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Nagaphani B. Aetukuri Shintaro Kitajima Edward Jung Leslie E. Thompson Kumar Virwani Maria‐Louisa Reich Miriam Kunze Meike Schneider Wolfgang Schmidbauer Winfried W. Wilcke Donald S. Bethune J. Campbell Scott Robert D. Miller Ho‐Cheol Kim 《Liver Transplantation》2015,5(14)
The use of metallic lithium anodes enables higher energy density and higher specific capacity Li‐based batteries. However, it is essential to suppress lithium dendrite growth during electrodeposition. Li‐ion‐conducting ceramics (LICC) can mechanically suppress dendritic growth but are too fragile and also have low Li‐ion conductivity. Here, a simple, versatile, and scalable procedure for fabricating flexible Li‐ion‐conducting composite membranes composed of a single layer of LICC particles firmly embedded in a polymer matrix with their top and bottom surfaces exposed to allow for ionic transport is described. The membranes are thin (<100 μm) and possess high Li‐ion conductance at thicknesses where LICC disks are mechanically unstable. It is demonstrated that these membranes suppress Li dendrite growth even when the shear modulus of the matrix is lower than that of lithium. It is anticipated that these membranes enable the use of metallic lithium anodes in conventional and solid‐state Li‐ion batteries as well as in future Li? S and Li? O2 batteries. 相似文献
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Mark Lipson Po-Ru Loh Sriram Sankararaman Nick Patterson Bonnie Berger David Reich 《PLoS genetics》2015,11(11)
The human mutation rate is an essential parameter for studying the evolution of our species, interpreting present-day genetic variation, and understanding the incidence of genetic disease. Nevertheless, our current estimates of the rate are uncertain. Most notably, recent approaches based on counting de novo mutations in family pedigrees have yielded significantly smaller values than classical methods based on sequence divergence. Here, we propose a new method that uses the fine-scale human recombination map to calibrate the rate of accumulation of mutations. By comparing local heterozygosity levels in diploid genomes to the genetic distance scale over which these levels change, we are able to estimate a long-term mutation rate averaged over hundreds or thousands of generations. We infer a rate of 1.61 ± 0.13 × 10−8 mutations per base per generation, which falls in between phylogenetic and pedigree-based estimates, and we suggest possible mechanisms to reconcile our estimate with previous studies. Our results support intermediate-age divergences among human populations and between humans and other great apes. 相似文献
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Klaus Schümann Nadia Herbach Christina Kerling Markus Seifert Carine Fillebeen Isabella Prysch Jens Reich Günter Weiss Kostas Pantopoulos 《Journal of trace elements in medicine and biology》2010,24(1):58-66
Hemizygous TNFΔARE/+ mice are a murine model for chronic inflammation. We utilized these animals to study iron-kinetics and corresponding protein expression in an iron-deficient and iron-adequate setting. 59Fe-absorption was determined in ligated duodenal loops in vivo. Whole body distribution of i.v. injected 59Fe was analysed, and the organ specific expression of ferroportin, transferrin receptor-1, hepcidin and duodenal DMT-1 was quantified by real-time PCR and Western blotting.Duodenal 59Fe-lumen-to-body transport was not affected by the genotype. Duodenal 59Fe-retention was increased in TNFΔARE/+ mice, suggesting higher 59Fe-losses with defoliated enterocytes. Iron-deficiency increased duodenal 59Fe-lumen-to-body transport, and higher duodenal 59Fe-tissue retention went along with higher duodenal DMT-1, ferroportin, and liver hepcidin expression. TNFΔARE/+ mice significantly increase their 59Fe-content in inflamed joints and ilea, and correspondingly reduce splenic 59Fe-content. Leukocyte infiltrations in the joints suggest a substantial shift of iron-loaded RES cells to inflamed tissues as the underlying mechanism. This finding was paralleled by increased non-haem iron content in joints and reduced haemoglobin and haematocrit concentrations in TNFΔARE/+ mice.In conclusion, erythropoiesis in inflamed TNFΔARE/+ mice could be iron-limited due to losses with exfoliated iron-loaded enterocytes and/or to increased iron-retention in RES cells that shift from the spleen to inflamed tissues. 相似文献
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Gali Arad-Haase Silvia G. Chuartzman Shlomi Dagan Maksim Kouza Hung Tien Nguyen Ziv Reich 《Biophysical journal》2010,99(1):238-247
Single-molecule manipulation methods provide a powerful means to study protein transitions. Here we combined single-molecule force spectroscopy and steered molecular-dynamics simulations to study the mechanical properties and unfolding behavior of the small enzyme acylphosphatase (AcP). We find that mechanical unfolding of AcP occurs at relatively low forces in an all-or-none fashion and is decelerated in the presence of a ligand, as observed in solution measurements. The prominent energy barrier for the transition is separated from the native state by a distance that is unusually long for α/β proteins. Unfolding is initiated at the C-terminal strand (βT) that lies at one edge of the β-sheet of AcP, followed by unraveling of the strand located at the other. The central strand of the sheet and the two helices in the protein unfold last. Ligand binding counteracts unfolding by stabilizing contacts between an arginine residue (Arg-23) and the catalytic loop, as well as with βT of AcP, which renders the force-bearing units of the protein resistant to force. This stabilizing effect may also account for the decelerated unfolding of ligand-bound AcP in the absence of force. 相似文献
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