The rapid increase in perovskite solar cell efficiencies has motivated massive experimental and theoretical efforts aimed at understanding and enhancing the performance. We apply machine learning to nonadiabatic molecular dynamics simulation of nonradiative charge recombination in MAPbI3 and discover that the I–I–I angle is the key structural parameter governing nonadiabatic electron–phonon coupling and the bandgap. Surprisingly, the structure of MAPbI3 is much more important that the motions of MAPbI3, even though the coupling depends explicitly on nuclear velocity. Also surprisingly, rotational and center-of-mass motions of MA influence charge recombination, even though MA does not contribute to electron or hole wave functions. The findings rationalize the unusual temperature dependence of carrier lifetimes in halide perovskites and emphasize inorganic lattice deformation and MA rotation during polaron formation. By detecting nontrivial correlations within complex data and providing accurate quantitative measures, machine learning surpasses traditional analyses and suggests that perovskite performance can be controlled by chemical changes that alter perovskite geometric structure.
We report epitaxial GaN layers grown on 6H-SiC (0001) substrates. A two stage substrate preparation procedure is described which effectively removes oxygen from the SiC substrate surface without the need of elaborate high temperature processing. In the first step, dangling Si bonds on the substrate surface are hydrogen passivated using a HF dip before introduction into vacuum. Second, the substrate is treated with a hydrogen plasma reducing the amount of oxygen-carbon bonding to below the x-ray photoemission detection limit. Upon heating in the molecular beam epitaxy (MBE) growth chamber, the SiC substrates are observed to have a sharp (1×1) reconstruction with Kikuchi lines readily visible. GaN epilayers deposited on AlN buffer layers by plasma enhanced MBE show sharp x-ray diffraction and photoluminescence peaks.
Acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary inflammation and endothelial barrier permeability. Omentin has been shown to benefit obesity-related systemic vascular diseases; however, its effects on ARDS are unknown. In the present study, the level of circulating omentin in patients with ARDS was assessed to appraise its clinical significance in ARDS. Mice were subjected to systemic administration of adenoviral vector expressing omentin (Ad-omentin) and one-shot treatment of recombinant human omentin (rh-omentin) to examine omentin's effects on lipopolysaccharide (LPS)-induced ARDS. Pulmonary endothelial cells (ECs) were treated with rh-omentin to further investigate its underlying mechanism. We found that a decreased level of circulating omentin negatively correlated with white blood cells and procalcitonin in patients with ARDS. Ad-omentin protected against LPS-induced ARDS by alleviating the pulmonary inflammatory response and endothelial barrier injury in mice, accompanied by Akt/eNOS pathway activation. Treatment of pulmonary ECs with rh-omentin attenuated inflammatory response and restored adherens junctions (AJs), and cytoskeleton organization promoted endothelial barrier after LPS insult. Moreover, the omentin-mediated enhancement of EC survival and differentiation was blocked by the Akt/eNOS pathway inactivation. Therapeutic rh-omentin treatment also effectively protected against LPS-induced ARDS via the Akt/eNOS pathway. Collectively, these data indicated that omentin protects against LPS-induced ARDS by suppressing inflammation and promoting the pulmonary endothelial barrier, at least partially, through an Akt/eNOS-dependent mechanism. Therapeutic strategies aiming to restore omentin levels may be valuable for the prevention or treatment of ARDS.
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