Vertex-Ball Spring Smoothing: An efficient method for unstructured dynamic hybrid meshes

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A new optimization algorithm for network component analysis based on convex programming

Proceedings of the IEEE International Conference on Acoustics, Speech and Signal Processing, 2009, p. 509-512Paper no. 2203Network component analysis (NCA) has been established as a promising tool for reconstructing gene regulatory networks from microarray data. NCA is a method that can resolve the problem of blind source separation when the mixing matrix instead has a known sparse structure despite the correlation among the source signals. The original NCA algorithm relies on alternating least squares (ALS) and suffers from local convergence as well as slow convergence. In this paper, we develop new and more robust NCA algorithms by incorporating additional signal constraints. In particular, we introduce the biologically sound constraints that all nonzero entries in the connectivity network are positive. Our new approach formulates a convex optimization problem which can be solved efficiently and effectively by fast convex programming algorithms. We verify the effectiveness and robustness of our new approach using simulations and gene regulatory network reconstruction from experimental yeast cell cycle microarray data. ©2009 IEEE.published_or_final_versio

Extra-hepatic fascioliasis with peritoneal malignancy tumor feature

Fascioliasis is a zoonose parasitic disease caused by Fasciola hepatica and Fasciola gigantica and is widespread in most regions of the world. Ectopic fascioliasis usually caused by juvenile Fasciola spp., but in recent years a few cases of tissue-embedded ova have been reported from different endemic areas. A 79-year-old Iranian man resident in Eird-e-Mousa village from Ardabil Province, north-west of Iran, complained with abdominal pain, nausea, and intestinal obstruction symptoms referred to Ardabil Fatemi hospital. In laparotomy multiple intestinal masses with peritoneal seeding resembling of a malignant lesion were seen. After appendectomy and peritoneal mass biopsy with numerous intraperitoneal adenopathy, paraffin embedded blocks were prepared from each tissues. A blood sample was taken from the patient 5 months later for serological diagnosis. Histopathological examination of sections showed fibrofatty stroma with dense mixed inflammatory cells infiltration and fibrosis in peritoneal masses. Large numbers of ova of Fasciola spp. were noted with typical circumscribed granulomas. Despite of anti-fasciola treatment, IHA test for detecting anti F. hepatica antibodies was positive 5 months after surgery with a titer of 1/128. Due to multiple clinical manifestation of extra-hepatic fascioliasis, its differential diagnosis from intraperitoneal tumors or other similar diseases should be considered

Finite-size corrections for logarithmic representations in critical dense polymers

We study (analytic) finite-size corrections in the dense polymer model on the strip by perturbing the critical Hamiltonian with irrelevant operators belonging to the tower of the identity. We generalize the perturbation expansion to include Jordan cells, and examine whether the finite-size corrections are sensitive to the properties of indecomposable representations appearing in the conformal spectrum, in particular their indecomposability parameters. We find, at first order, that the corrections do not depend on these parameters nor even on the presence of Jordan cells. Though the corrections themselves are not universal, the ratios are universal and correctly reproduced by the conformal perturbative approach, to first order.Comment: 5 pages, published versio

DNA end resection by Dna2–Sgs1–RPA and its stimulation by Top3–Rmi1 and Mre11–Rad50–Xrs2

The repair of DNA double-strand breaks (DSBs) by homologous recombination requires processing of broken ends. For repair to start, the DSB must first be resected to generate a 3′-single-stranded DNA (ssDNA) overhang, which becomes a substrate for the DNA strand exchange protein, Rad51 (ref. 1). Genetic studies have implicated a multitude of proteins in the process, including helicases, nucleases and topoisomerases. Here we biochemically reconstitute elements of the resection process and reveal that it requires the nuclease Dna2, the RecQ-family helicase Sgs1 and the ssDNA-binding protein replication protein-A (RPA). We establish that Dna2, Sgs1 and RPA constitute a minimal protein complex capable of DNA resection in vitro. Sgs1 helicase unwinds the DNA to produce an intermediate that is digested by Dna2, and RPA stimulates DNA unwinding by Sgs1 in a species-specific manner. Interestingly, RPA is also required both to direct Dna2 nucleolytic activity to the 5′-terminated strand of the DNA break and to inhibit 3′ to 5′ degradation by Dna2, actions that generate and protect the 3′-ssDNA overhang, respectively. In addition to this core machinery, we establish that both the topoisomerase 3 (Top3) and Rmi1 complex and the Mre11–Rad50–Xrs2 complex (MRX) have important roles as stimulatory components. Stimulation of end resection by the Top3–Rmi1 heterodimer and the MRX proteins is by complex formation with Sgs1 (refs 5, 6), which unexpectedly stimulates DNA unwinding. We suggest that Top3–Rmi1 and MRX are important for recruitment of the Sgs1–Dna2 complex to DSBs. Our experiments provide a mechanistic framework for understanding the initial steps of recombinational DNA repair in eukaryotes

The endothelial glycocalyx prefers albumin for evoking shear stress-induced, nitric oxide-mediated coronary dilatation

Background: Shear stress induces coronary dilatation via production of nitric oxide ( NO). This should involve the endothelial glycocalyx ( EG). A greater effect was expected of albumin versus hydroxyethyl starch ( HES) perfusion, because albumin seals coronary leaks more effectively than HES in an EG-dependent way. Methods: Isolated hearts ( guinea pigs) were perfused at constant pressure with Krebs-Henseleit buffer augmented with 1/3 volume 5% human albumin or 6% HES ( 200/0.5 or 450/0.7). Coronary flow was also determined after EG digestion ( heparinase) and with nitro-L-arginine ( NO-L-Ag). Results: Coronary flow ( 9.50 +/- 1.09, 5.10 +/- 0.49, 4.87 +/- 1.19 and 4.15 +/- 0.09 ml/ min/ g for `albumin', `HES 200', `HES 450' and `control', respectively, n = 5-6) did not correlate with perfusate viscosity ( 0.83, 1.02, 1.24 and 0.77 cP, respectively). NO-L-Ag and heparinase diminished dilatation by albumin, but not additively. Alone NO-L-Ag suppressed coronary flow during infusion of HES 450. Electron microscopy revealed a coronary EG of 300 nm, reduced to 20 nm after heparinase. Cultured endothelial cells possessed an EG of 20 nm to begin with. Conclusions: Albumin induces greater endothelial shear stress than HES, despite lower viscosity, provided the EG contains negative groups. HES 450 causes some NO-mediated dilatation via even a rudimentary EG. Cultured endothelial cells express only a rudimentary glycocalyx, limiting their usefulness as a model system. Copyright (c) 2007 S. Karger AG, Basel

Video enhancement using adaptive spatio-temporal connective filter and piecewise mapping

This paper presents a novel video enhancement system based on an adaptive spatio-temporal connective (ASTC) noise filter and an adaptive piecewise mapping function (APMF). For ill-exposed videos or those with much noise, we first introduce a novel local image statistic to identify impulse noise pixels, and then incorporate it into the classical bilateral filter to form ASTC, aiming to reduce the mixture of the most two common types of noises - Gaussian and impulse noises in spatial and temporal directions. After noise removal, we enhance the video contrast with APMF based on the statistical information of frame segmentation results. The experiment results demonstrate that, for diverse low-quality videos corrupted by mixed noise, underexposure, overexposure, or any mixture of the above, the proposed system can automatically produce satisfactory results

Time delay between images of the lensed quasar UM673

We study brightness variations in the double lensed quasar UM673 (Q0142-100) with the aim of measuring the time delay between its two images. In the paper we combine our previously published observational data of UM673 obtained during the 2003 - 2005 seasons at the Maidanak Observatory with archival and recently observed Maidanak and CTIO UM673 data. We analyze the V, R and I-band light curves of the A and B images of UM673, which cover ten observational seasons from August 2001 to November 2010. We also analyze the time evolution of the difference in magnitudes between images A and B of UM673 over more than ten years. We find that the quasar exhibits both short-term (with amplitude of \sim 0.1 mag in the R band) and high-amplitude (\sim 0.3 mag) long-term variability on timescales of about several months and several years, respectively. These brightness variations are used to constrain the time delay between the images of UM673. From cross-correlation analysis of the A and B quasar light curves and error analysis we measure the mean time delay and its error of 89 \pm11 days. Given the input time delay of 88 days, the most probable value of the delay that can be recovered from light curves with the same statistical properties as the observed R-band light curves of UM673 is 95{+5/-16}{+14/-29} days (68 and 95 % confidence intervals). Analysis of the V - I color variations and V, R and I-band magnitude differences of the quasar images does not show clear evidence of the microlensing variations between 1998 and 2010.Comment: Submitted to A&A, 11 pages, 9 figure

Epigenetics as a mechanism driving polygenic clinical drug resistance

Aberrant methylation of CpG islands located at or near gene promoters is associated with inactivation of gene expression during tumour development. It is increasingly recognised that such epimutations may occur at a much higher frequency than gene mutation and therefore have a greater impact on selection of subpopulations of cells during tumour progression or acquisition of resistance to anticancer drugs. Although laboratory-based models of acquired resistance to anticancer agents tend to focus on specific genes or biochemical pathways, such 'one gene : one outcome' models may be an oversimplification of acquired resistance to treatment of cancer patients. Instead, clinical drug resistance may be due to changes in expression of a large number of genes that have a cumulative impact on chemosensitivity. Aberrant CpG island methylation of multiple genes occurring in a nonrandom manner during tumour development and during the acquisition of drug resistance provides a mechanism whereby expression of multiple genes could be affected simultaneously resulting in polygenic clinical drug resistance. If simultaneous epigenetic regulation of multiple genes is indeed a major driving force behind acquired resistance of patients' tumour to anticancer agents, this has important implications for biomarker studies of clinical outcome following chemotherapy and for clinical approaches designed to circumvent or modulate drug resistance