Constraining the low-energy pion electromagnetic form factor with space-like and phase of time-like data

The Taylor coefficients c and d of the EM form factor of the pion are constrained using analyticity, knowledge of the phase of the form factor in the time-like region, 4m(pi)(2) <= t <= t(in) and its value at one space-like point, using as input the (g - 2) of the muon. This is achieved using the technique of Lagrange multipliers, which gives a transparent expression for the corresponding bounds. We present a detailed study of the sensitivity of the bounds to the choice of time-like phase and errors present in the space-like data, taken from recent experiments. We find that our results constrain c stringently. We compare our results with those in the literature and find agreement with the chiral perturbation-theory results for c. We obtain d similar to O(10) GeV-6 when c is set to the chiral perturbation-theory values.

Characterization of the human SLC22A18 gene promoter and its regulation by the transcription factor Sp1

SLC22A18, a poly-specific organic cation transporter, is paternally imprinted in humans and mice. It shows loss-of-heterozygosity in childhood and adult tumors, and gain-of-imprinting in hepatocarcinomas and breast cancers. Despite the importance of this gene, its transcriptional regulation has not been studied, and the promoter has not yet been characterized. We therefore set out to identify the potential cis-regulatory elements including the promoter of this gene. The luciferase reporter assay in human cells indicated that a region from -120 by to +78 by is required for the core promoter activity. No consensus TATA or CHAT boxes were found in this region, but two Sp1 binding sites were conserved in human, chimpanzee, mouse and rat. Mutational analysis of the two Sp1 sites suggested their requirement for the promoter activity. Chromatin-immunoprecipitation showed binding of Sp1 to the promoter region in vivo. Overexpression of Sp1 in Drosophila Sp1-null SL2 cells suggested that Sp1 is the transactivator of the promoter. The human core promoter was functional in mouse 3T3 and monkey COS7 cells. We found a CpG island which spanned the core promoter and exon 1. COBRA technique did not reveal promoter methylation in 10 normal oral tissues, 14 oral tumors, and two human cell lines HuH7 and A549. This study provides the first insight into the mechanism that controls expression of this imprinted tumor suppressor gene. A COBRA-based assay has been developed to look for promoter methylation in different cancers. The present data will help to understand the regulation of this gene and its role in tumorigenesis. (C) 2008 Elsevier B.V. All rights reserved.

Characterization of the human SLC22A18 gene promoter and its regulation by the transcription factor Sp1

SLC22A18, a poly-specific organic cation transporter, is paternally imprinted in humans and mice. It shows loss-of-heterozygosity in childhood and adult tumors, and gain-of-imprinting in hepatocarcinomas and breast cancers. Despite the importance of this gene, its transcriptional regulation has not been studied, and the promoter has not yet been characterized. We therefore set out to identify the potential cis-regulatory elements including the promoter of this gene. The luciferase reporter assay in human cells indicated that a region from -120 by to +78 by is required for the core promoter activity. No consensus TATA or CHAT boxes were found in this region, but two Sp1 binding sites were conserved in human, chimpanzee, mouse and rat. Mutational analysis of the two Sp1 sites suggested their requirement for the promoter activity. Chromatin-immunoprecipitation showed binding of Sp1 to the promoter region in vivo. Overexpression of Sp1 in Drosophila Sp1-null SL2 cells suggested that Sp1 is the transactivator of the promoter. The human core promoter was functional in mouse 3T3 and monkey COS7 cells. We found a CpG island which spanned the core promoter and exon 1. COBRA technique did not reveal promoter methylation in 10 normal oral tissues, 14 oral tumors, and two human cell lines HuH7 and A549. This study provides the first insight into the mechanism that controls expression of this imprinted tumor suppressor gene. A COBRA-based assay has been developed to look for promoter methylation in different cancers. The present data will help to understand the regulation of this gene and its role in tumorigenesis. (C) 2008 Elsevier B.V. All rights reserved.

Cooperative Regulation of NOTCH1 Protein-Phosphatidylinositol 3-Kinase (PI3K) Signaling by NOD1, NOD2, and TLR2 Receptors Renders Enhanced Refractoriness to Transforming Growth Factor-beta (TGF-beta)- or Cytotoxic T-lymphocyte Antigen 4 (CTLA-4)-mediated Impairment of Human Dendritic Cell Maturation

Dendritic cells (DCs) as sentinels of the immune system are important for eliciting both primary and secondary immune responses to a plethora of microbial pathogens. Cooperative stimulation of a complex set of pattern-recognition receptors, including TLR2 and nucleotide-binding oligomerization domain (NOD)-like receptors on DCs, acts as a rate-limiting factor in determining the initiation and mounting of the robust immune response. It underscores the need for ``decoding'' these multiple receptor interactions. In this study, we demonstrate that TLR2 and NOD receptors cooperatively regulate functional maturation of human DCs. Intriguingly, synergistic stimulation of TLR2 and NOD receptors renders enhanced refractoriness to TGF-beta- or CTLA-4-mediated impairment of human DC maturation. Signaling perturbation data suggest that NOTCH1-PI3K signaling dynamics assume critical importance in TLR2- and NOD receptor-mediated surmounting of CTLA-4- and TGF-beta -suppressed maturation of human DCs. Interestingly, the NOTCH1-PI3K signaling axis holds the capacity to regulate DC functions by virtue of PKC delta-MAPK-dependent activation of NF-kappa B. This study provides mechanistic and functional insights into TLR2-and NOD receptor-mediated regulation of DC functions and unravels NOTCH1-PI3K as a signaling cohort for TLR2 and NOD receptors. These findings serve in building a conceptual foundation for the design of improved strategies for adjuvants and immunotherapies against infectious diseases.

A constant factor approximation algorithm for boxicity of circular arc graphs

Boxicity of a graph G(V, E) is the minimum integer k such that G can be represented as the intersection graph of k-dimensional axis parallel boxes in Rk. Equivalently, it is the minimum number of interval graphs on the vertex set V such that the intersection of their edge sets is E. It is known that boxicity cannot be approximated even for graph classes like bipartite, co-bipartite and split graphs below O(n0.5-ε)-factor, for any ε > 0 in polynomial time unless NP = ZPP. Till date, there is no well known graph class of unbounded boxicity for which even an nε-factor approximation algorithm for computing boxicity is known, for any ε < 1. In this paper, we study the boxicity problem on Circular Arc graphs - intersection graphs of arcs of a circle. We give a (2+ 1/k)-factor polynomial time approximation algorithm for computing the boxicity of any circular arc graph along with a corresponding box representation, where k ≥ 1 is its boxicity. For Normal Circular Arc(NCA) graphs, with an NCA model given, this can be improved to an additive 2-factor approximation algorithm. The time complexity of the algorithms to approximately compute the boxicity is O(mn+n2) in both these cases and in O(mn+kn2) which is at most O(n3) time we also get their corresponding box representations, where n is the number of vertices of the graph and m is its number of edges. The additive 2-factor algorithm directly works for any Proper Circular Arc graph, since computing an NCA model for it can be done in polynomial time.

A Hybrid Parallel Algorithm for Computing and Tracking Level Set Topology

The contour tree is a topological abstraction of a scalar field that captures evolution in level set connectivity. It is an effective representation for visual exploration and analysis of scientific data. We describe a work-efficient, output sensitive, and scalable parallel algorithm for computing the contour tree of a scalar field defined on a domain that is represented using either an unstructured mesh or a structured grid. A hybrid implementation of the algorithm using the GPU and multi-core CPU can compute the contour tree of an input containing 16 million vertices in less than ten seconds with a speedup factor of upto 13. Experiments based on an implementation in a multi-core CPU environment show near-linear speedup for large data sets.

A constant factor approximation algorithm for boxicity of circular arc graphs

The boxicity (resp. cubicity) of a graph G(V, E) is the minimum integer k such that G can be represented as the intersection graph of axis parallel boxes (resp. cubes) in R-k. Equivalently, it is the minimum number of interval graphs (resp. unit interval graphs) on the vertex set V, such that the intersection of their edge sets is E. The problem of computing boxicity (resp. cubicity) is known to be inapproximable, even for restricted graph classes like bipartite, co-bipartite and split graphs, within an O(n(1-epsilon))-factor for any epsilon > 0 in polynomial time, unless NP = ZPP. For any well known graph class of unbounded boxicity, there is no known approximation algorithm that gives n(1-epsilon)-factor approximation algorithm for computing boxicity in polynomial time, for any epsilon > 0. In this paper, we consider the problem of approximating the boxicity (cubicity) of circular arc graphs intersection graphs of arcs of a circle. Circular arc graphs are known to have unbounded boxicity, which could be as large as Omega(n). We give a (2 + 1/k) -factor (resp. (2 + log n]/k)-factor) polynomial time approximation algorithm for computing the boxicity (resp. cubicity) of any circular arc graph, where k >= 1 is the value of the optimum solution. For normal circular arc (NCA) graphs, with an NCA model given, this can be improved to an additive two approximation algorithm. The time complexity of the algorithms to approximately compute the boxicity (resp. cubicity) is O(mn + n(2)) in both these cases, and in O(mn + kn(2)) = O(n(3)) time we also get their corresponding box (resp. cube) representations, where n is the number of vertices of the graph and m is its number of edges. Our additive two approximation algorithm directly works for any proper circular arc graph, since their NCA models can be computed in polynomial time. (C) 2014 Elsevier B.V. All rights reserved.

Context dependent non canonical WNT signaling mediates activation of fibroblasts by transforming growth factor-beta

Actions of transforming growth factor-beta are largely context dependent. For instance, TGF-beta is growth inhibitory to epithelial cells and many tumor cell-lines while it stimulates the growth of mesenchymal cells. TGF-beta also activates fibroblast cells to a myofibroblastic phenotype. In order to understand how the responsiveness of fibroblasts to TGF-beta would change in the context of transformation, we have compared the differential gene regulation by TGF-beta in immortal fibroblasts (hFhTERT), transformed fibroblasts (hFhTERT-LTgRAS) and a human fibrosarcoma cell-line (HT1080). The analysis revealed regulation of 6735, 4163, and 3478 probe-sets by TGF-beta in hFhTERT, hFhTERT-LTgRAS and HT1080 cells respectively. Intriguingly, 5291 probe-sets were found to be either regulated in hFhTERT or hFhTERT-LTgRAS cells while 2274 probe-sets were regulated either in hFhTERT or HT1080 cells suggesting that the response of immortal hFhTERT cells to TGF-beta is vastly different compared to the response of both the transformed cells hFhTERT-LTgRAS and HT1080 to TGF-beta. Strikingly, WNT pathway showed enrichment in the hFhTERT cells in Gene Set Enrichment Analysis. Functional studies showed induction of WNT4 by TGF-beta in hFhTERT cells and TGF-beta conferred action of these cells was mediated by WNT4. While TGF-beta activated both canonical and non-canonical WNT pathways in hFhTERT cells, Erk1/2 and p38 Mitogen Activated Protein Kinase pathways were activated in hFhTERT-LTgRAS and HT1080 cells. This suggests that transformation of immortal hFhTERT cells by SV40 large T antigen and activated RAS caused a switch in their response to TGF-beta which matched with the response of HT1080 cells to TGF-beta. These data suggest context dependent activation of non-canonical signaling by TGF-beta. (C) 2015 Published by Elsevier Inc.

The potential role of a late gene expression factor, lef2, from Bombyx mori nuclear polyhedrosis virus in very late gene transcription and DNA replication

Several late gene expression factors (Lefs) have been implicated in fostering high levels of transcription from the very late gene promoters of polyhedrin and p10 from baculoviruses. We cloned and characterized from Bombyx mori nuclear polyhedrosis virus a late gene expression factor (Bmlef2) that encodes a 209-amino-acid protein harboring a Cys-rich C-terminal domain. The temporal transcription profiles of lef2 revealed a 1.2-kb transcript in both delayed early and late periods after virus infection. Transcription start site mapping identified the presence of an aphidicolin-sensitive late transcript arising from a TAAG motif located at -352 nucleotides and an aphidicolin-insensitive early transcript originating from a TTGT motif located 35 nucleotides downstream to a TATA box at -312 nucleotides, with respect to the +1 ATG of lef2. BmLef2 trans-activated very late gene expression from both polyhedrin and p10 promoters in transient expression assays. Internal deletion of the Cys-rich domain from the C-terminal region abolished the transcriptional activation. Inactivation of Lef2 synthesis by antisense lef2 transcripts drastically reduced the very late gene transcription but showed little effect on the expression from immediate early promoter. Decrease in viral DNA synthesis and a reduction in virus titer were observed only when antisense lef2 was expressed under the immediate early (ie-1) promoter. Furthermore, the antisense experiments suggested that lef2 plays a direct role in very late gene transcription.

2.5-dimensional solution of the advective accretion disk:a self-similar approach

We provide a 2.5-dimensional solution to a complete set of viscous hydrodynamical equations describing accretion- induced outflows and plausible jets around black holes/compact objects. We prescribe a self-consistent advective disk-outflow coupling model, which explicitly includes the information of vertical flux. Inter-connecting dynamics of an inflow-outflow system essentially upholds the conservation laws. We provide a set of analytical family of solutions through a self-similar approach. The flow parameters of the disk-outflow system depend strongly on the viscosity parameter α and the cooling factor.

A Current Source Inverter Fed Induction Motor Drive with Power Factor Angle Control Using Microprocessor

This paper describes a method of adjusting the stator power factor angle for the control of an induction motor fed from a current source inverter (CSI) based on the concept of space vectors (or park vectors). It is shown that under steady state, if the torque angle is kept constant over the entire operating range, it has the advantage of keeping the slip frequency constant. This can be utilized to dispose of the speed feedback and simplify the control scheme for the drive, such that the stator voltage integral zero crossings alone can be used as a feedback for deciding the triggering instants of the CSI thyristors under stable operation of the system. A closed-loop control strategy is developed for the drive based on this principle, using a microprocessor-based control system and is implemented on a laboratory prototype CSI fed induction motor drive.

Hybrid constant factor incremental delta modulators

The paper presents a new adaptive delta modulator, called the hybrid constant factor incremental delta modulator (HCFIDM), which uses instantaneous as well as syllabic adaptation of the step size. Three instantaneous algorithms have been used: two new instantaneous algorithms (CFIDM-3 and CFIDM-2) and the third, Song's voice ADM (SVADM). The quantisers have been simulated on a digital computer and their performances studied. The figure of merit used is the SNR with correlated, /?C-shaped Gaussian signals and real speech as the input. The results indicate that the hybrid technique is superior to the nonhybrid adaptive quantisers. Also, the two new instantaneous algorithms developed have improved SNR and fast response to step inputs as compared to the earlier systems.

Modeling growth of hydrogen bubbles in aluminum castings using the level-set method

A new approach is proposed to solve for the growth as well as the movement of hydrogen bubbles during solidification in aluminum castings. A level-set methodology has been adopted to handle this multiphase phenomenon. A microscale domain is considered and the growth and movement of hydrogen bubbles in this domain has been studied. The growth characteristics of hydrogen bubbles have been evaluated under free growth conditions in a melt having a hydrogen input caused b solidification occurring around the microdomain.