Biomedical subjects

Stephen J Chapman

Publications and source records attributed to Stephen J Chapman.

7 recordsLinked to original sources

PubMed2005

Miniaturized test system for soil respiration induced by volatile pollutants.

A miniaturized method based on 96-well microtitre plates was developed and used to study respiration in pristine and contaminated soils following addition of volatile substrates. Small soil samples were exposed to fuel components, which were volatilized from spatially separate reservoirs of 2,2,4,4,6,8,8-heptamethylnonane (HMN) as an organic carrier. Respiration was determined as CO(2) production by means of a pH-indicator and bicarbonate-containing agar, or as (14)CO(2) evolution from (14)C-labelled substrates. Substrate concentrations inducing maximum microbial activity or inhibition were determined and CO(2) production profiles examined by multivariate analysis. When high concentrations of fuel components were applied, distinction of hydrocarbon exposed soils from unexposed soil was achieved within 6 h of incubation. With low concentrations, adequate distinction was achieved after 24 h, probably as a result of community adaptation. Nutrient limitation was identified with the (14)C method for toluene, and the optimal N and P amendment determined. Further potential applications of this rapid and inexpensive method are outlined.

Bacterial Physiological Phenomena↗

PubMed2005

Pleural effusion: a structured approach to care.

The accumulation of fluid in the pleural space is a common manifestation of a wide range of disease. This review provides a structured approach to the investigation of the patient with a pleural effusion. This should allow an accurate diagnosis to be made with the minimum number of invasive and time-consuming investigations.

Autoimmune Diseases↗

PubMed2004

Recent advances in parapneumonic effusion and empyema.

PURPOSE OF REVIEW: Complicated parapneumonic effusion and empyema continue to account for significant morbidity and mortality, and uncertainties remain regarding their optimal management. This review describes recent advances in this field, as well as areas for future research. RECENT FINDINGS: Recent advances have addressed the pathogenesis, bacteriology, and treatment of pleural infection. Key areas for research in the development of empyema include the interplay between inflammatory and coagulation cascades and development of fibrosis within the pleural space. The varied bacteriology of empyema has been more clearly defined, and in particular the differences between community- and hospital-acquired infection highlighted. Studies of treatment have focused particularly on the roles of intrapleural fibrinolytics and surgery. SUMMARY: Increased understanding of the pathogenesis of empyema may ultimately yield novel therapeutic targets. Comprehensive descriptions of the bacteriology of empyema aids antibiotic choice, and the use of intrapleural DNase shows promise in facilitating drainage of infected pleural fluid. Uncertainties remain, such as the role of intrapleural fibrinolytics and the optimal timing of surgical intervention.

Anti-Bacterial Agents↗

PubMed2004

The management of pleural space infections.

Pleural infection is responsible for significant morbidity and mortality worldwide, and its clinical management is challenging. The diagnosis of empyema and tuberculous pleurisy may be difficult, and these conditions may be confused with other causes of exudative pleural effusions. Complicated parapneumonic effusion or empyema may present with 'atypical' clinical features; delays in diagnosis are common and may contribute to the high mortality of these infections. Pleural aspiration is the key diagnostic step; pleural fluid that is purulent or that has a pH < 7.2, or organisms on Gram stain or culture, is an indication for formal intercostal drainage. In order to achieve a definitive diagnosis of tuberculous pleurisy, Mycobacterium tuberculosis must be isolated in the culture of pleural fluid, pleural tissue or sputum; demonstration of granulomas in pleural tissue is also suggestive of tuberculosis. The use of pleural fluid biochemical markers, such as adenosine deaminase, in the diagnosis of tuberculous pleurisy varies among clinicians; the diagnostic value of such markers is affected by the background prevalence of tuberculosis and the likelihood of an alternative diagnosis. Uncertainties also remain regarding the treatment of pleural infection. Treatment of complicated parapneumonic effusion and empyema involves prolonged courses of antibiotics and attention to the patient's nutritional state. The role of intrapleural fibrinolytics and the optimal timing of surgical intervention are unknown. The lack of clear predictors of clinical outcome in empyema contributes to the difficulty in treating this condition. The pharmacological treatment of tuberculous pleurisy is the same as for pulmonary tuberculosis; the precise role of steroids in the treatment of tuberculous pleurisy remains uncertain.

Chest Tubes↗

PubMed2003

Benign asbestos pleural diseases.

The global incidence of asbestos-related lung diseases is expected to continue to rise. Although much attention is devoted to malignant diseases induced by asbestos, benign asbestos pleural diseases (pleural plaques, benign asbestos-related pleural effusion, diffuse pleural thickening, and rounded atelectasis) are common in clinical practice and often produce diagnostic difficulties. The authors describe the clinical features of benign asbestos-related pleural disease, before focusing on recent advances in radiology and on controversies surrounding the pathogenesis of asbestos-induced pleural injury. Advances in computed tomography have assisted the understanding and diagnosis of these diseases, and increasing evidence suggests radiologic appearances on computed tomography can predict impairment in pulmonary function tests. The pathogenesis of asbestos-induced pleural diseases has also been subject to extensive investigation. Asbestos fibers can provoke pleural inflammation from direct toxicity to mesothelial cells. Inhaled asbestos fibers can also elicit pleural injury indirectly via the release of growth factors and inflammatory cytokines from within the lung. Although progress has been made in the understanding of the mechanisms of asbestos pleural injury, many important questions remain unanswered. The role of genetic factors and possible environmental cofactors (eg, simian virus 40) in the pathogenesis of benign asbestos pleural diseases requires further research.

Asbestos↗

PubMed2003

A rapid microtiter plate method to measure carbon dioxide evolved from carbon substrate amendments so as to determine the physiological profiles of soil microbial communities by using whole soil.

Sole-carbon-source tests (Biolog), designed to identify bacteria, have become very popular for metabolically fingerprinting soil microbial communities, despite disadvantages associated with the use of carbon source profiles that primarily select for fast-growing bacteria. In this paper we describe the use of an alternative method that combines the advantages of the Biolog community-level physiological profile (CLPP) method, in which microtiter-based detection plates are used, with the ability to measure carbon dioxide evolution from whole soil. This method facilitates measurement over short periods of time (4 to 6 h) and does not require the extraction and culturing of organisms. Deep-well microtiter plates are used as test wells into which soil is placed. The apparatus to fill the deep-well plates and interface it with a second removable detection plate is described. Two detection systems, a simple colorimetric reaction in absorbent alkali and scintillation counting with radioactive carbon sources, are described. The methods were compared to the Biolog-CLPP system by using soils under different vegetation types and soil treated with wastewater sludge. We aimed to test the hypothesis that using whole soil would have specific advantages over using extracts in that more immediate responses to substrates could be obtained that would reflect activity rather than growth. The whole-soil method was more rapid and gave earlier detection of C source use. Also, the metabolic fingerprints obtained could discriminate between sludge treatments.

Bacteria↗

PubMedDate not supplied

Pleural effusions.

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Humans↗