774 research outputs found
Current transport property of n-GaN/n-6H-SiC heterojunction: Influence of interface states
Heterostructures of n-GaNn-6H-SiC grown by hydride vapor phase epitaxy (HVPE) and molecular-beam epitaxy (MBE) are characterized with the current-voltage (I-V), capacitance-voltage (C-V), and deep level transient spectroscopy (DLTS) techniques. Using different contact configurations, the I-V results reveal a rectifying barrier in the n-GaNn-6H-SiC heterostructures. When GaN is negatively biased, the current is exponentially proportional to the applied voltage with the built-in barrier being 0.4-1.1 eV for the HVPE samples and 0.5 eV for the MBE sample. DLTS measurements reveal intense band-like deep level states in the interfacial region of the heterostructure, and the Fermi-level pinning by these deep level defects is invoked to account for the interfacial rectifying barrier of the heterostructures. © 2005 American Institute of Physics.published_or_final_versio
Deformation of the Fermi surface in the extended Hubbard model
The deformation of the Fermi surface induced by Coulomb interactions is
investigated in the t-t'-Hubbard model. The interplay of the local U and
extended V interactions is analyzed. It is found that exchange interactions V
enhance small anisotropies producing deformations of the Fermi surface which
break the point group symmetry of the square lattice at the Van Hove filling.
This Pomeranchuck instability competes with ferromagnetism and is suppressed at
a critical value of U(V). The interaction V renormalizes the t' parameter to
smaller values what favours nesting. It also induces changes on the topology of
the Fermi surface which can go from hole to electron-like what may explain
recent ARPES experiments.Comment: 5 pages, 4 ps figure
Modeling recursive RNA interference.
An important application of the RNA interference (RNAi) pathway is its use as a small RNA-based regulatory system commonly exploited to suppress expression of target genes to test their function in vivo. In several published experiments, RNAi has been used to inactivate components of the RNAi pathway itself, a procedure termed recursive RNAi in this report. The theoretical basis of recursive RNAi is unclear since the procedure could potentially be self-defeating, and in practice the effectiveness of recursive RNAi in published experiments is highly variable. A mathematical model for recursive RNAi was developed and used to investigate the range of conditions under which the procedure should be effective. The model predicts that the effectiveness of recursive RNAi is strongly dependent on the efficacy of RNAi at knocking down target gene expression. This efficacy is known to vary highly between different cell types, and comparison of the model predictions to published experimental data suggests that variation in RNAi efficacy may be the main cause of discrepancies between published recursive RNAi experiments in different organisms. The model suggests potential ways to optimize the effectiveness of recursive RNAi both for screening of RNAi components as well as for improved temporal control of gene expression in switch off-switch on experiments
Structural insight into SUMO chain recognition and manipulation by the ubiquitin ligase RNF4
The small ubiquitin-like modifier (SUMO) can form polymeric chains that are important signals in cellular processes such as meiosis, genome maintenance and stress response. The SUMO-targeted ubiquitin ligase RNF4 engages with SUMO chains on linked substrates and catalyses their ubiquitination, which targets substrates for proteasomal degradation. Here we use a segmental labelling approach combined with solution nuclear magnetic resonance (NMR) spectroscopy and biochemical characterization to reveal how RNF4 manipulates the conformation of the SUMO chain, thereby facilitating optimal delivery of the distal SUMO domain for ubiquitin transfer
Wall roughness induces asymptotic ultimate turbulence
Turbulence is omnipresent in Nature and technology, governing the transport
of heat, mass, and momentum on multiple scales. For real-world applications of
wall-bounded turbulence, the underlying surfaces are virtually always rough;
yet characterizing and understanding the effects of wall roughness for
turbulence remains a challenge, especially for rotating and thermally driven
turbulence. By combining extensive experiments and numerical simulations, here,
taking as example the paradigmatic Taylor-Couette system (the closed flow
between two independently rotating coaxial cylinders), we show how wall
roughness greatly enhances the overall transport properties and the
corresponding scaling exponents. If only one of the walls is rough, we reveal
that the bulk velocity is slaved to the rough side, due to the much stronger
coupling to that wall by the detaching flow structures. If both walls are
rough, the viscosity dependence is thoroughly eliminated in the boundary layers
and we thus achieve asymptotic ultimate turbulence, i.e. the upper limit of
transport, whose existence had been predicted by Robert Kraichnan in 1962
(Phys. Fluids {\bf 5}, 1374 (1962)) and in which the scalings laws can be
extrapolated to arbitrarily large Reynolds numbers
Mutations and SNPs of human cardiac sodium channel alpha subunit gene (SCN5A) in Japanese patients with Brugada syndrome
Background: Brugada syndrome is an inherited arrhythmogenic disease characterized by right bundle branch block pattern and ST segment elevation, leading to the change of V1 to V3 on electrocardiogram, and an increased risk of sudden cardiac death resulting from ventricular fibrillation. The sodium channel alpha 5 subunit (SCN5A) gene encodes a cardiac voltage-dependent sodium channel, and SCN5A mutations have been reported in Brugada syndrome. However, single nucleotide polymorphisms (SNPs) and gene mutations have not been well investigated in Japanese patients with Brugada syndrome.
Methods and Results: The SCN5A gene was examined in 58 patients by using PCR and the ABI 3130xl sequencer, revealing 17 SNP patterns and 13 mutations. Of the 13 mutations, 8 were missense mutations (with amino acid change), 4 were silent mutations (without amino acid change), and one case was a mutation within the splicing junction. Six of the eight missense mutations were novel mutations. Interestingly, we detected an R1664H mutation, which was identified originally in long QT syndrome.
Conclusion: We found 13 mutations of the SCN5A gene in 58 patients with Brugada syndrome. The disease may be attributable to some of the mutations and SNPs
Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay
The decay channel
is studied using a sample of events collected
by the BESIII experiment at BEPCII. A strong enhancement at threshold is
observed in the invariant mass spectrum. The enhancement can be fit
with an -wave Breit-Wigner resonance function with a resulting peak mass of
and a
narrow width that is at the 90% confidence level.
These results are consistent with published BESII results. These mass and width
values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics
53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility
Double-strand breaks activate the ataxia telangiectasia mutated (ATM) kinase, which promotes the accumulation of DNA damage factors in the chromatin surrounding the break. The functional significance of the resulting DNA damage foci is poorly understood. Here we show that 53BP1 (also known as TRP53BP1), a component of DNA damage foci, changes the dynamic behaviour of chromatin to promote DNA repair. We used conditional deletion of the shelterin component TRF2 (also known as TERF2) from mouse cells (TRF2fl/-) to deprotect telomeres, which, like double-strand breaks, activate the ATM kinase, accumulate 53BP1 and are processed by non-homologous end joining (NHEJ). Deletion of TRF2 from 53BP1-deficient cells established that NHEJ of dysfunctional telomeres is strongly dependent on the binding of 53BP1 to damaged chromosome ends. To address the mechanism by which 53BP1 promotes NHEJ, we used time-lapse microscopy to measure telomere dynamics before and after their deprotection. Imaging showed that deprotected telomeres are more mobile and sample larger territories within the nucleus. This change in chromatin dynamics was dependent on 53BP1 and ATM but did not require a functional NHEJ pathway. We propose that the binding of 53BP1 near DNA breaks changes the dynamic behaviour of the local chromatin, thereby facilitating NHEJ repair reactions that involve distant sites, including joining of dysfunctional telomeres and AID (also known as AICDA)-induced breaks in immunoglobulin class-switch recombination
Synthesis and White-Light Emission of ZnO/HfO2: Eu Nanocables
ZnO/HfO2:Eu nanocables were prepared by radio frequency sputtering with electrospun ZnO nanofibers as cores. The well-crystallized ZnO/HfO2:Eu nanocables showed a uniform intact core–shell structure, which consisted of a hexagonal ZnO core and a monoclinic HfO2 shell. The photoluminescence properties of the samples were characterized. A white-light band emission consisted of blue, green, and red emissions was observed in the nanocables. The blue and green emissions can be attributed to the zinc vacancy and oxygen vacancy defects in ZnO/HfO2:Eu nanocables, and the yellow–red emissions are derived from the inner 4f-shell transitions of corresponding Eu3+ ions in HfO2:Eu shells. Enhanced white-light emission was observed in the nanocables. The enhancement of the emission is ascribed to the structural changes after coaxial synthesis
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