222 research outputs found

    Stereodeficient subjects demonstrate non-linear stereopsis

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    AbstractThere appear to be two modes of stereoscopic processing: a conventional linear operation that is dependent on correspondence between local luminance components in the two eyes’ views, and a non-linear or second-order processing mode. This second mode may use disparity information provided by particular ‘non-Fourier’ features of the stimulus such as the contrast envelope. Preliminary results suggest that people who fail standard clinical stereotests are able to extract non-linear disparity information from Gabor stimuli [McColl & Mitchell, 1998. Vision Research, 38, 1889–1900]. Here we evaluate the status of the non-linear mechanism in such individuals by using two types of contrast enveloped stimuli, namely random line and Gabor micropatterns, in a task that requires near/far depth judgements [Ziegler & Hess, 1999. Vision Research, 39, 1491–1507]. Although our sample was small, three of our four subjects who had performed poorly on at least one standard clinical test of stereopsis could perform the task, as well as one ‘stereoblind’ subject who had failed all four standard clinical tests. The overall results suggest that individuals with stereoanomalies show a diversity of deficits, but some nevertheless can see depth using ‘non-linear’ mechanisms

    Can Blacklisting Reduce Terrorist Attacks?

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    Within global security governance, a number of governments monitor and label certain organizations as “terrorist groups” with the aim of curtailing their capacity. The most prominent example of this is the U.S. Foreign Terrorist Organization (FTO) list. Under what conditions is FTO listing an effective counterterrorism tool? We develop a theory of blacklisting in the context of FTOs, arguing that the impact of FTO designation depends on the types of support terrorist organizations rely on. We theorize that FTO blacklisting has capacity-curtailing effects on terrorist groups when funding sources are vulnerable to detection, sanctions, and stigmatization. Specifically, we hypothesize that groups with private funding (e.g. charities, diaspora networks) are more likely to reduce attacks after FTO designation, compared to groups with other funding sources such as criminal activities. Analysis of data on terrorist organizations between 1970 and 2014 takes into account the political processes of listing and provides support for the argument. The findings highlight the importance of understanding the nature of the target in evaluating the performance of global indicators

    Chronic pancreatitis in dogs: A retrospective study of clinical, clinicopathological, and histopathological findings in 61 cases

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    The objective of the present study was to characterize the clinical, clinicopathologic, and histopathologic findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histologic evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas, i.e. fibrosis and atrophy. Medical records and necropsy reports were retrieved and reviewed. A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both versus neither of these signs. All archived pancreata samples were evaluated histologically and scored using a published pancreatic scoring system. A total of 61 dogs with chronic pancreatitis were included in the study. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, and of the non-sporting/toy breed group and to have concurrent endocrine, hepatobiliary, or neurologic diseases. Clinical chronic pancreatitis cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis. Clinical chronic pancreatitis cases were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, and cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.http://www.elsevier.com/locate/tvjlam2013ab201

    Expressions 1983

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    The 1983 edition of Expressions magazine is the result of the efforts of students from several DMACC programs. Entrants in both the annual Creative Writing Contest and the Campus Chronicle Photography Contest as well as student in the commercial art program contributed material to the magazine. Layout, design and typesetting was done by the summer Publications Production class.https://openspace.dmacc.edu/expressions/1005/thumbnail.jp

    Polarizable Water Model for the Coarse-Grained MARTINI Force Field

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    Coarse-grained (CG) simulations have become an essential tool to study a large variety of biomolecular processes, exploring temporal and spatial scales inaccessible to traditional models of atomistic resolution. One of the major simplifications of CG models is the representation of the solvent, which is either implicit or modeled explicitly as a van der Waals particle. The effect of polarization, and thus a proper screening of interactions depending on the local environment, is absent. Given the important role of water as a ubiquitous solvent in biological systems, its treatment is crucial to the properties derived from simulation studies. Here, we parameterize a polarizable coarse-grained water model to be used in combination with the CG MARTINI force field. Using a three-bead model to represent four water molecules, we show that the orientational polarizability of real water can be effectively accounted for. This has the consequence that the dielectric screening of bulk water is reproduced. At the same time, we parameterized our new water model such that bulk water density and oil/water partitioning data remain at the same level of accuracy as for the standard MARTINI force field. We apply the new model to two cases for which current CG force fields are inadequate. First, we address the transport of ions across a lipid membrane. The computed potential of mean force shows that the ions now naturally feel the change in dielectric medium when moving from the high dielectric aqueous phase toward the low dielectric membrane interior. In the second application we consider the electroporation process of both an oil slab and a lipid bilayer. The electrostatic field drives the formation of water filled pores in both cases, following a similar mechanism as seen with atomistically detailed models

    Interactions Between a Voltage Sensor and a Toxin via Multiscale Simulations

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    Gating-modifier toxins inhibit voltage-gated ion channels by binding the voltage sensors (VS) and altering the energetics of voltage-dependent gating. These toxins are thought to gain access to the VS via the membrane (i.e., by partitioning from water into the membrane before binding the VS). We used serial multiscale molecular-dynamics (MD) simulations, via a combination of coarse-grained (CG) and atomistic (AT) simulations, to study how the toxin VSTx1, which inhibits the archeabacterial voltage-gated potassium channel KvAP, interacts with an isolated membrane-embedded VS domain. In the CG simulations, VSTx1, which was initially located in water, partitioned into the headgroup/water interface of the lipid bilayer before binding the VS. The CG configurations were used to generate AT representations of the system, which were subjected to AT-MD to further evaluate the stability of the complex and refine the predicted VS/toxin interface. VSTx1 interacted with a binding site on the VS formed by the C-terminus of S1, the S1-S2 linker, and the N-terminus of S4. The predicted VS/toxin interactions are suggestive of toxin-mediated perturbations of the interaction between the VS and the pore domain of Kv channels, and of the membrane. Our simulations support a membrane-access mechanism of inhibition of Kv channels by VS toxins. Overall, the results show that serial multiscale MD simulations may be used to model a two-stage process of protein-bilayer and protein-protein interactions within a membrane

    An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

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    For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

    Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

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    Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

    Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

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    Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN
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