Institution
University of Queensland
Education•Brisbane, Queensland, Australia•
About: University of Queensland is a education organization based out in Brisbane, Queensland, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 51138 authors who have published 155721 publications receiving 5717659 citations. The organization is also known as: UQ & The University of Queensland.
Papers published on a yearly basis
Papers
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TL;DR: A critical perspective on published studies of MP ingestion by aquatic biota is provided and there are significant mismatches between the types of MP most commonly found in the environment or reported in field studies and those used in laboratory experiments.
802 citations
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TL;DR: A review of the achievements and perspectives of anaerobic co-digestion within the period 2010-2013 is presented in this paper, which represents a continuation of the previous review made by the authors.
Abstract: Anaerobic digestion is a commercial reality for several kinds of waste. Nonetheless, anaerobic digestion of single substrates presents some drawbacks linked to substrate characteristics. Anaerobic co-digestion, the simultaneous digestion of two or more substrates, is a feasible option to overcome the drawbacks of mono-digestion and to improve plants economic feasibility. At present, since 50% of the publication has been published in the last two years, anaerobic co-digestion can be considered the most relevant topic within anaerobic digestion research. The aim of this paper is to present a review of the achievements and perspectives of anaerobic co-digestion within the period 2010-2013, which represents a continuation of the previous review made by the authors [3]. In the present review, the publications have been classified as for the main substrate, i.e., animal manures, sewage sludge and biowaste. Animal manures stand as the most reported substrate, agro-industrial waste and the organic fraction of the municipal solid waste being the most reported co-substrate. Special emphasis has been made to the effect of the co-digestion over digestate quality, since land application seems to be the best option for digestate recycling. Traditionally, anaerobic co-digestion between sewage sludge and the organic fraction of the municipal solid waste has been the most reported co-digestion mixture. However, between 2010 and 2013 the publications dealing with fats, oils and greases and algae as sludge co-substrate have increased. This is because both co-substrates can be obtained at the same wastewater treatment plant. In contrast, biowaste as a main substrate has not been as studied as manures or sewage sludge. Finally, three interdisciplinary sections have been written for addressing novelty aspects in anaerobic co-digestion, i.e., pre-treatments, microbial dynamics and modeling. However, much effort needs to be done in these later aspects to better understand and predict anaerobic co-digestion.
801 citations
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TL;DR: The effects of LPS on macrophages are examined by following events from the cell surface to the nucleus and the involvement of protein tyrosine kinase, mitogen‐activated protein kinases, protein kinase C, G proteins, Protein kinase A, ceramide‐activatedprotein kinase and microtubules in this process are reviewed.
Abstract: Through its action on macrophages, bacterial lipopolysaccharide (LPS) or endotoxin can trigger responses that are protective or injurious to the host. This review examines the effects of LPS on macrophages by following events from the cell surface to the nucleus. The involvement of protein tyrosine kinases, mitogen-activated protein kinases, protein kinase C, G proteins, protein kinase A, ceramide-activated protein kinase, and microtubules in this process are reviewed. At the nuclear level, rel, C/EBP, Ets, Egr, fos, and jun family members have been implicated in activation of LPS-inducible gene expression.
800 citations
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VU University Amsterdam1, Erasmus University Rotterdam2, Karolinska Institutet3, Charité4, Virginia Commonwealth University5, South London and Maudsley NHS Foundation Trust6, QIMR Berghofer Medical Research Institute7, King's College London8, University of Southern Denmark9, University of California, Riverside10, University of Southern California11, University of Minnesota12, University of Queensland13, University College London14, Johns Hopkins University15, University of California, Los Angeles16, University of Crete17, Icahn School of Medicine at Mount Sinai18, Harvard University19, Veterans Health Administration20, Yale University21, Haukeland University Hospital22, Trinity College, Dublin23, University of Edinburgh24, North Shore-LIJ Health System25, Hofstra University26, National Institutes of Health27, Oslo University Hospital28, University of Bergen29, National University of Ireland, Galway30, University of Helsinki31, University of Oslo32, Martin Luther University of Halle-Wittenberg33, Duke University34, Mental Health Research Institute35, National and Kapodistrian University of Athens36, University of Colorado Boulder37, Imperial College London38, University of Manchester39, Wellcome Trust40, Manchester Academic Health Science Centre41, Stanford University42, University of Oregon43, University of Toronto44, University of Michigan45, Erasmus University Medical Center46, Broad Institute47, University of North Carolina at Chapel Hill48
TL;DR: A large-scale genetic association study of intelligence identifies 190 new loci and implicates 939 new genes related to neurogenesis, neuron differentiation and synaptic structure, a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
Abstract: Intelligence is highly heritable1 and a major determinant of human health and well-being2. Recent genome-wide meta-analyses have identified 24 genomic loci linked to variation in intelligence3-7, but much about its genetic underpinnings remains to be discovered. Here, we present a large-scale genetic association study of intelligence (n = 269,867), identifying 205 associated genomic loci (190 new) and 1,016 genes (939 new) via positional mapping, expression quantitative trait locus (eQTL) mapping, chromatin interaction mapping, and gene-based association analysis. We find enrichment of genetic effects in conserved and coding regions and associations with 146 nonsynonymous exonic variants. Associated genes are strongly expressed in the brain, specifically in striatal medium spiny neurons and hippocampal pyramidal neurons. Gene set analyses implicate pathways related to nervous system development and synaptic structure. We confirm previous strong genetic correlations with multiple health-related outcomes, and Mendelian randomization analysis results suggest protective effects of intelligence for Alzheimer's disease and ADHD and bidirectional causation with pleiotropic effects for schizophrenia. These results are a major step forward in understanding the neurobiology of cognitive function as well as genetically related neurological and psychiatric disorders.
800 citations
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TL;DR: It is reported that a subset of children with medulloblastoma carry germline and somatic mutations in SUFU (encoding the human suppressor of fused) of the SHH pathway, accompanied by loss of heterozygosity of the wildtype allele.
Abstract: The sonic hedgehog (SHH) signaling pathway directs the embryonic development of diverse organisms and is disrupted in a variety of malignancies. Pathway activation is triggered by binding of hedgehog proteins to the multipass Patched-1 (PTCH) receptor, which in the absence of hedgehog suppresses the activity of the seven-pass membrane protein Smoothened (SMOH). De-repression of SMOH culminates in the activation of one or more of the GLI transcription factors that regulate the transcription of downstream targets. Individuals with germline mutations of the SHH receptor gene PTCH are at high risk of developmental anomalies and of basal-cell carcinomas, medulloblastomas and other cancers (a pattern consistent with nevoid basal-cell carcinoma syndrome, NBCCS). In keeping with the role of PTCH as a tumor-suppressor gene, somatic mutations of this gene occur in sporadic basal-cell carcinomas and medulloblastomas. We report here that a subset of children with medulloblastoma carry germline and somatic mutations in SUFU (encoding the human suppressor of fused) of the SHH pathway, accompanied by loss of heterozygosity of the wildtype allele. Several of these mutations encode truncated proteins that are unable to export the GLI transcription factor from nucleus to cytoplasm, resulting in the activation of SHH signaling. SUFU is a newly identified tumor-suppressor gene that predisposes individuals to medulloblastoma by modulating the SHH signaling pathway through a newly identified mechanism.
799 citations
Authors
Showing all 52145 results
Name | H-index | Papers | Citations |
---|---|---|---|
Graham A. Colditz | 261 | 1542 | 256034 |
George Davey Smith | 224 | 2540 | 248373 |
David J. Hunter | 213 | 1836 | 207050 |
Daniel Levy | 212 | 933 | 194778 |
Christopher J L Murray | 209 | 754 | 310329 |
Matthew Meyerson | 194 | 553 | 243726 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Nicholas G. Martin | 192 | 1770 | 161952 |
Paul M. Thompson | 183 | 2271 | 146736 |
Jie Zhang | 178 | 4857 | 221720 |
Alan D. Lopez | 172 | 863 | 259291 |
Ian J. Deary | 166 | 1795 | 114161 |
Steven N. Blair | 165 | 879 | 132929 |
Carlos Bustamante | 161 | 770 | 106053 |
David W. Johnson | 160 | 2714 | 140778 |