690 research outputs found

    Disproportionation Phenomena on Free and Strained Sn/Ge(111) and Sn/Si(111) Surfaces

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    Distortions of the 3×3\sqrt3\times\sqrt3 Sn/Ge(111) and Sn/Si(111) surfaces are shown to reflect a disproportionation of an integer pseudocharge, QQ, related to the surface band occupancy. A novel understanding of the (3×3)(3\times3)-1U (``1 up, 2 down'') and 2U (``2 up, 1 down'') distortions of Sn/Ge(111) is obtained by a theoretical study of the phase diagram under strain. Positive strain keeps the unstrained value Q=3 but removes distorsions. Negative strain attracts pseudocharge from the valence band causing first a (3×3)(3\times3)-2U distortion (Q=4) on both Sn/Ge and Sn/Si, and eventually a (3×3)(\sqrt3\times\sqrt3)-3U (``all up'') state with Q=6. The possibility of a fluctuating phase in unstrained Sn/Si(111) is discussed.Comment: Revtex, 5 pages, 3 figure

    Primary cutaneous anaplastic large cell lymphoma shows a distinct miRNA expression profile and reveals differences from tumor-stage mycosis fungoides

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    Copyright @ 2012 John Wiley & SonsThe miRNA expression profiles of skin biopsies from 14 primary cutaneous anaplastic large cell lymphoma (C-ALCL) patients were analysed with miRNA microarrays using the same control group of 12 benign inflammatory dermatoses (BID) as previously used to study the miRNA expression profile of tumor-stage mycosis fungoides (MF). We identified 13 differentially expressed miRNAs between C-ALCL and BID. The up-regulation of miR-155, miR-27b, miR-30c and miR-29b in C-ALCL was validated by miRNA-Q-PCR on independent study groups. Additionally, the miRNA expression profiles of C-ALCL were compared with those of tumor-stage MF. Although miRNA microarray analysis did not identify statistically significant differentially expressed miRNAs, miRNA-Q-PCR demonstrated statistically significantly differential expression of miR-155, miR-27b, miR-93, miR-29b and miR-92a between tumor-stage MF and C-ALCL. This study, the first describing the miRNA expression profile of C-ALCL, reveals differences with tumor-stage MF, suggesting a different contribution to the pathogenesis of these lymphomas.This work was funded by grants from Netherlands Organization for Scientific Research (NWO) (MHV) and the Fondation Rene´ Touraine (MvK), and grants from the Leukaemia and Lymphoma Research (EB) and the Julian Starmer-Smith Memorial Fund (CHL)

    Composition-Dependent Passivation Efficiency at the CdS/CuIn1-xGaxSe2 Interface

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    Multistep, sequential control of the trafficking and function of the multiple sulfatase deficiency gene product, SUMF1 by PDI, ERGIC-53 and ERp44.

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    Sulfatase modifying factor 1 (SUMF1) encodes for the formylglicine generating enzyme, which activates sulfatases by modifying a key cysteine residue within their catalytic domains. SUMF1 is mutated in patients affected by multiple sulfatase deficiency, a rare recessive disorder in which all sulfatase activities are impaired. Despite the absence of canonical retention/retrieval signals, SUMF1 is largely retained in the endoplasmic reticulum (ER), where it exerts its enzymatic activity on nascent sulfatases. Part of SUMF1 is secreted and paracrinally taken up by distant cells. Here we show that SUMF1 interacts with protein disulfide isomerase (PDI) and ERp44, two thioredoxin family members residing in the early secretory pathway, and with ERGIC-53, a lectin that shuttles between the ER and the Golgi. Functional assays reveal that these interactions are crucial for controlling SUMF1 traffic and function. PDI couples SUMF1 retention and activation in the ER. ERGIC-53 and ERp44 act downstream, favoring SUMF1 export from and retrieval to the ER, respectively. Silencing ERGIC-53 causes proteasomal degradation of SUMF1, while down-regulating ERp44 promotes its secretion. When over-expressed, each of three interactors favors intracellular accumulation. Our results reveal a multistep control of SUMF1 trafficking, with sequential interactions dynamically determining ER localization, activity and secretion

    Genomic imbalances are confined to non-proliferating cells in paediatric patients with acute myeloid leukaemia and a normal or incomplete karyotype

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    Copyright @ 2011 Ballabio et al.Leukaemia is often associated with genetic alterations such as translocations, amplifications and deletions, and recurrent chromosome abnormalities are used as markers of diagnostic and prognostic relevance. However, a proportion of acute myeloid leukaemia (AML) cases have an apparently normal karyotype despite comprehensive cytogenetic analysis. Based on conventional cytogenetic analysis of banded chromosomes, we selected a series of 23 paediatric patients with acute myeloid leukaemia and performed whole genome array comparative genome hybridization (aCGH) using DNA samples derived from the same patients. Imbalances involving large chromosomal regions or entire chromosomes were detected by aCGH in seven of the patients studied. Results were validated by fluorescence in situ hybridization (FISH) to both interphase nuclei and metaphase chromosomes using appropriate bacterial artificial chromosome (BAC) probes. The majority of these copy number alterations (CNAs) were confirmed by FISH and found to localize to the interphase rather than metaphase nuclei. Furthermore, the proliferative states of the cells analyzed by FISH were tested by immunofluorescence using an antibody against the proliferation marker pKi67. Interestingly, these experiments showed that, in the vast majority of cases, the changes appeared to be confined to interphase nuclei in a non-proliferative status.This work was supported by a grant from Leukaemia Research UK (grant no. 0253). SJLK and RR were supported by the NIHR Biomedical Research Centre, Oxford, with funding from the Department of Health’s NIHR Biomedical Research Centres funding schemeThis article is available through the Brunel Open Access Publishing Fund

    Mid-Infrared Plasmonic Platform Based on n-Doped Ge-on-Si: Molecular Sensing with Germanium Nano-Antennas on Si

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    CMOS-compatible, heavily-doped semiconductor films are very promising for applications in mid-infrared plasmonic devices because the real part of their dielectric function is negative and broadly tunable in this wavelength range. In this work we investigate n-type doped germanium epilayers grown on Si substrates. We design and realize Ge nanoantennas on Si substrates demonstrating the presence of localized plasmon resonances, and exploit them for molecular sensing in the mid-infrared

    The mechanism for the 3 x 3 distortion of Sn/ge (111)

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    We show that two distinct 3×33 \times 3 ground states, one nonmagnetic, metallic, and distorted, the other magnetic, semimetallic (or insulating) and undistorted, compete in α\alpha-phase adsorbates on semiconductor (111) surfaces. In Sn/Ge(111), LSDA/GGA calculations indicate, in agreement with experiment, that the distorted metallic ground state prevails. The reason for stability of this state is analysed, and is traced to a sort of bond density wave, specifically a modulation of the antibonding state filling between the adatom and a Ge-Ge bond directly underneath

    Optical properties of highly n-doped germanium obtained by in situ doping and laser annealing

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    High n-type doping in germanium is essential for many electronic and optoelectronic applications especially for high performance Ohmic contacts, lasing and mid-infrared plasmonics. We report on the combination of in situ doping and excimer laser annealing to improve the activation of phosphorous in germanium. An activated n-doping concentration of 8.8  ×  1019 cm−3 has been achieved starting from an incorporated phosphorous concentration of 1.1  ×  1020 cm−3. Infrared reflectivity data fitted with a multi-layer Drude model indicate good uniformity over a 350 nm thick layer. Photoluminescence demonstrates clear bandgap narrowing and an increased ratio of direct to indirect bandgap emission confirming the high doping densities achieved
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