13 research outputs found

    Fast kinetics of multivalent intercalation chemistry enabled by solvated magnesium-ions into self-established metallic layered materials

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    Rechargeable magnesium batteries are one of the most promising candidates for next-generation battery technologies. Despite recent significant progress in the development of efficient electrolytes, an on-going challenge for realization of rechargeable magnesium batteries remains to overcome the sluggish kinetics caused by the strong interaction between double charged magnesium-ions and the intercalation host. Herein, we report that a magnesium battery chemistry with fast intercalation kinetics in the layered molybdenum disulfide structures can be enabled by using solvated magnesium-ions ([Mg(DME)x]2+). Our study demonstrates that the high charge density of magnesium-ion may be mitigated through dimethoxyethane solvation, which avoids the sluggish desolvation process at the cathode-electrolyte interfaces and reduces the trapping force of the cathode lattice to the cations, facilitating magnesium-ion diffusion. The concept of using solvation effect could be a general and effective route to tackle the sluggish intercalation kinetics of magnesium-ions, which can potentially be extended to other host structures

    Ppm1b negatively regulates necroptosis through dephosphorylating ​Rip3

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    该研究论文发现蛋白磷酸酶Ppm1b 通过去磷酸化RIP3负调控程序性细胞坏死(necroptosis),阐明了RIP3磷酸化状态的精确调控对于细胞和机体在生理和病理状态下的存活至关重要。The auto-phosphorylation of murine ​receptor-interacting protein 3 (​Rip3) on Thr 231 and Ser 232 in the necrosome is required to trigger necroptosis. However, how ​Rip3 phosphorylation is regulated is still largely unknown. Here we identified ​protein phosphatase 1B (​Ppm1b) as a ​Rip3 phosphatase and found that ​Ppm1b restricts necroptosis in two settings: spontaneous necroptosis caused by ​Rip3 auto-phosphorylation in resting cells, and ​tumour necrosis factor-α (​TNF)-induced necroptosis in cultured cells. We revealed that ​Ppm1b selectively suppresses necroptosis through the dephosphorylation of ​Rip3, which then prevents the recruitment of ​mixed lineage kinase domain-like protein (​Mlkl) to the necrosome. We further showed that ​Ppm1b deficiency (​Ppm1bd/d) in mice enhanced ​TNF-induced death in a ​Rip3-dependent manner, and the role of ​Ppm1b in inhibiting necroptosis was evidenced by elevated ​Rip3 phosphorylation and tissue damage in the caecum of ​TNF-treated ​Ppm1bd/d mice. These data indicate that ​Ppm1b negatively regulates necroptosis through dephosphorylating ​Rip3 in vitro and in vivo

    Affiliation-hiding authenticated asymmetric group key agreement

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    We introduce the concept of Affiliation-Hiding Authenticated Asymmetric Group Key Agreement AH-AAGKA and construct a concrete one-round AH-AAGKA protocol. An AH-AAGKA protocol allows the participants of a group to establish a common encryption key associated with several decryption keys; each of which can only be computed by the corresponding legitimate group member. An AH-AAGKA protocol has the following privacy feature. For a member i of a group G, if i participates in an AH-AAGKA protocol, any protocol participant j cannot learn whether i is a member of G, unless j himself is a member of group G. Our scheme demonstrates new features in comparison with other existing AH-AGKA protocols. If non-group members participate in our protocol, honest parties can identify these non-group members. Our scheme also captures Unlinkability and Perfect Forward Secrecy PFS, which are missing in other existing schemes. We propose a novel security model to prove that our protocol holds PFS and present a new privacy model to prove that our scheme meets Affiliation-Hiding property

    A Bridge-Linked Phosphorus-Containing Flame Retardant for Endowing Vinyl Ester Resin with Low Fire Hazard

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    The high flammability of vinyl ester resin (VE) significantly limits its widespread application in the fields of electronics and aerospace. A new phosphorus-based flame retardant 6,6’-(1-phenylethane-1,2 diyl) bis (dibenzo[c,e][1,2]oxaphosphinine 6-oxide) (PBDOO), was synthesized using 9,10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide (DOPO) and acetophenone. The synthesized PBDOO was further incorporated with VE to form the VE/PBDOO composites, which displayed an improved flame retardancy with higher thermal stability. The structure of PBDOO was investigated using Fourier transformed infrared spectrometry (FTIR) and nuclear magnetic resonances (NMR). The thermal stability and flame retardancy of VE/PBDOO composites were investigated by thermogravimetric analysis (TGA), vertical burn test (UL-94), limiting oxygen index (LOI), and cone calorimetry. The impacts of PBDOO weight percentage (wt%) on the flame-retardant properties of the formed VE/PBDOO composites were also examined. When applying 15 wt% PBDOO, the formed VE composites can meet the UL-94 V-0 rating with a high LOI value of 31.5%. The peak heat release rate (PHRR) and the total heat release (THR) of VE loaded 15 wt% of PBDOO decreased by 76.71% and 40.63%, respectively, compared with that of untreated VE. In addition, the flame-retardant mechanism of PBDOO was proposed by analyzing pyrolysis behavior and residual carbon of VE/PBDOO composites. This work is expected to provide an efficient method to enhance the fire safety of VE

    VOCl as a Cathode for Rechargeable Chloride Ion Batteries

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    A novel room temperature rechargeable battery with VOCl cathode, lithium anode, and chloride ion transporting liquid electrolyte is described. The cell is based on the reversible transfer of chloride ions between the two electrodes. The VOCl cathode delivered an initial discharge capacity of 189 mAh g−1. A reversible capacity of 113 mAh g−1 was retained even after 100 cycles when cycled at a high current density of 522 mA g−1. Such high cycling stability was achieved in chloride ion batteries for the first time, demonstrating the practicality of the system beyond a proof of concept model. The electrochemical reaction mechanism of the VOCl electrode in the chloride ion cell was investigated in detail by ex situ X-ray diffraction (XRD), infrared spectroscopy (FTIR), transmission electron microscopy (TEM), and X-ray photoelectron spectroscopy (XPS). The results confirm reversible deintercalation–intercalation of chloride ions in the VOCl electrode

    Inherited DNA-Repair Defects in Colorectal Cancer

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    Colorectal cancer (CRC) heritability has been estimated to be around 30%. However, mutations in the known CRC-susceptibility genes explain CRC risk in fewer than 10% of affected individuals. Germline mutations in DNA-repair genes (DRGs) have recently been reported in CRC, but their contribution to CRC risk is largely unknown. We evaluated the gene-level germline mutation enrichment of 40 DRGs in 680 unselected CRC individuals and 27,728 ancestry-matched cancer-free adults. Significant findings were then examined in independent cohorts of 1,661 unselected CRC individuals and 1,456 individuals with early-onset CRC. Of the 680 individuals in the discovery set, 31 (4.56%) individuals harbored germline pathogenic mutations in known CRC-susceptibility genes, and another 33 (4.85%) individuals had DRG mutations that have not been previously associated with CRC risk. Germline pathogenic mutations in ATM and PALB2 were enriched in both the discovery (OR = 2.81 and p = 0.035 for ATM and OR = 4.91 and p = 0.024 for PALB2) and validation (OR = 2.97 and adjusted p = 0.0013 for ATM and OR = 3.42 and adjusted p = 0.034 for PALB2) sets. Biallelic loss of ATM was evident in all individuals with matched tumor profiling. CRC individuals also had higher rates of actionable mutations in the HR pathway, which can substantially increase the risk of developing cancers other than CRC. Our analysis provides evidence for ATM and PALB2 as CRC-risk genes, underscoring the importance of the homologous recombination pathway in CRC. In addition, we identified frequent complete homologous recombination deficiency in CRC tumors, representing a unique opportunity to explore targeted therapeutic interventions such as poly-ADP ribose polymerase inhibitor (PARPi)
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