Browsing by Subject "Lung"
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- ItemOpen AccessA Radiological study of the Right Lung(1943) Oosthuizen, Sarel FrancoisThe purpose of this thesis is to illustrate the author's observations on radiological investigations of the right lung both in the living body and at post-mortem, and to describe certain aspects of anatomical, clinical, pathological and radiological interest.
- ItemOpen AccessGuideline for the management of acute asthma in adults: 2013 update(2013) Lalloo, U G; Ainslie, G M; Abdool-Gaffar, M S; Awotedu, A A; Feldman, C; Greenblatt, M; IRUSEN, E M; Mash, R; Naidoo, S S; O\'Brien, J; Otto, W; Richards, G A; Wong,, M LAcute asthma attacks (asthma exacerbations) are increasing episodes of shortness of breath, cough, wheezing or chest tightness associated with a decrease in airflow that can be quantified and monitored by measurement of lung function (peak expiratory flow (PEF) or forced expiratory volume in the 1st second) and requiring emergency room treatment or admission to hospital for acute asthma and/or systemic glucocorticosteroids for management. The goals of treatment are to relieve hypoxaemia and airflow obstruction as quickly as possible, restore lung function, and provide a suitable plan to avoid relapse. Severe exacerbations are potentially life-threatening and their treatment requires baseline assessment of severity, close monitoring, and frequent reassessment using objective measures of lung function (PEF) and oxygen saturation. Patients at high risk of asthma-related death require particular attention. First-line therapy consists of oxygen supplementation, repeated administration of inhaled short-acting bronchodilators (beta-2-agonists and ipratropium bromide), and early systemic glucocorticosteroids. Intravenous magnesium sulphate and aminophylline are second- and third-line treatment strategies, respectively, for poorly responding patients. Intensive care is indicated for severe asthma that is not responsive to first-line treatment. Antibiotics are only indicated when there are definite features of bacterial infection. Factors that precipitated the acute asthma episode should be identified and preventive measures implemented. Acute asthma is preventable with optimal control of chronic asthma.
- ItemOpen AccessIs air pollution a risk factor for rheumatoid arthritis?(2015) Essouma, Mickael; Noubiap, Jean Jacques NRheumatoid arthritis is a chronic inflammatory debilitating disease triggered by a complex interaction involving genetic and environmental factors. Active smoking and occupational exposures such as silica increase its risk, suggesting that initial inflammation and generation of rheumatoid arthritis-related autoantibodies in the lungs may precede the clinical disease. This hypothesis paved the way to epidemiological studies investigating air pollution as a potential determinant of rheumatoid arthritis. Studies designed for epidemiology of rheumatoid arthritis found a link between traffic, a surrogate of air pollution, and this disease. Furthermore, a small case–control study recently found an association between wood smoke exposure and anticyclic citrullinated protein/peptide antibody in sera of patients presenting wood-smoke-related chronic obstructive pulmonary disease. However, reports addressing impact of specific pollutants on rheumatoid arthritis incidence and severity across populations are somewhat conflicting. In addition to the link reported between other systemic autoimmune rheumatic diseases and particulate matters/gaseous pollutants, experimental observation of exacerbated rheumatoid arthritis incidence and severity in mice models of collagen-induced arthritis after diesel exhaust particles exposure as well as hypovitaminosis D-related autoimmunity can help understand the role of air pollution in rheumatoid arthritis. All these considerations highlight the necessity to extend high quality epidemiological researches investigating different sources of atmospheric pollution across populations and particularly in low-and-middle countries, in order to further explore the biological plausibility of air pollution’s effect in the pathogenesis of rheumatoid arthritis. This should be attempted to better inform policies aiming to reduce the burden of rheumatoid arthritis.
- ItemOpen AccessLack of paradoxical bronchoconstriction after administration of tiotropium via Respimat® Soft Mist™ Inhaler in COPD(2011) Hodder, Rick; Lee, Angela; Bateman, EricBronchoconstriction has been reported in asthma and chronic obstructive pulmonary disease (COPD) patients after administration of some aqueous inhalation solutions. We investigated the incidence of this event during long-term clinical trials of tiotropium delivered via Respimat® Soft Mist™ Inhaler (SMI). We retrospectively analyzed pooled data from two identical Phase III clinical trials, in which 1990 patients with COPD received 48 weeks’ treatment with once-daily tiotropium (5 or 10 μg) or placebo inhaled via Respimat® SMI. We recorded the incidence of bronchospasm and of a range of respiratory events that could suggest bronchoconstriction during the first 30 minutes after inhalation of study treatment on each of the eight test days. No patients reported bronchospasm. Six patients (0.3%) reported a combination of at least two events suggestive of bronchoconstriction, and 21 (1.1%) reported either rescue medication use or a respiratory adverse event. Asymptomatic falls in forced expiratory volume in one second (FEV1) of ≥15% were recorded on all test days, with no change in incidence over time, and affected 8.2% of those in the tiotropium groups and 14.5% of those on placebo. In COPD patients receiving long-term treatment with tiotropium 5 or 10 μg via Respimat® SMI, no bronchospasm was recorded, and the number of events possibly indicative of paradoxical bronchoconstriction was very low.
- ItemOpen AccessProminent role for T cell-derived Tumour Necrosis Factor for sustained control of Mycobacterium tuberculosis infection(2013) Allie, Nasiema; Grivennikov, Sergei I; Keeton, Roanne; Hsu, Nai-Jen; Bourigault, Marie-Laure; Court, Nathalie; Fremond, Cecile; Yeremeev, Vladimir; Shebzukhov, Yuriy; Ryffel, Bernhard; Nedospasov, Sergei A; Quesniaux, Valérie F J; Jacobs, MuazzamTumour Necrosis Factor (TNF) is critical for host control of M. tuberculosis, but the relative contribution of TNF from innate and adaptive immune responses during tuberculosis infection is unclear. Myeloid versus T-cell-derived TNF function in tuberculosis was investigated using cell type-specific TNF deletion. Mice deficient for TNF expression in macrophages/neutrophils displayed early, transient susceptibility to M. tuberculosis but recruited activated, TNF-producing CD4+ and CD8+ T-cells and controlled chronic infection. Strikingly, deficient TNF expression in T-cells resulted in early control but susceptibility and eventual mortality during chronic infection with increased pulmonary pathology. TNF inactivation in both myeloid and T-cells rendered mice critically susceptible to infection with a phenotype resembling complete TNF deficient mice, indicating that myeloid and T-cells are the primary TNF sources collaborating for host control of tuberculosis. Thus, while TNF from myeloid cells mediates early immune function, T-cell derived TNF is essential to sustain protection during chronic tuberculosis infection.
- ItemOpen AccessSouth African tobacco smoking cessation clinical practice guideline(2013) van Zyl-Smit, Richard N; Allwood, Brian; Stickells, David; Symons, Gregory; Abdool-Gaffar, Sabs; Murphy, Kathy; Lalloo, Umesh; Vanker, Aneesa; Sabur, Natasha F; Richards, GuyTobacco smoking (i.e. cigarettes, rolled tobacco, pipes, etc.) is associated with significant health risks, reduced life expectancy and negative personal and societal economic impact. Smokers have an increased risk of cancer (i.e. lung, throat, bladder), chronic obstructive pulmonary disease (COPD), tuberculosis and cardiovascular disease (i.e. stroke, heart attack). Smoking affects unborn babies, children and others exposed to second hand smoke. Stopping or 'quitting' is not easy. Nicotine is highly addictive and smoking is frequently associated with social activities (e.g. drinking, eating) or psychological factors (e.g. work pressure, concerns about body weight, anxiety or depressed mood). The benefits of quitting, however, are almost immediate, with a rapid lowering of blood pressure and heart rate, improved taste and smell, and a longer-term reduction in risk of cancer, heart attack and COPD. Successful quitting requires attention to both the factors surrounding why an individual smokes (e.g. stress, depression, habit, etc.) and the symptoms associated with nicotine withdrawal. Many smokers are not ready or willing to quit and require frequent motivational input outlining the benefits that would accrue. In addition to an evaluation of nicotine dependence, co-existent medical or psychiatric conditions and barriers to quitting should be identified. A tailored approach encompassing psychological and social support, in addition to appropriate medication to reduce nicotine withdrawal, is likely to provide the best chance of success. Relapse is not uncommon and reasons for failure should be addressed in a positive manner and further attempts initiated when the individual is ready. Key steps in smoking cessation include: (i) identifying all smokers, alerting them to the harms of smoking and benefits of quitting; (ii) assessing readiness to initiate an attempt to quit; (iii) assessing the physical and psychological dependence to nicotine and smoking; (iv) determining the best combination of counselling/support and pharmacological therapy; (v) setting a quit date and provide suitable resources and support; (vi) frequent follow-up as often as possible via text/telephone or in person; (vii) monitoring for side-effects, relapse and on-going cessation; and (viii) if relapse occurs, providing the necessary support and encourage a further attempt when appropriate.