Thesis (Ph.D.)--Cleveland State University, 2008. / Abstract. Title from PDF t.p. (viewed on Mar. 4, 2009). Includes bibliographical references. Available online via the OhioLINK ETD Center. Also available in print.

The normal breathing pattern recorded in unanaesthetized, lightly re-strained turtles, Chrysemys picta, consisted of periods of continuous breathing interspersed with periods of breath holding. During each ventilatory period, respiratory frequency and tidal volume were controlled separately and independently of breath length, the total inspiratory interval, the active inspiratory interval and the expiratory interval. Increases in pulmonary minute ventilation during hypercapnia were caused by increases in respiratory frequency due solely to shortening of the intervals of breath holding. The frequency of breathing within each ventilatory period remained constant. There was a large variability in inspiratory and expiratory gas flow rates yet tidal volume was maintained within narrow limits by adjustment of the lengths of the active inspiratory and expiratory intervals. This mechanism was dependent upon lung volume information carried within the vagus nerve. Following vagotomy, changes in minute ventilation due to hypercapnia stemmed primarily from changes in tidal volume while changes in respiratory frequency were markedly reduced. Lung volume information carried within the vagus nerve arose from slowly adapting pulmonary stretch receptors. Single fibre nerve activity from pulmonary receptors was recorded from vagal slips in single-pithed tidally ventilated turtles. The major stimulus of these receptors was the change in lung volume throughout each breathing cycle. The rate and degree of change in transpulmonary pressure were without direct effect on receptor discharge. The functional characteristics of these receptors differed only quantitatively from those recorded in pulmonary stretch receptors of mammals and these differences probably stem from the lower body temperature of the turtle and the location of the receptors in the turtle lung. Most receptors were sensitive to CO₂, several sufficiently sensitive that both tonic and phasic receptor discharge were totally inhibited throughout the ventilatory cycle by 5 to 10% CO₂ in the inspired gas. Pulmonary mechanoreceptors in the frog were also shown to be sensitive to. The acute sensitivity to of a few receptors in turtles and frogs parallels that of the intrapulmonary receptors described-in birds and suggests that a pulmonary receptor with distinct mechano- and chemosensitive properties may represent the functional precursor of the variety of pulmonary receptor types which appear in modern day vertebrates. To examine the role of sensitivity of pulmonary receptors in the overall response of turtles to inhaled CO₂, ventilatory responses of unanaesthetized turtles to changes in the intrapulmonary CO₂ content of a vascularly isolated lung (constant PaCO₂ ) and an intact lung were measured during spontaneous breathing. The isocapnic hyperpnea associated with inhalation of CO₂ by the vascularly isolated lung was small and abolished by vagotomy. It is concluded that both inhibition of pulmonary stretch receptor discharge with increasing levels of FICO₂ and a functional increase in central inspiratory volume threshold contributed significantly to tidal volume increases during hypercapnia. The primary ventilatory response of intact turtles to increasing levels of FICO₂ was an increase in respiratory frequency and this response FICO₂ was greatly reduced when CO₂ was inspired only by the vascularly isolated lung. Thus the ventilatory response of turtles to increasing levels of FICO₂ is primarily dependent upon increased levels of arterial CO₂. The effect of vagotomy in producing apneusis in turtles supports suggestions they lack a pneumotaxic centre. The arrhythmic breathing pattern in turtles with intact vagal nerves, however, bears no similarity to the pattern of breathing in mammals with only the pneumotaxic centre ablated. It is concluded that the vagal input from pulmonary receptors to the respiratory centres in turtles is qualitatively similar to that in mammals yet the differences in central integration of lung volume information in turtles and mammals are not due solely to the absence of a pneumotaxic centre in the turtle. Many of the remaining differences may arise from the lower metabolic demand of turtles but how this affects central integration and respiratory pattern generation is unknown. / Science, Faculty of / Zoology, Department of / Graduate

No description available.

Call number: LD2668 .T4 1979 C73 / Master of Science

Thesis (M.Tech.: Chiropractic)-Dept. of Chiropractic, Durban Institute of Technology, 2003. x, 101 leaves / Anecdotal evidence and some developmental theory suggest that lower respiratory tract pathologies may be associated with thoracic spine pain and dysfunction. This hypothetical association may be better described either as respiratory conditions occurring as a result of musculoskeletal dysfunction of the thoracic spine, or as respiratory conditions causing thoracic musculoskeletal dysfunction. Optimal function of the lungs and the process of ventilation is dependant on the normal function of the thoracic spine and the rib cage. Disturbances of the musculoskeletal components of the thoracic spine may lead to increased respiratory efforts, decreased lung function and in turn affect bronchopulmonary function. Obstructive respiratory diseases such as asthma, bronchitis and emphysema place an increased demand on the musculoskeletal components involved in expiration, as air has to be forcefully expired. The purpose of this quantitative, non experimental, demographic retrospective clinical survey was to retrospectively describe lower respiratory tract disorders and thoracic spine pain and dysfunction in subjects presenting to the Durban Institute of Technology Chiropractic Day Clinic, in terms of the prevalence of lower respiratory tract disorders as well as any association between the presenting respiratory conditions and their vertebral distribution in the thoracic spine.

No description available.

Dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Chiropractic, Durban Institute of Technology, 2003. / Anecdotal evidence and some developmental theory suggest that lower respiratory tract pathologies may be associated with thoracic spine pain and dysfunction. This hypothetical association may be better described either as respiratory conditions occurring as a result of musculoskeletal dysfunction of the thoracic spine, or as respiratory conditions causing thoracic musculoskeletal dysfunction. Optimal function of the lungs and the process of ventilation is dependant on the normal function of the thoracic spine and the rib cage. Disturbances of the musculoskeletal components of the thoracic spine may lead to increased respiratory efforts, decreased lung function and in turn affect bronchopulmonary function. Obstructive respiratory diseases such as asthma, bronchitis and emphysema place an increased demand on the musculoskeletal components involved in expiration, as air has to be forcefully expired. The purpose of this quantitative, non experimental, demographic retrospective clinical survey was to retrospectively describe lower respiratory tract disorders and thoracic spine pain and dysfunction in subjects presenting to the Durban Institute of Technology Chiropractic Day Clinic, in terms of the prevalence of lower respiratory tract disorders as well as any association between the presenting respiratory conditions and their vertebral distribution in the thoracic spine. / M

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.

Includes bibliographical references (leaves 234-280) / xxviii, 292, [72] leaves : ill. (some col.), plates (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 2002

A safe, potent and broad-spectrum antiviral is urgently needed to combat emerging viral respiratory diseases such as avian influenza H5N1 and H7N9, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Previous studies carried out by PhD students in our lab found that mouse β-defenisn 4 (mBD4) shows highly antiviral activity in vitro. However, the recombinant mBD4 (rmBD4) expressed by E.coli is limited to very small scale of production and is very expensive. Thus, in this study, we firstly screened 16 short peptides derived from mBD4 and other mouse and human β-defensins for identifying their antiviral effects. One short peptide P9 (30 amino acids), derived from mBD4, exhibited potent and broad-spectrum antiviral effects against multiple respiratory viruses, including influenza A viruses H1N1, H3N2, H5N1, H7N7 and H7N9, SARS coronavirus (SARS-CoV)and MERS coronavirus (MERS-CoV). This P9 showed very high selectivity index (970), which was higher than that of the full-length peptide of synthetic mBD4 (smBD4) and rmBD4 in vitro. Secondly, the prophylactic and therapeutic effects of P9 against the infection of H1N1 virus were further detected in animal model. The survival rate of P9-pretreated mice challenged by lethal dose of H1N1 virus was 100%. The therapeutic effects of P9 protecting mice from lethal challenge of H1N1 virus were also statistically significant. The survival rate of mice could reach up to 67% by intranasal inoculation and 56% by intraperitoneal injection, respectively. To investigate the antiviral mechanism, we firstly elucidated that P9 could inhibit viral infection but not viral replication or release. Secondly, we detected whether P9 inhibited viral infection by binding to the surface of target cells or viral particles. The results showed that P9 only bound to viral particles but not to the cell surface. It was further identified that P9 bound to viral surface glycoprotein HA but not NA. Thirdly, we demonstrated that P9 did not inhibit virus binding to its receptor and block the virus entry into cells by endocytosis. Instead, P9 inhibited the acidification in late endosomes and thusP9 blocked virus-membrane fusion and subsequent viral disassembly and viral RNA release. Finally, we elucidated that the antiviral activity of P9 was attributed to its high binding affinity to viral HA and the abundance of basic amino acids in its composition. In this study, we have demonstrated that a short peptide P9, which is derived from mBD4, showed potent antiviral activity against multiple respiratory viruses. This peptide can be developed to a new promising prophylactic and therapeutic agent with broad-spectrum antiviral activity and low possibility to cause drug resistance. Moreover, this study has also revealed a novel antiviral mechanism for P9 and paved a path for the development of new antiviral agents with broad-spectrum antiviral activity against emerging respiratory viruses, such as avian influenza H5N1 and H7N9, as well as SARS-CoV and MERS-CoV. / published_or_final_version / Microbiology / Doctoral / Doctor of Philosophy