A generalization of heterochromatic graphs

In 2006, Suzuki, and Akbari & Alipour independently presented a necessary and sufficient condition for edge-colored graphs to have a heterochromatic spanning tree, where a heterochromatic spanning tree is a spanning tree whose edges have distinct colors. In this paper, we propose $f$-chromatic graphs as a generalization of heterochromatic graphs. An edge-colored graph is $f$-chromatic if each color $c$ appears on at most $f(c)$ edges. We also present a necessary and sufficient condition for edge-colored graphs to have an $f$-chromatic spanning forest with exactly $m$ components. Moreover, using this criterion, we show that a $g$-chromatic graph $G$ of order $n$ with $|E(G)|>\binom{n-m}{2}$ has an $f$-chromatic spanning forest with exactly $m$ ($1 \le m \le n-1$) components if $g(c) \le \frac{|E(G)|}{n-m}f(c)$ for any color $c$.Comment: 14 pages, 4 figure

Low Temperature Symmetry of Pyrochlore Oxide Cd2Re2O7

We report the X-ray study for the pyrochlore oxide Cd2Re2O7. Two symmetry-lowering structural transitions were observed at Ts1=200K and Ts2=120K. The former is of the second order from the ideal cubic pyrochlore structure with space group Fd-3m to a tetragonally distorted structure with I-4m2, while the latter is of the first order likely to another tetragonal space group I4122. We discuss the feature of the lattice deformation.Comment: 4 pages, 4 figure

Reprogramming of DNA methylation at NEUROD2-bound sequences during cortical neuron differentiation

The characteristics of DNA methylation changes that occur during neurogenesis in vivo remain unknown. We used whole-genome bisulfite sequencing to quantitate DNA cytosine modifications in differentiating neurons and their progenitors isolated from mouse brain at the peak of embryonic neurogenesis. Localized DNA hypomethylation was much more common than hypermethylation and often occurred at putative enhancers within genes that were upregulated in neurons and encoded proteins crucial for neuronal differ- entiation. The hypomethylated regions strongly overlapped with mapped binding sites of the key neuronal transcription factor NEUROD2. The 5-methylcytosine oxidase ten-eleven translocation 2 (TET2) interacted with NEUROD2, and its reaction product 5-hydroxymethylcytosine accumulated at the demethylated regions. NEUROD2-targeted differentially methylated regions retained higher methylation levels in Neurod2 knockout mice, and inducible expression of NEUROD2 caused TET2-associated demethylation at its in vivo binding sites. The data suggest that the reorganization of DNA methylation in developing neurons involves NEUROD2 and TET2-mediated DNA demethylation

Virtual Effects of Split SUSY in Higgs Productions at Linear Colliders

In split supersymmetry the gauginos and higgsinos are the only supersymmetric particles possibly accessible at foreseeable colliders like the CERN Large Hadron Collider (LHC) and the International Linear Collider (ILC). In order to account for the cosmic dark matter measured by WMAP, these gauginos and higgsinos are stringently constrained and could be explored at the colliders through their direct productions and/or virtual effects in some processes. The clean environment and high luminosity of the ILC render the virtual effects of percent level meaningful in unraveling the new physics effects. In this work we assume split supersymmetry and calculate the virtual effects of the WMAP-allowed gauginos and higgsinos in Higgs productions e+e- -> Z h and e+e- -> \nu_e \bar_\nu_e h through WW fusion at the ILC. We find that the production cross section of e+e- -> Zh can be altered by a few percent in some part of the WMAP-allowed parameter space, while the correction to the WW-fusion process e+e- -> \nu_e \bar_\nu_e h is below 1%. Such virtual effects are correlated with the cross sections of chargino pair productions and can offer complementary information in probing split supersymmetry at the colliders.Comment: more discussions added (7 pages, 10 figs

Differential spatial repositioning of activated genes in Biomphalaria glabrata snails infected with Schistosoma mansoni

Copyright @ 2014 Arican-Goktas et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This article has been made available through the Brunel Open Access Publishing Fund.Schistosomiasis is an infectious disease infecting mammals as the definitive host and fresh water snails as the intermediate host. Understanding the molecular and biochemical relationship between the causative schistosome parasite and its hosts will be key to understanding and ultimately treating and/or eradicating the disease. There is increasing evidence that pathogens that have co-evolved with their hosts can manipulate their hosts' behaviour at various levels to augment an infection. Bacteria, for example, can induce beneficial chromatin remodelling of the host genome. We have previously shown in vitro that Biomphalaria glabrata embryonic cells co-cultured with schistosome miracidia display genes changing their nuclear location and becoming up-regulated. This also happens in vivo in live intact snails, where early exposure to miracidia also elicits non-random repositioning of genes. We reveal differences in the nuclear repositioning between the response of parasite susceptible snails as compared to resistant snails and with normal or live, attenuated parasites. Interestingly, the stress response gene heat shock protein (Hsp) 70 is only repositioned and then up-regulated in susceptible snails with the normal parasite. This movement and change in gene expression seems to be controlled by the parasite. Other differences in the behaviour of genes support the view that some genes are responding to tissue damage, for example the ferritin genes move and are up-regulated whether the snails are either susceptible or resistant and upon exposure to either normal or attenuated parasite. This is the first time host genome reorganisation has been seen in a parasitic host and only the second time for any pathogen. We believe that the parasite elicits a spatio-epigenetic reorganisation of the host genome to induce favourable gene expression for itself and this might represent a fundamental mechanism present in the human host infected with schistosome cercariae as well as in other host-pathogen relationships.NIH and Sandler Borroughs Wellcome Travel Fellowshi

Prospects for heavy supersymmetric charged Higgs boson searches at hadron colliders

We investigate the production of a heavy charged Higgs boson at hadron colliders within the context of the MSSM. A detailed study is performed for all important production modes and basic background processes for the t\bar{t}b\bar{b} signature. In our analysis we include effects of initial and final state showering, hadronization, and principal detector effects. For the signal production rate we include the leading SUSY quantum effects at high \tan\beta>~ mt/mb. Based on the obtained efficiencies for the signal and background we estimate the discovery and exclusion mass limits of the charged Higgs boson at high values of \tan\beta. At the upgraded Tevatron the discovery of a heavy charged Higgs boson (MH^+ >~ 200 GeV) is impossible for the tree-level cross-section values. However, if QCD and SUSY effects happen to reinforce mutually, there are indeed regions of the MSSM parameter space which could provide 3\sigma evidence and, at best, 5\sigma charged Higgs boson discovery at the Tevatron for masses M_H^+<~ 300 GeV and M_H^+<~ 250 GeV, respectively, even assuming squark and gluino masses in the (500-1000) GeV range. On the other hand, at the LHC one can discover a H^+ as heavy as 1 TeV at the canonical confidence level of 5\sigma; or else exclude its existence at 95% C.L. up to masses ~ 1.5 TeV. Again the presence of SUSY quantum effects can be very important here as they may shift the LHC limits by a few hundred GeV.Comment: Latex2e, 44 pages, 15 figures, 6 tables, uses JHEP3.sty, axodraw.sty. Comments added. Discussion on QCD factors clarified. Added discussion on uncertainties. Change of presentation of Tables 4 and 5 and Fig.6. Results and conclusions unchanged. Version accepted in JHE

Reversing Blood Flows Act through klf2a to Ensure Normal Valvulogenesis in the Developing Heart

Heart valve anomalies are some of the most common congenital heart defects, yet neither the genetic nor the epigenetic forces guiding heart valve development are well understood. When functioning normally, mature heart valves prevent intracardiac retrograde blood flow; before valves develop, there is considerable regurgitation, resulting in reversing (or oscillatory) flows between the atrium and ventricle. As reversing flows are particularly strong stimuli to endothelial cells in culture, an attractive hypothesis is that heart valves form as a developmental response to retrograde blood flows through the maturing heart. Here, we exploit the relationship between oscillatory flow and heart rate to manipulate the amount of retrograde flow in the atrioventricular (AV) canal before and during valvulogenesis, and find that this leads to arrested valve growth. Using this manipulation, we determined that klf2a is normally expressed in the valve precursors in response to reversing flows, and is dramatically reduced by treatments that decrease such flows. Experimentally knocking down the expression of this shear-responsive gene with morpholine antisense oligonucleotides (MOs) results in dysfunctional valves. Thus, klf2a expression appears to be necessary for normal valve formation. This, together with its dependence on intracardiac hemodynamic forces, makes klf2a expression an early and reliable indicator of proper valve development. Together, these results demonstrate a critical role for reversing flows during valvulogenesis and show how relatively subtle perturbations of normal hemodynamic patterns can lead to both major alterations in gene expression and severe valve dysgenesis

Bax-Induced Apoptosis in Leber's Congenital Amaurosis: A Dual Role in Rod and Cone Degeneration

Pathogenesis in the Rpe65−/− mouse model of Leber's congenital amaurosis (LCA) is characterized by a slow and progressive degeneration of the rod photoreceptors. On the opposite, cones degenerate rapidly at early ages. Retinal degeneration in Rpe65−/− mice, showing a null mutation in the gene encoding the retinal pigment epithelium 65-kDa protein (Rpe65), was previously reported to depend on continuous activation of a residual transduction cascade by unliganded opsin. However, the mechanisms of apoptotic signals triggered by abnormal phototransduction remain elusive. We previously reported that activation of a Bcl-2-dependent pathway was associated with apoptosis of rod photoreceptors in Rpe65−/− mice during the course of the disease. In this study we first assessed whether activation of Bcl-2-mediated apoptotic pathway was dependent on constitutive activation of the visual cascade through opsin apoprotein. We then challenged the direct role of pro-apoptotic Bax protein in triggering apoptosis of rod and cone photoreceptors

Supersymmetric effects in top quark decay into polarized W-boson

We investigate the one-loop supersymmetric QCD (SUSY-QCD) and electroweak (SUSY-EW) corrections to the top quark decay into a b-quark and a longitudinal or transverse W-boson. The corrections are presented in terms of the longitudinal ratio \Gamma(t-->W_L b)/\Gamma(t--> W b) and the transverse ratio \Gamma(t-->W_- b)/\Gamma(t--> W b). In most of the parameter space, both SUSY-QCD and SUSY-EW corrections to these ratios are found to be less than 1% in magnitude and they tend to have opposite signs. The corrections to the total width \Gamma(t-->W b) are also presented for comparison with the existing results in the literature. We find that our SUSY-EW corrections to the total width differ significantly from previous studies: the previous studies give a large correction of more than 10% in magnitude for a large part of the parameter space while our results reach only few percent at most.Comment: Version in PRD (explanation and refs added