59 research outputs found

    Microstructural Shear Localization in Plastic Deformation of Amorphous Solids

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    The shear-transformation-zone (STZ) theory of plastic deformation predicts that sufficiently soft, non-crystalline solids are linearly unstable against forming periodic arrays of microstructural shear bands. A limited nonlinear analysis indicates that this instability may be the mechanism responsible for strain softening in both constant-stress and constant-strain-rate experiments. The analysis presented here pertains only to one-dimensional banding patterns in two-dimensional systems, and only to very low temperatures. It uses the rudimentary form of the STZ theory in which there is only a single kind of zone rather than a distribution of them with a range of transformation rates. Nevertheless, the results are in qualitative agreement with essential features of the available experimental data. The nonlinear theory also implies that harder materials, which do not undergo a microstructural instability, may form isolated shear bands in weak regions or, perhaps, at points of concentrated stress.Comment: 32 pages, 6 figure

    Ground-state phase diagram of the one-dimensional half-filled extended Hubbard model

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    We revisit the ground-state phase diagram of the one-dimensional half-filled extended Hubbard model with on-site (U) and nearest-neighbor (V) repulsive interactions. In the first half of the paper, using the weak-coupling renormalization-group approach (g-ology) including second-order corrections to the coupling constants, we show that bond-charge-density-wave (BCDW) phase exists for U \approx 2V in between charge-density-wave (CDW) and spin-density-wave (SDW) phases. We find that the umklapp scattering of parallel-spin electrons disfavors the BCDW state and leads to a bicritical point where the CDW-BCDW and SDW-BCDW continuous-transition lines merge into the CDW-SDW first-order transition line. In the second half of the paper, we investigate the phase diagram of the extended Hubbard model with either additional staggered site potential \Delta or bond alternation \delta. Although the alternating site potential \Delta strongly favors the CDW state (that is, a band insulator), the BCDW state is not destroyed completely and occupies a finite region in the phase diagram. Our result is a natural generalization of the work by Fabrizio, Gogolin, and Nersesyan [Phys. Rev. Lett. 83, 2014 (1999)], who predicted the existence of a spontaneously dimerized insulating state between a band insulator and a Mott insulator in the phase diagram of the ionic Hubbard model. The bond alternation \delta destroys the SDW state and changes it into the BCDW state (or Peierls insulating state). As a result the phase diagram of the model with \delta contains only a single critical line separating the Peierls insulator phase and the CDW phase. The addition of \Delta or \delta changes the universality class of the CDW-BCDW transition from the Gaussian transition into the Ising transition.Comment: 24 pages, 20 figures, published versio

    Pairing and Density Correlations of Stripe Electrons in a Two-Dimensional Antiferromagnet

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    We study a one-dimensional electron liquid embedded in a 2D antiferromagnetic insulator, and coupled to it via a weak antiferromagnetic spin exchange interaction. We argue that this model may qualitatively capture the physics of a single charge stripe in the cuprates on length- and time scales shorter than those set by its fluctuation dynamics. Using a local mean-field approach we identify the low-energy effective theory that describes the electronic spin sector of the stripe as that of a sine-Gordon model. We determine its phases via a perturbative renormalization group analysis. For realistic values of the model parameters we obtain a phase characterized by enhanced spin density and composite charge density wave correlations, coexisting with subleading triplet and composite singlet pairing correlations. This result is shown to be independent of the spatial orientation of the stripe on the square lattice. Slow transverse fluctuations of the stripes tend to suppress the density correlations, thus promoting the pairing instabilities. The largest amplitudes for the composite instabilities appear when the stripe forms an antiphase domain wall in the antiferromagnet. For twisted spin alignments the amplitudes decrease and leave room for a new type of composite pairing correlation, breaking parity but preserving time reversal symmetry.Comment: Revtex, 28 pages incl. 5 figure

    Multiethnic Meta-Analysis Identifies RAI1 as a Possible Obstructive Sleep Apnea-related Quantitative Trait Locus in Men.

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    Obstructive sleep apnea (OSA) is a common heritable disorder displaying marked sexual dimorphism in disease prevalence and progression. Previous genetic association studies have identified a few genetic loci associated with OSA and related quantitative traits, but they have only focused on single ethnic groups, and a large proportion of the heritability remains unexplained. The apnea-hypopnea index (AHI) is a commonly used quantitative measure characterizing OSA severity. Because OSA differs by sex, and the pathophysiology of obstructive events differ in rapid eye movement (REM) and non-REM (NREM) sleep, we hypothesized that additional genetic association signals would be identified by analyzing the NREM/REM-specific AHI and by conducting sex-specific analyses in multiethnic samples. We performed genome-wide association tests for up to 19,733 participants of African, Asian, European, and Hispanic/Latino American ancestry in 7 studies. We identified rs12936587 on chromosome 17 as a possible quantitative trait locus for NREM AHI in men (N = 6,737; P = 1.7 × 10 <sup>-8</sup> ) but not in women (P = 0.77). The association with NREM AHI was replicated in a physiological research study (N = 67; P = 0.047). This locus overlapping the RAI1 gene and encompassing genes PEMT1, SREBF1, and RASD1 was previously reported to be associated with coronary artery disease, lipid metabolism, and implicated in Potocki-Lupski syndrome and Smith-Magenis syndrome, which are characterized by abnormal sleep phenotypes. We also identified gene-by-sex interactions in suggestive association regions, suggesting that genetic variants for AHI appear to vary by sex, consistent with the clinical observations of strong sexual dimorphism

    Tracking early lung cancer metastatic dissemination in TRACERx using ctDNA

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    Circulating tumour DNA (ctDNA) can be used to detect and profile residual tumour cells persisting after curative intent therapy1. The study of large patient cohorts incorporating longitudinal plasma sampling and extended follow-up is required to determine the role of ctDNA as a phylogenetic biomarker of relapse in early-stage non-small-cell lung cancer (NSCLC). Here we developed ctDNA methods tracking a median of 200 mutations identified in resected NSCLC tissue across 1,069 plasma samples collected from 197 patients enrolled in the TRACERx study2. A lack of preoperative ctDNA detection distinguished biologically indolent lung adenocarcinoma with good clinical outcome. Postoperative plasma analyses were interpreted within the context of standard-of-care radiological surveillance and administration of cytotoxic adjuvant therapy. Landmark analyses of plasma samples collected within 120 days after surgery revealed ctDNA detection in 25% of patients, including 49% of all patients who experienced clinical relapse; 3 to 6 monthly ctDNA surveillance identified impending disease relapse in an additional 20% of landmark-negative patients. We developed a bioinformatic tool (ECLIPSE) for non-invasive tracking of subclonal architecture at low ctDNA levels. ECLIPSE identified patients with polyclonal metastatic dissemination, which was associated with a poor clinical outcome. By measuring subclone cancer cell fractions in preoperative plasma, we found that subclones seeding future metastases were significantly more expanded compared with non-metastatic subclones. Our findings will support (neo)adjuvant trial advances and provide insights into the process of metastatic dissemination using low-ctDNA-level liquid biopsy

    Genetic, Phenotypic, and Interferon Biomarker Status in ADAR1-Related Neurological Disease

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    We investigated the genetic, phenotypic, and interferon status of 46 patients from 37 families with neurological disease due to mutations in ADAR1. The clinicoradiological phenotype encompassed a spectrum of Aicardi-Goutières syndrome, isolated bilateral striatal necrosis, spastic paraparesis with normal neuroimaging, a progressive spastic dystonic motor disorder, and adult-onset psychological difficulties with intracranial calcification. Homozygous missense mutations were recorded in five families. We observed a p.Pro193Ala variant in the heterozygous state in 22 of 23 families with compound heterozygous mutations. We also ascertained 11 cases from nine families with a p.Gly1007Arg dominant-negative mutation, which occurred de novo in four patients, and was inherited in three families in association with marked phenotypic variability. In 50 of 52 samples from 34 patients, we identified a marked upregulation of type I interferon-stimulated gene transcripts in peripheral blood, with a median interferon score of 16.99 (interquartile range [IQR]: 10.64-25.71) compared with controls (median: 0.93, IQR: 0.57-1.30). Thus, mutations in ADAR1 are associated with a variety of clinically distinct neurological phenotypes presenting from early infancy to adulthood, inherited either as an autosomal recessive or dominant trait. Testing for an interferon signature in blood represents a useful biomarker in this context.0SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    A de novo p.Asp18Asn mutation in TREX1 in a patient with Aicardi-Goutieres syndrome.

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    Aicardi-Goutieres syndrome is a rare, genetically determined encephalopathy often resembling congenital infection. Mutations in the TREX1 gene are found in approximately 25% of patients. Aicardi-Goutieres syndrome is usually inherited as an autosomal recessive trait, although a single case of a heterozygous TREX1 mutation associated with the syndrome has been reported. We present a second case of a de novo heterozygous TREX1 mutation causing an autosomal dominant phenotype of Aicardi-Goutieres syndrome with additional features indicative of mitochondrial dysfunction. This report serves to enhance awareness of de novo heterozygous mutations underlying Aicardi-Goutieres syndrome-with a concomitant low risk of recurrence

    Crack tip fields in ductile crystals

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