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 'single biochemical mechanism for multiple physiological stressors' model is proposed, whereby the protective effect against abiotic stress is exerted through direct or indirect improvement in resistance to damage by reactive oxygen species.
Abstract: The sessile nature of plants has resulted in the evolution of an extraordinarily diverse suite of protective mechanisms against biotic and abiotic stresses. Though volatile isoprenoids are known to be involved in many types of biotic interactions, they also play important but relatively unappreciated roles in abiotic stress responses. We review those roles, discuss the proposed mechanistic explanations and examine the evolutionary significance of volatile isoprenoid emission. We note that abiotic stress responses generically involve production of reactive oxygen species in plant cells, and volatile isoprenoids mitigate the effects of oxidative stress by mediating the oxidative status of the plant. On the basis of these observations, we propose a 'single biochemical mechanism for multiple physiological stressors' model, whereby the protective effect against abiotic stress is exerted through direct or indirect improvement in resistance to damage by reactive oxygen species.
637 citations
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TL;DR: In this article, the authors developed a rationale for an empirical model based on Schein's conceptual model; the study reports a test of an empirically validated model, and the findings have implications for theory and practice, especially in relation to building an organizational culture within professional service firms that fosters innovative behavior.
637 citations
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QIMR Berghofer Medical Research Institute1, University of Queensland2, University of Glasgow3, Garvan Institute of Medical Research4, University of Padua5, Royal Brisbane and Women's Hospital6, Queensland University of Technology7, University of Newcastle8, Peking University9, Princess Alexandra Hospital10, St. Vincent's Health System11, Glasgow Royal Infirmary12, Human Genome Sequencing Center13, Baylor College of Medicine14, Children's Hospital at Westmead15, Children's Medical Research Institute16, University of Sydney17, Royal North Shore Hospital18, Royal Prince Alfred Hospital19, University of Western Sydney20, Fremantle Hospital21, Royal Adelaide Hospital22, St John of God Subiaco Hospital23, University of Western Australia24, University of Melbourne25
TL;DR: In this paper, the authors performed whole-genome sequencing of 102 primary pancreatic neuroendocrine tumours and defined the genomic events that characterize their pathogenesis, including a deficiency in G:C,>T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase.
Abstract: The diagnosis of pancreatic neuroendocrine tumours (PanNETs) is increasing owing to more sensitive detection methods, and this increase is creating challenges for clinical management. We performed whole-genome sequencing of 102 primary PanNETs and defined the genomic events that characterize their pathogenesis. Here we describe the mutational signatures they harbour, including a deficiency in G:C > T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase. Clinically sporadic PanNETs contain a larger-than-expected proportion of germline mutations, including previously unreported mutations in the DNA repair genes MUTYH, CHEK2 and BRCA2. Together with mutations in MEN1 and VHL, these mutations occur in 17% of patients. Somatic mutations, including point mutations and gene fusions, were commonly found in genes involved in four main pathways: chromatin remodelling, DNA damage repair, activation of mTOR signalling (including previously undescribed EWSR1 gene fusions), and telomere maintenance. In addition, our gene expression analyses identified a subgroup of tumours associated with hypoxia and HIF signalling.
637 citations
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TL;DR: Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host.
Abstract: Streptococcus pyogenes, also known as group A Streptococcus (GAS), causes mild human infections such as pharyngitis and impetigo and serious infections such as necrotizing fasciitis and streptococcal toxic shock syndrome. Furthermore, repeated GAS infections may trigger autoimmune diseases, including acute poststreptococcal glomerulonephritis, acute rheumatic fever, and rheumatic heart disease. Combined, these diseases account for over half a million deaths per year globally. Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host. This improved understanding of the contribution of individual virulence determinants to the disease process has led to the formulation of models of GAS disease progression, which may lead to better treatment and intervention strategies. While GAS remains sensitive to all penicillins and cephalosporins, rising resistance to other antibiotics used in disease treatment is an increasing worldwide concern. Several GAS vaccine formulations that elicit protective immunity in animal models have shown promise in nonhuman primate and early-stage human trials. The development of a safe and efficacious commercial human vaccine for the prophylaxis of GAS disease remains a high priority.
634 citations
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TL;DR: The results indicate that the mechanism of preparatory spinal control is altered in people with lower back pain for movement at a variety of speeds.
634 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 |