1,921 research outputs found
Large nuclear spin polarization in gate-defined quantum dots using a single-domain nanomagnet
The electron-nuclei (hyperfine) interaction is central to spin qubits in
solid state systems. It can be a severe decoherence source but also allows
dynamic access to the nuclear spin states. We study a double quantum dot
exposed to an on-chip single-domain nanomagnet and show that its inhomogeneous
magnetic field crucially modifies the complex nuclear spin dynamics such that
the Overhauser field tends to compensate external magnetic fields. This turns
out to be beneficial for polarizing the nuclear spin ensemble. We reach a
nuclear spin polarization of ~50%, unrivaled in lateral dots, and explain our
manipulation technique using a comprehensive rate equation model
Controlling the Local Spin-Polarization at the Organic-Ferromagnetic Interface
By means of ab initio calculations and spin-polarized scanning tunneling
microscopy experiments we show how to manipulate the local spin-polarization of
a ferromagnetic surface by creating a complex energy dependent magnetic
structure. We demonstrate this novel effect by adsorbing organic molecules
containing pi(pz)-electrons onto a ferromagnetic surface, in which the
hybridization of the out-of-plane pz atomic type orbitals with the d-states of
the metal leads to the inversion of the spin-polarization at the organic site
due to a pz - d Zener exchange type mechanism. As a key result, we demonstrate
that it is possible to selectively inject spin-up and spin-down electrons from
the same ferromagnetic surface, an effect which can be exploited in future
spintronic devices
High performance SERS platforms via parametric optimization of the laser-assisted photodeposition of silver and gold nanoparticles
Ablation and functionalization of flexographic printing forms using femtosecond lasers for additively manufactured polymer-optical waveguides
An efficient and low-cost approach to manufacture Opto-Mechatronic Interconnect Devices will be obligatory to handle the strongly increasing amount of data. The presented approach is based on a flexographic printing process. To adjust the transferred material the printing form is functionalized by means of laser-induced structures using an ultrashort-pulsed laser. The long-term goal is to adjust the printing result through microstructures in the printing form in order to create spatially resolved material transfer. In this work, first the ablation parameters are investigated at different repetition rates using a femtosecond laser. Further, a line structure is inserted in the material transferring areas of the printing form, which is consequently widened. Its influence on the printing result is presented. © 2020 The Authors. Published by Elsevier B.V
Atrial Natriuretic Peptide Protects against Histamine-Induced Endothelial Barrier Dysfunction in Vivo
Endothelial barrier dysfunction is a hallmark of many severe pathologies, including sepsis or atherosclerosis. The cardiovascular hormone atrial natriuretic peptide (ANP) has increasingly been suggested to counteract endothelial leakage. Surprisingly, the precise in vivo relevance of these observations has never been evaluated. Thus, we aimed to clarify this issue and, moreover, to identify the permeability-controlling subcellular systems that are targeted by ANP. Histamine was used as important pro-inflammatory, permeability-increasing stimulus. Measurements of fluorescein isothiocyanate (FITC)-dextran extravasation from venules of the mouse cremaster muscle and rat hematocrit values were performed to judge changes of endothelial permeability in vivo. It is noteworthy that ANP strongly reduced the histamine-evoked endothelial barrier dysfunction in vivo. In vitro, ANP blocked the breakdown of transendothelial electrical resistance (TEER) induced by histamine. Moreover, as judged by immunocytochemistry and Western blot analysis, ANP inhibited changes of vascular endothelial (VE)-cadherin, β-catenin, and p120ctn morphology; VE-cadherin and myosin light chain 2 (MLC2) phosphorylation; and F-actin stress fiber formation. These changes seem to be predominantly mediated by the natriuretic peptide receptor (NPR)-A, but not by NPR-C. In summary, we revealed ANP as a potent endothelial barrier protecting agent in vivo and identified adherens junctions and the contractile apparatus as subcellular systems targeted by ANP. Thus, our study highlights ANP as an interesting pharmacological compound opening new therapeutic options for preventing endothelial leakage
Reciprocal regulation of PKA and rac signaling
Activated G protein-coupled receptors (GPCRs) and receptor tyrosine kinases relay extracellular signals through spatial and temporal controlled kinase and GTPase entities. These enzymes are coordinated by multifunctional scaffolding proteins for precise intracellular signal processing. The cAMP-dependent protein kinase A (PKA) is the prime example for compartmentalized signal transmission downstream of distinct GPCRs. A-kinase anchoring proteins tether PKA to specific intracellular sites to ensure precision and directionality of PKA phosphorylation events. Here, we show that the Rho-GTPase Rac contains A-kinase anchoring protein properties and forms a dynamic cellular protein complex with PKA. The formation of this transient core complex depends on binary interactions with PKA subunits, cAMP levels and cellular GTP-loading accounting for bidirectional consequences on PKA and Rac downstream signaling. We show that GTP-Rac stabilizes the inactive PKA holoenzyme. However, β-adrenergic receptor-mediated activation of GTP-Rac–bound PKA routes signals to the Raf-Mek-Erk cascade, which is critically implicated in cell proliferation. We describe a further mechanism of how cAMP enhances nuclear Erk1/2 signaling: It emanates from transphosphorylation of p21-activated kinases in their evolutionary conserved kinase-activation loop through GTP-Rac compartmentalized PKA activities. Sole transphosphorylation of p21-activated kinases is not sufficient to activate Erk1/2. It requires complex formation of both kinases with GTP-Rac1 to unleash cAMP-PKA–boosted activation of Raf-Mek-Erk. Consequently GTP-Rac functions as a dual kinase-tuning scaffold that favors the PKA holoenzyme and contributes to potentiate Erk1/2 signaling. Our findings offer additional mechanistic insights how β-adrenergic receptor-controlled PKA activities enhance GTP-Rac–mediated activation of nuclear Erk1/2 signaling
A comparison of different Malaise trap types
Recent reports on insect decline have highlighted the need for long-term data on insect communities towards identifying their trends and drivers.
With the launch of many new insect monitoring schemes to investigate insect communities over large spatial and temporal scales, Malaise traps have become one of the most important tools due to the broad spectrum of species collected and reduced capture bias through passive sampling of insects day and night. However, Malaise traps can vary in size, shape, and colour, and it is unknown how these differences affect biomass, species richness, and composition of trap catch, making it difficult to compare results between studies.
We compared five Malaise trap types (three variations of the Townes and two variations of the Bartak Malaise trap) to determine their effects on biomass and species richness as identified by metabarcoding.
Insect biomass varied by 20%–55%, not strictly following trap size but varying with trap type. Total species richness was 20%–38% higher in the three Townes trap models compared to the Bartak traps. Bartak traps captured lower richness of highly mobile taxa but increased richness of ground-dwelling taxa. The white roofed Townes trap captured a higher richness of pollinators.
We find that biomass, total richness, and taxa group specific richness are all sensitive to Malaise trap type. Trap type should be carefully considered and aligned to match monitoring and research questions. Additionally, our estimates of trap type effects can be used to adjust results to facilitate comparisons across studies
Localized eigenmodes of the overlap operator and their impact on the eigenvalue distribution
In a system where chiral symmetry is spontaneously broken, the low energy
eigenmodes of the continuum Dirac operator are extended. On the lattice, due to
discretization effects, the Dirac operator can have localized eigenmodes that
affect physical quantities sensitive to chiral symmetry. While the infrared
eigenmodes of the Wilson Dirac operator are usually extended even on coarse
lattices, the chiral overlap operator has many localized eigenmodes in the
physical region, especially in mixed action simulations. Depending on their
density, these modes can introduce strong lattice artifacts. The effect can be
controlled by changing the parameters of the overlap operator, in particular
the clover improvement term and the center of the overlap projection.Comment: 16 pages, 6 figure
Cell death serum biomarkers are early predictors for survival in severe septic patients with hepatic dysfunction
Redox Responses in Patients with Sepsis: High Correlation of Thioredoxin-1 and Macrophage Migration Inhibitory Factor Plasma Levels
Background. Redox active substances (e.g., Thioredoxin-1, Macrophage Migration Inhibitory Factor) seem to be central hubs in the septic inflammatory process.
Materials and Methods. Blood samples from patients with severe sepsis or septic shock (n = 15) were collected at the time of sepsis diagnosis (t0), and 24 (t24) and 48 (t48) hours later; samples from healthy volunteers (n = 18) were collected once; samples from postoperative patients (n = 28) were taken one time immediately after surgery. In all patients, we measured plasma levels of IL-6, TRX1 and MIF.
Results. The plasma levels of MIF and TRX1 were significantly elevated in patients with severe sepsis or septic shock. Furthermore, TRX1 and MIF plasma levels showed a strong correlation (t0: rsp = 0.720, ρ = 0.698/t24: rsp = 0.771, ρ = 0.949).
Conclusions. Proinflammatory/~oxidative and anti-inflammatory/~oxidative agents show a high correlation in order to maintain a redox homeostasis and to avoid the harmful effects of an excessive inflammatory/oxidative response
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