Chest
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An increase in airway caliber (airway distensibility) with lung inflation is attenuated in COPD. Furthermore, some subjects have a decrease in airway caliber with lung inflation. We aimed to test the hypothesis that airway caliber increases are lower in subjects with emphysema-predominant (EP) compared with airway-predominant (AP) CT scan subtypes. Additionally, we compared clinical and CT scan features of subjects with (airway constrictors) and without a decrease in airway caliber. ⋯ Distensibility of large- to medium-sized airways is reduced in subjects with an EP CT scan subtype. Emphysema seems to alter airway-parenchyma interdependence.
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Endothelial dysfunction can develop in the context of both obesity and obstructive sleep apnea (OSA) in children. However, the potential interactions between OSA and obesity have not been defined. ⋯ Both obesity and OSA can independently increase the risk for endothelial dysfunction, and the concurrent presence of both markedly increases such risk. Although the mechanisms underlying endothelial dysfunction remain unclear, a potential role for MRP8/14 as an inflammatory biomarker of endothelial dysfunction is suggested.
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Obesity and asthma both cause breathlessness, and there is a risk of misdiagnosis of asthma in patients who are obese. Impaired health-related quality of life (HRQoL) and increased BMI increase physician attendance rates, increasing this risk. We explored the possibility of misdiagnosis and the relationship between BMI, HRQoL, and other traditional measures of asthma severity in subjects who were obese with a doctor's diagnosis of asthma. ⋯ We found evidence of misdiagnosis of asthma in subjects who were obese. The BMI in subjects who were obese and had asthma negatively correlates with the HRQoL, which may relate to the diagnostic uncertainty and requires further exploration.
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Comparative Study
Gene expression profiling in the lungs of patients with pulmonary hypertension associated with pulmonary fibrosis.
Pulmonary hypertension (PH) associated with pulmonary fibrosis (PF) is a severe condition with poor outcome. It is unknown whether patients with PF with associated PH (APH) represent a distinct phenotype of the disease. We hypothesized that the lung tissue gene expression pattern of patients with APH has a characteristic profile when compared with patients with PF without APH. We sought to determine if different gene expression signatures in PF could be determined based on pulmonary arterial pressures (PAPs) and to provide new insights into the pathobiology of APH. ⋯ Gene expression profiles distinguish PF phenotypes with and without APH. This observation can have important implications for future trials.