510 research outputs found

    Metal-semiconductor field-effect transistors fabricated using DVT grown n-MoSe2 crystals with Cu-Schottky gates

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    Metal-semiconductor field-effect transistors (MESFETs) based on DVT grown MoSe2 crystals and Cu Schottky gate have been fabricated and studied. When Schottky gate voltage (Vgs) changes from 0 to 10 V, the source-drain current (Ids) increases exponentially with Vgs and the conductance shows a drastic increase with positive Vgs. The fabricated n-MoSe2 MESFET have a saturated current level of about 100 mA and maximum transconductance of about 53 mA/V. Their results suggest a way of fabricating MESFETs from layered metal dichalcogenide semiconducting materials. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/2207

    LCCC 1025: a phase II study of everolimus, trastuzumab, and vinorelbine to treat progressive HER2-positive breast cancer brain metastases

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    Purpose: HER2 + breast cancer (BC) is an aggressive subtype with high rates of brain metastases (BCBM). Two-thirds of HER2 + BCBM demonstrate activation of the PI3K/mTOR pathway driving resistance to anti-HER2 therapy. This phase II study evaluated everolimus (E), a brain-permeable mTOR inhibitor, trastuzumab (T), and vinorelbine (V) in patients with HER2 + BCBM. Patients and methods: Eligible patients had progressive HER2 + BCBM. The primary endpoint was intracranial response rate (RR); secondary objectives were CNS clinical benefit rate (CBR), extracranial RR, time to progression (TTP), overall survival (OS), and targeted sequencing of tumors from enrolled patients. A two-stage design distinguished intracranial RR of 5% versus 20%. Results: 32 patients were evaluable for toxicity, 26 for efficacy. Intracranial RR was 4% (1 PR). CNS CBR at 6 mos was 27%; at 3 mos 65%. Median intracranial TTP was 3.9 mos (95% CI 2.2–5). OS was 12.2 mos (95% CI 0.6–20.2). Grade 3–4 toxicities included neutropenia (41%), anemia (16%), and stomatitis (16%). Mutations in TP53 and PIK3CA were common in BCBM. Mutations in the PI3K/mTOR pathway were not associated with response. ERBB2 amplification was higher in BCBM compared to primary BC; ERBB2 amplification in the primary BC trended toward worse OS. Conclusion: While intracranial RR to ETV was low in HER2 + BCBM patients, one-third achieved CNS CBR; TTP/OS was similar to historical control. No new toxicity signals were observed. Further analysis of the genomic underpinnings of BCBM to identify tractable prognostic and/or predictive biomarkers is warranted. Clinical Trial: (NCT01305941)

    Raditive decay of single charmed baryons

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    The electromagnetic transitions between (JP=3/2+J^{P}={3/2}^{+}) and (JP=1/2+J^{P}={1/2}^{+}) baryons are important decay modes to observe new hadronic states experimentally. For the estimation of these transitions widths, we employ a non-relativistic quark potential model description with color coulomb plus linear confinement potential. Such a description has been employed to compute the ground state masses and magnetic moments of the single heavy flavor baryons. The magnetic moments of the baryons are obtained using the spin-flavor structure of the constituting quark composition of the baryon. Here, we also define an effective constituent mass of the quarks (ecqm) by taking into account the binding effects of the quarks within the baryon. The radiative transition widths are computed in terms of the magnetic moments of the baryon and the photon energy. Our results are compared with other theoretical models.Comment: 06 Pages, Presented at XVIII DAE-BRNS symposium on High energy Physics, Banaras Hindu University, Varansi, INDI

    Measurement of νˉμ\bar{\nu}_{\mu} and νμ\nu_{\mu} charged current inclusive cross sections and their ratio with the T2K off-axis near detector

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    We report a measurement of cross section σ(νμ+nucleusμ+X)\sigma(\nu_{\mu}+{\rm nucleus}\rightarrow\mu^{-}+X) and the first measurements of the cross section σ(νˉμ+nucleusμ++X)\sigma(\bar{\nu}_{\mu}+{\rm nucleus}\rightarrow\mu^{+}+X) and their ratio R(σ(νˉ)σ(ν))R(\frac{\sigma(\bar \nu)}{\sigma(\nu)}) at (anti-)neutrino energies below 1.5 GeV. We determine the single momentum bin cross section measurements, averaged over the T2K νˉ/ν\bar{\nu}/\nu-flux, for the detector target material (mainly Carbon, Oxygen, Hydrogen and Copper) with phase space restricted laboratory frame kinematics of θμ\theta_{\mu}500 MeV/c. The results are σ(νˉ)=(0.900±0.029(stat.)±0.088(syst.))×1039\sigma(\bar{\nu})=\left( 0.900\pm0.029{\rm (stat.)}\pm0.088{\rm (syst.)}\right)\times10^{-39} and $\sigma(\nu)=\left( 2.41\ \pm0.022{\rm{(stat.)}}\pm0.231{\rm (syst.)}\ \right)\times10^{-39}inunitsofcm in units of cm^{2}/nucleonand/nucleon and R\left(\frac{\sigma(\bar{\nu})}{\sigma(\nu)}\right)= 0.373\pm0.012{\rm (stat.)}\pm0.015{\rm (syst.)}$.Comment: 18 pages, 8 figure

    An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

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    For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types
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