58 research outputs found

    A Study of the Lecompton Constitution in the Senate of the Thirty-Fifth Congress

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    CHD6 (chromodomain helicase DNA binding protein 6)

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    CHD6 is a chromatin remodeling protein characterized to play a role in transcriptional repression of genes and viruses. It occurs in a nuclear location as a component of a larger complex which associates with RNA Pol II. Mutations in CHD6 are associated with motor coordination defects, and development of cancers following substitutions and translocations

    Differential sphingosine-1-phosphate receptor-1 protein expression in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2

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    Understanding the etiology and treatment approaches in schizophrenia is challenged in part by the heterogeneity of this disorder. One encouraging progress is the growing evidence that there are subtypes of schizophrenia. Recen

    Misuse made plain: Evaluating concerns about neuroscience in national security

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    In this open peer commentary, we categorize the possible “neuroscience in national security” definitions of misuse of science and identify which, if any, are uniquely presented by advances in neuroscience. To define misuse, we first define what we would consider appropriate use: the application of reasonably safe and effective technology, based on valid and reliable scientific research, to serve a legitimate end. This definition presents distinct opportunities for assessing misuse: misuse is the application of invalid or unreliable science, or is the use of reliable scientific methods to serve illegitimate ends. Ultimately, we conclude that while national security is often a politicized issue, assessing the state of scientific progress should not be

    Alpha-synuclein (SNCA) polymorphisms exert protective effects on memory after mild traumatic brain injury

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    Problems with attention and short-term learning and memory are commonly reported after mild traumatic brain injury (mTBI). Due to the known relationships between α-synuclein (SNCA), dopaminergic transmission, and neurologic deficits, we hypothesized that SNCA polymorphisms might be associated with cognitive outcome after mTBI. A cohort of 91 mTBI patients one month after injury and 86 healthy controls completed a series of cognitive tests assessing baseline intellectual function, attentional function, and memory, and was genotyped at 13 common single nucleotide polymorphisms (SNPs) in the SNCA gene. Significant differences in two memory measures (p = 0.001 and 0.002), but not baseline intellectual function or attentional function tasks, were found between the mTBI group and controls. A highly significant protective association between memory performance and SNCA promoter SNP rs1372525 was observed in the mTBI patients (p = 0.006 and 0.029 for the long and short delay conditions of the California Verbal Learning Tests, respectively), where the presence of at least one copy of the A (minor) allele was protective after mTBI. These results may help elucidate the pathophysiology of cognitive alterations after mTBI, and thus warrant further investigation

    Intrinsic galaxy shapes and alignments I: Measuring and modelling COSMOS intrinsic galaxy ellipticities

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    The statistical properties of the ellipticities of galaxy images depend on how galaxies form and evolve, and therefore constrain models of galaxy morphology, which are key to the removal of the intrinsic alignment contamination of cosmological weak lensing surveys, as well as to the calibration of weak lensing shape measurements. We construct such models based on the halo properties of the Millennium Simulation and confront them with a sample of 90,000 galaxies from the COSMOS Survey, covering three decades in luminosity and redshifts out to z=2. The ellipticity measurements are corrected for effects of point spread function smearing, spurious image distortions, and measurement noise. Dividing galaxies into early, late, and irregular types, we find that early-type galaxies have up to a factor of two lower intrinsic ellipticity dispersion than late-type galaxies. None of the samples shows evidence for redshift evolution, while the ellipticity dispersion for late-type galaxies scales strongly with absolute magnitude at the bright end. The simulation-based models reproduce the main characteristics of the intrinsic ellipticity distributions although which model fares best depends on the selection criteria of the galaxy sample. We observe fewer close-to-circular late-type galaxy images in COSMOS than expected for a sample of randomly oriented circular thick disks and discuss possible explanations for this deficit.Comment: 18 pages, 8 figures; updated simulations and galaxy sample definition, more galaxy samples analysed; matches version published in MNRA

    Deletion of the Chd6 exon 12 affects motor coordination

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    Members of the CHD protein family play key roles in gene regulation through ATP-dependent chromatin remodeling. This is facilitated by chromodomains that bind histone tails, and by the SWI2/SNF2-like ATPase/helicase domain that remodels chromatin by moving histones. Chd6 is ubiquitously expressed in both mouse and human, with the highest levels of expression in the brain. The Chd6 gene contains 37 exons, of which exons 12-19 encode the highly conserved ATPase domain. To determine the biological role of Chd6, we generated mouse lines with a deletion of exon 12. Chd6 without exon 12 is expressed at normal levels in mice, and Chd6 Exon 12 −/− mice are viable, fertile, and exhibit no obvious morphological or pathological phenotype. Chd6 Exon 12 −/− mice lack coordination as revealed by sensorimotor analysis. Further behavioral testing revealed that the coordination impairment was not due to muscle weakness or bradykinesia. Histological analysis of brain morphology revealed no differences between Chd6 Exon 12 −/− mice and wild-type (WT) controls. The location of CHD6 on human chromosome 20q12 is overlapped by the linkage map regions of several human ataxias, including autosomal recessive infantile cerebellar ataxia (SCAR6), a nonprogressive cerebrospinal ataxia. The genomic location, expression pattern, and ataxic phenotype of Chd6 Exon 12 −/− mice indicate that mutations within CHD6 may be responsible for one of these ataxias
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