Enhanced Specular Andreev reflection in bilayer graphene

Andreev reflection in graphene is special since it can be of two types- retro or specular. Specular Andreev reflection (SAR) dominates when the position of the Fermi energy in graphene is comparable to or smaller than the superconducting gap. Bilayer graphene (BLG) is an ideal candidate to observe the crossover from retro to specular since the Fermi energy broadening near the Dirac point is much weaker compared to monolayer graphene. Recently, the observation of signatures of SAR in BLG have been reported experimentally by looking at the enhancement of conductance at finite bias near the Dirac point. However, the signatures were not very pronounced possibly due to the participation of normal quasi-particles at bias energies close to the superconducting gap. Here, we propose a scheme to observe the features of enhanced SAR even at zero bias at a normal metal (NM)-superconductor (SC) junction on BLG. Our scheme involves applying a Zeeman field to the NM side of the NM-SC junction on BLG (making the NM ferromagnetic), which energetically separates the Dirac points for up-spin and down-spin. We calculate the conductance as a function of chemical potential and bias within the superconducting gap and show that well-defined regions of specular- and retro-type Andreev reflection exist. We compare the results with and without superconductivity. We also investigate the possibility of the formation of a p-n junction at the interface between the NM and SC due to a work function mismatch.Comment: 9 pages, 10 captioned figures. Published versio

Fabry-P\'erot interference in Josephson junctions

Conductance of metallic heterostructures can be controlled by applying a gate voltage to a region in the transport channel. For sufficiently long phase coherent channels, oscillations appear in conductance versus chemical potential plot, which can be explained by Fabry-P\'erot interference. In this work, we study DC Josephson effect in a superconductor-normal metal-superconductor junctions. The chemical potential of the normal metal (NM) region can be tuned by an applied gate voltage. We numerically obtain the Andreev bound states formed within the superconducting gap and calculate Josephson current by summing up the currents carried by the occupied Andreev bound states. We find that the Josephson current oscillates as a function of the chemical potential in the NM region, and these oscillations can be explained by Fabry-P\'erot interference condition. We find that Josephson current carried by one bound state can be higher than that carried by two or more bound states.Comment: 4 pages, 3 captioned figure

Changes in Hypothalamic Gene Expression Associated with the Arrest of Pulsatile Gonadotropin-Releasing Hormone Release during Infancy in the Agonadal Male Rhesus Monkey (Macaca mulatta)

This study examined whether changes in the levels of the messenger RNAs (mRNAs) encoding the g-aminobutyric acid (GABA) synthesizing enzymes, glutamate decarboxylase (GAD)65 and GAD67 and transforming growth factor-a (TGFa) in the hypothalamus are correlated with the arrest of pulsatile GnRH release during infancy in the agonadal male monkey. This experiment also provided the opportunity to examine changes in hypothalamic GnRH gene expression during this critical phase of primate development. Male rhesus monkeys were castrated at 1 week of age: four were killed 4–7 weeks after orchidectomy while pulsatile GnRH release was robust as reflected by high circulating LH levels, and four were killed at 12–15 months of age after establishing that pulsatile GnRH release had been arrested. GAD65, GAD67, TGFa, and GnRH mRNA levels were estimated using RNase protection assays employing homologous probes and the results were expressed relative to cyclophilin mRNA levels. GnRH peptide was measured by RIA. GAD65 and GAD67 mRNA levels in the hypothalamus of juveniles were significantly greater than those in neonatal monkeys. On the other hand, hypothalamic TGFa and GnRH mRNA (and peptide) levels in agonadal neonate and juvenile monkeys were indistinguishable. These results indicate that the molecular concomitants associated with bringing the hypothalamic GnRH pulse generator into check in agonadal neonatal males are not a mirror image of those previously reported at the time this neuronal network is reactivated at puberty when TGFa and GnRH gene expression increase and GAD65 and GAD67 mRNA levels remain unchanged. Thus, the neurobiological mechanism that reactivates pulsatile GnRH release at puberty is likely to involve more than a simple reversal of that underlying inhibition of the same network in late infancy. (Endocrinology 141: 3273–3277, 2000

Neuropeptide Y: A hypothalamic brake restraining the onset of puberty in primates

The adult reproductive axis is driven by an intermittent discharge of gonadotropin-releasing hormone (GnRH) generated by a network of hypothalamic neurons known as the GnRH pulse generator. Although this signal generator is operational in infant primates, puberty in these species is delayed by activation shortly after birth of a central neural mechanism that holds GnRH release in check during juvenile development. Here, we show that, in the male rhesus monkey, the postnatal pattern in GnRH pulse generator activity is inversely related to that in neuropeptide Y (NPY) gene and protein expression in the mediobasal hypothalamus and that central administration of an NPY Y1 receptor antagonist to juvenile animals elicits precocious GnRH release. Cell imaging indicated that the developmentally regulated NPY neurons may be located in regions dorsal to the arcuate nucleus. These findings lead us to propose that NPY is a fundamental component of the neurobiological brake restraining the onset of puberty in primates

Development and organization of the hypophysiotropic hypothalamus driving the pituitary-gonadal axis in the rhesus monkey

Abstract Le but de cette revue est de décrire, tout particulièrement chez le singe rhésus, l\u27ontogenèse et l\u27organisation fonctionnelle du générateur de pulse à GnRH au niveau de l\u27hypothalamus. Cette fonction est assurée chez les primates, par un groupe d\u27environ 1 000 neurones répartis diffusément dans l\u27ensemble de l\u27hypothalamus. Le GnRH, initialement produit sous forme d\u27une préhormone, est déversé dans la circulation porte-hypothalamo-hypophysaire et va permettre la libération de FSH et LH. Abstract The purpose of the present review is to describe, with particular emphasis on the rhesus monkey, the ontogeny and functional organisation of the hypothalamic GnRH pulse generator. Control of pituitary-gonadal axis in higher primates is provided by a group of some 1,000 GnRH neurons that are diffusely distributed throughout the hypothalamus. After synthesis of a prehormone and formation of the mature decapeptide, GnRH is released in the hypophysial portal circulation and stimulates FSH and LH production

Neuronal suppressor of cytokine signaling-3 deficiency enhances hypothalamic leptin-dependent phosphatidylinositol 3-kinase signaling

Suppressor of cytokine signaling-3 (SOCS3) is thought to be involved in the development of central leptin resistance and obesity by inhibiting STAT3 pathway. Because phosphatidylinositol 3-kinase (PI3K) pathway plays an important role in transducing leptin action in the hypothalamus, we examined whether SOCS3 exerted an inhibition on this pathway. We first determined whether leptin sensitivity in the hypothalamic PI3K pathway was increased in brain-specific Socs3-deficient (NesKO) mice. In NesKO mice, hypothalamic insulin receptor substrate-1 (IRS1)-associated PI3K activity was significantly increased at 30 min and remained elevated up to 2 h after leptin intraperitoneal injection, but in wild-type (WT) littermates, the significant increase was only at 30 min. Hypothalamic p-STAT3 levels were increased up to 5 h in NesKO as opposed to 2 h in WT mice. In food-restricted WT mice with reduced body weight, leptin increased hypothalamic PI3K activity only at 30 min, and p-STAT3 levels at 30–120 min postinjection. These results suggest increased leptin sensitivity in both PI3K and STAT3 pathways in the hypothalamus of NesKO mice, which was not due to a lean phenotype. In the next experiment with a clonal hypothalamic neuronal cell line expressing proopiomelanocortin, we observed that whereas leptin significantly increased IRS1-associated PI3K activity and p-JAK2 levels in cells transfected with control vector, it failed to do so in SOCS3-overexpressed cells. Altogether, these results imply a SOCS3 inhibition of the PI3K pathway of leptin signaling in the hypothalamus, which may be one of the mechanisms behind the development of central leptin resistance and obesity

Enhanced shot noise at bilayer graphene-superconductor junction

Transport properties of graphene-superconductor junction have been studied extensively to understand the interplay of the relativistic Dirac quasiparticles and superconductivity. Though shot noise measurements in graphene have been performed to realize many theoretical predictions, both at zero magnetic field as well as quantum Hall (QH) regime, its junction with superconductor remain unexplored. Here, we have carried out the shot noise measurements in an edge contacted bilayer graphene-niobium superconductor junction at zero magnetic field as well as QH regime. At the Dirac point we have observed a Fano factor similar to 1/3 above the superconducting gap (Delta) and a transition to an enhanced Fano factor similar to 0.5 below the superconducting gap. By changing the carrier density we have found a continuous reduction of Fano factor for both types of carriers; however, the enhancement of Fano factor within the superconducting gap by a factor of similar to 1.5 is always preserved. The enhancement of shot noise is also observed in the QH regime, where the current is carried by the edge state, below the critical magnetic field and within the superconducting gap. These observations clearly demonstrate the enhanced charge transport at the graphene-superconductor interface