Magnetic Properties of Pr0.7Ca0.3MnO3/SrRuO3 Superlattices

High-quality Pr0.7Ca0.3MnO3/SrRuO3 superlattices were fabricated by pulsed laser deposition and were investigated by high-resolution transmission electron microscopy and SQUID magnetometry. Superlattices with orthorhombic and tetragonal SrRuO3 layers were investigated. The superlattices grew coherently; in the growth direction Pr0.7Ca0.3MnO3 layers were terminated by MnO2- and SrRuO3 layers by RuO2-planes. All superlattices showed antiferromagnetic interlayer coupling in low magnetic fields. The coupling strength was significantly higher for orthorhombic than for tetragonal symmetry of the SrRuO3 layers. The strong interlayer exchange coupling in the superlattice with orthorhombic SrRuO3 layers led to a magnetization reversal mechanism with a partially inverted hysteresis loop.Comment: 12 pages, 4 figure

Orthorhombic to tetragonal transition of SrRuO3 layers in Pr0.7Ca0.3MnO3/SrRuO3 superlattices

High-quality Pr0.7Ca0.3MnO3/SrRuO3 superlattices with ultrathin layers were fabricated by pulsed laser deposition on SrTiO3 substrates. The superlattices were studied by atomically resolved scanning transmission electron microscopy, high-resolution transmission electron microscopy, resistivity and magnetoresistance measurements. The superlattices grew coherently without growth defects. Viewed along the growth direction, SrRuO3 and Pr0.7Ca0.3MnO3 layers were terminated by RuO2 and MnO2, respectively, which imposes a unique structure to their interfaces. Superlattices with a constant thickness of the SrRuO3 layers, but varying thickness of the Pr0.7Ca0.3MnO3 layers showed a change of crystalline symmetry of the SrRuO3 layers. At a low Pr0.7Ca0.3MnO3 layer thickness of 1.5 nm transmission electron microscopy proved the SrRuO3 layers to be orthorhombic, whereas these were non-orthorhombic for a Pr0.7Ca0.3MnO3 layer thickness of 4.0 nm. Angular magnetoresistance measurements showed orthorhombic (with small monoclinic distortion) symmetry in the first case and tetragonal symmetry of the SrRuO3 layers in the second case. Mechanisms driving this orthorhombic to tetragonal transition are briefly discussed.Comment: 23 pages, 12 figure

Single-electron transitions in one-dimensional native nanostructures

Low-temperature measurements proved the existence of a two-dimensional electron gas at defined dislocation arrays in silicon. As a consequence, single-electron transitions (Coulomb blockades) are observed. It is shown that the high strain at dislocation cores modifies the band structure and results in the formation of quantum wells along dislocation lines. This causes quantization of energy levels inducing the formation of Coulomb blockades

On the electronic properties of a single dislocation

A detailed knowledge of the electronic properties of individual dislocations is necessary for next generation nanodevices. Dislocations are fundamental crystal defects controlling the growth of different nanostructures (nanowires) or appear during device processing. We present a method to record electric properties of single dislocations in thin silicon layers. Results of measurements on single screw dislocations are shown for the first time. Assuming a cross-section area of the dislocation core of about 1 nm2, the current density through a single dislocation is J = 3.8 × 1012 A/cm2 corresponding to a resistivity of ρ ≅ 1 × 10-8 Ω cm. This is about eight orders of magnitude lower than the surrounding silicon matrix. The reason of the supermetallic behavior is the high strain in the cores of the dissociated dislocations modifying the local band structure resulting in high conductive carrier channels along defect cores

A highly contiguous genome assembly of the bat hawkmoth Hyles vespertilio (Lepidoptera: Sphingidae)

Adapted to different ecological niches, moth species belonging to the Hyles genus exhibit a spectacular diversity of larval color patterns. These species diverged ∼7.5 million years ago, making this rather young genus an interesting system to study a wide range of questions including the process of speciation, ecological adaptation, and adaptive radiation

Six reference-quality genomes reveal evolution of bat adaptations

Bats possess extraordinary adaptations, including flight, echolocation, extreme longevity and unique immunity. High-quality genomes are crucial for understanding the molecular basis and evolution of these traits. Here we incorporated long-read sequencing and state-of-the-art scaffolding protocols to generate, to our knowledge, the first reference-quality genomes of six bat species (Rhinolophus ferrumequinum, Rousettus aegyptiacus, Phyllostomus discolor, Myotis myotis, Pipistrellus kuhlii and Molossus molossus). We integrated gene projections from our �Tool to infer Orthologs from Genome Alignments� (TOGA) software with de novo and homology gene predictions as well as short- and long-read transcriptomics to generate highly complete gene annotations. To resolve the phylogenetic position of bats within Laurasiatheria, we applied several phylogenetic methods to comprehensive sets of orthologous protein-coding and noncoding regions of the genome, and identified a basal origin for bats within Scrotifera. Our genome-wide screens revealed positive selection on hearing-related genes in the ancestral branch of bats, which is indicative of laryngeal echolocation being an ancestral trait in this clade. We found selection and loss of immunity-related genes (including pro-inflammatory NF-κB regulators) and expansions of anti-viral APOBEC3 genes, which highlights molecular mechanisms that may contribute to the exceptional immunity of bats. Genomic integrations of diverse viruses provide a genomic record of historical tolerance to viral infection in bats. Finally, we found and experimentally validated bat-specific variation in microRNAs, which may regulate bat-specific gene-expression programs. Our reference-quality bat genomes provide the resources required to uncover and validate the genomic basis of adaptations of bats, and stimulate new avenues of research that are directly relevant to human health and disease.s E.W.M. and M.P. were supported by the Max Planck Society and were partially funded by the Federal Ministry of Education and Research (grant 01IS18026C). All data produced in Dresden were funded directly by the Max Planck Society. S.C.V., P.D. and K.L. were funded by a Max Planck Research Group awarded to S.C.V. from the Max Planck Society, and a Human Frontiers Science Program (HFSP) Research grant awarded to S.C.V. (RGP0058/2016). M.H. was funded by the German Research Foundation (HI 1423/3-1) and the Max Planck Society. E.C.T. was funded by a European Research Council Research Grant (ERC2012-StG311000), UCD Wellcome Institutional Strategic Support Fund, financed jointly by University College Dublin and SFI-HRB-Wellcome Biomedical Research Partnership (ref 204844/Z/16/Z) and Irish Research Council Consolidator Laureate Award. G.M.H. was funded by a UCD Ad Astra Fellowship. G.J. and E.C.T. were funded from the Royal Society/Royal Irish Academy cost share programme. L.M.D. was supported by NSF-DEB 1442142 and 1838273, and NSF-DGE 1633299. D.A.R. was supported by NSF-DEB 1838283. E.D.J. and O.F. were funded by the Rockefeller University and the Howard Hughes Medical Institute. We thank Stony Brook Research Computing and Cyberinfrastructure, and the Institute for Advanced Computational Science at Stony Brook University for access to the high-performance SeaWulf computing system (which was made possible by a National Science Foundation grant (no. 1531492)); the Long Read Team of the DRESDEN-concept Genome Center, DFG NGS Competence Center, part of the Center for Molecular and Cellular Bioengineering (CMCB), Technische Universität Dresden; S. Kuenzel and his team of the Max Planck Institute of Evolutionary Biology; members of the Vertebrate Genomes Laboratory at The Rockefeller University for their support; L. Wiegrebe, U. Firzlaff and M. Yartsev, who gave us access to captive colonies of Phyllostomus and Rousettus bats and aided with tissue sample collection; and M. Springer, for completing the SVDquartet analyses, and providing phylogenetic input and expertise

Molecular mechanisms of vaspin action: from adipose tissue to skin and bone, from blood vessels to the brain

Visceral adipose tissue derived serine protease inhibitor (vaspin) or SERPINA12 according to the serpin nomenclature was identified together with other genes and gene products that  were specifically expressed or overexpressed in the intra abdominal or visceral adipose tissue  (AT) of the Otsuka Long-Evans Tokushima fatty rat. These rats spontaneously develop visceral  obesity, insulin resistance, hyperinsulinemia and ‐glycemia, as well as hypertension and thus represent a well suited animal model of obesity and related metabolic disorders such as type  2 diabetes.  The follow-up study reporting the cloning, expression and functional characterization of  vaspin suggested the great and promising potential of this molecule to counteract obesity induced insulin resistance and inflammation and has since initiated over 300 publications, clinical and experimental, that have contributed to uncover the multifaceted functions and molecular mechanisms of vaspin action not only in the adipose, but in many different cells, tissues and organs. This review will give an update on mechanistic and structural aspects of vaspin with a focus on its serpin function, the physiology and regulation of vaspin expression, and will summarize the latest on vaspin function in various tissues such as the different adipose tissue depots as well as the vasculature, skin, bone and the brain