Institution
University of Palermo
Education•Palermo, Italy•
About: University of Palermo is a education organization based out in Palermo, Italy. It is known for research contribution in the topics: Population & Cancer. The organization has 15621 authors who have published 40250 publications receiving 964384 citations. The organization is also known as: Università degli Studi di Palermo & Universita degli Studi di Palermo.
Topics: Population, Cancer, Catalysis, Diabetes mellitus, Volcano
Papers published on a yearly basis
Papers
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TL;DR: It is demonstrated that compression may be greatly improved by a particular reordering of the sequences in the collection and a novel 'implicit sorting' strategy is given that enables these benefits to be realized without the overhead of sorting the reads.
Abstract: Motivation: The Burrows–Wheeler transform (BWT) is the foundation of many algorithms for compression and indexing of text data, but the cost of computing the BWT of very large string collections has prevented these techniques from being widely applied to the large sets of sequences often encountered as the outcome of DNA sequencing experiments. In previous work, we presented a novel algorithm that allows the BWT of human genome scale data to be computed on very moderate hardware, thus enabling us to investigate the BWT as a tool for the compression of such datasets.
Results: We first used simulated reads to explore the relationship between the level of compression and the error rate, the length of the reads and the level of sampling of the underlying genome and compare choices of second-stage compression algorithm.
We demonstrate that compression may be greatly improved by a particular reordering of the sequences in the collection and give a novel ‘implicit sorting’ strategy that enables these benefits to be realized without the overhead of sorting the reads. With these techniques, a 45× coverage of real human genome sequence data compresses losslessly to under 0.5 bits per base, allowing the 135.3 Gb of sequence to fit into only 8.2 GB of space (trimming a small proportion of low-quality bases from the reads improves the compression still further).
This is >4 times smaller than the size achieved by a standard BWT-based compressor (bzip2) on the untrimmed reads, but an important further advantage of our approach is that it facilitates the building of compressed full text indexes such as the FM-index on large-scale DNA sequence collections.
Availability: Code to construct the BWT and SAP-array on large genomic datasets is part of the BEETL library, available as a github repository at https://github.com/BEETL/BEETL.
Contact: [email protected]
149 citations
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TL;DR: CD38 and CD49d can be thought of as parts of a consecutive chain of events ultimately leading to improved survival of CLL cells.
Abstract: CD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38(+)CD49d(+) versus CD38(-)CD49d(-) CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38(+)CD49d(+) but not CD38(-)CD49d(-) cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors for CCL3 and CCL4, were found in CLL-derived monocyte-macrophages. Consistently, CCL3 increased monocyte migration, and CD68(+) macrophage infiltration was particularly high in BMB from CD38(+)CD49d(+) CLL. Conditioned media from CCL3-stimulated macrophages induced endothelial cells to express vascular cell adhesion molecule-1 (VCAM-1), the CD49d ligand, likely through tumor necrosis factor alpha overproduction. These effects were apparent in BMB from CD38(+)CD49d(+) CLL, where lymphoid infiltrates were characterized by a prominent meshwork of VCAM-1(+) stromal/endothelial cells. Lastly, CD49d engagement by VCAM-1 transfectants increased viability of CD38(+)CD49d(+) CLL cells. Altogether, CD38 and CD49d can be thought of as parts of a consecutive chain of events ultimately leading to improved survival of CLL cells.
149 citations
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TL;DR: In this article, the transient dynamics of these ecosystems are analyzed through generalized Lotka-Volterra equations in the presence of multiplicative noise, which models the interaction between the species and the environment.
Abstract: Noise, through its interaction with the nonlinearity of the living systems, can give rise to counter-intuitive phenomena such as stochastic resonance, noise-delayed extinction, temporal oscillations, and spatial patterns. In this paper we briefly review the noise-induced effects in three different ecosystems: (i) two
competing species; (ii) three interacting species, one predator and two preys, and
(iii) N-interacting species. The transient dynamics of these ecosystems are analyzed through generalized Lotka-Volterra equations in the presence of multiplicative
noise, which models the interaction between the species and the environment. The
interaction parameter between the species is random in cases (i) and (iii), and a
periodical function, which accounts for the environmental temperature, in case (ii).
We find noise-induced phenomena such as quasi-deterministic oscillations, stochastic
resonance, noise-delayed extinction, and noise-induced pattern formation with non-monotonic behaviors of patterns areas and of the density correlation as a function
of the multiplicative noise intensity. The asymptotic behavior of the time average of
the$ i^{th}$
population when the ecosystem is composed of a great number of interacting
species is obtained and the effect of the noise on the asymptotic probability distri-
butions of the populations is discussed.
149 citations
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TL;DR: The data suggest that HLA-B27 misfolding occurs in the gut of AS patients and is accompanied by activation of autophagy rather than a UPR, which appears to be associated with intestinal modulation of IL-23 in AS.
Abstract: Objectives Interleukin (IL)-23 has been implicated in the pathogenesis of ankylosing spondylitis (AS). The aim of the study was to clarify the mechanisms underlying the increased IL-23 expression in the gut of AS patients. Methods Consecutive gut biopsies from 30 HLA-B27 + AS patients, 15 Crohn9s disease (CD) patients and 10 normal subjects were obtained. Evidence for HLA-B27 misfolding was studied. Unfolded protein response (UPR) and autophagy were assessed by RT-PCR and immunohistochemistry. The contribution of UPR and autophagy in the regulation of IL-23 expression was evaluated in in vitro experiments on isolated lamina propria mononuclear cells (LPMCs). Results Intracellular colocalisation of SYVN1 and FHCs but not a significant overexpression of UPR genes was observed in the gut of AS patients. Conversely, upregulation of the genes involved in the autophagy pathway was observed in the gut of AS and CD patients. Immunohistochemistry showed an increased expression of LC3II, ATG5 and ATG12 but not of SQSTM1 in the ileum of AS and CD patients. LC3II was expressed among infiltrating mononuclear cells and epithelial cells resembling Paneth cells (PC) and colocalised with ATG5 in AS and CD. Autophagy but not UPR was required to modulate the expression of IL-23 in isolated LPMCs of AS patients with chronic gut inflammation, CD patients and controls. Conclusions Our data suggest that HLA-B27 misfolding occurs in the gut of AS patients and is accompanied by activation of autophagy rather than a UPR. Autophagy appears to be associated with intestinal modulation of IL-23 in AS.
148 citations
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TL;DR: In this article, the authors consider the issue of performing statistical inference for Lorenz curve orderings, which involves testing for an ordered relationship in a multivariate context and making comparisons among more than two population distributions.
Abstract: In this paper we consider the issue of performing statistical inference for Lorenz curve orderings. This involves testing for an ordered relationship in a multivariate context and making comparisons among more than two population distributions. Our approach is to frame the hypotheses of interest as sets of linear inequality constraints on the vector of Lorenz curve ordinates, and apply order-restricted statistical inference to derive test statistics and their sampling distributions. We go on to relate our results to others which have appeared in recent literature, and use Monte Carlo analysis to highlight their respective properties and comparative performances. Finally, we discuss in general terms the issue and problems of framing hypotheses, and testing them, in the context of the study of income inequality, and suggest ways in which the distributional analyst could best proceed, illustrating with empiricalexamples.
148 citations
Authors
Showing all 15895 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robin M. Murray | 171 | 1539 | 116362 |
Frede Blaabjerg | 147 | 2161 | 112017 |
Jean Bousquet | 145 | 1288 | 96769 |
Zhanhu Guo | 128 | 886 | 53378 |
Jean Ballet | 115 | 263 | 46301 |
Antonio Facchetti | 111 | 602 | 51885 |
Michele Pagano | 97 | 306 | 42211 |
Frank Z. Stanczyk | 93 | 620 | 30244 |
Eleonora Troja | 91 | 271 | 30873 |
Francesco Sciortino | 90 | 536 | 28956 |
Zev Rosenwaks | 89 | 772 | 32039 |
Antonio Russo | 88 | 934 | 34563 |
Carlo Salvarani | 88 | 730 | 31699 |
Giuseppe Basso | 87 | 643 | 33320 |
Antonio Craxì | 86 | 659 | 39463 |