The VCCRI is proud to acknowledge the past graduates from the Institute and recognises their hard work and achievements.
|
|
Dr Christopher Semsarian A/Prof Christopher Semsarian graduated in medicine from the University of Sydney in 1990. After completing his medical and cardiology training at Royal Prince Alfred Hospital in Sydney, Dr Semsarian undertook his PhD with Professor Bob Graham at the Victor Chang Cardiac Research Institute. Following the completion of his PhD in 1999, Chris continued his research as a Research Associate in the Department of Genetics, Harvard Medical School, Boston, before returning to Australia in January 2002. His research interest over the last 10 years has focused on the molecular and genetic basis of heart disease and specifically, in understanding pathogenesis of inherited heart muscle disorders. Following his return to Sydney, A/Prof Semsarian established and is currently the Head of, the Ginges Centre for Molecular Cardiology at the Centenary Institute, is a Molecular Cardiologist at Royal Prince Alfred Hospital, and is an Associate Professor in the Faculty of Medicine at the University of Sydney. He is also chairman of the Cardiovascular Genetics Working Group of the CSANZ. |
|
|
Dr Cheng-Chun Wang Cheng-Chun completed his PhD in Professor Richard Harvey's Laboratory. His work was focused on the generation and subsequent analysis of the Nkx2.3 knockout mice. Cheng-Chun graduated from the University of Melboune in 2000, and upon graduation went to work at the Institute of Molecular and Cell Biology in Singapore. His current work is focused on determining the physiological role of some proteins thought to be important for vesicular transportation, such as SNAREs, Sorting Nexins and Rabs. |
|
|
Dr Andrew Owens Andrew trained in cardiothoracic surgery and transplantation in Newcastle, Middlesbrough and Cambridge in the UK. He recieved a research exchange fellowship through the Royal Australasian College of Surgeons / Royal College of Surgeons of England, and once arriving at the VCCRI he commenced work in the Molecular Cardiology Program. Andrew's main research interests at that time were the assessment of the cardiac physiology of genetically-modified mice, with an emphasis on cardiac contractility and hypertrophy, and an investigation into the genetic modification of skeletal muscle for use in the augmentation of cardiac function. |
|
|
Dr Nisha Nanda Nisha completed her PhD in Professor Robert Graham's Laboratory. Her theisis was focused on analysing the in vivo role of the tissue transglutamminase Gh. She was awarded her PhD in 2001 from the University of New South Wales, and upon graduation she went to work at a Biotechnology Company in California.
|
|
|
Dr Songhai Chen Songhai's main research interest was to investigate the molecular mechanisms of alpha-1A adrenergic receptor activation. His work was carried out in the Molecular Cardiology Program under the supervision of Professor RObert Graham. Songhai gained his MD (doctor of Medicine) in 2001, and upon graduation he moved to Vanderbilt University and now studies heterotrimeric G proteins and their associated interactions.
|
|
|
Dr Fang Lin Fang's main research interest was to understand the role of the alpha 1A adrenergic receptor in cardiac function. Fang worked in the Molecular Cardiology Program, under the supervision of Professor Graham. Upon graduation from the University of New South Wales in 2001, she moved to Vanderbilt University in the USA where she is currently working on heterotrimeric G proteins and associated interactions.
|
|
|
Dr David Elliott David completed his thesis in Professor Richard Havey's Laboratory. His main research interest was to understand the interactions of the C-terminal domains of the transcription factor Nkx2.5. He graduated from the University of Melbourne in 2002 and upon graduation went on to work at Cambridge University in the United Kingdom.
|
|
|
Dr Thomas Yeoh Upon completing his Cardiology training Dr Thomas Yeoh joined Professor Harvey's Laboratory where he began studying the differentiation of skeletal muscle. Upon his graduation in 2003 he joined Dr Diane Fatkin's Laboratory where he is currently co-ordinating a clinical trial in conjunction with St Vincent' Hospital. Thomas is also a Cardiologist at Concord Hospital (VMO), a Physician (VMO) at Catenbury Hospital, and has a private cardiology practice in Burwood. |
|
|
Dr Aaron Schindeler Aaron undertook his PhD at The Victor Chang Cardiac Research Institute from 1998-2003, where he investigated the role of the small muscle protein Csl in striated muscle development and function. Working under Prof. Richard Harvey, Aaron revealed that Csl can modify cytoskeletal dynamics (i.e. the structural elements of cells) involved with cell spreading in cultured muscle cells. He also identified several signalling pathways and binding partners potentially involved in Csl function. After leaving the VCCRI in 2003, Aaron was appointed as a Senior Research Officer at the Orthopaedics Research department at the Children's Hospital at Westmead. He is currently leading a team that is investigating the orthopaedic defects associated with type 1 Neurofibromatosis (NF1) and analysing the molecular basis of adjunctive drug therapies. This work utilises both mouse and cell culture models to understand and optimise present clinical treatments and has the potential for short-term and long-term impact on paediatric orthopaedics. |
|
|
Dr Donna Lai Donna's PhD project focused on the functions of NRG1 in the developing heart and the potential downstream pathways of NRG1 in heart cells. She generated a NRG1 transmembrane domain-specific knockout mice (NRG1TM). The homozygous NRG1TM/TM embryos died in utero. Differentiation of cardiomyocytes and development of the cardiac conduction system were severely interrupted in mutant hearts. Expression of a number of cardiac genes was down-regulated in mutant hearts in a region-specific and dose-dependent manner. Donna is currently working as a Postdoctoral Fellow in Professor Richard Harvey's Laboratory. Currently, she is involved in the establishment of an in vitro heart explant culture system to further investigate the downstream pathways of NRG1 in the developing heart. An improved understanding of the molecular mechanisms by which NRG1 and its downstream targets regulate heart function, will enable specific approaches for the control or prevention of heart disease. |
|
|
Dr Jennifer Cropley Jennifer's PhD project focused on analysing the behaviour of genetic elements called retrotransposons. Retrotransposons are not quite genes, because the body does not use them to function, in fact they can be considered parasites because they multiply and "hitch a ride" in our genome. However they are about the same size as genes, and there are millions of them in the DNA of pretty much every organism on earth (except for bacteria). In humans, retrotransposons have amplified over time to comprise almost 50% of our DNA. They often sit right next to genes, and can sometimes affect the function of these genes. To study how retrotransposons can do this, I used a model in mice where a particular retrotransposon affects the function of a gene called agouti, causing obesity and diabetes in affected mice. We found that the cell attempts to silence retrotransposon activity to prevent such diseases, and that the silencing mechanisms are very complex, partly involving addition of methyl molecules to the DNA. The title of her thesis was "Epigenetics of Retrotransposons in the Mouse" and her PhD was awarded in 2005. Jennifer has now moved to San Francisco to finish her PhD work with Professor David Martin. |
|
|
Dr Vesna Nikolova "Laminopathies" are a group of diverse human diseases caused by mutations in the LMNA gene, encoding the nuclear lamin A and C proteins. To evaluate molecular mechanisms of laminopathies we studied a mouse model with targeted delation of the Lmna-/- gene. We reported that Lmna-/- mice develop rapidly progressive dilated cardiomyopathy (DCM) characterised by left ventricular dilation and reduced systolic contraction. We showed that Lmna-/- cardiomyocyte nuclei developed marked alterations of shape and size with central displacement and fragmentation of heterochromatin. Electron microscopy of Lmna-/- cardiomyocytes showed disorganisation and detachment of desmin filaments from the nuclear surface with progressive disruption of the cytoskeletal desmin network. Alterations in the nuclear architecture were associated with defective nuclear function evidenced by decreased SREBP1 import, reduced PPARg expression, and a lack of hypertrophic gene activation. These findings suggested a model in which the primary pathophysiological mechanism in Lmna-/- mice is defective force transmission resulting from disruption of lamin interactions with the muscle-specific desmin network and loss of cytoskeletal tension. Despite severe DCM, defects in nuclear function prevented Lmna-/- cardiomyocytes from developing compensatory hypertrophy and accelerated disease progression. Vesna is completing her work at the VCCRI and once this is complete, she is planning on moving overseas and continuing her research in this field. |
|
|
Dr Rajesh Subbiah Raj Subbiah completed his PhD in the Electrophysiology and Biophysics Program. His PhD was awarded in 2005. |
|
|
Dr Bryony Mearns Bryony's PhD project was undertaken in Professor Bob Graham's Molecular Cardiology laboratory. Her work focussed on the role of transglutaminase II (TG2) in cell adhesion and migration, particularly with regards to wound healing. TG2 is a very complex protein with at least five different reported activities. Bryony used TG2-knockout murine embryonic fibroblasts and purified recombinant TG2 protein, containing various inactivating mutations, to try to tease out how TG2 performed this role. Bryony is planning to move to the US in the near future to undertake a post-doctoral position. |
|
|
Dr Suchitra Chandar Dr Suchitra Chandar graduated in medicine from University of Madras, India. Cardiology and specifically, heart failure, has captured her interest for quite some time. After completing her cardiology training, she joined A/Prof Diane Fatkin?s group to embark on a higher degree. Her research goal was to understand more about the pathogenetic mechanisms that underlie heart failure, which may help to identify novel pharmacologic targets and is the first step in improving the management of heart failure. The focus of her work was in evaluating disease-causing mechanisms and the role of exercise in dilated cardiomyopathy due to lamins A/C deficiency. She was awarded her PhD in May 2006, and has taken up a Senior Lecturer position at the University of Sydney, is a Cardiologist at Concord Repatriation General Hospital, Sydney, NSW, and has a private cardiology practice in Sydney. In the longer term, she aims to expand her research and teaching experience, in addition to maintaining a full and interesting clinical caseload. |
|
|
Ms Helen Hwang
Helen completed her honours year in Professor Graham's Laboratory. Her studies were focused on the molecular mechanisms involved in the release of Neuregulin signals. In 1998 Helen graduated from the School of Biochemistry and Molecular Genetics at the University of New South Wales. After graduation she went on to work as a research assistant in the Institute. |
|
|
Ms Gabrielle Thomson
Gabrielle completed her honours year in Professor David Martin's Lab, graduating in 2000. Her research focused on examining retroelements in mice and analysing their expression. At present she is undertaking a PhD in the same lab and is carrying this research further to examine if retroelements can interfere with expression of surrounding genes.
|
|
|
Ms Bryony Mearns
Bryony completed her Honours year in Professor Robert Graham's laboratory in 2000. Her thesis focused on signalling pathways stimulated by IGF-1 and VEGF in skeletal muscle cells. Bryony stayed on in Professor Graham's laboratory to undertake a PhD using a cell biology-based approach to try to elucidate the role of Transglutaminase II in wound healing.
|
|
|
Ms Vesna Nikolova
Vesna completed her honours year in the Laboratory of Dr Mingdong Zhou, studying intracellular signalling via erbB growth receptors of specific tyrosine kinases. Her specific area of interest was erbB2 receptor over-expression and cancer development. After completing her honours year, Vesna continued at the VCCRI as a PhD student. Under the supervision of Dr. Diane Fatkin she commenced work on a project investigating the molecular bases of dilated cardiomyopathy and conduction system disease. |
|
|
Ms Lisa Beeren Lisa completed her honours year in the Laboratory of Dr Thomas Preiss, studying translation initiation. She examined the proposal that ribavirin could inhibit the activity of a protein, eIF4E, a protein that is a key component of translation initiation in eukaryotes. The suggestion that ribavirin could inhibit eIF4E also implied that it was a potential anti-cancer treatment. Lisa found that ribavirin does not bind eIF4E and that it does not interfere with its function, and therefore was not a potential anti cancer therapy. Her work contributed to a paper that was published through the year (Westman B et al (2005) RNA 11:1505). Lisa was awarded a first class honours degree from the University of New South Wales in 2005. The title of her thesis was "Manipulating Translation Initiation: Can the Antiviral Drug Ribavirin Play a Role?". After completing her honours, Lisa has moved overseas and plans to complete her PhD in the United Kingdom. |
|
|
Mr Clive Yu
Clive completed his honours year in A/Professor Diane Fatkin's laboratory. His work was focused on establishing genes involved in Atrial Fibrilation, a common cadiac disease. Specifically, four genes have recently been identified as containing mutations that may contribute to the development of this disease. Clive examined whether these mutations were present in a group of families that have developed this disease. Clive was awarded his honours degree in 2005 from the UNiversity of New South Wales. He has since commenced work at the Victor Chang Cardiac Research Institute as a Research Assistant. |
Back to top
