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The mineral magnetite (Fe(3)O(4)) undergoes a complex structural distortion and becomes electrically insulating at temperatures less than 125 kelvin. Verwey proposed in 1939 that this transition is driven by a charge ordering of Fe(2+) and Fe(3+) ions, but the ground state of the low-temperature phase has remained contentious because twinning of crystal domains hampers diffraction studies of the structure. Recent powder diffraction refinements and resonant X-ray studies have led to proposals of a variety of charge-ordered and bond-dimerized ground-state models. Here we report the full low-temperature superstructure of magnetite, determined by high-energy X-ray diffraction from an almost single-domain, 40-micrometre grain, and identify the emergent order. The acentric structure is described by a superposition of 168 atomic displacement waves (frozen phonon modes), all with amplitudes of less than 0.24 ?ngstr?ms. Distortions of the FeO(6) octahedra show that Verwey's hypothesis is correct to a first approximation and that the charge and Fe(2+) orbital order are consistent with a recent prediction. However, anomalous shortening of some Fe-Fe distances suggests that the localized electrons are distributed over linear three-Fe-site units, which we call 'trimerons'. The charge order and three-site distortions induce substantial off-centre atomic displacements and couple the resulting large electrical polarization to the magnetization. Trimerons may be important quasiparticles in magnetite above the Verwey transition and in other transition metal oxides. 相似文献
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Jones FC Grabherr MG Chan YF Russell P Mauceli E Johnson J Swofford R Pirun M Zody MC White S Birney E Searle S Schmutz J Grimwood J Dickson MC Myers RM Miller CT Summers BR Knecht AK Brady SD Zhang H Pollen AA Howes T Amemiya C;Broad Institute Genome Sequencing Platform & Whole Genome Assembly Team Baldwin J Bloom T Jaffe DB Nicol R Wilkinson J Lander ES Di Palma F Lindblad-Toh K Kingsley DM 《Nature》2012,484(7392):55-61
Marine stickleback fish have colonized and adapted to thousands of streams and lakes formed since the last ice age, providing an exceptional opportunity to characterize genomic mechanisms underlying repeated ecological adaptation in nature. Here we develop a high-quality reference genome assembly for threespine sticklebacks. By sequencing the genomes of twenty additional individuals from a global set of marine and freshwater populations, we identify a genome-wide set of loci that are consistently associated with marine-freshwater divergence. Our results indicate that reuse of globally shared standing genetic variation, including chromosomal inversions, has an important role in repeated evolution of distinct marine and freshwater sticklebacks, and in the maintenance of divergent ecotypes during early stages of reproductive isolation. Both coding and regulatory changes occur in the set of loci underlying marine-freshwater evolution, but regulatory changes appear to predominate in this well known example of repeated adaptive evolution in nature. 相似文献
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The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups 总被引:1,自引:0,他引:1
Curtis C Shah SP Chin SF Turashvili G Rueda OM Dunning MJ Speed D Lynch AG Samarajiwa S Yuan Y Gräf S Ha G Haffari G Bashashati A Russell R McKinney S;METABRIC Group Langerød A Green A Provenzano E Wishart G Pinder S Watson P Markowetz F Murphy L Ellis I Purushotham A Børresen-Dale AL Brenton JD Tavaré S Caldas C Aparicio S 《Nature》2012,486(7403):346-352
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AA Pezzulo XX Tang MJ Hoegger MH Alaiwa S Ramachandran TO Moninger PH Karp CL Wohlford-Lenane HP Haagsman M van Eijk B Bánfi AR Horswill DA Stoltz PB McCray MJ Welsh J Zabner 《Nature》2012,487(7405):109-113
Cystic fibrosis (CF) is a life-shortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Although bacterial lung infection and the resulting inflammation cause most of the morbidity and mortality, how the loss of CFTR function first disrupts airway host defence has remained uncertain. To investigate the abnormalities that impair elimination when a bacterium lands on the pristine surface of a newborn CF airway, we interrogated the viability of individual bacteria immobilized on solid grids and placed onto the airway surface. As a model, we studied CF pigs, which spontaneously develop hallmark features of CF lung disease. At birth, their lungs lack infection and inflammation, but have a reduced ability to eradicate bacteria. Here we show that in newborn wild-type pigs, the thin layer of airway surface liquid (ASL) rapidly kills bacteria in vivo, when removed from the lung and in primary epithelial cultures. Lack of CFTR reduces bacterial killing. We found that the ASL pH was more acidic in CF pigs, and reducing pH inhibited the antimicrobial activity of ASL. Reducing ASL pH diminished bacterial killing in wild-type pigs, and, conversely, increasing ASL pH rescued killing in CF pigs. These results directly link the initial host defence defect to the loss of CFTR, an anion channel that facilitates HCO(3)(-) transport. Without CFTR, airway epithelial HCO(3)(-) secretion is defective, the ASL pH falls and inhibits antimicrobial function, and thereby impairs the killing of bacteria that enter the newborn lung. These findings suggest that increasing ASL pH might prevent the initial infection in patients with CF, and that assaying bacterial killing could report on the benefit of therapeutic interventions. 相似文献
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Moreno JA Radford H Peretti D Steinert JR Verity N Martin MG Halliday M Morgan J Dinsdale D Ortori CA Barrett DA Tsaytler P Bertolotti A Willis AE Bushell M Mallucci GR 《Nature》2012,485(7399):507-511
The mechanisms leading to neuronal death in neurodegenerative disease are poorly understood. Many of these disorders, including Alzheimer's, Parkinson's and prion diseases, are associated with the accumulation of misfolded disease-specific proteins. The unfolded protein response is a protective cellular mechanism triggered by rising levels of misfolded proteins. One arm of this pathway results in the transient shutdown of protein translation, through phosphorylation of the α-subunit of eukaryotic translation initiation factor, eIF2. Activation of the unfolded protein response and/or increased eIF2α-P levels are seen in patients with Alzheimer's, Parkinson's and prion diseases, but how this links to neurodegeneration is unknown. Here we show that accumulation of prion protein during prion replication causes persistent translational repression of global protein synthesis by eIF2α-P, associated with synaptic failure and neuronal loss in prion-diseased mice. Further, we show that promoting translational recovery in hippocampi of prion-infected mice is neuroprotective. Overexpression of GADD34, a specific eIF2α-P phosphatase, as well as reduction of levels of prion protein by lentivirally mediated RNA interference, reduced eIF2α-P levels. As a result, both approaches restored vital translation rates during prion disease, rescuing synaptic deficits and neuronal loss, thereby significantly increasing survival. In contrast, salubrinal, an inhibitor of eIF2α-P dephosphorylation, increased eIF2α-P levels, exacerbating neurotoxicity and significantly reducing survival in prion-diseased mice. Given the prevalence of protein misfolding and activation of the unfolded protein response in several neurodegenerative diseases, our results suggest that manipulation of common pathways such as translational control, rather than disease-specific approaches, may lead to new therapies preventing synaptic failure and neuronal loss across the spectrum of these disorders. 相似文献
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Marie Morelato Mark Barash Lucas Blanes Scott Chadwick Jessirie Dilag Unnikrishnan Kuzhiumparambil Katie D. Nizio Xanthe Spindler Sebastien Moret 《Foundations of Science》2017,22(4):799-825
Forensic science and its influence on policing and the criminal justice system have increased since the beginning of the twentieth century. While the philosophies of the forensic science pioneers remain the pillar of modern practice, rapid advances in technology and the underpinning sciences have seen an explosion in the number of disciplines and tools. Consequently, the way in which we exploit and interpret the remnant of criminal activity are adapting to this changing environment. In order to best exploit the trace, an interdisciplinary approach to both research and investigation is required. In this paper, nine postdoctoral research fellows from a multidisciplinary team discuss their vision for the future of forensic science at the crime scene, in the laboratory and beyond. This paper does not pretend to be exhaustive of all fields of forensic science, but describes a portion of the postdoctoral fellows’ interests and skills. 相似文献
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