Record Maximum Oscillation Frequency in C-face Epitaxial Graphene Transistors

The maximum oscillation frequency (fmax) quantifies the practical upper bound for useful circuit operation. We report here an fmax of 70 GHz in transistors using epitaxial graphene grown on the C-face of SiC. This is a significant improvement over Si-face epitaxial graphene used in the prior high frequency transistor studies, exemplifying the superior electronics potential of C-face epitaxial graphene. Careful transistor design using a high {\kappa} dielectric T-gate and self-aligned contacts, further contributed to the record-breaking fmax

Thick disk kinematics from RAVE and the solar motion

Radial velocity surveys such as the Radial Velocity Experiment (RAVE) provide us with measurements of hundreds of thousands of nearby stars most of which belong to the Galactic thin, thick disk or halo. Ideally, to study the Galactic disks (both thin and thick) one should make use of the multi-dimensional phase-space and the whole pattern of chemical abundances of their stellar populations. In this paper, with the aid of the RAVE Survey, we study the thin and thick disks of the Milky Way, focusing on the latter. We present a technique to disentangle the stellar content of the two disks based on the kinematics and other stellar parameters such as the surface gravity of the stars. Using the Padova Galaxy Model, we checked the ability of our method to correctly isolate the thick disk component from the Galaxy mixture of stellar populations. We introduce selection criteria in order to clean the observed radial velocities from the Galactic differential rotation and to take into account the partial sky coverage of RAVE. We developed a numerical technique to statistically disentangle thin and thick disks from their mixture. We deduce the components of the solar motion relative to the Local Standard of Rest (LSR) in the radial and vertical direction, the rotational lag of the thick disk component relative to the LSR, and the square root of the absolute value of the velocity dispersion tensor for the thick disk alone. The analysis of the thin disk is presented in another paper. We find good agreement with previous independent parameter determinations. In our analysis we used photometrically determined distances. In the Appendix we show that similar values can be found for the thick disk alone as derived in the main sections of our paper even without the knowledge of photometric distances.Comment: accepted on A&A, please see companion paper "THIN disk kinem...

Constraints on the Galactic bar from the Hercules stream as traced with RAVE across the Galaxy

Non-axisymmetries in the Galactic potential (spiral arms and bar) induce kinematic groups such as the Hercules stream. Assuming that Hercules is caused by the effects of the outer Lindblad resonance of the Galactic bar, we model analytically its properties as a function of position in the Galaxy and its dependence on the bar's pattern speed and orientation. Using data from the RAVE survey we find that the azimuthal velocity of the Hercules structure decreases as a function of Galactocentric radius, in a manner consistent with our analytical model. This allows us to obtain new estimates of the parameters of the Milky Way's bar. The combined likelihood function of the bar's pattern speed and angle has its maximum for a pattern speed of Omega(b) = (1.89 +/- 0.08) x Omega(0), where Omega(0) is the local circular frequency. Assuming a solar radius of 8.05 kpc and a local circular velocity of 238 km s(-1), this corresponds to Omega(b) = 56 +/- 2km s(-1) kpc(-1). On the other hand, the bar's orientation phi(b) cannot be constrained with the available data. In fact, the likelihood function shows that a tight correlation exists between the pattern speed and the orientation, implying that a better description of our best fit results is given by the linear relation Omega(b)/Omega(0) = 1.91+0.0044 (phi(b)(deg) - 48), with standard deviation of 0.02. For example, for an angle of phi(b) = 30 deg the pattern speed is 54.0 +/- 0.5 km s(-1) kpc(-1). These results are not very sensitive to the other Galactic parameters such as the circular velocity curve or the peculiar motion of the Sun, and are robust to biases in distance

Chemical gradients in the Milky Way from the RAVE data

Aims. We aim at measuring the chemical gradients of the elements Mg, Al, Si, and Fe along the Galactic radius to provide new constraints on the chemical evolution models of the Galaxy and Galaxy models such as the Besancon model. Thanks to the large number of stars of our RAVE sample we can study how the gradients vary as function of the distance from the Galactic plane. Methods. We analysed three different samples selected from three independent datasets: a sample of 19 962 dwarf stars selected from the RAVE database, a sample of 10 616 dwarf stars selected from the Geneva-Copenhagen Survey (GCS) dataset, and a mock sample (equivalent to the RAVE sample) created by using the GALAXIA code, which is based on the Besancon model. The three samples were analysed by using the very same method for comparison purposes. We integrated the Galactic orbits and obtained the guiding radii (R-g) and the maximum distances from the Galactic plane reached by the stars along their orbits (Z(max)). We measured the chemical gradients as functions of R-g at different Z(max). Results. We found that the chemical gradients of the RAVE and GCS samples are negative and show consistent trends, although they are not equal: at Z(max) < 0.4 kpc and 4.5 < R-g(kpc) < 9.5, the iron gradient for the RAVE sample is d[Fe/H]/dR(g) = -0.065 dex kpc(-1), whereas for the GCS sample it is d[Fe/H]/dR(g) = -0.043 dex kpc(-1) with internal errors of +/-0.002 and +/-0.004 dex kpc(-1), respectively. The gradients of the RAVE and GCS samples become flatter at larger Z(max). Conversely, the mock sample has a positive iron gradient of d[Fe/H]/dR(g) = +0.053 +/- 0.003 dex kpc(-1) at Z(max) < 0.4 kpc and remains positive at any Z(max). These positive and unrealistic values originate from the lack of correlation between metallicity and tangential velocity in the Besancon model. In addition, the low metallicity and asymmetric drift of the thick disc causes a shift of the stars towards lower R-g and metallicity which, together with the thin-disc stars with a higher metallicity and R-g, generates a fictitious positive gradient of the full sample. The flatter gradient at larger Z(max) found in the RAVE and the GCS samples may therefore be due to the superposition of thin-and thick-disc stars, which mimicks a flatter or positive gradient. This does not exclude the possibility that the thick disc has no chemical gradient. The discrepancies between the observational samples and the mock sample can be reduced by i) decreasing the density; ii) decreasing the vertical velocity; and iii) increasing the metallicity of the thick disc in the Besancon model

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism

Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcripts with elusive functions in metabolism. Here we show that a high fraction of lncRNAs, but not protein-coding mRNAs, are repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation induced lncRNAs in mouse liver. Similarly, lncRNAs are lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirm that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profile, improves glucose metabolism, de-represses lncRNAs and impairs mammalian target of rapamycin (mTOR) activation. We find that obesity-repressed LincIRS2 is controlled by MAFG and observe that genetic and RNAi-mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease

A MAFG-lncRNA axis links systemic nutrient abundance to hepatic glucose metabolism

Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcripts with elusive functions in metabolism. Here we show that a high fraction of lncRNAs, but not protein-coding mRNAs, are repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation induced lncRNAs in mouse liver. Similarly, lncRNAs are lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirm that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profile, improves glucose metabolism, de-represses lncRNAs and impairs mammalian target of rapamycin (mTOR) activation. We find that obesity-repressed LincIRS2 is controlled by MAFG and observe that genetic and RNAi-mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease

Neurosphere-Derived Cells Exert a Neuroprotective Action by Changing the Ischemic Microenvironment

BACKGROUND: Neurosphere-derived cells (NC), containing neural stem cells, various progenitors and more differentiated cells, were obtained from newborn C57/BL6 mice and infused in a murine model of focal ischemia with reperfusion to investigate if: 1) they decreased ischemic injury and restored brain function; 2) they induced changes in the environment in which they are infused; 3) changes in brain environment consequent to transient ischemia were relevant for NC action. METHODOLOGY/PRINCIPAL FINDINGS: NC were infused intracerebroventricularly 4 h or 7 d after 30 min middle cerebral artery occlusion. In ischemic mice receiving cells at 4 h, impairment of open field performance was significantly improved and neuronal loss significantly reduced 7–14 d after ischemia compared to controls and to ischemic mice receiving cells at 7 d. Infusion of murine foetal fibroblast in the same experimental conditions was not effective. Assessment of infused cell distribution revealed that they migrated from the ventricle to the parenchyma, progressively decreased in number but they were observable up to 14 d. In mice receiving NC at 7 d and in sham-operated mice, few cells could be observed only at 24 h, indicating that the survival of these cells in brain tissue relates to the ischemic environment. The mRNA expression of trophic factors such as Insulin Growth Factor-1, Vascular Endothelial Growth Factor-A, Transforming Growth Factor-β1, Brain Derived Neurotrophic Factor and Stromal Derived Factor−1α, as well as microglia/macrophage activation, increased 24 h after NC infusion in ischemic mice treated at 4 h compared to sham-operated and to mice receiving cells at 7 d. CONCLUSIONS/SIGNIFICANCE: NC reduce functional impairment and neuronal damage after ischemia/reperfusion injury. Several lines of evidence indicate that the reciprocal interaction between NC and the ischemic environment is crucial for NC protective actions. Based on these results we propose that a bystander control of the ischemic environment may be the mechanism used by NC to rapidly restore acutely injured brain function