Ballistic Josephson junctions in edge-contacted graphene

Hybrid graphene-superconductor devices have attracted much attention since the early days of graphene research. So far, these studies have been limited to the case of diffusive transport through graphene with poorly defined and modest quality graphene-superconductor interfaces, usually combined with small critical magnetic fields of the superconducting electrodes. Here we report graphene based Josephson junctions with one-dimensional edge contacts of Molybdenum Rhenium. The contacts exhibit a well defined, transparent interface to the graphene, have a critical magnetic field of 8 Tesla at 4 Kelvin and the graphene has a high quality due to its encapsulation in hexagonal boron nitride. This allows us to study and exploit graphene Josephson junctions in a new regime, characterized by ballistic transport. We find that the critical current oscillates with the carrier density due to phase coherent interference of the electrons and holes that carry the supercurrent caused by the formation of a Fabry-P\'{e}rot cavity. Furthermore, relatively large supercurrents are observed over unprecedented long distances of up to 1.5 $\mu$m. Finally, in the quantum Hall regime we observe broken symmetry states while the contacts remain superconducting. These achievements open up new avenues to exploit the Dirac nature of graphene in interaction with the superconducting state.Comment: Updated version after peer review. Includes supplementary material and ancillary file with source code for tight binding simulation

Quantum oscillations of the critical current and high-field superconducting proximity in ballistic graphene

Graphene-based Josephson junctions provide a novel platform for studying the proximity effect due to graphene's unique electronic spectrum and the possibility to tune junction properties by gate voltage. Here we describe graphene junctions with a mean free path of several micrometres, low contact resistance and large supercurrents. Such devices exhibit pronounced Fabry-P\'erot oscillations not only in the normal-state resistance but also in the critical current. The proximity effect is mostly suppressed in magnetic fields below 10mT, showing the conventional Fraunhofer pattern. Unexpectedly, some proximity survives even in fields higher than 1 T. Superconducting states randomly appear and disappear as a function of field and carrier concentration, and each of them exhibits a supercurrent carrying capacity close to the universal quantum limit. We attribute the high-field Josephson effect to mesoscopic Andreev states that persist near graphene edges. Our work reveals new proximity regimes that can be controlled by quantum confinement and cyclotron motion

Determinants of Complementary Feeding Practices Among Nepalese Children Aged 6-23 Months: Findings From Demographic and Health Survey 2011

Background: The adoption of inappropriate feeding practices is one of the reasons for under nutrition in Nepal and elsewhere. The objective of this study was to describe the rate of and identify the factors associated with providing the World Health Organization (WHO) recommended infant feeding practices of minimum dietary diversity, minimum meal frequency and minimum acceptable diet in Nepal amongst young children between 6–23 months in 2011. Methods: Data from Nepal Demographic and Health Survey (NDHS) 2011 was used. Prevalence of minimum dietary diversity, minimum meal frequency and minimum acceptable diet was obtained by using descriptive statistics. A Chi-square test (χ2) followed by multiple logistic regression analyses were used to determine the adjusted effect of potential factors on the outcome variables. Results: Of the 698 children aged 6–23 months; while 535 (76.6%) received the minimum meal frequency, only 212 (30.4%) children received the minimum dietary diversity, and 185 (26.5%) received an acceptable diet. Children of older mothers (>35 years); educated mothers and fathers; and mothers from all the development regions except the Mid-western region were more likely to have been provided with the recommended dietary diversity. Children of mothers who had attended ≥4 antenatal visits and who lived in the Eastern region were more likely to provide their child with the recommended meal frequency. Children of mothers, who attended ≥ 4 antenatal visits, were educated and whose fathers had at least a secondary education were more likely to meet the recommended acceptable diet standards.Conclusion: Young children aged less than two years in Nepal are at risk for not meeting the WHO recommended infant feeding standards given that only about one in three children were provided with the recommended dietary diversity and acceptable diet. This finding suggests that the majority of children are at risk of under nutrition. An appropriate mix of health education and food supplements could be a feasible option for Nepal to improve the number of children who meet the recommended infant feeding guidelines, reduce under nutrition and improve the survival rates of young children

Genomic expression profiling of human inflammatory cardiomyopathy (DCMi) suggests novel therapeutic targets

The clinical phenotype of human dilated cardiomyopathy (DCM) encompasses a broad spectrum of etiologically distinct disorders. As targeting of etiology-related pathogenic pathways may be more efficient than current standard heart failure treatment, we obtained the genomic expression profile of a DCM subtype characterized by cardiac inflammation to identify possible new therapeutic targets in humans. In this inflammatory cardiomyopathy (DCMi), a distinctive cardiac expression pattern not described in any previous study of cardiac disorders was observed. Two significantly altered gene networks of particular interest and possible interdependence centered around the cysteine-rich angiogenic inducer 61 (CYR61) and adiponectin (APN) gene. CYR61 overexpression, as in human DCMi hearts in situ, was similarly induced by inflammatory cytokines in vascular endothelial cells in vitro. APN was strongly downregulated in DCMi hearts and completely abolished cytokine-dependent CYR61 induction in vitro. Dysbalance between the CYR61 and APN networks may play a pathogenic role in DCMi and contain novel therapeutic targets. Multiple immune cell-associated genes were also deregulated (e.g., chemokine ligand 14, interleukin-17D, nuclear factors of activated T cells). In contrast to previous investigations in patients with advanced or end-stage DCM where etiology-related pathomechanisms are overwhelmed by unspecific processes, the deregulations detected in this study occurred at a far less severe and most probably fully reversible disease stage. ELECTRONIC SUPPLEMENTARY MATERIAL: Supplementary material is available in the online version of this article at http://dx.doi.org/10.1007/s00109-006-0122-9 and is accessible for authorized users

Aldose Reductase Inhibition Prevents Metaplasia of Airway Epithelial Cells

BACKGROUND: Goblet cell metaplasia that causes mucus hypersecretion and obstruction in the airway lumen could be life threatening in asthma and chronic obstructive pulmonary disease patients. Inflammatory cytokines such as IL-13 mediate the transformation of airway ciliary epithelial cells to mucin-secreting goblet cells in acute as well as chronic airway inflammatory diseases. However, no effective and specific pharmacologic treatment is currently available. Here, we investigated the mechanisms by which aldose reductase (AR) regulates the mucus cell metaplasia in vitro and in vivo. METHODOLOGY/FINDINGS: Metaplasia in primary human small airway epithelial cells (SAEC) was induced by a Th2 cytokine, IL-13, without or with AR inhibitor, fidarestat. After 48 h of incubation with IL-13 a large number of SAEC were transformed into goblet cells as determined by periodic acid-schiff (PAS)-staining and immunohistochemistry using antibodies against Mucin5AC. Further, IL-13 significantly increased the expression of Mucin5AC at mRNA and protein levels. These changes were significantly prevented by treatment of the SAEC with AR inhibitor. AR inhibition also decreased IL-13-induced expression of Muc5AC, Muc5B, and SPDEF, and phosphorylation of JAK-1, ERK1/2 and STAT-6. In a mouse model of ragweed pollen extract (RWE)-induced allergic asthma treatment with fidarestat prevented the expression of IL-13, phosphorylation of STAT-6 and transformation of epithelial cells to goblet cells in the lung. Additionally, while the AR-null mice were resistant, wild-type mice showed goblet cell metaplasia after challenge with RWE. CONCLUSIONS: The results show that exposure of SAEC to IL-13 caused goblet cell metaplasia, which was significantly prevented by AR inhibition. Administration of fidarestat to mice prevented RWE-induced goblet cell metaplasia and AR null mice were largely resistant to allergen induced changes in the lung. Thus our results indicate that AR inhibitors such as fidarestat could be developed as therapeutic agents to prevent goblet cell metaplasia in asthma and related pathologies