2,552 research outputs found
Structural characteristics of positionally-disordered lattices: relation to the first sharp diffraction peak in glasses
Positional disorder has been introduced into the atomic structure of certain
crystalline lattices, and the orientationally-averaged structure factor S(k)
and pair-correlation function g(r) of these disordered lattices have been
studied. Analytical expressions for S(k) and g(r) for Gaussian positional
disorder in 2D and 3D are confirmed with precise numerical simulations. These
analytic results also have a bearing on the unsolved Gauss circle problem in
mathematics. As the positional disorder increases, high-k peaks in S(k) are
destroyed first, eventually leaving a single peak, that with the lowest-k
value. The pair-correlation function for lattices with such high levels of
positional disorder exhibits damped oscillations, with a period equal to the
separation between the furthest-separated (lowest-k) lattice planes. The last
surviving peak in S(k) is, for example for silicon and silica, at a wavevector
nearly identical to that of the experimentally-observed first sharp diffraction
peak (FSDP) in the amorphous phases of those materials. Thus, for these
amorphous materials at least, the FSDP can be regarded as arising from
scattering from atomic configurations equivalent to the single family of
positionally-disordered local Bragg planes having the furthest separation.Comment: v2: changes in response to referees' comments: Figure 2 made more
readable, improved discussion of height of peaks in S(k), other minor changes
4 pages, 3 figures, submitted to Physical Review
Ariel - Volume 4 Number 2
Editors
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Gender, foundation degrees and the knowledge economy
This article questions the concept of âeducation for employmentâ, which constructs a discourse of individual and societal benefit in a knowledgeâdriven economy. Recent policy emphasis in the European Union promotes the expansion of higher education and shortâcycle vocational awards such as the intermediate twoâyear Foundation Degree recently introduced into England and Wales. Studies of vocational education and training (VET) and the knowledge economy have focused largely on the governance of education and on the development and drift of policy. Many VET programmes have also been considered for their classed, raced and gendered takeâup and subsequent effect on employment. This article builds on both fields of study to engage with the finer crossâanalyses of gender, social class, poverty, race and citizenship. In its analysis of policy texts the article argues that in spite of a discourse of inclusivity, an expanded higher education system has generated new inequalities, deepening social stratification. Drawing on early analyses of national quantitative data sets, it identifies emerging gendered, classed and raced patterns and considers these in relation to occupationally and hierarchically stratified labour markets, both within and without the knowledge economy
Evidence for replicative mechanism in a CHD7 rearrangement in a patient with CHARGE syndrome
Haploinsufficiency of CHD7 (OMIM# 608892) is known to cause CHARGE syndrome (OMIM# 214800). Molecular testing supports a definitive diagnosis in approximately 65-70% of cases. Most CHD7 mutations arise de novo, and no mutations affecting exon-7 have been reported to date. We report on an 8-year-old girl diagnosed with CHARGE syndrome that was referred to our laboratory for comprehensive CHD7 gene screening. Genomic DNA from the subject with a suspected diagnosis of CHARGE was isolated from peripheral blood lymphocytes and comprehensive Sanger sequencing, along with deletion/duplication analysis of the CHD7 gene using multiplex ligation-dependent probe amplification (MLPA), was performed. MLPA analysis identified a reduced single probe signal for exon-7 of the CHD7 gene consistent with potential heterozygous deletion. Long-range PCR breakpoint analysis identified a complex genomic rearrangement (CGR) leading to the deletion of exon-7 and breakpoints consistent with a replicative mechanism such as fork stalling and template switching (FoSTeS) or microhomology-mediated break-induced replication (MMBIR). Taken together this represents the first evidence for a CHD7 intragenic CGR in a patient with CHARGE syndrome leading to what appears to be also the first report of a mutation specifically disrupting exon-7. Although likely rare, CGR may represent an overlooked mechanism in subjects with CHARGE syndrome that can be missed by current sequencing and dosage assays
Cessation of biomechanical stretch model of C2C12 cells models myocyte atrophy and anaplerotic changes in metabolism using non-targeted metabolomics analysis
Studies of skeletal muscle disuse, either in patients on bed rest or experimentally in animals (immobilization), have demonstrated that decreased protein synthesis is common, with transient parallel increases in protein degradation. Muscle disuse atrophy involves a process of transition from slow to fast myosin fiber types. A shift toward glycolysis, decreased capacity for fat oxidation, and substrate accumulation in atrophied muscles have been reported, as has accommodation of the liver with an increased gluconeogenic capacity. Recent studies have modeled skeletal muscle disuse by using cyclic stretch of differentiated myotubes (C2C12), which mimics the loading pattern of mature skeletal muscle, followed by cessation of stretch. We utilized this model to determine the metabolic changes using non-targeted metabolomics analysis of the media. We identified increases in amino acids resulting from protein degradation (largely sarcomere) that occurs with muscle atrophy that are involved in feeding the Krebâs cycle through anaplerosis. Specifically, we identified increased alanine/proline metabolism (significantly elevated proline, alanine, glutamine, and asparagine) and increased Îą-ketoglutaric acid, the proposed Krebâs cycle intermediate being fed by the alanine/proline metabolic anaplerotic mechanism. Additionally, several unique pathways not clearly delineated in previous studies of muscle unloading were seen, including: 1) elevated keto-acids derived from branched chain amino aicds (i.e. 2-ketoleucine and 2-keovaline), which feed into a metabolic pathway supplying acetyl-CoA and 2-hydroxybutyrate (also significantly increased); and 2) elevated guanine, an intermediate of purine metabolism, was seen at 12 hours unloading. Given the interest in targeting different aspects of the ubiquitin proteasome system to inhibit protein degradation, this C2C12 system may allow the identification of direct and indirect alterations in metabolism due to anaplerosis or through other yet to be identified mechanisms using a non-targeted metabolomics approach
Lung injury-induced skeletal muscle wasting in aged mice is linked to alterations in long chain fatty acid metabolism
Older patients are more likely to acquire and die from acute respiratory distress syndrome (ARDS) and muscle weakness may be more clinically significant in older persons. Recent data implicate muscle ring finger protein 1 (MuRF1) in lung injury-induced skeletal muscle atrophy in young mice and identify an alternative role for MuRF1 in cardiac metabolism regulation through inhibition of fatty acid oxidation
Human amylin proteotoxicity impairs protein biosynthesis, and alters major cellular signaling pathways in the heart, brain and liver of humanized diabetic rat model in vivo
Chronic hypersecretion of the 37 amino acid amylin is common in type 2 diabetics (T2D). Recent studies implicate human amylin aggregates cause proteotoxicity (cell death induced by misfolded proteins) in both the brain and the heart
Exploiting Carbonyl Groups to Control Intermolecular Rhodium-Catalyzed Alkene and Alkyne Hydroacylation
Readily available β-carbonyl-substituted aldehydes are shown to be exceptional substrates for Rh-catalyzed intermolecular alkene and alkyne hydroacylation reactions. By using cationic rhodium catalysts incorporating bisphosphine ligands, efficient and selective reactions are achieved for β-amido, β-ester, and β-keto aldehyde substrates, providing a range of synthetically useful 1,3-dicarbonyl products in excellent yields. A correspondingly broad selection of alkenes and alkynes can be employed. For alkyne substrates, the use of a catalyst incorporating the Ampaphos ligand triggers a regioselectivity switch, allowing both linear and branched isomers to be prepared with high selectivity in an efficient manner. Structural data, confirming aldehyde chelation, and a proposed mechanism are provided
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