Sol-gel synthesis of Yb-doped NaLu(WO4)2 films

AbstractDense and (001)-textured thin films with composition NaLu1−xY bx(WO4)2 (x=0.01–0.5) have been prepared by multiple spincoating deposition of sol-gel synthesized solutions, followed by a sintering thermal annealing. Films with thickness above 1 μm are transparent and have photoluminescence properties similar to those of isostructural single crystals. The role of Yb composition, film thickness and purity of the raw Y b2O3 used on the Y b3+ fluorescence efficiency are discussed in relation to the application of the films as diode laser pumped solid-state laser media

Vibration analysis of the beam structure under the moving mass

Analytical solution of vibration of simply supported beam under the action of centralized moving mass and two numerical methods using life and death element method and displacement contact method are analyzed in this paper. The results show that vertical acceleration resulted from speed and centrifugal acceleration resulted from load moving must be taken into consideration for large quality and high speed. The characteristics and applicable situations of the two numerical methods are also studied to provide a basis for analyzing and considering structural dynamic problems of moving load mass

Crystal Structure Manipulation of the Exchange Bias in an Antiferromagnetic Film

Exchange bias is one of the most extensively studied phenomena in magnetism, since it exerts a unidirectional anisotropy to a ferromagnet (FM) when coupled to an antiferromagnet (AFM) and the control of the exchange bias is therefore very important for technological applications, such as magnetic random access memory and giant magnetoresistance sensors. In this letter, we report the crystal structure manipulation of the exchange bias in epitaxial hcp Cr2O3 films. By epitaxially growing twined (10-10) oriented Cr2O3 thin films, of which the c axis and spins of the Cr atoms lie in the film plane, we demonstrate that the exchange bias between Cr2O3 and an adjacent permalloy layer is tuned to in-plane from out-of-plane that has been observed in (0001) oriented Cr2O3 films. This is owing to the collinear exchange coupling between the spins of the Cr atoms and the adjacent FM layer. Such a highly anisotropic exchange bias phenomenon is not possible in polycrystalline films.Comment: To be published in Scientific Reports, 12 pages, 6 figure

Mobility-Aware Joint User Scheduling and Resource Allocation for Low Latency Federated Learning

As an efficient distributed machine learning approach, Federated learning (FL) can obtain a shared model by iterative local model training at the user side and global model aggregating at the central server side, thereby protecting privacy of users. Mobile users in FL systems typically communicate with base stations (BSs) via wireless channels, where training performance could be degraded due to unreliable access caused by user mobility. However, existing work only investigates a static scenario or random initialization of user locations, which fail to capture mobility in real-world networks. To tackle this issue, we propose a practical model for user mobility in FL across multiple BSs, and develop a user scheduling and resource allocation method to minimize the training delay with constrained communication resources. Specifically, we first formulate an optimization problem with user mobility that jointly considers user selection, BS assignment to users, and bandwidth allocation to minimize the latency in each communication round. This optimization problem turned out to be NP-hard and we proposed a delay-aware greedy search algorithm (DAGSA) to solve it. Simulation results show that the proposed algorithm achieves better performance than the state-of-the-art baselines and a certain level of user mobility could improve training performance

NQO1 targeting prodrug triggers innate sensing to overcome checkpoint blockade resistance

Lack of proper innate sensing inside tumor microenvironment (TME) limits T cell-targeted immunotherapy. NAD(P)H:quinone oxidoreductase 1 (NQO1) is highly enriched in multiple tumor types and has emerged as a promising target for direct tumor-killing. Here, we demonstrate that NQO1-targeting prodrug β-lapachone triggers tumor-selective innate sensing leading to T cell-dependent tumor control. β-Lapachone is catalyzed and bioactivated by NQO1 to generate ROS in NQO1high tumor cells triggering oxidative stress and release of the damage signals for innate sensing. β-Lapachone-induced high mobility group box 1 (HMGB1) release activates the host TLR4/MyD88/type I interferon pathway and Batf3 dendritic cell-dependent cross-priming to bridge innate and adaptive immune responses against the tumor. Furthermore, targeting NQO1 is very potent to trigger innate sensing for T cell re-activation to overcome checkpoint blockade resistance in well-established tumors. Our study reveals that targeting NQO1 potently triggers innate sensing within TME that synergizes with immunotherapy to overcome adaptive resistance

Energy-Efficient Wireless Federated Learning via Doubly Adaptive Quantization

Federated learning (FL) has been recognized as a viable distributed learning paradigm for training a machine learning model across distributed clients without uploading raw data. However, FL in wireless networks still faces two major challenges, i.e., large communication overhead and high energy consumption, which are exacerbated by client heterogeneity in dataset sizes and wireless channels. While model quantization is effective for energy reduction, existing works ignore adapting quantization to heterogeneous clients and FL convergence. To address these challenges, this paper develops an energy optimization problem of jointly designing quantization levels, scheduling clients, allocating channels, and controlling computation frequencies (QCCF) in wireless FL. Specifically, we derive an upper bound identifying the influence of client scheduling and quantization errors on FL convergence. Under the longterm convergence constraints and wireless constraints, the problem is established and transformed into an instantaneous problem with Lyapunov optimization. Solving Karush-Kuhn-Tucker conditions, our closed-form solution indicates that the doubly adaptive quantization level rises with the training process and correlates negatively with dataset sizes. Experiment results validate our theoretical results, showing that QCCF consumes less energy with faster convergence compared with state-of-the-art baselines

Genome plasticity of Vibrio parahaemolyticus: microevolution of the 'pandemic group'

<p>Abstract</p> <p>Background</p> <p>Outbreak of <it>V. parahaemolyticus </it>infections occurred since 1996 was linked to a proposed clonal complex, the pandemic group. The whole genome sequence provides an unprecedented opportunity for dissecting genome plasticity and phylogeny of the populations of <it>V. parahaemolyticus</it>. In the present work, a whole-genome cDNA microarray was constructed to compare the genomic contents of a collection of 174 strains of <it>V. parahaemolyticus</it>.</p> <p>Results</p> <p>Genes that present variably in the genome accounted for about 22% of the whole gene pool on the genome. The phylogenetic analysis of microarray data generated a minimum spanning tree that depicted the phylogenetic structure of the 174 strains. Strains were assigned into five complexes (C1 to C5), and those in each complex were related genetically and phylogenetically. C3 and C4 represented highly virulent clinical clones. C2 and C3 constituted two different clonal complexes 'old-O3:K6 clone' and 'pandemic clone', respectively. C3 included all the 39 pandemic strains tested (<it>trh</it>^-, <it>tdh</it>⁺and GS-PCR⁺), while C2 contained 12 pre-1996 'old' O3:K6 strains (<it>trh</it>⁺, <it>tdh</it>^-and GS-PCR^-) tested herein. The pandemic clone (post-1996 'new' O3:K6 and its derivates O4:K68, O1:K25, O1:KUT and O6:K18) might be emerged from the old-O3:K6 clone, which was promoted by acquisition of <it>toxRS</it>/new sequence and genomic islands. A phylogenetic intermediate O3:K6 clade (<it>trh</it>^-, <it>tdh</it>^-and GS-PCR⁺) was identified between the pandemic and old-O3:K6 clones.</p> <p>Conclusion</p> <p>A comprehensive overview of genomic contents in a large collection of global isolates from the microarray-based comparative genomic hybridization data enabled us to construct a phylogenetic structure of <it>V. parahaemolyticus </it>and an evolutionary history of the pandemic group (clone) of this pathogen.</p

FAK Promotes Early Osteoprogenitor Cell Proliferation by Enhancing mTORC1 Signaling

Focal adhesion kinase (FAK) has important functions in bone homeostasis but its role in early osteoprogenitor cells is unknown. We show herein that mice lacking FAK in Dermo1- expressing cells exhibited low bone mass and decreased osteoblast number. Mechanistically, FAK- deficient early osteoprogenitor cells had decreased proliferation and significantly reduced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, a central regulator of cell growth and proliferation. Furthermore, our data showed that the pharmacological inhibition of FAK kinase- dependent function alone was sufficient to decrease the proliferation and compromise the mineralization of early osteoprogenitor cells. In contrast to the Fak deletion in early osteoprogenitor cells, FAK loss in Col3.6 Cre- targeted osteoblasts did not cause bone loss, and Fak deletion in osteoblasts did not affect proliferation, differentiation, and mTORC1 signaling but increased the level of active proline- rich tyrosine kinase 2 (PYK2), which belongs to the same non- receptor tyrosine kinase family as FAK. Importantly, mTORC1 signaling in bone marrow stromal cells (BMSCs) was reduced if FAK kinase was inhibited at the early osteogenic differentiation stage. In contrast, mTORC1 signaling in BMSCs was not affected if FAK kinase was inhibited at a later osteogenic differentiation stage, in which, however, the concomitant inhibition of both FAK kinase and PYK2 kinase reduced mTORC1 signaling. In summary, our data suggest that FAK promotes early osteoprogenitor cell proliferation by enhancing mTORC1 signaling via its kinase- dependent function and the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2. © 2020 American Society for Bone and Mineral Research.Schematic model of the differential roles of FAK in the cells of osteoblast lineage. The model depicts the mechanisms of FAK action at three distinct stages of osteoblast lineage in which the roles of FAK have been addressed by genetic and pharmacological approaches as well as the respective Cre transgenes used to target Fak, including Dermo1- Cre (this study), Osterix- Cre,(10) Col3.6- Cre (this study), and Col2.3- Cre.(9) Red - indicates that the loss of FAK in osteoblasts can be compensated by the upregulated active PYK2.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/3/jbmr4029-sup-0001-Supinfo.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/2/jbmr4029_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162813/1/jbmr4029.pd