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: Using H2O2 as a model stress, further work revealed that this treatment induced a protease activity in isolated mitochondria, putatively responsible for the degradation of oxidatively damaged mitochondrial proteins and that O2 consumption by mitochondria was significantly decreased by H2 O2 treatment.
Abstract: Treatment of Arabidopsis cell culture for 16 h with H2O2, menadione or antimycin A induced an oxidative stress decreasing growth rate and increasing DCF fluorescence and lipid peroxidation products. Treated cells remained viable and maintained significant respiratory rates. Mitochondrial integrity was maintained, but accumulation of alternative oxidase and decreased abundance of lipoic acid-containing components during several of the treatments indicated oxidative stress. Analysis of the treatments was undertaken by IEF/SDS-PAGE, comparison of protein spot abundances and tandem mass spectrometry. A set of 25 protein spots increased >3-fold in H2O2/menadione treatments, a subset of these increased in antimycin A-treated samples. A set of 10 protein spots decreased significantly during stress treatments. A specific set of mitochondrial proteins were degraded by stress treatments. These damaged components included subunits of ATP synthase, complex I, succinyl CoA ligase, aconitase, and pyruvate and 2-oxoglutarate dehydrogenase complexes. Nine increased proteins represented products of different genes not found in control mitochondria. One is directly involved in antioxidant defense, a mitochondrial thioredoxin-dependent peroxidase, while another, a thioredoxin reductase-dependent protein disulphide isomerase, is required for protein disulfide redox homeostasis. Several others are generally considered to be extramitochondrial but are clearly present in a highly purified mitochondrial fraction used in this study and are known to play roles in stress response. Using H2O2 as a model stress, further work revealed that this treatment induced a protease activity in isolated mitochondria, putatively responsible for the degradation of oxidatively damaged mitochondrial proteins and that O2 consumption by mitochondria was significantly decreased by H2O2 treatment.
535 citations
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University of Leicester1, University of Nottingham2, Queen Mary University of London3, Medical Research Council4, Imperial College London5, King's College London6, Western General Hospital7, Uppsala University8, Wellcome Trust Sanger Institute9, University of Bristol10, St George's, University of London11, University of Helsinki12, University of Jyväskylä13, National Institutes of Health14, University of Zurich15, University of Split16, University of Zagreb17, University of Edinburgh18, University of Greifswald19, University of Gothenburg20, University of Western Australia21, Sir Charles Gairdner Hospital22, University College London23, University of London24, Glenfield Hospital25, University of Dundee26, National Institute for Health Research27, Southampton General Hospital28, Pasteur Institute29, University of Basel30, AstraZeneca31, University of Tampere32, University of St Andrews33, Health Protection Agency34
TL;DR: Genome-wide association with forced expiratory volume in 1 s (FEV1) and the ratio of FEV1 to forced vital capacity (FVC) in the SpiroMeta consortium offers mechanistic insight into pulmonary function regulation and indicate potential targets for interventions to alleviate respiratory disease.
Abstract: Pulmonary function measures are heritable traits that predict morbidity and mortality and define chronic obstructive pulmonary disease (COPD). We tested genome-wide association with forced expiratory volume in 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC) in the SpiroMeta consortium (n = 20,288 individuals of European ancestry). We conducted a meta-analysis of top signals with data from direct genotyping (n < or = 32,184 additional individuals) and in silico summary association data from the CHARGE Consortium (n = 21,209) and the Health 2000 survey (n < or = 883). We confirmed the reported locus at 4q31 and identified associations with FEV(1) or FEV(1)/FVC and common variants at five additional loci: 2q35 in TNS1 (P = 1.11 x 10(-12)), 4q24 in GSTCD (2.18 x 10(-23)), 5q33 in HTR4 (P = 4.29 x 10(-9)), 6p21 in AGER (P = 3.07 x 10(-15)) and 15q23 in THSD4 (P = 7.24 x 10(-15)). mRNA analyses showed expression of TNS1, GSTCD, AGER, HTR4 and THSD4 in human lung tissue. These associations offer mechanistic insight into pulmonary function regulation and indicate potential targets for interventions to alleviate respiratory disease.
535 citations
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TL;DR: It is shown that cadaver decomposition can have a greater, albeit localised, effect on belowground ecology than plant and faecal resources.
Abstract: A dead mammal (i.e. cadaver) is a high quality resource (narrow carbon:nitrogen ratio, high water content) that releases an intense, localised pulse of carbon and nutrients into the soil upon decomposition. Despite the fact that as much as 5,000 kg of cadaver can be introduced to a square kilometre of terrestrial ecosystem each year, cadaver decomposition remains a neglected microsere. Here we review the processes associated with the introduction of cadaver-derived carbon and nutrients into soil from forensic and ecological settings to show that cadaver decomposition can have a greater, albeit localised, effect on belowground ecology than plant and faecal resources. Cadaveric materials are rapidly introduced to belowground floral and faunal communities, which results in the formation of a highly concentrated island of fertility, or cadaver decomposition island (CDI). CDIs are associated with increased soil microbial biomass, microbial activity (C mineralisation) and nematode abundance. Each CDI is an ephemeral natural disturbance that, in addition to releasing energy and nutrients to the wider ecosystem, acts as a hub by receiving these materials in the form of dead insects, exuvia and puparia, faecal matter (from scavengers, grazers and predators) and feathers (from avian scavengers and predators). As such, CDIs contribute to landscape heterogeneity. Furthermore, CDIs are a specialised habitat for a number of flies, beetles and pioneer vegetation, which enhances biodiversity in terrestrial ecosystems.
535 citations
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Copenhagen University Hospital1, Brigham and Women's Hospital2, University of Western Australia3, Sahlgrenska University Hospital4, French Institute of Health and Medical Research5, Leiden University Medical Center6, University of Zurich7, University of Eastern Finland8, Innsbruck Medical University9, National Institutes of Health10, Harvard University11, Carlos III Health Institute12, Ghent University13
TL;DR: Non-fasting blood samples should be routinely used for the assessment of plasma lipid profiles and laboratory reports should flag abnormal values on the basis of desirable concentration cut-points to improve patient compliance with lipid testing.
Abstract: Aims To critically evaluate the clinical implications of the use of non-fasting rather than fasting lipid profiles and to provide guidance for the laboratory reporting of abnormal non-fasting or fasting lipid profiles.
Methods and results Extensive observational data, in which random non-fasting lipid profiles have been compared with those determined under fasting conditions, indicate that the maximal mean changes at 1–6 h after habitual meals are not clinically significant [+0.3 mmol/L (26 mg/dL) for triglycerides; −0.2 mmol/L (8 mg/dL) for total cholesterol; −0.2 mmol/L (8 mg/dL) for LDL cholesterol; +0.2 mmol/L (8 mg/dL) for calculated remnant cholesterol; −0.2 mmol/L (8 mg/dL) for calculated non-HDL cholesterol]; concentrations of HDL cholesterol, apolipoprotein A1, apolipoprotein B, and lipoprotein(a) are not affected by fasting/non-fasting status. In addition, non-fasting and fasting concentrations vary similarly over time and are comparable in the prediction of cardiovascular disease. To improve patient compliance with lipid testing, we therefore recommend the routine use of non-fasting lipid profiles, while fasting sampling may be considered when non-fasting triglycerides >5 mmol/L (440 mg/dL). For non-fasting samples, laboratory reports should flag abnormal concentrations as triglycerides ≥2 mmol/L (175 mg/dL), total cholesterol ≥5 mmol/L (190 mg/dL), LDL cholesterol ≥3 mmol/L (115 mg/dL), calculated remnant cholesterol ≥0.9 mmol/L (35 mg/dL), calculated non-HDL cholesterol ≥3.9 mmol/L (150 mg/dL), HDL cholesterol ≤1 mmol/L (40 mg/dL), apolipoprotein A1 ≤1.25 g/L (125 mg/dL), apolipoprotein B ≥1.0 g/L (100 mg/dL), and lipoprotein(a) ≥50 mg/dL (80th percentile); for fasting samples, abnormal concentrations correspond to triglycerides ≥1.7 mmol/L (150 mg/dL). Life-threatening concentrations require separate referral when triglycerides >10 mmol/L (880 mg/dL) for the risk of pancreatitis, LDL cholesterol >13 mmol/L (500 mg/dL) for homozygous familial hypercholesterolaemia, LDL cholesterol >5 mmol/L (190 mg/dL) for heterozygous familial hypercholesterolaemia, and lipoprotein(a) >150 mg/dL (99th percentile) for very high cardiovascular risk.
Conclusion We recommend that non-fasting blood samples be routinely used for the assessment of plasma lipid profiles. Laboratory reports should flag abnormal values on the basis of desirable concentration cut-points. Non-fasting and fasting measurements should be complementary but not mutually exclusive.
533 citations
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TL;DR: The purpose of this paper was to compare the repeatability of gait data obtained from two models, one based on ALs, and the other incorporating a functional method to define hip joint centres and a mean helical axis to define knee joint flexion/extension axes (FUN model).
533 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 |