Field Induced Nodal Order Parameter in the Tunneling Spectrum of YBa2_2Cu3_3O7−x_{7-x} Superconductor

We report planar tunneling measurements on thin films of YBa$_2$Cu$_3$O$_{7-x}$ at various doping levels under magnetic fields. By choosing a special setup configuration, we have probed a field induced energy scale that dominates in the vicinity of a node of the d-wave superconducting order parameter. We found a high doping sensitivity for this energy scale. At Optimum doping this energy scale is in agreement with an induced $id_{xy}$ order parameter. We found that it can be followed down to low fields at optimum doping, but not away from it.Comment: 9 pages, 8 figures, accepted for publication in Phys. Rev.

Determination of the critical current density in the d-wave superconductor YBCO under applied magnetic fields by nodal tunneling

We have studied nodal tunneling into YBa2Cu3O7-x (YBCO) films under magnetic fields. The films' orientation was such that the CuO2 planes were perpendicular to the surface with the a and b axis at 450 form the normal. The magnetic field was applied parallel to the surface and perpendicular to the CuO2 planes. The Zero Bias Conductance Peak (ZBCP) characteristic of nodal tunneling splits under the effect of surface currents produced by the applied fields. Measuring this splitting under different field conditions, zero field cooled and field cooled, reveals that these currents have different origins. By comparing the field cooled ZBCP splitting to that taken in decreasing fields we deduce a value of the Bean critical current superfluid velocity, and calculate a Bean critical current density of up to 3*10^7 A/cm2 at low temperatures. This tunneling method for the determination of critical currents under magnetic fields has serious advantages over the conventional one, as it avoids having to make high current contacts to the sample.Comment: 8 pages, 2 figure

Human herpesvirus multiplex ddPCR detection in brain tissue from low- and high-grade astrocytoma cases and controls.

BACKGROUND: Glioblastoma (GBM) is a fatal CNS malignancy, representing 50 % of all gliomas with approximately 12-18 months survival time after initial diagnosis. Recently, the human herpesvirus cytomegalovirus (CMV) has been suggested to have an oncogenic role, yet this association remains controversial. In addition, human herpesvirus 6 (HHV-6) and Epstein-Barr virus (EBV) have also been associated with low-grade gliomas, but few studies have examined HHV-6 and EBV in glioblastomas. Droplet digital PCR (ddPCR) is a highly precise diagnostic tool that enables the absolute quantification of target DNA. This study examines the association between multiple human herpesviruses and astrocytomas. METHODS: This study analyzed 112 brain tissue specimens, including 45 glioblastoma, 12 astrocytoma grade III, 2 astrocytoma grade II, 4 astrocytoma grade I, and 49 controls. All brain tissue samples were de-identified and pathologically confirmed. Each tissue block was sectioned for DNA extraction and CMV, EBV, HHV-6A and HHV-6B, and a cellular housekeeping gene were amplified by ddPCR. RESULTS: Neither CMV nor HHV-6A were detected in any of the astrocytoma samples. However, HHV-6B (p = 0.147) and EBV (p = 0.049) had a higher positivity frequency in the GBM compared to the controls. CONCLUSION: The undetectable CMV DNA in the astrocytoma cohort does not support the observation of an increased prevalence of CMV DNA in GBM, as reported in other studies. EBV has a significantly higher positivity in the GBM cohort compared to the controls, while HHV-6B has a higher but not statistically significant positivity in the case cohort. Whether these viruses play an oncogenic role in GBM remains to be further investigated

Scanning tunneling spectroscopy of a-axis YBa_2Cu_3O_7-\delta films:k-selectivity and the shape of the superconductor

Tunneling spectroscopy of epitaxial (100) oriented \chem{YBa_2Cu_3O_{7-\delta}} films was performed using an STM at 4.2 K. On atomically smooth areas, tunneling spectra revealing clear U-shaped gaps with relatively low zero bias conductance were measured. These spectra can be well fitted to the tunneling theory into a d-wave superconductor only when introducing a strong dependence of the tunneling probability on the wave-vector \emph{\textbf{k}}. Possible origins for this \emph{\textbf{k}}-selectivity in STM measurements will be discussed. On other areas, V-shaped gaps as well as zero bias conductance peaks are observed, indicating relaxation of \emph{\textbf{k}}-selectivity and the effect of nanofaceting, respectively.Comment: 7 epl pages, 4 embeded figure

Inhibition of Atrogin-1/MAFbx Mediated MyoD Proteolysis Prevents Skeletal Muscle Atrophy In Vivo

Ubiquitin ligase Atrogin1/Muscle Atrophy F-box (MAFbx) up-regulation is required for skeletal muscle atrophy but substrates and function during the atrophic process are poorly known. The transcription factor MyoD controls myogenic stem cell function and differentiation, and seems necessary to maintain the differentiated phenotype of adult fast skeletal muscle fibres. We previously showed that MAFbx mediates MyoD proteolysis in vitro. Here we present evidence that MAFbx targets MyoD for degradation in several models of skeletal muscle atrophy. In cultured myotubes undergoing atrophy, MAFbx expression increases, leading to a cytoplasmic-nuclear shuttling of MAFbx and a selective suppression of MyoD. Conversely, transfection of myotubes with sh-RNA-mediated MAFbx gene silencing (shRNAi) inhibited MyoD proteolysis linked to atrophy. Furthermore, overexpression of a mutant MyoDK133R lacking MAFbx-mediated ubiquitination prevents atrophy of mouse primary myotubes and skeletal muscle fibres in vivo. Regarding the complex role of MyoD in adult skeletal muscle plasticity and homeostasis, its rapid suppression by MAFbx seems to be a major event leading to skeletal muscle wasting. Our results point out MyoD as the second MAFbx skeletal muscle target by which powerful therapies could be developed

Plasma Dynamics

Contains reports on five research projects.U.S. Air Force - Office of Scientifc Research (Contract AFOSR 84-0026)National Science Foundation (Grant ECS 85-14517)Lawrence Livermore National Laboratory (Subcontract 6264005)National Science Foundation (Grant ECS 85-15032)U.S. Department of Energy (Contract DE-ACO2-78-ET-51013)U.S. Department of Energy (Contract DE-ACO2-ET-51013

Nuclear Receptor SHP Activates miR-206 Expression via a Cascade Dual Inhibitory Mechanism

MicroRNAs play a critical role in many essential cellular functions in the mammalian species. However, limited information is available regarding the regulation of miRNAs gene transcription. Microarray profiling and real-time PCR analysis revealed a marked down-regulation of miR-206 in nuclear receptor SHP−/− mice. To understand the regulatory function of SHP with regard to miR-206 gene expression, we determined the putative transcriptional initiation site of miR-206 and also its full length primary transcript using a database mining approach and RACE. We identified the transcription factor AP1 binding sites on the miR-206 promoter and further showed that AP1 (c-Jun and c-Fos) induced miR-206 promoter transactivity and expression which was repressed by YY1. ChIP analysis confirmed the physical association of AP1 (c-Jun) and YY1 with the endogenous miR-206 promoter. In addition, we also identified nuclear receptor ERRγ (NR3B3) binding site on the YY1 promoter and showed that YY1 promoter was transactivated by ERRγ, which was inhibited by SHP (NROB2). ChIP analysis confirmed the ERRγ binding to the YY1 promoter. Forced expression of SHP and AP1 induced miR-206 expression while overexpression of ERRγ and YY1 reduced its expression. The effects of AP1, ERRγ, and YY1 on miR-206 expression were reversed by siRNA knockdown of each gene, respectively. Thus, we propose a novel cascade “dual inhibitory” mechanism governing miR-206 gene transcription by SHP: SHP inhibition of ERRγ led to decreased YY1 expression and the de-repression of YY1 on AP1 activity, ultimately leading to the activation of miR-206. This is the first report to elucidate a cascade regulatory mechanism governing miRNAs gene transcription

Plasma Dynamics

Contains table of contents for Section 2 and reports on four research projects.Lawrence Livermore National Laboratory Subcontract 6264005National Science Foundation Grant ECS 84-13173National Science Foundation Grant ECS 85-14517U.S. Air Force - Office of Scientific Research Contract AFOSR 89-0082-AU.S. Army - Harry Diamond Laboratories Contract DAAL02-86-C-0050U.S. Navy - Office of Naval Research Contract N00014-87-K-2001Lawrence Livermore National Laboratory Subcontract B108472National Science Foundation Grant ECS 88-22475U.S. Department of Energy Contract DE-FG02-91-ER-54109National Aeronautics and Space Administration Grant NAGW-2048U.S. Department of Energy Contract DE-AC02-ET-51013U.S. Department of Energy Contract DE-AC02-78-ET-5101