Enhancement of thermovoltage and tunnel magneto-Seebeck effect in CoFeB based magnetic tunnel junctions by variation of the MgAl2_2O4_4 and MgO barrier thickness

We investigate the influence of the barrier thickness of Co$_{40}$Fe$_{40}$B$_{20}$ based magnetic tunnel junctions on the laser-induced tunnel magneto-Seebeck effect. Varying the barrier thickness from 1nm to 3nm, we find a distinct maximum in the tunnel magneto-Seebeck effect for 2.6nm barrier thickness. This maximum is independently measured for two barrier materials, namely MgAl$_2$O$_4$ and MgO. Additionally, samples with an MgAl$_2$O$_4$ barrier exhibit a high thermovoltage of more than 350$\mu$V in comparison to 90$\mu$V for the MTJs with MgO barrier when heated with the maximum laser power of 150mW. Our results allow for the fabrication of improved stacks when dealing with temperature differences across magnetic tunnel junctions for future applications in spin caloritronics, the emerging research field that combines spintronics and themoelectrics

Large magneto-Seebeck effect in magnetic tunnel junctions with half-metallic Heusler electrodes

Spin caloritronics studies the interplay between charge-, heat- and spin-currents, which are initiated by temperature gradients in magnetic nanostructures. A plethora of new phenomena has been discovered that promises, e.g., to make wasted heat in electronic devices useable or to provide new read-out mechanisms for information. However, only few materials have been studied so far with Seebeck voltages of only some {\mu}V, which hampers applications. Here, we demonstrate that half-metallic Heusler compounds are hot candidates for enhancing spin-dependent thermoelectric effects. This becomes evident when considering the asymmetry of the spin-split density of electronic states around the Fermi level that determines the spin-dependent thermoelectric transport in magnetic tunnel junctions. We identify Co$_2$FeAl and Co$_2$FeSi Heusler compounds as ideal due to their energy gaps in the minority density of states, and demonstrate devices with substantially larger Seebeck voltages and tunnel magneto-Seebeck effect ratios than the commonly used Co-Fe-B based junctions.Comment: 9 pages, 4 figure

Nlrp3 inflammasome activation and Gasdermin D-driven pyroptosis are immunopathogenic upon gastrointestinal norovirus infection.

Norovirus infection is the leading cause of food-borne gastroenteritis worldwide, being responsible for over 200,000 deaths annually. Studies with murine norovirus (MNV) showed that protective STAT1 signaling controls viral replication and pathogenesis, but the immune mechanisms that noroviruses exploit to induce pathology are elusive. Here, we show that gastrointestinal MNV infection leads to widespread IL-1β maturation in MNV-susceptible STAT1-deficient mice. MNV activates the canonical Nlrp3 inflammasome in macrophages, leading to maturation of IL-1β and to Gasdermin D (GSDMD)-dependent pyroptosis. STAT1-deficient macrophages displayed increased MAVS-mediated expression of pro-IL-1β, facilitating elevated Nlrp3-dependent release of mature IL-1β upon MNV infection. Accordingly, MNV-infected Stat1-/- mice showed Nlrp3-dependent maturation of IL-1β as well as Nlrp3-dependent pyroptosis as assessed by in vivo cleavage of GSDMD to its active N-terminal fragment. While MNV-induced diarrheic responses were not affected, Stat1-/- mice additionally lacking either Nlrp3 or GSDMD displayed lower levels of the fecal inflammatory marker Lipocalin-2 as well as delayed lethality after gastrointestinal MNV infection. Together, these results uncover new insights into the mechanisms of norovirus-induced inflammation and cell death, thereby revealing Nlrp3 inflammasome activation and ensuing GSDMD-driven pyroptosis as contributors to MNV-induced immunopathology in susceptible STAT1-deficient mice.Wellcome Trust BBSR

Temperature gradient-induced magnetization reversal of single ferromagnetic nanowires

In this study, we investigate the temperature- and temperature gradient-dependent magnetization reversal process of individual, single-domain Co39Ni61 and Fe15Ni85 ferromagnetic nanowires via the magneto-optical Kerr effect and magnetoresistance measurements. While the coercive fields (HC) and therefore the magnetic switching fields (HSW) generally decrease under isothermal conditions at elevated base temperatures (Tbase), temperature gradients (ΔT) along the nanowires lead to an increased switching field of up to 15% for ΔT  = 300 K in Co39Ni61 nanowires. This enhancement is attributed to a stress-induced, magneto-elastic anisotropy term due to an applied temperature gradient along the nanowire that counteracts the thermally assisted magnetization reversal process. Our results demonstrate that a careful distinction between locally elevated temperatures and temperature gradients has to be made in future heat-assisted magnetic recording devices

Physical and functional interaction between A20 and ATG16L1-WD40 domain in the control of intestinal homeostasis

Prevention of inflammatory bowel disease (IBD) relies on tight control of inflammatory, cell death and autophagic mechanisms, but how these pathways are integrated at the molecular level is still unclear. Here we show that the anti-inflammatory protein A20 and the critical autophagic mediator Atg16l1 physically interact and synergize to regulate the stability of the intestinal epithelial barrier. A proteomic screen using the WD40 domain of ATG16L1 (WDD) identified A20 as a WDD-interacting protein. Loss of A20 and Atg16l1 in mouse intestinal epithelium induces spontaneous IBD-like pathology, as characterized by severe inflammation and increased intestinal epithelial cell death in both small and large intestine. Mechanistically, absence of A20 promotes Atg16l1 accumulation, while elimination of Atg16l1 or expression of WDD-deficient Atg16l1 stabilizes A20. Collectively our data show that A20 and Atg16l1 cooperatively control intestinal homeostasis by acting at the intersection of inflammatory, autophagy and cell death pathways

Two distinct ubiquitin-binding motifs in A20 mediate its anti-inflammatory and cell-protective activities

Protein ubiquitination regulates protein stability and modulates the composition of signaling complexes. A20 is a negative regulator of inflammatory signaling, but the molecular mechanisms involved are ill understood. Here, we generated Tnfaip3 gene-targeted A20 mutant mice bearing inactivating mutations in the zinc finger 7 (ZnF7) and ZnF4 ubiquitin-binding domains, revealing that binding to polyubiquitin is essential for A20 to suppress inflammatory disease. We demonstrate that a functional ZnF7 domain was required for recruiting A20 to the tumor necrosis factor receptor 1 (TNFR1) signaling complex and to suppress inflammatory signaling and cell death. The combined inactivation of ZnF4 and ZnF7 phenocopied the postnatal lethality and severe multiorgan inflammation of A20-deficient mice. Conditional tissue-specific expression of mutant A20 further revealed the key role of ubiquitin-binding in myeloid and intestinal epithelial cells. Collectively, these results demonstrate that the anti-inflammatory and cytoprotective functions of A20 are largely dependent on its ubiquitin-binding properties. van Loo and colleagues provide insights into the action of the anti-inflammatory protein A20. The ZnF7 and ZnF4 ubiquitin-binding domains of A20 are both required to suppress inflammatory signaling and cell death; however, these zinc fingers operate via distinct mechanisms

Anomalous Nernst effect and three-dimensional temperature gradients in magnetic tunnel junctions

Understanding nanoscale temperature gradients in magnetic materials and how it affects their properties can help widen their potential applications. The authors analyze the anomalous Nernst effect in magnetic tunnel junctions and report how temperature gradients influence the thermomagnetic properties in three dimensions

Visions for a walking and cycling focussed urban transport system

Walking and cycling can make a considerable contribution to sustainable transport goals, building healthier and more sustainable communities and contributing to traffic and pollution reduction. There have been many national and local initiatives to promote walking and cycling, but without a long term vision and consistent strategy it is difficult to see how a significant change may be achieved. This paper presents three alternative visions for the role of walking and cycling in urban areas for the year 2030: each vision illustrates a ‘desirable’ walking- and cycling-oriented transport system against a different ‘exogenous social background’. These visions have been developed through a process of expert discussion and review and are intended to provide a stimulus for debate on the potential for and desirability of such alternative futures. Each is based on the UK and represents a substantial change to the current situation: in particular, each of the visions presents a view of a society where walking and cycling are considerably more important than is currently the case and where these modes cater for a much higher proportion of urban transport needs than at present. The visions show pictures of urban environments where dependence on motor vehicles has been reduced, in two of the visions to very low levels. The methodological approach for devising visions is informed by work on ‘utopian thinking’: a key concept underlying this approach is one of viewing the future in social constructivist terms (i.e. the future is what ‘we’, as a society, make it) rather than considering the future as something that can be ‘scientifically’ predicted by the extrapolation of current trends