Institution
University of Western Australia
Education•Perth, Western Australia, Australia•
About: University of Western Australia is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 29613 authors who have published 87405 publications receiving 3064466 citations. The organization is also known as: UWA & University of WA.
Topics: Population, Poison control, Galaxy, Context (language use), Medicine
Papers published on a yearly basis
Papers
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TL;DR: Recent insights into the regulatory roles of the untranslated gene regions and non-coding RNAs in the control of complex gene expression are discussed, as well as the implications of this in terms of organism complexity and evolution.
Abstract: There is now compelling evidence that the complexity of higher organisms correlates with the relative amount of non-coding RNA rather than the number of protein-coding genes. Previously dismissed as “junk DNA”, it is the non-coding regions of the genome that are responsible for regulation, facilitating complex temporal and spatial gene expression through the combinatorial effect of numerous mechanisms and interactions working together to fine-tune gene expression. The major regions involved in regulation of a particular gene are the 5′ and 3′ untranslated regions and introns. In addition, pervasive transcription of complex genomes produces a variety of non-coding transcripts that interact with these regions and contribute to regulation. This review discusses recent insights into the regulatory roles of the untranslated gene regions and non-coding RNAs in the control of complex gene expression, as well as the implications of this in terms of organism complexity and evolution.
489 citations
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TL;DR: If endothelial dysfunction is an integral component of the pathogenesis of vascular disease, as currently believed, this study supports the value of an exercise program in the management of type 2 diabetes.
489 citations
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TL;DR: Using genetic parentage analyses, patterns of larval dispersal for two species of exploited coral reef fish within a network of marine reserves on the Great Barrier Reef are resolved and provide compelling evidence that adequately protected reserve networks can make a significant contribution to the replenishment of populations on both reserve and fished reefs at a scale that benefits local stakeholders.
488 citations
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Royal Brisbane and Women's Hospital1, University of Queensland2, Princess Alexandra Hospital3, National University of Singapore4, Nanyang Technological University5, Tan Tock Seng Hospital6, Istanbul Medipol University7, King Saud bin Abdulaziz University for Health Sciences8, Sapienza University of Rome9, University of Udine10, Monash University11, American University of Beirut12, North Shore Hospital13, University of Sydney14, Westmead Hospital15, University of Cape Town16, Illawarra Health & Medical Research Institute17, Wollongong Hospital18, University of Wollongong19, Middlemore Hospital20, King Fahad Specialist Hospital21, St. Vincent's Health System22, Fiona Stanley Hospital23, University of Western Australia24, Sunnybrook Health Sciences Centre25, Mater Health Services26, QIMR Berghofer Medical Research Institute27, Deakin University28, Monash University, Clayton campus29
TL;DR: Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in a noninferior 30-day mortality, and findings do not support use of piperACillin- tazobactsam in this setting.
Abstract: Importance Extended-spectrum β-lactamases mediate resistance to third-generation cephalosporins (eg, ceftriaxone) in Escherichia coli and Klebsiella pneumoniae. Significant infections caused by these strains are usually treated with carbapenems, potentially selecting for carbapenem resistance. Piperacillin-tazobactam may be an effective “carbapenem-sparing” option to treat extended-spectrum β-lactamase producers. Objectives To determine whether definitive therapy with piperacillin-tazobactam is noninferior to meropenem (a carbapenem) in patients with bloodstream infection caused by ceftriaxone-nonsusceptible E coli or K pneumoniae . Design, Setting, and Participants Noninferiority, parallel group, randomized clinical trial included hospitalized patients enrolled from 26 sites in 9 countries from February 2014 to July 2017. Adult patients were eligible if they had at least 1 positive blood culture with E coli or Klebsiella spp testing nonsusceptible to ceftriaxone but susceptible to piperacillin-tazobactam. Of 1646 patients screened, 391 were included in the study. Interventions Patients were randomly assigned 1:1 to intravenous piperacillin-tazobactam, 4.5 g, every 6 hours (n = 188 participants) or meropenem, 1 g, every 8 hours (n = 191 participants) for a minimum of 4 days, up to a maximum of 14 days, with the total duration determined by the treating clinician. Main Outcomes and Measures The primary outcome was all-cause mortality at 30 days after randomization. A noninferiority margin of 5% was used. Results Among 379 patients (mean age, 66.5 years; 47.8% women) who were randomized appropriately, received at least 1 dose of study drug, and were included in the primary analysis population, 378 (99.7%) completed the trial and were assessed for the primary outcome. A total of 23 of 187 patients (12.3%) randomized to piperacillin-tazobactam met the primary outcome of mortality at 30 days compared with 7 of 191 (3.7%) randomized to meropenem (risk difference, 8.6% [1-sided 97.5% CI, −∞ to 14.5%]; P = .90 for noninferiority). Effects were consistent in an analysis of the per-protocol population. Nonfatal serious adverse events occurred in 5 of 188 patients (2.7%) in the piperacillin-tazobactam group and 3 of 191 (1.6%) in the meropenem group. Conclusions and relevance Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in a noninferior 30-day mortality. These findings do not support use of piperacillin-tazobactam in this setting. Trial Registration anzctr.org.au Identifiers:ACTRN12613000532707andACTRN12615000403538and ClinicalTrials.gov Identifier:NCT02176122
487 citations
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TL;DR: It is shown here that factors secreted by macrophages stimulate RGCs to regenerate their axons, and the effects of macrophage activation can be optimized by the timing of their activation.
Abstract: After optic nerve injury in mature mammals, retinal ganglion cells (RGCs) are normally unable to regenerate their axons and undergo delayed apoptosis However, if the lens is damaged at the time of nerve injury, many RGCs survive axotomy and regenerate their axons into the distal optic nerve Lens injury induces macrophage activation, and we show here that factors secreted by macrophages stimulate RGCs to regenerate their axons When macrophages were activated by intravitreal injections of Zymosan, a yeast cell wall preparation, the number of RGC axons regenerating into the distal optic nerve was even greater than after lens injury These effects were further enhanced if Zymosan was injected 3 d after nerve crush In a grafting paradigm, intravitreal Zymosan increased the number of RGCs that regenerated their axons through a 15 cm peripheral nerve graft twofold relative to uninjected controls and threefold if injections were delayed 3 d In cell culture, media conditioned by activated macrophages stimulated adult rat RGCs to regenerate their axons; this effect was potentiated by a low molecular weight factor that is constitutively present in the vitreous humor After gel-filtration chromatography, macrophage-derived proteins > or =30 kDa were found to be toxic to RGCs, whereas proteins <30 kDa reversed this toxicity and promoted axon regeneration The protein(s) that stimulated axon growth is distinct from identified polypeptide trophic factors that were tested Thus, macrophages produce proteins with both positive and negative effects on RGCs, and the effects of macrophages can be optimized by the timing of their activation
487 citations
Authors
Showing all 29972 results
Name | H-index | Papers | Citations |
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Nicholas G. Martin | 192 | 1770 | 161952 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Steven N. Blair | 165 | 879 | 132929 |
David W. Bates | 159 | 1239 | 116698 |
Mark E. Cooper | 158 | 1463 | 124887 |
David Cameron | 154 | 1586 | 126067 |
Stephen T. Holgate | 142 | 870 | 82345 |
Jeremy K. Nicholson | 141 | 773 | 80275 |
Xin Chen | 139 | 1008 | 113088 |
Graeme J. Hankey | 137 | 844 | 143373 |
David Stuart | 136 | 1665 | 103759 |
Joachim Heinrich | 136 | 1309 | 76887 |
Carlos M. Duarte | 132 | 1173 | 86672 |
David Smith | 129 | 2184 | 100917 |