369 research outputs found
Change blindness in a dynamic scene due to endogenous override of exogenous attentional cues
Change blindness is a failure to detect changes if the change occurs during a mask or distraction. Without distraction, it is assumed that the visual transients associated with the change will automatically capture attention (exogenous control) leading to detection. However, visual transients are a defining feature of naturalistic dynamic scenes. Are artificial distractions needed to hide changes to a dynamic scene? Do the temporal demands of the scene instead lead to greater endogenous control that may result in viewers missing a change in plain sight? In the present study we pitted endogenous and exogenous factors against each other during a card trick. Complete change blindness was demonstrated even when a salient highlight was inserted coincident with the change. These results indicate strong endogenous control of attention during dynamic scene viewing and its ability to override exogenous influences even when it is to the detriment of accurate scene representation
Where science and magic meet: the illusion of a “science of magic”
Recent articles calling for a scientific study of magic have been the subject of widespread interest. This article considers the topic from a broader perspective and argues that to engage in a science of magic, in any meaningful sense, is misguided. It argues that those who have called for a scientific theory of magic have failed to explain either how or why such a theory might be constructed, that a shift of focus to a neuroscience of magic is simply unwarranted, and that a science of magic is itself an inherently unsound idea. It seeks to provide a more informed view of the relationship between science and magic and suggests a more appropriate way forward for scientists
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
TRIM32 is a E3 ubiquitin -ligase containing RING, B-box, coiled-coil and six C-terminal NHL domains. Mutations
involving NHL and coiled-coil domains result in a pure myopathy (LGMD2H/STM) while the only described
mutation in the B-box domain is associated with a multisystemic disorder without myopathy (Bardet-Biedl
syndrome type11), suggesting that these domains are involved in distinct processes. Knock-out (T32KO) and knockin
mice carrying the c.1465G > A (p.D489N) involving the NHL domain (T32KI) show alterations in muscle regrowth
after atrophy and satellite cells senescence. Here, we present phenotypical description and functional
characterization of mutations in the RING, coiled-coil and NHL domains of TRIM32 causing a muscle dystrophy.
Reduced levels of TRIM32 protein was observed in all patient muscle studied, regardless of the type of mutation
(missense, single amino acid deletion, and frameshift) or the mutated domain. The affected patients presented with
variable phenotypes but predominantly proximal weakness. Two patients had symptoms of both muscular
dystrophy and Bardet-Biedl syndrome. The muscle magnetic resonance imaging (MRI) pattern is highly variable
among patients and families. Primary myoblast culture from these patients demonstrated common findings
consistent with reduced proliferation and differentiation, diminished satellite cell pool, accelerated senescence of
muscle, and signs of autophagy activation.Health Institute Carlos III PI16-01843 JR15/00042FEDER PI16-01843 JR15/00042Fundación Progreso y Salud, Junta de Andalucía PI-0085-2016Australian National Health and Medical Research Council (NHMRC) APP1122952 APP111751
Altered myogenesis and premature senescence underlie human TRIM32-related myopathy
TRIM32 is a E3 ubiquitin -ligase containing RING, B-box, coiled-coil and six C-terminal NHL domains. Mutations
involving NHL and coiled-coil domains result in a pure myopathy (LGMD2H/STM) while the only described
mutation in the B-box domain is associated with a multisystemic disorder without myopathy (Bardet-Biedl
syndrome type11), suggesting that these domains are involved in distinct processes. Knock-out (T32KO) and knockin
mice carrying the c.1465G > A (p.D489N) involving the NHL domain (T32KI) show alterations in muscle regrowth
after atrophy and satellite cells senescence. Here, we present phenotypical description and functional
characterization of mutations in the RING, coiled-coil and NHL domains of TRIM32 causing a muscle dystrophy.
Reduced levels of TRIM32 protein was observed in all patient muscle studied, regardless of the type of mutation
(missense, single amino acid deletion, and frameshift) or the mutated domain. The affected patients presented with
variable phenotypes but predominantly proximal weakness. Two patients had symptoms of both muscular
dystrophy and Bardet-Biedl syndrome. The muscle magnetic resonance imaging (MRI) pattern is highly variable
among patients and families. Primary myoblast culture from these patients demonstrated common findings
consistent with reduced proliferation and differentiation, diminished satellite cell pool, accelerated senescence of
muscle, and signs of autophagy activation.Health Institute Carlos III PI16-01843 JR15/00042FEDER PI16-01843 JR15/00042Fundación Progreso y Salud, Junta de Andalucía PI-0085-2016Australian National Health and Medical Research Council (NHMRC) APP1122952 APP111751
Longitudinal double-spin asymmetry and cross section for inclusive neutral pion production at midrapidity in polarized proton collisions at sqrt(s) = 200 GeV
We report a measurement of the longitudinal double-spin asymmetry A_LL and
the differential cross section for inclusive Pi0 production at midrapidity in
polarized proton collisions at sqrt(s) = 200 GeV. The cross section was
measured over a transverse momentum range of 1 < p_T < 17 GeV/c and found to be
in good agreement with a next-to-leading order perturbative QCD calculation.
The longitudinal double-spin asymmetry was measured in the range of 3.7 < p_T <
11 GeV/c and excludes a maximal positive gluon polarization in the proton. The
mean transverse momentum fraction of Pi0's in their parent jets was found to be
around 0.7 for electromagnetically triggered events.Comment: 6 pages, 3 figures, submitted to Phys. Rev. D (RC
Single Spin Asymmetry in Polarized Proton-Proton Elastic Scattering at GeV
We report a high precision measurement of the transverse single spin
asymmetry at the center of mass energy GeV in elastic
proton-proton scattering by the STAR experiment at RHIC. The was measured
in the four-momentum transfer squared range \GeVcSq, the region of a significant interference between the
electromagnetic and hadronic scattering amplitudes. The measured values of
and its -dependence are consistent with a vanishing hadronic spin-flip
amplitude, thus providing strong constraints on the ratio of the single
spin-flip to the non-flip amplitudes. Since the hadronic amplitude is dominated
by the Pomeron amplitude at this , we conclude that this measurement
addresses the question about the presence of a hadronic spin flip due to the
Pomeron exchange in polarized proton-proton elastic scattering.Comment: 12 pages, 6 figure
Kaon Production and Kaon to Pion Ratio in Au+Au Collisions at \snn=130 GeV
Mid-rapidity transverse mass spectra and multiplicity densities of charged
and neutral kaons are reported for Au+Au collisions at \snn=130 GeV at RHIC.
The spectra are exponential in transverse mass, with an inverse slope of about
280 MeV in central collisions. The multiplicity densities for these particles
scale with the negative hadron pseudo-rapidity density. The charged kaon to
pion ratios are and
for the most central collisions. The ratio is lower than the same
ratio observed at the SPS while the is higher than the SPS result.
Both ratios are enhanced by about 50% relative to p+p and +p
collision data at similar energies.Comment: 6 pages, 3 figures, 1 tabl
Azimuthal anisotropy and correlations in p+p, d+Au and Au+Au collisions at 200 GeV
We present the first measurement of directed flow () at RHIC. is
found to be consistent with zero at pseudorapidities from -1.2 to 1.2,
then rises to the level of a couple of percent over the range . The latter observation is similar to data from NA49 if the SPS rapidities
are shifted by the difference in beam rapidity between RHIC and SPS.
Back-to-back jets emitted out-of-plane are found to be suppressed more if
compared to those emitted in-plane, which is consistent with {\it jet
quenching}. Using the scalar product method, we systematically compared
azimuthal correlations from p+p, d+Au and Au+Au collisions. Flow and non-flow
from these three different collision systems are discussed.Comment: Quark Matter 2004 proceeding, 4 pages, 3 figure
Azimuthal anisotropy: the higher harmonics
We report the first observations of the fourth harmonic (v_4) in the
azimuthal distribution of particles at RHIC. The measurement was done taking
advantage of the large elliptic flow generated at RHIC. The integrated v_4 is
about a factor of 10 smaller than v_2. For the sixth (v_6) and eighth (v_8)
harmonics upper limits on the magnitudes are reported.Comment: 4 pages, 6 figures, contribution to the Quark Matter 2004 proceeding
Partonic flow and -meson production in Au+Au collisions at = 200 GeV
We present first measurements of the -meson elliptic flow
() and high statistics distributions for different
centralities from = 200 GeV Au+Au collisions at RHIC. In
minimum bias collisions the of the meson is consistent with the
trend observed for mesons. The ratio of the yields of the to those of
the as a function of transverse momentum is consistent with a model
based on the recombination of thermal quarks up to GeV/,
but disagrees at higher momenta. The nuclear modification factor () of
follows the trend observed in the mesons rather than in
baryons, supporting baryon-meson scaling. Since -mesons are
made via coalescence of seemingly thermalized quarks in central Au+Au
collisions, the observations imply hot and dense matter with partonic
collectivity has been formed at RHIC.Comment: 6 pages, 4 figures, submit to PR
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