1,633 research outputs found

    Distinction between the Poole-Frenkel and tunneling models of electric field-stimulated carrier emission from deep levels in semiconductors

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    The enhancement of the emission rate of charge carriers from deep-level defects in electric field is routinely used to determine the charge state of the defects. However, only a limited number of defects can be satisfactorily described by the Poole-Frenkel theory. An electric field dependence different from that expected from the Poole-Frenkel theory has been repeatedly reported in the literature, and no unambiguous identification of the charge state of the defect could be made. In this article, the electric field dependencies of emission of carriers from DX centers in AlxGa1-xAs:Te, Cu pairs in silicon, and Ge:Hg have been studied applying static and terahertz electric fields, and analyzed by using the models of Poole-Frenkel and phonon assisted tunneling. It is shown that phonon assisted tunneling and Poole-Frenkel emission are two competitive mechanisms of enhancement of emission of carriers, and their relative contribution is determined by the charge state of the defect and by the electric-field strength. At high-electric field strengths carrier emission is dominated by tunneling independently of the charge state of the impurity. For neutral impurities, where Poole-Frenkel lowering of the emission barrier does not occur, the phonon assisted tunneling model describes well the experimental data also in the low-field region. For charged impurities the transition from phonon assisted tunneling at high fields to Poole-Frenkel effect at low fields can be traced back. It is suggested that the Poole-Frenkel and tunneling models can be distinguished by plotting logarithm of the emission rate against the square root or against the square of the electric field, respectively. This analysis enables one to unambiguously determine the charge state of a deep-level defect

    Search for Magnetic Monopoles Trapped in Matter

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    There have been many searches for magnetic monopoles in flight, but few for monopoles in matter. We have searched for magnetic monopoles in meteorites, schists, ferromanganese nodules, iron ores and other materials. The detector was a superconducting induction coil connected to a SQUID (Superconducting Quantum Interference Device) with a room temperature bore 15 cm in diameter. We tested a total of more than 331 kg of material including 112 kg of meteorites. We found no monopole and conclude the overall monopole/nucleon ratio in the samples is <1.2×1029<1.2 \times 10^{-29} with a 90\% confidence level.Comment: 6 pages, rev tex, no figure

    Virtual screening for inhibitors of the human TSLP:TSLPR interaction

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    The pro-inflammatory cytokine thymic stromal lymphopoietin (TSLP) plays a pivotal role in the pathophysiology of various allergy disorders that are mediated by type 2 helper T cell (Th2) responses, such as asthma and atopic dermatitis. TSLP forms a ternary complex with the TSLP receptor (TSLPR) and the interleukin-7-receptor subunit alpha (IL-7Ra), thereby activating a signaling cascade that culminates in the release of pro-inflammatory mediators. In this study, we conducted an in silico characterization of the TSLP: TSLPR complex to investigate the drugability of this complex. Two commercially available fragment libraries were screened computationally for possible inhibitors and a selection of fragments was subsequently tested in vitro. The screening setup consisted of two orthogonal assays measuring TSLP binding to TSLPR: a BLI-based assay and a biochemical assay based on a TSLP: alkaline phosphatase fusion protein. Four fragments pertaining to diverse chemical classes were identified to reduce TSLP: TSLPR complex formation to less than 75% in millimolar concentrations. We have used unbiased molecular dynamics simulations to develop a Markov state model that characterized the binding pathway of the most interesting compound. This work provides a proof-ofprinciple for use of fragments in the inhibition of TSLP: TSLPR complexation

    Weight Loss after Roux-en-Y Gastric Bypass in Obese Patients Heterozygous for MC4R Mutations

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    BackgroundHeterozygous mutations in melanocortin-4 receptor (MC4R) are the most frequent genetic cause of obesity. Bariatric surgery is a successful treatment for severe obesity. The mechanisms of weight loss after bariatric surgery are not well understood.MethodsNinety-two patients who had Roux-en-Y gastric bypass (RYGB) surgery were screened for MC4R mutations. We compared percent excess weight loss (%EWL) in the four MC4R mutation carriers with that of two control groups: 8 matched controls and with the remaining 80 patients who underwent RYGB.ResultsFour patients were heterozygous for functionally significant MC4R mutations. In patients with MC4R mutations, the %EWL after RYGB (66% EWL) was not significantly different compared to matched controls (70% EWL) and non-matched controls (60% EWL) after 1 year of follow-up.ConclusionsThis study suggests that patients with heterozygous MC4R mutations also benefit from RYGB and that weight loss may be independent of the presence of such mutations

    A gene signature for post-infectious chronic fatigue syndrome

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    Background: At present, there are no clinically reliable disease markers for chronic fatigue syndrome. DNA chip microarray technology provides a method for examining the differential expression of mRNA from a large number of genes. Our hypothesis was that a gene expression signature, generated by microarray assays, could help identify genes which are dysregulated in patients with post-infectious CFS and so help identify biomarkers for the condition. Methods: Human genome-wide Affymetrix GeneChip arrays (39,000 transcripts derived from 33,000 gene sequences) were used to compare the levels of gene expression in the peripheral blood mononuclear cells of male patients with post-infectious chronic fatigue (n = 8) and male healthy control subjects (n = 7). Results: Patients and healthy subjects differed significantly in the level of expression of 366 genes. Analysis of the differentially expressed genes indicated functional implications in immune modulation, oxidative stress and apoptosis. Prototype biomarkers were identified on the basis of differential levels of gene expression and possible biological significance Conclusion: Differential expression of key genes identified in this study offer an insight into the possible mechanism of chronic fatigue following infection. The representative biomarkers identified in this research appear promising as potential biomarkers for diagnosis and treatment

    SSA-Based Register Allocation with PBQP

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    Abstract. Recent research shows that maintaining SSA form allows to split register allocation into separate phases: spilling, register assign-ment and copy coalescing. After spilling, register assignment can be done in polynomial time, but copy coalescing is NP-complete. In this pa-per we present an assignment approach with integrated copy coalescing, which maps the problem to the Partitioned Boolean Quadratic Problem (PBQP). Compared to the state-of-the-art recoloring approach, this re-duces the relative number of swap and copy instructions for the SPEC CINT2000 benchmark to 99.6 % and 95.2%, respectively, while taking 19 % less time for assignment and coalescing

    Mild Pd-Catalyzed Aminocarbonylation of (Hetero)Aryl Bromides with a Palladacycle Precatalyst

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    A palladacyclic precatalyst is employed to cleanly generate a highly active XantPhos-ligated Pd-catalyst. Its use in low temperature aminocarbonylations of (hetero)aryl bromides provides access to a range of challenging products in good to excellent yields with low catalyst loading and only a slight excess of CO. Some products are unattainable by traditional carbonylative coupling.National Institutes of Health (U.S.) (Award GM46059)Danish National Research Foundation (Grant DNRF59)Villum FoundationDanish Council for Independent Researc

    Linkage of cystic fibrosis to the proα2(I) collagen gene, COL1A2, on chromosome 7

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    A linkage has been detected between the locus for cystic fibrosis (CF) and the proα2(I) collagen gene (COL1A2) which is located in the region q21.3→q22.1 of chromosome 7. Based on the combined linkage data derived from 50 informative two-generation nuclear families collected in Canada and Denmark, the distance between COL1A2 and CF is estimated to be 19 centiMorgans. Close lilnkage has also been detected between COL1A2 and the DNA market D7S15 (formerly D0CRI-917) and the serum enzyme activity marker paraoxonase (PON), both of which have previously been found linked to CF. The results of the two-oint and three-point linkage analyses indicate that the most probable order of these four genetic loci is COL1A2-D7S15-PON-CF.published_or_final_versio
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