1,126 research outputs found
Atomic matter wave scanner
We report on the experimental realization of an atom optical device, that
allows scanning of an atomic beam. We used a time-modulated evanescent wave
field above a glass surface to diffract a continuous beam of metastable Neon
atoms at grazing incidence. The diffraction angles and efficiencies were
controlled by the frequency and form of modulation, respectively. With an
optimized shape, obtained from a numerical simulation, we were able to transfer
more than 50% of the atoms into the first order beam, which we were able to
move over a range of 8 mrad.Comment: 4 pages, 4 figure
GAUSS - genesis of asteroids and evolution of the solar system
The goal of Project GAUSS (Genesis of Asteroids and evolUtion of the Solar System) is to return samples from the dwarf planet Ceres. Ceres is the most accessible candidate of ocean worlds and the largest reservoir of water in the inner Solar System. It shows active volcanism and hydrothermal activities in recent history. Recent evidence for the existence of a subsurface ocean on Ceres and the complex geochemistry suggest past habitability and even the potential for ongoing habitability. GAUSS will return samples from Ceres with the aim of answering the following top-level scientific questions:
What is the origin of Ceres and what does this imply for the origin of water and other volatiles in the inner Solar System?
What are the physical properties and internal structure of Ceres? What do they tell us about the evolutionary and aqueous alteration history of dwarf planets?
What are the astrobiological implications of Ceres? Is it still habitable today?
What are the mineralogical connections between Ceres and our current collections of carbonaceous meteorites
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015
Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as âaccidental cell deathâ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. âRegulated cell deathâ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death
TNF-induced necroptosis in L929 cells is tightly regulated by multiple TNFR1 complex I and II members
TNF receptor 1 signaling induces NF-ÎşB activation and necroptosis in L929 cells. We previously reported that cellular inhibitor of apoptosis protein-mediated receptor-interacting protein 1 (RIP1) ubiquitination acts as a cytoprotective mechanism, whereas knockdown of cylindromatosis, a RIP1-deubiquitinating enzyme, protects against tumor necrosis factor (TNF)-induced necroptosis. We report here that RIP1 is a crucial mediator of canonical NF-ÎşB activation in L929 cells, therefore questioning the relative cytoprotective contribution of RIP1 ubiquitination versus canonical NF-ÎşB activation. We found that attenuated NF-ÎşB activation has no impact on TNF-induced necroptosis. However, we identified A20 and linear ubiquitin chain assembly complex as negative regulators of necroptosis. Unexpectedly, and in contrast to RIP3, we also found that knockdown of RIP1 did not block TNF cytotoxicity. Cell death typing revealed that RIP1-depleted cells switch from necroptotic to apoptotic death, indicating that RIP1 can also suppress apoptosis in L929 cells. Inversely, we observed that Fas-associated protein via a death domain, cellular FLICE inhibitory protein and caspase-8, which are all involved in the initiation of apoptosis, counteract necroptosis induction. Finally, we also report RIP1-independent but RIP3-mediated necroptosis in the context of TNF signaling in particular conditions
Measurements of branching fraction ratios and CP-asymmetries in suppressed B^- -> D(-> K^+ pi^-)K^- and B^- -> D(-> K^+ pi^-)pi^- decays
We report the first reconstruction in hadron collisions of the suppressed
decays B^- -> D(-> K^+ pi^-)K^- and B^- -> D(-> K^+ pi^-)pi^-, sensitive to the
CKM phase gamma, using data from 7 fb^-1 of integrated luminosity collected by
the CDF II detector at the Tevatron collider. We reconstruct a signal for the
B^- -> D(-> K^+ pi^-)K^- suppressed mode with a significance of 3.2 standard
deviations, and measure the ratios of the suppressed to favored branching
fractions R(K) = [22.0 \pm 8.6(stat)\pm 2.6(syst)]\times 10^-3, R^+(K) =
[42.6\pm 13.7(stat)\pm 2.8(syst)]\times 10^-3, R^-(K)= [3.8\pm 10.3(stat)\pm
2.7(syst]\times 10^-3, as well as the direct CP-violating asymmetry A(K) =
-0.82\pm 0.44(stat)\pm 0.09(syst) of this mode. Corresponding quantities for
B^- -> D(-> K^+ pi^-)pi^- decay are also reported.Comment: 8 pages, 1 figure, accepted by Phys.Rev.D Rapid Communications for
Publicatio
Performance of CMS muon reconstruction in pp collision events at sqrt(s) = 7 TeV
The performance of muon reconstruction, identification, and triggering in CMS
has been studied using 40 inverse picobarns of data collected in pp collisions
at sqrt(s) = 7 TeV at the LHC in 2010. A few benchmark sets of selection
criteria covering a wide range of physics analysis needs have been examined.
For all considered selections, the efficiency to reconstruct and identify a
muon with a transverse momentum pT larger than a few GeV is above 95% over the
whole region of pseudorapidity covered by the CMS muon system, abs(eta) < 2.4,
while the probability to misidentify a hadron as a muon is well below 1%. The
efficiency to trigger on single muons with pT above a few GeV is higher than
90% over the full eta range, and typically substantially better. The overall
momentum scale is measured to a precision of 0.2% with muons from Z decays. The
transverse momentum resolution varies from 1% to 6% depending on pseudorapidity
for muons with pT below 100 GeV and, using cosmic rays, it is shown to be
better than 10% in the central region up to pT = 1 TeV. Observed distributions
of all quantities are well reproduced by the Monte Carlo simulation.Comment: Replaced with published version. Added journal reference and DO
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