144 research outputs found

    Chiral-even axial twist-3 GPDs of the proton from lattice QCD

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    This work presents the first lattice-QCD calculation of the twist-3 axial quark GPDs for the proton using the large-momentum effective theory approach. We calculate matrix elements with momentum-boosted proton states and a non-local axial operator. The calculation is performed using one ensemble of two degenerate light, a strange and a charm quark (Nf=2+1+1N_f=2+1+1) of maximally twisted mass fermions with a clover term. The ensemble has a volume 323×6432^3\times64, lattice spacing 0.0934 fm, and corresponds to a pion mass of 260 MeV. The matrix elements are calculated for three values of the proton momentum, namely 0.83, 1.25, and 1.67 GeV. The light-cone GPDs are defined in the symmetric frame, which we implement here with a (negative) 4-momentum transfer squared of 0.69, 1.38, and 2.76 GeV2^2, all at zero skewness. We also conduct several consistency checks, including assessing the local limit of the twist-3 GPDs and examining the Burkhardt-Cottingham-type as well as Efremov-Teryaev-Leader-type sum rules.Comment: 22 pages, 17 figure

    Advancing the Development of the Magneto-Active Slosh Control (MaSC) System for Spacecraft and Launch Vehicles

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    The Magneto-Active Propellant Management Device (MAPMD) system is designed to address safety hazards in liquid-propellant spaceflight caused by sloshing. This innovative system of Magneto-Active Slosh Control surpasses traditional passive slosh baffles by reducing mass, improving surface wave suppression, and minimizing volumetric intrusion (Santhanam 2012). In prior fight experiments conducted in collaboration between Embry-Riddle Aeronautical University and Carthage College, remnant slosh suppression was observed, however the effective slosh damping did not meet our expectations due to inadequate control forces. We are redesigning the magnetic membrane with multiple layers of ultrahigh-permeability metallic glass film and are developing an optimized configuration of current-carrying coils to increase magnetic force and field performance. These advancements are expected to elevate the MAPMD system\u27s Technology Readiness Level (TRL) from 3 to 4 in order to pave the way for microgravity flight testing. The MAPMD system promises to enhance the safety and performance of liquid-propellant spaceflight by actively managing slosh dynamics

    Downregulation of 26S proteasome catalytic activity promotes epithelial-mesenchymal transition.

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    The epithelial-mesenchymal transition (EMT) endows carcinoma cells with phenotypic plasticity that can facilitate the formation of cancer stem cells (CSCs) and contribute to the metastatic cascade. While there is substantial support for the role of EMT in driving cancer cell dissemination, less is known about the intracellular molecular mechanisms that govern formation of CSCs via EMT. Here we show that β2 and β5 proteasome subunit activity is downregulated during EMT in immortalized human mammary epithelial cells. Moreover, selective proteasome inhibition enabled mammary epithelial cells to acquire certain morphologic and functional characteristics reminiscent of cancer stem cells, including CD44 expression, self-renewal, and tumor formation. Transcriptomic analyses suggested that proteasome-inhibited cells share gene expression signatures with cells that have undergone EMT, in part, through modulation of the TGF-β signaling pathway. These findings suggest that selective downregulation of proteasome activity in mammary epithelial cells can initiate the EMT program and acquisition of a cancer stem cell-like phenotype. As proteasome inhibitors become increasingly used in cancer treatment, our findings highlight a potential risk of these therapeutic strategies and suggest a possible mechanism by which carcinoma cells may escape from proteasome inhibitor-based therapy

    Generalized Parton Distributions from Lattice QCD

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    In recent years, there has been a breakthrough in lattice calculations of xx-dependent partonic distributions. This encompasses also distributions describing the 3D structure of the nucleon, such as generalized parton distributions (GPDs). We report a new method of accessing GPDs in asymmetric frames of reference, relying on a novel Lorentz-covariant parametrization of the accessed off-forward matrix elements in boosted nucleon states. The approach offers the possibility of computationally more efficient determination of the full parameter dependence of GPDs and as such, it can contribute to better understanding of nucleon's structure.Comment: Proceedings of XXIX Cracow Epiphany Conference on Physics at the EIC and Future Facilities, 16-19 January 2023; 15 pages, 7 figure

    NPTX2 and cognitive dysfunction in Alzheimer’s Disease

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    This is the final version of the article. Available from eLife Sciences Publications via the DOI in this record.Memory loss in Alzheimer’s disease (AD) is attributed to pervasive weakening and loss of synapses. Here, we present findings supporting a special role for excitatory synapses connecting pyramidal neurons of the hippocampus and cortex with fast-spiking parvalbumin (PV) interneurons that control network excitability and rhythmicity. Excitatory synapses on PV interneurons are dependent on the AMPA receptor subunit GluA4, which is regulated by presynaptic expression of the synaptogenic immediate early gene NPTX2 by pyramidal neurons. In a mouse model of AD amyloidosis, Nptx2-/- results in reduced GluA4 expression, disrupted rhythmicity, and increased pyramidal neuron excitability. Postmortem human AD cortex shows profound reductions of NPTX2 and coordinate reductions of GluA4. NPTX2 in human CSF is reduced in subjects with AD and shows robust correlations with cognitive performance and hippocampal volume. These findings implicate failure of adaptive control of pyramidal neuron-PV circuits as a pathophysiological mechanism contributing to cognitive failure in AD.DNA.This study was supported by NIMH MH100024 (PFW), (R35 NS-097966) (PFW), P50 AG005146-27 (PFW, JCT), Down Syndrome Research and Treatment Foundation and Research Down Syndrome (MX and RR), NIA AG05131 (DS, SE, DG), Alzheimer’s Disease Drug Discovery Foundation (DX, DG) and in part by the Intramural Research Program, National Institute on Aging, and National Institutes on Child Health and Development, NIH
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