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Institution

Flinders University

EducationAdelaide, South Australia, Australia
About: Flinders University is a education organization based out in Adelaide, South Australia, Australia. It is known for research contribution in the topics: Population & Health care. The organization has 12033 authors who have published 32831 publications receiving 973172 citations. The organization is also known as: Flinders University of South Australia.


Papers
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Journal ArticleDOI
TL;DR: This review is aimed at comprehensively collating the current available published evidence and clinical correlates of magnesium disorders and its role as a cofactor for more than 300 enzymatic reactions.
Abstract: Magnesium is the fourth most abundant cation in the body. It has several functions in the human body including its role as a cofactor for more than 300 enzymatic reactions. Several studies have shown that hypomagnesemia is a common electrolyte derangement in clinical setting especially in patients admitted to intensive care unit where it has been found to be associated with increase mortality and hospital stay. Hypomagnesemia can be caused by a wide range of inherited and acquired diseases. It can also be a side effect of several medications. Many studies have reported that reduced levels of magnesium are associated with a wide range of chronic diseases. Magnesium can play important therapeutic and preventive role in several conditions such as diabetes, osteoporosis, bronchial asthma, preeclampsia, migraine, and cardiovascular diseases. This review is aimed at comprehensively collating the current available published evidence and clinical correlates of magnesium disorders.

206 citations

Journal ArticleDOI
TL;DR: Recent progress and problems with respect to Abeta clearance mechanisms are discussed and strategies for the development of therapeutics targeting Abeta Clearance are proposed.

205 citations

Journal ArticleDOI
TL;DR: Statin therapy before PCI is associated with a marked reduction in mortality among patients with high hsCRP levels and an improved targeting of statin therapy and clinical outcome among patients undergoing PCI is recommended.
Abstract: Background— Beyond lipid lowering, statins are known to possess antiinflammatory and antithrombotic properties. Recent studies suggested an association between statins and early reduction in death or myocardial infarction (MI) after percutaneous coronary interventions (PCIs). We sought to examine the interrelationship between inflammation, statin use, and PCI outcomes. Methods and Results— In the year 2000, 1552 consecutive United States residents underwent elective or urgent PCI at the Cleveland Clinic and were prospectively followed for 1 year. Preprocedural serum high-sensitivity C-reactive protein (hsCRP) levels were routinely measured. Patients who had statins initiated before the procedure (39.6%) had a lower median hsCRP level (0.40 versus 0.50 mg/dL, P=0.012) independent of the baseline cholesterol levels and had less frequent periprocedural MI (defined by CKMB ≥3×upper limit of normal, 5.7% versus 8.1%, P=0.038). At 1 year, statin pretreatment was predictive of survival predominantly among patien...

205 citations

Journal ArticleDOI
TL;DR: It is demonstrated that there is insufficient evidence to definitively state that RAS WT/BRAF MT individuals attain a different treatment benefit from anti-EGFR mAbs for mCRC compared with RASWT/B RAF WT individuals, and there are insufficient data to justify the exclusion of anti- EGFR mAb therapy for patients with MCRC.
Abstract: Metastatic colorectal cancer (mCRC) that harbours a BRAF V600E mutation (BRAF MT) is associated with poorer outcomes. However, whether this mutation is predictive of treatment benefit from anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) is uncertain. We conducted a systematic review and meta-analysis of randomised controlled trials (RCTs) published up to July 2014 that evaluated the effect of BRAF MT on the treatment benefit from anti-EGFR mAbs for mCRC. Seven RCTs met the inclusion criteria for assessment of overall survival (OS), whereas eight RCTs met the inclusion criteria for assessment of progression-free survival (PFS). For RAS WT/BRAF MT tumours, the hazard ratio for OS benefit with anti-EGFR mAbs was 0.97 (95% CI; 0.67–1.41), whereas the hazard ratio was 0.81 (95% CI; 0.70–0.95) for RAS WT/BRAF WT tumours. However, the test of interaction (P=0.43) was not statistically significant, highlighting that the observed differences in the effect of anti-EGFR mAbs on OS according to the BRAF mutation status may be due to chance alone. Regarding PFS benefit with anti-EGFR mAbs, the hazard ratio was 0.86 (95% CI; 0.61–1.21) for RAS WT/BRAF MT tumours as compared with 0.62 (95% CI; 0.50–0.77) for RAS WT/BRAF WT tumours (test of interaction, P=0.07). This meta-analysis demonstrates that there is insufficient evidence to definitively state that RAS WT/BRAF MT individuals attain a different treatment benefit from anti-EGFR mAbs for mCRC compared with RAS WT/BRAF WT individuals. As such, there are insufficient data to justify the exclusion of anti-EGFR mAb therapy for patients with RAS WT/BRAF MT mCRC.

205 citations

Journal ArticleDOI
Jessica N. Cooke Bailey1, Stephanie Loomis2, Jae H. Kang2, R. Rand Allingham3, Puya Gharahkhani4, Chiea Chuen Khor5, Chiea Chuen Khor6, Kathryn P. Burdon7, Kathryn P. Burdon8, Hugues Aschard2, Daniel I. Chasman2, Robert P. Igo1, Pirro G. Hysi9, Craig A. Glastonbury9, Allison E. Ashley-Koch3, Murray H. Brilliant10, Andrew A. Brown11, Donald L. Budenz12, Alfonso Buil11, Ching-Yu Cheng13, Ching-Yu Cheng5, Hyon K. Choi14, William G. Christen2, Gary C. Curhan2, Immaculata De Vivo2, John H. Fingert15, Paul J. Foster16, Paul J. Foster17, Charles S. Fuchs2, Douglas E. Gaasterland, Terry Gaasterland18, Alex W. Hewitt19, Frank B. Hu2, David J. Hunter2, Anthony P Khawaja20, Richard K. Lee21, Zheng Li6, Paul R. Lichter22, David A. Mackey23, David A. Mackey24, Peter McGuffin9, Paul Mitchell25, Sayoko E. Moroi22, Shamira A. Perera5, Shamira A. Perera13, Keating W. Pepper, Qibin Qi26, Tony Realini27, Julia E. Richards22, Paul M. Ridker2, Eric B. Rimm2, Robert Ritch28, Marylyn D. Ritchie29, Joel S. Schuman30, William K. Scott21, Kuldev Singh31, Arthur J. Sit32, Yeunjoo E. Song1, Rulla M. Tamimi2, Fotis Topouzis33, Ananth C. Viswanathan16, Shefali S. Verma29, Douglas Vollrath31, Jie Jin Wang25, Nicole Weisschuh34, Bernd Wissinger34, Gadi Wollstein30, Tien Yin Wong5, Tien Yin Wong13, Brian L. Yaspan35, Donald J. Zack36, Kang Zhang18, Robert N. Weinreb18, Margaret A. Pericak-Vance21, Kerrin S. Small9, Christopher J Hammond9, Tin Aung5, Tin Aung13, Yutao Liu37, Eranga N. Vithana5, Eranga N. Vithana13, Stuart MacGregor4, Jamie E Craig8, Peter Kraft2, Gareth R. Howell, Michael A. Hauser3, Louis R. Pasquale2, Jonathan L. Haines1, Janey L. Wiggs2 
TL;DR: New pathways underlying POAG susceptibility are identified and new targets for preventative therapies are suggested, including TXNRD2 and ATXN2 expression in retinal ganglion cells and the optic nerve head.
Abstract: Primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide. To identify new susceptibility loci, we performed meta-analysis on genome-wide association study (GWAS) results from eight independent studies from the United States (3,853 cases and 33,480 controls) and investigated the most significantly associated SNPs in two Australian studies (1,252 cases and 2,592 controls), three European studies (875 cases and 4,107 controls) and a Singaporean Chinese study (1,037 cases and 2,543 controls). A meta-analysis of the top SNPs identified three new associated loci: rs35934224[T] in TXNRD2 (odds ratio (OR) = 0.78, P = 4.05 × 10(-11)) encoding a mitochondrial protein required for redox homeostasis; rs7137828[T] in ATXN2 (OR = 1.17, P = 8.73 × 10(-10)); and rs2745572[A] upstream of FOXC1 (OR = 1.17, P = 1.76 × 10(-10)). Using RT-PCR and immunohistochemistry, we show TXNRD2 and ATXN2 expression in retinal ganglion cells and the optic nerve head. These results identify new pathways underlying POAG susceptibility and suggest new targets for preventative therapies.

205 citations


Authors

Showing all 12221 results

NameH-indexPapersCitations
Matthew Jones125116196909
Robert Edwards12177574552
Justin C. McArthur11343347346
Peter Somogyi11223242450
Glenda M. Halliday11167653684
Jonathan C. Craig10887259401
Bruce Neal10856187213
Alan Cooper10874645772
Robert J. Norman10375545147
John B. Furness10359737668
Richard J. Miller10341935669
Michael J. Brownstein10227447929
Craig S. Anderson10165049331
John Chalmers9983155005
Kevin D. Hyde99138246113
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202368
2022336
20212,761
20202,320
20191,943
20181,806