107 research outputs found
Ecosystem effects of variant rabbit hemorrhagic disease virus, Iberian Peninsula
Letter to the Editor.The Aragón monitoring scheme is run by the Fish and Game Department, Government of Aragón. M.D.M. was supported by a JAE-DOC contract (Programa Junta para la Ampliación de Estudios), funded by CSIC and the European Social Fund. C.F. was supported by a Post-Doctoral Fellowship funded by NSERC, Government of Canada. C.G. acknowledges EU-FP7 grant ANTIGONE (#278976) and the EMIDA ERA-NET and INIA grant APHAEA.Peer Reviewe
Giants On Deformed Backgrounds
We study giant graviton probes in the framework of the three--parameter
deformation of the AdS_5 x S^5 background. We examine both the case when the
brane expands in the deformed part of the geometry and the case when it blows
up into AdS. Performing a detailed analysis of small fluctuations around the
giants, the configurations turn out to be stable. Our results hold even for the
supersymmetric Lunin-Maldacena deformation.Comment: LaTex, 28 pages, uses JHEP3; v2: minor corrections, references added;
v3: final version accepted for publication in JHE
Mesons in marginally deformed AdS/CFT
We study the embedding of spacetime filling D7-branes in beta-deformed
backgrounds which, according to the AdS/CFT dictionary, corresponds to
flavoring beta-deformed N=4 super Yang-Mills. We consider supersymmetric and
more general non-supersymmetric three parameter deformations. The equations of
motion for quadratic fluctuations of a probe D7-brane wrapped on a deformed
three-sphere exhibit a non-trivial coupling between scalar and vector modes
induced by the deformation. Nevertheless, we manage to solve them analytically
and find that the mesonic mass spectrum is discrete, with a mass gap and a
Zeeman-like splitting occurs. Finally we propose the action for the dual field
theory as obtained by star-product deformation of super Yang-Mills with
fundamental matter.Comment: LaTex, 42 pages, 3 figures, uses JHEP
InSAR-Based Mapping to Support Decision-Making after an Earthquake
It has long been recognized that earthquakes change the stress in the upper crust around
the fault rupture and can influence the behaviour of neighbouring faults and volcanoes. Rapid
estimates of these stress changes can provide the authorities managing the post-disaster situation
with valuable data to identify and monitor potential threads and to update the estimates of seismic
and volcanic hazard in a region. Here we propose a methodology to evaluate the potential
influence of an earthquake on nearby faults and volcanoes and create easy-to-understand maps
for decision-making support after large earthquakes. We apply this methodology to the Mw 7.8,
2016 Ecuador earthquake. Using Sentinel-1 Interferometric Synthetic Aperture Radar (InSAR) and
continuous GPS data, we measure the coseismic ground deformation and estimate the distribution
of slip over the fault rupture. We also build an alternative source model using the Global Centroid
Moment Tensor (CMT) solution. Then we use these models to evaluate changes of static stress
on the surrounding faults and volcanoes and produce maps of potentially activated faults and
volcanoes. We found, in general, good agreement between our maps and the seismic and volcanic
events that occurred after the Pedernales earthquake. We discuss the potential and limitations of
the methodology.This work is supported by the European Commission, Directorate-General Humanitarian
Aid and Civil Protection (ECHO) under the SAFETY (Sentinel for Geohazards regional monitoring and forecasting)
project (ECHO/SUB/2015/718679/Prev02) and by the Spanish Ministry of Economy and Competitiveness under
INTERGEOSIMA (CGL2013-47412) and ACTIVESTEP (CGL2017-83931-C3), QUAKESTEP (1-P) + 3GEO(2-P)
+ GEOACTIVA (3-P) projects
On the perturbative chiral ring for marginally deformed N=4 SYM theories
For \cal{N}=1 SU(N) SYM theories obtained as marginal deformations of the
\cal{N}=4 parent theory we study perturbatively some sectors of the chiral ring
in the weak coupling regime and for finite N. By exploiting the relation
between the definition of chiral ring and the effective superpotential we
develop a procedure which allows us to easily determine protected chiral
operators up to n loops once the superpotential has been computed up to (n-1)
order. In particular, for the Lunin-Maldacena beta-deformed theory we determine
the quantum structure of a large class of operators up to three loops. We
extend our procedure to more general Leigh-Strassler deformations whose chiral
ring is not fully understood yet and determine the weight-two and weight-three
sectors up to two loops. We use our results to infer general properties of the
chiral ring.Comment: LaTex, 40 pages, 4 figures, uses JHEP3; v2: minor correction
Thermodynamics of SU(N) Yang-Mills theories in 2+1 dimensions II - The deconfined phase
We present a non-perturbative study of the equation of state in the
deconfined phase of Yang-Mills theories in D=2+1 dimensions. We introduce a
holographic model, based on the improved holographic QCD model, from which we
derive a non-trivial relation between the order of the deconfinement phase
transition and the behavior of the trace of the energy-momentum tensor as a
function of the temperature T. We compare the theoretical predictions of this
holographic model with a new set of high-precision numerical results from
lattice simulations of SU(N) theories with N=2, 3, 4, 5 and 6 colors. The
latter reveal that, similarly to the D=3+1 case, the bulk equilibrium
thermodynamic quantities (pressure, trace of the energy-momentum tensor, energy
density and entropy density) exhibit nearly perfect proportionality to the
number of gluons, and can be successfully compared with the holographic
predictions in a broad range of temperatures. Finally, we also show that, again
similarly to the D=3+1 case, the trace of the energy-momentum tensor appears to
be proportional to T^2 in a wide temperature range, starting from approximately
1.2 T_c, where T_c denotes the critical deconfinement temperature.Comment: 2+36 pages, 10 figures; v2: comments added, curves showing the
holographic predictions included in the plots of the pressure and energy and
entropy densities, typos corrected: version published in JHE
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Symmorphosis through dietary regulation: a combinatorial role for proteolysis, autophagy and protein synthesis in normalising muscle metabolism and function of hypertrophic mice after acute starvation
Animals are imbued with adaptive mechanisms spanning from the tissue/organ to the cellular scale which insure that processes of homeostasis are preserved in the landscape of size change. However we and others have postulated that the degree of adaptation is limited and that once outside the normal levels of size fluctuations, cells and tissues function in an aberant manner. In this study we examine the function of muscle in the myostatin null mouse which is an excellent model for hypertrophy beyond levels of normal growth and consequeces of acute starvation to restore mass. We show that muscle growth is sustained through protein synthesis driven by Serum/Glucocorticoid Kinase 1 (SGK1) rather than Akt1. Furthermore our metabonomic profiling of hypertrophic muscle shows that carbon from nutrient sources is being channelled for the production of biomass rather than ATP production. However the muscle displays elevated levels of autophagy and decreased levels of muscle tension. We demonstrate the myostatin null muscle is acutely sensitive to changes in diet and activates both the proteolytic and autophagy programmes and shutting down protein synthesis more extensively than is the case for wild-types. Poignantly we show that acute starvation which is detrimental to wild-type animals is beneficial in terms of metabolism and muscle function in the myostatin null mice by normalising tension production
Parkinson's Disease DJ-1 L166P Alters rRNA Biogenesis by Exclusion of TTRAP from the Nucleolus and Sequestration into Cytoplasmic Aggregates via TRAF6
Mutations in PARK7/DJ-1 gene are associated to autosomal recessive early onset forms of Parkinson's disease (PD). Although large gene deletions have been linked to a loss-of-function phenotype, the pathogenic mechanism of missense mutations is less clear. The L166P mutation causes misfolding of DJ-1 protein and its degradation. L166P protein may also accumulate into insoluble cytoplasmic aggregates with a mechanism facilitated by the E3 ligase TNF receptor associated factor 6 (TRAF6). Upon proteasome impairment L166P activates the JNK/p38 MAPK apoptotic pathway by its interaction with TRAF and TNF Receptor Associated Protein (TTRAP). When proteasome activity is blocked in the presence of wild-type DJ-1, TTRAP forms aggregates that are localized to the cytoplasm or associated to nucleolar cavities, where it is required for a correct rRNA biogenesis. In this study we show that in post-mortem brains of sporadic PD patients TTRAP is associated to the nucleolus and to Lewy Bodies, cytoplasmic aggregates considered the hallmark of the disease. In SH-SY5Y neuroblastoma cells, misfolded mutant DJ-1 L166P alters rRNA biogenesis inhibiting TTRAP localization to the nucleolus and enhancing its recruitment into cytoplasmic aggregates with a mechanism that depends in part on TRAF6 activity. This work suggests that TTRAP plays a role in the molecular mechanisms of both sporadic and familial PD. Furthermore, it unveils the existence of an interplay between cytoplasmic and nucleolar aggregates that impacts rRNA biogenesis and involves TRAF6
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