Chest
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Human rhinoviruses (RVs) are picornaviruses that can cause a variety of upper and lower respiratory tract illnesses, including the common cold, bronchitis, pneumonia, and exacerbations of chronic respiratory diseases such as asthma. There are currently > 160 known types of RVs classified into three species (A, B, and C) that use three different cellular membrane glycoproteins expressed in the respiratory epithelium to enter the host cell. These viral receptors are intercellular adhesion molecule 1 (used by the majority of RV-A and all RV-B types), low-density lipoprotein receptor family members (used by 12 RV-A types), and cadherin-related family member 3 (CDHR3; used by RV-C). ⋯ A single nucleotide polymorphism (rs6967330) in CDHR3 increases cell surface expression of this protein and, as a result, also promotes RV-C infections and illnesses. There are currently no approved vaccines or antiviral therapies available to treat or prevent RV infections, which is a major unmet medical need. Understanding interactions between RV and cellular receptors could lead to new insights into the pathogenesis of respiratory illnesses as well as lead to new approaches to control respiratory illnesses caused by RV infections.
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Systemic markers of inflammation in smokers with symptoms despite preserved spirometry in SPIROMICS.
Chronic respiratory symptoms and exacerbation-like events are common among ever-smokers without airflow limitation on spirometry. The pathobiology of respiratory disease in this subgroup remains poorly defined, but may be due to underlying inflammation that overlaps with COPD or asthma. We hypothesized that symptoms, exacerbations, and functional measures of disease severity among smokers with preserved spirometry would be associated with markers of systemic inflammation, similar to what is reported in bone fide COPD, rather than elevated type 2 inflammation, which is often present in asthma. ⋯ Markers of inflammation including CRP and sTNFRSF1A are enriched among symptomatic smokers with preserved spirometry, suggesting an overlap with the underlying pathophysiology of COPD.
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Lobar atelectasis (or collapse) is an exceedingly common, rather predictable, and potentially pathogenic companion to many forms of acute illness, postoperative care, and chronic debility. Readily diagnosed by using routine chest imaging and bedside ultrasound, the consequences from lobar collapse may be minor or serious, depending on extent, mechanism, patient vulnerability, abruptness of onset, effectiveness of hypoxic vasoconstriction, and compensatory reserves. Measures taken to reduce secretion burden, assure adequate secretion clearance, maintain upright positioning, reverse lung compression, and sustain lung expansion accord with a logical physiologic rationale. Both classification and logical approaches to prophylaxis and treatment of lobar atelectasis derive from a sound mechanistic knowledge of its causation.
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The impact of antibiotic timing on sepsis outcomes remains controversial due to conflicting results from previous studies. ⋯ Delays in ED antibiotic initiation time are associated with clinically important increases in long-term, risk-adjusted sepsis mortality.