560 research outputs found
Effect of thermal treatment on the growth, structure and luminescence of nitride-passivated silicon nanoclusters
Silicon nanoclusters (Si-ncs) embedded in silicon nitride films have been studied to determine the effects that deposition and processing parameters have on their growth, luminescent properties, and electronic structure. Luminescence was observed from Si-ncs formed in silicon-rich silicon nitride films with a broad range of compositions and grown using three different types of chemical vapour deposition systems. Photoluminescence (PL) experiments revealed broad, tunable emissions with peaks ranging from the near-infrared across the full visible spectrum. The emission energy was highly dependent on the film composition and changed only slightly with annealing temperature and time, which primarily affected the emission intensity. The PL spectra from films annealed for duration of times ranging from 2 s to 2 h at 600 and 800°C indicated a fast initial formation and growth of nanoclusters in the first few seconds of annealing followed by a slow, but steady growth as annealing time was further increased. X-ray absorption near edge structure at the Si K- and L3,2-edges exhibited composition-dependent phase separation and structural re-ordering of the Si-ncs and silicon nitride host matrix under different post-deposition annealing conditions and generally supported the trends observed in the PL spectra
Improved Measurement of the Pseudoscalar Decay Constant
We present a new determination of the Ds decay constant, f_{Ds} using 5
million continuum charm events obtained with the CLEO II detector. Our value is
derived from our new measured ratio of widths for Ds -> mu nu/Ds -> phi pi of
0.173+/- 0.021 +/- 0.031. Taking the branching ratio for Ds -> phi pi as (3.6
+/- 0.9)% from the PDG, we extract f_{Ds} = (280 +/- 17 +/- 25 +/- 34){MeV}. We
compare this result with various model calculations.Comment: 23 page postscript file, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
First Observation of and Decays
We have observed new channels for decays with an in the final
state. We study 3-prong tau decays, using the and
\eta\to 3\piz decay modes and 1-prong decays with two \piz's using the
channel. The measured branching fractions are
\B(\tau^{-}\to \pi^{-}\pi^{-}\pi^{+}\eta\nu_{\tau})
=(3.4^{+0.6}_{-0.5}\pm0.6)\times10^{-4} and \B(\tau^{-}\to
\pi^{-}2\piz\eta\nu_{\tau}
=(1.4\pm0.6\pm0.3)\times10^{-4}. We observe clear evidence for
substructure and measure \B(\tau^{-}\to
f_1\pi^{-}\nu_{\tau})=(5.8^{+1.4}_{-1.3}\pm1.8)\times10^{-4}. We have also
searched for production and obtain 90% CL upper limits
\B(\tau^{-}\to \pi^{-}\eta'\nu_\tau)<7.4\times10^{-5} and \B(\tau^{-}\to
\pi^{-}\piz\eta'\nu_\tau)<8.0\times10^{-5}.Comment: 11 page postscript file, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
Search for the Decays B^0 -> D^{(*)+} D^{(*)-}
Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays
B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one
candidate signal event, with an expected background of 0.022 +/- 0.011 events.
This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) =
(5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0
-> D^{*+} D^{*-}) D^{*\pm} D^\mp and
B^0 -> D^+ D^-, no significant excess of signal above the expected background
level is seen, and we calculate the 90% CL upper limits on the branching
fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+
D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through
http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter
Production in Two-Photon Interactions at CLEO
Using the CLEO detector at the Cornell storage ring, CESR, we study
the two-photon production of , making the first
observation of . We present the
cross-section for as a function of
the center of mass energy and compare it to that predicted by
the quark-diquark model.Comment: 10 pages, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
Observation of the Decay
Using e+e- annihilation data collected by the CLEO~II detector at CESR, we
have observed the decay Ds+ to omega pi+. This final state may be produced
through the annihilation decay of the Ds+, or through final state interactions.
We find a branching ratio of [Gamma(Ds+ to omega pi+)/Gamma(Ds+ to eta
pi+)]=0.16+-0.04+-0.03, where the first error is statistical and the second is
systematic.Comment: 9 pages, postscript file also available through
http://w4.lns.cornell.edu/public/CLN
BRIT1/MCPH1 links chromatin remodelling to DNA damage response
To detect and repair damaged DNA, DNA damage response proteins need to overcome the barrier of condensed chromatin to gain access to DNA lesions1. ATP-dependent chromatin remodeling is one of the fundamental mechanisms used by cells to relax chromatin in DNA repair2–3. However, the mechanism mediating their recruitment to DNA lesions remains largely unknown. BRIT1 (also known as MCPH1) is an early DNA damage response protein that is mutated in human primary microcephaly4–8. We report here a previously unknown function of BRIT1 as a regulator of ATP-dependent chromatin remodeling complex SWI/SNF in DNA repair. Upon DNA damage, BRIT1 increases its interaction with SWI/SNF through the ATM/ATR-dependent phosphorylation on the BAF170 subunit. This increase of binding affinity provides a means by which SWI/SNF can be specifically recruited to and maintained at DNA lesions. Loss of BRIT1 causes impaired chromatin relaxation owing to reduced association of SWI/SNF with chromatin. This explains the decreased recruitment of repair proteins to DNA lesions and reduced efficiency of repair in BRIT1-deficient cells, resulting in impaired survival from DNA damage. Our findings, therefore, identify BRIT1 as a key molecule that links chromatin remodeling with DNA damage response in the control of DNA repair, and its dysfunction contributes to human disease
Integrated Proteomic and Transcriptomic Investigation of the Acetaminophen Toxicity in Liver Microfluidic Biochip
Microfluidic bioartificial organs allow the reproduction of in vivo-like properties such as cell culture in a 3D dynamical micro environment. In this work, we established a method and a protocol for performing a toxicogenomic analysis of HepG2/C3A cultivated in a microfluidic biochip. Transcriptomic and proteomic analyses have shown the induction of the NRF2 pathway and the related drug metabolism pathways when the HepG2/C3A cells were cultivated in the biochip. The induction of those pathways in the biochip enhanced the metabolism of the N-acetyl-p-aminophenol drug (acetaminophen-APAP) when compared to Petri cultures. Thus, we observed 50% growth inhibition of cell proliferation at 1 mM in the biochip, which appeared similar to human plasmatic toxic concentrations reported at 2 mM. The metabolic signature of APAP toxicity in the biochip showed similar biomarkers as those reported in vivo, such as the calcium homeostasis, lipid metabolism and reorganization of the cytoskeleton, at the transcriptome and proteome levels (which was not the case in Petri dishes). These results demonstrate a specific molecular signature for acetaminophen at transcriptomic and proteomic levels closed to situations found in vivo. Interestingly, a common component of the signature of the APAP molecule was identified in Petri and biochip cultures via the perturbations of the DNA replication and cell cycle. These findings provide an important insight into the use of microfluidic biochips as new tools in biomarker research in pharmaceutical drug studies and predictive toxicity investigations
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