238 research outputs found
The duty cycle of radio galaxies revealed by LOFAR : remnant and restarted radio source populations in the Lockman Hole
14 pages, 7 figures, accepted for publication in MNRAS. Companion paper to Jurlin et al., also in today's arXiv postingFeedback from radio jets associated with Active Galactic Nuclei (AGN) plays a profound role in the evolution of galaxies. Kinetic power of these radio jets appears to show temporal variation, but the mechanism(s) responsible for this process are not yet clear. Recently, the LOw Frequency ARray (LOFAR) has uncovered large populations of active, remnant and restarted radio jet populations. By focusing on LOFAR data in the Lockman Hole, in this work we use the Radio AGN in Semi-Analytic Environments (RAiSE) dynamical model to present the first self-consistent modelling analysis of active, remnant and restarted radio source populations. Consistent with other recent work, our models predict that remnant radio lobes fade quickly. Any high (>10 percent) observed fraction of remnant and restarted sources therefore requires a dominant population of short-lived jets. We speculate that this could plausibly be provided by feedback-regulated accretion.Peer reviewe
Estimating Residential Solar Potential Using Aerial Data
Project Sunroof estimates the solar potential of residential buildings using
high quality aerial data. That is, it estimates the potential solar energy (and
associated financial savings) that can be captured by buildings if solar panels
were to be installed on their roofs. Unfortunately its coverage is limited by
the lack of high resolution digital surface map (DSM) data. We present a deep
learning approach that bridges this gap by enhancing widely available
low-resolution data, thereby dramatically increasing the coverage of Sunroof.
We also present some ongoing efforts to potentially improve accuracy even
further by replacing certain algorithmic components of the Sunroof processing
pipeline with deep learning
Relief Macroforms of South America
O relevo sulamericano representado no Mapa das Macroformas do Relevo da America do Sul pode ser interpretado a partir dos processos geológicos e geomorfológicos pós-gondwânicos, aos quais estão relacionadas, a abertura do Oceano Atlântico e a formação da Cadeia Orogenética dos Andes. A tectônica por meio da epirogênese meso-cenozóica, afetou o centro-leste do continente e desencadeou, em conjunto com as atividades climáticas, os processos morfogenéticos denudacionais e estabeleceram a compartimentação do relevo, a qual está aqui representada pelas macroformas também denominadas de Morfoestruturas. Essas macroformas associam-se também às megaestruturas dos Crátons, Cinturões Orogenéticos e Bacias Sedimentares herdadas do Gondwana, produzidas pelas fases erosivas pré e pós-Cretáceo. No oeste do continente com a ocorrência da orogenia e no centro-leste a epirogenia e consequentes arqueamentos e falhamentos criaram desníveis de antigas superfícies de erosão, acompanhadas de processos erosivos e deposicionais mais recentes datados do Terciário e do Quaternário. A esses processos associam-se os períodos glaciais e interglaciais, os quais no mundo tropical se manifestaram por meio dos climas secos e pouco mais frios seguidos de períodos quentes e úmidos alternando-se ao longo do Pleistoceno/Holoceno. Todas as formas interpretadas e analisadas nesta pesquisa são resultantes de processos geomorfológicos exógenos atuantes sobre os materiais que sustentam o relevo da América do Sul.The South American relief represented by this Map of Macroforms can be understood from the geological and geomorphological processes post gondwanico with wich they are related by the opening of the Atlantic Ocean and the formation of the Andean Orogenic Chain. The tectonics through the meso-cenozoic epirogenesis affected the eastern central part of the continent and started the erosion processes and established the division of the relief. Macroforms are associated with the mega-structures of the Cratons, Orogenic Belts and Sedimentary Basins inherited from Gondwana, produced by the pre- and post-Cretaceous erosive phases. In the west of the continent the orogeny and in the center-east epirogenia with archings and faults that created uneven of old surfaces of erosion, accompanied by erosive and depositional processes Tertiary and Quaternary, associated to the glacial and interglacial periods that in the tropical world were manifested through the climates dry and slightly colder followed by hot and humid that alternated along the Pleistocene / Holocene. Thus, all the forms interpreted and analyzed in this research are due to exogenous processes on the materials that sustain the relief of South America
A genetic chronology for the Indian Subcontinent points to heavily sex-biased dispersals
Background
India is a patchwork of tribal and non-tribal populations that speak many different languages from various language families. Indo-European, spoken across northern and central India, and also in Pakistan and Bangladesh, has been frequently connected to the so-called “Indo-Aryan invasions” from Central Asia ~3.5 ka and the establishment of the caste system, but the extent of immigration at this time remains extremely controversial. South India, on the other hand, is dominated by Dravidian languages. India displays a high level of endogamy due to its strict social boundaries, and high genetic drift as a result of long-term isolation which, together with a very complex history, makes the genetic study of Indian populations challenging.
Results
We have combined a detailed, high-resolution mitogenome analysis with summaries of autosomal data and Y-chromosome lineages to establish a settlement chronology for the Indian Subcontinent. Maternal lineages document the earliest settlement ~55–65 ka (thousand years ago), and major population shifts in the later Pleistocene that explain previous dating discrepancies and neutrality violation. Whilst current genome-wide analyses conflate all dispersals from Southwest and Central Asia, we were able to tease out from the mitogenome data distinct dispersal episodes dating from between the Last Glacial Maximum to the Bronze Age. Moreover, we found an extremely marked sex bias by comparing the different genetic systems.
Conclusions
Maternal lineages primarily reflect earlier, pre-Holocene processes, and paternal lineages predominantly episodes within the last 10 ka. In particular, genetic influx from Central Asia in the Bronze Age was strongly male-driven, consistent with the patriarchal, patrilocal and patrilineal social structure attributed to the inferred pastoralist early Indo-European society. This was part of a much wider process of Indo-European expansion, with an ultimate source in the Pontic-Caspian region, which carried closely related Y-chromosome lineages, a smaller fraction of autosomal genome-wide variation and an even smaller fraction of mitogenomes across a vast swathe of Eurasia between 5 and 3.5 ka
A multiplexed protein microarray for the simultaneous serodiagnosis of human immunodeficiency virus/hepatitis C virus infection and typing of whole blood
All donor blood samples must be tested pretransfusion to determine the donor blood type. Standard testing protocols require that assays be performed for important bloodborne pathogens such as hepatitis C, syphilis, hepatitis B, and human immunodeficiency virus. We have demonstrated proof of the concept that a protein microarray can type whole blood and detect antibody to significant pathogens simultaneously from the same donor blood sample. The data collected demonstrate the ability of the array to accurately type blood samples while also detecting the presence of antibodies against both human immunodeficiency virus and hepatitis C virus. In conclusion, we have successfully developed a platform capable of typing human whole blood samples, while at the same time testing for the presence of antibodies specific for human immunodeficiency virus/hepatitis C virus. The major benefits of this system are its amenability to expansion with additional assays, for example, rhesus typing and syphilis and/or hepatitis B virus detection, and also the adaptability of the assay to higher-throughput analysis, currently 16 individual samples per slide, but readily expandable to a 96-well format
Integrated genomics and proteomics define huntingtin CAG length-dependent networks in mice.
To gain insight into how mutant huntingtin (mHtt) CAG repeat length modifies Huntington's disease (HD) pathogenesis, we profiled mRNA in over 600 brain and peripheral tissue samples from HD knock-in mice with increasing CAG repeat lengths. We found repeat length-dependent transcriptional signatures to be prominent in the striatum, less so in cortex, and minimal in the liver. Coexpression network analyses revealed 13 striatal and 5 cortical modules that correlated highly with CAG length and age, and that were preserved in HD models and sometimes in patients. Top striatal modules implicated mHtt CAG length and age in graded impairment in the expression of identity genes for striatal medium spiny neurons and in dysregulation of cyclic AMP signaling, cell death and protocadherin genes. We used proteomics to confirm 790 genes and 5 striatal modules with CAG length-dependent dysregulation at the protein level, and validated 22 striatal module genes as modifiers of mHtt toxicities in vivo
Natural History of Very Early Onset Inflammatory Bowel Disease in North America: A Retrospective Cohort Study
Background: The incidence of very early onset inflammatory bowel disease (VEOIBD) is increasing, yet the phenotype and natural history of VEOIBD are not well described. Methods: We performed a retrospective cohort study of patients diagnosed with VEOIBD (6 years of age and younger) between 2008 and 2013 at 25 North American centers. Eligible patients at each center were randomly selected for chart review. We abstracted data at diagnosis and at 1, 3, and 5 years after diagnosis. We compared the clinical features and outcomes with VEOIBD diagnosed younger than 3 years of age with children diagnosed with VEOIBD at age 3 to 6 years. Results: The study population included 269 children (105 [39%] Crohn\u27s disease, 106 [39%] ulcerative colitis, and 58 [22%] IBD unclassified). The median age of diagnosis was 4.2 years (interquartile range 2.9-5.2). Most (94%) Crohn\u27s disease patients had inflammatory disease behavior (B1). Isolated colitis (L2) was the most common disease location (70% of children diagnosed younger than 3 years vs 43% of children diagnosed 3 years and older; P = 0.10). By the end of follow-up, stricturing/penetrating occurred in 7 (6.6%) children. The risk of any bowel surgery in Crohn\u27s disease was 3% by 1 year, 12% by 3 years, and 15% by 5 years and did not differ by age at diagnosis. Most ulcerative colitis patients had pancolitis (57% of children diagnosed younger than 3 years vs 45% of children diagnosed 3 years and older; P = 0.18). The risk of colectomy in ulcerative colitis/IBD unclassified was 0% by 1 year, 3% by 3 years, and 14% by 5 years and did not differ by age of diagnosis. Conclusions: Very early onset inflammatory bowel disease has a distinct phenotype with predominantly colonic involvement and infrequent stricturing/penetrating disease. The cumulative risk of bowel surgery in children with VEOIBD was approximately 14%-15% by 5 years. These data can be used to provide anticipatory guidance in this emerging patient population
Massively distributed authorship of academic papers
Wiki-like or crowdsourcing models of collaboration can provide a number of benefits to academic work. These techniques may engage expertise from different disciplines, and potentially increase productivity. This paper presents a model of massively distributed collaborative authorship of academic papers. This model, developed by a collective of thirty authors, identifies key tools and techniques that would be necessary or useful to the writing process. The process of collaboratively writing this paper was used to discover, negotiate, and document issues in massively authored scholarship. Our work provides the first extensive discussion of the experiential aspects of large-scale collaborative research.Peer ReviewedPostprint (author's final draft
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Population stratification may bias analysis of PGC-1α as a modifier of age at Huntington disease motor onset
Huntington’s disease (HD) is an inherited neurodegenerative disorder characterized by motor, cognitive and behavioral disturbances, caused by the expansion of a CAG trinucleotide repeat in the HD gene. The CAG allele size is the major determinant of age at onset (AO) of motor symptoms, although the remaining variance in AO is highly heritable. The rs7665116 SNP in PPARGC1A, encoding the mitochondrial regulator PGC-1α, has been reported to be a significant modifier of AO in three European HD cohorts, perhaps due to affected cases from Italy. We attempted to replicate these findings in a large collection of (1,727) HD patient DNA samples of European origin. In the entire cohort, rs7665116 showed a significant effect in the dominant model (p value = 0.008) and the additive model (p value = 0.009). However, when examined by origin, cases of Southern European origin had an increased rs7665116 minor allele frequency (MAF), consistent with this being an ancestry-tagging SNP. The Southern European cases, despite similar mean CAG allele size, had a significantly older mean AO (p < 0.001), suggesting population-dependent phenotype stratification. When the generalized estimating equations models were adjusted for ancestry, the effect of the rs7665116 genotype on AO decreased dramatically. Our results do not support rs7665116 as a modifier of AO of motor symptoms, as we found evidence for a dramatic effect of phenotypic (AO) and genotypic (MAF) stratification among European cohorts that was not considered in previously reported association studies. A significantly older AO in Southern Europe may reflect population differences in genetic or environmental factors that warrant further investigation
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Candidate glutamatergic and dopaminergic pathway gene variants do not influence Huntington’s disease motor onset
Huntington’s disease (HD) is a neurodegenerative disorder characterized by motor, cognitive, and behavioral disturbances. It is caused by the expansion of the HTT CAG repeat, which is the major determinant of age at onset (AO) of motor symptoms. Aberrant function of N-methyl-D-aspartate receptors and/or overexposure to dopamine has been suggested to cause significant neurotoxicity, contributing to HD pathogenesis. We used genetic association analysis in 1,628 HD patients to evaluate candidate polymorphisms in N-methyl-D-aspartate receptor subtype genes (GRIN2A rs4998386 and rs2650427, and GRIN2B rs1806201) and functional polymorphisms in genes in the dopamine pathway (DAT1 3′ UTR 40-bp variable number tandem repeat (VNTR), DRD4 exon 3 48-bp VNTR, DRD2 rs1800497, and COMT rs4608) as potential modifiers of the disease process. None of the seven polymorphisms tested was found to be associated with significant modification of motor AO, either in a dominant or additive model, after adjusting for ancestry. The results of this candidate-genetic study therefore do not provide strong evidence to support a modulatory role for these variations within glutamatergic and dopaminergic genes in the AO of HD motor manifestations
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