Evidence of spontaneous spin polarized transport in magnetic nanowires

The exploitation of the spin in charge-based systems is opening revolutionary opportunities for device architecture. Surprisingly, room temperature electrical transport through magnetic nanowires is still an unresolved issue. Here, we show that ferromagnetic (Co) suspended atom chains spontaneously display an electron transport of half a conductance quantum, as expected for a fully polarized conduction channel. Similar behavior has been observed for Pd (a quasi-magnetic 4d metal) and Pt (a non-magnetic 5d metal). These results suggest that the nanowire low dimensionality reinforces or induces magnetic behavior, lifting off spin degeneracy even at room temperature and zero external magnetic field.Comment: 4 pages, 3 eps fig

Application of laser in seam welding of dissimilar steel to aluminium joints for thick structural components

Laser welding-brazing technique, using a continuous wave (CW) fibre laser with 8000 W of maximum power, was applied in conduction mode to join 2 mm thick steel (XF350) to 6 mm thick aluminium (AA5083-H22), in a lap joint configuration with steel on the top. The steel surface was irradiated by the laser and the heat was conducted through the steel plate to the steel-aluminium interface, where the aluminium melts and wets the steel surface. The welded samples were defect free and the weld micrographs revealed presence of a brittle intermetallic compounds (IMC) layer resulting from reaction of Fe and Al atoms. Energy Dispersive Spectroscopy (EDS) analysis indicated the stoichiometry of the IMC as Fe2Al5 and FeAl3, the former with maximum microhardness measured of 1145 HV 0.025/10. The IMC layer thickness varied between 4 to 21 μm depending upon the laser processing parameters. The IMC layer showed an exponential growth pattern with the applied specific point energy (Esp) at a constant power density (PD). Higher PD values accelerate the IMC layer growth. The mechanical shear strength showed a narrow band of variation in all the samples (with the maximum value registered at 31.3 kN), with a marginal increase in the applied Esp. This could be explained by the fact that increasing the Esp results into an increase in the wetting and thereby the bonded area in the steel-aluminium interface

Axonal stress kinase activation and tau misbehavior induced by kinesin-1 transport defects

Many neurodegenerative diseases exhibit axonal pathology, transport defects, and aberrant phosphorylation and aggregation of the microtubule binding protein tau. While mutant tau protein in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP17) causes aberrant microtubule binding and assembly of tau into filaments, the pathways leading to tau-mediated neurotoxicity in Alzheimer's disease and other neurodegenerative disorders in which tau protein is not genetically modified remain unknown. To test the hypothesis that axonal transport defects alone can cause pathological abnormalities in tau protein and neurodegeneration in the absence of mutant tau or amyloid β deposits, we induced transport defects by deletion of the kinesin light chain 1 (KLC1) subunit of the anterograde motor kinesin-1. We found that upon aging, early selective axonal transport defects in mice lacking the KLC1 protein (KLC1-/-) led to axonopathies with cytoskeletal disorganization and abnormal cargo accumulation. In addition, increased c-jun N-terminal stress kinase activation colocalized with aberrant tau in dystrophic axons. Surprisingly, swollen dystrophic axons exhibited abnormal tau hyperphosphorylation and accumulation. Thus, directly interfering with axonal transport is sufficient to activate stress kinase pathways initiating a biochemical cascade that drives normal tau protein into a pathological state found in a variety of neurodegenerative disorders including Alzheimer's disease.Fil: Falzone, Tomas Luis. Howard Hughes Medical Institute; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Stokin, Gorazd B.. University Psychiatric Hospital; EsloveniaFil: Lillo, Concepción. University of California at San Diego; Estados UnidosFil: Rodrigues, Elizabeth M.. Howard Hughes Medical Institute; Estados UnidosFil: Westerman, Eileen L.. Howard Hughes Medical Institute; Estados UnidosFil: Williams, David S.. University of California at San Diego; Estados UnidosFil: Goldstein, Lawrence S. B.. Howard Hughes Medical Institute; Estados Unido

Honey Bee Gut Microbiome Is Altered by In-Hive Pesticide Exposures

Honey bees (Apismellifera) are the primary pollinators of major horticultural crops. Over the last few decades, a substantial decline in honey bees and their colonies have been reported. While a plethora of factors could contribute to the putative decline, pathogens, and pesticides are common concerns that draw attention. In addition to potential direct effects on honey bees, indirect pesticide effects could include alteration of essential gut microbial communities and symbionts that are important to honey bee health (e.g.,immunesystem). The primary objective of this study was to determine the microbiome associated with honey bees exposed to commonly used in-hive pesticides: coumaphos, tau-fluvalinate, and chlorothalonil. Treatments were replicated at three independent locations near Blacksburg Virginia, and included ano-pesticide amended control at each location. The microbiome was characterized through pyrosequencing of V2–V3 regions of the bacterial 16S rRNA gene and fungal ITS region. Pesticide exposure significantly affected the structure of bacterial but not fungal communities. The bee bacteriome, similar to other studies, was dominated by sequences derived from Bacilli, Actinobacteria, α-, β-, γ-proteobacteria. The fungal community sequences were dominated by Ascomycetes and Basidiomycetes. The Multi-response permutation procedures (MRPP) and subsequent Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) analysis indicated that chlorothalonil caused significant change to the structure and functional potential of the honey bee gut bacterial community relative to control. Putative genes for oxidative phosphorylation, for example, increased while sugar metabolism and peptidase potential declined in the microbiome of chlorothalonil exposed bees. The results of this field-based study suggest the potential for pesticide induced changes to the honey bee gut microbiome that warrant further investigation