Biomedical subjects
Publications and source records attributed to T M O'Connor.
Pulmonary eosinophilia responds very quickly to steroid treatment. Chronic pulmonary eosinophilia is common in middle aged females. We report on a patient who presented with subacute onset of shortness of breath, severe weight loss associated with a rise in the peripheral eosinophil count. She was treated successfully with steroids resulting in complete resolution of the pulmonary infiltrates.
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SETTING: The Southwest of Ireland (Counties Cork and Kerry) 1987-2000, average population 549,500. OBJECTIVE: Nontuberculous mycobacteria (NTM) cause significant morbidity worldwide and the study of epidemiology and characteristics helps in their prevention and treatment. This study was performed to determine the incidence of NTM disease in comparison to Mycobacterium tuberculosis (M. tuberculosis) and Mycobacterium bovis (M. bovis) in Southwest Ireland, over the above time period. DESIGN: A retrospective study was carried out in all human isolates of NTM, M. tuberculosis and M. bovis between 1987 and 2000, in the Southwest Region of Ireland. RESULTS: The mean incidence of NTM (0.4/100,000 population) has risen since 1995, principally of pulmonary Mycobacterium avium intracellulare complex (MAC). The annual incidence of M. tuberculosis in humans over 14 years in the same region was 971/100,000 population with a significant reduction since 1994 and M. bovis remained constant at 0.5/100,000 population. CONCLUSION: The increasing incidence of disease causing NTM noted in Southwest Ireland reflects global data and is surmised to be due to an ageing population, increased incidence related to chronic fibrotic lung disease, and environmental mycobacterial factors.
Aspergillus fumigatus is one of the most ubiquitous of the airborne saprophytic fungi. Allergic bronchopulmonary aspergillosis (ABPA) is a syndrome seen in patients with asthma and cystic fibrosis, and is characterized by hypersensitivity to chronic colonization of the airways with A. fumigatus. We report the case of a patient with ABPA presenting with pleural effusion. A 27-year-old male was referred with recurrent right pleural effusion. Past medical history was remarkable for asthma, allergic sinusitis, and recurrent pleurisy. Investigations revealed peripheral eosinophilia with elevated serum immunoglobulin E and bilateral pleural effusions with bilateral upper lobe proximal bronchiectasis. Precipitating serum antibodies to A. fumigatus were positive and the A. fumigatus immediate skin test yielded a positive reaction. A diagnosis of ABPA associated with bilateral pleural effusions was made and the patient was commenced on prednisolone. At review, the patient's symptoms had considerably improved and his pleural effusions had resolved. ABPA may present with diverse atypical syndromes, including paratracheal and hilar adenopathy, obstructive lung collapse, pneumothorax and bronchopleural fistula, and allergic sinusitis. Allergic bronchopulmonary aspergillosis is a rare cause of pleural effusion and must be considered in the differential diagnosis of patients presenting with a pleural effusion, in particular those with a history of asthma.
OBJECTIVES: Occupational asthma is the principal cause of respiratory disease in the workplace. The enzymes phytase and beta-glucanase are used in the agricultural industry to optimise the nutritional value of animal feeds. A relation between these enzymes and occupational asthma in a 43 year old man was suspected. METHODS: Inhalation challenge tests were performed with the enzymes phytase, beta-glucanase, and amylase. Skin prick tests were performed with the enzymes diluted to a concentration of 1 mg/ml and 5 mg/ml. Specific IgE to phytase and beta-glucanase were measured with a radioallergosorbent test. RESULTS: Baseline spirometry values were normal. A histamine challenge test showed bronchial hyperreactivity. Exposure to phytase and beta-glucanase led to significant reductions in forced vital capacity and forced expired volume in 1 second. No significant differences were noted after exposure to amylase. Skin tests showed a positive reaction to beta-glucanase (5 mm) at a concentration of 1 mg/ml and positive reactions to beta-glucanase (7 mm) and phytase (5 mm) at a concentration of 5 mg/ml. Similarly specific IgE was present against both phytase and beta-glucanase, at 2.5% and 9.3% binding respectively (2% binding is considered positive). CONCLUSIONS: This is the first description of occupational asthma due to the enzymes phytase and beta-glucanase. Their addition to the ever increasing list of substances associated with occupational asthma will have notable implications for those exposed to these enzymes.
Organisms survive by maintaining equilibrium with their environment. The stress system is critical to this homeostasis. Glucocorticoids modulate the stress response at a molecular level by altering gene expression, transcription, and translation, among other pathways. The effect is the inhibition of the functions of inflammatory cells, predominantly mediated through inhibition of cytokines, such as IL-1, IL-6, and TNF-alpha. The central effectors of the stress response are the corticotrophin-releasing hormone (CRH) and locus coeruleus-norepinephrine (LC-NE)/sympathetic systems. The CRH system activates the stress response and is subject to modulation by cytokines, hormones, and neurotransmitters. Glucocorticoids also modulate the growth, reproductive and thyroid axes. Abnormalities of stress system activation have been shown in inflammatory diseases such as rheumatoid arthritis, as well as behavioural syndromes such as melancholic depression. These disorders are comparable to those seen in rats whose CRH system is genetically abnormal. Thus, the stress response is central to resistance to inflammatory and behavioural syndromes. In this review, we describe the response to stress at molecular, cellular, neuroendocrine and behavioural levels, and discuss the disease processes that result from a dysregulation of this response, as well as recent developments in their treatment.
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BACKGROUND: The ligase chain reaction Mycobacterium tuberculosis assay uses ligase chain reaction technology to detect tuberculous DNA sequences in clinical specimens. A study was undertaken to determine its sensitivity and specificity as a primary screening tool for the detection of culture positive tuberculosis. METHODS: The study was conducted on 2420 clinical specimens (sputum, bronchoalveolar lavage fluid, pleural fluid, urine) submitted for primary screening for Mycobacterium tuberculosis to a regional medical microbiology laboratory. Specimens were tested in parallel with smear, ligase chain reaction, and culture. RESULTS: Thirty nine patients had specimens testing positive by the ligase chain reaction assay. Thirty two patients had newly diagnosed tuberculosis, one had a tuberculosis relapse, three had tuberculosis (on antituberculous therapy when tested), and three had healed tuberculosis. In the newly diagnosed group specimens were smear positive in 21 cases (66%), ligase chain reaction positive in 30 cases (94%), and culture positive in 32 cases (100%). Using a positive culture to diagnose active tuberculosis, the ligase chain reaction assay had a sensitivity of 93.9%, a specificity of 99.8%, a positive predictive value of 83.8%, and a negative predictive value of 99.9%. CONCLUSIONS: This study is the largest clinical trial to date to report the efficacy of the ligase chain reaction as a primary screening tool to detect Mycobacterium tuberculosis infection. The authors conclude that ligase chain reaction is a useful primary screening test for tuberculosis, offering speed and discrimination in the early stages of diagnosis and complementing traditional smear and culture techniques.
INTRODUCTION: Patients with Type 1 diabetes mellitus have a high prevalence of coeliac disease, symptoms of which are often mild, atypical, or absent. Untreated coeliac disease is associated with an increased risk of malignancy, particularly of lymphoma. We describe four patients with Type 1 diabetes mellitus and coeliac disease who developed lymphoma. CASE REPORTS: Two patients were male and two female. In three patients, coeliac disease and lymphoma were diagnosed simultaneously. Enteropathy-associated T cell lymphoma occurred in two patients, Hodgkin's disease in one, and B cell lymphoma in one. Response to treatment was in general poor, and three patients died soon after the diagnosis of lymphoma was made. CONCLUSION: As the relative risk of lymphoma is reduced by a gluten-free diet, a high index of suspicion for coeliac disease should exist in all Type 1 diabetic patients with unexplained constitutional or gastrointestinal symptoms.
The photoresponse in retinal photoreceptors begins when a molecule of rhodopsin is excited by a photon of light. Photoexcited rhodopsin activates an enzymatic cascade including the G-protein transducin and cyclic GMP phosphodiesterase. As a result, cytoplasmic cyclic GMP concentration is decreased and the photoresponse is initiated. This process is terminated when rhodopsin is phosphorylated by rhodopsin kinase and subsequently blocked by a protein called arrestin. It has been noted by several investigators that light can cause phosphorylation of not only photoexcited but also non-excited rhodopsin in rod photoreceptors. A goal of this study was to determine how much non-bleached rhodopsin is phosphorylated. To determine how the structural integrity of the photoreceptor influences the extent of non-bleached rhodopsin phosphorylation, we studied the reaction in electropermeabilized rod outer segments, in rod outer segments still attached to isolated retinas and in living frogs. In the first two preparations, we found that the maximum extent of non-bleached rhodopsin phosphorylation was approximately 1% of the total rhodopsin pool. In living frogs, the maximal amount of non-bleached rhodopsin phosphorylation was approximately 2% of the total rhodopsin pool and occurred after prolonged illumination by the relatively dim light intensity of 20 lux. These data appear to exclude models for light adaptation that postulate high levels of phosphorylation of non-bleached rhodopsin in rod photoreceptors.
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Controversy surrounds the issue of screening for the human immunodeficiency virus in pregnancy. The question remains: Which pregnant women should be tested? To answer this question, it is clear that local prevalence data of seropositivity must be known. At present, these figures are unavailable for midwestern metropolitan areas such as ours. Therefore an obstetric human immunodeficiency virus screening committee was formed to determine the prevalence of seropositivity of this virus in our obstetric clinic population. During a 14-month period of time all patients registering for prenatal care were offered human immunodeficiency virus antibody testing. A total of 585 out of 751 patients (78%) gave informed consent. Forty-two of these patients had risk factors for human immunodeficiency virus infection. The rate of seropositivity in this group was 7.1% (3 of 42). The remaining 543 patients had no risk factors and none of these patients had positive test results. From our preliminary results, screening only those prenatal patients with identified risk factors appears to be justified.
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Neuronal microtubules in a variety of nerve cell types are unaffected by high hydrostatic pressures over a range of 1400-10,000 pounds/inch(2) and periods of 10-45 min. Similarly, purified tubulin polymerized to form microtubules in vitro were not depolymerized by the same range of pressures. The depolymerization of microtubules in several types of non-neuronal cells, which has been reported, may have been over-generalized with regard to the direct action of pressure on microtubule stability.
The events which occur in the death of visceromotor neurons of the cervical region of the chick embryo's spinal cord have been analyzed by electron microscopy. These normal degenerative events are compared with those in the lumbosacral cord where nerve cell death was induced by removal of peripheral organs. The initial set of degenerative changes include a decrease in nuclear size, the clumping of chromatin beneath the nuclear envelope, an increase in electron opacity of the cells, the disappearance of Golgi bodies, and the disaggregation of polysomes. These events are followed by the loss of the nuclear envelope and most of the endoplasmic reticulum, the appearance of bundles of filaments, and the formation of many ribosome crystals. Ribosome crystals are seen only in the dying cells. Their abundance may indicate a drastic reduction in RNA synthesis as one of the initial events which lead to the death of these neurons. The neurons are finally subdivided and engulfed by cells of the normal glial population, and further breakdown of the cell fragments occurs in large phagocytic vesicles of the gliocytes.