic pharmacokinetic (PK) parameters obtained from intravenous (IV) studies in the literature. While large variations in tobramycin’s clearance precluded accurate assessment of its bioavailability, the results were indicative of substantial pulmonary absorption, in spite of its hydrophilic and poly cationic properties. To explore its disposition kinetics and mechanisms following airway administration, tobramycin absorption was investigated as a function of dose in the IPRL. The cumulative fraction of the administered tobramycin dose reaching the perfusate versus time, was bi-exponential and dose-dependent, unlike that of the marker solutes fluorescein and mannitol, both of which showed first-order and dose-independent kinetics. A kinetic model that incorporated lung tissue binding (or sequestration) alongside passive absorption was employed successfully to describe the aminoglycoside’s disposition in the IPRL following airway administration. Tobramycin’s absorption was fast with the first-order absorption rate constants (0.065-0.070 min-1) close to those seen with fluorescein (0.076 min-1), but a dose-, and concentration-dependent slow onset tissue binding prolonged its presence in the rat lung. Binding was confirmed by independent dynamic dialysis experiments using sliced lung prepared from the intact IPRL, immediately following airway administration using an identical technique as that used in tobramycin absorption studies. Dosing solution osmolality and pH had negligible effects on the drug’s disposition in the IPRL, when these were investigated over experimental ranges that could be used clinically. While tobramycin itself was found to accelerate mannitol’s absorption, and thus affect airway epithelial integrity when administered at high doses, the effect was undetectable at a dose level in rat lungs that was believed to produce airway concentrations corresponding to those in human patients using TOBI®. These findings may partly explain the apparent success of inhaled tobramycin therapy in the treatment of pulmonary infections.

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31

Chakravorty, Indranil. "Health technology assessment of continuous positive airway pressure devices in sleep apnoea hypopnoea syndrome". Thesis, University of Warwick, 2005. http://wrap.warwick.ac.uk/38056/.

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A. 1 Background The need to assess safety as well as clinical and economic effectiveness of health care innovations and thus prioritise health care provision, created the need for structured health technology assessment (HTA) programs [Gafni et al. 1993b; Henshall et al. 1997; Stevens et al. 20041. Sleep apnoea hypopnoea syndrome (SAHS) affects 2-4% of the adult population [Young et al. 1993] who are disabled by daytime dysfunction [Hardinge et al. 1995; Johns 1993b; Mitler 1993; Sauter et al. 200l and a heightened mortality and morbidity [Greenberg et al. 1995; Kiely et al. 2000; Peker et al. 1999; Sanner et al. 1997; Tremel et al. 1999; Wilcox et al. 1998; Moruzzi et al 1999; Malone et al. 1991]. The advent of continuous positive airway pressure devices (CPAP) [Sullivan et al 1981] made it possible to treat safely, patients over a wider spectrum of disease severity [Borak et al. 1996; Mar et al. 2003; Engleman et al 1997a], yet its diffusion and adoption appears to follow a heterogenous pattern. A. 2 Study design A retrospective case-control study of 603 SAHS patients was followed by a prospective, randomised, parallel group trial (RCT) of CPAP compared to lifestyle intervention (including weight reduction and sleep hygiene strategy) comparing clinical, health related quality of life (HRQL) and cost-utility ratios (CUR). The final study is a qualitative survey assessing the factors influencing the diffusion and adoption of CPAP among 303 Primary care trusts (PCT) and 261 Respiratory physicians in the UYA. 3 Results SAHS patients had a (5x) higher risk of death and (2x) of hypertension, compared to controls. Among 71 SAHS patients in the RCT, those on CPAP demonstrated greater clinical effectiveness (sleep latency, apnoea hypopnoea index, excessive daytime sleepiness & neuropsychiatriefunction) and HRQL (social functioning, mental health & energylvitality) compared to lifestyle intervention. Utilities improved on CPAP and the CUR were lower (E'716-E2027 vs. F-326444243). The diffusion survey demonstrated that the characteristics of CPAP as an innovation, would favour its adoption compared to alternative therapies, except in patient tolerability (PCT respondents). However there appeared to be no regular system for the diffusion of innovation knowledge within the NHS and hindrances in SAHS management due to deficiencies in resources, specialists and facilities. A. 4 Conclusions The results presented in this thesis provide a logical framework for the assessment of the progression of an innovation from the stage of establishing the clinical burden of disease and treatment needs, to its adoption and may help identify potentially modifiable factors in slow diffusion scenarios.

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32

Laing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma". University of Western Australia. School of Paediatrics and Child Health, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0097.

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[Truncated abstract] Asthma genetic studies have identified many genes that contribute to the pathogenesis of asthma and related variables. Members of the secretoglobin family appear to play an important role in controlling airway inflammation but they have received relatively little attention in asthma genetic research. In this thesis, I have investigated the genes of two members of the secretoglobin family (16 kDa Clara cell secretory protein (CC16) and secretoglobin 3A2 (SCGB3A2)) that are expressed at high levels in the airways and are important anti-inflammatory agents. The overall aim of these studies was to investigate the genetic variability of the CC16 and SCGB3A2 genes and their influence on airway inflammatory disease. The main hypothesis was that genetic variability in the genes for CC16 and SCGB3A2 exert an influence on airway inflammatory disease. Three populations were investigated: (1) a paediatric case control population (n=99), (2) an unselected birth cohort followed longitudinally at ages 1 month (n=244), six (n=123) and 11 years (n=195) and (3) an unselected Aboriginal Australian population (n=251). The case-control population was screened for novel DNA sequence variants in the CC16 promoter and the SCGB3A2 5’UTR and exons. No novel sequence variants were identified in the CC16 promoter and two were identified in the SCGB3A2 5’UTR (G- 811A and G-205A). A single nucleotide polymorphism previously identified in the CC16 gene (A38G) and the two polymorphisms identified in the SCGB3A2 gene were genotyped in both unselected populations. Genotype/phenotype associations were identified with adjustment for potential confounders such as age, gender, height and maternal tobacco smoking, where appropriate. This was due to the contribution of these factors to the aetiology of asthma, atopy and related phenotypes. All three polymorphism frequencies were significantly different between these two ethnically diverse populations

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33

Haji, Sadeghi Mahboobeh. "The emerging role of the eosinophil and its measurement in chronic cough : airway inflammation in chronic cough". Thesis, University of Hull, 2017. http://hydra.hull.ac.uk/resources/hull:16543.

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Although the aetiology of chronic cough in guidelines is clearly stated as asthma and related syndromes, gastro-oesophageal reflux disease, and upper airways disease, the inflammatory mechanisms underlying these conditions differ. Recent studies on asthma have increasingly focused on its molecular phenotypes instead of clinical characteristics. Predominantly in this thesis I hypothesize that by dividing cough patients into the clinical characteristics of eosinophilic and neutrophilic groups will enhance our ability to recognise the type of airway inflammation, and consequently will lead us to more targeted treatment approaches. To investigate this hypothesis I conducted a randomized, single centre, open label, controlled, clinical trial to examine the outcome of anti-inflammatory therapy with either montelukast or prednisolone in 50 patients with chronic cough. Furthermore, I studied the epidemiology of 137 chronic cough patients attending the Hull cough clinic. Results from the clinical study demonstrated that patients with FeNO≤20ppb had twice the number of coughs compared with patients with FeNO≥30ppb. This was reflected on quality of life as assessed by the LCQ and HARQ. Confirming this finding I found in the epidemiological study, that patients attending the hull cough clinic with FeNO≤25ppb scored significantly higher in HARQ compared with FeNO≥25ppb. In the clinical trial study I have shown that FeNO was a good marker for eosinophilic inflammation. There was a high degree of correlation with FeNO, blood and sputum eosinophilia thus confirming phenotypic identity. Whether the FeNO can be used to identify the different characteristics between eosinophilic and non-eosinophilic coughs needs further investigation. Cough patients in both low and high FeNO groups have shown a similar response to montelukast despite anticipating little or no effect in those without eosinophilic inflammation. These results suggest that response to montelukast may not be predicted by presence of eosinophilic biomarkers alone but may be act by effecting localised leukotriene mediated inflammation.

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34

Marino, Rafael. "Genetic dissection of airway responsiveness and its impact on the susceptibility to allergic asthma". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97030.

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Asthma is a chronic and inflammatory disease of the airways determined by genetic and environmental factors which trigger an uncontrolled immune response. Airway hyperresponsiveness (AHR) is inherited as a complex trait and associated with asthma. We assessed AHR in naïve A/J and C57BL/6J mice using the non-invasive method and demonstrated its correlation with invasive method evaluating AHR in non-sensitized mice. Aditionally, we studied the genetic causes underlying AHR using six F2 backcrosses generated from recombinant congenic strains (RCS) created from A/J and C57BL/6J parental strains. Our genetic study allowed us to narrow down the significant regions previously identified in the RCS, as associated with AHR. Quantitative trait loci analysis of BcA86xC57BL/6J (F2) and BcA86xC3H/HeJ (F2) crosses shows 3 significant regions on chromosome 12. These significant regions contain 232 genes, of which 9 genes have been identified as potential candidates. Those genes include the Arhgap5, Foxa1, Clec14a, Ctage5, Rtn1, Gpx2, Rsad2, Prkd1 and Adam21. Additionally, increased levels of secretory leukocyte protease inhibitor (SLPI), an anti-inflammatory mediator, have been observed in asthmatic patients compared to healthy controls. We investigated the role of SLPI in the development of phenotypes associated with allergic asthma and the effect of resiquimod on SLPI expression. Our results demonstrated that over expression of SLPI leads to a lower degree of airway inflammation and higher lung resistance, whereas the ablation of SLPI has the opposite effect on allergic asthma phenotypes. We also demonstrated that the treatment with resiquimod is independent of SLPI expression. Overall, the results presented in this thesis demonstrate how the non-invasive method is a reliable tool for the assessment of AHR in naïve A/J and C57Bl/6J mice. Furthermore, loci on mouse chromosome 12 are linked to the susceptibility to develop AHR. Candidate genes have been identified in these loci and remain to be explored. Finally, we demonstrate the immunoregulatory activity of SLPI in the airways by diminishing inflammation and improving lung function in allergic asthma. Taken together, our results provide a better understanding of the inheritance and molecular mechanisms of phenotypes of asthma as well as provide insights for the design of new therapies.
L'asthme est une maladie chronique et inflammatoire des voies respiratoires déterminée par des facteurs génétiques et environnementaux qui déclenchent une réponse immunitaire non contrôlée. L'hyper-responsivité aérienne (HRA) est hérité comme un trait complexe et est associée à l'asthme. Nous avons évalué HRA dans des souris de souches A/J et C57BL/6J suivant la méthode non-invasive et nous avons démontré sa corrélation avec la méthode invasive en évaluant l'HRA dans des souris non-sensibilisés. En outre, nous avons étudié la cause génétique de l'HRB en utilisant six croissement en retour (F2) générer avec des souches de souris cogéniques recombinantes (SCR) et les souches parentales, A/J ou C57BL/6J. Notre étude génétique nous a permis de rétrécisse les régions signifiantes identifier dans les SCR. L'analyse des locus quantitatifs des croisements BcA86xC57BL/6J (F2) et BcA86xC3H/HeJ (F2) prouve trois régions significative sur le chromosome 12. Cette région significative contient 232 gènes dont neuf ont été identifié comme gènes candidats. Ces gènes incluent Arhgap5, Foxa1, Clec14a, Ctage5, Rtn1, Gpx2, Rsad2, Prkd1 and Adam21. En outre, une augmentation du niveau de l'inhibiteur de la protéase des leucocytes sécrétoire (IPLS), un médiateur anti-inflammatoire, a été observée dans des patients souffrant de l'asthme comparé à des contrôles sains. Nous avons étudié le rôle de l'IPLS dans le développent des phénotypes associe avec l'asthme allergique et l'effet de resiquimod sur l'expression de l'IPLS. Nos résultats démontrent que l'hyper-expression de l'IPLS réduit le degré d'inflammation dans les voies respiratoires et augmente la résistance des poumons, tandis que l'ablation de l'IPLS a l'effet opposé sur les phénotypes associés avec l'asthme allergique. Nous avons aussi démontré que le traitement avec resiquimod est indépendant de l'expression de l'IPLS.En somme, les résultats présentés dans cette thèse démontrent que la méthode non-invasive est une technique fiable pour l'évaluation de l'HRA dans des souris des souches A/J et C57BL/6J non-sensibilises. De plus, des locus sur le chromosome 12 des souris sont liés à la susceptibilité pour développer l'HRA. Des gènes candidats on été identifié dans ces locus et restent à être explorés. Finalement, on a démontré la propriété immuno-modulatrice de l'IPLS dans les voies respiratoires, en diminuant l'inflammation et en améliorant la performance des poumons des individus souffrant de l'asthme allergique. En tout, nos résultats fournissent une meilleure compréhension de l'hérédité et le mécanisme moléculaire des phénotypes de l'asthme et aux développements de nouvelles stratégies thérapeutiques.

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Kitaev, Timur. "Evaluating Perceived Barriers to Cognitive Aid Use Among Anesthesia Providers During Malignant Hyperthermia, Myocardial Ischemia, and Unanticipated Difficult Airway". Thesis, University of Southern California, 2021. http://pqdtopen.proquest.com/#viewpdf?dispub=28002089.

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Background: A cognitive aid is defined by the Stanford Anesthesia Cognitive Aid Group as a visual in any form intended to enhance cognition and improve adherence to medical best practices. While the efficacy of cognitive aid use during simulated, intraoperative emergencies is well supported in the current literature, their use in anesthesia practice remains limited. Aim: The aim of this doctoral capstone paper is to investigate perceived barriers to cognitive aid use in the operating room among anesthesia providers during various emergency situations. Methodology: An anonymous survey was disseminated to 149 certified registered nurse anesthetists and anesthesiologists at two large academic institutions to explore actual and potential barriers that preclude cognitive aid use during three specific intraoperative emergencies: malignant hyperthermia, myocardial ischemia, and unanticipated difficult airway. Results: The survey was completed by 35 anesthesia providers. The three most frequently reported perceived barriers to cognitive aid use for all three emergency scenarios were: (a) would have distracted/delayed patient care, (b) did not know a cognitive aid was available, and (c) not enough help in the room (nobody available as the reader). Conclusion: While the current literature vastly supports the use of cognitive aids during simulated, intraoperative emergency scenarios, studies investigating their use in practice is limited. Our survey identified barriers to cognitive aid use in three specific emergency situations. Future research should focus on interdisciplinary cognitive aid training, access to cognitive aids, and use of a reader.

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Chang, Michael K. "Three-dimensional conebeam CT analysis of pharyngeal airway changes after orthognathic surgery". Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1465479.

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37

Leow, Li Pyn. "Mechanisms of airway protection in ageing and Parkinson's disease". Thesis, University of Canterbury. Communication Disorders, 2007. http://hdl.handle.net/10092/1461.

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Safe and efficient swallowing requires integrity of both motor and sensory systems. Prior studies have established that motor impairment in individuals with PD frequently manifests as abnormalities in swallowing biomechanics. In contrast, very few studies have investigated the contribution of sensory impairment towards pharyngeal biomechanics and airway protection in this patient cohort. This area should be addressed in light of evidence that the severity of limb motor dysfunction in PD does not reliably predict severity of dysphagia. Emerging data suggests that dysphagia in PD cannot be solely attributed to motor impairment, but may also be influenced by deficits in sensory aspects of airway protection. As an example, silent aspiration in up to 100% has been reported in individuals with PD due to laryngopharyngeal sensory deficits have. Even so, current research lacks information on the integration of both motor and sensory components that make up the swallowing process. The aim of this study was to document changes in airway protection with age, in PD and across severity levels of PD. The project was comprised of two parts. In part one, three parallel studies were conducted to assess a series of both motor and sensory airway mechanism (Chapters 4 to 9). In the first study, 16 young (8 males, age range 21.3 - 32.4) and 16 elder adults (8 males, age range 61.5 - 84.7), were assessed to investigate changes in airway protection that accompany ageing. In the second study, data from individuals diagnosed with PD across severity levels (Hoehn-Yahr 1 - 4, age range 64.2 - 84.5) were age and gender-matched to 16 healthy elders in order to examine the effects of PD on airway protection. In the third, the impact of disease severity was studied with data from 16 individuals in the earlier stages (Hoehn-Yahr ≤ 2, 13 males, age range 51.3 - 82.5, ) compared to 16 individuals in the later stages (Hoehn-Yahr ≥ 2.5, 10 males, age range 61.5 - 78.9). In part two of this project, two smaller, pilot studies were completed to probe the influence of pharmacologic and behavioural treatments on airway protection mechanisms. In the first pilot study, the effect of pharmacotherapy on airway protection was investigated in 10 patients 'on' and 'off' levodopa (Chapter 10). In the second study, 5 patients were assessed before and after completing the Lee Silverman Voice Treatment (LSVT) to document effects of speech rehabilitation on airway protection (Chapter 11). Multimodality assessment elicited data from all participants on both motor and sensory components of airway protection (Chapter 3). Specifically, breathing-swallowing coordination (BSC) and swallowing apnoea (SA) were captured using simultaneous directional nasal airflow and surface electromyography (sEMG). Standard, closed-loop spirometry was used to assess pulmonary function. Swallowing biomechanics were screened using a validated timed test of swallowing efficiency and further evaluated using fibreoptic endoscopic evaluation of swallowing (FEES). Finally, chemo-sensation of the laryngopharynx was determined with the administration of the inhalation cough challenge while mechanosensation was examined using FEES. Results suggest that motor control for airway protection is reasonably robust in PD, although sensory response is impaired. The predominant pattern for swallowing respiratory coordination was mid-expiration for all participants regardless of age and disease severity (Chapter 4). Individuals with PD demonstrated a reduction in average time and volume per swallow, leading to an overall decrease in swallowing capacity (Chapter 5). No difference was found for swallowing efficiency between those in early and later stages of PD. Pulmonary function measures were not significantly different as a function of age, PD or PD severity (Chapter 6). In summary, results from motor assessments contributing to airway protection support the robustness of breathing-swallowing coordination (BSC) and pulmonary function across research groups, but identify a reduction in overall swallowing efficiency in PD. Results from sensory assessments contributing to airway protection revealed that chemosensation was not different between age groups but base of tongue mechano-sensation was diminished in individuals with PD. Natural cough thresholds did not differ between young adults and elders but when asked to stifle coughing, elders were less able to do so compared to young adults (Chapter 7). For the first time, a reduction in mechano-reception at the base of tongue was recorded in individuals with PD (Chapter 8). These patients also demonstrated increased post swallow residual (Chapter 5), which offers an explanation for the complaint of globus in this population. These assessments highlight some compromise to sensory aspects of airway protection in PD. Overall, dysphagia had a negative impact on the quality of life of individuals with PD and even more as disease severity progresses (Chapter 9). Results from part two of the study looking at the effects of therapeutic interventions on airway protection revealed some unexpected findings. In chapter 10, results showed a reduction in pulmonary function when 'on' levodopa, but no differences in swallowing efficiency, BSC, or laryngopharyngeal chemo- and mechano-reception were observed. These results suggested a reduction in pulmonary function with levodopa without any increase in risk of airway protection compromise1. Unexpectedly and documented for the first time, the percentage of post swallow inspiration increased after LSVT (Chapter 11) but as with the levodopa study, this was also not accompanied by any apparent increase in aspiration risk. An increase in submental surface electromyography (sEMG) amplitude across all 5 participants may serve as a proxy measure of improvement in hyolaryngeal excursion. Finally, participants reported an overall improvement in social functioning and communication after LSVT. In conclusion, this study provided evidence that mechano-sensory aspect of airway protection is diminished in individuals with PD, possibly compromising airway protection. Patients not only demonstrated increased residue but the lack of sensation may prevent clearing or spontaneous multiple swallows. Overall, airway protection is maintained in ageing but swallowing efficiency declines in the presence of PD. This study contributes significantly to current research efforts in PD by expanding on existing reports regarding motor aspects of airway protection. Specifically, BSC, swallowing efficiency and evaluation of biomechanics using FEES research have never before been investigated exclusively in the PD population. Finally, the chemo- and mechano-sensation evaluated in this study are an important addition to the limited evidence that sensory impairment in individuals with PD potentially compromises airway protection. Results of the present study will serve as a platform upon which future studies may compare and expand.

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38

Cunningham, Jason Owen. "Variation in airway remodelling genes and their role on asthma severity in children and young adults". Thesis, University of Sussex, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590080.

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Background: Asthma affects approximately 300 million people worldwide ', 5.2 million of these people live in the UK2, 1.1 million of these are children" Asthma is one of the most common chronic diseases and is the fourth leading cause of morbidity worldwide, and there is no indication of a decline in prevalence. It is hypothesised that a range of gene- environmental interactions may influence the susceptibility, severity and medication response of asthma in children and young adults". Methods: To explore these issues, two studies have been established to create datasets that will describe the phenotypic and genotypic characteristics of children with asthma in the paediatric population across Sussex and Scotland. This thesis is the output of doctoral research using data from these studies (BREATHE and PAGES) that aims to explore the interactions between variants of six genes implicated in airway remodelling and relevant environmental factors and their influence on the severity of asthma in children and young adults. This thesis is divided by analysis of individual variants. The thesis included one variant of Chitinase 3-Like-1, two variants of Matrix metalloproteinase 9, two variants of Matrix metalloproteinase 12, one variant of Matrix metalloproteinase 9, one variant of Glutathione S-tronsferase mu-1, one variant of Glutathione S-transferase theta-1 and one variant of Glutathione S-transferase pi-1. A total of eight variants were investigated. Variants were analysed for effect on multiple proxy measures of asthma severity, including asthma exacerbations, asthma treatment steps, pulmonary function and quality of life. Variants were also analysed for their effect on allergy.

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Sikuvi, Kaveto Andreas. "The availability and perceived knowledge of use of airway management devices in emergency centres at referral hospitals in Namibia". Master's thesis, Faculty of Health Sciences, 2017. http://hdl.handle.net/11427/31225.

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Introduction Maintaining the airway is an essential element in the care of any ill or injured patient. Inadequate management of the airway may lead to hypoxia and hypercarbia with subsequent secondary brain injury, cardiopulmonary arrest, and ultimately death. The aim of the study was to identify which airway devices are available in public emergency centres of referral hospitals in Namibia and to determine the perceived level of knowledge of use regarding these devices. Methods A cross-sectional study was conducted in four emergency centres of referral hospitals in Namibia. Data regarding the availability of airway devices were collected on a standardised data sheet by means of a site inspection. A questionnaire was also distributed to emergency centre doctors to assess their perceived knowledge of use of airway devices. Descriptive statistics of all variables are reported. Results Twenty-two different airway devices were documented at study hospitals. All centres had some form of basic airway devices. Only one (25%) had venturi-masks. Two centres (50%) had one type of introducer (Gum elastic bougie) whilst none of the centres had video laryngoscopes, surgical airway devices or laryngeal tubes. Twelve participants (32.4%) had received formal training on airway devices (senior clinicians n=6, junior clinicians n=6), and 25 (67.6%) had no formal training (senior clinicians n=11, junior clinicians n=12). Majority of the clinicians lacked perceived knowledge in the use of alternative airway devices which were not available in their respective emergency centres, with a frequency of 81.4%. Conclusion The study indicates that basic airway devices are available in referral emergency centres in Namibia, however most of the alternative airway devices are not adequately stocked in the sampled emergency centres. Furthermore, a large number of clinicians had perceived knowledge of the basic airway devices. However, the perceived level of knowledge of use in alternative airway devices was inadequate.

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40

Chong, Mei-man y 臧薇敏. "Three-dimensional comparison of the upper airway in various types of dentofacial deformities". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48542027.

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Objectives 1. To define the normative airway of Chinese population using three-dimensional imaging and computer analysis 2. To evaluate the upper airway differences in patients with normal facial profile and those with skeletal class III deformity 3. To evaluate the differences in upper airway models among patients with different dentofacial deformities and describe the role of computational fluid dynamics (CFD) in the human upper airway Materials and Methods Part I : Three-Dimensional Analysis of the Normative Upper Airway in Chinese This was a cross-sectional observational study. Cone beam computerized tomography (CBCT) scans of one hundred patients were analyzed. Computer analysis of the different upper airway parameters were studied including airway length and volume, as well as airway dimensions at the axial level of the soft palate, hard palate, base of tongue, and epiglottis. The most constricted airway location was identified and correlation analysis with variables of interest was done. Part II: A Cone Beam Computerized Tomography Study of Airway in Skeletal Class I and Class III Cone-beam computed tomography (CBCT) records of 200 patients were used to evaluate the upper airway dimensions. This sample consisted of patients with normal facial profile (Class I) and those demonstrating skeletal class III deformities. Computer analysis of the upper airway parameters such as airway length, airway volume, airway anterior-posterior and cross-sectional area dimensions at the hard palate, soft palate, base of tongue and epiglottis were performed. The most constricted airway sites were identified. Part III: Computational fluid dynamics study of upper airway in different dentofacial deformities Cone-beam computed tomography records of 12 patients were used to evaluate the upper airway. This sample consisted of facial skeletal Class I, II and III subjects. The upper airway models were constructed to allow CFD simulations in the airway from the epiglottis to the hard palate. Cross-sectional area, pressure, velocity and resistance were measured based on the reconstructed meshed models. Results Part I : Three-Dimensional Analysis of the Normative Upper Airway in Chinese In 100 subjects (40 males, 60 females) aged 16-40 years with normal facial profile, we found that the most constricted site occurs at the level of the soft palate. This surface area of this site was found to be linearly correlated to the airway volume, suggesting a significant relationship between the most constricted area and the total airway volume. Gender differences were found in airway length, volume, and in the dimensions at the base of tongue and epiglottis region. The mean airway length was 54.12 mm + 6.19 for males and 49.25 mm + 4.86 for females; airway volume of 15.09 cm3 + 4.92 for males and 13.12 cm3 + 4.72 for females. Part II: A Cone Beam Computerized Tomography Study of Airway in Skeletal Class I and Class III The sample consisted of 100 Class I (41 males, 59 females) with a mean age of 25.4 years and 100 Class III (38 males, 62 females) with a mean age of 23.5 years. Gender differences were noted in the airway length, airway volume and dimensions at the base of tongue and epiglottis for both groups. Males showed longer airway length, larger airway volume, larger airway dimensions at the base of tongue and epiglottis compared to females. Significant differences in all the airway parameters between the two groups were found except for airway length. The soft palate was found to be the most constricted airway site observed in the Class I subjects while Class III subjects showed restriction in both the soft palate and epiglottis region. Part III: Computational fluid dynamics study of upper airway in different dentofacial deformities The airflow was variable among airway in different skeletal deformities. The pressure changes along airway of Class II were the largest, followed by Class I. The pressure drop in the airway of Class III subjects were the smallest. The larger pressure differences would cause greater resistance in the airway. The highest resistance was observed in the airway of Class II subjects. Conclusion Part I : Three-Dimensional Analysis of the Normative Upper Airway in Chinese This airway data provide a normative reference that can be used in various dentofacial analysis as well as for diagnosis and treatment planning for related dentofacial deformities and in understanding the pathophysiology for sleep-related breathing disorders. Part II: A Cone Beam Computerized Tomography Study of Airway in Skeletal Class I and Class III The upper airway is larger in patients with Class III deformity than those with a normal facial profile. The site of restriction is commonly observed at the soft palate in the Class I group whereas patients with Class III deformity, the airway restriction sites are at both the soft palate and epiglottis. Understanding of the upper airway differences in between class I and class III facial deformities can have implications on treatment planning for orthognathic surgery. Part III: Computational fluid dynamics study of upper airway in different dentofacial deformities The results in this study suggest that skeletal pattern showed a significant correlation with pressure and resistance along the upper airway.
published_or_final_version
Dental Surgery
Master
Master of Dental Surgery

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41

Pourazar, Jamshid. "Activation of epithelial signal transduction pathways, cytokine production and airway inflammation following diesel exhaust exposure". Doctoral thesis, Umeå : Department of Public Health and Clinical Medicine, Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-795.

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42

Stolarski, Bartosz. "The role of IL 33/ST2 pathway in innate immune response in airway inflammation". Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2961/.

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Asthma is a common and complex inflammatory disease of the airways characterized by deregulated immune responses that involves activation of multiple cell types including Th2 cells, IgE producing B cells, mast cells, basophils and eosinophils as well as resident lung cells such as epithelial, smooth muscle cells and macrophages. Despite intensive research, there are still unmet needs in the treatment of asthma. Recently, a new cytokine of IL 1 family, named IL 33 emerged as a potentially important factor in the immunopathogenesis of allergy and asthma. It was recently shown in our laboratory that intranasal administration of IL 33 can induce certain physiological features that are characteristic of experimental asthma, such as eosinophilic inflammation, Th2 cytokine and antibody production as well as increased airway hyperresponsiveness. The effect of IL 33 on the activation and differentiation of allergen specific Th2 cells has been well studied. However, the contribution of IL 33 to the activation of lung resident and inflammatory innate cells remains undefined. In this project I focused on alveolar macrophages and eosinophils as both cell types were reported to express IL 33R, ST2L and are thought to play a crucial role in asthma pathogenesis. I raised the hypothesis that IL 33 released locally in the lungs may trigger symptoms resembling asthma through the activation of airway alveolar macrophages. Furthermore, I hypothesize that IL 33 may exacerbate and maintain inflammation in the lungs by the direct activation of eosinophils. In our previous study we showed that IL 33 could switch the quiescent phenotype of alveolar macrophages toward the alternatively activated phenotype (M2, AAM). In the first part of my thesis I looked at the consequences of this phenomenon for airway inflammation. Using clodronate liposomes in vivo I was able to eliminate macrophage population from the lungs and demonstrated that resident alveolar macrophages are crucial for the development of IL 33 induced eosinophilic inflammation in the airways. I then examined the contribution of IL 13, a known M2 differentiation factor, to airway inflammation. Using anti IL 13 neutralizing antibodies I showed that IL 13 is required for the IL 33 triggered differentiation of alveolar macrophages toward M2 phenotype as well as for eosinophilic inflammation. Next, I looked at how IL 33/ST2 pathway modulates the differentiation and activation of eosinophil. I demonstrated that bone marrow hematopoietic progenitors CD117+ express ST2L and that IL 33 is able to differentiate these cells toward eosinophils. By employing deficient mice or neutralizing antibodies I found that this process is ST2 and IL 5 dependent and independent of IL 13. I then extended my research interests to include mature mouse and human eosinophils. I showed that both human and mouse resting eosinophils express low levels of ST2L which can be markedly increased by IL 33. Moreover, I demonstrated that eosinophils that are recruited to the lungs during experimental allergic airway inflammation express high levels of ST2L. Furthermore, I carried out a study on effector function of eosinophils. I found that IL 33 induces IL 13, IL 6 and increases TARC, TGF production by mouse eosinophils. In addition, IL 33 exacerbated IgG induced human and mouse eosinophil degranulation, likely by enhancing FcRII expression. Having shown earlier that IL 13 is requited for the polarization of alveolar macrophages toward AAM by IL 33 in vitro and in light of the fact that IL 33 stimulated eosinophils can be a significant source of IL 13; I went on to investigate the interaction between macrophages and eosinophils. Using co cultures of ST2 / macrophages with WT eosinophils in Transwell system, I demonstrated that IL 33 but not IL 5 activated eosinophils can support macrophage polarization toward the pro inflammatory AAM phenotype, partially through the production of IL 13. Finally, given the role of IL 33/ST2L axis in eosinophil activation in vitro, I investigated the contribution of IL 33 activated eosinophils to airway inflammation in vivo. Using adoptive transfer protocol I showed that the contribution of IL 33 activated eosinophils to airway inflammation is mediated primarily by the release of cytokines from these cells which, in turn, recruits other inflammatory cells and supports the differentiation of alveolar macrophages towards AAM. These data show that IL 33/ST2 pathway regulates multiple features of alveolar macrophage and eosinophil biology that can have a significant impact on asthma pathophysiology in the airways. Studies carried out in our laboratory and elsewhere suggest that IL 33 is equally capable of activating other cell types that have been implicated in asthma pathology such as Th2, B1 cells, DCs, mast cells and basophils. Therefore, targeting IL 33/ST2 pathway may potentially offer a promising therapeutic approach to asthma and allergy.

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43

Govindaraju, Vasanthi. "Actions of interleukin-8 and extracellular nucleotides on airway smooth muscle from normal and CF subjects". Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85553.

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Cystic fibrosis (CF) patients have airway neutrophilic inflammation associated with high levels of interleukin-8 (IL-8) and often develop airway hyperresponsiveness (AHR). Aerosolized uridine triphosphate (UTP) has been used to improve mucosal clearance by inducing Cl- secretion. However, nucleotides such as UTP and ATP (adenine triphosphate) also evoke the release of intracellular Ca2+ ([Ca2+]i), which are enhanced by pro-inflammatory mediators, such as IL-1beta. Since most of the CF airway epithelium is lost during infection and inflammation, the underlying airway smooth muscle cells (ASMC) are exposed to IL-8 and extracellular nucleotides. Thus, we were particularly interested in evaluating the effects of IL-8, extracellular ATP and UTP on contractile responses of ASMC. For this study, cultured ASM from normal and CF lung specimens were used. We have found that human ASM cells (HASMC) express mRNA and protein for IL-8 receptors (CXCR1 and CXCR2) and IL-8 causes an increase in [Ca2+]; as well as cellular contraction and migration. Furthermore, changes in the [Ca2+] i were abrogated on blocking IL-8 receptors with specific neutralizing antibodies, and were also decreased following inhibition of phospholipase C (PLC), indicating that changes in [Ca2+]i were likely mediated by inositol trisphosphate. The effects of IL-8 on HASMC prompted us to investigate whether IL-8 induced ASMC contraction in CF was different from normal. IL-8 caused larger ASM contractions and greater phosphorylation of myosin light chain (MLC20) compared to normal cells. CF cells expressed more MLC20 compared to normal cells. However, the expression of CXCR1, CXCR2, IL-8 induced changes in [Ca2+]i and ASMC migration in CF cells were similar to normal cells. We also found that normal HASMC express receptors (subtypes of P2Y) for ATP and UTP, which stimulated the release of intracellular Ca2+. Brief exposure of normal HASMC with UTP enhanced Ca2+ transients in response t

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44

Armstrong, Julian. "Anatomical optical coherence tomography in the human upper airway". University of Western Australia. School of Electrical, Electronic and Computer Engineering, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0022.

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[Truncated abstract] This thesis describes the development, clinical validation and initial application of a technique for taking measurements of the shape and dimensions of the human upper airway, called anatomical optical coherence tomography (aOCT). The technique uses a transparent catheter containing a rotating optical probe which is introduced transnasally and positioned in the airway and oesophagus. Optical coherence tomography is used to take calibrated cross-sectional images of the airway lumen as the probe rotates. The probe can also be advanced or withdrawn within the catheter during scanning to build up three-dimensional information. The catheter remains stationary so that the subject is not aware of the probe motion. The initial application of the system is research into obstructive sleep apnoea (OSA), a serious condition characterized by repetitive collapse of the upper airway during sleep and an independent risk factor for deaths by heart disease, strokes or car accidents. Measurement of upper airway size and shape is important for the investigation of the pathophysiology of OSA, and for the development and assesment of new treatments. . . We have used aOCT to capture three-dimensional data sets of the airway shape from upper oesophagus to the nasal cavity, undertaken measurements of compliance and other airway characteristics, and recorded dynamic airway shape during confirmed sleep apnoea events in a hospital sleep laboratory. We have shown that aOCT generates quantitative, real-time measurements of upper airway size and shape, allowing study over lengthy periods during both sleep and wakefulness. These features should make it useful for study of upper airway behavior to investigate OSA pathophysiology, and aid clinical management and treatment development.

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45

Craig, Daniel John. "Low Frequency Airway Epithelial Cell Mutation Pattern Associated with Lung Cancer Risk". University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1556918218571742.

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46

Castle, Nicholas. "What airway and vascular access skills can be performed whilst wearing the NHS issued chemical, biological, radiation, and nuclear personal protective equipment?" Thesis, City University London, 2014. http://openaccess.city.ac.uk/15163/.

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The introduction of chemical, biological, radiation and nuclear personal protective equipment (CBRN-PPE) across the National Health Service (NHS), in 2007, represented an increase in the capacity to treat patients following a CBRN incident. However, little was known on what impact the NHS CBRN-PPE would have on skill performance. To date a number of studies have evaluated various skills performed whilst wearing a range of CBRN-PPE, none of which resembles the NHS CBRN-PPE. This gap in the evidence prompted a series of research studies addressing the following research question, ‘What airway and vascular access skills can be performed whilst wearing the NHS issued chemical, biological, radiation, and nuclear personal protective equipment? The resulting nine published peer-reviewed papers are presented with a critical commentary in three chapters: Chapter 3 (Papers 1 to 4) assesses what clinical skills can be performed using the NHS CBRN-PPE; Chapter 4 (Papers 5 & 6) explores clinicians’ views on the preferences and experiences of airway management whilst wearing CBRN-PPE; and Chapter 5 (Papers 7 to 9) evaluates the optimal strategies of airway management whilst wearing the NHS CBRN-PPE. Chapter 6 is a summary of the findings presented in this thesis and presents a number of new research questions to further expand our knowledge-base, regarding skill performance whilst wearing NHS CBRN-PPE, reflecting the developmental nature of this area of research. The research contained in this thesis utilises a combination of randomised controlled trials, interviews and questionnaires, to ascertain the impact of the NHS CBRN-PPE on skill completion. Papers 1 to 4 recruited a group of mixed clinicians allowing subgroup analysis observing for inter-professional differences regarding skill performance. Whereas, Papers 7 to 9 recruited student paramedics ensuring similar levels of airway management skills, thereby isolating prior expertise as a variable. The research presented in this thesis has been used during simulation training as part preparations for the 2012 Olympics, in the development of a CBRN training DVD and incorporated into a textbook. The results have also been shared with NHS England working party on CBRN-PPE and, are being incorporated into CBRN treatment protocols by an overseas ambulance service.

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47

Burke, Jan. "Prehospital advanced airway management practices by advanced life support providers: A retrospective observational study of emergency medical service providers in South Africa". Master's thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/32596.

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Introduction: The skill of endotracheal intubation to achieve a definitive airway for critically ill and injured patients in the prehospital setting is frequently performed by advanced life support providers. Several methods may be utilised, including intubation without the use of medication, the use of sedatives or a rapid sequence intubation. There is a paucity of data available that assesses prehospital advanced airway intubation practices in South Africa. The aim of this study is to describe the advanced airway management practices of advanced life support providers across South Africa. Methods: A retrospective, observational study method was used (chart review). Electronic patient care records were sourced from private and public emergency medical services companies and collated accordingly. Results: A total of 704 cases were included. Intubation during cardiac arrest was the most common approach to airway management (n=280, 40%) followed by rapid sequence intubation (n=202, 28%), medication-facilitated intubations (n=152, 22%) and a nomedication approach (n=70, 10%). Successful intubation using an endotracheal tube was reported in 197 (98%) of rapid sequence intubation cases, 134 (88%) of the medication facilitated cases, 61 (87%) of no-medication cases and 228 (81%) of cardiac arrest cases. A first-pass success rate was described in 260 (79%) cases, with the cardiac arrest group having a first-pass success of 85%, followed by the rapid sequence intubation group (83%), the nomedication group (71%) and the medication facilitated group (61%). Hypotension and cardiac arrest were the most common adverse events. A total of 496 (70%) patients were alive at hospital handover. The average scene time and transportation time was 42 minutes and 24 minutes respectively for the rapid sequence intubation group, 42min and 27min for the medication facilitated group, 44min and 25min for the no-medication group and 57min and 16min for the cardiac arrest group. Discussion: The study described the prehospital airway management practices by advanced life support providers in South Africa. Rapid sequence intubation had the highest endotracheal intubation success rate overall and the lowest prevalence of adverse events. There was no statistical difference in survival between the rapid sequence intubation, medication facilitated and no-medication group. Due to a lack in standardised treatment guidelines, differences in fluid administration, post-intubation care, confirmation of placement and ventilation were noted. No standard approach to record keeping was found, with the quality of patient care records being variable. A standardised advanced airway management report would be beneficial as it would improve the quality of data recorded and allow for better comparisons to be made.

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48

Hotchkiss, Joel W. "Quantitative epidemiological studies on recurrent airway obstruction in the horse population of Great Britain using a risk-screening questionnaire". Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/2607/.

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The principal aim of this study was to investigate the epidemiology of recurrent airway obstruction (RAO) in horses in Great Britain using risk-screening questionnaires (RSQ). Three processes were used to aid construction of the RSQ for RAO, namely: a review of the scientific literature, a survey of equine practitioners in the UK and a modified Delphi consultation with experts in the field of RAO. The demographic information, generated by the questionnaire, enabled investigation of risk factors associated with the disease using multilevel, multivariable logistic regression. Two models were constructed. The first related to host and environmental risk factors and the second explored the effect of early life factors. The host and environmental model identified an increased risk of RAO in association with increasing age and the horse residing in an urban or semi-urban environment. There were also some associations that were contrary to what would be expected from knowledge of the aetiology of RAO. In particular, horses fed soaked (wet) hay had increased odds of having RAO, whilst horses fed dry hay had decreased odds. The early life model identified an increased risk of a horse having RAO if its owner had acquired them after the age of two years or that in early life it had been fed hay or had a respiratory infection. The final stage of the study was to develop and assess an educational package for horse owners regarding the disease. RAO appears to be worryingly prevalent in the horse population of Great Britain; a real concern in terms of welfare. Much can be done to alleviate this chronic disease by controlling a horse’s environment to reduce respiratory challenge. Greater emphasis could be placed on assisting horse owners in making this transition by providing detailed guidance.

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49

Cameron, Euan John. "Effects of azithromycin on asthma control, airway inflammation and bacterial colonisation in smokers with asthma : a randomised control trial". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4575/.

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Smokers with asthma represent an important sub-group of asthmatics displaying both reduced response to inhaled and oral corticosteroids as well as demonstrating accelerated decline in lung function and increased use of health care services. Clinical and laboratory studies have suggested that macrolide antibiotics may exhibit anti-inflammatory properties in a variety of airways disease including asthma. The anti-inflammatory properties of macrolides have been recognised for almost 50 years. Indirect evidence from both pre-clinical and clinical studies suggests that the mechanism of action may be of particular benefit in smokers with asthma. A proof of concept study was designed to test the hypothesis that the macrolide antibiotic azithromycin improves measures of asthma control, airway inflammation and bacterial colonisation in smokers with asthma. Azithromycin was chosen for its convenience of once daily dosing and its oral tolerability in addition to its more limited interactions. Seventy-seven adults with allergic asthma were recruited to a 12-week parallel group randomised controlled trial comparing the effects on asthma control, airway inflammation and bacterial colonisation of oral azithromycin 250 mg daily with matched placebo. The primary outcome measure was peak expiratory flow at the final study visit. Secondary outcome measures included spirometry, asthma control questionnaire [ACQ] score, asthma quality of life questionnaire [AQLQ], Leicester cough questionnaire [LCQ] score, provocation concentration to methacholine PC20, and inflammatory markers: exhaled nitric oxide, sputum differential cell counts, sputum supernatant and serum inflammatory markers such as interleukin-1β [IL-1β], IL-2, -4, -5, -6, -10, TNF-α, IFN-γ, GM-CSF, Leukotriene B4, and high sensitivity C-reactive protein. Microbiological culture and PCR of sputum was also performed to assess for any changes associated with treatment. At 12 weeks, the change in PEF at the final study visit, as compared with baseline, did not differ significantly between the azithromycin and placebo treatment groups [mean difference azithromycin-placebo -10.3L/min, 95% CI -47.1 to 26.4, p=0.58]. No statistically significant difference was observed between the azithromycin and placebo groups in each of the measures of spirometry, ACQ, AQLQ, LCQ, PC20, or evening PEF. The LCQ-psychological domain did reach statistical significance, [mean difference azithromycin-placebo -0.46, 95%CI -0.9 to 0.02 p=0.04], however this indicates a deterioration in the treatment group. No change was seen in exhaled nitric oxide. The total cell counts recovered from sputum were similar following treatment with azithromycin compared to placebo. In addition, differential cell counts remained unchanged and lymphocyte proliferation assays did not demonstrate any statistically significant changes following 12 weeks of treatment with azithromycin when compared to placebo. There was no substantial difference in any of the measured sputum supernatant or plasma cytokines. Peripheral blood monocyte stimulation was performed, with supernatant being measured against a panel of cytokines. There was again no substantial difference in any of the measured panel of cytokines collected from the monocyte stimulation assays when the azithromycin group was compared to placebo. There was no correlation between changes in ACQ, AQLQ, LCQ, PC20, sputum macrophage count, sputum neutrophil count, sputum eosinophil count, and PEF. Adverse event rates were similar in patients taking azithromycin compared with placebo. A total of 4 patients were lost to follow up [1 in the azithromycin group, 3 in the placebo group]. One patient died of a cardiovascular cause. This occurred following completion of the study but within the pre-specified regulatory reporting period. In conclusion there were no clinically important improvements in a range of clinical indices of asthma control, airway inflammation or bacterial colonisation following 12 weeks treatment with azithromycin when compared with placebo in smokers with asthma. The lack of any evidence of clinical benefit of azithromycin in smokers with asthma is a new finding and extends the current knowledge base and evidence for the use of macrolides in asthma. There exists no firm evidence to suggest the widespread use of macrolides in asthma and the current study suggests that no benefit will be observed in the sub-group of asthmatics whom are current smokers.

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50

Hart, Matthew Thomas. "The Effects of Aerosol Drug Delivery on Airway Resistance through Heat-Moisutre Exchangers". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/rt_theses/4.

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Introduction: The use of heat moisture exchangers (HMEs) is becoming more popular with many institutions delivering aerosolized medications between the HME and the endotracheal tube of patients being mechanically ventilated. When HMEs become saturated resistance can increase which can cause changes that can lead to patient-ventilator dysnchrony, development of intrinsic PEEP, and weaning difficulty. The purpose of this study was to determine the effects of aerosol drug delivery on resistance through heat-moisture exchangers. Method: An in-vitro model to simulate exhaled heat and humidity from a patient’s lungs was developed by connecting the test lung to a cascade humidifier that was placed between the endotracheal tube and the test lung. Temperature (37 ºC) and relative humidity (100%) were held constant through all test runs. Ventilator settings used for the study were as follows: Tidal volume 500 mL, frequency 15/min, PEF 60 L/min, PEEP 5 cmH2O, bias flow 2 L/min and I:E ratio 1:3.The pressurized metered-dose inhaler (pMDI; ProAir HFA) with a minispacer (Thayer Medical), hand-held nebulizer (HHN; Salter Labs) and placebo (No aerosol generator or medication) were compared. Albuterol sulfate (2.5 mg/3 ml) was administered through continuous HHN and six puffs of albuterol were given from a pMDI equaling one treatment. Neither medication nor aerosol device was used with the placebo group in order to determine the effect of HME on airway resistance during mechanical ventilation. Six aerosolized treatments were given to simulate a patient receiving albuterol every four hours over a twenty-four hour period. While five minutes was allowed between treatments, airway resistance was measured via the ventilator before and after the administration of the placebo, pMDI and HHN, which equaled five-minute intervals. Data Analysis: Descriptive statistics, dependent t-tests, one-way analysis of variance (ANOVA), repeated measures ANOVA and post-hoc multiple comparisons were utilized for the data analysis of this study, using SPSS version 16.0. A p-value<0.05 was considered significant. Results: There is a linear time effect with means of airway resistance increasing overtime not only with the placebo but also with the pMDI and nebulizer. At the end of all treatments, the means of resistance with the placebo, pMDI and nebulizer were 9.31 cmH2O/L/sec, 9.37 cmH2O/L/sec and 11.20 cmH2O/L/sec, respectively. While no significant difference was found between the placebo and the pMDI (p=0.452), the nebulizer significantly increased airway resistance when compared to placebo (p=0.004) and the pMDI (p=0.02). Conclusion: Airway resistance increases with use of the placebo, pMDI, and JN groups. Aerosol generators showed a greater increase in resistance when compared to placebo with the greater increase in resistance by HHN.

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