A method for improving the crack resistance of aluminum alloy aircraft skin inspired by plant leaf

Abstract(#br)Aircraft skins are likely to experience cracks and fracture failure due to the combined action of shear, bending, and torsional load. Inspired by the crack resistance exhibited by plant leaf, a method is proposed to improve the crack resistance of aluminum alloy aircraft skin. The characteristic parameters of main and secondary leaf veins are extracted by image edge detection and analysis methods. According to a constructed collection of self-similar fractal sets, a bio-inspired residual stress field with fractal characteristics extracted from leaf veins is applied to specimens ahead of crack tip by using laser peening. The effects of fractal parameters on crack retardation are analyzed using interaction integral. The results show that the stress intensity factor ahead of crack tip is reduced by applying a bio-inspired residual stress field, whereas the plastic zone area ahead of crack tip is enlarged. The correlation between these two trends reveals the mechanism of stress intensity decrease after the introduction of bio-inspired residual stress field. The optimal crack retardation effect is achieved at a fractal angle of 55°, at which the residual fatigue life is increased by up to 203.0%. Compared with square-shaped laser peening, full-coverage laser peening, square criss-cross pattern method, and single-edge notched tensile (SENT) specimen repair method, the proposed method achieves the longest residual fatigue life, which is almost three times that of the square-shaped laser peening method. Therefore, this theoretical study presents a potential method for improving the crack resistance of aluminum alloy aircraft skin

Correction of narrow nostril deformity secondary to cleft lip: indications for different surgical methods and a retrospective study

BackgroundCleft lip and/or palate (CLP) can lead to severe nasolabial deformities that significantly affect the appearance of the patient. Among all types of nasolabial deformities, narrow nostril deformities are the most troublesome, causing poor and unstable surgical outcomes. The purpose of this study was to develop an algorithm for surgical method selection for revision of narrow nostril deformities secondary to CLP based on retrospective clinical data.Materials and methodsPatients with narrow nostril deformities secondary to CLP were enrolled in the study. Before surgery, patients' clinical data were collected and the width of the nasal floor and the length of the alar rim were measured. Surgical methods were determined according to the measurements. After surgery, a nostril retainer was applied for 6 months to consolidate and maintain the nostril shape. The surgical method and postsurgical changes were recorded for the final summary of the algorithm to select surgical methods for narrow nostril deformities.ResultsThe data from 9 patients were analyzed. According to the width of the nasal floor and the length of the alar rim, correct surgical methods were determined. Four patients received nasolabial skin flaps to widen the soft tissue of the nasal floor. Three patients received upper lip scar tissue flaps to treat the narrow nasal floor. For the short alar rim, free alar composite tissue flap or narrowing of the nostril of the noncleft side was recommended.ConclusionThe width of the nasal floor and the length of the alar rim are critical elements to consider when selecting the correct surgical method for revising narrow nostril deformities secondary to CLP. The proposed algorithm provides a reference for selecting surgical methods in future clinical practice

Mechanical antihypersensitivity effect induced by repeated spinal administrations of a TRPA1 antagonist or a gap junction decoupler in peripheral neuropathy

Spinal transient receptor potential ankyrin 1 (TRPA1) channel is associated with various pain hypersensitivity conditions. Spinally, TRPA1 is expressed by central terminals of nociceptive nerve fibers and astrocytes. Among potential endogenous agonists of TRPA1 is H2O2 generated by D-amino acid oxidase (DAAO) in astrocytes. Here we studied whether prolonged block of the spinal TRPA1 or astrocytes starting at time of injury attenuates development and/or maintenance of neuropathic hypersensitivity. Additionally, TRPA1 and DAAO mRNA were determined in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH). Experiments were performed in rats with spared nerve injury (SNI) and chronic intrathecal catheter. Drugs were administered twice daily for the first seven injury days or only once seven days after injury. Mechanical hypersensitivity was assessed with monofilaments. Acute and prolonged treatment with Chembridge-5861528 (a TRPA1 antagonist), carbenoxolone (an inhibitor of activated astrocytes), or gabapentin (a comparison drug) attenuated tactile allodynia-like responses evoked by low (2 g) stimulus. However, antihypersensitivity effect of these compounds was short of significance at a high (15 g) stimulus intensity. No preemptive effects were observed. In healthy controls, carbenoxolone failed to prevent hypersensitivity induced by spinal cinnamaldehyde, a TRPA1 agonist TRPA1 and DAAO mRNA in the DRG but not SDH were slightly increased in SNI, independent of drug treatment The results indicate that prolonged peri-injury block of spinal TRPA1 or inhibition of spinal astrocyte activation attenuates maintenance but not development of mechanical (tactile allodynia-like) hypersensitivity after nerve injury. (C) 2016 Elsevier Inc. All rights reserved.Peer reviewe

Interface passivation using ultrathin polymer–fullerene films for high-efficiency perovskite solar cells with negligible hysteresis

Interfacial carrier recombination is one of the dominant loss mechanisms in high efficiency perovskite solar cells, and has also been linked to hysteresis and slow transient responses in these cells. Here we demonstrate an ultrathin passivation layer consisting of a PMMA:PCBM mixture that can effectively passivate defects at or near to the perovskite/TiO2 interface, significantly suppressing interfacial recombination. The passivation layer increases the open circuit voltage of mixed-cation perovskite cells by as much as 80 mV, with champion cells achieving Voc ∼ 1.18 V. As a result, we obtain efficient and stable perovskite solar cells with a steady-state PCE of 20.4% and negligible hysteresis over a large range of scan rates. In addition, we show that the passivated cells exhibit very fast current and voltage response times of less than 3 s under cyclic illumination. This new passivation approach addresses one of the key limitations of current perovskite cells, and paves the way to further efficiency gains through interface engineering.Australian Renewable Energy Agency; Australian Research Council; MSTC (Grant No. 2016YFA0301300), NNSFC (Grant No. 11674402) and GSTP (Grant No. 201607010044, 201607020023

Triptriolide Alleviates Lipopolysaccharide-Induced Liver Injury by Nrf2 and NF-κB Signaling Pathways

Nrf2 (Nuclear Factor Erythroid 2 Related Factor 2) transcription factor not only regulates oxidative stress response, but also represses inflammation by regulating cytokines production and cross-talking with NF-κB signaling pathways. Nrf2 plays an essential role in liver injury induced by oxidative stress and inflammation. Triptriolide (T11) is a minor component of Tripterygium wilfordii Hook F. (TwHF), which can be obtained by hydrolysis reaction of triptolide (T9). The major purpose of this study is to clarify the regulating effects of T11 on oxidative stress and inflammation in vivo and in vitro. LPS-stimulated RAW 264.7 cells were used to verify the regulating effects of T11 on oxidative stress (ROS and Nrf2 signaling pathway) and inflammatory cytokines production (TNF-α, IL-6 and IL-1β). The antioxidant responsive element (ARE) luciferase assay was employed to evaluate Nrf2 activation effect of T11 in HEK-293T cells. Lipopolysaccharides (LPS) induced acute liver injury (ALI) in BALB/c mice were used to study the protective effects (ALT, AST, MDA, SOD, histopathology and neutrophils/macrophages filtration) and the underlying protection mechanisms of ALI amelioration (Nrf2 and NF-κB signaling pathway) of T11. Firstly, the results showed that T11 can not only effectively decrease the productions of inflammatory cytokines (TNF-α, IL-6 and IL-1β), ROS and NO in LPS-stimulated RAW 264.7 cells, but also further significantly increase the activity of Nrf2 in HEK-293T cells. Secondly, the results suggested that T11 could dramatically decrease the oxidative stress responses (SOD and MDA) and inflammation (histopathology, neutrophils/macrophages filtration, TNF-α, IL-6 and IL-1β production) in LPS-induced ALI in BALB/c mice. Finally, the results implied that T11 could dramatically increase Nrf2 protein expression and decrease p-TAK1, p-IκBα and NF-κB protein expression both in vivo and in vitro. In conclusion, our findings indicated that T11 could alleviate LPS induced oxidative stress and inflammation by regulating Nrf2 and NF-κB signaling pathways in vitro and in vivo, which offers a novel insights for the application of TwHF in clinical