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Institution

University of Western Australia

EducationPerth, 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.


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Journal ArticleDOI
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

Journal ArticleDOI
Emmanouela Repapi1, Ian Sayers2, Louise V. Wain1, Paul Burton1, Toby Johnson3, Ma'en Obeidat2, Jing Hua Zhao4, Adaikalavan Ramasamy5, Guangju Zhai6, Veronique Vitart7, Jennifer E. Huffman7, Wilmar Igl8, E Albrecht, Panagiotis Deloukas9, John Henderson10, Raquel Granell10, Wendy L. McArdle10, Alicja R. Rudnicka11, Inês Barroso9, Loos Rjf.4, Nicholas J. Wareham4, Linda Mustelin12, Taina Rantanen13, Ida Surakka14, Ida Surakka12, Medea Imboden15, H E Wichmann16, Ivica Grković16, Stipan Janković16, Lina Zgaga17, Hartikainen A-L.9, Hartikainen A-L.14, Hartikainen A-L.12, Leena Peltonen12, Leena Peltonen14, Leena Peltonen9, Ulf Gyllensten8, Åsa Johansson8, Ghazal Zaboli8, Harry Campbell18, Sarah H. Wild18, James F. Wilson18, Sven Gläser19, Georg Homuth19, Henry Völzke19, Massimo Mangino6, Nicole Soranzo6, Nicole Soranzo9, Tim D. Spector6, Ozren Polasek17, Igor Rudan16, Igor Rudan18, Alan F. Wright7, Markku Heliövaara14, Samuli Ripatti14, Samuli Ripatti12, Anneli Pouta14, Åsa Torinsson Naluai20, Olin A-C.20, Kjell Torén20, Mark E. Cooper21, Alan James22, Lyle J. Palmer22, Lyle J. Palmer21, Aroon D. Hingorani23, S.G. Wannamethee11, Peter H. Whincup11, George Davey Smith10, Shah Ebrahim24, Tricia M. McKeever2, Ian D. Pavord25, Andrew K. MacLeod7, Andrew D. Morris26, David J. Porteous7, Cyrus Cooper27, Cyrus Cooper28, Elaine M. Dennison28, Seif O. Shaheen14, Stefan Karrasch, E Schnabel, Holger Schulz, H Grallert, Nabila Bouatia-Naji29, Jérôme Delplanque29, Philippe Froguel5, Philippe Froguel29, John D Blakey2, John Britton2, Richard W Morris23, John W. Holloway28, Debbie A Lawlor10, Jennie Hui22, Jennie Hui30, Fredrik Nyberg20, Fredrik Nyberg31, Jarvelin M-R.32, Catherine Jackson33, Mika Kähönen32, Jaakko Kaprio14, Jaakko Kaprio12, Nicole Probst-Hensch15, Nicole Probst-Hensch30, Beate Koch19, Caroline Hayward7, David M. Evans10, Paul Elliott34, Paul Elliott5, David P. Strachan11, Ian P. Hall2, Martin D. Tobin1 
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

NameH-indexPapersCitations
Nicholas G. Martin1921770161952
Cornelia M. van Duijn1831030146009
Kay-Tee Khaw1741389138782
Steven N. Blair165879132929
David W. Bates1591239116698
Mark E. Cooper1581463124887
David Cameron1541586126067
Stephen T. Holgate14287082345
Jeremy K. Nicholson14177380275
Xin Chen1391008113088
Graeme J. Hankey137844143373
David Stuart1361665103759
Joachim Heinrich136130976887
Carlos M. Duarte132117386672
David Smith1292184100917
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023138
2022656
20215,967
20205,589
20195,452
20184,923