Transit timing variation analysis of the low-mass brown dwarf KELT-1 b

We investigate whether there is a variation in the orbital period of the short-period brown dwarf-mass KELT-1 b, which is one of the best candidates to observe orbital decay. We obtain 19 high-precision transit light curves of the target using six different telescopes. We add all precise and complete transit light curves from open databases and the literature, as well as the available Transiting Exoplanet Survey Satellite (TESS) observations from sectors 17 and 57, to form a transit timing variation (TTV) diagram spanning more than 10 yr of observations. The analysis of the TTV diagram, however, is inconclusive in terms of a secular or periodic variation, hinting that the system might have synchronized. We update the transit ephemeris and determine an informative lower limit for the reduced tidal quality parameter of its host star of Q ′⋆>(8.5±3.9)×106 assuming that the stellar rotation is not yet synchronized. Using our new photometric observations, published light curves, the TESS data, archival radial velocities, and broadband magnitudes, we also update the measured parameters of the system. Our results are in good agreement with those found in previous analyses

Generalized Phase Synchronization in unidirectionally coupled chaotic oscillators

We investigate phase synchronization between two identical or detuned response oscillators coupled to a slightly different drive oscillator. Our result is that phase synchronization can occur between response oscillators when they are driven by correlated (but not identical) inputs from the drive oscillator. We call this phenomenon Generalized Phase Synchronization (GPS) and clarify its characteristics using Lyapunov exponents and phase difference plots.Comment: 4 pages, 5 figure

Interruption of torus doubling bifurcation and genesis of strange nonchaotic attractors in a quasiperiodically forced map : Mechanisms and their characterizations

A simple quasiperiodically forced one-dimensional cubic map is shown to exhibit very many types of routes to chaos via strange nonchaotic attractors (SNAs) with reference to a two-parameter $(A-f)$ space. The routes include transitions to chaos via SNAs from both one frequency torus and period doubled torus. In the former case, we identify the fractalization and type I intermittency routes. In the latter case, we point out that atleast four distinct routes through which the truncation of torus doubling bifurcation and the birth of SNAs take place in this model. In particular, the formation of SNAs through Heagy-Hammel, fractalization and type--III intermittent mechanisms are described. In addition, it has been found that in this system there are some regions in the parameter space where a novel dynamics involving a sudden expansion of the attractor which tames the growth of period-doubling bifurcation takes place, giving birth to SNA. The SNAs created through different mechanisms are characterized by the behaviour of the Lyapunov exponents and their variance, by the estimation of phase sensitivity exponent as well as through the distribution of finite-time Lyapunov exponents.Comment: 27 pages, RevTeX 4, 16 EPS figures. Phys. Rev. E (2001) to appea

Fractal Properties of Robust Strange Nonchaotic Attractors in Maps of Two or More Dimensions

We consider the existence of robust strange nonchaotic attractors (SNA's) in a simple class of quasiperiodically forced systems. Rigorous results are presented demonstrating that the resulting attractors are strange in the sense that their box-counting dimension is N+1 while their information dimension is N. We also show how these properties are manifested in numerical experiments.Comment: 9 pages, 14 figure

Mitochondrial carrier homolog 1 (Mtch1) antibodies in neuro-Behçet's disease

Cataloged from PDF version of article.Efforts for the identification of diagnostic autoantibodies for neuro-Behcet's disease (NBD) have failed. Screening of NBD patients' sera with protein macroarray identified mitochondrial carrier homolog 1 (Mtch1), an apoptosis-related protein, as a potential autoantigen. ELISA studies showed serum Mtch1 antibodies in 68 of 144 BD patients with or without neurological involvement and in 4 of 168 controls corresponding to a sensitivity of 47.2% and specificity of 97.6%. Mtch1 antibody positive NBD patients had more attacks, increased disability and lower serum nucleosome levels. Mtch1 antibody might be involved in pathogenic mechanisms of NBD rather than being a coincidental byproduct of autoinflammation. © 2013 Elsevier B.V

Visual pattern recognition as a means to optimising building performance?

Visual pattern recognition as a means to optimising building performance

Gastrointestinal dysfunction in patients and mice expressing the autism-associated R451C mutation in neuroligin-3

Gastrointestinal (GI) problems constitute an important comorbidity in many patients with autism. Multiple mutations in the neuroligin family of synaptic adhesion molecules are implicated in autism, however whether they are expressed and impact GI function via changes in the enteric nervous system is unknown. We report the GI symptoms of two brothers with autism and an R451C mutation in Nlgn3 encoding the synaptic adhesion protein, neuroligin-3. We confirm the presence of an array of synaptic genes in the murine GI tract and investigate the impact of impaired synaptic protein expression in mice carrying the human neuroligin-3 R451C missense mutation (NL3R451C ). Assessing in vivo gut dysfunction, we report faster small intestinal transit in NL3R451C compared to wild-type mice. Using an ex vivo colonic motility assay, we show increased sensitivity to GABAA receptor modulation in NL3R451C mice, a well-established Central Nervous System (CNS) feature associated with this mutation. We further show increased numbers of small intestine myenteric neurons in NL3R451C mice. Although we observed altered sensitivity to GABAA receptor modulators in the colon, there was no change in colonic neuronal numbers including the number of GABA-immunoreactive myenteric neurons. We further identified altered fecal microbial communities in NL3R451C mice. These results suggest that the R451C mutation affects small intestinal and colonic function and alter neuronal numbers in the small intestine as well as impact fecal microbes. Our findings identify a novel GI phenotype associated with the R451C mutation and highlight NL3R451C mice as a useful preclinical model of GI dysfunction in autism. LAY SUMMARY: People with autism commonly experience gastrointestinal problems, however the cause is unknown. We report gut symptoms in patients with the autism-associated R451C mutation encoding the neuroligin-3 protein. We show that many of the genes implicated in autism are expressed in mouse gut. The neuroligin-3 R451C mutation alters the enteric nervous system, causes gastrointestinal dysfunction, and disrupts gut microbe populations in mice. Gut dysfunction in autism could be due to mutations that affect neuronal communication.This work was supported by an Idea Development Award from the United States Department of Defense’s Congressionally Directed Medical Research Programs (CDMRP) Autism Research Program (AR110134) to E.L.H.-Y. and J.C.B.; the Victorian Government through the Operational Infrastructure Scheme, National Health and Medical Research Council (NHMRC) project grants (APP566642 to J.C.B. and APP1047674 to E.L.H.-Y.) and the Royal Melbourne Hospital Neuroscience Foundation. E.L.H.-Y. also received an ARC Future Fellowship (FT160100126) and an RMIT Vice Chancellor’s Senior Research Fellowship which supported G.K.B. and S.H. T.S., P.U., and N.Y. were funded by grants RO1AI100914, P30-DK56338, and U01-AI24290 awards to Baylor College of Medicine funded from the National Institute of Allergy and Infectious Diseases and National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health (T.C.S.)

Megalencephalic leukoencephalopathy with subcortical cysts: Characterization of disease variants

OBJECTIVE: To provide an overview of clinical and MRI characteristics of the different variants of the leukodystrophy megalencephalic leukoencephalopathy with subcortical cysts (MLC) and identify possible differentiating features. METHODS: We performed an international multi-institutional, cross-sectional observational study of the clinical and MRI characteristics in patients with genetically confirmed MLC. Clinical information was obtained by questionnaires for physicians and retrospective chart review. RESULTS: We included 204 patients with classic MLC, 187 of whom had recessive mutations in MLC1 (MLC1 variant) and 17 in GLIALCAM (MLC2A variant) and 38 patients with remitting MLC caused by dominant GLIALCAM mutations (MLC2B variant). We observed a relatively wide variability in neurologic disability among patients with classic MLC. No clinical differences could be identified between patients with MLC1 and MLC2A. Patients with MLC2B invariably had a milder phenotype with preservation of motor function, while intellectual disability and autism were relatively frequent. Systematic MRI review revealed no MRI features that distinguish between MLC1 and MLC2A. Radiologic improvement was observed in all patients with MLC2B and also in 2 patients with MLC1. In MRIs obtained in the early disease stage, absence of signal abnormalities of the posterior limb of the internal capsule and cerebellar white matter and presence of only rarefied subcortical white matter instead of true subcortical cysts were suggestive of MLC2B. CONCLUSION: Clinical and MRI features did not distinguish between classic MLC with MLC1 or GLIALCAM mutations. Absence of signal abnormalities of the internal capsule and cerebellar white matter are MRI findings that point to the remitting phenotype