Institution
University of Adelaide
Education•Adelaide, South Australia, Australia•
About: University of Adelaide is a education organization based out in Adelaide, South Australia, Australia. It is known for research contribution in the topics: Population & Pregnancy. The organization has 27251 authors who have published 79167 publications receiving 2671128 citations. The organization is also known as: The University of Adelaide & Adelaide University.
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TL;DR: In this paper, anisotropy was measured by the fraction of arrival directions that are less than 3.1 degrees from the position of an active galactic nucleus within 75 Mpc (using the Veron-Cetty and Veron 12th catalog).
404 citations
University of Washington1, Creighton University2, Central South University3, Huazhong University of Science and Technology4, Radboud University Nijmegen5, Karolinska Institutet6, Katholieke Universiteit Leuven7, Leiden University Medical Center8, University of Adelaide9, South Australia Pathology10, Boston Children's Hospital11, University of South Australia12, University of Antwerp13, University of California, San Diego14, University of California, Davis15, University of Melbourne16, Florey Institute of Neuroscience and Mental Health17, Howard Hughes Medical Institute18
TL;DR: Twenty-five genes showing a bias for autism versus intellectual disability and a network associated with high-functioning autism are highlighted, and clinical follow-up for NAA15, KMT5B, and ASH1L highlighted new syndromic and nonsyndromic forms of disease.
Abstract: Gene-disruptive mutations contribute to the biology of neurodevelopmental disorders (NDDs), but most of the related pathogenic genes are not known. We sequenced 208 candidate genes from >11,730 cases and >2,867 controls. We identified 91 genes, including 38 new NDD genes, with an excess of de novo mutations or private disruptive mutations in 5.7% of cases. Drosophila functional assays revealed a subset with increased involvement in NDDs. We identified 25 genes showing a bias for autism versus intellectual disability and highlighted a network associated with high-functioning autism (full-scale IQ >100). Clinical follow-up for NAA15, KMT5B, and ASH1L highlighted new syndromic and nonsyndromic forms of disease.
404 citations
TL;DR: The degree of inequality in the levels of well-being of its citizens tells us a great deal about a society and enables us to judge its social and economic system, identify those citizens with a claim on community compassion, to identify the sources of hardship, and to devise strategies for reducing levels of hardship.
Abstract: The degree of inequality in the levels of well-being of its citizens tells us a great deal about a society It enables us to judge its social and economic system, to identify those citizens with a claim on community compassion, to identify the sources of hardship, and to devise strategies for reducing levels of hardship The value of such information is undoubted But we confront a severe practical problem in first defining, and then measuring, what we mean by well-being It is surely multi-dimensional, and difficult to reduce to a scalar-valued index
403 citations
TL;DR: The failure to resolve epithelial damage in chronic obstructive pulmonary disease may result, at least partially, from specific defects in phagocytic ability of alveolar macrophages to ingest apoptotic airway epithelial cells.
Abstract: Chronic obstructive pulmonary disease is a highly prevalent, complex disease, usually caused by cigarette smoke. It causes serious morbidity and mortality and costs the global community billions of dollars per year. While chronic inflammation, extracellular matrix destruction and increased airway epithelial cell apoptosis are reported in chronic obstructive pulmonary disease, the understanding of the basic pathogenesis of the disease is limited and there are no effective treatments. We hypothesized that the accumulation of apoptotic airway epithelial cells chronic obstructive pulmonary disease in could be due to defective phagocytic clearance by alveolar macrophages. There have been no previous studies of the phagocytic capacity of alveolar macrophages in chronic obstructive pulmonary disease using physiologically relevant apoptotic airway epithelial cells as phagocytic targets. We developed a phagocytosis assay whereby cultured 16HBE airway epithelial cells were induced to apoptosis with ultraviolet radiation and stained with mitotracker green. Alveolar macrophages from bronchoalveolar lavage from eight control and six chronic obstructive pulmonary disease subjects were analysed following 1.5 h incubation with apoptotic airway epithelial cells, then staining with macrophage marker anti CD33. CD33+/mitotracker green + events (i.e., alveolar macrophages which had phagocytosed apoptotic airway epithelial cells) were analysed using flow cytometry. Phagocytosis of polystyrene microbeads was investigated in parallel. A significantly reduced proportion of alveolar macrophages from chronic obstructive pulmonary disease subjects ingested apoptotic airway epithelial cells compared with controls (11.6 +/- 4.1% for chronic obstructive pulmonary disease versus 25.6 +/- 9.2% for control group). Importantly, the deficiency was not observed using polystyrene beads, suggesting that the failure to resolve epithelial damage in chronic obstructive pulmonary disease may result, at least partially, from specific defects in phagocytic ability of alveolar macrophages to ingest apoptotic airway epithelial cells.
402 citations
McMaster University1, University of Pennsylvania2, University of Adelaide3, University of Copenhagen4, Population Health Research Institute5, University of Miyazaki6, University of Queensland7, University of Birmingham8, University of Toronto9, University of Calgary10, University of British Columbia11, University of Brescia12, University of Western Ontario13, Charles University in Prague14, Kyoto University15, Kyoto Prefectural University of Medicine16, Imperial College London17, University of Cambridge18
TL;DR: Among patients with severe ANCA-associated vasculitis, the use of plasma exchange did not reduce the incidence of death or ESKD, and a reduced-dose regimen of glucocorticoids was noninferior to a standard- dose regimen with respect to death orESKD.
Abstract: Background More effective and safer treatments are needed for antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis. Methods We conducted a randomized trial with a 2-by-2 factor...
402 citations
Authors
Showing all 27579 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Martin White | 196 | 2038 | 232387 |
| Nicholas G. Martin | 192 | 1770 | 161952 |
| David W. Johnson | 160 | 2714 | 140778 |
| Nicholas J. Talley | 158 | 1571 | 90197 |
| Mark E. Cooper | 158 | 1463 | 124887 |
| Xiang Zhang | 154 | 1733 | 117576 |
| John E. Morley | 154 | 1377 | 97021 |
| Howard I. Scher | 151 | 944 | 101737 |
| Christopher M. Dobson | 150 | 1008 | 105475 |
| A. Artamonov | 150 | 1858 | 119791 |
| Timothy P. Hughes | 145 | 831 | 91357 |
| Christopher Hill | 144 | 1562 | 128098 |
| Shi-Zhang Qiao | 142 | 523 | 80888 |
| Paul Jackson | 141 | 1372 | 93464 |
| H. A. Neal | 141 | 1903 | 115480 |