Institution
Flinders University
Education•Adelaide, 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 published on a yearly basis
Papers
More filters
••
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
••
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
••
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
••
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
••
Case Western Reserve University1, Harvard University2, Duke University3, QIMR Berghofer Medical Research Institute4, National University of Singapore5, Agency for Science, Technology and Research6, University of Tasmania7, Flinders University8, King's College London9, Marshfield Clinic10, University of Geneva11, University of North Carolina at Chapel Hill12, Singapore National Eye Center13, Boston University14, University of Iowa15, Moorfields Eye Hospital16, University College London17, University of California, San Diego18, University of Melbourne19, University of Cambridge20, University of Miami21, University of Michigan22, Menzies Research Institute23, University of Western Australia24, University of Sydney25, Yeshiva University26, West Virginia University27, New York Eye and Ear Infirmary28, Pennsylvania State University29, University of Pittsburgh30, Stanford University31, Mayo Clinic32, Aristotle University of Thessaloniki33, University of Tübingen34, Genentech35, Johns Hopkins University36, Georgia Regents University37
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
Name | H-index | Papers | Citations |
---|---|---|---|
Matthew Jones | 125 | 1161 | 96909 |
Robert Edwards | 121 | 775 | 74552 |
Justin C. McArthur | 113 | 433 | 47346 |
Peter Somogyi | 112 | 232 | 42450 |
Glenda M. Halliday | 111 | 676 | 53684 |
Jonathan C. Craig | 108 | 872 | 59401 |
Bruce Neal | 108 | 561 | 87213 |
Alan Cooper | 108 | 746 | 45772 |
Robert J. Norman | 103 | 755 | 45147 |
John B. Furness | 103 | 597 | 37668 |
Richard J. Miller | 103 | 419 | 35669 |
Michael J. Brownstein | 102 | 274 | 47929 |
Craig S. Anderson | 101 | 650 | 49331 |
John Chalmers | 99 | 831 | 55005 |
Kevin D. Hyde | 99 | 1382 | 46113 |