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| 1 | Ultrabroadband and multiband infrared/terahertz photodetectors with high sensitivity显示文摘Broadband response is pursued in both infrared(IR)and terahertz(THz)detection technologies,which find their applications in both terrestrial and astronomical realms.Herein,we report an ultrabroadband and multiband IR/THz detector based on blocked-impurity-band detecting principle.The detectors are prepared by implanting phosphorus into germanium(Ge:P),where photoresponses with a P impurity band,a self-interstitial defect band,and a vacancy-P(V-P)pair defect band are realized simultaneously.The response spectra of the detectors show ultrabroad and dual response bands in a range of 3-28μm(IR band)and 40-165μm(THz band),respectively.Additionally,a tiny mid-IR(MIR)band within 3-4.2μm is embedded in the IR band.The THz band arises from the P impurity band,whereas the IR and the MIR bands are ascribed to the two defect bands.At150 m V and 4.5 K,the peak detectivities of the three bands are obtained as 2.9×10^(12) Jones(at 3.9μm),6.8×10^(12) Jones(at 16.3μm),and 9.9×10^(12) Jones(at 116.5μm),respectively.The impressive coverage andsensitivity of the detectors are promising for applications in IR and THz detection technologies. | JIAQI ZHU HE ZHU MENGJUAN LIU YAO WANG HANLUN XU NASIR ALI HUIYONG DENG ZHIYONG TAN JUNCHENG CAO NING DAI HUIZHEN WU | 2021 | Photonics Research2021，9，11： | 2 |
| 2 | BRD4 interacts with PML/RARα in acute promyelocytic leukemia显示文摘Bromodomain-containing 4(BRD4)has been considered as an important requirement for disease maintenance and an attractive therapeutic target for cancer therapy.This protein can be targeted by JQ1,a selective small-molecule inhibitor.However,few studies have investigated whether BRD4influenced acute promyelocytic leukemia (APL),and whether BRD4had interaction with promyelocytic leukemia-retinoic acid receptor a (PML/RARa)fusion protein to some extent.Results from cell viability assay,cell cycle analysis,and Annexin-V/PI analysis indicated that JQ1inhibited the growth of NB4cells,an APL-derived cell line,and induced NB4cell cycle arrest at G1and apoptosis.Then,we used co-immunoprecipitation (co-IP)assay and immunoblot to demonstrate the endogenous interaction of BRD4and PML/RARa in NB4cells.Moreover,downregulation of PML/RARa at the mRNA and protein levels was observed upon JQ1treatment.Furthermore,results from the RT-qPCR,ChIP-qPCR,and re-ChIP-qPCR assays showed that BRD4and PML/RARu co-existed on the same regulatory regions of their target genes.Hence,we showed a new discovery of the interaction of BRD4and PML/ RARa,as well as the decline of PML/RARa expression,under JQ1treatment. | Qun Luo Wanglong Deng Haiwei Wang Huiyong Fan Ji Zhang | 2018 | Frontiers of Medicine2018，12，6： | 1 |
| 3 | An Adaptive Task Creation Pruning Strategy for Optimizing Irregular Applications显示文摘The Open MP task directive makes it possible to efficiently parallelize irregular applications, with task granularity as one of the most critical issues. To implement Open MP specification on multi-core architecture,a model is presented specializing in the execution of irregular applications. The model captures computation and communication within a node with host cores and accelerator cores. Based on this model, we propose an adaptive task creation pruning strategy including two stages to adjust dynamically task granularity. The first stage is task creation in breadth-first manner until getting to a threshold, which utilizes potential parallelism of multi-core processor. The second stage is starvation-triggered task regeneration once some worker thread becomes starved, which ensures work-stealing and thus achieves load balance. The evaluation is conducted with a series of typical irregular benchmarks, and the results indicate that our approach offers more effective performance in parallel execution of irregular benchmarks. | CAO Qian LI Huiyong ZUO Min DENG Yun YU Yuan | 2015 | Chinese Journal of Electronics2015，24，3： | 0 |
| 4 | Compressive Behaviour and Failure Mechanisms of GFRP Composite at High Strain Rates显示文摘Experimental investigations into the compressive behavior of glass fiber reinforced polymer(GFRP)composite at high strain rates were carried out using a split Hopkinson pressure bar(SHPB)setup.The GFRP laminates were made from E-glass fibers and epoxy resins by vacuum assisted compression molding machine.The results of the compressive tests indicated that the mechanical behavior of the GFRP composite depends highly on the strain rate.The compressive peak stress,toughness and Young's modulus of the GFRP composite increased with the increase of strain rate,while the strain level at the initial stages of damage was shortened with the increase of strain rate.In addition,the dynamic deformation behavior and failure process of the specimens were observed directly by using a high-speed camera.Following the experiments,the fracture morphologies and damage modes were examined by scanning electron microscopy(SEM)to explore the possible failure mechanisms of the specimens.The results showed that multiple failure mechanisms appeared,such as matrix crack,fiber-matrix debonding,fiber failure and shear fracture. | Dejun Yin Jian Zheng Chao Xiong Junhui Yin Huiyong Deng Xiaobo Su | 2019 | Journal of Beijing Institute of Technology2019，28，1： | 0 |
| 5 | Regulatory mechanism and functional analysis of S100A9 in acute promyelocytic leukemia cells显示文摘S100A9,钙绑定蛋白质,参予各种各样的肿瘤的煽动性的进程和开发,因此在癌症的领域里吸引许多注意生物学。这研究试图在 APL 调查 S100A9 和它的功能参与的规章的机制。我们使用了即时量的 PCR 决定 PML/RAR 是否在 ATRA 治疗之上在 NB4 和 PR9 房间影响 S100A9 的表示。基于薄片的 PCR 和双酶的记者试金系统被用来检测 PML/RAR 和 PU.1 怎么调整 S100A9 倡导者活动。当 S100A9 是 overexpressed 时, CCK-8 试金和流动 cytometry 被采用观察 NB4 房间的生存能力和 apoptosis。结果证明 S100A9 是 ATRA 应答的基因,并且 PML/RAR 为在 APL 房间的 S100A9 的导致 ATRA 的表示是必要的。另外, PU.1 能绑在 S100A9 的倡导者,特别当在 NB4 房间与 ATRA 对待时,并且支持它的活动。更重要地, S100A9 的 overexpression 导致了 NB4 房间的 apoptosis 并且禁止了房间生长。一起,我们的数据显示了那 PML/RAR, PU.1 为在 APL 房间的 S100A9 的导致 ATRA 的表达式是必要的。而且, S100A9 在 APL 房间支持了 apoptosis 并且影响了房间生长。 | Yonglan Zhu Fang Zhang Shanzhen Zhang Wanglong Deng Huiyong Fan Haiwei Wang Ji Zhang | 2017 | Frontiers of Medicine2017，11，1： | 0 |
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