Institution
Victor Chang Cardiac Research Institute
Nonprofit•Sydney, New South Wales, Australia•
About: Victor Chang Cardiac Research Institute is a nonprofit organization based out in Sydney, New South Wales, Australia. It is known for research contribution in the topics: Mechanosensitive channels & Heart failure. The organization has 708 authors who have published 1599 publications receiving 70035 citations.
Papers published on a yearly basis
Papers
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San Francisco VA Medical Center1, University of California, San Francisco2, Duke University3, British Heart Foundation4, Brigham and Women's Hospital5, University of North Carolina at Chapel Hill6, Robertson Centre for Biostatistics7, National Institutes of Health8, University of Alberta9, Sofia Medical University10, Victor Chang Cardiac Research Institute11, University of Brescia12, Goethe University Frankfurt13, Vilnius University14, Masaryk University15, St John of God Health Care16, University of Groningen17, Amgen18
TL;DR: Omecamtiv mecarbil dosing guided by pharmacokinetics achieved plasma concentrations associated with improved cardiac function and decreased ventricular diameter, and the frequency of adverse clinical events did not differ between groups.
216 citations
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TL;DR: It is demonstrated that Dll3(neo) and Dll 3(pu) are functionally equivalent alleles with respect to the skeletal dysplasia, and it is suggested that the three human DLL3 mutations associated with spondylocostal Dysplasia are also functionally equivalent to the Dll2(neO) null allele.
Abstract: A loss-of-function mutation in the mouse delta-like3 (Dll3) gene has been generated following gene targeting, and results in severe axial skeletal defects These defects, which consist of highly disorganised vertebrae and costal defects, are similar to those associated with the Dll3-dependent pudgy mutant in mouse and with spondylocostal dysplasia (MIM 277300) in humans This study demonstrates that Dll3neo and Dll3pu are functionally equivalent alleles with respect to the skeletal dysplasia, and we suggest that the three human DLL3 mutations associated with spondylocostal dysplasia are also functionally equivalent to the Dll3neo null allele Our phenotypic analysis of Dll3neo/Dll3neo mutants shows that the developmental origins of the skeletal defects lie in delayed and irregular somite formation, which results in the perturbation of anteroposterior somite polarity As the expression of Lfng, Hes1, Hes5 and Hey1 is disrupted in the presomitic mesoderm, we suggest that the somitic aberrations are founded in the disruption of the segmentation clock that intrinsically oscillates within presomitic mesoderm
214 citations
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TL;DR: Recurrence risks vary between different types of non‐syndromal CHD with multifactorial inheritance, and can be as high as 10% when two or more siblings are affected, and the recurrence risk increases if a parent rather than a sibling is affected, particularly when the affected parent is the mother.
Abstract: About 80% of congenital heart disease (CHD) is multifactorial and arises through various combinations of genetic and environmental contributors. About 20% of cases can be attributed to chromosomal anomalies, Mendelian syndromes, non-syndromal single gene disorders or teratogens. Down syndrome and velocardiofacial syndrome are the most commonly seen syndromes in patients with CHD. To date, more than 30 genes have been linked to non-syndromal forms of CHD. Their contribution to CHD remains unknown but is presumed to be relatively small. There is limited evidence for the contribution of specific environmental factors to CHD causation. However, folic acid supplementation in the pre- and peri-conception period, ensuring rubella vaccination has been completed before pregnancy, and maintaining good glycaemic control in mothers with diabetes may reduce the risk of CHD in infants. Recurrence risks vary between different types of non-syndromal CHD with multifactorial inheritance, and can be as high as 10% when two or more siblings are affected. Generally, the recurrence risk increases if a parent rather than a sibling is affected, particularly when the affected parent is the mother. Individualised recurrence risks can be generated for members of families affected by CHD after obtaining a detailed family history, including accurate cardiac diagnoses for all affected members. High-throughput genetic techniques can accelerate gene discovery and improve our ability to provide individualised genetic counselling.
210 citations
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TL;DR: It is found that glioma microvesicles are predominantly of exosomal origin and contain complex populations of coding and noncoding RNAs in proportions that are distinct from those in the cells from which they are derived.
Abstract: Interactions between glioma cells and their local environment are critical determinants of brain tumor growth, infiltration and neovascularisation. Communication with host cells and stroma via microvesicles represents one pathway by which tumors can modify their surroundings to achieve a tumor-permissive environment. Here we have taken an unbiased approach to identifying RNAs in glioma-derived microvesicles, and explored their potential to regulate gene expression in recipient cells. We find that glioma microvesicles are predominantly of exosomal origin and contain complex populations of coding and noncoding RNAs in proportions that are distinct from those in the cells from which they are derived. Microvesicles show a relative depletion in microRNA compared with their cells of origin, and are enriched in unusual or novel noncoding RNAs, most of which have no known function. Short-term exposure of brain microvascular endothelial cells to glioma microvesicles results in many gene expression changes in the endothelial cells, most of which cannot be explained by direct delivery of transcripts. Our data suggest that the scope of potential actions of tumor-derived microvesicles is much broader and more complex than previously supposed, and highlight a number of new classes of small RNA that remain to be characterized.
209 citations
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Garvan Institute of Medical Research1, University of New South Wales2, Victor Chang Cardiac Research Institute3, St. Vincent's Health System4, Illawarra Health & Medical Research Institute5, University of Sydney6, Royal Prince Alfred Hospital7, Royal North Shore Hospital8, Glasgow Royal Infirmary9, University of Glasgow10, University of California, San Diego11, University of South Australia12
TL;DR: A graded response to priming is demonstrated in stratified patient-derived tumors, indicating that fine-tuned tissue manipulation before chemotherapy may offer opportunities in both primary and metastatic targeting of pancreatic cancer.
Abstract: The emerging standard of care for patients with inoperable pancreatic cancer is a combination of cytotoxic drugs gemcitabine and Abraxane, but patient response remains moderate. Pancreatic cancer development and metastasis occur in complex settings, with reciprocal feedback from microenvironmental cues influencing both disease progression and drug response. Little is known about how sequential dual targeting of tumor tissue tension and vasculature before chemotherapy can affect tumor response. We used intravital imaging to assess how transient manipulation of the tumor tissue, or “priming,” using the pharmaceutical Rho kinase inhibitor Fasudil affects response to chemotherapy. Intravital Forster resonance energy transfer imaging of a cyclin-dependent kinase 1 biosensor to monitor the efficacy of cytotoxic drugs revealed that priming improves pancreatic cancer response to gemcitabine/Abraxane at both primary and secondary sites. Transient priming also sensitized cells to shear stress and impaired colonization efficiency and fibrotic niche remodeling within the liver, three important features of cancer spread. Last, we demonstrate a graded response to priming in stratified patient-derived tumors, indicating that fine-tuned tissue manipulation before chemotherapy may offer opportunities in both primary and metastatic targeting of pancreatic cancer.
209 citations
Authors
Showing all 728 results
Name | H-index | Papers | Citations |
---|---|---|---|
Bruce D. Walker | 155 | 779 | 86020 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Matthias W. Hentze | 110 | 319 | 41879 |
Roland Stocker | 92 | 331 | 34364 |
Richard P. Harvey | 83 | 403 | 27060 |
Michael F. O'Rourke | 81 | 451 | 35355 |
Robert Terkeltaub | 80 | 284 | 21034 |
Robert M. Graham | 69 | 319 | 16342 |
Sunil Gupta | 69 | 440 | 33856 |
Anne Keogh | 64 | 337 | 20268 |
Filip K. Knop | 61 | 437 | 13614 |
Peter S. Macdonald | 57 | 455 | 12988 |
Boris Martinac | 56 | 245 | 14121 |
Carolyn L. Geczy | 55 | 187 | 8987 |
Christopher J. Ormandy | 54 | 131 | 8757 |