190 research outputs found
On the critical level-curvature distribution
The parametric motion of energy levels for non-interacting electrons at the
Anderson localization critical point is studied by computing the energy
level-curvatures for a quasiperiodic ring with twisted boundary conditions. We
find a critical distribution which has the universal random matrix theory form
for large level-curvatures corresponding to
quantum diffusion, although overall it is close to approximate log-normal
statistics corresponding to localization. The obtained hybrid distribution
resembles the critical distribution of the disordered Anderson model and makes
a connection to recent experimental data.Comment: 4 pages, 3 figure
An evolving network model with community structure
Many social and biological networks consist of communities—groups of nodes within which connections are dense, but between which connections are sparser. Recently, there has been considerable interest in designing algorithms for detecting community structures in real-world complex networks. In this paper, we propose an evolving network model which exhibits community structure. The network model is based on the inner-community preferential attachment and inter-community preferential attachment mechanisms. The degree distributions of this network model are analysed based on a mean-field method. Theoretical results and numerical simulations indicate that this network model has community structure and scale-free properties
Antibiotic susceptibility and molecular identification of antibiotic resistance genes of staphylococci isolated from bovine mastitis in algeri
A network biology approach to prostate cancer
There is a need to identify genetic mediators of solid-tumor cancers, such as prostate cancer, where invasion and distant metastases determine the clinical outcome of the disease. Whole-genome expression profiling offers promise in this regard, but can be complicated by the challenge of identifying the genes affected by a condition from the hundreds to thousands of genes that exhibit changes in expression. Here, we show that reverse-engineered gene networks can be combined with expression profiles to compute the likelihood that genes and associated pathways are mediators of a disease. We apply our method to non-recurrent primary and metastatic prostate cancer data, and identify the androgen receptor gene (AR) among the top genetic mediators and the AR pathway as a highly enriched pathway for metastatic prostate cancer. These results were not obtained on the basis of expression change alone. We further demonstrate that the AR gene, in the context of the network, can be used as a marker to detect the aggressiveness of primary prostate cancers. This work shows that a network biology approach can be used advantageously to identify the genetic mediators and mediating pathways associated with a disease
An approach for the identification of targets specific to bone metastasis using cancer genes interactome and gene ontology analysis
Metastasis is one of the most enigmatic aspects of cancer pathogenesis and is
a major cause of cancer-associated mortality. Secondary bone cancer (SBC) is a
complex disease caused by metastasis of tumor cells from their primary site and
is characterized by intricate interplay of molecular interactions.
Identification of targets for multifactorial diseases such as SBC, the most
frequent complication of breast and prostate cancers, is a challenge. Towards
achieving our aim of identification of targets specific to SBC, we constructed
a 'Cancer Genes Network', a representative protein interactome of cancer genes.
Using graph theoretical methods, we obtained a set of key genes that are
relevant for generic mechanisms of cancers and have a role in biological
essentiality. We also compiled a curated dataset of 391 SBC genes from
published literature which serves as a basis of ontological correlates of
secondary bone cancer. Building on these results, we implement a strategy based
on generic cancer genes, SBC genes and gene ontology enrichment method, to
obtain a set of targets that are specific to bone metastasis. Through this
study, we present an approach for probing one of the major complications in
cancers, namely, metastasis. The results on genes that play generic roles in
cancer phenotype, obtained by network analysis of 'Cancer Genes Network', have
broader implications in understanding the role of molecular regulators in
mechanisms of cancers. Specifically, our study provides a set of potential
targets that are of ontological and regulatory relevance to secondary bone
cancer.Comment: 54 pages (19 pages main text; 11 Figures; 26 pages of supplementary
information). Revised after critical reviews. Accepted for Publication in
PLoS ON
Erratum to the “Use of pleural fluid C-reactive protein in diagnosis of pleural effusions” [Respiratory medicine 94(5) 432–435]
Vascular Wall-Resident CD44+ Multipotent Stem Cells Give Rise to Pericytes and Smooth Muscle Cells and Contribute to New Vessel Maturation
Here, we identify CD44(+)CD90(+)CD73(+)CD34(−)CD45(−) cells within the adult human arterial adventitia with properties of multipotency which were named vascular wall-resident multipotent stem cells (VW-MPSCs). VW-MPSCs exhibit typical mesenchymal stem cell characteristics including cell surface markers in immunostaining and flow cytometric analyses, and differentiation into adipocytes, chondrocytes and osteocytes under culture conditions. Particularly, TGFß1 stimulation up-regulates smooth muscle cell markers in VW-MPSCs. Using fluorescent cell labelling and co-localisation studies we show that VW-MPSCs differentiate to pericytes/smooth muscle cells which cover the wall of newly formed endothelial capillary-like structures in vitro. Co-implantation of EGFP-labelled VW-MPSCs and human umbilical vein endothelial cells into SCID mice subcutaneously via Matrigel results in new vessels formation which were covered by pericyte- or smooth muscle-like cells generated from implanted VW-MPSCs. Our results suggest that VW-MPSCs are of relevance for vascular morphogenesis, repair and self-renewal of vascular wall cells and for local capacity of neovascularization in disease processes
Paying for parking : improving stated-preference surveys
This article describes an experiment which introduced random ranges into the variables used for the design of a stated preference survey and its effects on willingness to pay for parking. User behaviour at the time of parking was modelled to determine their willingness to pay in order to get to their final destination more quickly. Calculating willingness to pay is fundamental during the social and economic assessment of projects. It is important to correctly model how car parks and their users interact in order to get values which represent reality as closely as possible. Willingness to pay is calculated using a stated preference survey and by calibrating multinomial logit models, taking variable tastes into account. It is shown that a value with a low variability can be obtained for willingness to pay by correctly establishing the context of the choice and randomly changing the variables around an average value
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