University of British Columbia

About: University of British Columbia is a education organization based out in Vancouver, British Columbia, Canada. It is known for research contribution in the topics: Population & Health care. The organization has 89939 authors who have published 209679 publications receiving 9226862 citations. The organization is also known as: UBC & The University of British Columbia.

SATzilla: portfolio-based algorithm selection for SAT

Abstract: It has been widely observed that there is no single "dominant" SAT solver; instead, different solvers perform best on different instances. Rather than following the traditional approach of choosing the best solver for a given class of instances, we advocate making this decision online on a per-instance basis. Building on previous work, we describe SATzilla, an automated approach for constructing per-instance algorithm portfolios for SAT that use so-called empirical hardness models to choose among their constituent solvers. This approach takes as input a distribution of problem instances and a set of component solvers, and constructs a portfolio optimizing a given objective function (such as mean runtime, percent of instances solved, or score in a competition). The excellent performance of SATzilla was independently verified in the 2007 SAT Competition, where our SATzilla07 solvers won three gold, one silver and one bronze medal. In this article, we go well beyond SATzilla07 by making the portfolio construction scalable and completely automated, and improving it by integrating local search solvers as candidate solvers, by predicting performance score instead of runtime, and by using hierarchical hardness models that take into account different types of SAT instances. We demonstrate the effectiveness of these new techniques in extensive experimental results on data sets including instances from the most recent SAT competition.

Preattentive processing in vision

Abstract: Visual analysis appears to be functionally divided between an early preattentive level of processing at which simple features are coded spatially in parallel and a later stage at which focused attention is required to conjoin the separate features into coherent objects. Evidence supporting this dichotomy comes from behavioral studies of visual search, from differences in the ease of texture segregation, from reports of illusory conjunctions when attention is overloaded, from subjects' ability to identify simple features correctly even when they mislocate them, and from the substantial benefit of pre-cuing the location of a relevant item when the task requires that features be conjoined but not when simple features are sufficient. Some further studies of search have revealed a striking asymmetry between several pairs of stimuli which differ in the presence or absence of a single part or property. The asymmetry depends solely on which of the pair is allocated the role of target and which is replicated to form the background items. It suggests that search for the presence of a visual primitive is automatic and parallel, whereas search for the absence of the same feature is serial and requires focused attention. The search asymmetry can be used as an additional diagnostic to help define the functional features extracted by the visual system.

Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes.

Abstract: Huntingtin protein is mutated in Huntington disease. We previously reported that wild-type but not mutant huntingtin stimulates transcription of the gene encoding brain-derived neurotrophic factor (BDNF; ref. 2). Here we show that the neuron restrictive silencer element (NRSE) is the target of wild-type huntingtin activity on BDNF promoter II. Wild-type huntingtin inhibits the silencing activity of NRSE, increasing transcription of BDNF. We show that this effect occurs through cytoplasmic sequestering of repressor element-1 transcription factor/neuron restrictive silencer factor (REST/NRSF), the transcription factor that binds to NRSE. In contrast, aberrant accumulation of REST/NRSF in the nucleus is present in Huntington disease. We show that wild-type huntingtin coimmunoprecipitates with REST/NRSF and that less immunoprecipitated material is found in brain tissue with Huntington disease. We also report that wild-type huntingtin acts as a positive transcriptional regulator for other NRSE-containing genes involved in the maintenance of the neuronal phenotype. Consistently, loss of expression of NRSE-controlled neuronal genes is shown in cells, mice and human brain with Huntington disease. We conclude that wild-type huntingtin acts in the cytoplasm of neurons to regulate the availability of REST/NRSF to its nuclear NRSE-binding site and that this control is lost in the pathology of Huntington disease. These data identify a new mechanism by which mutation of huntingtin causes loss of transcription of neuronal genes.