109 research outputs found

    Note: Scale-free center-of-mass displacement correlations in polymer films without topological constraints and momentum conservation

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    We present here computational work on the center-of-mass displacements in thin polymer films of finite width without topological constraints and without momentum conservation obtained using a well-known lattice Monte Carlo algorithm with chain lengths ranging up to N=8192. Computing directly the center-of-mass displacement correlation function C_N(t) allows to make manifest the existence of scale-free colored forces acting on a reference chain. As suggested by the scaling arguments put forward in a recent work on three-dimensional melts, we obtain a negative algebraic decay C_N(t) \sim -1/(Nt) for times t << T_N with T_N being the chain relaxation time. This implies a logarithmic correction to the related center-of-mass mean square-displacement h_N(t) as has been checked directly

    The relationship between case-control differential gene expression from brain tissue and genetic associations in schizophrenia

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    This is the final version. Available on open access from Wiley via the DOI in this recordData availability statement: The data that supports the findings of this study are available in the supplementary material of this article.Large numbers of genetic loci have been identified that are known to contain common risk alleles for schizophrenia, but linking associated alleles to specific risk genes remains challenging. Given that most alleles that influence liability to schizophrenia are thought to do so by altered gene expression, intuitively, case-control differential gene expression studies should highlight genes with a higher probability of being associated with schizophrenia and could help identify the most likely causal genes within associated loci. Here, we test this hypothesis by comparing transcriptome analysis of the dorsolateral prefrontal cortex from 563 schizophrenia cases and 802 controls with genome-wide association study (GWAS) data from the third wave study of the Psychiatric Genomics Consortium. Genes differentially expressed in schizophrenia were not enriched for common allelic association statistics compared with other brain-expressed genes, nor were they enriched for genes within associated loci previously reported to be prioritized by genetic fine-mapping. Genes prioritized by Summary-based Mendelian Randomisation were underexpressed in cases compared to other genes in the same GWAS loci. However, the overall strength and direction of expression change predicted by SMR were not related to that observed in the differential expression data. Overall, this study does not support the hypothesis that genes identified as differentially expressed from RNA sequencing of bulk brain tissue are enriched for those that show evidence for genetic associations. Such data have limited utility for prioritizing genes in currently associated loci in schizophrenia.Medical Research Council (MRC)National Institute of Mental Health (USA

    Siketnémák és Vakok Oktatásügye 32 (1930) 07-08

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    A Siketnémák és Vakok Tanárai Országos Egyesületének hivatalos lapja 32. évfolyam, 7-8. szám Budapest, 1930. Előzménye a "Magyar Siketnéma-Oktatás a siketnémák oktatásával foglalkozók szakközlönye". A lap 1=41. évfolyam 1. számától (1939) "Magyar gyógypedagógiai tanárok közlönye a Magyar Gyógypedagógiai Tanárok Országos Egyesületének hivatalos lapja és szakfolyóirata" cím alatt folytatódott

    Lectures on the functional renormalization group method

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    These introductory notes are about functional renormalization group equations and some of their applications. It is emphasised that the applicability of this method extends well beyond critical systems, it actually provides us a general purpose algorithm to solve strongly coupled quantum field theories. The renormalization group equation of F. Wegner and A. Houghton is shown to resum the loop-expansion. Another version, due to J. Polchinski, is obtained by the method of collective coordinates and can be used for the resummation of the perturbation series. The genuinely non-perturbative evolution equation is obtained in a manner reminiscent of the Schwinger-Dyson equations. Two variants of this scheme are presented where the scale which determines the order of the successive elimination of the modes is extracted from external and internal spaces. The renormalization of composite operators is discussed briefly as an alternative way to arrive at the renormalization group equation. The scaling laws and fixed points are considered from local and global points of view. Instability induced renormalization and new scaling laws are shown to occur in the symmetry broken phase of the scalar theory. The flattening of the effective potential of a compact variable is demonstrated in case of the sine-Gordon model. Finally, a manifestly gauge invariant evolution equation is given for QED.Comment: 47 pages, 11 figures, final versio

    Scale-free static and dynamical correlations in melts of monodisperse and Flory-distributed homopolymers: A review of recent bond-fluctuation model studies

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    It has been assumed until very recently that all long-range correlations are screened in three-dimensional melts of linear homopolymers on distances beyond the correlation length ξ\xi characterizing the decay of the density fluctuations. Summarizing simulation results obtained by means of a variant of the bond-fluctuation model with finite monomer excluded volume interactions and topology violating local and global Monte Carlo moves, we show that due to an interplay of the chain connectivity and the incompressibility constraint, both static and dynamical correlations arise on distances rξr \gg \xi. These correlations are scale-free and, surprisingly, do not depend explicitly on the compressibility of the solution. Both monodisperse and (essentially) Flory-distributed equilibrium polymers are considered.Comment: 60 pages, 49 figure

    Profiling CpG island field methylation in both morphologically normal and neoplastic human colonic mucosa

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    Aberrant CpG island (CGI) methylation occurs early in colorectal neoplasia. Quantitative methylation-specific PCR profiling applied to biopsies was used to quantify low levels of CGI methylation of 18 genes in the morphologically normal colonic mucosa of neoplasia-free subjects, adenomatous polyp patients, cancer patients and their tumours. Multivariate statistical analyses distinguished tumour from mucosa with a sensitivity of 78.9% and a specificity of 100% (P=3 × 10−7). In morphologically normal mucosa, age-dependent CGI methylation was observed for APC, AXIN2, DKK1, HPP1, N33, p16, SFRP1, SFRP2 and SFRP4 genes, and significant differences in CGI methylation levels were detected between groups. Multinomial logistic regression models based on the CGI methylation profiles from normal mucosa correctly identified 78.9% of cancer patients and 87.9% of non-cancer (neoplasia-free+polyp) patients (P=4.93 × 10−7) using APC, HPP1, p16, SFRP4, WIF1 and ESR1 methylation as the most informative variables. Similarly, CGI methylation of SFRP4, SFRP5 and WIF1 correctly identified 61.5% of polyp patients and 78.9% of neoplasia-free subjects (P=0.0167). The apparently normal mucosal field of patients presenting with neoplasia has evidently undergone significant epigenetic modification. Methylation of the genes selected by the models may play a role in the earliest stages of the development of colorectal neoplasia

    Siketnémák és Vakok Oktatásügye 31 (1929) 03-06

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    A Siketnémák és Vakok Tanárai Országos Egyesületének hivatalos lapja 31. évfolyam, 3-6. szám Budapest, 1929. Előzménye a "Magyar Siketnéma-Oktatás a siketnémák oktatásával foglalkozók szakközlönye". A lap 1=41. évfolyam 1. számától (1939) "Magyar gyógypedagógiai tanárok közlönye a Magyar Gyógypedagógiai Tanárok Országos Egyesületének hivatalos lapja és szakfolyóirata" cím alatt folytatódott

    Genomic analysis of genetic heterogeneity and evolution in high-grade serous ovarian carcinoma

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    Resistance to chemotherapy in ovarian cancer is poorly understood. Evolutionary models of cancer predict that, following treatment, resistance emerges either because of outgrowth of an intrinsically resistant sub-clone or evolves in residual disease under the selective pressure of treatment. To investigate genetic evolution in high-grade serous (HGS) ovarian cancers, we first analysed cell line series derived from three cases of HGS carcinoma before and after platinum resistance had developed (PEO1, PEO4 and PEO6; PEA1 and PEA2; and PEO14 and PEO23). Analysis with 24-colour fluorescence in situ hybridisation and single nucleotide polymorphism (SNP) array comparative genomic hybridisation (CGH) showed mutually exclusive endoreduplication and loss of heterozygosity events in clones present at different time points in the same individual. This implies that platinum-sensitive and -resistant disease was not linearly related, but shared a common ancestor at an early stage of tumour development. Array CGH analysis of six paired pre- and post-neoadjuvant treatment HGS samples from the CTCR-OV01 clinical study did not show extensive copy number differences, suggesting that one clone was strongly dominant at presentation. These data show that cisplatin resistance in HGS carcinoma develops from pre-existing minor clones but that enrichment for these clones is not apparent during short-term chemotherapy treatment
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