230 research outputs found
Eikonal methods applied to gravitational scattering amplitudes
We apply factorization and eikonal methods from gauge theories to scattering
amplitudes in gravity. We hypothesize that these amplitudes factor into an
IR-divergent soft function and an IR-finite hard function, with the former
given by the expectation value of a product of gravitational Wilson line
operators. Using this approach, we show that the IR-divergent part of the
n-graviton scattering amplitude is given by the exponential of the one-loop IR
divergence, as originally discovered by Weinberg, with no additional subleading
IR-divergent contributions in dimensional regularization.Comment: 16 pages, 3 figures; v2: title change and minor rewording (published
version); v3: typos corrected in eqs.(3.2),(4.1
Next-to-eikonal corrections to soft gluon radiation: a diagrammatic approach
We consider the problem of soft gluon resummation for gauge theory amplitudes
and cross sections, at next-to-eikonal order, using a Feynman diagram approach.
At the amplitude level, we prove exponentiation for the set of factorizable
contributions, and construct effective Feynman rules which can be used to
compute next-to-eikonal emissions directly in the logarithm of the amplitude,
finding agreement with earlier results obtained using path-integral methods.
For cross sections, we also consider sub-eikonal corrections to the phase space
for multiple soft-gluon emissions, which contribute to next-to-eikonal
logarithms. To clarify the discussion, we examine a class of log(1 - x) terms
in the Drell-Yan cross-section up to two loops. Our results are the first steps
towards a systematic generalization of threshold resummations to
next-to-leading power in the threshold expansion.Comment: 66 pages, 19 figure
Wall-Crossing in Coupled 2d-4d Systems
We introduce a new wall-crossing formula which combines and generalizes the
Cecotti-Vafa and Kontsevich-Soibelman formulas for supersymmetric 2d and 4d
systems respectively. This 2d-4d wall-crossing formula governs the
wall-crossing of BPS states in an N=2 supersymmetric 4d gauge theory coupled to
a supersymmetric surface defect. When the theory and defect are compactified on
a circle, we get a 3d theory with a supersymmetric line operator, corresponding
to a hyperholomorphic connection on a vector bundle over a hyperkahler space.
The 2d-4d wall-crossing formula can be interpreted as a smoothness condition
for this hyperholomorphic connection. We explain how the 2d-4d BPS spectrum can
be determined for 4d theories of class S, that is, for those theories obtained
by compactifying the six-dimensional (0,2) theory with a partial topological
twist on a punctured Riemann surface C. For such theories there are canonical
surface defects. We illustrate with several examples in the case of A_1
theories of class S. Finally, we indicate how our results can be used to
produce solutions to the A_1 Hitchin equations on the Riemann surface C.Comment: 170 pages, 45 figure
Factorization Properties of Soft Graviton Amplitudes
We apply recently developed path integral resummation methods to perturbative
quantum gravity. In particular, we provide supporting evidence that eikonal
graviton amplitudes factorize into hard and soft parts, and confirm a recent
hypothesis that soft gravitons are modelled by vacuum expectation values of
products of certain Wilson line operators, which differ for massless and
massive particles. We also investigate terms which break this factorization,
and find that they are subleading with respect to the eikonal amplitude. The
results may help in understanding the connections between gravity and gauge
theories in more detail, as well as in studying gravitational radiation beyond
the eikonal approximation.Comment: 35 pages, 5 figure
Time separation as a hidden variable to the Copenhagen school of quantum mechanics
The Bohr radius is a space-like separation between the proton and electron in
the hydrogen atom. According to the Copenhagen school of quantum mechanics, the
proton is sitting in the absolute Lorentz frame. If this hydrogen atom is
observed from a different Lorentz frame, there is a time-like separation
linearly mixed with the Bohr radius. Indeed, the time-separation is one of the
essential variables in high-energy hadronic physics where the hadron is a bound
state of the quarks, while thoroughly hidden in the present form of quantum
mechanics. It will be concluded that this variable is hidden in Feynman's rest
of the universe. It is noted first that Feynman's Lorentz-invariant
differential equation for the bound-state quarks has a set of solutions which
describe all essential features of hadronic physics. These solutions explicitly
depend on the time separation between the quarks. This set also forms the
mathematical basis for two-mode squeezed states in quantum optics, where both
photons are observable, but one of them can be treated a variable hidden in the
rest of the universe. The physics of this two-mode state can then be translated
into the time-separation variable in the quark model. As in the case of the
un-observed photon, the hidden time-separation variable manifests itself as an
increase in entropy and uncertainty.Comment: LaTex 10 pages with 5 figure. Invited paper presented at the
Conference on Advances in Quantum Theory (Vaxjo, Sweden, June 2010), to be
published in one of the AIP Conference Proceedings serie
Abnormal Changes in NKT Cells, the IGF-1 Axis, and Liver Pathology in an Animal Model of ALS
Amyotrophic lateral sclerosis (ALS) is a rapidly progressing fatal neurodegenerative disorder characterized by the selective death of motor neurons (MN) in the spinal cord, and is associated with local neuroinflammation. Circulating CD4+ T cells are required for controlling the local detrimental inflammation in neurodegenerative diseases, and for supporting neuronal survival, including that of MN. T-cell deficiency increases neuronal loss, while boosting T cell levels reduces it. Here, we show that in the mutant superoxide dismutase 1 G93A (mSOD1) mouse model of ALS, the levels of natural killer T (NKT) cells increased dramatically, and T-cell distribution was altered both in lymphoid organs and in the spinal cord relative to wild-type mice. The most significant elevation of NKT cells was observed in the liver, concomitant with organ atrophy. Hepatic expression levels of insulin-like growth factor (IGF)-1 decreased, while the expression of IGF binding protein (IGFBP)-1 was augmented by more than 20-fold in mSOD1 mice relative to wild-type animals. Moreover, hepatic lymphocytes of pre-symptomatic mSOD1 mice were found to secrete significantly higher levels of cytokines when stimulated with an NKT ligand, ex-vivo. Immunomodulation of NKT cells using an analogue of α-galactosyl ceramide (α-GalCer), in a specific regimen, diminished the number of these cells in the periphery, and induced recruitment of T cells into the affected spinal cord, leading to a modest but significant prolongation of life span of mSOD1 mice. These results identify NKT cells as potential players in ALS, and the liver as an additional site of major pathology in this disease, thereby emphasizing that ALS is not only a non-cell autonomous, but a non-tissue autonomous disease, as well. Moreover, the results suggest potential new therapeutic targets such as the liver for immunomodulatory intervention for modifying the disease, in addition to MN-based neuroprotection and systemic treatments aimed at reducing oxidative stress
Antibodies Targeted to the Brain with Image-Guided Focused Ultrasound Reduces Amyloid-β Plaque Load in the TgCRND8 Mouse Model of Alzheimer's Disease
Immunotherapy for Alzheimer's disease (AD) relies on antibodies directed against toxic amyloid-beta peptide (Aβ), which circulate in the bloodstream and remove Aβ from the brain [1], [2]. In mouse models of AD, the administration of anti-Aβ antibodies directly into the brain, in comparison to the bloodstream, was shown to be more efficient at reducing Aβ plaque pathology [3], [4]. Therefore, delivering anti-Aβ antibodies to the brain of AD patients may also improve treatment efficiency. Transcranial focused ultrasound (FUS) is known to transiently-enhance the permeability of the blood-brain barrier (BBB) [5], allowing intravenously administered therapeutics to enter the brain [6]–[8]. Our goal was to establish that anti-Aβ antibodies delivered to the brain using magnetic resonance imaging-guided FUS (MRIgFUS) [9] can reduce plaque pathology. To test this, TgCRND8 mice [10] received intravenous injections of MRI and FUS contrast agents, as well as anti-Aβ antibody, BAM-10. MRIgFUS was then applied transcranially. Within minutes, the MRI contrast agent entered the brain, and BAM-10 was later found bound to Aβ plaques in targeted cortical areas. Four days post-treatment, Aβ pathology was significantly reduced in TgCRND8 mice. In conclusion, this is the first report to demonstrate that MRIgFUS delivery of anti-Aβ antibodies provides the combined advantages of using a low dose of antibody and rapidly reducing plaque pathology
Regulation of Cancer Aggressive Features in Melanoma Cells by MicroRNAs
MicroRNAs (miRNAs) are small non-coding RNAs with regulatory roles, which are involved in a broad spectrum of physiological and pathological processes, including cancer. A common strategy for identification of miRNAs involved in cell transformation is to compare malignant cells to normal cells. Here we focus on identification of miRNAs that regulate the aggressive phenotype of melanoma cells. To avoid differences due to genetic background, a comparative high-throughput miRNA profiling was performed on two isogenic human melanoma cell lines that display major differences in their net proliferation, invasion and tube formation activities. This screening revealed two major cohorts of differentially expressed miRNAs. We speculated that miRNAs up-regulated in the more-aggressive cell line contribute oncogenic features, while the down-regulated miRNAs are tumor suppressive. This assumption was further tested experimentally on five candidate tumor suppressive miRNAs (miR-31, -34a, -184, -185 and -204) and on one candidate oncogenic miRNA (miR-17-5p), all of which have never been reported before in cutaneous melanoma. Remarkably, all candidate Suppressive-miRNAs inhibited net proliferation, invasion or tube formation, while miR-17-5p enhanced cell proliferation. miR-34a and miR-185 were further shown to inhibit the growth of melanoma xenografts when implanted in SCID-NOD mice. Finally, all six candidate miRNAs were detected in 15 different metastatic melanoma specimens, attesting for the physiological relevance of our findings. Collectively, these findings may prove instrumental for understanding mechanisms of disease and for development of novel therapeutic and staging technologies for melanoma
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