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Sydney, Australia

Lal S.,University of Sydney | Li A.,University of Sydney | Allen D.,University of Sydney | Allen P.D.,University of California at Davis | And 6 more authors.
Biophysical Reviews | Year: 2015

This review provides a guide to researchers who wish to establish a biobank. It also gives practical advice to investigators seeking access to samples of healthy or diseased human hearts. We begin with a brief history of the Sydney Heart Bank (SHB) from when it began in 1989, including the pivotal role played by the late Victor Chang. We discuss our standard operating procedures for tissue collection which include cryopreservation and the quality assurance needed to maintain the long-term molecular and cellular integrity of the samples. The SHB now contains about 16,000 heart samples derived from over 450 patients who underwent isotopic heart transplant procedures and from over 100 healthy organ donors. These enable us to provide samples from a wide range of categories of heart failure. So far, we have delivered heart samples to more than 50 laboratories over two decades, and we answer their most frequently asked questions. Other SHB services include the development of tissue microarrays (TMA). These enable end users to perform preliminary examinations of the expression and localisation of target molecules in diseased or aging donor hearts, all in a single section of the TMA. Finally, the processes involved in managing tissue requests from external users and logistics considerations for the shipment of human tissue are discussed in detail. © 2015, International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag Berlin Heidelberg. Source


Vallely M.P.,Cardiothoracic Surgical Unit | Vallely M.P.,Baird Institute | Vallely M.P.,University of Sydney | Edelman J.J.B.,Cardiothoracic Surgical Unit | And 2 more authors.
Interventional Cardiology (London) | Year: 2013

Recent trials have shown that coronary artery bypass grafting remains the standard-of-care for multivessel coronary artery disease. However, the main criticism of surgery in these trials has been the higher rate of stroke. Off-pump coronary artery bypass grafting (OPCAB) has been suggested as a technique to reduce the rate of stroke. However, large randomized trials comparing coronary artery bypass grafting with OPCAB have failed to show any neurological benefit, most probably because surgeons in these trials fail to avoid manipulation of the ascending aorta. Herein, the authors review a technique of OPCAB surgery where manipulation of the ascending aorta is completely avoided - 'anaortic OPCAB - facilitated by the use of composite and in situ grafts using bilateral internal mammary arteries. © 2013 Future Medicine Ltd. Source


Edelman J.J.,Baird Institute | Edelman J.J.,University of Sydney | Edelman J.J.,ANZAC Research Institute | Reddel C.J.,ANZAC Research Institute | And 10 more authors.
Journal of Thoracic and Cardiovascular Surgery | Year: 2014

Objectives The balance between hyper- and hypocoagulable states is critical after coronary artery surgery both with (coronary artery bypass grafting [CABG]) and without (off-pump coronary artery bypass [OPCAB]) cardiopulmonary bypass to prevent thrombotic or bleeding complications. We aimed to quantify novel parameters of coagulation, fibrinolysis, and overall hemostasis 6 months after CABG and OPCAB and to determine the influences on these parameters. Methods A total of 63 patients (30 CABG, 33 OPCAB) had blood collected before and at various points 6 months after surgery. Fibrin and fibrinolysis time curves were generated by measuring the absorption of 405 nm each minute for 100 minutes after the addition of tissue factor and tissue plasminogen activator to cell-free plasma. The parameters were compared with those from a group of healthy controls. Results The patients' preoperative prothrombotic assay parameters were compared with those from healthy controls. Both CABG and OPCAB patients were hypercoagulable until at least day 10 after surgery, with elevation of fibrin generation (CABG, peak day 3, +28.9%; OPCAB, peak day 1, +16.3% vs preoperative baseline) and impairment of fibrinolysis capacity (CABG, day 1, -58.4%; OPCAB, day 1, -22.6%). Surgical revascularization resulted in resolution of preoperative hypercoagulability by 6 months postoperatively. Patients with preoperative myocardial infarction (MI) had prolonged hypercoagulability after surgery that was most exaggerated after CABG (overall hemostatic potential day 5, no MI, +64.1% vs with MI, +128.9% compared with baseline; P =.013). Conclusions Patients will be vulnerable to thrombotic events for ≤6 weeks after coronary surgery yet will have resolution of hypercoagulability by 6 months. Preoperative factors, such as MI, could require individualized management of thrombosis prophylaxis in the postoperative period. Copyright © 2014 by The American Association for Thoracic Surgery. Source


Dignan R.,University of New South Wales | Keech A.C.,University of Sydney | Gebski V.J.,University of Sydney | Mann K.P.,University of Sydney | And 2 more authors.
International Journal of Cardiology | Year: 2013

Aims The Warfarin Self-Management Anticoagulation Research Trial (Warfarin SMART) was designed to determine whether patients self-managing warfarin (PSM) using the CoaguChek device and a dosing algorithm developed for the trial could keep the INR (International Normalised Ratio) test in target range at least as often as patients managed by usual care by the family doctor or hospital clinic. Methods and results 310 patients were randomly assigned to PSM or usual care. The PSM group was trained to perform home INR testing and warfarin dosing using a validated ColourChart algorithm. The primary endpoint was the proportion of times over 12 months that a monthly, blinded "outcome INR test", measured in a central laboratory, was outside the patient's target therapeutic range. The rate of out-of-range outcome INRs was lower in PSM, and non-inferior to the usual care group (PSM: 36% vs. usual care: 41%, P < 0.001 for non-inferiority; P = 0.08 for superiority in closed-loop testing). The deviations from the patient's midpoint of target INR range (P = 0.02) and number of extreme INRs (P = 0.03) were significantly less in the PSM group than the usual-care group. There was no significant difference between groups in rates of bleeding or thrombotic adverse events. Conclusion Patient self-management performed at least as well as usual care in maintaining the INR within the target range, without any safety concerns. This treatment modality for the long-term use of warfarin has the potential to change current local and international practice. © 2013 Elsevier Ireland Ltd © 2013 Published by Elsevier Ireland Ltd. Source


Padang R.,Centenary Institute | Padang R.,University of Sydney | Padang R.,Baird Institute | Bagnall R.D.,Centenary Institute | And 7 more authors.
Physiological Genomics | Year: 2015

Intrinsic valvular degeneration and dysfunction is the most common complication of bicuspid aortic valve (BAV) disease. Phenotypically, it ranges from calcific aortic stenosis to redundant or prolapsing regurgitant leaflets. The underlying molecular mechanism underpinning phenotype heterogeneity of valvular degeneration in BAV is poorly understood. We used RNA sequencing (RNA-seq) to identify genes and pathways responsible for the development of valvular degeneration in BAV, compared with tricuspid aortic valve (TAV). Comparative transcriptome analysis was performed on total RNA of aortic valve tissues of patients with diseased BAV (n = 5) and calcified TAV (n = 3). RNA-seq findings were validated by RT-qPCR. A total of 59 and 177 genes were significantly up- and downregulated, respectively, in BAV compared with TAV. Hierarchical clustering indicated heterogeneity within the BAV group, separating those with heavy calcification (BAVc) from those with redundant leaflets and/or minimal calcification (BAVr). Interestingly, the gene expression profile of the BAVc group closely resembled the TAV, with shared up- and downregulation of inflammatory andNOTCH1signaling pathways, respectively. Downregulation of matrix protease ADAMTS9 and protein aggrecan were observed in BAVr compared with TAV. Dysregulation of fetal gene programs were also present, with notable downregulation ofSEMA6BandSEMA3Fin BAVr and BAVc compared with TAV, respectively. Upregulation ofTBX20was observed exclusively in BAVr compared with BAVc. In conclusion, diverging molecular mechanisms underpin phenotype heterogeneity of valvular degeneration in BAV and data from the present study suggest that there may be shared mechanisms leading to calcification in BAV and TAV. Recognition of these pathways is fundamental to improve our understanding of the molecular basis of human BAV disease. © 2015 the American Physiological Society Source

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