2,422 research outputs found

    LSR/angulin-1 is a tricellular tight junction protein involved in blood-brain barrier formation.

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    The blood-brain barrier (BBB) is a term used to describe the unique properties of central nervous system (CNS) blood vessels. One important BBB property is the formation of a paracellular barrier made by tight junctions (TJs) between CNS endothelial cells (ECs). Here, we show that Lipolysis-stimulated lipoprotein receptor (LSR), a component of paracellular junctions at points in which three cell membranes meet, is greatly enriched in CNS ECs compared with ECs in other nonneural tissues. We demonstrate that LSR is specifically expressed at tricellular junctions and that its expression correlates with the onset of BBB formation during embryogenesis. We further demonstrate that the BBB does not seal during embryogenesis in Lsr knockout mice with a leakage to small molecules. Finally, in mouse models in which BBB was disrupted, including an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and a middle cerebral artery occlusion (MCAO) model of stroke, LSR was down-regulated, linking loss of LSR and pathological BBB leakage

    Super-lattice, rhombus, square, and hexagonal standing waves in magnetically driven ferrofluid surface

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    Standing wave patterns that arise on the surface of ferrofluids by (single frequency) parametric forcing with an ac magnetic field are investigated experimentally. Depending on the frequency and amplitude of the forcing, the system exhibits various patterns including a superlattice and subharmonic rhombuses as well as conventional harmonic hexagons and subharmonic squares. The superlattice arises in a bicritical situation where harmonic and subharmonic modes collide. The rhombic pattern arises due to the non-monotonic dispersion relation of a ferrofluid

    Perturbative QCD analysis of BϕKB \to \phi K^* decays

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    We study the first observed charmless BVVB\to VV modes, the BϕKB\to\phi K^* decays, in perturbative QCD formalism. The obtained branching ratios B(BϕK)15×106B(B\to\phi K^*)\sim 15 \times 10^{-6} are larger than 9×106\sim 9\times 10^{-6} from QCD factorization. The comparison of the predicted magnitudes and phases of the different helicity amplitudes, and branching ratios with experimental data can test the power counting rules, the evaluation of annihilation contributions, and the mechanism of dynamical penguin enhancement in perturbative QCD, respectively.Comment: 14 pages, 2 tables, brief disscussion on hard sacle added, version to appear in PR

    Innovation Contests with Entry Auction

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    We consider procurement of an innovation from heterogeneous sellers. Innovations are random but depend on unobservable effort and private information. We compare two procurement mechanisms where potential sellers first bid in an auction for admission to an innovation contest. After the contest, an innovation is procured employing either a fixed prize or a first-price auction. We characterize Bayesian Nash equilibria such that both mechanisms are payoff-equivalent and induce the same efforts and innovations. In these equilibria, signaling in the entry auction does not occur since contestants play a simple strategy that does not depend on rivals' private information

    Effect of a reduction in glomerular filtration rate after nephrectomy on arterial stiffness and central hemodynamics: rationale and design of the EARNEST study

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    Background: There is strong evidence of an association between chronic kidney disease (CKD) and cardiovascular disease. To date, however, proof that a reduction in glomerular filtration rate (GFR) is a causative factor in cardiovascular disease is lacking. Kidney donors comprise a highly screened population without risk factors such as diabetes and inflammation, which invariably confound the association between CKD and cardiovascular disease. There is strong evidence that increased arterial stiffness and left ventricular hypertrophy and fibrosis, rather than atherosclerotic disease, mediate the adverse cardiovascular effects of CKD. The expanding practice of live kidney donation provides a unique opportunity to study the cardiovascular effects of an isolated reduction in GFR in a prospective fashion. At the same time, the proposed study will address ongoing safety concerns that persist because most longitudinal outcome studies have been undertaken at single centers and compared donor cohorts with an inappropriately selected control group.<p></p> Hypotheses: The reduction in GFR accompanying uninephrectomy causes (1) a pressure-independent increase in aortic stiffness (aortic pulse wave velocity) and (2) an increase in peripheral and central blood pressure.<p></p> Methods: This is a prospective, multicenter, longitudinal, parallel group study of 440 living kidney donors and 440 healthy controls. All controls will be eligible for living kidney donation using current UK transplant criteria. Investigations will be performed at baseline and repeated at 12 months in the first instance. These include measurement of arterial stiffness using applanation tonometry to determine pulse wave velocity and pulse wave analysis, office blood pressure, 24-hour ambulatory blood pressure monitoring, and a series of biomarkers for cardiovascular and bone mineral disease.<p></p> Conclusions: These data will prove valuable by characterizing the direction of causality between cardiovascular and renal disease. This should help inform whether targeting reduced GFR alongside more traditional cardiovascular risk factors is warranted. In addition, this study will contribute important safety data on living kidney donors by providing a longitudinal assessment of well-validated surrogate markers of cardiovascular disease, namely, blood pressure and arterial stiffness. If any adverse effects are detected, these may be potentially reversed with the early introduction of targeted therapy. This should ensure that kidney donors do not come to long-term harm and thereby preserve the ongoing expansion of the living donor transplant program.<p></p&gt

    Nonfactorizable contributions to BD()MB \to D^{(*)} M decays

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    While the factorization assumption works well for many two-body nonleptonic BB meson decay modes, the recent measurement of BˉD()0M0\bar B\to D^{(*)0}M^0 with M=πM=\pi, ρ\rho and ω\omega shows large deviation from this assumption. We analyze the BD()MB\to D^{(*)}M decays in the perturbative QCD approach based on kTk_T factorization theorem, in which both factorizable and nonfactorizable contributions can be calculated in the same framework. Our predictions for the Bauer-Stech-Wirbel parameters, a2/a1=0.43±0.04|a_2/a_1|= 0.43\pm 0.04 and Arg(a2/a1)42Arg(a_2/a_1)\sim -42^\circ and a2/a1=0.47±0.05|a_2/a_1|= 0.47\pm 0.05 and Arg(a2/a1)41Arg(a_2/a_1)\sim -41^\circ, are consistent with the observed BDπB\to D\pi and BDπB\to D^*\pi branching ratios, respectively. It is found that the large magnitude a2|a_2| and the large relative phase between a2a_2 and a1a_1 come from color-suppressed nonfactorizable amplitudes. Our predictions for the Bˉ0D()0ρ0{\bar B}^0\to D^{(*)0}\rho^0, D()0ωD^{(*)0}\omega branching ratios can be confronted with future experimental data.Comment: 25 pages with Latex, axodraw.sty, 6 figures and 5 tables, Version published in PRD, Added new section 5 and reference
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