Oscillatory dependence of current-driven magnetic domain wall motion on current pulse length

Magnetic domain walls, in which the magnetization direction varies continuously from one direction to another, have long been objects of considerable interest. New concepts for devices based on such domain walls are made possible by the direct manipulation of the walls using spin-polarized electrical current through the phenomenon of spin momentum transfer. Most experiments to date have considered the current-driven motion of domain walls under quasi-static conditions, whereas for technological applications, the walls must be moved on much shorter timescales. Here we show that the motion of domain walls under nanosecond-long current pulses is surprisingly sensitive to the pulse length. In particular, we find that the probability of dislodging a domain wall, confined to a pinning site in a permalloy nanowire, oscillates with the length of the current pulse, with a period of just a few nanoseconds. Using an analytical model and micromagnetic simulations, we show that this behaviour is connected to a current-induced oscillatory motion of the domain wall. The period is determined by the wall's mass and the slope of the confining potential. When the current is turned off during phases of the domain wall motion when it has enough momentum, the domain wall is driven out of the confining potential in the opposite direction to the flow of spin angular momentum. This dynamic amplification effect could be exploited in magnetic nanodevices based on domain wall motion.     

Hidden magnetism and quantum criticality in the heavy fermion superconductor CeRhIn5

With only a few exceptions that are well understood, conventional superconductivity does not coexist with long-range magnetic order (for example, ref. 1). Unconventional superconductivity, on the other hand, develops near a phase boundary separating magnetically ordered and magnetically disordered phases. A maximum in the superconducting transition temperature T(c) develops where this boundary extrapolates to zero Kelvin, suggesting that fluctuations associated with this magnetic quantum-critical point are essential for unconventional superconductivity. Invariably, though, unconventional superconductivity masks the magnetic phase boundary when T < T(c), preventing proof of a magnetic quantum-critical point. Here we report specific-heat measurements of the pressure-tuned unconventional superconductor CeRhIn5 in which we find a line of quantum-phase transitions induced inside the superconducting state by an applied magnetic field. This quantum-critical line separates a phase of coexisting antiferromagnetism and superconductivity from a purely unconventional superconducting phase, and terminates at a quantum tetracritical point where the magnetic field completely suppresses superconductivity. The T --> 0 K magnetic field-pressure phase diagram of CeRhIn5 is well described with a theoretical model developed to explain field-induced magnetism in the high-T(c) copper oxides, but in which a clear delineation of quantum-phase boundaries has not been possible. These experiments establish a common relationship among hidden magnetism, quantum criticality and unconventional superconductivity in copper oxides and heavy-electron systems such as CeRhIn5.     

Bone histology indicates insular dwarfism in a new Late Jurassic sauropod dinosaur

Sauropod dinosaurs were the largest animals ever to inhabit the land, with truly gigantic forms in at least three lineages. Small species with an adult body mass less than five tonnes are very rare, and small sauropod bones generally represent juveniles. Here we describe a new diminutive species of basal macronarian sauropod, Europasaurus holgeri gen. et sp. nov., and on the basis of bone histology we show it to have been a dwarf species. The fossils, including excellent skull material, come from Kimmeridgian marine beds of northern Germany, and record more than 11 individuals of sauropods 1.7 to 6.2 m in total body length. Morphological overlap between partial skeletons and isolated bones links all material to the same new taxon. Cortical histology of femora and tibiae indicates that size differences within the specimens are due to different ontogenetic stages, from juveniles to fully grown individuals. The little dinosaurs must have lived on one of the large islands around the Lower Saxony basin. Comparison with the long-bone histology of large-bodied sauropods suggests that the island dwarf species evolved through a decrease in growth rate from its larger ancestor.     

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

On activation, T cells undergo distinct developmental pathways, attaining specialized properties and effector functions. T-helper (T(H)) cells are traditionally thought to differentiate into T(H)1 and T(H)2 cell subsets. T(H)1 cells are necessary to clear intracellular pathogens and T(H)2 cells are important for clearing extracellular organisms. Recently, a subset of interleukin (IL)-17-producing T (T(H)17) cells distinct from T(H)1 or T(H)2 cells has been described and shown to have a crucial role in the induction of autoimmune tissue injury. In contrast, CD4+CD25+Foxp3+ regulatory T (T(reg)) cells inhibit autoimmunity and protect against tissue injury. Transforming growth factor-beta (TGF-beta) is a critical differentiation factor for the generation of T(reg) cells. Here we show, using mice with a reporter introduced into the endogenous Foxp3 locus, that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ T(reg) cells induced by TGF-beta. We also demonstrate that IL-23 is not the differentiation factor for the generation of T(H)17 cells. Instead, IL-6 and TGF-beta together induce the differentiation of pathogenic T(H)17 cells from naive T cells. Our data demonstrate a dichotomy in the generation of pathogenic (T(H)17) T cells that induce autoimmunity and regulatory (Foxp3+) T cells that inhibit autoimmune tissue injury.     

Defective acidification of intracellular organelles in cystic fibrosis.

The phenotype of cystic fibrosis (CF) includes abnormalities in transepithelial transport of Cl- (refs 1-5), decreased sialylation and increased sulphation and fucosylation of glycoproteins, and lung colonization with Pseudomonas. It is not apparent how these abnormalities are interrelated, nor how they result from loss of function of the CF gene-encoded transmembrane regulator (CFTR). We have previously shown that that the pH of a secretory granule is regulated by the vesicular conductance for Cl- (ref. 11). Here we find defective acidification in CF cells of the trans-Golgi/trans-Golgi network, of prelysosomes and of endosomes as a result of diminished Cl- conductance. Sialytation of proteins and lipids is reduced and ligand traffic altered. These abnormalities can result from defective acidification because vacuolar pH regulates glycoprotein processing and ligand transport. The CF phenotype is similar to that of alkalinized cells and acidification-defective mutatants.