Lung
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Comparative Study
Longitudinal assessment of high versus low levels of fractional exhaled nitric oxide among children with asthma and atopy.
Fractional exhaled nitric oxide (FeNO) has emerged as an important biomarker in asthma. Increasing evidence points to atopy as a confounding factor in the interpretation of elevated FeNO. We conducted a longitudinal study to understand the clinical significance of FeNO as an inflammatory biomarker. ⋯ An elevation of FeNO appears to indicate an atopic phenotype regardless of an asthma diagnosis, clinical symptoms, or corticosteroid use. An elevation of FeNO also is associated with a systemic elevation in inflammatory cytokines.
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Cocaine is the most commonly used illicit drug among patients presenting at hospital emergency departments and the most frequent cause of drug-related deaths reported by medical examiners. Various respiratory problems temporally associated with cocaine use have been reported. ⋯ Although most imaging findings are nonspecific, they may raise suspicion of a cocaine-related etiology when considered together with patients' profiles and medical histories. This literature review describes cocaine-induced diseases with pulmonary involvement, with an emphasis on high-resolution chest computed tomographic findings and patterns.
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Comparative Study Observational Study
Comparison of severe healthcare-associated pneumonia with severe community-acquired pneumonia.
We compared the demographic characteristics and outcomes of patients with severe healthcare-associated pneumonia (HCAP) to those with severe community-acquired pneumonia (CAP). ⋯ The severity of illness rather than the type of pneumonia might be associated with in-hospital mortality in patients with severe pneumonia.
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Receptor for advanced glycation end products (RAGE), a multiple-ligands receptor, is implicated in chronic obstructive pulmonary disease (COPD). This study was designed to investigate the potential role of RAGE in nitric oxide (NO) generation, an endogenous marker of nitrosative stress in COPD. ⋯ These findings suggest that overexpression of RAGE contributes to CS-induced NO generation in COPD with involvement in NF-κB activation.