American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Oct 2012
Obesity and asthma: an inflammatory disease of adipose tissue not the airway.
Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese. ⋯ Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.
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Am. J. Respir. Crit. Care Med. · Oct 2012
Vitamin D deficiency, smoking, and lung function in the Normative Aging Study.
Vitamin D has immunomodulatory and antiinflammatory effects that may be modified by cigarette smoke and may affect lung function. ⋯ Vitamin D deficiency was associated with lower lung function and more rapid lung function decline in smokers over 20 years in this longitudinal cohort of elderly men. This suggests that vitamin D sufficiency may have a protective effect against the damaging effects of smoking on lung function. Future studies should seek to confirm this finding in the context of smoking and other exposures that affect lung function.
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Am. J. Respir. Crit. Care Med. · Oct 2012
Multicenter StudyImpact of intensive care unit organ failures on mortality during the five years after a critical illness.
The relationship between organ failure during critical illness and long-term survival is uncertain, especially among intensive care unit (ICU) survivors. ⋯ Cardiovascular, respiratory, and liver failures during critical illness strongly predict subsequent 5-year survival. Acute organ failure burden is associated with long-term mortality even among patients who survive up to 1 year after ICU admission.
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Am. J. Respir. Crit. Care Med. · Oct 2012
A critical role for p130Cas in the progression of pulmonary hypertension in humans and rodents.
Pulmonary arterial hypertension (PAH) is a progressive and fatal disease characterized by pulmonary arterial muscularization due to excessive pulmonary vascular cell proliferation and migration, a phenotype dependent upon growth factors and activation of receptor tyrosine kinases (RTKs). p130(Cas) is an adaptor protein involved in several cellular signaling pathways that control cell migration, proliferation, and survival. ⋯ Our findings demonstrate that p130(Cas) signaling plays a critical role in experimental and idiopathic PAH by modulating pulmonary vascular cell migration and proliferation and by acting as an amplifier of RTK downstream signals.
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Am. J. Respir. Crit. Care Med. · Oct 2012
Carbon monoxide induces cardiac arrhythmia via induction of the late Na+ current.
Clinical reports describe life-threatening cardiac arrhythmias after environmental exposure to carbon monoxide (CO) or accidental CO poisoning. Numerous case studies describe disruption of repolarization and prolongation of the QT interval, yet the mechanisms underlying CO-induced arrhythmias are unknown. ⋯ Our data indicate that the proarrhythmic effects of CO arise from activation of NO synthase, leading to NO-mediated nitrosylation of Na(V)1.5 and to induction of the late Na(+) current. We also show that the antianginal drug ranolazine can abolish CO-induced early after-depolarizations, highlighting a novel approach to the treatment of CO-induced arrhythmias.