146 research outputs found
Various Improvements to Operate the 1.5GeV HDSM at MAMI
During the last three years at the 1.5GeV Harmonic Double Sided Microtron HDSM, [1] of MAMI a lot of improvements concerning the longitudinal operation of the accelerator were tested and installed. To monitor the rf power dissipated in the accelerating sections, their cooling water flow and its temperature rise are now continuously logged. Phase calibration measurements of the linacs and the phase intensity monitors p i monitors revealed nonlinearities of the high precision step motor driven waveguide phase shifters. They were recalibrated to deliver precise absolute values. Thereby it is now possible to measure not only the first turn s phase very exactly, but also to determine the linac s rf amplitude within an error of less than 5 using the well known longitudinal dispersion of the bending system. These results are compared to the thermal load measurements. For parity violation experiments the beam energy has to be stabilised to some 10 amp; 8722;6. A dedicated system measuring the time of flight through a bending magnet is now used in routine operation and controls the output energy via the linac phase
Measurement of the Transverse Beam Spin Asymmetry in Elastic Electron Proton Scattering and the Inelastic Contribution to the Imaginary Part of the Two-Photon Exchange Amplitude
We report on a measurement of the asymmetry in the scattering of transversely
polarized electrons off unpolarized protons, A, at two Q values of
\qsquaredaveragedlow (GeV/c) and \qsquaredaveragedhighII (GeV/c) and a
scattering angle of . The measured transverse
asymmetries are A(Q = \qsquaredaveragedlow (GeV/c)) =
(\experimentalasymmetry alulowcorr \statisticalerrorlow
\combinedsyspolerrorlowalucor) 10 and
A(Q = \qsquaredaveragedhighII (GeV/c)) = (\experimentalasymme
tryaluhighcorr \statisticalerrorhigh
\combinedsyspolerrorhighalucor) 10. The first
errors denotes the statistical error and the second the systematic
uncertainties. A arises from the imaginary part of the two-photon
exchange amplitude and is zero in the one-photon exchange approximation. From
comparison with theoretical estimates of A we conclude that
N-intermediate states give a substantial contribution to the imaginary
part of the two-photon amplitude. The contribution from the ground state proton
to the imaginary part of the two-photon exchange can be neglected. There is no
obvious reason why this should be different for the real part of the two-photon
amplitude, which enters into the radiative corrections for the Rosenbluth
separation measurements of the electric form factor of the proton.Comment: 4 figures, submitted to PRL on Oct.
Measurement of Strange Quark Contributions to the Nucleon's Form Factors at Q^2=0.230 (GeV/c)^2
We report on a measurement of the parity-violating asymmetry in the
scattering of longitudinally polarized electrons on unpolarized protons at a
of 0.230 (GeV/c)^2 and a scattering angle of \theta_e = 30^o - 40^o.
Using a large acceptance fast PbF_2 calorimeter with a solid angle of
\Delta\Omega = 0.62 sr the A4 experiment is the first parity violation
experiment to count individual scattering events. The measured asymmetry is
A_{phys} =(-5.44 +- 0.54_{stat} +- 0.27_{\rm sys}) 10^{-6}. The Standard Model
expectation assuming no strangeness contributions to the vector form factors is
. The difference is a direct measurement of the
strangeness contribution to the vector form factors of the proton. The
extracted value is G^s_E + 0.225 G^s_M = 0.039 +- 0.034 or F^s_1 + 0.130 F^s_2
= 0.032 +- 0.028.Comment: 5 pages, 3 figures, submitted to Phys. Rev. Letters on Dec 11, 200
Self-organization and Mechanical Properties of Active Filament Bundles
A phenomenological description for active bundles of polar filaments is
presented. The activity of the bundle results from crosslinks, that induce
relative displacements between the aligned filaments. Our generic description
is based on momentum conservation within the bundle. By specifying the internal
forces, a simple minimal model for the bundle dynamics is obtained, capturing
generic dynamic behaviors. In particular, contracted states as well as solitary
and oscillatory waves appear through dynamic instabilities. The introduction of
filament adhesion leads to self-organized persistent filament transport.
Furthermore, calculating the tension, homogeneous bundles are shown to be able
to actively contract and to perform work against external forces. Our
description is motivated by dynamic phenomena in the cytoskeleton and could
apply to stress-fibers and self-organization phenomena during cell-locomotion.Comment: 19 pages, 10 figure
Evidence for Strange Quark Contributions to the Nucleon's Form Factors at = 0.108 (GeV/c)
We report on a measurement of the parity violating asymmetry in the elastic
scattering of polarized electrons off unpolarized protons with the A4 apparatus
at MAMI in Mainz at a four momentum transfer value of = \Qsquare
(GeV/c) and at a forward electron scattering angle of 30. The measured asymmetry is = (\Aphys
\Deltastat \Deltasyst) 10. The
expectation from the Standard Model assuming no strangeness contribution to the
vector current is A = (\Azero \DeltaAzero) 10. We
have improved the statistical accuracy by a factor of 3 as compared to our
previous measurements at a higher . We have extracted the strangeness
contribution to the electromagnetic form factors from our data to be +
\FakGMs = \GEsGMs \DeltaGEsGMs at = \Qsquare (GeV/c).
As in our previous measurement at higher momentum transfer for + 0.230
, we again find the value for + \FakGMs to be positive,
this time at an improved significance level of 2 .Comment: 4 pages, 3 figure
Myeloid Differentiation Primary Response Gene 88 Is Required for the Resolution of Otitis Media
Signaling defects in the Toll-like receptor (TLR) pathway, such as interleukin-1 receptorâassociated kinase 4 deficiency, highlight the prominence of TLR signaling in the defense against bacterial disease. Because myeloid differentiation primary response gene 88 (MyD88) can transduce signals from almost all TLRs, we studied its role in otitis media (OM), the most common upper respiratory tract bacterial infectious disease in young children
Kinetochore fiber formation in animal somatic cells : dueling mechanisms come to a draw
Author Posting. © The Author, 2005. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Chromosoma 114 (2005): 310-318, doi:10.1007/s00412-005-0028-2.The attachment to and movement of a chromosome on the mitotic spindle is
mediated by the formation of a bundle of microtubules (MTs) that tethers the
kinetochore on the chromosome to a spindle pole. The origin of these âkinetochore
fibersâ (K-fibers) has been investigated for over 125 years. As noted in 1944 by
Schrader, there are only three possible ways to form a K-fiber: either it a) grows from
the pole until it contacts the kinetochore; b) grows directly from the kinetochore; or c)
it forms as a result of an interaction between the pole and the chromosome. Since
Schraderâs time it has been firmly established that K-fibers in centrosome-containing
animal somatic cells form as kinetochores capture MTs growing from the spindle pole
(route a). It is now similarly clear that in cells lacking centrosomes, including plants
and many animal oocytes, K-fibers âself-assembleâ from MTs generated by the
chromosomes (route b). Can animal somatic cells form K-fibers in the absence of
centrosomes by the âself-assemblyâ pathway? In 2000 the answer to this question
was shown to be a resounding âyesâ. With this result, the next question became
whether the presence of a centrosome normally suppresses K-fiber self-assembly, or
if this route works concurrently with centrosome-mediated K-fiber formation. This
question, too, has recently been answered: observations on untreated live animal cells
expressing GFP-tagged tubulin clearly show that kinetochores can nucleate the
formation of their associated MTs in the presence of functional centrosomes. The
concurrent operation of these two âduelingâ routes for forming K-fibers in animals
helps explain why the attachment of kinetochores and the maturation of K-fibers
occur as quickly as it does on all chromosomes within a cell.The work is sponsored by
NIH grant GMS 40198
Prioritization and Evaluation of Depression Candidate Genes by Combining Multidimensional Data Resources
Large scale and individual genetic studies have suggested numerous susceptible genes for depression in the past decade without conclusive results. There is a strong need to review and integrate multi-dimensional data for follow up validation. The present study aimed to apply prioritization procedures to build-up an evidence-based candidate genes dataset for depression.Depression candidate genes were collected in human and animal studies across various data resources. Each gene was scored according to its magnitude of evidence related to depression and was multiplied by a source-specific weight to form a combined score measure. All genes were evaluated through a prioritization system to obtain an optimal weight matrix to rank their relative importance with depression using the combined scores. The resulting candidate gene list for depression (DEPgenes) was further evaluated by a genome-wide association (GWA) dataset and microarray gene expression in human tissues.A total of 5,055 candidate genes (4,850 genes from human and 387 genes from animal studies with 182 being overlapped) were included from seven data sources. Through the prioritization procedures, we identified 169 DEPgenes, which exhibited high chance to be associated with depression in GWA dataset (Wilcoxon rank-sum test, pâ=â0.00005). Additionally, the DEPgenes had a higher percentage to express in human brain or nerve related tissues than non-DEPgenes, supporting the neurotransmitter and neuroplasticity theories in depression.With comprehensive data collection and curation and an application of integrative approach, we successfully generated DEPgenes through an effective gene prioritization system. The prioritized DEPgenes are promising for future biological experiments or replication efforts to discover the underlying molecular mechanisms for depression
An analysis of binary microlensing event OGLE-2015-BLG-0060
We present the analysis of stellar binary microlensing event OGLE-2015-BLG-0060 based on observations obtained from 13 different telescopes. Intensive coverage of the anomalous parts of the light curve was achieved by automated follow-up observations from the robotic telescopes of the Las Cumbres Observatory. We show that, for the first time, all main features of an anomalous microlensing event are well covered by follow-up data, allowing us to estimate the physical parameters of the lens. The strong detection of second-order effects in the event light curve necessitates the inclusion of longer-baseline survey data in order to constrain the parallax vector. We find that the event was most likely caused by a stellar binary-lens with masses Mâ1=0.87±0.12Mâ and Mâ2=0.77±0.11Mââ . The distance to the lensing system is 6.41 ± 0.14 kpc and the projected separation between the two components is 13.85 ± 0.16 AU. Alternative interpretations are also considered
Defective Sphingosine-1-phosphate metabolism is a druggable target in Huntington's disease
Huntington's disease is characterized by a complex and heterogeneous pathogenic profile. Studies have shown that disturbance in lipid homeostasis may represent a critical determinant in the progression of several neurodegenerative disorders. The recognition of perturbed lipid metabolism is only recently becoming evident in HD. In order to provide more insight into the nature of such a perturbation and into the effect its modulation may have in HD pathology, we investigated the metabolism of Sphingosine-1-phosphate (S1P), one of the most important bioactive lipids, in both animal models and patient samples. Here, we demonstrated that S1P metabolism is significantly disrupted in HD even at early stage of the disease and importantly, we revealed that such a dysfunction represents a common denominator among multiple disease models ranging from cells to humans through mouse models. Interestingly, the in vitro anti-apoptotic and the pro-survival actions seen after modulation of S1P-metabolizing enzymes allows this axis to emerge as a new druggable target and unfolds its promising therapeutic potential for the development of more effective and targeted interventions against this incurable condition
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