Design of Two-Channel Low-Delay FIR Filter Banks using Constrained Optimization

This paper shows the efficiency of using constrained optimization for designing two-channel low-delay finite impulse response filter banks. The filter banks under consideration are quadrature mirror filter (QMF) banks and perfect reconstruction (PR) biorthogonal filter banks. The design problems for both types of banks are stated as constrained minimization problems in forms that enable us to minimize the maximum of the stopband energies of the analysis filter(s) subject to the given passband and transition band constraints of the filter(s) as well as subject to the given allowable reconstruction error for QMF banks or the PR property for biorthogonal filter banks. For solving the given optimization problems a modified Dutta-Vidyasagar optimization technique has been used. The efficiency of the proposed design methods is illustrated by means of some examples

Improved technique for design of perfect reconstruction FIR QMF banks with lossless polyphase matrices

A technique is developed for the design of analysis filters in an M-channel maximally decimated, perfect reconstruction, finite-impulse-response quadrature mirror filter (FIR QMF) bank that has a lossless polyphase-component matrix E(z). The aim is to optimize the parameters characterizing E(z) until the sum of the stopband energies of the analysis filters is minimized. There are four novel elements in the procedure reported here. The first is a technique for efficient initialization of one of the M analysis filters, as a spectral factor of an Mth band filter. The factorization itself is done in an efficient manner using the eigenfilters approach, without the need for root-finding techniques. The second element is the initialization of the internal parameters which characterize E(z), based on the above spectral factor. The third element is a modified characterization, mostly free from rotation angles, of the FIR E(z). The fourth is the incorporation of symmetry among the analysis filters, so as to minimize the number of unknown parameters being optimized. The resulting design procedure always gives better filter responses than earlier ones (for a given filter length) and converges much faste

Spectral and network methods in the analysis of correlation matrices of stock returns

Correlation matrices inferred from stock return time series contain information on the behaviour of the market, especially on clusters of highly correlating stocks. Here we study a subset of New York Stock Exchange (NYSE) traded stocks and compare three different methods of analysis: i) spectral analysis, i.e. investigation of the eigenvalue-eigenvector pairs of the correlation matrix, ii) asset trees, obtained by constructing the maximal spanning tree of the correlation matrix, and iii) asset graphs, which are networks in which the strongest correlations are depicted as edges. We illustrate and discuss the localisation of the most significant modes of fluctuation, i.e. eigenvectors corresponding to the largest eigenvalues, on the asset trees and graphs.Comment: 6 pages, 2 figure

Mapping of the chromosomal amplification 1p21-22 in bladder cancer

Background The aim of the study was to characterize a recurrent amplification at chromosomal region 1p21-22 in bladder cancer. Methods ArrayCGH (aCGH) was performed to identify DNA copy number variations in 7 clinical samples and 6 bladder cancer cell lines. FISH was used to map the amplicon at 1p21-22 in the cell lines. Gene expression microarrays and qRT-PCR were used to study the expression of putative target genes in the region. Results aCGH identified an amplification at 1p21-22 in 10/13 (77%) samples. The minimal region of the amplification was mapped to a region of about 1 Mb in size, containing a total of 11 known genes. The highest amplification was found in SCaBER squamous cell carcinoma cell line. Four genes, TMED5, DR1, RPL5 and EVI5, showed significant overexpression in the SCaBER cell line compared to all the other samples tested. Oncomine database analysis revealed upregulation of DR1 in superficial and infiltrating bladder cancer samples, compared to normal bladder. Conclusions In conclusions, we have identified and mapped chromosomal amplification at 1p21-22 in bladder cancer as well as studied the expression of the genes in the region. DR1 was found to be significantly overexpressed in the SCaBER, which is a model of squamous cell carcinoma. However, the overexpression was found also in a published clinical sample cohort of superficial and infiltrating bladder cancers. Further studies with more clinical material are needed to investigate the role of the amplification at 1p21-22.BioMed Central open acces

Detecting modules in dense weighted networks with the Potts method

We address the problem of multiresolution module detection in dense weighted networks, where the modular structure is encoded in the weights rather than topology. We discuss a weighted version of the q-state Potts method, which was originally introduced by Reichardt and Bornholdt. This weighted method can be directly applied to dense networks. We discuss the dependence of the resolution of the method on its tuning parameter and network properties, using sparse and dense weighted networks with built-in modules as example cases. Finally, we apply the method to data on stock price correlations, and show that the resulting modules correspond well to known structural properties of this correlation network.Comment: 14 pages, 6 figures. v2: 1 figure added, 1 reference added, minor changes. v3: 3 references added, minor change

Recurrent SKIL-activating rearrangements in ETS-negative prostate cancer

Prostate cancer is the third most common cause of male cancer death in developed countries, and one of the most comprehensively characterized human cancers. Roughly 60% of prostate cancers harbor gene fusions that juxtapose ETS-family transcription factors with androgen regulated promoters. A second subtype, characterized by SPINK1 overexpression, accounts for 15% of prostate cancers. Here we report the discovery of a new prostate cancer subtype characterized by rearrangements juxtaposing the SMAD inhibitor SKIL with androgen regulated promoters, leading to increased SKIL expression. SKIL fusions were found in 6 of 540 (1.1%) prostate cancers and 1 of 27 (3.7%) cell lines and xenografts. 6 of 7 SKIL-positive cancers were negative for ETS overexpression, suggesting mutual exclusivity with ETS fusions. SKIL knockdown led to growth arrest in PC-3 and LNCaP cell line models of prostate cancer, and its overexpression led to increased invasiveness in RWPE-1 cells. The role of SKIL as a prostate cancer oncogene lends support to recent studies on the role of TGF-β signaling as a rate-limiting step in prostate cancer progression. Our findings highlight SKIL as an oncogene and potential therapeutic target in 1-2% of prostate cancers, amounting to an estimated 10,000 cancer diagnoses per year worldwide.This article has supplementary files, which can be found here:http://dx.doi.org/10.18632/oncotarget.335