127 research outputs found
Second Generation Leptoquark Search in p\bar{p} Collisions at = 1.8 TeV
We report on a search for second generation leptoquarks with the D\O\
detector at the Fermilab Tevatron collider at = 1.8 TeV.
This search is based on 12.7 pb of data. Second generation leptoquarks
are assumed to be produced in pairs and to decay into a muon and quark with
branching ratio or to neutrino and quark with branching ratio
. We obtain cross section times branching ratio limits as a function
of leptoquark mass and set a lower limit on the leptoquark mass of 111
GeV/c for and 89 GeV/c for at the 95%\
confidence level.Comment: 18 pages, FERMILAB-PUB-95/185-
The Drift Chambers Of The Nomad Experiment
We present a detailed description of the drift chambers used as an active
target and a tracking device in the NOMAD experiment at CERN. The main
characteristics of these chambers are a large area, a self supporting structure
made of light composite materials and a low cost. A spatial resolution of 150
microns has been achieved with a single hit efficiency of 97%.Comment: 42 pages, 26 figure
Jet Production via Strongly-Interacting Color-Singlet Exchange in Collisions
A study of the particle multiplicity between jets with large rapidity
separation has been performed using the D{\O}detector at the Fermilab Tevatron
Collider operating at TeV. A significant excess of
low-multiplicity events is observed above the expectation for color-exchange
processes. The measured fractional excess is , which is consistent with a strongly-interacting
color-singlet (colorless) exchange process and cannot be explained by
electroweak exchange alone. A lower limit of 0.80% (95% C.L.) is obtained on
the fraction of dijet events with color-singlet exchange, independent of the
rapidity gap survival probability.Comment: 15 pages (REVTeX), 3 PS figs (uuencoded/tar compressed, epsf.sty)
Complete postscript available at http://d0sgi0.fnal.gov/d0pubs/journals.html
Submitted to Physical Review Letter
The NOMAD experiment at the CERN SPS
The NOMAD experiment is a short base-line search for oscillations in the CERN neutrino beam. The 's are searched for through their charged-current interactions followed by the observation of the resulting through its electronic, muonic or hadronic decays. These decays are recognized using kinematical criteria necessitating the use of a light target which enables the reconstruction of individual particles produced in the neutrino interactions. This paper describes the various components of the NOMAD detector: the target and muon drift chambers, the electromagnetic and hadronic calorimeters, the preshower and transition radiation detectors, and the veto and trigger scintillation counters. The beam and data acquisition system are also described. The quality of the reconstruction of individual particles is demonstrated through the ability of NOMAD to observe K's, 's and 's. Finally, the observation of through its electronic decay being one of the most promising channels in the search, the identification of electrons in NOMAD is discussed
The NOMAD Experiment at the CERN SPS
The NOMAD experiment is a short base-line search for ν<sub>μ</sub> − ν<sub>τ</sub> oscillations in the CERN neutrino beam. The ν<sub>τ</sub>'s are searched for through their charged current interactions followed by the observation of the resulting τ− through its electronic, muonic or hadronic decays. These decays are recognized using kinematical criteria necessitating the use of a light target which enables the reconstruction of individual particles produced in the neutrino interactions. This paper describes the various components of the NOMAD detector: the target and muon drift chambers, the electromagnetic and hadronic calorimeters, the preshower and transition radiation detectors and the veto and trigger scintillation counters. The beam and data acquisition system are also described. The quality of the reconstruction and individual particles is demonstrated through the ability of NOMAD to observe K<sub>s</sub><sup>0</sup>'s, Λ<sup>0</sup>'s and π<sup>0</sup>'s. Finally, the observation of τ− through its electronic decay being one of the most promising channels in the search, the identification of electrons in NOMAD is discussed
Search for a new gauge boson in pi(0) decays
A search was made for a new light gauge boson X which might be produced in pi(0) -->, gamma + X decay from neutral pions generated by 450 GeV protons in the CERN SPS neutrino target. The X's would penetrate the downstream shielding and be observed in the NOMAD detector via the Primakoff effect, in the process of X --> pi(0) conversion in the external Coulomb field of a nucleus. With 1.45 x 10(18) protons on target, 20 candidate events with energy between 8 and 140 GeV were found from the analysis of neutrino data. This number is in agreement with the expectation of 18.1 +/- 2.8 background events from standard neutrino processes. A new 90% C.L. upper limit on the branching ratio Br(pi(0) --> Y + X)< (3.3 to 1.9)X 10(-5) for X masses ranging from 0 to 120 MeV/c(2) is obtained
The cytoprotective drug amifostine modifies both expression and activity of the pro-angiogenic factor VEGF-A
Peer reviewedPublisher PD
Differential modulatory effects of GSK-3β and HDM2 on sorafenib-induced AIF nuclear translocation (programmed necrosis) in melanoma
<p>Abstract</p> <p>Background</p> <p>GSK-3β phosphorylates numerous substrates that govern cell survival. It phosphorylates p53, for example, and induces its nuclear export, HDM2-dependent ubiquitination, and proteasomal degradation. GSK-3β can either enhance or inhibit programmed cell death, depending on the nature of the pro-apoptotic stimulus. We previously showed that the multikinase inhibitor sorafenib activated GSK-3β and that this activation attenuated the cytotoxic effects of the drug in various BRAF-mutant melanoma cell lines. In this report, we describe the results of studies exploring the effects of GSK-3β on the cytotoxicity and antitumor activity of sorafenib combined with the HDM2 antagonist MI-319.</p> <p>Results</p> <p>MI-319 alone increased p53 levels and p53-dependent gene expression in melanoma cells but did not induce programmed cell death. Its cytotoxicity, however, was augmented in some melanoma cell lines by the addition of sorafenib. In responsive cell lines, the MI-319/sorafenib combination induced the disappearance of p53 from the nucleus, the down modulation of Bcl-2 and Bcl-x<sub>L</sub>, the translocation of p53 to the mitochondria and that of AIF to the nuclei. These events were all GSK-3β-dependent in that they were blocked with a GSK-3β shRNA and facilitated in otherwise unresponsive melanoma cell lines by the introduction of a constitutively active form of the kinase (GSK-3β-S9A). These modulatory effects of GSK-3β on the activities of the sorafenib/MI-319 combination were the exact reverse of its effects on the activities of sorafenib alone, which induced the down modulation of Bcl-2 and Bcl-x<sub>L </sub>and the nuclear translocation of AIF only in cells in which GSK-3β activity was either down modulated or constitutively low. In A375 xenografts, the antitumor effects of sorafenib and MI-319 were additive and associated with the down modulation of Bcl-2 and Bcl-x<sub>L</sub>, the nuclear translocation of AIF, and increased suppression of tumor angiogenesis.</p> <p>Conclusions</p> <p>Our data demonstrate a complex partnership between GSK-3β and HDM2 in the regulation of p53 function in the nucleus and mitochondria. The data suggest that the ability of sorafenib to activate GSK-3β and alter the intracellular distribution of p53 may be exploitable as an adjunct to agents that prevent the HDM2-dependent degradation of p53 in the treatment of melanoma.</p
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