325 research outputs found

    From Verlaine

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    7 new translations of Paul Verlaine

    Capability by Stacking: The Current Design Heuristic for Soft Robots

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    Soft robots are a new class of systems being developed and studied by robotics scientists. These systems have a diverse range of applications including sub-sea manipulation and rehabilitative robotics. In their current state of development, the prevalent paradigm for the control architecture in these systems is a one-to-one mapping of controller outputs to actuators. In this work, we define functional blocks as the physical implementation of some discrete behaviors, which are presented as a decomposition of the behavior of the soft robot. We also use the term ‘stacking’ as the ability to combine functional blocks to create a system that is more complex and has greater capability than the sum of its parts. By stacking functional blocks a system designer can increase the range of behaviors and the overall capability of the system. As the community continues to increase the capabilities of soft systems—by stacking more and more functional blocks—we will encounter a practical limit with the number of parallelized control lines. In this paper, we review 20 soft systems reported in the literature and we observe this trend of one-to-one mapping of control outputs to functional blocks. We also observe that stacking functional blocks results in systems that are increasingly capable of a diverse range of complex motions and behaviors, leading ultimately to systems that are capable of performing useful tasks. The design heuristic that we observe is one of increased capability by stacking simple units—a classic engineering approach. As we move towards more capability in soft robotic systems, and begin to reach practical limits in control, we predict that we will require increased amounts of autonomy in the system. The field of soft robotics is in its infancy, and as we move towards realizing the potential of this technology, we will need to develop design tools and control paradigms that allow us to handle the complexity in these stacked, non-linear systems

    Poemas irlandeses

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    Tradução de: Marcelo Tápi

    Integrated model of the vertebrate augmin complex

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    Accurate segregation of chromosomes is required to maintain genome integrity during cell division. This feat is accomplished by the microtubule-based spindle. To build a spindle rapidly and with high fidelity, cells take advantage of branching microtubule nucleation, which rapidly amplifies microtubules during cell division. Branching microtubule nucleation relies on the hetero-octameric augmin complex, but lack of structure information about augmin has hindered understanding how it promotes branching. In this work, we combine cryo-electron microscopy, protein structural prediction, and visualization of fused bulky tags via negative stain electron microscopy to identify the location and orientation of each subunit within the augmin structure. Evolutionary analysis shows that augmin\u27s structure is highly conserved across eukaryotes, and that augmin contains a previously unidentified microtubule binding site. Thus, our findings provide insight into the mechanism of branching microtubule nucleation

    Genetic Overlap Between Alzheimer’s Disease and Bipolar Disorder Implicates the MARK2 and VAC14 Genes

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    Background: Alzheimer's disease (AD) and bipolar disorder (BIP) are complex traits influenced by numerous common genetic variants, most of which remain to be detected. Clinical and epidemiological evidence suggest that AD and BIP are related. However, it is not established if this relation is of genetic origin. Here, we applied statistical methods based on the conditional false discovery rate (FDR) framework to detect genetic overlap between AD and BIP and utilized this overlap to increase the power to identify common genetic variants associated with either or both traits. Methods: We obtained genome wide association studies data from the International Genomics of Alzheimer's Project part 1 (17,008 AD cases and 37,154 controls) and the Psychiatric Genetic Consortium Bipolar Disorder Working Group (20,352 BIP cases and 31,358 controls). We used conditional QQ-plots to assess overlap in common genetic variants between AD and BIP. We exploited the genetic overlap to re-rank test-statistics for AD and BIP and improve detection of genetic variants using the conditional FDR framework. Results: Conditional QQ-plots demonstrated a polygenic overlap between AD and BIP. Using conditional FDR, we identified one novel genomic locus associated with AD, and nine novel loci associated with BIP. Further, we identified two novel loci jointly associated with AD and BIP implicating the MARK2 gene (lead SNP rs10792421, conjunctional FDR=0.030, same direction of effect) and the VAC14 gene (lead SNP rs11649476, conjunctional FDR=0.022, opposite direction of effect). Conclusions: We found polygenic overlap between AD and BIP and identified novel loci for each trait and two jointly associated loci. Further studies should examine if the shared loci implicating the MARK2 and VAC14 genes could explain parts of the shared and distinct features of AD and BIP

    The genetics of the mood disorder spectrum:genome-wide association analyses of over 185,000 cases and 439,000 controls

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    Background Mood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders. Methods To clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424). Results Seventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell-types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder. Conclusions The mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum

    Bipolar multiplex families have an increased burden of common risk variants for psychiatric disorders.

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    Multiplex families with a high prevalence of a psychiatric disorder are often examined to identify rare genetic variants with large effect sizes. In the present study, we analysed whether the risk for bipolar disorder (BD) in BD multiplex families is influenced by common genetic variants. Furthermore, we investigated whether this risk is conferred mainly by BD-specific risk variants or by variants also associated with the susceptibility to schizophrenia or major depression. In total, 395 individuals from 33 Andalusian BD multiplex families (166 BD, 78 major depressive disorder, 151 unaffected) as well as 438 subjects from an independent, BD case/control cohort (161 unrelated BD, 277 unrelated controls) were analysed. Polygenic risk scores (PRS) for BD, schizophrenia (SCZ), and major depression were calculated and compared between the cohorts. Both the familial BD cases and unaffected family members had higher PRS for all three psychiatric disorders than the independent controls, with BD and SCZ being significant after correction for multiple testing, suggesting a high baseline risk for several psychiatric disorders in the families. Moreover, familial BD cases showed significantly higher BD PRS than unaffected family members and unrelated BD cases. A plausible hypothesis is that, in multiplex families with a general increase in risk for psychiatric disease, BD development is attributable to a high burden of common variants that confer a specific risk for BD. The present analyses demonstrated that common genetic risk variants for psychiatric disorders are likely to contribute to the high incidence of affective psychiatric disorders in the multiplex families. However, the PRS explained only part of the observed phenotypic variance, and rare variants might have also contributed to disease development

    Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes

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    publisher: Elsevier articletitle: Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes journaltitle: Cell articlelink: https://doi.org/10.1016/j.cell.2018.05.046 content_type: article copyright: © 2018 Elsevier Inc

    Orpheus Ascending The Berlin Wall Café by Paul Durcan

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    "Orpheus Ascending The Berlin Wall Café by Paul Durcan", by Derek Mahon. The Irish Review, 1986 Published with the kind permission of Gallery Press. "Orpheus Ascending The Berlin Wall Café by Paul Durcan", by Derek Mahon. The Irish Review, 1986. Publicado com a permissão de Gallery Press.&nbsp

    MacNeice, the war and the BBC

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    One evening in the autumn of 1940, as MacNeice recounts in his unfinished autobiography, The Strings Are False, he went into the country for dinner beside the Hudson River outside New York: "The ice in my whiskey tinkled like a sheep-bell", he remembers, "and the boats on the night river were like sheep on an endless moor, and the lights of Tarrytown and the noises of trains called me to the further bank — ripae ulterioris amore — but it was more than the bank of the Hudson or even the easter..
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