1,030 research outputs found
Algebraic Aspects of Abelian Sandpile Models
The abelian sandpile models feature a finite abelian group G generated by the
operators corresponding to particle addition at various sites. We study the
canonical decomposition of G as a product of cyclic groups G = Z_{d_1} X
Z_{d_2} X Z_{d_3}...X Z_{d_g}, where g is the least number of generators of G,
and d_i is a multiple of d_{i+1}. The structure of G is determined in terms of
toppling matrix. We construct scalar functions, linear in height variables of
the pile, that are invariant toppling at any site. These invariants provide
convenient coordinates to label the recurrent configurations of the sandpile.
For an L X L square lattice, we show that g = L. In this case, we observe that
the system has nontrivial symmetries coming from the action of the cyclotomic
Galois group of the (2L+2)th roots of unity which operates on the set of
eigenvalues of the toppling matrix. These eigenvalues are algebraic integers,
whose product is the order |G|. With the help of this Galois group, we obtain
an explicit factorizaration of |G|. We also use it to define other simpler,
though under-complete, sets of toppling invariants.Comment: 39 pages, TIFR/TH/94-3
Statoviruses, a novel taxon of RNA viruses present in the gastrointestinal tracts of diverse mammals
Periodic One-Dimensional Hopping Model with one Mobile Directional Impurity
Analytic solution is given in the steady state limit for the system of Master
equations describing a random walk on one-dimensional periodic lattices with
arbitrary hopping rates containing one mobile, directional impurity (defect
bond). Due to the defect, translational invariance is broken, even if all other
rates are identical. The structure of Master equations lead naturally to the
introduction of a new entity, associated with the walker-impurity pair which we
call the quasi-walker. The velocities and diffusion constants for both the
random walker and impurity are given, being simply related to that of the
quasi-particle through physically meaningful equations. Applications in driven
diffusive systems are shown, and connections with the Duke-Rubinstein reptation
models for gel electrophoresis are discussed.Comment: 31 LaTex pages, 5 Postscript figures included, to appear in Journal
of Statistical Physic
Domain wall QCD with physical quark masses
We present results for several light hadronic quantities (, ,
, , , , ) obtained from simulations of 2+1
flavor domain wall lattice QCD with large physical volumes and nearly-physical
pion masses at two lattice spacings. We perform a short, O(3)%, extrapolation
in pion mass to the physical values by combining our new data in a simultaneous
chiral/continuum `global fit' with a number of other ensembles with heavier
pion masses. We use the physical values of , and to
determine the two quark masses and the scale - all other quantities are outputs
from our simulations. We obtain results with sub-percent statistical errors and
negligible chiral and finite-volume systematics for these light hadronic
quantities, including: = 130.2(9) MeV; = 155.5(8) MeV; the
average up/down quark mass and strange quark mass in the scheme
at 3 GeV, 2.997(49) and 81.64(1.17) MeV respectively; and the neutral kaon
mixing parameter, , in the RGI scheme, 0.750(15) and the
scheme at 3 GeV, 0.530(11).Comment: 131 pages, 30 figures. Updated to match published versio
The rural non-farm economy and poverty alleviation in Armenia, Georgia and Romania: A synthesis of findings
Motion of a driven tracer particle in a one-dimensional symmetric lattice gas
We study the dynamics of a tracer particle subject to a constant driving
force in a one-dimensional lattice gas of hard-core particles whose
transition rates are symmetric. We show that the mean displacement of the
driven tracer grows in time, , as , rather than the linear
time dependence found for driven diffusion in the bath of non-interacting
(ghost) particles. The prefactor is determined implicitly, as the
solution of a transcendental equation, for an arbitrary magnitude of the
driving force and an arbitrary concentration of the lattice gas particles. In
limiting cases the prefactor is obtained explicitly. Analytical predictions are
seen to be in a good agreement with the results of numerical simulations.Comment: 21 pages, LaTeX, 4 Postscript fugures, to be published in Phys. Rev.
E, (01Sep, 1996
You turn me cold: evidence for temperature contagion
Introduction
During social interactions, our own physiological responses influence those of others. Synchronization of physiological (and behavioural) responses can facilitate emotional understanding and group coherence through inter-subjectivity. Here we investigate if observing cues indicating a change in another's body temperature results in a corresponding temperature change in the observer.
Methods
Thirty-six healthy participants (age; 22.9±3.1 yrs) each observed, then rated, eight purpose-made videos (3 min duration) that depicted actors with either their right or left hand in visibly warm (warm videos) or cold water (cold videos). Four control videos with the actors' hand in front of the water were also shown. Temperature of participant observers' right and left hands was concurrently measured using a thermistor within a Wheatstone bridge with a theoretical temperature sensitivity of <0.0001°C. Temperature data were analysed in a repeated measures ANOVA (temperature × actor's hand × observer's hand).
Results
Participants rated the videos showing hands immersed in cold water as being significantly cooler than hands immersed in warm water, F(1,34) = 256.67, p0.1). There was however no evidence of left-right mirroring of these temperature effects p>0.1). Sensitivity to temperature contagion was also predicted by inter-individual differences in self-report empathy.
Conclusions
We illustrate physiological contagion of temperature in healthy individuals, suggesting that empathetic understanding for primary low-level physiological challenges (as well as more complex emotions) are grounded in somatic simulation
PURA syndrome: clinical delineation and genotype-phenotype study in 32 individuals with review of published literature
Background De novo mutations in PURA have recently been described to cause PURA syndrome, a neurodevelopmental disorder characterized by severe intellectual disability (ID), epilepsy, feeding difficulties and neonatal hypotonia. Objectives To delineate the clinical spectrum of PURA syndrome and study genotype-phenotype correlations. Methods Diagnostic or research-based Exome or Sanger sequencing was performed in individuals with ID. We systematically collected clinical and mutation data on newly ascertained PURA syndrome individuals, evaluated data of previously reported individuals, and performed a computational analysis of photographs. We classified mutations based on predicted effect using 3D in silico models of crystal structures of Drosophila-derived Pur-alpha homologues. Finally, we explored genotype-phenotype correlations by analysis of both recurrent mutations as well as mutation classes. Results We report mutations in PURA in 32 individuals, the largest cohort described so far. Evaluation of clinical data, including 22 previously published cases, revealed that all have moderate to severe ID and neonatal-onset symptoms, including hypotonia (96%), respiratory problems (57%), feeding difficulties (77%), exaggerated startle response (44%), hypersomnolence (66%) and hypothermia (35%). Epilepsy (54%), gastro-intestinal- (69%), ophthalmological- (51%), and endocrine problems (42%) were observed frequently. Computational analysis of facial photographs showed subtle facial dysmorphism. No strong genotype-phenotype correlation was identified by subgrouping mutations into functional classes. Conclusion We delineate the clinical spectrum of PURA syndrome with the identification of 32 additional individuals. The identification of one individual through targeted Sanger sequencing points towards the clinical recognizability of the syndrome. Genotype-phenotype analysis showed no significant correlation between mutation classes and disease severity
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