American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Apr 2016
Randomized Controlled TrialLung Deflation and Cardiovascular Structure and Function in COPD: A Randomized Controlled Trial.
Patients with chronic obstructive pulmonary disease develop increased cardiovascular morbidity with structural alterations. ⋯ Pharmacologic treatment of chronic obstructive pulmonary disease has consistent beneficial and plausible effects on cardiac function and pulmonary vasculature that may contribute to favorable effects of inhaled therapies. Future studies should investigate the effect of prolonged lung deflation on intrinsic myocardial function. Clinical trial registered with www.clinicaltrials.gov (NCT 01691885).
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Am. J. Respir. Crit. Care Med. · Apr 2016
Membrane and Capillary Components of Lung Diffusion in Infants with Bronchopulmonary Dysplasia.
Autopsied lungs of infants with bronchopulmonary dysplasia (BPD) demonstrate impaired alveolar development with larger and fewer alveoli, which is consistent with our previous physiologic findings of lower pulmonary diffusing capacity of the lung for carbon monoxide (DL(CO)) in infants and toddlers with BPD compared with healthy controls born at full term (FT). However, it is not known whether the decreased DL(CO) in infants with BPD results from a reduction in both components of DL(CO): pulmonary membrane diffusing capacity (D(M)) and Vc. ⋯ Our findings are consistent with infants with BPD having impaired alveolar development with fewer but larger alveoli, as well as a reduced Vc.
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Am. J. Respir. Crit. Care Med. · Apr 2016
Small-molecule, T315, Promotes CBL-dependent Degradation of EGFR via Y1045 Autophosphorylation.
Despite the fact that tyrosine kinase inhibitors (TKIs) have been found effective in treating patients harboring activating mutations of epidermal growth factor receptor (EGFR), an acquired secondary mutation, T790M, which lowers the affinity to TKIs, can lead to EGFR TKI resistance after this standard treatment. ⋯ Our evidence suggests that T315 is a novel class of anticancer drug that is able to inhibit the growth of EGFR-TKI-resistant lung adenocarcinoma cells by inducing the degradation of EGFR.