Bio-Inspired Pangolin Design for Self-Healable Flexible Perovskite Light-Emitting Diodes.

Despite tremendous developments in the luminescene performance of perovskite light-emitting diodes (PeLEDs), the brittle nature of perovskite crystals and their poor crystallinity on flexible substrates inevitably lead to inferior performance. Inspired by pangolins' combination of rigid scales and soft flesh, we propose a bionic structure design for self-healing flexible PeLEDs by employing a polymer-assisted crystal regulation method with a soft elastomer of diphenylmethane diisocyanate polyurethane (MDI-PU). The crystallinity and flexural strain resistance of such perovskite films on plastics with silver-nanowire-based flexible transparent electrodes are highly enhanced. The detrimental cracks induced during repeated deformation can be effectively self-healed under heat treatment via intramolecular/intermolecular hydrogen bonds with MDI-PU. Upon collective optimization of the perovskite films and device architecture, the blue-emitting flexible PeLEDs can achieve a record external quantum efficiency of 13.5% and high resistance to flexural strain, which retain 87.8 and 80.7% of their initial efficiency after repeated bending and twisting operations of 2000 cycles, respectively.

Interfacial "Anchoring Effect" Enables Efficient Large-Area Sky-Blue Perovskite Light-Emitting Diodes.

While tremendous progress has recently been made in perovskite light-emitting diodes (PeLEDs), large-area blue devices feature inferior performance due to uneven morphologies and vast defects in the solution-processed perovskite films. To alleviate these issues, a facile and reliable interface engineering scheme is reported for manipulating the crystallization of perovskite films enabled by a multifunctional molecule 2-amino-1,3-propanediol (APDO)-triggered "anchoring effect" at the grain-growth interface. Sky-blue perovskite films with large-area uniformity and low trap states are obtained, showing the distinctly improved radiative recombination and hole-transport capability. Based on the APDO-induced interface engineering, synergistical boost in device performance is achieved for large-area sky-blue PeLED (measuring at 100 mm2 ) with a peak external quantum efficiency (EQE) of 9.2% and a highly prolonged operational lifetime. A decent EQE up to 6.1% is demonstrated for the largest sky-blue device emitting at 400 mm2 .

Surface-induced phase engineering and defect passivation of perovskite nanograins for efficient red light-emitting diodes.

Organic-inorganic hybrid lead halide perovskites are potential candidates for next-generation light-emitting diodes (LEDs) in terms of tunable emission wavelengths, high electroluminescence efficiency, and excellent color purity. However, the device performance is still limited by severe non-radiative recombination losses and operational instability due to a high degree of defect states on the perovskite surface. Here, an effective surface engineering method is developed via the assistance of guanidinium iodide (GAI), which allows the formation of surface-2D heterophased perovskite nanograins and surface defect passivation due to the bonding with undercoordinated halide ions. Efficient and stable red-emission LEDs are realized with the improved optoelectronic properties of GAI-modified perovskite nanograins by suppressing the trap-mediated non-radiative recombination loss. The champion device with a high color purity at 692 nm achieves an external quantum efficiency of 17.1%, which is 2.3 times that of the control device. Furthermore, the operational stability is highly improved, showing a half-lifetime of 563 min at an initial luminance of 1000 cd m-2. The proposed GAI-assisted surface engineering is a promising approach for defect passivation and phase engineering in perovskite films to achieve high-performance perovskite LEDs.

Pharmacological characterisation and functional roles for egg-laying of a ß-adrenergic-like octopamine receptor in the brown planthopper Nilaparvata lugens.

Octopamine, the invertebrate counterpart of adrenaline and noradrenaline, controls and modulates many physiological and behavioral processes in protostomes. It mediates its effects by binding to specific receptors belonging to the superfamily of G-protein coupled receptors. We report the cloning of a cDNA from the brown planthopper (Nloa2b2) sharing high similarity with members of the OA2B2 receptor class. Activation of NlOA2B2 by octopamine increased the production of cAMP in a dose-dependent manner (EC50 = 114 nM). Tyramine also activated the receptor but with much less potency than octopamine. Using a series of known agonists and antagonists of octopamine receptors and cAMP measurements, we observed a rather unique pharmacological profile of NlOA2B2. The potency ranking of the tested agonists was naphazoline > clonidine. The activated effect of octopamine is abolished by co-incubation with epinastine, mianserin, phentolamine, methiothepin, butaclamol or methysergide. Nloa2b2 was expressed in different developmental stages and in various tissues including female reproductive regions known to be involved in egg-laying behavior. Using in vivo pharmacology and RNAi methodology, we demonstrated that interference of NlOA2B2 signaling pathway had a strong impact on the egg-laying behavior of female brown planthopper. The data presented here mark the first comprehensive study-from gene to behavior-of a OA2B2 receptor in the rice brown planthopper.

Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.

MicroRNA­106b (miR­106b) is reported to correlate closely with skeletal muscle insulin resistance. In the current study the effect of miR­106b on palmitic acid (PA)­induced mitochondrial dysfunction and insulin resistance was investigated in C2C12 myotubes via the silencing of miR­106b. MiR­106b expression was increased under PA treatment, while miR­106b loss of function improved insulin sensitivity by upregulating its target mitofusin­2 (Mfn2) in C2C12 myocytes. Furthermore, miR­106b loss of function partly improved mitochondrial morphological lesions and increased the levels of mitochondial DNA and intracellular adenosine triphosphate that had been impaired by PA exposure in C2C12 myocytes. MiR­106b loss of function attenuated the levels of intracellular reactive oxygen species (ROS), and upregulated the expression levels of the estrogen­related receptor (ERR)­α/peroxisome proliferative activated receptor γ coactivator (PGC)­1α/Mfn2 axis under PA exposure. In addition, miR­106b negatively regulated skeletal muscle mitochondrial function and insulin sensitivity under PA­induced insulin resistance by targeting Mfn2, which may be associated with reduced ROS and upregulation of the ERR­α/PGC­1α/Mfn2 axis.

MicroRNA-106b induces mitochondrial dysfunction and insulin resistance in C2C12 myotubes by targeting mitofusin-2.

MicroRNA-106b (miR-106b) is reported to correlate closely with skeletal muscle insulin resistance and type 2 diabetes. The aim of this study was to identify an mRNA targeted by miR-106b which regulates skeletal muscle insulin sensitivity. MiR-106b was found to target the 3' untranslated region (3' UTR) of mitofusin-2 (Mfn2) through miR-106b binding sites and to downregulate Mfn2 protein abundance at the post-transcriptional level by luciferase activity assay combined with mutational analysis and immunoblotting. Overexpression of miR-106b resulted in mitochondrial dysfunction and insulin resistance in C2C12 myotubes. MiR-106b was increased in insulin-resistant cultured C2C12 myotubes induced by TNF-α, and accompanied by increasing Mfn2 level, miR-106b loss of function improved mitochondrial function and insulin sensitivity impaired by TNF-α in C2C12 myotubes. In addition, both overexpression and downregulation of miR-106b upregulated peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α and estrogen-related receptor (ERR)-α expression. MiR-106b targeted Mfn2 and regulated skeletal muscle mitochondrial function and insulin sensitivity. Therefor, Inhibition of miR-106b may be a potential new strategy for treating insulin resistance and type 2 diabetes.