A planar-like Fe 2 N 6 structure with distinguished catalytic mechanism was highlighted as a high-efficiency oxygen reduction catalyst. Accelerated catalytic kinetics and highly suppressed side reaction enabled the planar-like Fe 2 N 6 structure to exhibit over 700% increase in mass activity than traditional isolated iron-nitrogen sites. Proton-exchange membrane fuel cells built with this catalyst also achieved a large peak power density of 845 mW cm À2 , representing a critical breakthrough for the practical application of metal-nitrogen-carbon materials in PEMFC systems.

Background Long non-coding RNA (LncRNA) controls cell proliferation and plays a significant role in the initiation and progression of esophageal squamous cell carcinoma (ESCC). N6-methyladenosine (m6A) modification now is recognized as a master driver of RNA function to maintain homeostasis in cancer cells. However, how m6A regulates LncRNA function and its role in tumorigenesis of ESCC remain unclear. Methods Multiple ESCC datasets were used to analyze gene expression in tumor tissues and normal tissues. Kaplan-Meier method and the ROC curve were conducted to evaluate the prognostic value and diagnostic value of LINC00022 in ESCC, respectively. Both gain-of-function and loss-of-function experiments were employed to investigate the effects of LINC00022 on ESCC growth in vitro and in vivo. Bioinformatics analysis, colorimetric m6A assay, RIP, MeRIP and co-IP was performed to explore the epigenetic mechanism of LINC00022 up-regulation in ESCC. Results Here we report that m6A demethylation of LncRNA LINC00022 by fat mass and obesity-associated protein (FTO) promotes tumor growth of ESCC in vivo. Clinically, we revealed that LINC00022 was up-regulated in primary ESCC samples and was predictive of poor clinical outcome for ESCC patients. Mechanistically, LINC00022 directly binds to p21 protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation. Further, the elevated FTO in ESCC decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. Over-expression of FTO was shown to drive LINC00022-dependent cell proliferation and tumor growth of ESCC. Conclusions Thus, this study demonstrated m6A-mediated epigenetic modification of LncRNA contributes to the tumorigenesis in ESCC and LINC00022, specific target of m6A, serves as a potential biomarker for this malignancy.

The nonradiating nature of anapole modes owing to the compositions of electric and toroidal dipole moments makes them distinct from conversional radiative resonances, and they have been suggested for the design of nanophotonic devices such as nanolasers based on light−matter interactions tailor by nanodisks. Therefore, the investigation of resonance coupling between molecular excitons and anapole modes is not only of fundamental interest, but is also promising for practical applications. To this end, a heterostructure composed of a silicon nanodisk and a uniform molecular J-aggregate ring is used to achieve the resonance coupling between the exciton transition and the anapole mode. In contrast with that of the conversional resonances, the resonance coupling is evidenced by a scattering peak around the exciton transition frequency, and the anapole mode splits into a pair of eigenmodes characterized as pronounced scattering dips, which are termed as the formation of two hybrid anapole modes caused by the coherent energy exchange in the heterostructure, and it has been verified by the multipole decompositions and the near-field distributions. An anticrossing behavior with a mode splitting of 161 meV is observed on the energy diagram, indicating that the strong coupling regime is achieved. Furthermore, due to the unique near-field distribution associated with the anapole mode, there is a much larger upper limit value for the width of the J-aggregate ring to enhance the resonance coupling, and the molecules located around the apexes of the disk perpendicular to the incident polarization play the dominate role for the resonance coupling.

We report the development of an optofluidic laser array fabricated on a chip using stable plano-concave Fabry-Pérot (FP) microcavities, which are far less susceptible to optical misalignment during device assembly than commonly used plano-plano FP microcavities. The concave mirrors in our FP microcavities were created by first generating an array of microwells of a few micrometers in depth and a few tens of micrometers in diameter on a fused silica chip using a CO2 laser, followed by coating of distributed Bragg reflection (DBR) layers. The planoconcave FP microcavity had a Q-factor of 5.6×105 and finesse of 4×103, over 100 times higher than those for the FP microcavities in existing optofluidic lasers. 1 mM R6G dye in ethanol was used to test the plano-concave FP microcavities, showing an ultralow lasing threshold of only 90 nJ/mm2, over 10 times lower than that in the corresponding unstable plano-plano FP microcavities formed by the same DBR coatings on the same chip. Simultaneous laser emission from the optofluidic laser array on the chip and single-mode lasing operation were also demonstrated. Our work will lead to the development of optofluidic laser based biochemical sensors and novel on-chip photonic devices with extremely low lasing thresholds (nJ/mm2) and mode volumes (fL).

Biolasers are an emerging technology for next generation biochemical detection and clinical applications. Progress has recently been made to achieve lasing from biomolecules and single living cells. Tissues, which consist of cells embedded in extracellular matrix, mimic more closely the actual complex biological environment in a living body and therefore are of more practical significance. Here, we developed a highly versatile tissue laser platform, in which tissues stained with fluorophores are sandwiched in a high-Q Fabry-Pérot microcavity. Distinct lasing emissions from muscle and adipose tissues stained respectively with fluorescein isothiocyanate (FITC) and boron-dipyrromethene (BODIPY), and hybrid muscle/adipose tissue with dual-staining were achieved with a threshold of only ~10 μJ/mm2. Additionally, we investigated how tissue structure/geometry, tissue thickness, and staining dye concentration affect the tissue laser. Lasing emission from FITC conjugates (FITC-phalloidin) that target specifically F-actin in muscle tissues was also realized. It is further found that, despite large fluorescence spectral overlap between FITC and BODIPY in tissues, their lasing emissions could be clearly distinguished and controlled due to their narrow lasing bands and different lasing thresholds, thus enabling highly multiplexed detection. Our tissue laser platform can be broadly applicable to various types of tissues/diseases. It provides a new tool for a wide range of biological and biomedical applications, such as diagnostics/screening of tissues and identification/monitoring of biological transformations in tissue engineering.

Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor with poor prognosis. And different individuals respond to the same drug differently. Increasing evidence has confirmed that metabolism reprogramming was involved in the drug sensitivity of tumor cells. However, the potential molecular mechanism of 5‐fluorouracil (5‐FU) sensitivity remains to be elucidated in ESCC cells. In this study, we found that the 5‐FU sensitivity of TE1 cells was lower than that of EC1 and Eca109 cells. Gas chromatography‐mass spectrometry analysis results showed that nicotinate and nicotinamide metabolism and tricarboxylic acid cycle were significantly different in these three cell lines. Nicotinamide N‐methyltransferase (NNMT), a key enzyme of nicotinate and nicotinamide metabolism, was significantly higher expressed in TE1 cells than that in EC1 and Eca109 cells. Therefore, the function of NNMT on 5‐FU sensitivity was analyzed in vitro and in vivo. NNMT downregulation significantly increased 5‐FU sensitivity in TE1 cells. Meanwhile, the glucose consumption and lactate production were decreased, and the expression of glycolysis‐related enzymes hexokinase 2, lactate dehydrogenase A, and phosphoglycerate mutase 1 were downregulated in NNMT knockdown TE1 cells. Besides, overexpression of NNMT in EC1 and Eca109 cells caused the opposite effects. Moreover, when glycolysis was inhibited by 2‐deoxyglucose, the roles of NNMT on 5‐FU sensitivity was weakened. In vivo experiments showed that NNMT knockdown significantly increased the sensitivity of xenografts to 5‐FU and suppressed the Warburg effect. Overall, these results demonstrated that NNMT decreases 5‐FU sensitivity in human ESCC cells through promoting the Warburg effect, suggesting that NNMT may contribute to predict the treatment effects of the clinical chemotherapy in ESCC.

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Endogenous heterojunction of 2D MXenes with unique structure shows inspiring potential in energy applications, which is impeded by complex synthesis method and finite MAX materials. Herein, an in situ hydrothermal strategy is implemented to successfully synthesize unique endogenous hetero‐MXenes of amorphous MoS2 coupling with fluoride‐free Mo2CTx (hetero‐Mo2C) directly from Mo2Ga2C MAX. The distinctive morphology and heterojunction structure caused by the introduction of MoS2 endow the hetero‐MXenes with extraordinary structural stability and optimized Li+ storage mechanism with improved charge transport and lithium ion adsorption capabilities. As a result, hetero‐Mo2C exhibits excellent electrochemical performance with a high discharge specific capacity of 1242 mAh g‐1 at 0.1 A g−1 and long cycle stability of 683.9 mAh g−1 after 1200 cycling. This work provides new insights into rational design of novel MXenes heterojunctions, practically important for the development of MXenes and their applications in high‐performance energy storage systems.