6,109 research outputs found
Lie point symmetries and the geodesic approximation for the Schr\"odinger-Newton equations
We consider two problems arising in the study of the Schr\"odinger-Newton
equations. The first is to find their Lie point symmetries. The second, as an
application of the first, is to investigate an approximate solution
corresponding to widely separated lumps of probability. The lumps are found to
move like point particles under a mutual inverse-square law of attraction
FEDERAL COURTS-REMOVAL JURISDICTION-COUNTERCLAIM AS THE SOLE BASIS FOR REMOVAL
Plaintiff brought an action for damages in a state court Defendant filed pleas to the declaration, and also filed a counterclaim arising out of the same cause of action. On this date defendant also filed a motion with the Federal District Court asking removal of the case based solely upon his counterclaim. On plaintiff\u27s motion, held, case remanded to the state court. Defendant has no right under the United States Judicial Code to have a case removed from the state court to the federal court when his motion is based upon his own counterclaim. Collins v. Faucett, (D.C. Fla. 1949) 87 F. Supp. 254
A method to assess compositional bias in biological sequences and its application to prion-like glutamine/asparagine-rich domains in eukaryotic proteomes
We have derived a novel method to assess compositional biases in biological sequences, which is based on finding the lowest-probability subsequences for a given residue-type set. As a case study, the distribution of prion-like glutamine/asparagine-rich ((Q+N)-rich) domains (which are linked to amyloidogenesis) was assessed for budding and fission yeasts and four other eukaryotes. We find more than 170 prion-like (Q+N)-rich regions in budding yeast, and, strikingly, many fewer in fission yeast. Also, some residues, such as tryptophan or isoleucine, are unlikely to form biased regions in any eukaryotic proteome
Visual Working Memory Is Independent of the Cortical Spacing Between Memoranda.
The sensory recruitment hypothesis states that visual short-term memory is maintained in the same visual cortical areas that initially encode a stimulus' features. Although it is well established that the distance between features in visual cortex determines their visibility, a limitation known as crowding, it is unknown whether short-term memory is similarly constrained by the cortical spacing of memory items. Here, we investigated whether the cortical spacing between sequentially presented memoranda affects the fidelity of memory in humans (of both sexes). In a first experiment, we varied cortical spacing by taking advantage of the log-scaling of visual cortex with eccentricity, presenting memoranda in peripheral vision sequentially along either the radial or tangential visual axis with respect to the fovea. In a second experiment, we presented memoranda sequentially either within or beyond the critical spacing of visual crowding, a distance within which visual features cannot be perceptually distinguished due to their nearby cortical representations. In both experiments and across multiple measures, we found strong evidence that the ability to maintain visual features in memory is unaffected by cortical spacing. These results indicate that the neural architecture underpinning working memory has properties inconsistent with the known behavior of sensory neurons in visual cortex. Instead, the dissociation between perceptual and memory representations supports a role of higher cortical areas such as posterior parietal or prefrontal regions or may involve an as yet unspecified mechanism in visual cortex in which stimulus features are bound to their temporal order.SIGNIFICANCE STATEMENT Although much is known about the resolution with which we can remember visual objects, the cortical representation of items held in short-term memory remains contentious. A popular hypothesis suggests that memory of visual features is maintained via the recruitment of the same neural architecture in sensory cortex that encodes stimuli. We investigated this claim by manipulating the spacing in visual cortex between sequentially presented memoranda such that some items shared cortical representations more than others while preventing perceptual interference between stimuli. We found clear evidence that short-term memory is independent of the intracortical spacing of memoranda, revealing a dissociation between perceptual and memory representations. Our data indicate that working memory relies on different neural mechanisms from sensory perception
Follow the Leader: Adoption Behavior in Food Retailers' Decision to Offer Fresh Irradiated Ground Beef
During the 14-month period from May 2002 to June 2003, approximately 10 percent of U.S. supermarkets began to offer fresh irradiated ground beef under the stores' own labels. Using a survey of supermarket store managers from this time period, this paper investigates the factors that influenced new product offerings and adoptions. Results from the adoption model show that factors associated with competition and structure in the food retailing industry play a strong role in the decision. Among other results, we find that variables relating to a competitor's adoption status and proximity significantly affect a store's decision to offer fresh irradiated ground beef.Marketing,
Adoption Behavior in Food Retailers' Decision to Offer Fresh Irradiated Ground Beef
During the 14-month period from May 2002 to June 2003, approximately 10 percent of U.S. supermarkets began to offer fresh irradiated ground beef under the stores' own labels. Using a survey of supermarket store managers from this time period, this paper investigates the factors that influenced stores' adoption of irradiated ground beef. Results from the adoption model show that factors associated with competition, merchandising philosophy, and structure in the food retailing industry play a strong role in the decision. Among other results, we find that variables relating to a competitor's adoption status and proximity can increase the likelihood of a store's adoption decision.Marketing,
GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia
Involvement of the glutamate system, particularly N-methyl-D-aspartate (NMDA) receptor hypofunction, has long been postulated to be part of the pathophysiology of schizophrenia. An important development is provided by recent data that strongly implicate GRIN2A, the gene encoding the NR2A (GluN2A) NMDA receptor subunit, in the aetiology of the disorder. Rare variants and common variants are both robustly associated with genetic risk for schizophrenia. Some of the rare variants are point mutations likely affecting channel function, but most are predicted to cause protein truncation and thence result, like the common variants, in reduced gene expression. We review the genomic evidence, and the findings from Grin2a mutant mice and other models which give clues as to the likely phenotypic impacts of GRIN2A genetic variation. We suggest that one consequence of NR2A dysfunction is impairment in a form of hippocampal synaptic plasticity, producing deficits in short-term habituation and thence elevated and dysregulated levels of attention, a phenotype of relevance to schizophrenia and its cognitive aspects
Genomic evidence for non-random endemic populations of decaying exons from mammalian genes
<p>Abstract</p> <p>Background</p> <p>Functional diversification of genes in mammalian genomes is engendered by a number of processes, <it>e.g</it>., gene duplication and alternative splicing. Gene duplication is classically discussed as leading to <it>neofunctionalization </it>(generation of new functions), <it>subfunctionalization </it>(generation of a varied function), or <it>pseudogenization </it>(loss of the gene and its function).</p> <p>Results</p> <p>Here, we focus on the process of pseudogenization, but specifically for individual exons from genes. It is at present unclear to what extent pseudogenization of individual exon duplications affects gene evolution, <it>i.e</it>., is it a random phenomenon, or is it associated with specific types of genes and encoded proteins, and positions in gene structures? We gathered genomic evidence for <it>pseudogenic exons </it>(ΨEs, <it>i.e</it>., exons disabled by frameshifts and premature stop codons), to examine for significant trends in their distribution across four mammalian genomes (specifically human, cow, mouse and rat). Across these four genomes, we observed a consistent population of ΨEs, associated with 0.4–1.0% of genes. These ΨE populations exhibit codon substitution patterns that are typical of an endemic population of decaying sequences. In human, ΨEs have significant over-representation for functional categories related to 'ion binding' and 'nucleic-acid binding', compared to duplicated exons in general. Also, ΨEs tend to be associated with some protein domains that are abundant generally, <it>e.g</it>., Zinc-finger and immunoglobulin protein domains, but not others, <it>e.g</it>., EGF-like domains. Positionally, ΨEs are also significantly associated with the 5' end of genes, but despite this, individual stop codons are positioned so that there is significant avoidance of potential targeting to nonsense-mediated decay. In human, ΨEs are often associated with alternative splicing (in 22 out of 284 genes with ΨEs in their milieu), and can have different parts of their sequence differentially spliced in alternative transcripts. Some unusual cases of ΨEs embedded within 5' and 3' non-coding exons are observed.</p> <p>Conclusion</p> <p>Our results indicate the types of genes that harbour ΨEs, and demonstrate that ΨEs have non-random distribution within gene structures. These ΨEs may function in gene regulation through generation of transcribed pseudogenes, or regulatory alternate transcripts.</p
Assessing the genomic evidence for conserved transcribed pseudogenes under selection
<p>Abstract</p> <p>Background</p> <p><it>Transcribed pseudogenes </it>are copies of protein-coding genes that have accumulated indicators of coding-sequence decay (such as frameshifts and premature stop codons), but nonetheless remain transcribed. Recent experimental evidence indicates that transcribed pseudogenes may regulate the expression of homologous genes, through antisense interference, or generation of small interfering RNAs (siRNAs). Here, we assessed the genomic evidence for such transcribed pseudogenes of potential functional importance, in the human genome. The most obvious indicators of such functional importance are significant evidence of conservation and selection pressure.</p> <p>Results</p> <p>A variety of pseudogene annotations from multiple sources were pooled and filtered to obtain a subset of sequences that have significant mid-sequence disablements (frameshifts and premature stop codons), and that have clear evidence of full-length mRNA transcription. We found 1750 such transcribed pseudogene annotations (TPAs) in the human genome (corresponding to ~11.5% of human pseudogene annotations). We checked for syntenic conservation of TPAs in other mammals (rhesus monkey, mouse, rat, dog and cow). About half of the human TPAs are conserved in rhesus monkey, but strikingly, very few in mouse (~3%). The TPAs conserved in rhesus monkey show evidence of selection pressure (relative to surrounding intergenic DNA) on: <it>(i) </it>their GC content, and <it>(ii) </it>their rate of nucleotide substitution. This is in spite of distributions of Ka/Ks (ratios of non-synonymous to synonymous substitution rates), congruent with a lack of protein-coding ability. Furthermore, we have identified 68 human TPAs that are syntenically conserved in at least two other mammals. Interestingly, we observe three TPA sequences conserved in dog that have intermediate character (<it>i.e.</it>, evidence of both protein-coding ability and pseudogenicity), and discuss the implications of this.</p> <p>Conclusion</p> <p>Through evolutionary analysis, we have identified candidate sequences for functional human transcribed pseudogenes, and have pinpointed 68 strong candidates for further investigation as potentially functional transcribed pseudogenes across multiple mammal species.</p
Strong association between pseudogenization mechanisms and gene sequence length
<p>Abstract</p> <p>Pseudogenes arise from the decay of gene copies following either RNA-mediated duplication (processed pseudogenes) or DNA-mediated duplication (nonprocessed pseudogenes). Here, we show that long protein-coding genes tend to produce more nonprocessed pseudogenes than short genes, whereas the opposite is true for processed pseudogenes. Protein-coding genes longer than 3000 bp are 6 times more likely to produce nonprocessed pseudogenes than processed ones.</p> <p>Reviewers</p> <p>This article was reviewed by Dr. Dan Graur and Dr. Craig Nelson (nominated by Dr. J Peter Gogarten).</p
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