Trace doping of multiple elements enables stable battery cycling of LiCoO2 at 4.6 V

LiCoO2 is a dominant cathode material for lithium-ion (Li-ion) batteries due to its high volumetric energy density, which could potentially be further improved by charging to high voltages. However, practical adoption of high-voltage charging is hindered by LiCoO2’s structural instability at the deeply delithiated state and the associated safety concerns. Here, we achieve stable cycling of LiCoO2 at 4.6 V (versus Li/Li+) through trace Ti–Mg–Al co-doping. Using state-of-the-art synchrotron X-ray imaging and spectroscopic techniques, we report the incorporation of Mg and Al into the LiCoO2 lattice, which inhibits the undesired phase transition at voltages above 4.5 V. We also show that, even in trace amounts, Ti segregates significantly at grain boundaries and on the surface, modifying the microstructure of the particles while stabilizing the surface oxygen at high voltages. These dopants contribute through different mechanisms and synergistically promote the cycle stability of LiCoO2 at 4.6 V

Double In Situ Approach for the Preparation of Polymer Nanocomposite with Multi-functionality

A novel one-step synthetic route, the double in situ approach, is used to produce both TiO2nanoparticles and polymer (PET), and simultaneously forming a nanocomposite with multi-functionality. The method uses the release of water during esterification to hydrolyze titanium (IV) butoxide (Ti(OBu)4) forming nano-TiO2in the polymerization vessel. This new approach is of general significance in the preparation of polymer nanocomposites, and will lead to a new route in the synthesis of multi-functional polymer nanocomposites

Polymerase δ replicates both strands after homologous recombination-dependent fork restart

To maintain genetic stability DNA must be replicated only once and replication completed even when individual replication forks are inactivated. Because fork inactivation is common, the passive convergence of an adjacent fork is insufficient to rescue all inactive forks. Thus, eukaryotic cells have evolved homologous recombination-dependent mechanisms to restart persistent inactive forks. Completing DNA synthesis via Homologous Recombination Restarted Replication (HoRReR) ensures cell survival, but at a cost. One such cost is increased mutagenesis caused by HoRReR being more error prone than canonical replication. This increased error rate implies that the HoRReR mechanism is distinct from that of a canonical fork. Here we exploit the fission yeast Schizosaccharomyces pombe to demonstrate that a DNA sequence duplicated by HoRReR during S phase is replicated semi-conservatively, but that both the leading and lagging strands are synthesised by DNA polymerase delta

Search for a Light Sterile Neutrino at Daya Bay

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The muon system of the Daya Bay Reactor antineutrino experiment

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Independent measure of the neutrino mixing angle θ13 via neutron capture on hydrogen at Daya Bay

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Improved Measurement of Electron Antineutrino Disappearance at Daya Bay

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Plx1 is required for chromosomal DNA replication under stressful conditions

Polo-like kinase (Plk)1 is required for mitosis progression. However, although Plk1 is expressed throughout the cell cycle, its function during S-phase is unknown. Using Xenopus laevis egg extracts, we demonstrate that Plx1, the Xenopus orthologue of Plk1, is required for DNA replication in the presence of stalled replication forks induced by aphidicolin, etoposide or reduced levels of DNA-bound Mcm complexes. Plx1 binds to chromatin and suppresses the ATM/ATR-dependent intra-S-phase checkpoint that inhibits origin firing. This allows Cdc45 loading and derepression of DNA replication initiation. Checkpoint activation increases Plx1 binding to the Mcm complex through its Polo box domain. Plx1 recruitment to chromatin is independent of checkpoint mediators Tipin and Claspin. Instead, ATR-dependent phosphorylation of serine 92 of Mcm2 is required for the recruitment of Plx1 to chromatin and for the recovery of DNA replication under stress. Depletion of Plx1 leads to accumulation of chromosomal breakage that is prevented by the addition of recombinant Plx1. These data suggest that Plx1 promotes genome stability by regulating DNA replication under stressful conditions