American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · May 2014
Clinical TrialShould we view COPD Differently after ECLIPSE? A Clinical Perspective from the Study Team.
Chronic obstructive pulmonary disease (COPD) seems to be a heterogeneous disease with a variable course. ⋯ By following a large, well characterized cohort of patients with COPD over 3 years, we have a clearer picture of a heterogeneous disease with clinically important subtypes ("phenotypes") and a variable and not inherently progressive course. Clinical trial registered with www.clinicaltrials.gov (NCT00292552).
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The risk of cardiovascular events after severe sepsis is not known, and these events may explain increased long-term mortality in survivors of severe sepsis. ⋯ Survivors of severe sepsis have high risk of cardiovascular events. The higher risk is mainly due to poor prehospitalization health status, and is also seen in a broader population of acutely ill patients.
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Am. J. Respir. Crit. Care Med. · May 2014
Functional Prostacyclin Synthase Promoter Polymorphisms: Impact in Pulmonary Arterial Hypertension.
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary artery pressure, vascular remodeling, and ultimately right ventricular heart failure. PAH can have a genetic component (heritable PAH), most often through mutations of bone morphogenetic protein receptor 2, and idiopathic and associated forms. Heritable PAH is not completely penetrant within families, with approximately 20% concurrence of inactivating bone morphogenetic protein receptor 2 mutations and delayed onset of PAH disease. Because one of the treatment options is using prostacyclin analogs, we hypothesized that prostacyclin synthase promoter sequence variants associated with increased mRNA expression may play a protective role in the bone morphogenetic protein receptor 2 unaffected carriers. ⋯ Prostacyclin synthase promoter sequence variants exhibit a range of transcriptional activities. We discovered a significant bias for more active prostacyclin synthase promoter variants in unaffected carriers as compared with affected patients with PAH.