12 research outputs found

    Selenium‐doping induced two antiferromagnetic transitions in thiospinel compounds CuCo₂S_(4‐x)Se_x (0 ≀ x ≀ 0.8)

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    A series of copper thiospinels compounds, CuCo₂S_(4‐x)Se_x (x = 0, 0.2, 0.4, 0.6, 0.8), have been successfully synthesized by solid state reaction and their structure and magnetic properties have been studied. The Rietveld refinements of X‐Ray diffractions indicate that both the lattice constants and the nearest neighbor Cu‐Cu distances increase with increasing selenium doping. A weakly antiferromagnetic transition occurring at about 4 K is observed in CuCo₂S₄. Two antiferromagnetic transitions at about 3.5 K and 6 K are observed in selenium‐doped samples, which suggest that the exchange couplings associated with Cu‐S(Se)‐Cu and Cu‐Se(S)‐Cu, respectively, are responsible for the two antiferromagnetic transitions. Detailed analysis of the experimental results further indicate that the nearest‐neighbor molecular field coefficient is comparable to the next‐neighbor molecular field coefficient. We propose a reasonable model to explain this phenomenon

    Evidences for pressure-induced two-phase superconductivity and mixed structures of NiTe₂ and NiTe in type-II Dirac semimetal NiTe_(2-x) (x = 0.38 ± 0.09) single crystals

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    Bulk NiTe₂ is a type-II Dirac semimetal with non-trivial Berry phases associated with the Dirac fermions. Theory suggests that monolayer NiTe₂ is a two-gap superconductor, whereas experimental investigation of bulk NiTe_(1.98) for pressures (P) up to 71.2 GPa do not reveal any superconductivity. Here we report experimental evidences for pressure-induced two-phase superconductivity as well as mixed structures of NiTe₂ and NiTe in Te-deficient NiTe_(2-x) (x = 0.38±0.09) single crystals. Hole-dominant multi-band superconductivity with the P3M1 hexagonal-symmetry structure of NiTe₂ appears at P ≄ 0.5 GPa, whereas electron-dominant single-band superconductivity with the P2/m monoclinic-symmetry structure of NiTe emerges at 14.5 GPa < P < 18.4 GPa. The coexistence of hexagonal and monoclinic structures and two-phase superconductivity is accompanied by a zero Hall coefficient up to ∌ 40 GPa, and the second superconducting phase prevails above 40 GPa, reaching a maximum T_c = 7.8 K and persisting up to 52.8 GPa. Our findings suggest the critical role of Te-vacancies in the occurrence of superconductivity and potentially nontrivial topological properties in NiTe_(2-x)

    Students' perceptions, attitudes and behaviour towards academic dishonesty.

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    A study of students perceptions, attitudes, environmental factors and how they relate to the propensity to cheat

    On the Shoulders of Giants: Incremental Influence Maximization in Evolving Social Networks

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    Influence maximization problem aims to identify the most influential individuals so as to help in developing effective viral marketing strategies over social networks. Previous studies mainly focus on designing efficient algorithms or heuristics on a static social network. As a matter of fact, real-world social networks keep evolving over time and a recalculation upon the changed network inevitably leads to a long running time. In this paper, we propose an incremental approach, IncInf, which can efficiently locate the top-K influential individuals in evolving social networks based on previous information instead of calculation from scratch. In particular, IncInf quantitatively analyzes the influence spread changes of nodes by localizing the impact of topology evolution to only local regions, and a pruning strategy is further proposed to narrow the search space into nodes experiencing major increases or with high degrees. To evaluate the efficiency and effectiveness, we carried out extensive experiments on real-world dynamic social networks: Facebook, NetHEPT, and Flickr. Experimental results demonstrate that, compared with the state-of-the-art static algorithm, IncInf achieves remarkable speedup in execution time while maintaining matching performance in terms of influence spread

    Recent advances in microfluidic technology of arterial thrombosis investigations

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    AbstractMicrofluidic technology has emerged as a powerful tool in studying arterial thrombosis, allowing researchers to construct artificial blood vessels and replicate the hemodynamics of blood flow. This technology has led to significant advancements in understanding thrombosis and platelet adhesion and aggregation. Microfluidic models have various types and functions, and by studying the fabrication methods and working principles of microfluidic chips, applicable methods can be selected according to specific needs. The rapid development of microfluidic integrated system and modular microfluidic system makes arterial thrombosis research more diversified and automated, but its standardization still needs to be solved urgently. One key advantage of microfluidic technology is the ability to precisely control fluid flow in microchannels and to analyze platelet behavior under different shear forces and flow rates. This allows researchers to study the physiological and pathological processes of blood flow, shedding light on the underlying mechanisms of arterial thrombosis. In conclusion, microfluidic technology has revolutionized the study of arterial thrombosis by enabling the construction of artificial blood vessels and accurately reproducing hemodynamics. In the future, microfluidics will place greater emphasis on versatility and automation, holding great promise for advancing antithrombotic therapeutic and prophylactic measures

    Hyperbolic polaritonic crystals with configurable low-symmetry Bloch modes

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    Photonic crystals (PhCs) are a kind of artificial structures that can mold the flow of light at will. Polaritonic crystals (PoCs) made from polaritonic media offer a promising route to controlling nano-light at the subwavelength scale. Conventional bulk PhCs and recent van der Waals PoCs mainly show highly symmetric excitation of Bloch modes that closely rely on lattice orders. Here, we experimentally demonstrate a type of hyperbolic PoCs with configurable and low-symmetry deep-subwavelength Bloch modes that are robust against lattice rearrangement in certain directions. This is achieved by periodically perforating a natural crystal α-MoO3 that hosts in-plane hyperbolic phonon polaritons. The mode excitation and symmetry are controlled by the momentum matching between reciprocal lattice vectors and hyperbolic dispersions. We show that the Bloch modes and Bragg resonances of hyperbolic PoCs can be tuned through lattice scales and orientations while exhibiting robust properties immune to lattice rearrangement in the hyperbolic forbidden directions. Our findings provide insights into the physics of hyperbolic PoCs and expand the categories of PhCs, with potential applications in waveguiding, energy transfer, biosensing and quantum nano-optics.Nanyang Technological UniversityPublished versionThis project was supported by the Science and Technology Development Fund, Macau SAR (No. 0116/2022/A3), the Australian Research Council (DE220100154 and CE170100039), the National Natural Science Foundation of China (Grant No. 62105058) and the Fundamental Research Funds for the Central Universities Key Scientific Research Guidance Project (Grant No. N2023005). The work at Zhejiang University was sponsored by the Key Research and Development Program of the Ministry of Science and Technology (Grants Nos. 2022YFA1404704, 2022YFA1405200, and 2022YFA1404902), the National Natural Science Foundation of China (Grant No. 61975176), the Key Research and Development Program of Zhejiang Province (Grant No. 2022C01036), and the Fundamental Research Funds for the Central Universities. G.H. acknowledges the startup grant from Nanyang Technological University. S.A.M. additionally acknowledges the Lee-Lucas Chair in Physics. This work was performed in part at the Melbourne Centre for Nanofabrication (MCN) in the Victorian Node of the Australian National Fabrication Facility (ANFF)

    Glia maturation factor beta deficiency protects against diabetic osteoporosis by suppressing osteoclast hyperactivity

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    Abstract Excessive osteoclast activation, which depends on dramatic changes in actin dynamics, causes osteoporosis (OP). The molecular mechanism of osteoclast activation in OP related to type 1 diabetes (T1D) remains unclear. Glia maturation factor beta (GMFB) is considered a growth and differentiation factor for both glia and neurons. Here, we demonstrated that Gmfb deficiency effectively ameliorated the phenotype of T1D-OP in rats by inhibiting osteoclast hyperactivity. In vitro assays showed that GMFB participated in osteoclast activation rather than proliferation. Gmfb deficiency did not affect osteoclast sealing zone (SZ) formation but effectively decreased the SZ area by decreasing actin depolymerization. When GMFB was overexpressed in Gmfb-deficient osteoclasts, the size of the SZ area was enlarged in a dose-dependent manner. Moreover, decreased actin depolymerization led to a decrease in nuclear G-actin, which activated MKL1/SRF-dependent gene transcription. We found that pro-osteoclastogenic factors (Mmp9 and Mmp14) were downregulated, while anti-osteoclastogenic factors (Cftr and Fhl2) were upregulated in Gmfb KO osteoclasts. A GMFB inhibitor, DS-30, targeting the binding site of GMFB and Arp2/3, was obtained. Biocore analysis revealed a high affinity between DS-30 and GMFB in a dose-dependent manner. As expected, DS-30 strongly suppressed osteoclast hyperactivity in vivo and in vitro. In conclusion, our work identified a new therapeutic strategy for T1D-OP treatment. The discovery of GMFB inhibitors will contribute to translational research on T1D-OP

    Targeting PPAR-gamma counteracts tumour adaptation to immune-checkpoint blockade in hepatocellular carcinoma

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    Therapy-induced tumour microenvironment (TME) remodelling poses a major hurdle for cancer cure. As the majority of patients with hepatocellular carcinoma (HCC) exhibits primary or acquired resistance to antiprogrammed cell death (ligand)-1 (anti-PD-[L]1) therapies, we aimed to investigate the mechanisms underlying tumour adaptation to immune-checkpoint targeting.Published versionThis project is supported by the Collaborative Research Fund (C4045-18W to AS-LC), the General Research Fund (14115820 and 14120621 to AS-LC), the Li Ka Shing Foundation (grant number not applicable to YMDL, AS-LC), the Health and Medical Research Fund (07180556 to JZ), the Terry Fox Foundation—Terry Fox Run, Hong Kong (I1008 to SLC, AS-LC), the CUHK Strategic Seed Funding for Collaborative Research Scheme (grant number not applicable to AS-LC) and the Charlie Lee Charitable Foundation (grant number not applicable). We also acknowledge support (funding and study medications) by Merck Sharp and Dohme (MSD-IIS 55253 to SLC) for the clinical trial (NCT03419481)
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