In Situ Coupling of Strung Co₄N and Intertwined N–C Fibers toward Free-Standing Bifunctional Cathode for Robust, Efficient, and Flexible Zn–Air Batteries

Flexible power sources with high energy density are crucial for the realization of next-generation flexible electronics. Theoretically, rechargeable flexible zinc–air (Zn–air) batteries could provide high specific energy, while their large-scale applications are still greatly hindered by high cost and resources scarcity of noble-metal-based oxygen evolution reaction (OER)/oxygen reduction reaction (ORR) electrocatalysts as well as inferior mechanical properties of the air cathode. Combining metallic Co₄N with superior OER activity and Co–N–C with perfect ORR activity on a free-standing and flexible electrode could be a good step for flexible Zn–air batteries, while lots of difficulties need to be overcome. Herein, as a proof-of-concept experiment, we first propose a strategy for in situ coupling of strung Co₄N and intertwined N–C fibers, by pyrolyzation of the novel pearl-like ZIF-67/polypyrrole nanofibers network rooted on carbon cloth. Originating from the synergistic effect of Co₄N and Co–N–C and the stable 3D interconnected conductive network structure, the obtained free-standing and highly flexible bifunctional oxygen electrode exhibits excellent electrocatalytic activity and stability for both OER and ORR in terms of low overpotential (310 mV at 10 mA cm^–2) for OER, a positive half-wave potential (0.8 V) for ORR, and a stable current density retention for at least 20 h, and especially, the obtained Zn–air batteries exhibit a low discharge–charge voltage gap (1.09 V at 50 mA cm^–2) and long cycle life (up to 408 cycles). Furthermore, the perfect bendable and twistable and rechargeable properties of the flexible Zn–air battery particularly make it a potentially power portable and wearable electronic device

Supported Cu/Ni Bimetallic Cluster Electrocatalysts Boost CO₂ Reduction

Supported metal clusters with the integrated advantages of single-atom catalysts and conventional nanoparticles held great promise in the electrocatalytic carbon dioxide reduction (ECO2R) operated at low overpotential and high current density. However, its precise synthesis and the understanding of synergistically catalytic effects remain challenging. Herein, we report a facile method to synthesize the bimetallic Cu and Ni clusters anchored on porous carbon (Cu/Ni–NC) and achieve an enhanced ECO2R. The aberration-corrected high-angle annular dark-field scanning transmission electron microscopy and synchrotron X-ray absorption spectroscopy were employed to verify the metal dispersion and the coordination of Cu/Ni clusters on NC. As a result of this route, the target Cu/Ni–NC exhibits excellent electrocatalytic performance including a stable 30 h electrolysis at 200 mA cm–2 with carbon monoxide Faradaic efficiency of ∼95.1% using a membrane electrode assembly electrolysis cell. Combined with the in situ analysis of the surface-enhanced Fourier transform infrared spectroelectrochemistry, we propose that the synergistic effects between Ni and Cu can effectively promote the H2O dissociation, thereby accelerate the hydrogenation of CO2 to *COOH and the overall reaction process

NO donor dose dependently decreases cell number induced by PDGF-BB and blocks survivin expression and <i>in vitro</i>.

<p>(A), Rat SMC were treated or not with PDGF (10 ng/ml), in the absence or presence of the NO donor, DETA/NO (10, 30, and 100 µM) and cell number quantified after 48 h. (B), NO reduces PDGF induced survivin levels. VSM were treated with PDGF (10 ng/ml) with or withoutt DETA/NONO (10, 30 and 100 µM) and the levels of survivin assessed by Western blotting. DETA/NO dose dependently decreased survivin levels relative to Hsp90 (a protein loading control). Densitometric values of the ratio of survivin to Hsp90 are shown below the blots. * P<0.05, ** P<0.01 with one way ANOVA with Bonferroni posttest.</p

Ad-T34A survivin transduction blocks cell proliferation and restores normal remodeling in eNOS (−/−) mice.

<p>(A) LCs were transduced with Ad-GFP or Ad-T34A survivin at the time of LEC ligation. Lumen diameter and wall thickness were calculated from 10 sections of contralateral RC and infected LC of eNOS (−/−) mice. Upper panel shows lumen diameter of Ad-T34A transduced LC was significantly decreased compared to RC. Ad-T34A transduction also blocks the wall thickening in transduced LC (lower panel). (B), Ad T34A suvivin reduces the number of BrdU positive cells in LC. (C), BrdU labeling index shows significant increase of BrdU positive cell/total nuclei ratio in Ad-GFP transduced LC compare to RC in eNOS (−/−) mice. This activation of cell proliferation was blocked by Ad-T34A transduction. Values are mean ± SEM; * P<0.05, ** P<0.01, and † P<0.001 with one way ANOVA with Bonferroni posttest; n = 5 for each group of mice. Scale bar equals to 25 µm.</p

SU9518 selectively inhibits PDGFR.

<p>SU9518 selectively inhibits PDGFR.</p

Molecular Mechanism Behind the Resistance of the G1202R-Mutated Anaplastic Lymphoma Kinase to the Approved Drug Ceritinib

Anaplastic lymphoma kinase (ALK) has been regarded as an essential target for the treatment of nonsmall cell lung cancer (NSCLC). However, the emergence of the G1202R solvent front mutation that confers resistance to the drugs was reported for the first as well as the second generation ALK inhibitors. It was thought that the G1202R solvent front mutation might hinder the drug binding. In this study, a different fact could be clarified by multiple molecular modeling methodologies through a structural analogue of ceritinib (compound 10, Cpd-10) that is reported to be a potent inhibitor against the G1202R mutation. Herein, molecular docking, accelerated molecular dynamics (aMD) simulations in conjunction with principal component analysis (PCA), and free energy map calculations were used to produce reasonable and representative initial conformations for the conventional MD simulations. Compared with Cpd-10, the binding specificity of ceritinib between ALK wild-type (ALK^WT) and ALK G1202R (ALK^G1202R) are primarily controlled by the conformational change of the P-loop- and A-loop-induced energetic redistributions, and the variation is nonpolar interactions, as indicated by conventional MD simulations, PCA, dynamic cross-correlation map (DCCM) analysis, and free energy calculations. Furthermore, the umbrella sampling (US) simulations were carried out to make clear the principle of the dissociation processes of ceritinib and Cpd-10 toward ALK^WT and ALK^G1202R. The calculation results suggest that Cpd-10 has similar dissociation processes from both ALK^WT and ALK^G1202R, but ceritinib is more easily dissociated from ALK^G1202R than from ALK^WT, thus less residence time is responsible for the ceritinib resistance. Our results suggest that both the binding specificity and the drug residence time should be emphasized in rational drug design to overcome the G1202R solvent front mutation of ALK resistance

SU9518 decreases cell proliferation and restore normal remodeling in eNOS (−/−) mice.

<p>(A), Lumen diameters (upper panel) of LC in SU9518 treated eNOS (−/−) mice were reduced in response to a remodeling stimulus but not in LC of vehicle treated eNOS (−/−) mice. Wall thickness (lower panel) of vehicle treated LC was significantly increased and, SU9518 restored the normal wall remodeling in LC. Values are mean ± SEM; n = 7 for each group of mice; * P<0.05, ** P<0.001 with one way ANOVA with Bonferroni posttest. (B) Representative hematoxylin and eosin stained LC cross sections of vehicle or SU9518 treated mice. Inward remodeling can be seen in SU9518 treated LC. Scale bar represents 100 µm. (C), Immunostaining shows BrdU positive cells were detected in all layers of ligated LC in vehicle treated mice (left panel), which blocked by SU9518 treatment as shown on the right panel. Scale bar represents 25 µm. (D), Quantitative BrdU index shows cell proliferation was significantly increased in vehicle treated LCs of eNOS (−/−) mice, but not in vessels from SU9518 treated eNOS (−/−) mice. (E) PDGF-BB receptor tyrosine kinase inhibitor decreases immunoreactive survivin levels in LC of eNOS (−/−) mice, compared to vehicle treated eNOS (−/−) mice (left panel). Right panel shows the quantification of percentage of suvivin positive staining in total vessel area. Values are mean ± SEM; n = 5. * P<0.05, ** P<0.001 with one way ANOVA with Bonferroni posttest.</p

Impaired vascular remodeling in congenic eNOS knockout mice.

<p>(A) Morphometric analysis showing reductions in lumen diameter of LC in C57BL/6J mice with no change in wall thickness in response to a remodeling stimulus, yet no change in lumen diameter but an increase in wall thickness in LC of eNOS (−/−) mice. (B) Hematoxylin and eosin staining showing RC and remodeled LC from a C57BL/6J mouse (upper panel) and RC and remodeled LC from an eNOS (−/−) mouse (lower panel). Scale bar represents 25 µm. Values are mean ± SEM; * P<0.05, ** P<0.01 with one way ANOVA with Bonferroni posttest; n = 5 for each group of mice.</p

Cation Segregation of A‑Site Deficiency Perovskite La_0.85FeO_3−δ Nanoparticles toward High-Performance Cathode Catalysts for Rechargeable Li‑O₂ Battery

Cation segregation of perovskite oxide is crucial to develop high-performance catalysts. Herein, we achieved the exsolution of α-Fe₂O₃ from parent La_0.85FeO_3−δ by a simple heat treatment. Compared to α-Fe₂O₃ and La_0.85FeO_3−δ, α-Fe₂O₃-LaFeO_3–<i>x</i> achieved a significant improvement of lithium-oxygen battery performance in terms of discharge specific capacity and cycling stability. The promotion can be attributed to the interaction between α-Fe₂O₃ and LaFeO_3–<i>x</i>. During the cycling test, α-Fe₂O₃-LaFeO_3–<i>x</i> can be stably cycled for 108 cycles at a limited discharge capacity of 500 mAh g^–1 at a current density of 100 mA g^–1, which is remarkably longer than those of La_0.85FeO_3−δ (51 cycles), α-Fe₂O₃ (21 cycles), and mechanical mixing of LaFeO₃ and α-Fe₂O₃ (26 cycles). In general, these results suggest a promising method to develop efficient lithium-oxygen battery catalysts via segregation