65 research outputs found
Performance-based regulation and its applications
2002-2003 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe
Search for Kaluza-Klein Graviton Emission in Collisions at TeV using the Missing Energy Signature
We report on a search for direct Kaluza-Klein graviton production in a data
sample of 84 of \ppb collisions at = 1.8 TeV, recorded
by the Collider Detector at Fermilab. We investigate the final state of large
missing transverse energy and one or two high energy jets. We compare the data
with the predictions from a -dimensional Kaluza-Klein scenario in which
gravity becomes strong at the TeV scale. At 95% confidence level (C.L.) for
=2, 4, and 6 we exclude an effective Planck scale below 1.0, 0.77, and 0.71
TeV, respectively.Comment: Submitted to PRL, 7 pages 4 figures/Revision includes 5 figure
Measurement of the average time-integrated mixing probability of b-flavored hadrons produced at the Tevatron
We have measured the number of like-sign (LS) and opposite-sign (OS) lepton
pairs arising from double semileptonic decays of and -hadrons,
pair-produced at the Fermilab Tevatron collider. The data samples were
collected with the Collider Detector at Fermilab (CDF) during the 1992-1995
collider run by triggering on the existence of and candidates
in an event. The observed ratio of LS to OS dileptons leads to a measurement of
the average time-integrated mixing probability of all produced -flavored
hadrons which decay weakly, (stat.)
(syst.), that is significantly larger than the world average .Comment: 47 pages, 10 figures, 15 tables Submitted to Phys. Rev.
Longitudinal Molecular Trajectories of Diffuse Glioma in Adults
The evolutionary processes that drive universal therapeutic resistance in adult patients with diffuse glioma remain unclear ¹² . Here we analysed temporally separated DNA-sequencing data and matched clinical annotation from 222 adult patients with glioma. By analysing mutations and copy numbers across the three major subtypes of difuse glioma, we found that driver genes detected at the initial stage of disease were retained at recurrence, whereas there was little evidence of recurrence-specifc gene alterations. Treatment with alkylating agents resulted in a hypermutator phenotype at diferent rates across the glioma subtypes, and hypermutation was not associated with diferences in overall survival. Acquired aneuploidy was frequently detected in recurrent gliomas and was characterized by IDH mutation but without co-deletion of chromosome arms 1p/19q, and further converged with acquired alterations in the cell cycle and poor outcomes. The clonal architecture of each tumour remained similar over time, but the presence of subclonal selection was associated with decreased survival. Finally, there were no differences in the levels of immunoediting between initial and recurrent gliomas. Collectively, our results suggest that the strongest selective pressures occur during early glioma development and that current therapies shape this evolution in a largely stochastic manner
Glucose Transporter 1 and Monocarboxylate Transporters 1, 2, and 4 Localization within the Glial Cells of Shark Blood-Brain-Barriers
Although previous studies showed that glucose is used to support the metabolic activity of the cartilaginous fish brain, the distribution and expression levels of glucose transporter (GLUT) isoforms remained undetermined. Optic/ultrastructural immunohistochemistry approaches were used to determine the expression of GLUT1 in the glial blood-brain barrier (gBBB). GLUT1 was observed solely in glial cells; it was primarily located in end-feet processes of the gBBB. Western blot analysis showed a protein with a molecular mass of 50 kDa, and partial sequencing confirmed GLUT1 identity. Similar approaches were used to demonstrate increased GLUT1 polarization to both apical and basolateral membranes in choroid plexus epithelial cells. To explore monocarboxylate transporter (MCT) involvement in shark brain metabolism, the expression of MCTs was analyzed. MCT1, 2 and 4 were expressed in endothelial cells; however, only MCT1 and MCT4 were present in glial cells. In neurons, MCT2 was localized at the cell membrane whereas MCT1 was detected within mitochondria. Previous studies demonstrated that hypoxia modified GLUT and MCT expression in mammalian brain cells, which was mediated by the transcription factor, hypoxia inducible factor-1. Similarly, we observed that hypoxia modified MCT1 cellular distribution and MCT4 expression in shark telencephalic area and brain stem, confirming the role of these transporters in hypoxia adaptation. Finally, using three-dimensional ultrastructural microscopy, the interaction between glial end-feet and leaky blood vessels of shark brain was assessed in the present study. These data suggested that the brains of shark may take up glucose from blood using a different mechanism than that used by mammalian brains, which may induce astrocyte-neuron lactate shuttling and metabolic coupling as observed in mammalian brain. Our data suggested that the structural conditions and expression patterns of GLUT1, MCT1, MCT2 and MCT4 in shark brain may establish the molecular foundation of metabolic coupling between glia and neurons
Measurement of the Ratio of b Quark Production Cross Sections in Antiproton-Proton Collisions at 630 GeV and 1800 GeV
We report a measurement of the ratio of the bottom quark production cross
section in antiproton-proton collisions at 630 GeV to 1800 GeV using bottom
quarks with transverse momenta greater than 10.75 GeV identified through their
semileptonic decays and long lifetimes. The measured ratio
sigma(630)/sigma(1800) = 0.171 +/- .024 +/- .012 is in good agreement with
next-to-leading order (NLO) quantum chromodynamics (QCD)
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