478 research outputs found
The Omega Deformation From String and M-Theory
We present a string theory construction of Omega-deformed four-dimensional
gauge theories with generic values of \epsilon_1 and \epsilon_2. Our solution
gives an explicit description of the geometry in the core of Nekrasov and
Witten's realization of the instanton partition function, far from the
asymptotic region of their background. This construction lifts naturally to
M-theory and corresponds to an M5-brane wrapped on a Riemann surface with a
selfdual flux. Via a 9-11 flip, we finally reinterpret the Omega deformation in
terms of non-commutative geometry. Our solution generates all modified
couplings of the \Omega-deformed gauge theory, and also yields a geometric
origin for the quantum spectral curve of the associated quantum integrable
system.Comment: LaTeX, 35 pages, 1 figure. Appendix on couplings of hypermultiplets
in N=4 SYM adde
Manganese toxicity with ephedrone abuse manifesting as parkinsonism: a case report
Introduction: Neurologic consequences of manganese toxicity have been recognized since 1837. A new form of presumed manganese poisoning has been reported in drug addicted persons from Eastern Europe and the Baltic states who have intravenously injected self-prepared methcathinone hydrochloride (ephedrone), which is synthesized from pseudoephedrine hydrochloride using potassium permanganate as a potent oxidant. This clinical syndrome is under-recognized in Western Europe and there are no reported cases in the literature from Ireland.
Case presentation: We report a 30-year-old Eastern European man who presented with a two-year history of gait disturbance. A neurological assessment revealed features of parkinsonism which included hypophonia, hypomimia, mild bradykinesia and rigidity with no resting tremor. He held his arms slightly abducted from his sides when walking, with a reduction in arm swing. Magnetic resonance imaging of his brain showed a high signal on T1 in the globus pallidus and serum manganese levels were raised. He had no response to levodopa.
Conclusion: Manganism secondary to ephedrone abuse causing parkinsonism has emerged in Western Europe in recent years due to mass immigration and often remains unrecognized. This paper highlights the various features of this rare cause of parkinsonism and aids in its recognition and subsequent diagnosis. Neurologists in Western Europe will increasingly encounter such patients
Wall Crossing, Quivers and Crystals
We study the spectrum of BPS D-branes on a Calabi-Yau manifold using the 0+1
dimensional quiver gauge theory that describes the dynamics of the branes at
low energies. The results of Kontsevich and Soibelman predict how the
degeneracies change. We argue that Seiberg dualities of the quiver gauge
theories, which change the basis of BPS states, correspond to crossing the
"walls of the second kind." There is a large class of examples, including local
del Pezzo surfaces, where the BPS degeneracies of quivers corresponding to one
D6 brane bound to arbitrary numbers of D4, D2 and D0 branes are counted by
melting crystal configurations. We show that the melting crystals that arise
are a discretization of the Calabi-Yau geometry. The shape of the crystal is
determined by the Calabi-Yau geometry and the background B-field, and its
microscopic structure by the quiver Q. We prove that the BPS degeneracies
computed from Q and Q' are related by the Kontsevich Soibelman formula, using a
geometric realization of the Seiberg duality in the crystal. We also show that,
in the limit of infinite B-field, the combinatorics of crystals arising from
the quivers becomes that of the topological vertex. We thus re-derive the
Gromov-Witten/Donaldson-Thomas correspondence
Nuclear receptor REVERBα is a state-dependent regulator of liver energy metabolism
The nuclear receptor REVERBα is a core component of the circadian clock and proposed to be a dominant regulator of hepatic lipid metabolism. Using antibody-independent ChIP-sequencing of REVERBα in mouse liver, we reveal a high-confidence cistrome and define direct target genes. REVERBα-binding sites are highly enriched for consensus RORE or RevDR2 motifs and overlap with corepressor complex binding. We find no evidence for transcription factor tethering and DNA-binding domain-independent action. Moreover, hepatocyte-specific deletion of Reverbα drives only modest physiological and transcriptional dysregulation, with derepressed target gene enrichment limited to circadian processes. Thus, contrary to previous reports, hepatic REVERBα does not repress lipogenesis under basal conditions. REVERBα control of a more extensive transcriptional program is only revealed under conditions of metabolic perturbation (including mistimed feeding, which is a feature of the global Reverbα -/- mouse). Repressive action of REVERBα in the liver therefore serves to buffer against metabolic challenge, rather than drive basal rhythmicity in metabolic activity
D-branes Wrapped on Fuzzy del Pezzo Surfaces
We construct classical solutions in quiver gauge theories on D0-branes
probing toric del Pezzo singularities in Calabi-Yau manifolds. Our solutions
represent D4-branes wrapped around fuzzy del Pezzo surfaces. We study the
fluctuation spectrum around the fuzzy CP^2 solution in detail. We also comment
on possible applications of our fuzzy del Pezzo surfaces to the fuzzy version
of F-theory, dubbed F(uzz) theory.Comment: 1+42 pages, 9 figures v2: references added v3: statements on the
structure of the Yukawa couplings weakened. published versio
Non-abelian Action for Multiple Five-Branes with Self-Dual Tensors
We construct an action for non-abelian 2-form in 6-dimensions. Our action
consists of a non-abelian generalization of the abelian action of Perry and
Schwarz for a single five-brane. It admits a self-duality equation on the field
strength as the equation of motion. It has a modified 6d Lorentz symmetry. On
dimensional reduction on a circle, our action gives the standard 5d Yang-Mills
action plus higher order corrections. Based on these properties, we propose
that our theory describes the gauge sector of multiple M5-branes in flat space.Comment: LaTeX, 26 pages. v2: improved discussion of Lorentz symmetry. ref
added. v3: add comments in the discussion section on the inclusion of scalar
fields and supersymmetry; title changed to a more suitable one; version
published in JHE
Photo-antagonism of the GABAA receptor
Neurotransmitter receptor trafficking is fundamentally important for synaptic transmission and neural network activity. GABAA receptors and inhibitory synapses are vital components of brain function, yet much of our knowledge regarding receptor mobility and function at inhibitory synapses is derived indirectly from using recombinant receptors, antibody-tagged native receptors and pharmacological treatments. Here we describe the use of a set of research tools that can irreversibly bind to and affect the function of recombinant and neuronal GABAA receptors following ultraviolet photoactivation. These compounds are based on the competitive antagonist gabazine and incorporate a variety of photoactive groups. By using site-directed mutagenesis and ligand-docking studies, they reveal new areas of the GABA binding site at the interface between receptor β and α subunits. These compounds enable the selected inactivation of native GABAA receptor populations providing new insight into the function of inhibitory synapses and extrasynaptic receptors in controlling neuronal excitation
On instantons as Kaluza-Klein modes of M5-branes
Instantons and W-bosons in 5d maximally supersymmetric Yang-Mills theory
arise from a circle compactification of the 6d (2,0) theory as Kaluza-Klein
modes and winding self-dual strings, respectively. We study an index which
counts BPS instantons with electric charges in Coulomb and symmetric phases. We
first prove the existence of unique threshold bound state of (noncommutative)
U(1) instantons for any instanton number, and also show that charged instantons
in the Coulomb phase correctly give the degeneracy of SU(2) self-dual strings.
By studying SU(N) self-dual strings in the Coulomb phase, we find novel
momentum-carrying degrees on the worldsheet. The total number of these degrees
equals the anomaly coefficient of SU(N) (2,0) theory. We finally show that our
index can be used to study the symmetric phase of this theory, and provide an
interpretation as the superconformal index of the sigma model on instanton
moduli space.Comment: 54 pages, 2 figures. v2: references added, figure improved, added
comments on self-dual string anomaly, added new materials on the symmetric
phase index, other minor correction
Effect of malaria infection on hematological profiles of people living with human immunodeficiency virus in Gambella, southwest Ethiopia
Who fans the flames of Alzheimer's disease brains? Misfolded tau on the crossroad of neurodegenerative and inflammatory pathways
Neurodegeneration, induced by misfolded tau protein, and neuroinflammation, driven by glial cells, represent the salient features of Alzheimer's disease (AD) and related human tauopathies. While tau neurodegeneration significantly correlates with disease progression, brain inflammation seems to be an important factor in regulating the resistance or susceptibility to AD neurodegeneration. Previously, it has been shown that there is a reciprocal relationship between the local inflammatory response and neurofibrillary lesions. Numerous independent studies have reported that inflammatory responses may contribute to the development of tau pathology and thus accelerate the course of disease. It has been shown that various cytokines can significantly affect the functional and structural properties of intracellular tau. Notwithstanding, anti-inflammatory approaches have not unequivocally demonstrated that inhibition of the brain immune response can lead to reduction of neurofibrillary lesions. On the other hand, our recent data show that misfolded tau could represent a trigger for microglial activation, suggesting the dual role of misfolded tau in the Alzheimer's disease inflammatory cascade. On the basis of current knowledge, we can conclude that misfolded tau is located at the crossroad of the neurodegenerative and neuroinflammatory pathways. Thus disease-modified tau represents an important target for potential therapeutic strategies for patients with Alzheimer's disease
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