6,894 research outputs found

    An O(N) symmetric extension of the Sine-Gordon Equation

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    We discuss an O(N) exension of the Sine-Gordon (S-G)equation which allows us to perform an expansion around the leading order in large-N result using Path-Integral methods. In leading order we show our methods agree with the results of a variational calculation at large-N. We discuss the striking differences for a non-polynomial interaction between the form for the effective potential in the Gaussian approximation that one obtains at large-N when compared to the N=1 case. This is in contrast to the case when the classical potential is a polynomial in the field and no such drastic differences occur. We find for our large-N extension of the Sine-Gordon model that the unbroken ground state is unstable as one increases the coupling constant (as it is for the original S-G equation) and we determine the stability criteria.Comment: 21 pages, Latex (Revtex4) v3:minor grammatical changes and addition

    Star Formation and the Growth of Stellar Mass

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    Recent observations have demonstrated a significant growth in the integrated stellar mass of the red sequence since z=1, dominated by a steadily increasing number of galaxies with stellar masses M* < 10^11 M_sun. In this paper, we use the COMBO-17 photometric redshift survey in conjunction with deep Spitzer 24 micron data to explore the relationship between star formation and the growth of stellar mass. We calculate `star formation rate functions' in four different redshift slices, splitting also into contributions from the red sequence and blue cloud for the first time. We find that the growth of stellar mass since z=1 is consistent with the integrated star formation rate. Yet, most of the stars formed are in blue cloud galaxies. If the stellar mass already in, and formed in, z<1 blue cloud galaxies were to stay in the blue cloud the total stellar mass in blue galaxies would be dramatically overproduced. We explore the expected evolution of stellar mass functions, finding that in this picture the number of massive M* > 3x10^10 M_sun blue galaxies would also be overproduced; i.e., most of the new stars formed in blue cloud galaxies are in the massive galaxies. We explore a simple truncation scenario in which these `extra' blue galaxies have their star formation suppressed by an unspecified mechanism or mechanisms; simple cessation of star formation in these extra blue galaxies is approximately sufficient to build up the red sequence at M*<10^11 M_sun.Comment: 9 Pages; ApJ in pres

    On the Nonlinear Geometric Behaviour of Flared Folding Wingtips

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    The netrin receptor DCC is required in the pubertal organization of mesocortical dopamine circuitry

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    Netrins are guidance cues involvedinneural connectivity.Wehave shownthat the netrin-1 receptor DCC (deletedin colorectal cancer) is involvedinthefunctionalorganizationofthemesocorticolimbic dopamine(DA)system.Adult micewithaheterozygousloss-of-function mutation in dcc exhibit changes in indexes of DA function, including DA-related behaviors. These phenotypes are only observed after puberty,acritical periodinthe maturationofthe mesocortical DAprojection. Here, weexamined whether dcc heterozygous mice exhibit structural changes in medial prefrontal cortex (mPFC) DA synaptic connectivity, before and after puberty. Stereological counts of tyrosine-hydroxylase (TH)-positive varicosities were increased in the cingulate 1 and prelimbic regions of the pregenual mPFC. dcc heterozygous mice also exhibited alterations in the size, complexity, and dendritic spine density of mPFC layer V pyramidal neuron basilar dendritic arbors. Remarkably, these presynaptic and postsynaptic partner phenotypes were not observed in juvenile mice, suggesting that DCC selectively influences the extensive branching and synaptic differentiation that occurs in the maturing mPFC DA circuitatpuberty.Immunolabelingexperimentsinwild-typemice demonstratedthat DCCissegregatedtoTH-positivefibersinnervating the nucleus accumbens, with only scarce DCC labeling in mPFC TH-positive fibers. Netrin had an inverted target expression pattern. Thus, DCC-mediated netrin-1 signaling may influence the formation/maintenance of mesocorticolimbic DA topography. In support of this, we report that dcc heterozygous mice exhibit a twofold increase in the density of mPFC DCC/TH-positive varicosities. Our results implicate DCC-mediated netrin-1 signaling in the establishment of mPFC DA circuitry during puberty

    Experimental and Numerical Nonlinear Stability Analysis of Wings Incorporating Flared Folding Wingtips

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    Recent studies have considered the use of wings incorporating flared folding wingtips (FFWTs) to enable higher aspect ratios (reducing overall induced drag) while also reducing gust loading and meeting airport operational requirements. This paper presents the first experimental research into the nonlinear dynamic behavior of a wing incorporating an FFWT. Wind-tunnel tests were conducted at a range of velocities below and beyond the linear flutter boundary. The experimental findings are compared with results obtained from continuation and bifurcation analyses on a representative low-fidelity numerical model. The results show that beyond the linear flutter boundary, stable limit cycle oscillations form, which is dependent on the flare angle, are bounded by either geometric or aerodynamic nonlinearities. Also presented is the effect of a wingtip trim tab on the stability boundary of a wing incorporating FFWTs. It is found that the tab angle can significantly alter the stability boundary of the system, indicating that the choice of camber is an important parameter when considering the stability boundary of FFWTs and that a moveable control surface on an FFWT could be used “in flight” to extend the stability boundary of an aircraft

    Folding Wingtips for Improved Roll Performance

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    The lack of star formation gradients in galaxy groups up to z~1.6

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    In the local Universe, galaxy properties show a strong dependence on environment. In cluster cores, early type galaxies dominate, whereas star-forming galaxies are more and more common in the outskirts. At higher redshifts and in somewhat less dense environments (e.g. galaxy groups), the situation is less clear. One open issue is that of whether and how the star formation rate (SFR) of galaxies in groups depends on the distance from the centre of mass. To shed light on this topic, we have built a sample of X-ray selected galaxy groups at 0<z<1.6 in various blank fields (ECDFS, COSMOS, GOODS). We use a sample of spectroscopically confirmed group members with stellar mass M >10^10.3 M_sun in order to have a high spectroscopic completeness. As we use only spectroscopic redshifts, our results are not affected by uncertainties due to projection effects. We use several SFR indicators to link the star formation (SF) activity to the galaxy environment. Taking advantage of the extremely deep mid-infrared Spitzer MIPS and far-infrared Herschel PACS observations, we have an accurate, broad-band measure of the SFR for the bulk of the star-forming galaxies. We use multi-wavelength SED fitting techniques to estimate the stellar masses of all objects and the SFR of the MIPS and PACS undetected galaxies. We analyse the dependence of the SF activity, stellar mass and specific SFR on the group-centric distance, up to z~1.6, for the first time. We do not find any correlation between the mean SFR and group-centric distance at any redshift. We do not observe any strong mass segregation either, in agreement with predictions from simulations. Our results suggest that either groups have a much smaller spread in accretion times with respect to the clusters and that the relaxation time is longer than the group crossing time.Comment: Accepted for publication in MNRA

    The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology

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    The role of endomyocardial biopsy (EMB) in the diagnosis and treatment of adult and pediatric cardiovascular disease remains controversial, and the practice varies widely even among cardiovascular centers of excellence. A need for EMB exists because specific myocardial disorders that have unique prognoses and treatment are seldom diagnosed by noninvasive testing.1 Informed clinical decision making that weighs the risks of EMB against the incremental diagnostic, prognostic, and therapeutic value of the procedure is especially challenging for nonspecialists because the relevant published literature is usually cited according to specific cardiac diseases, which are only diagnosed after EM

    EGF regulates survivin stability through the Raf-1/ERK pathway in insulin-secreting pancreatic β-cells

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    <p>Abstract</p> <p>Background</p> <p>Postnatal expansion of the pancreatic β-cell mass is required to maintain glucose homeostasis immediately after birth. This β-cell expansion is regulated by multiple growth factors, including glucose, insulin, insulin-like growth factor (IGF-1) and epidermal growth factor (EGF). These mitogens signal through several downstream pathways (AKT, ERK, STAT3, and JNK) to regulate the survival and proliferation of β-cells. Survivin, an oncofetal protein with both pro-proliferative and anti-apoptotic properties, is a known transcriptional target of both IGF-1 and EGF in cancer cells. Here, we analyzed the effects of the β-cell mitogens IGF-1 and EGF on survivin regulation in the established pancreatic β-cell model cell lines, MIN6 and INS-1 and in primary mouse islets.</p> <p>Results</p> <p>In pancreatic β-cells, treatment with glucose, insulin, or EGF increased survivin protein levels at early time points. By contrast, no significant effects on survivin were observed following IGF-1 treatment. EGF-stimulated increases in survivin protein were abrogated in the presence of downstream inhibitors of the Raf-1/MEK/ERK pathway. EGF had no significant effect on <it>survivin </it>transcription however it prolonged the half-life of the survivin protein and stabilized survivin protein levels by inhibiting surviving ubiquitination.</p> <p>Conclusions</p> <p>This study defines a novel mechanism of survivin regulation by EGF through the Raf-1/MEK/ERK pathway in pancreatic β-cells, via prolongation of survivin protein half-life and inhibition of the ubiquitin-mediated proteasomal degradation pathway. This mechanism may be important for regulating β-cell expansion after birth.</p
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