19 research outputs found

    Fast convergence to equilibrium for long-chain polymer melts using a MD/continuum hybrid method

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    Effective and fast convergence toward an equilibrium state for long-chain polymer melts is realized by a hybrid method coupling molecular dynamics and the elastic continuum. The required simulation time to achieve the equilibrium state is reduced drastically compared with conventional equilibration methods. The polymers move on a wide range of the energy landscape due to large-scale fluctuation generated by the elastic continuum. A variety of chain structures is generated in the polymer melt which results in the fast convergence to the equilibrium state.Comment: 13 page

    Chloroplast acquisition without the gene transfer in kleptoplastic sea slugs, Plakobranchus ocellatus

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    Some sea slugs sequester chloroplasts from algal food in their intestinal cells and photosynthesize for months. This phenomenon, kleptoplasty, poses a question of how the chloroplast retains its activity without the algal nucleus. There have been debates on the horizontal transfer of algal genes to the animal nucleus. To settle the arguments, this study reported the genome of a kleptoplastic sea slug, Plakobranchus ocellatus, and found no evidence of photosynthetic genes encoded on the nucleus. Nevertheless, it was confirmed that light illumination prolongs the life of mollusk under starvation. These data presented a paradigm that a complex adaptive trait, as typified by photosynthesis, can be transferred between eukaryotic kingdoms by a unique organelle transmission without nuclear gene transfer. Our phylogenomic analysis showed that genes for proteolysis and immunity undergo gene expansion and are up-regulated in chloroplast-enriched tissue, suggesting that these molluskan genes are involved in the phenotype acquisition without horizontal gene transfer

    A Model for Triboluminescence from Fracture Surfaces of Silica Glass

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    Spotted Fever Group Rickettsiae in Inner Mongolia, China, 2015–2016

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    We found Rickettsia raoultii infection in 6/261 brucellosis-negative patients with fever of unknown origin in brucellosis-endemic Inner Mongolia, China. We further identified Hyalomma asiaticum ticks associated with R. raoultii, H. marginatum ticks associated with R. aeschlimannii, and Dermacentor nuttalli ticks associated with both rickettsiae species in the autonomous region

    Inorganic carbon uptake genes in the gill of the deep-sea clam Calyptogena okutanii

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    http://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt08-08/ehttp://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt11-09/ehttp://www.godac.jamstec.go.jp/darwin/cruise/kairei/kr12-05/

    Expression of genes involved in the uptake of inorganic carbon in the gill of a deep-sea vesicomyid clam harboring intracellular thioautotrophic bacteria

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    http://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt08-03/ehttp://www.godac.jamstec.go.jp/darwin/cruise/natsushima/nt11-09/ehttp://www.godac.jamstec.go.jp/darwin/cruise/kairei/kr12-05/

    A Hereditary Enteropathy Caused by Mutations in the <i>SLCO2A1</i> Gene, Encoding a Prostaglandin Transporter

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    <div><p>Previously, we proposed a rare autosomal recessive inherited enteropathy characterized by persistent blood and protein loss from the small intestine as chronic nonspecific multiple ulcers of the small intestine (CNSU). By whole-exome sequencing in five Japanese patients with CNSU and one unaffected individual, we found four candidate mutations in the <i>SLCO2A1</i> gene, encoding a prostaglandin transporter. The pathogenicity of the mutations was supported by segregation analysis and genotyping data in controls. By Sanger sequencing of the coding regions, 11 of 12 other CNSU patients and 2 of 603 patients with a diagnosis of Crohn’s disease were found to have homozygous or compound heterozygous <i>SLCO2A1</i> mutations. In total, we identified recessive <i>SLCO2A1</i> mutations located at seven sites. Using RT-PCR, we demonstrated that the identified splice-site mutations altered the RNA splicing, and introduced a premature stop codon. Tracer prostaglandin E2 uptake analysis showed that the mutant SLCO2A1 protein for each mutation exhibited impaired prostaglandin transport. Immunohistochemistry and immunofluorescence analyses revealed that SLCO2A1 protein was expressed on the cellular membrane of vascular endothelial cells in the small intestinal mucosa in control subjects, but was not detected in affected individuals. These findings indicate that loss-of-function mutations in the <i>SLCO2A1</i> gene encoding a prostaglandin transporter cause the hereditary enteropathy CNSU. We suggest a more appropriate nomenclature of “chronic enteropathy associated with <i>SLCO2A1</i> gene” (CEAS).</p></div
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