Lung
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Undifferentiated connective tissue disease (UCTD) is a distinct clinical entity that may be accompanied by interstitial lung disease (ILD). The natural history of UCTD-ILD is unknown. We hypothesized that patients with UCTD-ILD would be more likely to have improvement in lung function than those with idiopathic pulmonary fibrosis (IPF) during longitudinal follow-up. ⋯ After accounting for baseline pulmonary function tests, treatment, and duration between studies, UCTD was associated with substantial improvement in FVC (odds ratio = 8.23, 95% confidence interval, 1.27-53.2; p = 0.03) during follow-up (median, 8 months) compared with IPF. Patients with UCTD-ILD are more likely to have improved pulmonary function during follow-up than those with IPF. These findings demonstrate the clinical importance of identifying UCTD in patients presenting with an "idiopathic" interstitial pneumonia.
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The purpose of this review is to cover the definition and mechanism of airway pressure release ventilation, its advantages, and applications in acute lung injury.
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Talc is a mineral widely used in the ceramic, paper, plastics, rubber, paint, and cosmetic industries. Four distinct forms of pulmonary disease caused by talc have been defined. Three of them (talcosilicosis, talcoasbestosis, and pure talcosis) are associated with aspiration and differ in the composition of the inhaled substance. ⋯ The characteristic histopathologic feature in talc pneumoconiosis is the striking appearance of birefringent, needle-shaped particles of talc seen within the giant cells and in the areas of pulmonary fibrosis with the use of polarized light. In conclusion, computed tomography can play an important role in the diagnosis of pulmonary talcosis, since suggestive patterns may be observed. The presence of these patterns in drug abusers or in patients with an occupational history of exposure to talc is highly suggestive of pulmonary talcosis.
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Sneezing, cough, mucus secretion, and bronchoconstriction represent the main components of a coordinated and efficient reaction direct to expel or neutralize irritant agents from the respiratory system. A dense network of sensory nerves localized from the nose to the lower airways beneath the epithelium subserves this function. A variety of receptors and channels present in sensory nerve terminals by sensing irritant stimuli activate the system in emergence and initiate protective reflex responses, including cough. Previous and recent literature highlights the prominent role of some transient receptor potential (TRP) ion channels, and specifically the vanilloid 1 (TRPV1) and the ankyrin 1 (TRPA1) as sensors of airway irritation and initiators of the cough reflex.
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In healthy nonsmokers, inhalation of one single puff of cigarette smoke immediately evoked airway irritation and cough, which were either prevented or markedly diminished after premedication with hexamethonium. Single-fiber recording experiments performed in anesthetized animals showed that both C fibers and rapidly adapting receptors in the lungs and airways were stimulated by inhalation of one breath of cigarette smoke. Application of nicotine evoked an inward current and triggered depolarization and action potentials in a concentration-dependent manner in a subset of isolated vagal pulmonary sensory neurons. ⋯ In contrast to the observations in animal studies, both enhanced and diminished cough sensitivities to tussive agents have been reported in chronic smokers. This discrepancy is probably related to the history of chronic smoking of the individual smokers and the severity of existing airway inflammation and dysfunction. Furthermore, several other factors possibly contributing to the regulation of cough receptor sensitivity in chronic smokers should also be considered.