New tests for tuberculosis: local immune responses have greater specificity.

Urinary leukotriene E4 concentrations increase after aspirin challenge in aspirin-sensitive asthmatic subjects. of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma. Effect of endobronchial aspirin challenge on inflammatory cells in bronchial biopsy samples from aspirin-sensitive asthmatic subjects. Expression of interleukin-5 and granulocyte-macrophage colony-stimulating factor in aspirin-sensitive and non-aspirin-sensitive asthmatic airways.mediated inhibition of 5-lipoxygenase translocation and leukotriene biosynthesis in human neutrophils. prevents aspirin-induced bronchoconstriction and urinary LTE 4 excretion in aspirin-sensitive asthma. Aspirin-sensitive rhinosinusitis is associated with reduced E-prostanoid 2 receptor expression on nasal mucosal inflammatory cells. Release of leukotrienes, prostaglandins, and histamine into nasal secretions of aspirin-sensitive asthmatics during reaction to aspirin. Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. Differential metabolism of arachidonic acid in nasal polyp epithelial cells cultured from aspirin-sensitive and aspirin-tolerant patients. Deficient prostaglandin E2 production by bronchial fibroblasts of asthmatic patients, with special reference to aspirin-induced asthma. Differential effects of aspirin and misoprostol on 15-hydroxyeicosatetraenoic acid generation by leukocytes from aspirin-sensitive asthmatic patients. Prostaglandin E 2 systemic production in patients with asthma with and without aspirin hypersensitivity. Safety of meloxicam in aspirin-hypersensitive patients with asthma and/or nasal polyps. A challenge-proven study. Biochemical and clinical evidence that aspirin-intolerant asthmatic subjects tolerate the cyclooxygenase 2-selective analgetic drug celecoxib. Cyclooxygenase-2 mRNA is down expressed in nasal polyps from aspirin-sensitive asthmatics. Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma. Enhanced expression of cyclo-oxygenase isoenzyme 2 (COX-2) in asthmatic airways and its cellular distribution in aspirin-sensitive asthma. We all want a good test for tuberculosis. Sputum smears are negative in half of those with lung involvement. 1 How can we detect tuberculosis if there are ,10 5 bacilli per ml of sputum? We could use either a more sensitive test for something the tubercle bacillus produces or use the host's response to amplify the signal. Mycobacterial culture, DNA-based amplification , 2 breath tests for volatile organic chemicals 3 and lipid profiles 4 5 exhibit the first approach. Chest radiographs, non-specific inflammatory markers and tests based on the specific immune response (such as tuberculin testing) exploit the second option. Local immune responses have previously been shown to have greater potential for diagnostic assays than sys-temic responses from peripheral blood. 6 7 Studies using cells isolated from human granulomas have demonstrated the importance of early secretory antigen target-6 (ESAT-6) in the CD4+ T …