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Institution

Monash University

EducationMelbourne, Victoria, Australia
About: Monash University is a education organization based out in Melbourne, Victoria, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 35920 authors who have published 100681 publications receiving 3027002 citations.


Papers
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Journal ArticleDOI
TL;DR: When the observed data for the Vanuatu avifauna and the Antillean bat communities are compared, it is found that these communities have significantly large checkerboard distributions, making implausible the hypothesis that their species distributions are a product of random colonisation.
Abstract: There has been an ongoing controversy over how to decide whether the distribution of species is “random” — i.e., whether it is not greatly different from what it would be if species did not interact. We recently showed (Roberts and Stone (1990)) that in the case of the Vanuatu (formerly New Hebrides) avifauna, the number of islands shared by species pairs was incompatible with a “random” null hypothesis. However, it was difficult to determine the causes or direction of the community's exceptionality. In this paper, the latter problem is examined further. We use Diamond's (1975) notion of checkerboard distributions (originally developed as an indicator of competition) and construct a C-score statistic which quantifies “checkerboardedness”. This statistic is based on the way two species might colonise a pair of islands; whenever each species colonises a different island this adds 1 to the C-score. Following Connor and Simberloff (1979) we generate a “control group” of random colonisation patterns (matrices), and use the C-score to determine their checkerboard characteristics. As an alternative mode of enquiry, we make slight alterations to the observed data, repeating this process many times so as to obtain another “control group”. In both cases, when we compare the observed data for the Vanuatu avifauna and the Antillean bat communities with that given by their respective “control group”, we find that these communities have significantly large checkerboard distributions, making implausible the hypothesis that their species distributions are a product of random colonisation.

948 citations

Journal ArticleDOI
Jian Feng Nie1
TL;DR: In this article, the Orowan equation for magnesium alloys strengthened by rationally-oriented, shear-resistant precipitate plates/rods was developed and compared with identical volume fractions and number densities of precipitates per unit volume.

947 citations

Posted Content
TL;DR: In this paper, the authors present a framework analysis for applied policy research that is adapted to research that has specific questions, a limited time frame, a pre-designed sample and a priori issues.
Abstract: Policies and procedures govern organizations whether they are private or public, for-profit or not-for profit. Review of such policies and procedures are done periodically to ensure optimum efficiency within the organization. Framework analysis is a qualitative method that is aptly suited for applied policy research. Framework analysis is better adapted to research that has specific questions, a limited time frame, a pre-designed sample and a priori issues. In the analysis, data is sifted, charted and sorted in accordance with key issues and themes using five steps: familiarization; identifying a thematic framework; indexing; charting; and mapping and interpretation. Framework analysis provides an excellent tool to assess policies and procedures from the very people that they affect.

945 citations

Journal ArticleDOI
TL;DR: It is time to ease the strain on healthcare systems through clear policy initiatives that prioritize heart failure prevention and champion equity of care for all.
Abstract: Heart failure is a life-threatening disease and addressing it should be considered a global health priority. At present, approximately 26 million people worldwide are living with heart failure. The outlook for such patients is poor, with survival rates worse than those for bowel, breast or prostate cancer. Furthermore, heart failure places great stresses on patients, caregivers and healthcare systems. Demands on healthcare services, in particular, are predicted to increase dramatically over the next decade as patient numbers rise owing to ageing populations, detrimental lifestyle changes and improved survival of those who go on to develop heart failure as the final stage of another disease. It is time to ease the strain on healthcare systems through clear policy initiatives that prioritize heart failure prevention and champion equity of care for all. Despite the burdens that heart failure imposes on society, awareness of the disease is poor. As a result, many premature deaths occur. This is in spite of the fact that most types of heart failure are preventable and that a healthy lifestyle can reduce risk. Even after heart failure has developed, premature deaths could be prevented if people were taught to recognize the symptoms and seek immediate medical attention. Public awareness campaigns focusing on these messages have great potential to improve outcomes for patients with heart failure and ultimately to save lives. Compliance with clinical practice guidelines is also associated with improved outcomes for patients with heart failure. However, in many countries, there is considerable variation in how closely physicians follow guideline recommendations. To promote equity of care, improvements should be encouraged through the use of hospital performance measures and incentives appropriate to the locality. To this end, policies should promote the research required to establish an evidence base for performance measures that reflect improved outcomes for patients. Continuing research is essential if we are to address unmet needs in caring for patients with heart failure. New therapies are required for patients with types of heart failure for which current treatments relieve symptoms but do not address the disease. More affordable therapies are desperately needed in the economically developing world. International collaborative research focusing on the causes and treatment of heart failure worldwide has the potential to benefit tens of millions of people. Change at the policy level has the power to drive improvements in prevention and care that will save lives. It is time to make a difference across the globe by confronting the problem of heart failure. A call to action: policy recommendations We urge policymakers at local, national and international levels to collaborate and act on the following recommendations. Promote heart failure prevention Support the development and implementation of public awareness programmes about heart failure. These should define heart failure in simple and accessible language, explain how to recognize the symptoms and emphasize that most types of heart failure are preventable. Highlight the need for healthcare professionals across all clinical disciplines to identify patients with illnesses that increase the risk of heart failure and to prescribe preventive medications. Prioritize the elimination of infectious diseases in parts of the world where they still cause heart failure. Improve heart failure awareness amongst healthcare professionals Encourage the development and use of heart failure education programmes for all appropriate healthcare professionals. These should aim to improve the prevention, diagnosis, treatment and long-term management of heart failure and raise awareness of clinical practice guidelines. Ensure equity of care for all patients with heart failure Provide a healthcare system that delivers timely access to diagnostic services and treatment of heart failure, as well as a seamless transition to long-term management. Ensure that the best available and most appropriate care is consistently provided to all patients with heart failure through efficient use of resources. Support and empower patients and their caregivers Provide resources for the education and practical support of patients with heart failure and their families or other caregivers, empowering them to engage proactively in long-term care. Promote heart failure research Fund and encourage international collaborative research to improve understanding of the patterns, causes and effects of modern day heart failure and how the disease can be prevented across the globe. Fund and encourage research into new and more affordable therapies and medical devices for all types of heart failure. Fund and encourage research into evidence-based healthcare performance measures that reflect improved clinical outcomes for patients with heart failure.

944 citations

Journal ArticleDOI
04 Mar 2021-Nature
TL;DR: The GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2244 critically ill Covid-19 patients from 208 UK intensive care units is reported, finding evidence in support of a causal link from low expression of IFNAR2, and high expression of TYK2, to life-threatening disease.
Abstract: Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10−8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10−8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10−12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10−8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte–macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice. A genome-wide association study of critically ill patients with COVID-19 identifies genetic signals that relate to important host antiviral defence mechanisms and mediators of inflammatory organ damage that may be targeted by repurposing drug treatments.

941 citations


Authors

Showing all 36568 results

NameH-indexPapersCitations
Bert Vogelstein247757332094
Kenneth W. Kinzler215640243944
David J. Hunter2131836207050
David R. Williams1782034138789
Yang Yang1712644153049
Lei Jiang1702244135205
Dongyuan Zhao160872106451
Christopher J. O'Donnell159869126278
Leif Groop158919136056
Mark E. Cooper1581463124887
Theo Vos156502186409
Mark J. Smyth15371388783
Rinaldo Bellomo1471714120052
Detlef Weigel14251684670
Geoffrey Burnstock141148899525
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023250
20221,020
20219,402
20208,420
20197,409
20186,438