Baker Heart Research Institute | | Institute Research Heart Baker
Annual Report 2005 Annual Report 2005 Report Annual Contents
2 The Baker story 4 Organisational Structure 6 Director’s Report 8 President’s Report 9 A word from our patron 10 The Board 12 Baker History 14 Summary of Baker relationships
15 Research & Divisions 16 Baker Clinical 17 ABMU
18 Experimental Cardiology and Heart Failure 19 Wynn Department of Cardiology 20 Cellular Biochemistry 21 Experimental Cardiology 22 Cardiac Hypertrophy 23 Cardiac Surgery 24 Applied Cardiovascular Research 25 Molecular Endocrinology 26 Molecular Pharmacology
27 Atherothrombosis and Vascular 28 Thrombosis & Myocardial Infarction 29 Cell Biology 30 Clinical Physiology 31 Vascular Pharmacology 32 Cell Biology & Diabetes 33 Lipoproteins & Atherosclerosis 34 Human & Vascular Biology
35 JDRF Diabetes and Metabolism 36 Oxidative Stress 37 Human Epigenetics 38 Biochemistry of Diabetic Complications 39 Kidney Disease in Diabetic Complications 40 Advanced Glycation in Diabetic Complications 41 Genomics of Diabetic Complications 42 Proliferation & Fibrosis in Diabetic Complications 43 Atherosclerosis in Diabetic Complications
44 Cardiovascular Neuroscience 45 Neuropharmacology 46 Translational Proteomics Ramaciotti Centre 47 Human Neurotransmitters
48 Commercialisation 60 Core Facilities 62 Staff & Students 66 Monthly Baker Science Awards 68 Development 67 Donors 70 Financial Report 73 Publications 76 Location & Contact details now in its 80th year, the Baker A comprehensive research Heart Research Institute is program with a strategic focus: The Baker story… Australia’s most distinguished Research at the Baker is broadly cardiovascular research centre divided into four divisions: and one of the world’s leading Experimental Cardiology and Heart organisations investigating Failure; Atherothrombosis and the causes and complications, Vascular; Diabetes and Metabolism treatment and prevention of heart, and Cardiovascular Neuroscience. stroke and vascular disease. Four associate directors of the Baker, each of them internationally At the Baker we are devoted renowned scientists and clinicians, to the prevention and cure of lead these divisions. Together they cardiovascular disease. Every oversee the research activities of research dollar we attract and 2005 Report Annual Institute Research Heart Baker the Baker’s 26 laboratories. spend goes into finding out why A researcher who is at the top of people are getting sick and dying their field in turn heads each of and the best ways we might help these labs. Their research focus them get better and stay alive. ranges from the study of blood The Baker’s close links with The Alfred, We are finding out more about vessels to the complex relationship who is at risk and how we might an outstanding hospital specialising between molecules, from ways stop heart attack, stroke, to improve the health of people sudden cardiac death and the in the most complex and serious acute undergoing or waiting for heart like from ever happening. In this surgery to the organ damage way, explaining what we do is health problems, gives it a special place caused by diabetes. simple. Why we do it, sadly, in cardiovascular research in Australia is even simpler. The figures One of the Baker’s great strengths remain shocking: is that this disparate research, and puts it among the leading research highlighted in the following pages, • An Australian dies every 10 is highly collaborative. Together, facilities in the world. minutes from cardiovascular our specialised staff use state-of- disease, representing more than the-art facilities to build a better 40 per cent of all deaths in understanding of the causes and this country. effects of cardiovascular disease • Cardiovascular disease is the than we’ve ever had. leading cause of death and The Baker’s close links with disability, not only in Australia The Alfred Hospital, an outstanding but also around the world. It is hospital specialising in the most on the rise in developing nations complex and serious acute health and expected to reach epidemic problems, gives it a special place in proportions by the middle of cardiovascular research in Australia this century. and puts it among the leading • More than 3.2 million people research facilities in the world. in Australia are affected by With only a third floor walkway cardiovascular – 67 per cent of separating the two buildings, all families. the unique relationship between the institute and the hospital • Throughout the world, is pivotal to the Baker’s work. cardiovascular disease accounts Some of our scientists are also for more than 16 million clinicians, and this “wearing two deaths every year – more than hats” ensures our research remains cancer, and all respiratory, clinically relevant. digestive and non-communicable diseases combined. Every day Baker staff witness the effects of cardiovascular disease in • Cardiovascular disease is Alfred patients and their families. Australia’s leading health This link is a constant, powerful problem. At a cost of $7 billion reminder of the value and the a year, it makes up 11 per cent urgency of their work and it keeps of Australia’s total direct health the Baker very close to changes care expenditure. in disease trends and treatments. • Over the last decade, the Just as importantly, the Alfred prevalence of cardiovascular connection gives our researchers disease in Australia rose by access to a huge patient database almost 20 per cent. and to human samples of tissue and cells. In return the clinical Our work has never been more services have access to the important. latest ideas and treatments. The combined effect is a strongly committed, disease-focused, well-informed research community with the highest degree of empathy for those suffering from cardiovascular disease. Organisational Structure
DIrector Garry Jennings Annual Report 2005 Report Annual Institute Research Heart Baker Chief Associate Director Operating Officer Cardiovascular Neurosciences David Lloyd Murray Esler Annual Report 2005
Chief Head Financial Officer Neuropharmacology Baker Heart Research Institute Associate Director Associate Director Anita Furnell Experimental Geoff Head JDRF Diabetes & Cardiology & Metabolism Head Heart Failure Associate Director Director Translational Associate DIrector Atherothrombosis Mark Cooper Commercialisation David Kaye Proteomics Baker Clinical & Vascular & Research Contracts Ramaciotti Centre Tony Dart Karlheinz Peter Chris Nave Greg Rice Head Head Director Wynn Head Lab Manager Oxidative Stress Fundraising Department of Head Human Baker Clinical Development Cardiology Thrombosis Judy de Haan Neurotransmitters (ABMU) Lyn Brodie David Kaye & Myocardial Gavin Lambert Head Elizabeth Dewar Infarction Cellular Head Human Epigenetics Manager HR Head of Biochemistry Karlheinz Peter Biological Preventative Media Preparation Assam El-Osta Annette Crawford Cardiology Elizabeth Woodcock Head Cell Biology Amy Gatt TBA Head Head Alex Bobik Manager Experimental Biochemistry Media Cardiology of Diabetic Risk Clinic/ Head Complications Ebru Yaman Xiao-Jun Du Clinical Gene Bank Merlin Thomas Head Physiology Head Kidney Disease Cardiac Bronwyn Kingwell Manager OH&S Hypertrophy in Diabetes Head Adrian Quintarelli Julie McMullen Vascular Karin Jandeleit-Dahm Head Pharmacology Advanced Manager Head Jaye Glycation Information Cardiac Surgery Chin-Dusting in Diabetic Systems Head Complications Salvatore Pepe Cell Biology & Jamie Howard Head Josephine Forbes Head Diabetes Applied Genomics Cardiovascular Peter Little of Diabetic Manager IT Complications Research Head Ian Briggs John Power Lipoproteins & Phillip Kantharidis Head Atherosclerosis Head Manager Molecular Dmitri Sviridov Proliferation & Building Endocrinology Fibrosis in Diabetic Infrastructure Head Complications Walter Thomas Human & Steve Droste Zhonglin Chai Vascular Biology Head Head Molecular Stephen Duffy Diabetic Hypertension Atherosclerosis Zygmunt Head Terri Allen Krozowski Proteomics Centre Head Head Molecular Gert Talbo Precinct Animal Pharmacology Centre Rebecca Ritchie Head Debra Ramsey Confocal Imaging Head Alan HIbbs Adenovirus Facility Walter Thomas
Head Head Small DNA Sequencing Animal Facility Walter Thomas Xiao-Jun Du Director’s Report › Professor Garry Jennings
growth and consolidation have Further growth has occurred Achieving these objectives however By now almost everyone is aware Each year the Institute receives The applications in the Institute Four new companies contributed
been key for the Baker this year, with the strategic recruitment of will still leave many people in that obesity and diabetes will a grant from the Thomas Baker of this epigenetic approach so to an important year of progress 2005 Report Annual Institute Research Heart Baker now 80 years old, but in many new scientific groups – strategic the community living with the keep cardiovascular disease at the Foundation. In 2005, at the far range from cancer, to rare in the commercialisation of Baker ways becoming younger by the because they not only share the combined effects of an ageing forefront of community health suggestion of the trustees, a new inherited forms of autism that research. V-Kardia Pty Ltd and day. In part the growth has been mission of the Baker - to reduce and damaged heart. All of us concern for the foreseeable future. initiative was the Thomas Baker appear suddenly in childhood, its US subsidiary V-Kardia Inc are organic, driven by outstanding death and disability from heart, have family members, friends But awareness is not enough and Award for Research Excellence, diabetes, and even to neurogenic developing the research ideas of Annual Report 2005 success in grant applications to stroke and vascular disease, but or colleagues in this situation. we need breakthroughs, more recognising an outstanding piece hypertension. The latter is Professor David Kaye and Dr John national and international peer also because they bring new Heart failure is the most serious than a few, and at many levels. of research published during a term applied by Professor Power. The exciting potential of review granting bodies (over $10M skills and technologies that manifestation and research on Professor Mark Cooper leads our the year. The bar was set very Murray Esler to a common form gene and cell therapy to repair and Baker Heart Research Institute in new National Health & Medical match and complement those heart failure and advanced disease diabetes and metabolism theme. high and the winner, Dr Assam of high blood pressure that is restore damaged heart muscle can Research Council grants), supported of our existing groups. Professor is another major theme at the He and his large group work El-Osta and his colleagues had caused by overactivity of the only be realised with the aid of an by a good year for fundraising Karlheinz Peter relocated from the Baker involving a large team of on preventing the damage that their paper featured on the cover nervous system and may be a efficient delivery system that takes and for investment income. Were University of Freiberg in Germany; molecular scientists, physiologists high sugar levels do to arteries of the prestigious journal Nature product of protracted or extreme the new therapies to the heart we not a group of hard-nosed he brings strengths in thrombosis and cardiologists. Professor leading to the high risk of heart Genetics. Sam has introduced mental stress. Murray heads our without spilling over to other parts scientists and the like, and aware research and in applying high- David Kaye leads the group, which disease, stroke, vascular disease, epigenetics to the Institute - the Cardiovascular Neurosciences of the body. A V-Kardia device of the hard work and planning of class molecular research to the includes the Wynn Department, blindness and kidney failure that study of the modification of gene theme. We all know that there is scheduled to go into clinical the Board and staff that got us in development of new treatments established investigators such as is characteristic of diabetes and function by chromatin. This has is interdependence between trials this year. Another company, this position we might be saying and diagnostic tools for the clinic. Walter Thomas, Elizabeth Woodcock the main reason diabetes is such proven important in many of the health of the mind and the ElaCor Pty Ltd was formed jointly that 2005 was a year when all the and Xiao-Jun Du as well as some a significant health problem. The the questions of interest to our body and there has long been with the Institute for Molecular Together with our strong stars lined up for the Baker. who are developing their careers award of a Diabetes Complications laboratories in every division in the a suspicion that in many cases Bioscience in Queensland and complement of vascular biologists like Rebecca Ritchie. New arrivals Centre grant, the only one outside Institute and there are many more heart attack has a psychological Geoff Head is leading the research already at the Baker we have in this division have also hit the the USA by the New York-based high impact publications to come. or psychosocial element. Recently on development of a new drug for formed a new scientific theme, ground running, and include Juvenile Diabetes Research Fund expert evidence has accepted heart failure treatment. also referred to as a division, Most of the diseases we seek to Julie McMullen who is working was great news and strong depression as a risk factor for heart working on the link between prevent and cure have both genetic Nucleus Network is the Victorian We exist in the cause of scientific on understanding why heart recognition of the international attack, independent of other risk atherosclerosis and thrombosis. and environmental causes and clinical trials platform formed from growth (hypertrophy) from exercise stature of the group. factors and our Cardiovascular These key events turn an individual understanding their interaction is a the merger of Clinical Trials Victoria excellence, especially science that training is good for you, and Neuroscience division is pursuing who is apparently healthy - albeit Exercise, obesity, nutrition, key step in understanding disease. and the Centre for Clinical Studies. protects the heart, whereas heart this link using advanced clinical contributes to our community. This with some risk factors like high diabetes and other cardiovascular Epigenetic changes as simple as a New CEO Andrew Giddy leads a growth due to disease is not. research technologies, many of blood pressure, diabetes, high risk factors are closely linked chemical modification, methylation team that is building the clinical which were developed here at involves doing good science now and also cholesterol or a family history - We exist in the cause of scientific through metabolic pathways, and provides a genetic on/off switch. trials capability of Australia and the Institute. training future generations of scientists into a cardiac emergency, suffering excellence, especially science that the Institute is making a major This may be a critical link between helps biotech companies make a sudden catastrophic event like contributes to our community. investment in these areas. At the the environment and whether a Our students and postdoctoral the transition from pre clinical and clinicians. a heart attack or major stroke. This involves doing good science clinical end Professor Kerin O’Dea, cell faithfully produces the proteins fellows did us proud at many to human studies, providing Understanding the biological now and also training future one of our most distinguished programmed by its genes. national and international regulatory support, education and processes that occur both in the generations of scientists and alumni, has joined us part time to conferences during the year as accreditation as well as a modern years when trouble in the arteries clinicians. Our 80th anniversary assist us in developing a program did the eminence gris. Enzo Porelli early phase clinical trials facility on is brewing and in the last few also brings to light the many of research on nutrition and won the Young Investigators Award the Alfred campus. minutes before an acute cardiac people, particularly with a diabetes. Professor Mark Febbraio of the High Blood Pressure Research event is a key Baker objective in scientific background, who have will soon establish his Molecular Council (HBPRCA). Judy De Haan the coming years. passed through the Baker and now Metabolism laboratory. His work was successful at a major National contribute to the community in a on changes in cell signalling in Heart Foundation conference and Every year, almost 20 million variety of ways: in government and diabetes and with exercise has Xiao-Jun Du was their inaugural people suffer these events. In industry, in developing policy, in had a major impact in the field. Ross Hohnen Award recipient Australia, most people who running biotechnology companies The strong collaborations he has for the top rated project in the eventually die from cardiovascular or working in occupations such already with many existing Baker country. At the same meeting Paul disease have previously suffered as stock market analysts, as laboratories will further enhance Nestel also received an inaugural heart attack or stroke. Our aim at journalists, or in the non-profit this research. award, the NHF Medal for Lifetime the Baker is to use the new biology sector. Last year we had a record Research Achievement. Professor to develop predictive tests and number of students at the Baker, Colin Johnston was recognised treatments that are individualised, around 70. All were enrolled for for lifetime achievement with the more specific and more pre- postgraduate degrees at Monash naming of an annual lecture at emptive than tests and treatments University, the University of HBPRCA meetings in his honour. that we now have. Melbourne and other universities, and all benefited from a highly active mentoring and support program led by our Scholars Executive, now chaired by Jaye Chin-Dusting. President’s A word from Report our patron › Mr Robert Stewart › Sir Laurence Muir
it has been a tremendous year In his decade as President, And last but not least, Norman has i have been privileged to be As patron I congratulate the
for the Baker. Our dedicated team Norman saw the Institute through had the privilege of working with associated with the Baker Heart board and staff on all that has 2005 Report Annual Institute Research Heart Baker of scientists continue to have a period of great change. One two outstanding Baker directors. Research Institute for over half been achieved in 2005. It has great success in their pursuit of of the most significant of those John Funder’s retirement in 2000, its life. As we move into our 80th been a year of expansion and of finding ways to prevent, cure changes was the move from the after a stellar career and great year it is timely to reflect on our successes in the laboratories. and treat heart disease. Many of building now known as “the old leadership, ushered in new director rich partnerships – with The I pay tribute to all of our partners Annual Report 2005 their successes are highlighted Baker” to our state-of-the art Garry Jennings. Garry’s steady Alfred Hospital, with state and and say a sincere thank you to throughout the pages of this new building, officially opened guidance and inspiring vision has commonwealth governments, Norman O’Bryan, our recently annual report in 2002. Our new premises, at the heralded in an exciting new era for with corporations and charitable retired president who has been an Baker Heart Research Institute heart of the rapidly expanding the Baker, as this report will attest. institutions, with the community inspirational leader. While I am delighted to be taking AMREP, Melbourne’s newest and and its generous volunteers. These over the reins from Norman I would like here to report Finally a warm welcome and most exciting medical research partnerships have enabled us to O’Bryan, who served as Board some changes that occurred sincere best wishes to our new precinct, befit the high-tech, employ 180 dedicated scientists President for 10 energetic and on the Board in 2005: Gerry president Robert Stewart. leading edge research conducted and 40 support staff in 26 research capable years, I am aware that Johnson, Philip Munz, and here. Quite aside from the complex laboratories, devoted to both his is a hard act to follow. It is Paula Campbell-Tuckfield all logistics and planning such a move clinical and basic research. fitting to be reflecting on some of resigned during the year. Gerry entailed, it would not have been the Baker’s achievements during had served on the Board for 14 Thanks to the brilliance of our possible without a significant his presidency in the year of the years, including a valuable term scientists and the outstanding injection of capital. While Norman Baker’s 80th anniversary. as vice president. Philip was leadership of Professor Garry has previously thanked many of a Board member for 10 years, Jennings, the Baker is a leading the people and organisations that making a particular contribution international cardiovascular helped raise those funds, I’d like to the commercialisation of Baker research institute at the hub of Our dedicated team of scientists to extend here our most sincere research. Although Paula had only a major medical research and thanks to him, for his leadership been on the Board for a short creative centre of excellence on continue to have great success in their throughout the process and his period her contribution during The Alfred campus. tireless dedication to the project. pursuit of finding ways to prevent, that time was well valued. It is surely one of his most Baker scientists today remain We thank them for their service significant legacies. passionate about improving cure and treat heart disease. and wish them well in their quality of life through their But that wasn’t the only big future endeavours. discoveries. Collaborating with the change of Norman’s decade: it was New appointments to the Board best researchers in the world and also during Norman’s time that include Lindsay Maxsted who has using innovative, cutting edge the medical research community joined our ranks as Treasurer, John technology and research methods underwent the transition from Allen, Justin Arter and the newly they continue to strive towards our block funding of research to appointed Chief Operating Officer one goal: the prevention, cure and competitive, grant-based funding. of the Institute, David Lloyd. treatment of heart disease. At the time the Baker approached I am delighted that Paula Dwyer this new regime with some has agreed to take on the role of trepidation, but it has proven to Vice President, after serving as be a system under which the Baker Treasurer for three years. The very has excelled. This has been a result strong financial performance of of the outstanding leadership of the Institute in 2006 is a credit to the Institute and the excellence her work, as well as to the strong of the scientific and support staff oversight of Norman O’Bryan and working at the Baker. all of the Board. It’s a wonderful time to be involved with the Baker and I look forward to contributing to its great future. Board members L-R: Rob Stewart David Lloyd The Board Professor Garry Jennings Paula Dwyer Anita Furnell (by invitation) Lindsay Maxsted Justin Arter John Allen
Board Members absent: Greg Hywood Richard Smallwood Peter Scott Graeme Ryan Edward Byrne
10 Robert Stewart Paula Dwyer Lindsay Maxsted John Allen Justin Arter Professor Edward Byrne Professor Garry Jennings Greg Hywood David Lloyd Professor Graeme Ryan Peter Scott Professor Richard Smallwood 11 President Vice President Honorary Treasurer AM AC AO Annual Report 2005 Report Annual Institute Research Heart Baker
Rob Stewart was National Paula Dwyer’s background is Lindsay Maxsted is the John Allen is Deputy Chair Justin Arter is Managing Ed Byrne is Dean of Medicine, Garry Jennings is director. Gregory Hywood spent nearly David Lloyd is Chief Operating Graeme Ryan is currently part- Peter Scott leads the Richard Smallwood is Managing Partner of Minter in investment management Australian CEO and former of Austral Credit Union, Director Firmwide Strategy of Nursing and Health Sciences He is an internationally 30 years in the newspaper Officer of the Baker Heart time director of Research Melbourne Investment an Emeritus Professor of Ellison, one of Australia’s and investment banking. In managing partner of the Director to Aust Photo Goldman Sachs JBWere, and a at Monash University and recognised authority in industry. He joined the Research Institute. He took up Strategy at The Alfred Hospital. Banking team of UBS and has Medicine, University
Annual Report 2005 leading law firms, for particular, Paula specialised Australian Corporate Recovery Supply and Trustee of Kodak member of the firm’s Board, has had an active career in cardiology. His background Australian Financial Review this position in August 2005 For more than 20 years, more than 20 years experience of Melbourne. 11 years, retiring in June 1999. in the provision of corporate practice of the International Superannuation Fund. Management Committee, clinical neurology and basic is both a clinical cardiologist in 1976. He was variously and joined the Baker Board in Graeme has had senior in providing financial advice As Professor of Medicine He spent five years with financial advice to companies Audit, Tax and Advisory firm Risk Committee, Commitments neurological research. Ed was and an academic with Canberra Bureau Chief, January 2006. leadership and management to large Australian companies John concluded a 29 year with the University of Pacific Dunlop from 1976 to operating in regulated of KPMG. He is a member of Committee, IT Steering the Founding Director of the broad clinical experience European Correspondent and roles in medical research, and governments. 1981 in a variety of general industries, including financial KPMG Australia’s National career with Kodak at the Committee, Compliance and research ranging from Washington Correspondent He holds a BA (Hons) in medical education and health Melbourne, Richard was Baker Heart Research Institute Melbourne Neuromuscular end of 2004, where he had Philosophy from the University He has extensive experience head of the Department of management positions within institutions and utilities. Board and KPMG’s ASPAC Committee and Discretionary Research Institute. He was community prevention to before becoming Editor in care. These roles include a been chairman and CEO since of Stirling and a Master of in Mergers and Acquisitions Medicine and Chairman of the Footwear Group. She provided corporate Regional Board. Portfolio Service the Founding Director of the fundamental research on 1992 and then Publisher and period of 10 years, from 1986 1999. His career covered Public Administration from the (including public company the Division of Medicine advice to major private and Investment Committee. Centre for Neuroscience and mechanisms and treatments Editor in Chief in 1996. In 1998 to 1995, as dean of Medicine He is Chairman of Melbourne His principal area of practice a wide and diverse set of University of Tasmania. takeovers), corporate financial at the Austin and Repatriation government sector clients in Professor of Experimental of high blood pressure, he was appointed Publisher at the University of Melbourne IT Limited, an ecommerce prior to his becoming CEO management skills including Justin graduated from restructuring, joint ventures, Medical Centre. He was also areas including the reform of Neurology at the University atherosclerosis and heart and Editor in Chief of the and then, from 1996 to 2000, infrastructure company was in the Corporate Recovery finance, consumer marketing, Melbourne University in He began his career in the asset sales and purchases, Director of Gastroenterology public infrastructure, private of Melbourne. As Director of failure. He has published Sydney Morning Herald and as Chief of Clinical Services providing key products and field managing a number of divisional and general 1984 with degrees in Law New Zealand Ministry of public floats, equity and debt at the centre, and has sector investment in public the Centre for Neuroscience, well over 300 scientific in 2000 Publisher and and board member, Inner services such as domain Australia’s largest insolvency/ management. John came to and Commerce. Soon after Foreign Affairs, then served issues and privatisations. had over 30 years infrastructure, mergers and he played a major role in papers in fields including Editor in Chief of the Age and Eastern Health Care names on the internet workout/turnaround Australia in 1999 to assume he completed his Articles of in the New Zealand Trade The sectors and industries involvement in the teaching acquisitions advisory and driving the establishment of exercise, cardiac and vascular and Group Publisher of Network, Melbourne. required by companies engagements. Some of the the leadership of Kodak Clerkship and practised as a Development Board from in which he has worked of undergraduates and equity capital market raisings. Neurosciences Victoria and hypertrophy, the neurobiology Fairfax Magazines. entering the digital assignments which he has Australasia after managing solicitor for a short time. 1986 to 1990. As well as his role at with clients include health postgraduates. He has She has extensive experience Neurosciences Australia. His of cardiovascular disease and economy; Chairman of handled include International Kodak NZ very successfully He is CEO of Tourism Victoria. The Alfred since 2000, he is care, building materials, published over 250 clinical in the securities and research group has made heart failure. He moved into higher Meditech Research Limited, Trucks Australia Ltd; 1992-1998. In 1986 he entered the He is a Board member of the also currently chairman of financial services, health care, and scientific papers, investment industries. significant contributions education administration in a biotechnology company companies associated with stockbroking industry as a He is Cardiovascular and Geelong Football Club, the Board of Directors, Royal manufacturing, media primarily in the field of the in muscular dystrophy and 1990, first in the New Zealand focused on developing and Paula is presently a director Abraham Goldberg including His particular forte is strategy research analyst focusing Respiratory Co-Director The State Library and the Victorian Eye and Ear Hospital, and telecommunications, liver and its diseases. He mitochondrial research. Polytechnic Sector and then commercialising drugs that of Tabcorp Holdings Limited, Linter Textiles Corporation Ltd, and business development on the food and household for Bayside Health, which Baker Institute. a Governor of the Ian Potter public utilities, resources was President of the Royal and he applying these skills goods, entrepreneurs, as Director, International and improve the health and Promina Group Limited the shareholder company of He is a board member includes the Alfred Hospital, Foundation, chairman of and transport. Australasian College of to the companies and other transport and paper and Commercial Services at the quality of life of patients (Chairman of the Board businesses such as Speedo, of Cochlear Pty Ltd, and is a Professor of Medicine the NHMRC Special Expert Physicians from 1996 to 1998. interests he is currently packaging sectors. University of Tasmania from Peter has been a member of with cancer and other Audit, Risk and Compliance King Gee, Hilton Hosiery etc. Neurosciences Australia and at Monash University. Committee on Transmissible involved with. 1993 to 1998. the Takeovers Panel since 2002 In addition to his extensive chronic diseases; deputy Committee), David Jones companies within The Bell Neurosciences Victoria and He heads a World Health Spongiform Encephalopathies, He joined Goldman Sachs and is also a director of Australian and international chairman of Emitch Limited, Limited and Babcock and Group Ltd, including the immediate past Editor-in- Organisation Collaborating In 1998 he was appointed and a member of the He has been chairman and JBWere in 1991 as the research UWC Limited. clinical and research an online advertising and Brown Japan Property owner of West Australian Chief of the Internal Medicine Centre for Research and CEO of Melbourne Enterprises Commonwealth Plasma CEO Kodak Australia, Director analyst responsible for the experience, Richard had a media placement company; Management Limited. Newspapers; the McEwans Journal. He is a member of Training in Cardiovascular International Ltd, the Fractionation Review of HPA Pty Ltd and President Transport sector as well as long standing association chairman of C E Bartlett, one Hardware group of companies, the Neuromuscular Steering Diseases and a National commercial arm of the Committee. Past appointments include of Photo Imaging Council BTR Nylex, Foster’s Brewing, with the National Health and of the leading manufacturers and Brashs Pty Ltd. Group of the World Federation Health and Medical Research University of Melbourne. serving as a director of RACV Australia (PICA). Southcorp Holdings and the Medical Research Council. in Australia of quality products of Neurology and was Council Centre of Clinical When that company was Ltd., as a member of the At the request of the Victorian Telecommunications and He was chair of the council in the fabrication of synthetic Secretary General and Chair Research Excellence (the Alfred merged with Melbourne Victorian Casino and Gaming State Government, he joined Wine sectors. He was voted in from 1994 to 1997 and has and canvas fabrics; and a of the program committee and Baker Medical Unit). University Private in 2001 he Authority and of the Victorian the Board of the Public numerous surveys as the top been member or chair of director of QSR International of the 9th International Garry Chairs CVHAC, the peak became CEO of MUP until his Gaming Commission, as a Transport Corporation (“PTC”) analyst in the Transport and several committees. He was Pty Ltd, which produces Neuromuscular Congress, committee overseeing the appointment to the Baker deputy director of Emergency in December 1995 and was Diversified Industrials sectors. a member of the Australian qualitative research software. governor of BHP Billiton National Heart Foundation in 2005. Services Superannuation, appointed its chairman on Health Ministers Advisory He was also a non-executive Following research, Justin Charitable Trustees and Board research and cardiovascular VicSuper and Government 1 January 1997. As chairman Council from 1993 to 1997. director of Memtec Ltd, a high worked in corporate finance Member of Prince Henry’s health programs. He David is also a director of the technology filtration company, Superannuation Office and he had the responsibility of represents the Cardiac Society Chifley Business School. for a short period, primarly Institute, Burnet Centre for In November 1999 he was from 1988 until 1997. Memtec as a committee member of guiding the Public Transport on the National Heart, Stroke on the Telstra 1 Float in both a Medical Research, Monash seconded to Canberra as listed on NASDAQ and then the Chartered Accountants in Corporation through the and Vascular Health Strategies corporate finance and equity Institute of Medical Research, Australia’s Chief Medical New York Stock Exchange prior Business. final stages of a significant Group and has been President capital markets capacity. and Southern Health. He has Officer, a position he held to being taken over by a US reform process. The end of the High Blood Pressure been awarded the Queen’s until July 2003. He also company in 1997. process of that reform was the Appointed Head of Research Research Council of Australia. Square prize for Neurological provided consultation and corporatisation and ultimate and Strategist in 1998, he He is a Director of several Research (1982), Bethlehem advice on international He is also President of the privatisation of the business formulated equity market biotechnology companies Griffiths Research Medal aspects of health, and in Business/Higher Education units within the PTC. strategy. Throughout the time and has chaired Steering (2003) and Sir Louis Pyke 2000 was a Vice President Round Table, a member of the that Justin led this group, the Committees of large multi- He is also a Director of Racing Award for contribution to of the World Health Assembly Council of Wesley College and strategy team rated as the centre trials. Victoria Limited, Chairman of Multiple Sclerosis (2004). in Geneva. a director of the Australasian number one team in many Cardiac Surgery Research VicRacing Pty Ltd and Deputy In 2005 he was awarded the private and public surveys. Present appointments Institution Limited. President on the Board of honour ‘Member in the Order include chair of the National Directors at Ruyton Girls’ School. In 2001, he was appointed of Australia’. Blood Authority, Chair of Joint Managing Director the Ministerial Taskforce – Equities Products Group for Cancer in Victoria, chair with institutional cash of the Specialist Education equities, derivatives and Accreditation Committee of research reporting to him. the Australian Medical Council and Member of the Board of VicHealth. › Director › Director Virologist Frank Fenner › US physician Jonas Salk develops the › Norman Watkins, 21, The early years – 1938-1949 1949-1974 releases the myxoma virus, first polio vaccine survives Australia’s first Arthur Basil Corkill Tom E.Lowe to control rabbits, in the › February 6, first use of a mechanical organ transplant, a kidney Murray River Valley. heart in a human patient. graft operation at Royal important people and Melbourne Hospital. › Director › Charles Richter and Beno › First assembly (and › US physician Jonas Salk develops the › First organ transplant Richard › April 18, death of › April 12, Russian some landmark papers 1926-1938 Gutenberg develop the Richter calculations) of a general first polio vaccine Herrick received a kidney from Albert Einstein. cosmonaut Yuri W.S. Penfold scale for measuring earthquakes. purpose electronic › February 6, first use of a mechanical his twin brother Ronald at Gagarin becomes first computer, covering 1800 heart in a human patient. Boston’s Peter Bent Brigham human in space. feet of floor space. Hospital on December 23, 1954.
1926-48 1926 1932 1938 1949 1950 1951 1952 1953 1954 1955 1957 1961 1962 1963
12 13 April 1, 1926: The Baker service for the hospital but and colleagues into better Venous Occlusion Fluid Balance in Congestive The Vectorelectrocardiogram The Nature of the Total Body Perfusion Experimental Pancreatitis: should also have facilities for techniques for x-rays of the 2005 Report Annual Institute Research Heart Baker Medical Research Institute Plethysmography: Cardiac Failure two in Bundle Branch Block Pigmentary Disturbance G.R. Stirling, K.N. Morris and Use of a new Antiproteolytic medical research. The Baker cerebrospinal fluid and studies is established. A critical study Mechanisms in Diuresis T.E. Lowe and J.M. Gardiner in Addison’s Disease F. Kincross substance, Trasylol 80 Medical Research Institute of its cell content and chemistry :&"340' When John F. Mackeddie, a Alfred J. Barnett T.E. Lowe, Bryan Hudson and A.D. McCutcheon, was born. in various diseases. Their Dr JM Gardiner, MD, FRCP, FRACP, FACC Dr George Stirling, clinical doctor and medical 3&4&"3$) work greatly improved the MD, FRACP, FRCP, MD, DSc Melb, FRACP, MRCP Geoff Bentley MBBS, FRACS, FACS (1955-1962) MD, FRACP and D Race, MBBS researcher, had the idea for Research 1926 – 1948: › Dr Gardiner was a superb cardiologist diagnostic ability for diseases › Kimpton Research Scholar, › First director of the Clinical Professor Bryan Hudson, › Dr Doug McCutcheon worked improving the laboratory The institute’s relationship with who brought modern cardiology › Dr Stirling pioneered research
Annual Report 2005 of the central nervous system. facilities of The Alfred Hospital, Clinical Research Unit, Alfred Research Unit (now known as to Melbourne in the 1950s and DSc, MD, FRCP, FRACP into the beginnings of at the Baker at various times The Alfred Hospital from its very From this base, Laurence the Baker Heart Research Institute he wanted the hospital be able Hospital, Melbourne and ABMU), 1949. established the Cardiovascular › A most distinguished modern cardiac surgery – from 1950 until 1961. formation suggested it would Cox, between 1930 and 1938, to keep up with the exciting associate director of the › Director of the Baker Diagnostic Service. endocrinologist with heart-lung perfusion systems, is Australia’s largest heart research evolve as a place of clinically was able to relate clinical new advances that were Baker. institute and one of this nation’s relevant research. An overview observations with pathological 1949-1974. A great teacher. major findings on pituitary myocardial preservation, and occurring overseas, especially in › Major contributions hormones and first Monash hyperthermia. Baker Heart Research Institute of early research projects, findings in a large series of relation to the management of An Anti-Insulin Factor in the Gastric, Duodenal and Jejunal Motility most important resources in before cardiovascular disease brain tumours. His research in peripheral arterial professor of medicine. diabetes and other metabolic Plasma of Diabetic Patients in Man: Physiological studies by Dr. Ken Morris the fight against cardiovascular became the main focus in 1975, was reviewed in the American disease, hypertension and disorders. He was able to Joseph Bornstein and Balloon-Kymography Associate professor › Performed the first open- confirms this was the case. Journal of Pathology in 1933. scleroderma. Geoff Bentley, PhD disease. Over the years our persuade his friend, the Early Baker research pursuits Phyllis Trewhella Roderick Andrew AO, MD, FRCP, FRACP heart operation in Australia Work in infectious diseases pharmacist and philanthropist range from surgery to asthma › Led pharmacology research in 1957. researchers have been responsible by the Baker’s first director, Professor Joseph Bornstein, › Professor Andrew probably had the Thomas Baker and his wife, and infectious diseases. from 1952-1955. for many groundbreaking Alice and sister-in-law, Eleanor William J Penfold, led to a new MD, DSc, FRACP longest association with the Baker, from 1947 until his death in the mid- advances including: Shaw, to assume financial Important early projects ranged technique for bacteriological › At the Baker from 1948 -1952. responsibility for a medical in focus from the central research: “blood culture”, by 90s. An eminent gastroenterologist › Probably the first to recognise institute. Together they decided nervous system and pioneering which organisms circulating in and first medical dean at Monash the distinction between Types › Establishing open heart surgery that the institute should not work by Mackeddie the bloodstream were grown University. 1954 – The Mechanism of in Australia (in collaboration with only provide a better laboratory in the laboratory. 1 and 2 diabetes. Arterial Hypertension: A Comparison of the Effects of Hexamethonium The Alfred Hospital) Bromide in Hypertensive and Normotensive Patients. › Proving that exercise can lower › Director blood pressure 1975-1989 › January 11, › July 20, First manned Paul I. Korner › July 20, 1976: Viking 1 › Improving preservation US surgeon- moon landing. lands on mars, sends › British › Director › Bill Gates and Paul Allen back first clear images of general makes first › US Department of computer 2000 techniques for the long distance form company called planet’s surface. › Scientists at Garry Jennings announcement that Defence invents the programmer transport of donor hearts for Micro Soft. Edinburgh’s Roslin smoking may be bad internet. Tim Berners- › Perth researchers Barry Institute clone first transplantation for health. › Immunologist Peter › Director › US launches › May, first › Space shuttle Lee invents Marshall and Robin Warren › January 2, first › May 14, launch of › First vaccine for adult animal, Dolly Doherty describes how 1990-2000 space shuttle report of the Challenger the world win the Nobel Prize for successful human the first US space pneumonia. the sheep. the body recognises virus- John W. Columbia. virus that explodes, killing all wide web. Medicine for their discovery › Proving that mental stress heart transplant. station, Skylab. infected cells. Funder causes AIDS. seven on board. of a bacterium that causes and cigarette smoking both gastritis and stomach ulcers. provide powerful, selective and potentially harmful stimulation of 1964 1968 1969 1973 1975-80 1976 1977 1980-90 1981 1983 1986 1989 1990-06 1996 2000 2004 the nerves of the heart
› Developing techniques to assess A Structural Study of Abnormal Myocardial Function during Some proud achievements › Improvements in the clinical Some proud achievements › Demonstration that › The opening up of new blood Some proud achievements Haemoglobins Occurring in b-Adrenergic Blockade 1975 to 1980 diagnosis and treatment of 1980 - 1990 adrenoceptors (alpha and beta) vessels is found to account for 1990 - 2006 stiffness of arteries, enabling New Guinea Winifred G. Naylor › Hypertension Evaluation Clinic circulatory abnormalities › Development of radiotracer are regulated in an inverse falls in blood pressure that occur › Defining the genetic basis of the reliable early detection of C.C. Curtain associated with autonomic manner during chronic changes in training individuals. Later Professor Gwen Naylor, was expanded methodology to study pseudohypoaldosteronism atherosclerosis and hypertension dysfunction. sympathetic function in humans. in sympathetic nerve activity. reductions in sympathetic nerve Dr Cyril Curtain, DSc (1955-1972) › Garry Jennings, Alex Bobik, activity also contribute. › Pets associated with lower PhD, DSc (1955-1966) Alf Burnett and Paul › Epidemiological studies › Examination of the feasibility of › Increases in physical activity cardiovascular risk factors › Developing a method to repair › Professor Naylor was one of demonstrate that low HDL induce favourable reductions in › Demonstration that exercise › Dr Curtain was a protein the Institute’s most prolific Korner introduced clinical using beta-adrenoceptor pro- › Enzyme actions provide pharmacological methods plasma levels are associated drugs to prolong the duration of cardiovascular risk. lowers blood pressure in heart valves without surgery chemist and biochemist and innovative scientists and with significant risk of hypertensives without a novel mechanism of who conducted outstanding an international authority to optimise antihyper- the beta-adrenoceptor blockade. › Evidence to suggest that cardiac selectivity of action of tensive therapy. coronary heart disease. sympathetic nervous activity demonstrable changes in › Identifying key factors involved research on blood proteins in on myocardial metabolism, › Development of analytical the structure or compliance steroids. clinical disorders. › Establishment in humans that contributes to arrhythmia in clotting function and pharmacology. › Paul Nestel recruited to take methods for measuring of the heart. › 11BHSD cloned for the first Her work contributed greatly charge of atherosclerosis cholesterol leaving tissues is noradrenaline metabolites. development during ischaemia. immediately and primarily › Demonstration in animals time to the introduction of calcium research. › First ever measurements of › Demonstration from › Defining the differences between channel blockers, a keystone transferred to HDL in plasma noradrenaline spillover studies with genetic hypertension that › The hypertension of renal › Lipid Clinic was established (study in obese subjects regional sympathetic nerve early prevention of cardiac artery narrowing defined the two forms of diabetes, type 1 of treatment for high blood activity in humans. that, in congestive heart failure, pressure and angina. › Exercise testing centre for undergoing weight loss) clearance of noradrenaline and vascular hypertrophy and type 2. results in markedly attenuated › Leptin shown to be produced detecting ischaemic heart › Demonstration that moderate › Observation that the severity is reduced and release from in the human brain disease was established. long-term exercise with of coronary heart disease in men sympathetic nerves is increased. hypertension later in life. is more linked to cholesterol- › Hypertension has several › Heart Risk evaluation clinic apparent insulin resistance › Demonstration that a new › Echo-Doppler methods improved insulin resistance rich lipoproteins, while in women introduced to study aortic causes in many patients was established (with the transport system- sodium proven by unique new Victorian division of the and lowered plasma it is more linked to triglyceride- distensibility. rich fractions. hydrogen exchange- is the methods of studying human National Heart Foundation) triglycerides without affecting major sodium transport process › Impairments in vascular body weight. brain release of amines › Commencement of › Investigations into the usefulness responsible for sodium influx function (contraction and collaborative studies between › Studies focus on of partial beta-adrenoceptor into vascular smooth muscle and relaxation) identified in patients the Clinical Research Unit (now environmental factors agonists for the treatment of cardiac cells. with heart failure. heart failure. ABMU) and the Circulatory and that may play key roles in › Sympathetic nervous activity › Transforming growth factor-beta Hypertension Experimental precipitating obesity and › Enalapril is useful for the increased in cirrhosis of the liver. is identified as a key factor unit at the Baker Medical diabetes in humans. treatment of congestive › Demonstration that most people which contributes to vascular Research Institute. This › Dr Murray Esler demonstrates heart failure. hypertrophy and collagen collaboration leads to world with high blood pressure have a neural defective › Demonstration of defective some structural and functional deposition in arteries of leadership in aspects noradrenaline uptake thermogenesis in obese people hypertensives. of hypertension research cardiac abnormality. system in some hypertensive › First demonstration that and treatment. patients. › Marine polyenoic acids are potent › Exercise may modify renal triglyceride lowering agents. sympathetic function which is sodium-hydrogen exchange is a › First demonstration that › New treatment is introduced major intracellular pH regulatory it may be possible to › Fish oils lower plasma important for control of vascular to postural hypotension. resistance pathway in cardiac and vascular normalise the structure of triglycerides. smooth muscle cells. arteries disease when blood › Beta-adrenoceptors are found › Exercise is recognised as one pressure is well controlled in to be increased in patients of the most reliable life-style › First ever measurement of hypertensive patients. with autonomic neuropathy, methods for lowering blood noradrenaline release from brain correlating with their greater pressure in sedentary people in human subjects. › Introduction of the ACE response to beta-adrenergic inhibitor enalapril to manage stimulation. patients with essential hypertension resistant to standard therapies. Research Partners Research
14 The Burnet Institute /the Austin State and Federal Governments the Baker leads the fight against We are recognised as one of 15
The highly regarded Burnet Locally, we receive strong support heart disease. Cardiovascular the world’s leading medical 2005 Report Annual Institute Research Heart Baker Institute has merged with the from the Victorian Government disease is Australia’s most research centres. Four divisions: Austin Research Institute, and Department of Infrastructure, serious health problem. Over Experimental Cardiology and Heart this merger is bringing the Austin Industry and Regional Development the last decade the prevalence Failure, Atherothrombosis and to the AMREP site. This brings (DIIRD) in the form of vital of cardiovascular disease rose by Vascular, JDRF and Metabolism Annual Report 2005 with it opportunities for greater infrastructure funding to support close to 20 per cent and at a cost and Cardiovascular Neurosciences collaboration, and makes it the Baker’s research profile. At a of more than $7 billion a year, it oversee the work of 26 labs. necessary also for the Baker to federal level, the National Health demands 11 per cent of the nation’s Their work is dedicated to the Baker Heart Research Institute respond to the greater call that and Medical Research Council total health care expenditure. prevention and cure of heart will now be made on jointly provides substantial funding that is disease by concentration on the The major areas of research at the funded core services. crucial to the continuing work of themes outlined above. The work Baker are: our scientists. of these labs and our talented Monash University › The risk factors and prevention scientists is crucially supported The substance of the Baker’s National Heart Foundation (NHF) of heart disease by a series of core services that collaboration with Monash is with The work of the National Heart each play an important part in the the components of the university Foundation intersects with that of › Coronary heart disease, translation of our research from based on AMREP – the Inner the Baker at a number of levels; heart attack and sudden bench top to bedside. the Baker is a member of the The Alfred Hospital and Eastern Medical School and as a provider of research funds, as coronary death Alfred Medical Research and The Baker and The Alfred have the Australian Centre for Blood a collaborator on certain projects, › Heart failure Education Precinct (AMREP) and been integrally linked for 80 years, Diseases. At an institutional level, and as a co-contributor to has advanced relationships with particularly since the establishment the Baker’s formal affiliation with national awareness of risk factors › Diabetes and its complications other AMREP tenants – The Burnet of the Clinical Research Unit in Monash is managed out of its of cardiovascular disease and › Cardiovascular disease and Institute, The Alfred Hospital, 1948 (which became the Alfred Clayton campus. Just over half of preventive health measures. the PhD students being supervised the brain Monash University, The Australian Baker Medical Unit in 1989). Much World Health Organisation at the Baker are enrolled with Centre for Blood Diseases, Nucleus of the research profile of the Baker The Baker is a World Health Monash, and the university Network (a wholly owned Baker has depended on access to clinical Organisation Centre for provides access to academic status subsidiary offering phase 1-4 practice, patient data and human Cardiovascular Research and 4 Divisions, 26 Labs – dedicated to the for Baker research staff. clinical trials), the Centre for Health tissue provided by The Alfred; Training - recognition of its role Care Innovation and The National and The Alfred’s service reputation The University of Melbourne at the forefront of heart disease prevention and cure of heart disease. Trauma Research Institute – as well as a hospital has been built in The Baker benefits from the research, and of its focus on In addition, Baker Clinical weaves together as other academic and research large measure around the university’s willingness to support prevention and cure. institutions outside of AMREP. research strengths of the the institute in its research activity The Juvenile Diabetes the institute’s research pursuits with our These alliances are critical to the Baker, including catheter through student enrolment, Research Foundation Baker’s success: good science does laboratories, heart and lung credentialing of staff, the provision clinical goals, many of which are realised The philanthropic, US-based not thrive in isolation and these transplants, vascular medicine, of core services (such as proteomics JDRF is a major supporter of mutually beneficial relationships biochemistry, endinocrinology through Bio21) and research through our collaboration with research at the Baker, recognised are key to our standing as the and clinical pharmacology. collaboration in general. nation’s premier cardiovascular in the JDRF Diabetes and The Alfred Hospital. research institute. Atherosclerosis Research Trust Metabolism division of the This UK Trust has supported the institute, led by Professor Mark work of Professor David Kaye Cooper. JDRF grants in 2005 The Baker is a member of the Alfred since 2001 under the Wynn exceeded $4 million. Department. The grant honours Medical Research and Education Precinct a distinguished Melbourne-born clinician-scientist, Professor Victor (AMREP) and has advanced relationships Wynn. Since its establishment, the department has conducted with other AMREP tenants research into various aspects of heart failure prevention and cure. Baker The Alfred & Clinical Baker Medical Unit (ABMU)
16 associate director of Baker Clinical Clinical studies in the past have the Alfred and Baker Medical 17
and head of Cardiovascular been strongly focused in large Unit (ABMU), established in 1949, 2005 Report Annual Institute Research Heart Baker The pioneering work of Tony and his team Medicine at The Alfred Hospital, arteries and systolic hypertension represents decades of rewarding Professor Anthony Dart oversees in endothelial function – the lining collaboration between the Baker of researchers from the Baker has added clinical research across all divisions of blood vessels and how they Heart Research Institute and of the Baker. As both a clinical affect blood vessel function and The Alfred Hospital. This partnership, Annual Report 2005 significantly to the way cardiovascular cardiologist and distinguished the regulation of blood pressure. unique in Australian medical disease risk is assessed and how disease researcher, Tony also works in More recently clinical studies have research, plays an important collaboration with the Baker’s been moved more prominently part in securing the Baker’s Baker Heart Research Institute is treated. Experimental Cardiology lab, run into the area of atherosclerosis, position as a world leader in by Xiao-Jun Du. the development of plaques in cardiovascular research. coronary blood vessels. As the head of Baker Clinical, Tony Positioned in The Alfred Hospital’s oversees the direction and function Alfred-Baker collaborative clinical third floor Heart Centre, the ABMU of the Alfred & Baker Medical Unit, studies in large arteries have is the hub of joint research and the hub of collaborative studies made a major contribution to clinical activity between the two between The Alfred and the the fight against cardiovascular institutions. The Alfred is renowned Baker; the Cardiovascular Disease disease. The study of large arteries for its treatment and care of heart Prevention Unit (CVDPU) and the was far from mainstream when disease patients. In turn, the Risk Clinic and Gene Bank. it became Tony’s area of research Baker’s scientists are leaders in focus some 15 years ago. The cardiovascular disease research. pioneering work of Tony and his Their combined force ensures that team of researchers from the Baker Baker research remains directly has added significantly to the relevant - both to disease as it is way cardiovascular disease risk is experienced by those who are sick assessed and how disease and to community needs is treated. and priorities.
In recent years clinical and The vast database of patient The Risk Reduction Clinic focuses experimental research has clinical information held by on the prevention of cardiovascular This partnership, unique in Australian focused more on acute coronary The Alfred is available, with the disease and identifies links syndromes - the causes of acute consent that almost all patients between nutrition, exercise and medical research, plays an important part heart attacks. As time goes on, give, to Baker researchers daily. heart disease. Staff at the Risk this body of work is contributing This network of information allows Reduction Clinic run heart disease in securing the Baker’s position as a world to our understanding of such broad and up-to-date profiles of risk assessments for members of coronary events in a number of patients and disease as well as the community and are involved leader in cardiovascular research. ways. These include establishing the effectiveness of treatments. in research studies. With consent, a methodology for studying acute It is also a resource that allows information gathered in this clinic coronary disease by obtaining scientists to identify suitable is added to samples collected blood samples from the coronary candidates for participation in for The Alfred and Baker Gene circulation in patients, and relating research – from the effect of Bank, an invaluable store of findings to the structure of disease exercise on blood sugar levels genetic samples that can provide plaque. There have also been to the relationship between researchers with a genetic novel findings both in substances depression and cardiovascular “snapshot” of health and disease released by coronary plaques and disease risk. over time. in the structural changes that The ABMU also fulfils a health plaques undergo. Inpatients and outpatients at The promotion and risk assessment Alfred’s Heart Centre are invited to Ongoing research projects role for the Baker, through the participate in ABMU research. Many include an investigation of the Risk Reduction Clinic and take up this option, which gives triggers of symptomatic coronary the Cardiovascular Disease Baker scientists access to the most atherosclerosis while another Prevention Unit. clinically relevant groups for their major area of investigation is studies. State-of-the-art facilities related to understanding the and equipment at the Heart Centre causes of heart rupture, a deadly are used for clinical treatment and complication of heart attack. These for clinical research equally. projects, running across different labs at the Baker with a different clinical and experimental focus in each, all aim to determine how such complications can be predicted and prevented. Experimental Wynn Department Cardiology and Heart of Cardiology Failure Division › David Kaye
18 heart failure – a debilitating, David Kaye’s own research 19
progressive condition in which concentrates on the investigation 2005 Report Annual Institute Research Heart Baker Professor David Kaye the heart muscle deteriorates and of the development and fails to adequately pump blood progression of congestive heart is an associate around the body – can occur in failure, with an emphasis on people who have suffered some designing therapies that are of Annual Report 2005 director of the damage to the heart, commonly direct use in the treatment of Baker and head of after a heart attack. As more this condition. In addition, by people survive heart attack, heart exploring what can be done to Baker Heart Research Institute the Experimental failure is becoming more common. regenerate hearts that have failed, The quality of life of heart failure and specifically how the heart Cardiology and Heart patients is dramatically reduced muscle can be rebuilt to make it and in many cases it leads to function better, David and his team Failure Division. death. It is currently estimated hope to find a way to cure heart to affect 300,000 Australians and failure, not just treat it. up to 30,000 new cases develop In association with the Baker’s each year. John Power, David has developed a non-surgical method for mitral valve repair: For many patients with advanced heart failure, Professor David Kaye is an associate director secondary failure of the mitral valve to function normally results of the Baker and heads the institute’s in a considerable worsening of the disease because of the effect Experimental Cardiology and Heart Failure of mitral regurgitation. When division. He is also head of the institute’s this circumstance arises, the risk of death, hospitalisation and Wynn Department of Metabolic Cardiology, disabling symptoms increases. Unfortunately for these patients, a laboratory within the division, and works the risk of reparative cardiac surgery is too high. as a cardiologist at The Alfred. Having recognised this significant clinical problem, with an unmet need, David and his team developed a novel technique for research across this division The broad work of David’s team The research of this team ranges The following pages will give mitral valve repair which could be aims to find ways of stopping is centred on understanding the from work on the cellular, some details on the work of the performed via catheter, removing the deterioration of heart failure processes of heart failure in order molecular and genetic under- individual labs within this division, the need for open heart surgery. patients through a range of means to identify those who might be pinnings of the progression from and the way their research fits into The first patient implant was - from better understanding the at risk of the condition and to halt initial heart muscle damage to the work of the Baker as a whole. successfully conducted in 2004 cellular mechanisms involved in its progression in those already heart failure, to large animal and the device is now under trial the process of heart failure itself to suffering. In extreme cases, heart studies with immediate clinical internationally. This development developing therapeutic devices to failure patients require heart relevance and the development was nominated as one of ’10 of the improve the health of those living transplants if they are to have any of therapeutic devices to improve best’ Australian medical research with the condition. chance of survival. The cardiac the lives of those living with developments by the federal surgery laboratory works on the condition. Our labs are Government and the National Heart failure is a debilitating, ways of improving the health of studying the mechanics of the Health and Medical Research progressive condition that can people who must undergo surgery heart and heart muscle across Council in 2005. begin as a response to injury of for heart failure and other a range of disciplines. the heart muscle, for example cardiac disease. after heart attack. Heart failure Projects underway include has devastating consequences for studies of the enlarged heart patients, representing a host of (cardiac hypertrophy) - why it is secondary conditions that result beneficial to athletes but a harmful from the failing heart’s inability development in heart failure; the to adequately pump blood around effects of diabetes on the muscle the body. It is the third largest of the heart; the effects of the cause of death among the various hormone relaxin on fibrotic heart forms of cardiovascular disease in tissue and the investigation of Australia, and the major cause of better cardiac surgical techniques. disability in the elderly. Cellular Experimental Biochemistry Cardiology › Elizabeth Woodcock › Xiao-Jun Du
20 associate Professor Elizabeth du’s research group at the Baker The contribution of these new This significant discovery has led to Until now however, the function 21
Woodcock is a Principal Research was established in 1995, when, classes of genetically modified mice ongoing research by Du and his lab of this hormone had only been 2005 Report Annual Institute Research Heart Baker Fellow of the National Health in a first for Australia, he shifted to cardiovascular disease research into ways of eliminating the risk of investigated in relation to the and Medical Research Council his research focus from classical cannot be overstated. Eliminating this complication - understanding reproductive system. Developing and heads the institute’s Cellular models to genetically modified or over expressing a gene in a why ruptures occur in the first a model of mouse without the Biochemistry laboratory. mouse models: animals which mouse and then inducing a range place and which drug treatments relaxin gene, Du discovered its Annual Report 2005 have been genetically altered, of conditions from diabetes to heart might stop them occurring. absence causes a build up of scar Liz is known primarily for studies allowing the close examination attack in the animal allows detailed tissue in the heart, a condition of mechanisms where the heart Another key research area for Du of the effects of specific genes study of the behaviours of that gene known as fibrosis and the hallmark
Baker Heart Research Institute responds to stimulation, and is on the peptide hormone relaxin, in heart disease. Du’s research is and the mechanisms affected by it. of heart disease in humans. how these processes contribute a study that is continuing and pivotal to the work at the Baker: Crossing these animals would also Fibrosis is one of the body’s most to heart disease. In particular this expanding in its collaboration application and discovery in vivo allow for research on gene- basic responses to heart disease laboratory studies mechanisms with the Howard Florey Institute is critical to understanding genetic gene interactions. and greatly contributes to the associated with the regulation in Melbourne. While it has long and molecular mechanisms. decline of heart function. The of intracellular calcium and the Du’s stamp on this field has been associated with reproduction, importance of reducing fibrosis is maintenance of ion channels. been the development of intricate its increase in the female body well documented but as yet there The laboratory is best known research techniques on these in pregnancy allowing the is no effective drug treatment. for defining a new cause of animals. The heart of a mouse enlargement of the uterus and Most recent research has found arrhythmogenesis, leading to is roughly the size of a soybean the safe delivery of a baby, it that treating animals with relaxin sudden cardiac death. Their and weighs about 0.1 gram. appears that relaxin, which breaks for a period as short as two weeks research concentrates on Microsurgery, open chest surgery down collagen in the reproductive significantly reduced their fibrosis. pinpointing the exact mechanisms and other sophisticated procedures system, may also help prevent Plans are now underway for a involved in atrial and ventricular such as heart catheterisation and heart disease. clinical trial. fibrillation, where the heart muscle echocardiography, the estimation cells beat out of synchrony and of the size and shape of the thus the heart is unable to pump heart, are infinitely complicated blood effectively. by the very tininess of the organ. Performing these procedures is an The long term aim is to develop exacting technical process and one treatments for sudden cardiac that Du has pioneered. His is the Associate professor Elizabeth Woodcock death that are well tolerated. Liz’s only group in Australia capable of laboratory is also investigating performing this surgery and one of is a principal fellow of the National novel mechanisms to increase the only a few in the world with such strength of the heart beat. This Health and Medical Research Council expertise. Du is regularly called will improve quality of life for upon to train other scientists and heart failure patients. They are and heads the institute’s Cellular internationally his skills are in also hoping to identify factors that high demand. Biochemistry laboratory. may reduce damage to the heart during a heart attack. Reduction The importance of mice to in damage to the heart will reduce cardiovascular disease research the incidence of heart failure in was also highlighted with the the longer term. discovery in 1997 by Du’s team that the mouse was the only animal model to develop one of the most serious complications known in heart attack: rupture of the Xiao-Jun Du is a medical doctor by ventricular wall. This event almost always leads to sudden death and training and switched his focus from the accounts for 5~25% of total deaths clinic to the laboratory early in his career, during the acute phase. While many other areas of heart disease when he was still living in China. have seen great improvements, this, one of the most malignant complications, has been out of reach of researchers because none of the other species used in heart research develop ruptures after heart attack is induced. Cardiac Cardiac Hypertrophy Surgery › Julie McMullen › Salvatore Pepe
22 this lab focuses on understanding Her research is novel in its this research unit is devoted to 23
heart enlargement, cardiac suggestion that it is possible to improving the condition of patients 2005 Report Annual Institute Research Heart Baker hypertrophy, through comparisons promote and activate “good” before, during and after heart between models of health and genes in the heart as opposed surgery by better understanding disease: examining the enlarged to just inhibiting “bad” genes the biology and metabolism of athletic heart in comparison to that cause the growth of the both the diseased and the Annual Report 2005 heart enlargement associated diseased heart. healthy heart. with disease. Her research involves genetically Based at the Baker, the lab is
Baker Heart Research Institute It is well understood that the modified mouse models of heart closely tied to its clinical research hearts of athletes grow: the failure. By over expressing a gene unit, headed by Professor Franklin super fit have a heart size greater involved in the growth of the Rosenfeldt, a surgeon in the than the average person. This athlete’s heart in a mouse model Department of Cardiothoracic enlargement is of benefit to them with heart failure, Julie hopes to Surgery at The Alfred Hospital. in their training and works to understand whether this gene Although heart surgery is often enable them to continue their level might be of use to patients with undergone in an emergency after a of exercise and fitness. When they heart disease, and whether its sudden heart attack, or in chronic Salvatore Pepe, stop training that healthy heart promotion and growth can negate conditions such as heart failure growth stops and the heart returns the effects of the “bad” when other medical approaches a scientist by to a normal size. Conversely, growth genes. have been exhausted, elective training, heads Julie McMullen trained at the heart failure patients commonly surgery occurs far more frequently In understanding what is making experience heart growth but this when the patient has stabilised the heart pump well in the the Cardiac University of NSW and completed a change is devastating. It wreaks and involves coronary artery athlete’s case, Julie’s research is havoc and is usually impossible bypass grafting, heart valve repair Surgery postdoctoral research fellowship in going a long way towards trying to reverse. or replacement. By its nature the to find a cure for the failing heart. cardiac surgery patient’s profile laboratory. the US at Harvard before joining the From this observation, Julie’s Current therapeutics are largely is one where surgery is a risk and research has focused on treating heart failure-her aim is Baker early in 2005. health is compromised by other understanding the changes in the to help find a cure. symptoms of heart disease or by athlete’s heart that might benefit the advanced age of the patient, people with heart disease, whose with most being over 60 years old. heart growth might be caused by hypertension and/or heart failure. Salvatore’s lab is investigating the molecular deficiencies of the This research group is taking a new Salvatore has been recently funded Julie’s studies demonstrate there human heart that can give rise to approach to tackle post-operative by the National Health and Medical are changes in genes that occur in the metabolic dysfunction that atrial fibrillation by targeting Research Council, starting in 2006, people with cardiac hypertrophy occurs in ischaemic heart disease, before surgery the factors that to conduct a three year clinical associated with heart failure that heart failure and atrial fibrillation. make atrial fibrillation more likely trial to test whether omega-3 fatty do not occur in the athlete’s Atrial fibrillation, where the heart to occur. The lab’s previous work acid pre-treatment of elective heart. She has established that beats irregularly and ineffectively, established that the ageing process cardiac surgery patients can reduce even though there are comparable is one debilitating and expensive creates a deficiency in the capacity the incidence of post-operative increases in heart size, there are complication of surgery being of human heart muscle to recover atrial fibrillation, reduce the clear molecular and histological investigated by this research unit. from the metabolic stress of heart length of hospital stay and other changes between the two. About 30 per cent of patients suffer disease and of surgery itself. This related clinical and molecular Julie is working to identify genes this complication after surgery. is mainly due to deficiencies in complications. Positive results causing heart enlargement that Atrial fibrillation can be treated the heart’s natural antioxidants from this trial will provide an are good for the heart, as opposed but the drugs used have potent and related enzymes. The group inexpensive, drug free approach to to those genes causing heart side effects, are used after the recently demonstrated in a clinical minimising a major complication enlargement with detrimental condition arises, and can often trial of Coenzyme Q10 that it of heart surgery. effects. In doing so she hopes to be ineffective. Consequently, afforded elective cardiac surgery reproduce the work of the “good in-hospital recovery and care patients improved metabolic genes” in the failing heart. is usually greatly extended and benefits and greater tolerance of more expensive. Although atrial stresses imposed by heart surgery. fibrillation is itself not fatal, left untreated it leads to blood clot formation, substantially increasing the risk of serious complications such as stroke and heart failure. Applied Cardiovascular Molecular Research Endocrinology › John Power › Walter Thomas
24 john’s focus is on the develop- John and David’s research uses a 25
ment of novel devices to treat and small device to reduce the size of 2005 Report Annual Institute Research Heart Baker manage the failing heart the valve. The device is inserted Walter Thomas did his PhD in and problems associated with it. through the jugular vein under He runs a large animal facility at local anaesthetic, avoiding the Queensland and postdoctoral training Werribee and conducts need for major surgery in patients Annual Report 2005 studies that are immediately with this condition, most of whom in the US. His research focuses on the clinically applicable. are elderly and for whom general renin angiotensin system. anaesthesia presents a great risk.
Baker Heart Research Institute John’s work translates directly Human trials continue at The into human disease. His research Alfred Hospital and it is hoped the focuses on therapeutic devices to procedure will become available to treat and manage heart failure. the general community within Heart failure, where a weak heart a few years. is unable to pump effectively, creates a syndrome of debilitating This lab regularly conducts conditions, ranging from research for overseas companies arrhythmia to muscle wastage who come to John for his large and weight loss. animal expertise and use of his facility at Werribee where he has walter has worked at the Baker The Molecular Endocrinology team The hormone angiotensin, like Understanding the mechanism Most of the work conducted in developed many models of heart since his return to Australia at the Baker study the regulation hundreds of other hormones in behind how two different families John’s lab goes on to testing in failure, mostly in sheep. Research from the US in 1996. His team of blood pressure by studying our body, cannot work without of receptors can communicate is humans. He is the co-founder, directions in this lab are now of molecular and cell biologists the mechanisms of the renin interacting with its own receptor, the subject of the next phase of with the Baker’s David Kaye, of two focused on the rapidly expanding work exclusively on the G-protein angiotensin system. This is an or “lock”. It is this protein research for this lab, which has start-up companies with therapies areas of gene and cell therapy, coupled family of receptors, acute system, triggered by the receptor that is the main focus of recently secured an NHMRC grant to now in, and close to, clinical trial. and on a holistic approach to specifically, on the renin kidneys, that recognises a sudden research for Walter and his team, investigate this link further. V-Kardia Pty Ltd has patented a heart failure using these new angiotensin system. drop in blood pressure – due to as a means of understanding the revolutionary system that allows Walter and his team hope technologies. There is a strong injury or disease - and adjusts the relationship between other the delivery of drugs directly to Angiotensin is a vital hormone in that better understanding drive to understand better the body’s functions to compensate for G-protein coupled receptors in the heart, with little systemic the body, but an excess of it can the mechanisms of the renin causes of the various devastating it. It does this by releasing into the the body, of which angiotensin circulation of that drug. By lead to high blood pressure and angiotensin system will lead to the symptoms heart failure, such as blood vast amounts of a protein is just one. isolating the coronary circulation heart attack. Research is focused development of better targeted fluid retention, or cardiac cachexia, called renin. The renin attaches from the general circulation, toxic on better understanding how It is known that people with treatments that would allow blood where fat is retained but vital itself to a precursor protein in effects and dangers to other organs angiotensin works, so treatments high blood pressure overproduce pressure regulation but inhibit John Power trained as a vet and muscle is lost. By focusing research the blood, angiotensinogen, of the spread of a drug intended can be found that retain the angiotensin, but drug treatments heart growth or vice versa. This on the underlying hormonal and effectively cuts a bit off it. worked in rural private practice for for the heart are substantially benefits of angiotensin while currently work by blocking would allow heart growth - which mechanisms responsible for This protein is not usually active reduced. V-Kardia has established limiting its production – not the angiotensin receptor and is necessary after heart attack symptoms, John hopes that the but it is converted into an active 17 years before returning to the city a US subsidiary, V-Kardia Inc, to blocking it entirely. inhibiting production of the – but stop the excessive production lack of knowledge about heart hormone – angiotensin - by develop close relationships with hormone. Because it is known that of renin angiotensisn that leads and undertaking a PhD at The Alfred failure can begin to be addressed. coming into contact with renin the renin angiotensin system is an to hypertension. world-leading researchers in the under these extreme conditions. important one, Walter’s team is Hospital. He has worked in heart area of gene therapy for heart This newly activated hormone finding out all they can about this failure, and this company is circulates through the blood at very system. For example, by regulating failure for his entire research career. expanding its collaborations with high levels, constricting the blood blood pressure and constricting groups specialising in gene therapy vessels to slow down blood loss blood vessels, angiotensin causes for other major organs. and at the same time inducing heart growth in the longer term. an extreme thirst and a craving for Cardiac Dimensions Inc represents While that has some benefits, it is salt. In so doing, it is trying to get another significant discovery for detrimental over time. By studying the body to correct the salt and John and David. For many patients what it is about angiotensin that fluid loss caused by the dramatic with advanced heart failure, causes heart growth, Walter’s loss of blood. secondary failure of the mitral team discovered that the hormone valve compounds their illness and didn’t itself directly cause this decline. Mitral valve failure, where growth, but did so by taking a valve does not close properly, over another receptor, called the causes blood to leak during each epidermal growth factor receptor, heartbeat, putting greater pressure a hormone indicated in 25 per cent on the failing heart and further of breast cancer cases. increasing the risk of heart attack. Molecular Atherothrombosis Pharmacology and Vascular Division › Rebecca Ritchie
26 scientist Rebecca Ritchie heads Rebecca’s work in cardiac 27
the Molecular Pharmacology hypertrophy has focused on 2005 Report Annual Institute Research Heart Baker lab, pursuing three main identifying elements within the Professor Karlheinz areas of research: the cellular heart muscle cells themselves mechanisms responsible for cardiac that might prevent this unwanted Peter oversees the hypertrophy, or heart growth growth. Her most recent research Annual Report 2005 associated with disease; heart showed that a different chemical research of seven complications related to diabetes, form of nitric oxide, gas released labs in his role as an and addressing reperfusion injury, by the innermost layer of the blood Baker Heart Research Institute the damage caused to the heart vessel wall, prevents hypertrophy associate director of after a heart attack. by elevating levels of the cyclic GMP chemical within the cells. the Baker and head of Work is building on their discovery Continuing research will look at that elevated levels of a small whether this gas has other effects the Atherothrombosis heart cell chemical called cyclic not related to cyclic GMP which GMP, a natriuretic peptide, will nonetheless protects against and Vascular division. prevent abnormal heart growth. heart failure. It is well known They also have evidence that other that one of the contributing such hormones also increase in factors to hypertrophy and heart The damage to the heart caused Rebecca’s hypothesis is that response to this heart growth or failure is oxidative stress, where by diabetes is often characterised a naturally occurring, anti- cardiac hypertrophy, and work the metabolic balance of a cell is by hypertrophy, myocardial inflammatory protein called to stop it from worsening or disrupted and there is an increase fibrosis (stiffening) and impaired annexin-1 improves how the progressing to heart failure. in the body of harmful free pumping. Furthermore, diabetics heart recovers from a heart radicals. The powerful antioxidant with heart complications fare attack. She believes that it may action of this gas, occurring worse than non-diabetics with reduce the accumulation of naturally where there is injury comparable cardiovascular inflammatory white blood cells to the heart, will be the focus of disease. Work conducted in this and also maintain the viability further study and has implications lab suggests that free radicals and pumping action of the heart for the development of drugs play an important role and their muscle following the event. Her that promote the production and presence has implications for the research involves administering release of these natriuretic most appropriate way to treat heart annexin-1 to mice and rats in peptide hormones. disease specifically in diabetes. The which heart attack has been changes in structure and function induced. Mouse models lacking occurring in the hearts of rats with annexin-1 are also studied for Scientist Rebecca Ritchie heads the diabetes have been characterised comparison, and in an effort to Molecular Pharmacology lab pursuing and their research has shown that isolate its function. Understanding heart attack is a sudden The Atherothrombosis and Vascular This division hopes to address Karlheinz’s division, like all both the levels of free radicals the protective role played by catastrophic event in the lives of division comprises a diverse range these public health concerns from divisions of the Baker, is highly three main areas of research and the enzymes that generate annexin-1 opens exciting new many people in our community. of labs with research interests that a number of angles, including collaborative. The overall aim them are increased in rats and possibilities for reducing long-term The direct cost of coronary heart are addressing these problems working towards the design of a of prevention and cure of mice with both type 1 and type 2 damage from human heart attack. disease in Australia is the largest in a range of ways: from the new class of “intelligent “ drugs. cardiovascular disease is realised diabetes. Studies are now focusing of any single cardiovascular investigation of those cells that These will prevent clotting, or by overlapping research that is on whether boosting the genes condition, at $1.76 billion, or 28.6 play an important role in plaque dissolve clots that have caused a molecular, cellular, physiological thought to reduce the production per cent, of all costs associated development to the study of heart attack or stroke without the and highly translational – research and numbers of free radicals in the with heart disease. Stroke is the nutritional approaches that might excessive bleeding complications that has a strong clinical focus. body will improve the health of second largest at $1.08 billion, prevent atherosclerosis and even that are a feature of currently The following pages give more diabetics with these complications. or 16.5 per cent. It is the single the prevention and reversal of available drugs. The division is also detail on the research focus of most common cause of death in cholesterol accumulation in working towards the identification labs within this division. Reperfusion injury can occur after a Australia and is most commonly blood vessels. of biomarkers (such as elevated heart attack. Reduced blood supply manifest as angina, heart attack levels of certain proteins in the to the heart, known as myocardial or sudden death. For a growing blood) which, when added to ischaemia, can lead to heart attack number of elderly Australians, existing knowledge of family during which cells can die. But atherosclerosis, the development history and lifestyle risk, help the damage does not always stop of plaques, fatty deposits in predict coronary plaque rupture. with a return of blood flow: in blood vessel walls, and its fact the death of cells can create complications – such as coronary its own havoc, releasing their own heart disease and stroke – will “nasties”, and restoring blood be the major health care problem flow – reperfusion – can cause in terms of mortality, reduction additional damage. in quality of life, and cost to the public health system. Thrombosis & Cell Myocardial Infarction Biology › Karlheinz Peter › Alex Bobik
28 Using basic molecular biology The lab’s other main area of this lab pursues two main Other cell types are also being 29
techniques, Karlheinz’s lab is research looks into inflammation areas of research: (1) cellular studied, in particular cells that 2005 Report Annual Institute Research Heart Baker studying how platelets responsible mechanisms. Inflammation is and molecular mechanisms that cause inflammation and promote for blood clots that lead to recognised as a major driving promote atherosclerosis (inflamed the development of atherosclerotic heart attack and stroke can be force of atherosclerosis, the fatty lesions that develop in blood lesions that are rich in fat and inhibited without causing the accumulation of fatty deposits, vessels and cause strokes and heart low in collagen. These lesions are Annual Report 2005 potentially fatal side effect of plaques, in blood vessels. Rupture attacks), and (2) mechanisms that weak and highly susceptible to excessive bleeding. Current of these plaques can cause lead to development of cardiac rupture, which can cause a blood therapies used for treatment in heart attack and stroke and it is fibrosis (where excessive collagen clot and lead to strokes and heart Baker Heart Research Institute myocardial infarction (heart attack) understood that inflammation stiffens the heart muscle and attacks. These include immune and stroke are very aggressive is the process that drives this impedes electrical conduction cells called natural killer T cells and are themselves responsible rupture. Inflammatory cells in the leading frequently to sudden (NKT) cells. Alex and his team have for disability and even death. blood such as neutrophils and death) and (3) understanding how shown that a specific type of NKT One group of drugs now in use monocytes are being investigated bone marrow-derived stem cells cell, which can be identified by prevent the coagulation function for clues that might lead to a can be used to repair the heart expression of the marker CD4, of platelets so they cannot form better understanding of their role after damage from a heart attack. promotes development of these a network – a clot – by stopping in plaque rupture. The ability to lesions. Research is continuing into During 2005 Alex was able to them from binding to certain inhibit inflammation in these how they do this. Other studies on show that a specific cell type the development of “intelligent plasma molecules. It is this plaques offers an opportunity atherosclerosis focus on proteins of the immune system called a Studies on the role of bone marrow Another area of study is the drugs”, drugs that can target and binding function that creates to prevent heart attack. Peter’s that are secreted by macrophages, regulatory T cell is important in derived cells in healing the heart possibility of using genetically dissolve blood clots but do not the network. Activated platelets team is looking into how these cells in the body’s circulation that controlling the development of after a heart attack have shown modified bone marrow stem cells carry the devastating side effect of attach to fibrinogen, a plasma inflammatory cells are activated. accumulate in lesions and take atherosclerosis. These cells, which that a substance which Alex’s lab to attract heart stem cells into uncontrolled bleeding is a major protein, causing a blockage They have developed an antibody up fats. One such protein called can be identified by the expression has shown improves healing, called damaged regions of the heart to research focus. that leads to heart attack and that recognises this monocyte high mobility group box protein-1 of specific markers on their cell granulocyte-colony stimulating further improve cardiac repair. stroke. This relationship forms activation and this is now being appears to be a potent stimulator The work of Karlheinz and his team surface called CD4 and CD25, were factor (G-CSF), increases the the basic architecture of a blood used as a tool to understand of atherosclerosis. of researchers can be broadly shown to reduce the development number of blood vessels in the clot and treatment inhibits the inflammatory stimuli and how divided into two areas: thrombosis of atherosclerosis in genetically Studies on cardiac fibrosis have led damaged region. It does this by binding function of the fibrinogen these might regulate the activation – the blood clots that are a cause modified mice. When these to the identification of unexpected stimulating the production of molecule, inactivating the of cells such as monocytes. of heart attack and stroke, cells are removed mice develop mechanisms that promote fibrosis. growth factor systems that promote coagulation function of platelets. and inflammation. The long term goal of this lab is more severe atherosclerosis. When the heart has to pump the development and growth of But in so doing the treatment to develop an anti-inflammatory These studies have important against high pressure, such as in new blood vessels. These include blocks every available platelet, drug better than ones currently implications for the treatment hypertension, the heart muscle vascular endothelial cell growth of which there are hundreds of available, for example those used of atherosclerosis and have the produces proteins that attract factor-A, placental growth factor Professor Karlheinz Peter, an associate billions in the blood of a single to treat rheumatoid arthritis, potential to be used in conjunction specific bone marrow derived cells and thymidine phosphorylase. patient, causing the excessive director of the Baker and head of the as they have been linked to an with other therapies to prevent from the circulation. Alex and his This lab is currently studying bleeding that is itself increased risk of heart attack. development of severe lesions. team have identified two such bone marrow-derived cells that a complication. Atherothrombosis and Vascular division, This is currently being studied. proteins called secondary lymphoid invade the damaged region and leads research in the Thrombosis and Karlheinz’s studies are working on chemokine and monocyte their contribution to development the development of “intelligent chemotactic protein-1. These of new blood vessels are Myocardial Infarction laboratory. drugs”; drugs that will block attract several circulating cell types producing these. only activated platelets - the into regions of developing fibrosis He is a practising internationally ones involved in clot formation. including lymphocytes that express Professor Alex Bobik heads the Cell Laboratory research conducted to the marker CD4, macrophages, recognised cardiologist familiar with both date shows a reduction in overall and an as yet unidentified cell Biology Laboratory in the Baker’s bleeding time while clot formation that produces large amounts molecular research and acute clinical at the site of injury is allowed to of collagen. Current studies are Atherothrombosis and Vascular division. cardiology practice. occur. Another research avenue focused on depleting these cell being investigated is concentrating types in mice and examining how on techniques that will make use this affects the development of of activated platelets by allowing fibrosis and proteins that regulate them to enrich the action of drugs collagen production, in particular at the site of the blood clot. transforming growth factor-beta The lab has developed an antibody and interleukin-10. molecule that recognises only activated platelets and can be fused to different products, for example a clot-dissolving drug, so its action is enriched at the site and does not circulate through the blood. Clinical Vascular Physiology Pharmacology › Bronwyn Kingwell › Jaye Chin-Dusting
30 The difficulty with this type of of the pain associated with From this starting point, the 31
plaque growth is that standard physical activity. This lab tested Vascular Pharmacology team have 2005 Report Annual Institute Research Heart Baker diagnostic techniques – the use the effects of an Angiotensin- investigated cellular mechanisms of an angiogram, where dye is Converting Enzyme (ACE) inhibitor in a range of cardiovascular released into the middle of an drug on patients with PVD. This diseases. It was the work of this artery to identify problems – are group of drugs is commonly used lab that established a new form Annual Report 2005 not effective because the artery to treat other forms of heart of treatment for people with looks clear. The introduction of disease, but has never before been cirrhosis, or scarring, of the liver. intravascular ultrasound has made examined in relation to symptoms The observation that cirrhotic Baker Heart Research Institute diagnosis of this type of plaque of this leg disease. Results in this jaye Chin-Dusting came to the patients have exactly the opposite possible by examining the blood relatively small but groundbreaking Baker as a postdoctoral scholar physiological profile to patients vessel wall and it’s a technique study have been startling: 20 in 1990. Since then, the Vascular with CVD, for example low blood used in the research conducted patients in the study taking the ACE Pharmacology lab conducts pressure as opposed to high was in this lab. inhibitor increased their walking experimental drug studies in taken further by Jaye and her distance by as much as 200 per animal models of disease and team. While this opposite profile Predicting the stability of coronary cent over 24 weeks: this group translates them directly into work had been noted, Jaye’s lab was plaques is a major research interest doubled their treadmill walking in human blood vessels, tissue the first to look at the role of nitric of Bronwyn’s team. Understanding time, from 300 to 600 seconds. and cells. oxide in these two patient groups, why some people have unstable The 20 patients in the other half and whether there was an over- Postdoctoral researcher Kevin during endothelial cell damage. plaques and others do not will They study the relationship of the study took the placebo production of nitric oxide in the Woollard has been working These proteins, only expressed in go a long way towards preventing between blood vessels and research in this lab is focused on It is understood that most people drug and no change was evident cirrhotic patients responsible with the lab on the effect of the cell injury, are of interest because heart attacks. Looking at what the cardiovascular disease, in two main areas: coronary plaque have plaques in these arteries by a in the distance they could walk for the low blood pressure and endothelium on the blood, a their presence in the blood at high plaque releases into the blood particular the innermost layer of stability (in collaboration with certain age, but in roughly half of without pain. This study has major other complications. new direction for Jaye’s team. levels is understood to be a marker might hold clues as to why some blood vessels, known as Dr Stephen Duffy and Professor that group the plaques don’t cause implications for the treatment of While previously work has been of disease. Kevin and the Vascular plaques rupture. the endothelium. They hypothesised that the scarring Anthony Dart) and diabetes. Work any problems – they are stable. For patients with PVD and by providing focused on the influence of Pharmacology lab are particularly is largely driven by the goals of the other half though, those with of the liver in cirrhotic patients Using intravascular ultrasound them with a treatment that makes Jaye and her team of researchers the endothelium on muscle interested in the protein selectin, better management of existing unstable disease, plaques rupture, interfered with the process of techniques, researchers have it easier for them to exercise, have significantly built on the constrictions and dilations, and research is focusing on the disease and the development of exposing the soft substance within blood cleansing that occurs in identified plaques in patients their own ability to manage their discovery more than 25 years research is now turning to the discovery that selectin is not better predictive tools against it. it to the blood flowing through the the portal system, where blood and collected blood samples disease is dramatically improved. ago that the endothelium – the release of nitric oxide into the merely an inactive biomarker but artery. Once there, this substance is transferred from the gut to the The formation of plaques, from either side of the deposit. This work was recently published in innermost layer of the blood blood. When the endothelium a significant contributor to disease forms a clot, also known as a liver. Cirrhosis congested this flow known as atherosclerosis, inside A recently completed three-year the high impact medical journal, vessels, separating the blood from is damaged blood cells start to in its own right and as such, drug thrombus. That clot can block off and new blood vessels formed to the heart’s blood vessels is a study, collecting blood samples Annals of Internal Medicine. the muscle - was not a passive stick together forming plaques. treatments for disease indicated by the whole blood vessel, causing compensate, allowing the transfer major contributor to heart attack. from about 200 patients, has barrier as it had been assumed Kevin’s research is looking at the its presence can focus on switching a heart attack by stopping blood Exercise is also a key factor in of blood from the gut directly Plaques, essentially small fatty shown that people with a but in fact a very active structure production of “sticky” proteins off the effects of this protein. supply to some of the heart the prevention and management into the systemic circulation, deposits, are characterised by a particular genetic version of in its own right. The discovery muscle. Some plaques, however, of diabetes; another of this bypassing an important cleansing thick, fibrous layer, like a scab, an enzyme in the blood seem that nitric oxide was released grow outside of the blood vessel. group’s major research interests. process. In patients with alcohol- containing a soft, semi-liquid core. to be more susceptible to by the endothelium, expanding While this type of plaque doesn’t Bronwyn’s team has been trying induced cirrhosis, diet is often plaque rupture. In a recently blood vessels, during activity was Jaye came to the Baker as a obstruct blood flow it is prone to understand what it is about poor, resulting in an increase in submitted paper, Bronwyn and significant. During exercise the to rupture causing a sudden exercise that helps to prevent bacteria levels in the gut that in her research team argue this heart needs more oxygen and postdoctoral scholar in 1990. Since then, heart attack. diabetes and why exercise is turn compounds the effects of enzyme is associated with positive pumps harder. As a result the critical to managing the illness. liver dysfunction. The Vascular remodelling – where the plaque blood flows harder and the sheer the Vascular Pharmacology lab has Understanding that exercise serves Pharmacology team surmised that grows outside the blood vessel stress of movement along the the same function as insulin the high level of endotoxins in this conducted experimental drug studies in A physiologist by training, associate wall – and increases the patient’s endothelium triggers this release – that is, to move glucose from group – toxins released from cells susceptibility to unstable disease, of nitric oxide. This release of professor Bronwyn Kingwell is head of the the bloodstream into the muscles - was responsible for the copious animal models of disease and translates or sudden heart attack. This nitric oxide expands the muscles that need it – was the platform release of nitric oxide, as these finding will significantly contribute allowing more oxygen to go to the Baker’s clinical physiology lab. In 2005 she for the identification of some of toxins switched on an enzyme them directly into work in human blood to heart attack risk prediction. heart as is needed. When there is was president of the Australian Society of the molecules in muscle that, disease, however – hypertension, triggering the inappropriate vessels, tissue and cells. Another significant research activated by exercise, coax the diabetes, heart failure – there is production of this gas in cirrhotic Medical Research, spearheading advocacy study has focused on patients glucose from the blood to that impairment of the endothelium patients. To test their hypothesis, with peripheral vascular disease muscle. This team is continuing and the release of nitric oxide is they recruited a group of cirrhotic for research support nationally. (PVD). This group suffers from its important work on identifying impaired. Without its release there patients and treated them with the formation of these plaques the exact effects of exercise on the is not the necessary dilation and an antibiotic, to great effect. – atherosclerosis – in the top body because doing so will enable sometimes there is a restriction The successful outcomes for liver of their legs. A symptom of this the development of drugs that can of the vessel, causing angina. The patients with a treatment model disease is great pain on walking, activate the molecules stimulated lack of nitric oxide can limit the developed at a cardiovascular essentially angina of the leg. Drug by physical activity and replicate carriage of oxygen to the heart, institute is a prime example of treatments, such as anti-platelet their beneficial effects in people resulting in heart damage. how the work of Baker researchers therapy to stop the blood clotting, who can’t, or won’t exercise. feeds into the improvement of are available but not very effective. health in the community on One of the best treatments is many different levels. exercise but getting this group to exercise is difficult because Cell Biology Lipoproteins & & Diabetes Atherosclerosis › Peter Little › Dmitri Sviridov
32 research in this lab is focused The development of atherosclerosis Statins are possibly the most One of the lab’s most significant 33
on better understanding the is accelerated in people with successful drug in the history of ongoing projects is concerned with 2005 Report Annual Institute Research Heart Baker causes of atherosclerosis, the diabetes, who often suffer medicine. They have been a very the development of atherosclerosis build up of fatty plaques in blood from high blood pressure and effective therapy in the reduction in HIV patients. While people with vessels, particularly in people other complications as well of blood cholesterol levels and HIV are living longer with better with diabetes. Little’s lab is as high glucose levels. As the are generally prescribed to people drug treatments, heart disease Annual Report 2005 working towards the development incidence of diabetes continues with high cholesterol levels that is a major complication. Other of a drug that can prevent the its alarming rise, complications put them at risk of heart attack. research has established that they formation of atherosclerotic such as cardiovascular disease are They are also prescribed to people have anywhere from three to 100 Baker Heart Research Institute plaques by preventing changes in becoming more commonplace. who have suffered a heart attack, times greater risk of cardiovascular proteoglycans, protein molecules as a way of preventing a second disease than the rest of The Cell Biology and Diabetes that exist in the blood vessel wall. event. The combination of this the community. laboratory focuses on basic drug and better diet has greatly The major cause of premature research into the causes of Dmitri’s group has discovered that improved life expectancy in death in people in Western and atherosclerosis, and is contributing in HIV patients there is a severe developed nations, and decreased now developing societies is the to existing hypotheses for how this disregulation of the pathways the incidence of heart disease by formation of atherosclerotic process occurs. One theory most that remove cholesterol. His as much as 40 per cent. But for plaques in blood vessels. The relevant to Peter’s work is called pioneering work has found that it the 60 per cent whose lives are rupture of those plaques causes a response to retention, and suggests is most likely HIV itself, and not its The key element of the formation not saved by statins and dietary heart attack if they are in the heart that while lipoproteins – balls of lipoproteins are responsible for treatment, that is responsible for of an atherosclerotic block is modification, the work by Dmitri Professor Peter Little is head of the Cell or a stroke if the rupture is in the fat in the blood also known as the accumulation of cholesterol in this imbalance. When combined change in the metabolism of and his team is crucial. brain. Commonly prescribed drugs lipids – would usually pass straight blood. This accumulation causes with HIV drugs which increase the cholesterol, which is the main area Biology and Diabetes laboratory in the to prevent this process lower blood through a healthy blood vessel fatty deposits in the blood vessel The Lipoproteins and delivery of cholesterol and impair of investigation for this laboratory. Atherosclerosis and Vascular division. pressure or lower cholesterol levels, wall, under some circumstances wall, known as atherosclerotic Atherosclerosis lab is focusing the mechanism in the body that but research has shown that these the blood vessels become plaques. This lab investigates the Cholesterol is moved around in on the pathway within the removes it, the development of He is also president of Diabetes Australia drugs are not entirely effective and sticky and that lipid gets stuck. metabolism of cholesterol and the blood with lipoproteins. An body responsible for removing atherosclerosis is dangerously a significant amount of disease Molecules called proteoglycans the mechanisms responsible for imbalance of elements in the cholesterol from the blood vessel accelerated. Work is continuing to occurs despite the use are responsible for the stickiness. its accumulation. blood inhibits the transfer of wall, known as reverse cholesterol establish the independent roles of of medication. These molecules contain long Lipoproteins and atherosclerosis cholesterol through the blood transport. Research is focused on both HIV and its treatments in this sugar chains that are negatively form the basis of one of the oldest vessel wall to the liver, the only the balance between the delivery process with the aim of developing charged, while the lipid is research areas at the Baker. For part of the body with the ability to of cholesterol to blood and its drugs that can compensate for positively charged, and as a result the last four years Dmitri has led break down cholesterol. removal. Dmitri’s work aims to these effects. they stick together. Research in this research. Atherosclerosis, the combine current therapies with the Peter’s lab has added to growing development of fatty plaques manipulation of this cholesterol evidence that the stickiness of in the blood vessel wall is the delivery pathway: allowing less blood vessels is caused by changes direct cause of about half of all cholesterol to pass through the in proteoglycans and is the cardiovascular diseases and as such liver while boosting its removal. initiating step in atherosclerosis. is probably the major single cause Reverse cholesterol transport depends on two processes, both Work in 2005 continued on of death in humans. of which are examined by this understanding the synthesis lab: the ability of cells to remove and structure of proteoglycans, cholesterol from themselves, studying the factors that make Dr Dmitri Sviridov trained as a and the tendency of plasma to these molecules stickier and the accept cholesterol from the cells. processes by which they might doctor in Russia and now heads one The balance between these two be able to be prevented from mechanisms is what essentially becoming sticky at all – with a of the longest established research determines healthy or unhealthy view to stopping atherosclerosis. areas at the Baker, the Lipoproteins blood cholesterol. So far Peter and his team have discovered a new area of signalling and Atherosclerosis laboratory. molecules and last year completed a study in atherosclerotic mice, giving them a specially designed drug which stopped changes occurring in proteoglycans. They found a statistically significant reduction in the degree of atherosclerosis in those animals. Patents are in place and research is continuing on the development of this drug. Human JDRF Diabetes Vascular Biology and Metabolism › Stephen Duffy Division
34 Traditionally, risk is predicted It is thought high iron levels might 35
by family history, lifestyle and be implicated in heart disease 2005 Report Annual Institute Research Heart Baker whether there are other known because of iron’s ability to increase Baker Heart risk factors present. These include oxidative stress and free radical diabetes, high cholesterol and high production. Oxidative stress is in Research Institute blood pressure; but the process of turn linked to atherosclerosis. Annual Report 2005 assessing the stability of plaques associate director This lab hopes to investigate themselves is very invasive and the role iron stores play in the and professor Mark expensive and not an option on a
Baker Heart Research Institute development of heart disease and broader community scale. whether decreasing iron levels in Cooper heads the This group is working on the vital certain patient groups could reduce JDRF Diabetes and and rapidly expanding area of their risk of heart disease. biomarkers, identifying measurable Stephen is also involved in a Metabolism Division, and reliable physiological changes long-term collaborative project that can predict plaque rupture. the leading research looking at cardiac patient health They are investigating new markers after successful intervention of unstable disease by studying group of its kind in and discharge from hospital. protein molecules that are released one area of focus for Stephen’s lab At present there are very few by plaques into the blood. To Australia and one of is the better prediction of unstable long-term follow up studies on date increased levels of MMP-3 coronary disease - the rupture of patient health after a coronary the most prominent and MMP-9 have been associated coronary plaques, a major cause of event. Stephen’s work as part with unstable disease. MMPs are heart attack and stroke. Plaques, of the Melbourne Intervention in the world. of broad interest because they are essentially fatty deposits in the Group, a collaboration between 12 known to have the ability to break coronary arteries, can be stable hospitals in the Victorian public down the blood vessel wall and and as such not cause problems and private health systems, will might be a mechanism by which but their rupture can cause blood go towards establishing a large the fibrous cap of the plaque is clots. This can lead to heart attack clinical database that will be able broken down. But they are only and stroke. to track the efficacy of existing and one example of investigation into new cardiovascular procedures by biomarkers. It is believed there monitoring the health of patients are dozens of other proteins in after discharge. So far the registry the blood, the elevated levels of contains more than 3000 patients which might even be masked by eligible for follow-up. the presence of other proteins. Stephen Duffy heads the Human Advancing techniques to isolate diabetes is a serious public health The main aim of this division is to The current focus of this division His work on the combination of these proteins is another area of issue and the dramatic rise of understand why people develop is the development of new ACE inhibitors and A2 antagonists Vascular Biology research unit at the interest to the lab, as they could diabetes in the community is a complications from diabetes, a techniques for early diagnosis of for use in the treatment of diabetic hold a significant contribution to major concern. The complications high blood glucose level, and the complications, primarily gene and kidney disease has seen this Baker. He divides his time between the better prediction of disease. of diabetes include kidney disease, mechanisms responsible for those proteomic approaches to diagnosis. therapy become widespread and eye disease and vascular disease. complications. Research feeds is reducing the risk of end-stage Stephen’s position as a cardiologist Mark himself has received many cardiovascular disease research and Diabetes is a major factor in directly into the development renal failure. gives the research conducted in awards and is an eminent cardiovascular disease and the of new treatments to target and this lab a significant edge. Access researcher in the field of diabetes Mark’s group derives funding seeing patients at The Alfred, where he most common cause of kidney prevent the development of to heart disease patients at The and its complications. His work from the New York-based Juvenile failure in the western world. diabetes-related disease. Mark’s works as a clinical cardiologist. Alfred ensures a wide and clinically has profoundly improved our Diabetes Research Foundation as group has recently secured a relevant range of blood samples are understanding of this disease well as from NHMRC grants. multi-million dollar grant from collected, studied and compared. and has been of direct benefit to the prestigious US-based National millions of sufferers around the A controversial area, of interest to Institutes for Health to explore the world. His distinguished body of Stephen’s team, is the effect of causes of glycation - a biochemical research has led to new treatments iron in blood vessels. Iron is a vital process brought on by an excess of for sufferers of diabetes that are component of blood and it has sugar – and atherosclerosis in Type today considered standard. He been noted that the iron stores of 1 diabetes. was involved in very early studies people at risk of heart disease are using Angiotensin-Converting higher than average. Enzyme (ACE) inhibitors in diabetic complications, now a routine treatment, and was also involved in the original description of microalbuminuria, now used as a tool in predicting diabetic complications. Oxidative Human Stress Epigenetics › Judy de Haan › Assam El-Osta
36 oxidative stress has been Beginning her studies by this lab is working hard to In 2005 Sam and his team 37
linked to atherosclerosis, the examining the presence of certain understand the behaviour and generated a great deal of 2005 Report Annual Institute Research Heart Baker Judy de Haan, an expert in the harmful accumulation of fatty deposits enzymes in the normal ageing “misbehaviour” of genes in interest among the international in the lining of blood vessels. process, Judy’s research team disease, with a particular focus scientific community with their effects of oxidative stress on the body, This group is investigating the developed a mouse model lacking on diabetes, cancer and discovery, which was highlighted genetic component of oxidative an important antioxidant enzyme, chromosomal disorders such as on the cover of the prestigious Annual Report 2005 originally trained in South Africa and then stress in atherosclerosis and one that is usually present to Fragile X syndrome. scientific journal Nature Genetics, in diabetes. They are working remove an excess of free radicals. of a master regulator, a class completed her PhD at Monash University. Epigenetics is the study of on the development of dietary Experiments showed that these of molecules that control the
Baker Heart Research Institute reversible changes in gene interventions or drug compounds mice could function quite normally “switching on” or “switching She has been with the Baker since 2003. function, changes that occur to increase the activity of until they were stressed in some off” of genes. His discovery without any mutation in the antioxidant enzymes, reducing the way. From there studies moved has significantly increased our sequence of the DNA itself. effects of atherosclerosis. on to trying to better understand understanding of the way that Epigenetics concerns itself the link between oxidative stress, genes are controlled and may Judy started her research in with trying to understand how injury and disease. represent. This may be a critical the area of oxidative stress and information that regulates gene link between the environment Down Syndrome. Oxidative stress For the last five years Judy behaviour but that is not expressed and whether a cell faithfully describes a state characterised by has focused exclusively on in DNA sequences can be passed on produces the proteins programmed an excess of unstable elements, atherosclerosis, both within and from one generation to the next. by its genes. By uncovering known as free radicals, in the outside the setting of diabetes, Most of the diseases we seek to how genes are manipulated in body. Free radicals can be and the role that oxidative stress Assam El-Osta is head of the Human prevent and cure at the Baker have this way, researchers have a better overproduced as a result of plays in the development of both genetic and environmental chance of preventing genetic exposure to some environmental atherosclerotic disease. Oxidative Epigenetics laboratory within the JDRF causes. Understanding their diseases or, when they haven’t toxins and are believed to be stress is understood to play an interaction is a key step in Diabetes and Metabolism division. been prevented, designing involved in the premature ageing important role in atherosclerosis. developing our research. better treatments. of organs and in cellular damage. Increased glucose levels in Sam and his team focus on Sam’s research has uncovered very diabetic patients predispose understanding why genes are distinct patterns in the way these them to oxidative stress and “switched on” or “switched off” genes “misbehave”, regardless diabetics are at a far greater risk in certain diseases. His research of the disease being studied. He of developing atherosclerosis. in this area began with looking has focused his work on the need Judy’s work is now focused on the at what happens to genes in to understand why the gene is relationship between the two, cancer, particularly the behaviour switched off. By understanding the using the mouse models already of genes in people who suffer modus operandi of, for example, developed. Studying atherosclerotic from drug resistance. Resistance the Fragile X gene “silencing”, or diabetic mice that are missing the to chemotherapy drugs, which “switch off” mechanism, in the antioxidant enzyme, which would is often part of a multi-drug future we may be able to interrupt otherwise mop up the free radicals, resistance, is a serious problem that mechanism and reactivate this lab is investigating whether for cancer patients. Understanding that gene, and genes in other there are increased components of the way genes act in this condition devastating diseases. atherosclerosis in these animals, may help researchers find a way increased lesions, for example. of developing treatments and therapies that are more effective. This study has established the But more than that, the framework for the next important findings can lead to a better phase of Judy’s research: the understanding of gene behaviour effects in mice carrying an over in other diseases. expression of the antioxidant enzyme – more than would normally be present – and whether that reduces the effects of diabetic atherosclerosis. From there, this lab will look into the development of drugs that can mimic the effects of these antioxidants, as well as dietary supplements that can boost their presence thereby reducing atherosclerosis. Biochemistry of Kidney Disease in Diabetic Complications Diabetic Complications › Merlin Thomas › Karin Jandeleit-Dahm
38 karin’s lab primarily focuses By using drugs to inhibit AGEs, 39
on the link between kidney and kidney damage and atherosclerosis 2005 Report Annual Institute Research Heart Baker Associate professor Merlin Thomas cardiovascular disease, particularly might be controlled. The Kidney in people with diabetes. Research Disease in Diabetic Complications heads the Biochemistry of Diabetic extends to the relationship lab is investigating the effectiveness between diabetes, kidney disease of existing and novel drugs to Annual Report 2005 Complications lab. and atherosclerosis, and finding investigate the cardio-renal ways to predict the development protection of these interventions. of these diseases in those at risk.
Baker Heart Research Institute Another area of this research is People with kidney disease have focusing on why some people a higher risk of cardiovascular with diabetes are more likely to disease, and kidney disease is a develop complications than others. major risk factor of diabetes. Using the same screening process The kidney is a very vascular and group of patients, attempts organ and findings in disease are being made to understand there translate into cardiovascular what genetic or other factors in disease. In this way the work of the blood might protect against Karin and her team is of benefit diabetic complications. Identifying the growing epidemic of diabetes His research has concentrated on For Merlin, the best way of This group is also coordinating the both to understanding kidney markers of resistance to disease already affects over 1.3 million Advanced Glycation End-products reducing the impact of diabetes NEFRON study, the largest study of Dr Karin Jandeleit-Dahm is a disease but also more broadly in those at risk will allow early, Australians and twice that number (AGEs), formed when sugars bind is to break the link between high patients with type 2 diabetes across to the prevention and cure of preventative treatment. This is a again is at risk of developing to protein, making it sticky, sweet sugar levels and the damage they Australia. NEFRON is a collaborative nephrologist, currently working cardiovascular disease. major driver of research, which diabetes in the next 5–10 years. and brown. In food like chocolate cause because even with the best effort of the Baker Heart Research aims to ward off disease altogether Despite the clear and present and caramel, this reaction is treatment, patients can suffer from Institute, Kidney Health Australia with patients at The Alfred Advanced glycation end products by stopping the accumulation of danger of diabetes, the role of high appetizing. But when sugar kidney failure, amputations and and Servier Australia, that aims to (AGEs) are formed in diabetes at AGEs or halt its progression before sugars in causing blindness, kidney accumulates in diabetes, this same blindness from their diabetes. define the prevalence and severity Hospital. As a researcher she heads a very high rate and are believed damage is irreversible. failure and heart disease is poorly process contributes to blindness, AGEs are one of those links. For of complications of diabetes in the Kidney Disease in Diabetic to be responsible for irreversible understood. Merlin is working on kidney failure and heart disease. the millions with diabetes who Australian general practice. Already damage to the kidney and to the breaking the links between sugar Merlin’s research has shown that struggle to control their sugars this study has been able to show Complications laboratory. cardiovascular system. Karin’s and the damage it causes. this reaction leads to changes in every day, an understanding of this that every second individual lab has studied these substances the shape and function of AGE- pathway will provide an important with type 2 diabetes in Australian and found that they play an modified proteins. In the same advance to their care. currently has chronic kidney important role in the development way that lamb is more tender than disease, with clear potential to of atherosclerosis as well as the Another key focus of the mutton, AGE-modified proteins influence their health and well development of kidney disease. Biochemistry of Diabetic tend to be inelastic. being, as well as contribute to Complications lab is the renin Work in 2005 focused on measuring This means that AGEs gradually premature mortality. angiotensin system (RAS), a pivotal AGEs and markers of inflammation build up in tissues, making element of vascular function in and oxidative stress in diabetic them in turn more stiff; literally both health and disease. Many patients and comparing those ‘hardening’ the arteries. Where the patients with diabetes are already levels to control subjects (people sugar concentration is high, AGEs taking drugs that block the RAS, who do not have diabetes) to see accumulate much more quickly. in an attempt to prevent some if AGE levels or other markers can This is one reason why strong sugar of the complications of diabetes. be used as a predictor or marker of control is so important in diabetes. However, these agents are only cardiovascular disease in diabetic partly effective. Merlin and his patients. So far, about 150 diabetic team are working to define novel patients have been screened. regulators of the RAS, using unique methods to disrupt the RAS, with the aim of making current interventions for diabetes even more effective. Advanced Glycation Genomics of in Diabetic Complications Diabetic Complications › Josephine Forbes › Phillip Kantharidis
40 research in this lab focuses One of the major research 41
on kidney disease in diabetes, interests of this group is to 2005 Report Annual Institute Research Heart Baker specifically, the effects of advanced better understand how advanced Dr Phillip Kantharidis has a PhD in glycation on the diabetic kidney. glycation occurs and the very Kidney disease is one of the most process by which sugar attaches molecular virology and joined the Baker important risk factors for itself to proteins in the blood. Annual Report 2005 heart attack. They are trying to find out if they four years ago. He heads the Genomics can inhibit the process once it has Advanced glycation is a of Diabetic Complications lab. begun and crucially, whether it
Baker Heart Research Institute biochemical process brought on can be reversed. One of the main by an excess of sugar – we see it difficulties in this area is that many in the browning of fruit and the people who present with kidney process is also apparent in the problems have been suffering from ageing of collagen, resulting in diabetes for many years but have the gradual formation of wrinkles not known it. As a result, their and lines on our skin as we grow kidney dysfunction has not been older. Glycation is a major problem addressed and is at an advanced in diabetes, and these molecules stage. The challenge taken up by resulting from an excess circulating Josephine’s team is to find some blood sugar have the capacity to research for this lab focuses on Another project of this group The third major interest of the way of undoing the damage in Josephine Forbes did her PhD in kidney do major damage to the organs genes that regulate cell growth focuses on the response of cells group is the study of proteins these patients. of a diabetic person over several and differentiation in response to to the diabetic environment. Of called histones, which may be disease at the Royal Children’s Hospital decades. Essentially, it speeds up A significant research area for diabetic disease, with a particular particular interest is the activation affected by advanced glycation. the ageing process, and can lead to this group is the development of focus on kidney disease. of key regulatory molecules called These proteins form the scaffolding in Melbourne and heads the Advanced transcriptional repressors that on which DNA is tethered in the a “caramelisation” of major organs a new drug, expected to enter The lab is primarily concerned control cell differentiation through nucleus, playing an intricate such as the kidney. Kidney disease clinical trials in 2007, known as with the investigation of genes Glycation in Diabetes Complications lab a process called epithelial to and extremely important role in is an important risk factor for “the scissors”. This compound has and their products that are altered mesenchymal transition (EMT). regulating which genes are active at the Baker. heart attack. It is estimated that as the ability to go to the protein as a consequence of diabetes, The lab has demonstrated that and which genes get switched many as 70 per cent of people with and literally break off the sugar. with particular interest in genes this process can occur as a result off. The focus of this project is to diabetes die from heart attack In so doing, it has the capacity to that regulate the activity and of high glucose and exposure to investigate whether modification or stroke. renew the protein and return it expression of factors that result in to its normal state, reversing the advanced glycation end products, of histones in the context of One of the major functions of kidney fibrosis, where the tissue detrimental effects of advanced influencing the cell phenotype diabetes affects their normal the kidney is to regulate blood becomes scarred and hardened. glycation. The drug alagebrium is in the kidney and potentially nuclear function and hence pressure, and blood pressure is currently in clinical trials in other Many small and large molecules in contributing to fibrotic kidney contributes to diabetic disease. directly related to heart attack diseases but this will be its first our bodies undergo modifications disease. Focusing on the kidney, and stroke. The kidneys also application in kidney disease. in the context of diabetic disease. this team is investigating when regulate fluid volume, important DNA is often damaged as a result these cells change from their in determining how hard the heart Josephine’s team is also looking of oxidative stress in diabetes, original state and start producing pumps and serve as the body’s at ways to predict who in the resulting in the activation of a things that make the kidney waste filter, removing toxins from community might be at risk of number of proteins. One of these harden and eventually fail. The the blood stream before they reach developing diabetic complications. proteins, PARP, is known to modify group hopes eventually to prevent the heart. Poor kidney function The main complications involve the other proteins in the nucleus of the the progression of disease caused has devastating effects on health, eyes, heart, kidneys and nerves. cell in response to DNA damage. by diabetic complications and also particularly on the heart, and By investigating genetic risk factors While some of the effects of these prevent the worsening of disease advanced glycation irreversibly in people with diabetes who modifications are known, many in those already suffering. harms kidney function. are as yet not suffering from any are not. Better understanding related health problems but have of these modifications and the a diabetic relative with eye, kidney protein targets may help to contain or heart disease, they hope to help diabetic kidney disease and prevent the progress of this disease eventually prevent it. in a new generation of sufferers. Proliferation & Atherosclerosis Fibrosis in Diabetic in Diabetic Complications Complications › Zhonglin Chai › Terri Allen
42 terri’s lab focuses exclusively on Ongoing research projects, many 43
atherosclerosis, the accumulation conducted in collaboration with 2005 Report Annual Institute Research Heart Baker Zhonglin Chai Dr Terri Allen heads the Atherosclerosis of fatty deposits in the heart’s pharmaceutical companies, include blood vessels, in diabetes. Heart the study of a new application of trained as a vet in Diabetes lab in the JDRF Diabetes and disease is a major complication of the hormone endothelin, which diabetes, and its greatest cause of constricts blood vessels, in diabetic Annual Report 2005 in China and in Metabolism division of the Baker. Terri has death in people with the disease. kidney disease and atherosclerosis. People with diabetes generally Australia completed a PhD in diabetic kidney disease and has In conjunction with the Baker’s have an abnormal cholesterol
Baker Heart Research Institute Paul Nestel, Terri’s lab has level, known as a lipid profile. So a PhD in molecular been working in the area of atherosclerosis conducted research into the even though, compared to the rest controversial notion of reducing biology with CSIRO since 2000. Terri is also chair of the of the population, diabetics have cholesterol and the incidence of higher cholesterol levels, atherosclerosis by boosting cow’s before going on AMREP Animal Ethics Committee. they run a greater risk of going milk with a specific oil. Their on to have a heart attack than a finding, that the effects on disease to postdoctoral person with a higher cholesterol were unremarkable, will add to the reading but who does not have studies at Monash body of information on this topic. diabetes. The presence of diabetes University. is a risk factor for heart disease Research now underway, as great as family history, high conducted in collaboration cholesterol and even having had with the Australian Centre for a heart attack previously. Blood Diseases, will look at the relationship between changes Terri’s lab, which works in in platelets, manufactured in the collaboration with many bone marrow and associated other Baker labs on projects, with the blood’s ability to clot, investigates the effectiveness and atherosclerosis. of drug treatments in diabetic chai is currently building on his Building on earlier work that both By better understanding how CDA1 atherosclerosis, as well as earlier, groundbreaking work identified this molecule, and works, and understanding its exact the effectiveness of dietary where he identified a new recognised its anti-proliferation molecular mechanisms, Chai and interventions. Using a genetically molecule, CDA1. CDA1 is understood properties, Chai and his team are his team will come a step closer to modified mouse model with to have an anti-proliferation currently investigating CDA1 and targeting it for the treatment and diabetes and high cholesterol, function: increasing the level its role in diabetic complications. prevention of disease, slow down Terri’s group monitors the effects of this protein in a cell stops The team has established that CDA1 the injury or prevent it altogether. of diet and drugs on the cell division. CDA1 is present in interferes with TGF (transforming His previous research has indicated development of atherosclerosis and elevated levels at sites in the body, growth factor)-beta signalling. that CDA1 levels are related to the also studies what has taken place particularly blood vessels and the TGF-beta is known as a pro-fibrotic severity of disease and therefore at a cellular and molecular level. kidneys, where there is damage factor: it stimulates extra cellular may play a role in mediating This approach gives insight into caused by diabetes. Chai aims to matrix proteins, thereby promoting its development. why a particular intervention may understand the biological function fibrosis, or tissue scarring. Chai or may not have proved effective of CDA1, how it works and its role and his team believe that far from and does so in a condensed in disease. being purely the result of diabetic space of time: in humans injury, CDA1 actively promotes diabetic complications such as damage where it is present in atherosclerosis can take 15-20 raised levels. Research is centred years to develop. on understanding the biological function of this molecule and its relationship with other proteins and pathways within the body. Cardiovascular Neuropharmacology Neurosciences Division › Geoff Head › Murray Esler
44 the influence of the central Geoff’s computer program allows 45
nervous system on long-term analysis of the impact of everyday 2005 Report Annual Institute Research Heart Baker As an associate blood pressure levels and the life on the blood pressure of relationship between blood a large number of patients. director of the pressure and stress pathways Continuing research has shown in the brain is a major focus of that in people with hypertension, Annual Report 2005 Baker and head of Geoff’s studies. the morning rise in blood pressure is steeper than usual at first, and the Cardiovascular Research in this lab centres on then plateaus more slowly.
Baker Heart Research Institute cardiovascular neuroscience and Neurosciences fills a niche between the clinic and Another research focus of Geoff’s Division, Professor basic research. Work is carried out lab is looking into a better to understand the mechanisms treatment for congestive heart Murray Esler leads that trigger cardiovascular failure. People with heart failure diseases through environmental -a serious, progressive disease - the institute’s factors. Stress is a main area of have as little as a 50 per cent five- investigation, and research is also year survival rate. ElaCor Pty Ltd is extraordinary being conducted on the effects a company established in 2005 to on the central nervous system further develop research conducted research into and control of the cardiovascular in collaboration with IMBCom at the relationship system of obesity and other the University of Queensland. The Associate Professor Geoff metabolic disorders. Elacor technology is based on the discovery of a group of natriuretic between the brain Geoff hopes that better Head leads research at the peptides - part of the body’s understanding circadian patterns, and heart health. natural response to heart failure Baker’s Neuropharmacology the day/night oscillations of blood - isolated from the venom of the pressure, will shed light on why Taipan snake. The lead compound lab in the Cardiovascular people are two to three times is showing great promise as a more likely to have a stroke or Neurosciences division. treatment for congestive heart other cardiovascular event in the failure and has outperformed early part of the day. Geoff and human natriuretic peptides in his team have developed the early studies. first mathematical model used to estimate the rate of blood pressure rise in the morning. While this morning surge has been previously documented, Geoff’s work, which a clinical cardiologist practising at Data that has come to light In collaboration with the Human Previous groundbreaking work by involves a relatively simple but The Alfred, Murray also has a PhD during earthquakes, though, Neurotransmitters lab, led by the Murray on heart failure patients, robust mathematical program, in neuroscience. has gradually silenced sceptics. Baker’s Gavin Lambert, Murray which showed their sympathetic will go towards proving the Multiple international studies oversees an active research nervous system was active without relationship between these natural Research is conducted in humans have shown that the incidence of program on depressive illness. relief, led to the lifesaving use elevations in blood pressure and and in animals and focuses on sudden cardiac death is increased Major depression is known to be of beta-blockers in this group the incidence of cardiovascular the importance of psychological manifold, up to seven times, a major cause of heart attacks and patients. It was this previous events. By analysing ambulatory mechanisms and mental on the day of a major quake. sudden death. As an isolated risk discovery that led Murray to look blood pressure in patients against stress in heart disease and high Earthquake data is compelling in factor it is equally high to the risk into whether the sympathetic his mathematical model the blood pressure. that some people seem to thrive posed by high blood pressure or nervous system has a role in the underlying mechanisms that trigger The brain-heart link in on forms of stress that may have a high cholesterol. Investigations by increased risk of heart attack heart attack and stroke can be cardiovascular disease has harmful effect on others but during Murray and Gavin, in association in patients with depressive better understood. Research in this come into the medical research an earthquake it is accepted that with psychiatrist and PhD illness. The findings, that there is area is focusing on the role played mainstream in the last 10 – 15 people are stressed and frightened candidate David Barton, have abnormal activity in 40 per cent by hormones and the nervous years, but only after many years of without exception, and the measured the brain transmitters of sufferers, have direct system on this phenomenon and being relegated to the sidelines: increased rate of heart attack and in people newly diagnosed with implications for future treatment whether arteries stiffened by stress and psychological illness as sudden death during such natural depressive illness and found of sufferers of depression and atherosclerosis lead to a greater causes of heart disease have long phenomena has been apparent that in about 40 per cent of this this anomaly in their risk of heart surge in morning blood pressure. been accepted by the public but since the 1960s. group the sympathetic nervous attack may hold clues about the body of science supporting this system – our “flight or flight‘ different types of depression. folk wisdom is relatively new. response – is permanently switched on, placing the heart under unrelieved pressure. Translational Proteomics Human Ramaciotti Centre Neurotransmitters › Greg Rice › Gavin Lambert
46 greg’s work in the rapidly In collaboration with the Mercy research in Gavin’s lab focuses Research conducted by Gavin’s 47
expanding discipline of proteomics Perinatal Research Centre at the on the link between factors such team suggests that an important 2005 Report Annual Institute Research Heart Baker is not confined to one disease Mercy Hospital for Women, Greg as different forms of stress and link between heart disease and setting. Although much of his has developed a new screening heart disease. body fat might be due to an research and background is in the method for the early detection of overactive sympathetic nervous In addition to the groundbreaking development of new diagnostic complications in pregnancy. Major system. The sympathetic nervous Annual Report 2005 work on depression and heart tools for use in female reproductive complications of pregnancy include system is associated with the disease, conducted with health and in gynaecological miscarriage; pre-eclampsia; body’s response to stress and in Professor Murray Esler, Gavin’s cancers, his appointment to the preterm labour; premature rupture an active state the stress hormone
Baker Heart Research Institute lab is investigating the way that Baker will see his research expand of membranes; intra-uterine noradrenaline is released, which obesity contributes to raised into cardiovascular disease. growth restriction, gestational raises blood pressure. Studies blood pressure. While it is well diabetes and stillbirth. Despite conducted on overweight and One of the strengths of proteomics known that an excess of body many other advances in pregnancy obese volunteers and published in is to allow the measurement fat distributed around the healthcare, the incidence of these 2005 have shown that weight loss and comparison of a wide range abdomen increases the risk of complications has not changed and exercise not only improved of different biomarkers in one heart disease, the precise reasons and most cannot be diagnosed every symptom of metabolic sample. Research into the features for this are not yet understood. until late in the pregnancy. Greg’s syndrome but an average weight of proteins in health and in disease High cholesterol, high blood team has identified 10 different loss of 6.5 kg in 22 volunteers led as well as their changes, both pressure and high blood sugar substances present in the blood to an average reduction in the over time and in the presence of levels are all commonly found in of pregnant women that could release of noradrenaline of 43 different stages of disease, will overweight and obese people and be used develop a new test for Associate professor Greg Rice is a new per cent. Research is continuing Dr Gavin Lambert is head of the Baker’s give rise to the development of this cluster of symptoms, referred pregnant women who might be at into whether the process of new and better predictive and to as “metabolic syndrome”, risk of later complications. Such recruit to the Baker. With his appointment weight loss or a stable lower Human Neurotransmitters laboratory. diagnostic tests. significantly increases the risk of a test would be used at the first weight is more important in in 2005 as head of the institute’s heart attack and the development antenatal visit. modifying sympathetic nervous of diabetes. system activity. In 2005 Greg’s team completed a Translational Proteomics Ramaciotti small Phase 1 trial of a series of Centre, he brings to the Baker an Another area of study examines biomarkers. That trial established the link between panic disorder that more 90 per cent of the expertise in the area of proteomics, the and cardiovascular disease. It is women in the study who were believed that the risk of heart going to develop a complication study and identification of proteins disease is increased in people of their pregnancy could suffering from panic disorder and be identified. and their functions. is due to an over stimulation of their sympathetic nervous system. By establishing risk of complication Gavin’s lab has shown that during early in a pregnancy, a woman has a panic attack, patients display the best chance to tailor care to some symptoms similar to those her needs and minimise the effect experienced when somebody of the complication – or avoid is experiencing a myocardial it altogether. infarction or heart attack. Gavin’s team is studying the effects on heart risk of two different types of treatment: cognitive behavioural therapy and selective serotonin reuptake inhibitor medication Commercialisation The Baker exists to reduce death and disability from cardiovascular disease, and technology transfer – the transfer of laboratory findings to the community – is vital in realising its mission. Commercialisation
50 the commercialisation of 2005 marked a boost in our His appointment supports a Under Chris’s guidance, the Baker’s 2005 marked a boost in our 51 research activities is one of the involvement in research contracts, broader strategy for the Baker that newly revitalised commercialisation 2005 Report Annual Institute Research Heart Baker most effective ways we have of which will continue throughout encompasses technology transfers team is offering an unparalleled involvement in research contracts, ensuring that knowledge and 2006. The commercial partnerships and associated intellectual support service to the institute’s ideas developed by scientists at we develop through such contracts property issues, contract research scientific community. Their job is which will continue throughout 2006. the Baker Heart Research Institute provide us with an opportunity and commercial research. A strong to ensure that our most exciting Annual Report 2005 improve the lives of people living to interact with scientists and and experienced team, also newly bench top research is transformed The commercial partnerships we with, and at risk of, cardiovascular research in the commercial sector. recruited to the Baker, will support into viable treatments and disease. The Baker exists to Chris in his new role. therapies for people living with, develop through such contracts
Baker Heart Research Institute This is one useful indicator of the reduce death and disability from and at risk of, cardiovascular currency of our own research, and Commercialisation manager provide us with an opportunity to cardiovascular disease. To do disease. Their combined experience an important source of funding Bev Thomas has both academic this successfully the Baker needs offers business development for our research activity. It also and industrial pharmaceutical interact with scientists and research to ensure that laboratory expertise, access to research ensures our scientific work is development experience and has findings are translated into good development funds and superior connected with and informed by worked on industry funded projects in the commercial sector. results for patients. project management skills. The the best science underway in the as a research fellow in preclinical establishment of this high level of A hierarchy of principles informs commercial sector – this pharmacokinetics and disposition support to the Baker’s scientific the way the Baker enters into kind of work ensures we are before working for the drug delivery community in 2005 is an indication technology transfer initiatives connected with the commercial start-up company Acrux. of the Institute’s commitment to and these are considered in every scientific mainstream. Chris and Bev are also joined encouraging an atmosphere in commercialisation venture. The appointment in December in 2006 by Elise Needham, who which commercialisation is well They include: 2005 of Dr Chris Nave as the has taken on the position of understood, and in which success › The attraction of commercial Baker’s commercialisation commercial contracts manager and is celebrated for the benefits funding to support basic R&D director put the institute at the Zoe Kristall, business development it brings to the community at the Baker. forefront of the biotechnology associate. Elise, who has a PhD and researchers. sector in Victoria. Chris has in medical research from the › Seeing the generation of new international experience in the University of Melbourne, has ideas applied and taken up in pharmaceutical/biotechnology previously worked as a clinical the commercial world in a way industries, with particular focus in trial coordinator at the Royal which ensures they are used to the areas of business development Melbourne Hospital and as a improve health; and commercialisation of new research project manager at the › The mitigation of risk associated technology. Most recently he Royal Australian and New Zealand with commercialisation pursuits. was the biotechnology manager College of Psychiatrists. at Melbourne Ventures, the Zoe holds an honours degree in › Profit from the commercialisation commercialisation arm of the chemical engineering and an of technology developed at the University of Melbourne and one MBA in Entrepreneurship and Baker directly returned to support of the state’s most respected Innovation. She previously worked future research. biotechnology development in IP commercialisation for QPSX/ agencies. He has been co-founder, › Providing an appropriate level Offspring Ventures and has held director and business development of personal reward and incentive technical, operational and sales manager of various start-up to individual researchers involved roles in the mining industry. in the development of biotechnology companies and has new technologies. worked for Leiras Pharmaceuticals (Finland), a fully owned subsidiary of Schering AG (Germany). He is currently the director of three biotechnology companies and plays an active role in their business development and management, and has previously worked as a professional scientific consultant for government organisations and private corporations.
L-R. Bev Thomas, Paul Howie, Chris Nave, Zoe Kristall and Elise Needham V-Kardia Pty Ltd & ElaCor Pty Ltd V-Kardia Inc
52 v-kardia Pty Ltd and its sister Drug delivery has become an 53
US operation V-Kardia Inc, a integral part of drug development 2005 Report Annual Institute Research Heart Baker fully owned Baker subsidiary, strategies. Some of the most are medical device companies promising new therapeutic dedicated to the development agents are gene-based and when of V-FocusTM, a new, minimally successfully delivered to the Annual Report 2005 invasive, percutaneous (delivered patient can restore the function through the skin) system for of the failing organ. But because the selective administration of these drugs can have dangerous Baker Heart Research Institute genetic, cellular or pharmaceutical side effects when delivery is agents to targeted organs without systemic, localised delivery is the systemic leakage. V-Kardia key to their effectiveness. Both overcomes a major problem with new drugs and existing drugs that heart disease therapies: it allows are known to be effective but that drugs to be delivered directly have toxic side effects when they to the heart, with little leakage circulate through the body will around the rest of the body. By benefit from the development of isolating the coronary circulation this technology, which is the work from general circulation, the of Baker scientists David Kaye and toxic effects and dangers to other John Power. organs of drugs intended for the The first disease targeted for heart are substantially reduced. V-Kardia is heart failure. This This catheter-based system allows progressive disease, there the heart the circulation of the heart to cannot pump blood to meet the be isolated from the systemic requirements of the body, can be a circulation. V-Kardia’s first consequence of all forms of serious therapeutic target is the treatment cardiac disease but coronary heart of heart failure, a disease of disease and cardiomyopathy are elacor Pty Ltd is a spin-off Natriuretic peptides (NPs) are epidemic proportions. The system the most common underlying company established to further part of the body’s natural may also be used to deliver drugs ElaCor is a spin-off company established conditions. Patients with heart develop work from the Baker Heart response to heart failure and as to other organs. failure have impaired quality of Research Institute’s Geoff Head such they have been adopted to further develop work from the Baker life, with median survival of only working in collaboration with the as treatment for the disease. 1.7 years in men and 3.2 years in Institute for Molecular Bioscience However they have a number of Heart Research Institute’s Geoff Head women. Heart failure is a growing at the University of Queensland. inadequacies as drugs, including problem around the world: in ElaCor is focused on developing a short life span in the body, working in collaboration with the the US, it costs the US health care a novel and effective therapy for which restrict their usefulness. Institute for Molecular Bioscience at the system $40 billion a year. There is congestive heart failure, (CHF). There is a demonstrated need for new NP therapies and the no cure for heart failure short of CHF is an often fatal condition in University of Queensland. ElaCor technology is based on the heart transplant and treatment which the heart muscle becomes discovery of a new group of NPs that can improve heart function weakened and lacks the strength isolated from the venom of the carries the serious challenge of to adequately pump blood around Taipan snake. The lead compound systemic leakage, which David the body. It is usually a chronic is showing great promise for and John’s technology has been disease – a long-term condition drug development. developed to overcome. While that gradually becomes worse. clinical trials are planned for use Conversely, acute CHF has a sudden of the device in delivering drugs and severe onset and requires to the heart, studies to develop immediate hospitalisation. It is its effectiveness in use with other drastically increasing in prevalence organs are continuing. all over the world and now causes more than 10,000 deaths per year in Australia and more than 260,000 in the US. It is a condition that causes long term disability and requires ongoing treatment. Nucleus Network Australia in total has only 0.25% of the global early phase clinical trial market. We have a › A wholly owned Baker subsidiary offering phase 1-4 clinical trials strong belief that Australia can significantly increase its share of this international market. Working closely with Australian industry, Nucleus Network is promoting Australia as 54 a destination for clinical studies. 55 Annual Report 2005 Report Annual Institute Research Heart Baker Annual Report 2005 Baker Heart Research Institute Nucleus Network
56 2004 and early 2005 was a time Since August Nucleus Network 57
when the business was becoming has shown impressive growth in 2005 Report Annual Institute Research Heart Baker established and beginning to clinical study numbers. There has undertake significant business also been good growth in both development activity to bring the consulting business and the clinical research investments eduction business. A three-year Annual Report 2005 to Victoria. In 2004 it ran an growth plan that will see Nucleus Australian Clinical Trials Symposium Network grow to conduct over in San Francisco, an event that is 30 studies per year. Baker Heart Research Institute running again in April 2006. We Australia in total has only 0.25% have also joined the Victorian of the global early phase clinical delegation to BIO2004, BIO2005 trial market. Australia can and BIO2006, the world’s largest significantly increase its share of biotechnology congress. In 2005 we this international market. This joined with the state government belief is a driving force for all and BioMelbourne in a biotech Nucleus Network staff. road show to China. We also established relationships with nucleus Network is a wholly The business is active in industry over forty alliance partners within owned Baker subsidiary, offering building activities including Australia to deliver a full range of phase 1-4 clinical trials and has international promotion, drug development services. evolved significantly in the last participation in the Pharmaceutical In early 2005, CTVL was facing 18 months. It is a tribute to the Industry Action Agenda (PIAA), expiration of initial grant funding. dedication and talent of the staff and establishing the Australian In March three of the founding and to the goodwill and support chapter of ACRP. Nucleus Network members; Monash, Neurosciences shown by the founding members also established a marketing and Victoria and Melbourne Health of both the Centre for Clinical business development presence withdrew from membership and Studies (CCS) and Clinical Trials in San Francisco. the Baker Heart Research Institute Victoria (CTV). In July 2004 the Centre for took control. In order to grow both Clinical Trials Victoria and Centre Clinical Studies, at that time a CCS and CTVL it was agreed by the for Clinical Studies were conceived joint venture between The Alfred, partners of CCS that it should merge by clinicians and researchers to Monash and the Baker moved into with CTV. CTV had also by this time provide a framework for a newly built, world class, 24 bed established a successful clinical world-class clinical research clinical trial facility in the Burnet development consulting business, services for the Australian and Tower at AMREP. At the same time Clinical Trials Consulting and a International Pharmaceutical and Clinical Trials Victoria Limited fledgling training business in Good Biotechnology industries. This moved in to share the office Clinical Practice Education. was a platform was created to space. Clinical Trials Victoria was The formal merge of CCS Ltd and help clinicians and researchers then a business to build clinical CTV Ltd occurred on 1st July 2005, market Australia’s capabilities in trials capability within Victoria. the entity continued as CTVL. clinical research to domestic and The founding members on CTVL In August 2005, The Hon. John international industry. were Melbourne Health, Cancer Brumby, Minister for Innovation, Trials Australia (CTA), Neurosciences Nucleus Network is now a fully re-launched the business Victoria and Centre for Clinical self supporting business without under a new trading name Studies. CTVL initially administered any reliance on government grant of Nucleus Network. seed funding from the Victorian funding. It remains a commercially A platform was created to help Government that provided some This re-launch was a significant operating not-for-profit company, capital investment to establish event for Nucleus Network as it and reinvests earnings in market Australia’s capabilities in important technologies including marked the clear establishment developing the business itself and PET scanning facilities at Callan of Nucleus as a member of the clinical research. supporting research and industry Institute, Peter Mac for oncology Baker family. initiatives on the AMREP site, in research, an analytic laboratory Victoria and nationally. at the Royal Melbourne Hospital and the CCS clinical trial unit. The majority of this funding was for capital equipment and fit-out with significant staff resource contributions in-kind from the founding members of CTVL and CCS. Nucleus Network
58 59 Annual Report 2005 Report Annual Institute Research Heart Baker The unit has shown rapid growth in both in-patient and outpatient studies and
Annual Report 2005 is attracting a significant flow of work internationally. Over 70% of revenue has
Baker Heart Research Institute come from overseas investment.
Nucleus Network Education: In 2005 a licensing arrangement The unit also benefits from a Clinical Trials Consulting: The consulting business also Finally the consulting business Nucleus Network has established was established to deliver the close and supportive relationship The CTC business has grown creates a significant flow of work also provides commercial an exclusive arrangement with ACRP GCP course in Queensland and with Monash and The Alfred from strength to strength and has for the CCS business through sponsorship services to off-shore the Association of Clinical and plans are underway for a similar hospital. The Alfred provides become a core part of business. establishing trusted relationships companies who do not have an Research Professionals (ACRP), arrangement in NSW. Modules medical services including It is also key to one of the original at the very early stage of drug established entity in Australia. which is the leading global on GCP within the University of emergency support, pathology goals of building a platform to developments. It will eventually These services can range from industry association with over Melbourne graduate programs in laboratory, medical imaging and support clinical research and provide these services to simple sponsorship through to full 20,000 members. Nucleus Network clinical research are offered. biomedical engineering. development for Australian discoveries and new treatments project and site management. companies. This consulting arising from discoveries made Education offers an Australian Across all consulting work, Centre for Clinical Studies: The Alfred’s patients also benefit as business focuses on the transition by the Baker Heart Research significant achievements and adaptation of the ACRP course in the business is engaging with The unit has shown rapid many of our studies provide access from bench research to clinical Institute. An additional aspect of events within each line of Good Clinical Practice (GCP). GCP is additional Australian clinical growth in both in-patient to new treatments that would research in human subjects. One the consulting business combines business include: the standard by which all research research service providers and outpatient studies. CCS is otherwise be unavailable. Nucleus element of this is combining an experience in managing trial involving humans is required to be to offer a full spectrum of attracting a significant flow of Network enjoys strong support from understanding of pre-clinical, sites and business management. undertaken. Australia has a strong services. This provides good work internationally, over 70% the Baker Heart Research Institute trials, stock manufacture and Staff are engaged in a number of international reputation for the spin-off benefits to Australian of revenues have come from particularly in strategy, specialist regulatory strategy. Many small projects that support development quality of its medical and clinical industry, particularly in terms overseas investment. CCS has analytics, business development Australian biotech companies do of the clinical research industry as research, however many staff have of manufacturing, bioanalytic strong relationships with two and contract resources. Monash not have sufficient experience in a whole. These projects include not received formal training in GCP. services, pharmacogenomics, site top 10 global pharmaceutical Department of Epidemiology and these areas to efficiently enter infrastructure developments as well management and monitoring and The focus of these programs companies, each of them placing Preventive Medicine and Clinical human clinical development. We as helping additional trials sites to general laboratory services. is to train investigational site multiple studies with the unit. CCS Pharmacology are also have assembled a team of highly become established and operate staff in GCP and then encourage also has relationships with and is close collaborators. experienced consultants who to international standards. CTC has have provided consultancy them to undertake certification conducting studies for some of the have significant experience in services to over 20 Australian by examination. Developing largest global biotech companies as regulatory, pre-clinical, clinical companies and have acted the number of GCP qualified well as many Australian biotechs. and manufacturing scale up as international sponsor for researchers in Australia will The unit has grown from around strategy. We also have a great deal five companies. increase Australian competitiveness 10 staff in 2004 to a regular staff of experience in later phase studies in the international market place. of over 40, comprising permanent and are able to offer advisory and sessional staff. services to create a full clinical development plan and regulatory The unit is now supported by filings for international agencies full-time medical and nursing such as FDA and EMEA. staff, dedicated subject recruitment staff, project coordinators, full- time technical laboratory and quality management staff. Core Facilities
60 DNA sequencing. Adenovirus facility. Confocal imaging. 61
the Baker’s DNA sequencing The institute’s virus facility, run New graphics software was 2005 Report Annual Institute Research Heart Baker service has been integrated with by the Baker’s Walter Thomas, head purchased for the Baker’s confocal that of the commercially run IDI of the Molecular Endocrinology imaging equipment in 2004 facility, and is involved in a broad lab, has been developed to and more recently a consortium range of collaborations with the produce medically modified of AMREP partners has been Annual Report 2005 laboratories of the institute and adeno-associated viruses and established to bring together elsewhere. As well as providing an lenitvirus capabilities that crucially imaging equipment under a new essential support to the Baker’s support Baker research. The work imaging joint secretariat. This has Baker Heart Research Institute laboratories it has been the source of this core facility has become greatly enhanced access to high of several successful publications in increasingly important as several level imaging capabilities across its own right. Baker labs are now exploring more the precinct. specific targeting of gene therapies which can use the viruses created to carry the therapies into the circulation.
Proteomics become vital. A range of functional Proteomics, the study and and microsurgical methodologies identification of proteins, is a has been developed which are now critical service for Baker scientists available to other laboratories. Dr and underpins much of their Xiao-Jun Du, head of the institute’s research. The Clive and Vera Experimental Cardiology lab and a Ramaciotti Proteomics Centre world leader in mouse cardiology, was expanded in 2005 with the runs this core facility. recruitment of associate professor Precinct Animal Centre (PAC). Greg Rice from the University of The Animal Centre plays a vital role Melbourne. In 2005 we purchased in research at the AMREP precinct, new Bruker Daltonics Mass conducting scientific research and Spectroscopy equipment. This breeding animals for research. has enabled the proteomics core There are approximately 350 facility to develop more precise users of the facility, all part of the and wide-ranging predictive process of delivering science from tests, and has supported the the “bench top to the bedside.” identification of new biomarkers Managed by the Baker under the of cardiovascular disease and guidance of Debra Ramsey, PAC diabetes. Distinguished proteomics serves the animal needs of all expert Dr Gert Talbo heads the partners of AMREP. Each piece of institute’s proteomics centre research involving animals requires and provides crucial support approval by the National Health that enables scientists to better and Medical Research Council and understand their lab findings. the precinct’s own animal ethics Mouse Surgery/Cardiology committee. Some examples of The Mouse Cardiology Core procedures that were researched Facility provides collaborative by the facility include cardio support to other groups at the myoplasty procedures used by Baker Institute in conducting surgeons today and bypass surgery, cardiovascular research using mice. which has evolved to a point The selective use of genetically where the procedure is carried out manipulated animals allows Baker by keyhole surgery. scientists to determine the role of significant genes and proteins in cardiovascular physiology and disease. Because mice are the most common choice of species for this type of research, determining mouse heart and vascular function and reproducing cardiovascular diseases in small animals have Staff & Students 2005
62 Director Associate Professor Geoff Head - Students Thrombosis & Myocardial Vascular Pharmacology Laboratory Human & Vascular Experimental Cardiology 63
Professor Garry Jennings - BSc (Hons), PhD Swati Mukherjee - PhD (Monash) Infarction Laboratory Biology Laboratory & Heart Failure Division 2005 Report Annual Institute Research Heart Baker Head of Laboratory AM -MD, MBBS, FRCP, FRACP, FAHA Professor David Kaye - Risk Clinic / Gene Bank Head Of Laboratory Dr Jaye Chin-Dusting - Head of Laboratory Head MBBS, PhD, FRACP, FACC Associate Directors Unit Manager Professor Karlheinz Peter BSc (Hons), PhD Stephen Duffy - Professor David Kaye - Associate Professor Professor Anthony Dart - Janis Jennings - SRN MB, BS (Hons), PhD, FRACP, MRCP MBBS, PhD, FRACP, FACC Bronwyn Kingwell - Professional & Technical Staff Senior Scientific Annual Report 2005 BA, Dphil, BMBCh, FRCP BSc (Hons), PhD Professional & Technical Staff Dexing Huang Kevin Wollard - PhD Professional & Technical Staff Wynn Department Professor David Kaye - Associate Professor Bernadette Chiodi - BSc (Hons) Steffen Eisenhardt Lovisa Dousha of Cardiology MBBS, PhD, FRACP, FACC Professional & Technical Staff Zygmunt Krozowski - Christoph Hagemeyer
Baker Heart Research Institute Professor Karlheinz Peter Risk Reduction Clinic Nurses Ann-Maree Jefferis - BSc Cell Biology & Diabetes Laboratory Head of Laboratory BSc (Hons), PhD Nicole Bassler Professor Mark Cooper - Elizabeth Jenkins - SRN Margaret Vincent - AssDipAppSci Professor David Kaye - Dr Dmitri Sviridov - BSc (Hons), Head of Laboratory MBBS, FRACP, PhD, FAHA, FASN Marijke Tress - SRN Students Emma Jones - BSc (Hons) MBBS, PhD, FRACP, FACC MBBS, FAHA, PhD Professor Peter Little - Professor Murray Esler - Melissa Leung - UROP Student Dr Walter Thomas - Cardiovascular Disease Students B Pham, MSc, PhD, ASIA Administrative BmediSci, MBBS, PhD Yung Chen - MBioTech (RMIT) BSc (Hons), PhD Prevention Unit Nathan Connelly - PhD (Melbourne) Kate Knight - Personal Assistant Professional & Technical Staff Senior Faculty Associate Professor Visiting Scientist Andrew Murphy - PhD (Monash) Head of Unit Narin Osman Senior Scientific Staff Elizabeth Woodcock - Natela Jakhutashvili - Rajesh Nair - PhD (Monash) Senior Principal Research Fellows Colin Johnston - Soniya Survase Wei-Zheng Zhang - MSc, PhD BSc (Hons), PhD University of Freiburg, Germany Ngan Huynh - PhD (Monash) Professor Alex Bobik - AO - MBBS, MD (Hon), FRACP, FAHA Mandy Ballinger Zhiyong Yang Christoph Ellwanger - Bpham, Msc, PhD Professor Gregory Rice - Cell Biology Laboratory University of Freiburg, Germany Professor Mark Cooper - PhD, Grad Dip Management, Senior Scientific Students Professional & Technical Staff Fabian Albrecht - MBBS, FRACP, PhD, FAHA, FASN Masters Health Administration Christopher Reid - Head of Laboratory Mandy Ballinger - PhD (Monash) Carla Enriquez - BSc (Hons) University of Freiburg, Germany Professor Anthony Dart - BA, DipEd, MSc, PhD Professor Alex Bobik - Melanie Ivey - PhD (Monash) Tannaele Marshall - BSc (Hons) JDRF Fellows Patrick Stoll - BA, Dphil, BMBCh, FRCP Bpham, Msc, PhD Nelly Cemerlang - Samara Finch - BSc (Hons) Dr Josephine Forbes - Professional & Technical Staff University of Freiburg, Germany Professor Murray Esler - Pharmaceutical Science (RMIT) Kylie Venardos BSc, PhD Anne Bruce - SRN Senior Scientific BmediSci, MBBS, PhD Abigail Chong Chris Tikellis - Claudia Retegan - Dip SC, BA Clinical Physiology Alex Agritos - BSc (Hons), PhD Lipoproteins & Professor Colin I Johnston - BSCc (Hons), PhD Diem Dinh - BSc (Hons), Atherosclerosis Laboratory Students Head of Laboratory Professional & Technical Staff AO - MBBS, MD (Hon), FRACP, FAHA PhD, Peter Doherty Fellow Justin Marini - PhD (Monash) Associate Professor Giovanna Pomilio - BSc (Hons) Head of Laboratory Professor Paul J Nestel - Career Development Fellows Kathryn Murphy - SRN Kristy Jackson - Bronwyn Kingwell - Peter Kanellakis - BSc Dr Dmitri Sviridov - AO - MD, FTE, FRACP, FAHA Dr Terri Allen - Ann Nadonza - BSc Pharmaceutical Science (RMIT) BSc, PhD BSc (Hons), PhD Georgia Kostolias - BSc (Hons) BSc (Hons), MBBS, FAHA, PhD Principal Research Fellows Jessele Vinluan - BA Dr Stephen Duffy - Associate Professor Geoffrey Head - Robyn Berry Senior Scientific Student Professional & Technical Staff MB, BS (Hons), PhD, FRACP, MRCP BSc (Hons), PhD Susan Montgomery Barbora de Courten - Kelly To - PhD (Monash) Anh Hoang - BSc (Hons) Dr Gavin Lambert - PhD Associate Professor Anita Wluka - MD PhD Michael Ditiatkowski - Urbain Tchoua - PhD Dr Rebecca Ritchie - Zygmunt Krozowski - Public Health Fellowship PhD (Monash) Wilissa D’Souza BSc (Hons), PhD Professional & Technical Staff BSc (Hons), PhD Nigora Mukhamedova Students Brian Drew - BSc (Hons) Visiting Student Associate Professor Consultant Scientist Jessica Chellappah - PhD (Monash) Melissa Formosa - BSc Anastasia Efimenko - Students Elizabeth Woodcock - Derek Denton Mehernaz Sadafi - Sally Penfold - BSc (Hons) Cardiology Research Centre & Honor Rose - PhD (Monash) BSc (Hons), PhD Baker Clinical Pharmaceutical Science (RMIT) Alaina Natoli - BSc (Hons) Moscow State Uni, Russia Amy Gatt - Hons (Deakin) NHMRC Fellows (Alfred Baker Medical Unit) Tanya Medley Atherothrombosis Proteomics Core Facility Dr Xiao-Jun Du - Sonia Dougherty Head & Vascular Division MBBS, M Med, PhD Head Professor Anthony Dart - Students Dr Jay Chin-Dusting - Head Gert Talbo - PhD BA, Dphil, BMBCh, FRCP Darren Henstridge - PhD (Monash) BSc (Hons), PhD Professor Karlheinz Peter Anna Ahimastos - PhD (Monash) Professional & Technical Staff Professor Anthony Dart - Professional & Technical Staff Anthony White - PhD (Monash) Mustafa Ayhan - PhD BA, Dphil, BMBCh, FRCP Elizabeth Dewar Brian Drew - PhD (Monash) Vincent Strangis - BSc (Hons) Professor Murray Esler - Jenny Starr BmediSci, MBBS, PhD Sally Kay - SRN, BBm Students Irene Chum Nathan Connelly - James Shaw PhD (Melbourne) Rodney Reddy Andrew Murphy - PhD (Monash) Rajesh Nair - PhD (Monash) Ngan Huynh - PhD (Monash) Staff & Students 2005 › Continued
64 Cellular Biochemistry Laboratory Oxidative Stress Sara Hatsi Molecular Students Students Students Human Resources 65
Laboratory Megan Fettke Endocrinology Laboratory Wendy Burns - PhD (Melbourne) Brooke Harcourt - Hons (Monash) Kristy Jackson - MSc (RMIT) Annette Crawford - 2005 Report Annual Institute Research Heart Baker Head of Laboratory Elissa Wells William Tu - PhD (Monash) Felicia Yap - (Hons (Monash) John-Luis Moretti - MSc (Monash) Human Resources Manager Associate Professor Head of Laboratory Head of Laboratory Kylie Lewis Yogeshwar Rajaram - Katrina Rajic - Elizabeth Woodcock - Dr Judy De Haan Dr Walter Thomas - BSc (Hons), PhD Visiting Scientist Translational Proteomics Kirsty Lee AMS (Melbourne) Human Resources Advisor BSc (Hons), PhD Kei Fukami - Ramaciotti Centre Professional & Technical Staff Fiona Keurentjes - Senior Scientific Vicki Bonke -PhD (Melbourne) P/T Annual Report 2005 Kurume University School of Development Professional & Scientific Staff Nada Stefanovic AppSci (Animal Tech) Hongwei Qian - PhD Yen Pham - PhD (Monash) Head of Laboratory Medicine, Japan Bobbie Renard - Huy Huynh - BApplSciBiotech Associate Professor Students Animal Ethics Secretary Professional & Technical Staff Genomics of Diabetic Aino Soro-Paavonen - Manager Community Relations Fatemeh Amirahmadi - Greg Rice -
Baker Heart Research Institute Fatma Ahmet - Hons (Melbourne) Leia Demtschyna Luisa Pipolo - AssDipAppSc Complications Laboratory Department of Medicine, Helsinki Elizabeth Veal - MSc, PhD PhD, Grad Dip Management, Paul Lewis - Hons (Melbourne) Tamara Paravicini University, Finland Fundraising Projects Manager Alfred Lanzafame - Cardiac Hypertrophy Laboratory Head of Laboratory Masters Health Administration Margherita Boemo - BSc (Hons), PhD Atherosclerosis in Students Dr Phillip Kantharidis Cardiovascular Head of Laboratory Professional & Technical Staff Marketing & Events Coordinator Diabetic Complications Nicola Smith - PhD (Melbourne) Neurosciences Division Students Dr Julie McMullen - BSc (Hons), PhD Professional & Technical Staff Karen Oliva - DipAppSci Trish Roath - Enzo Porrello - PhD (Melbourne) Oliver Vasilevski - PhD Head of Laboratory Wenzhen Huo Head Fundraising Manager Professional & Technical Staff Cristina Oro - PhD (Melbourne) Biological Media Preparation (Swinburne University of Technology) Dr Terri Allen - BSc, PhD Josefa Pete - BS (Hons) Professor Murray Esler - Marisa Morabito - Russell Bouwman - BSc (Hons) Hsiu-Wen Chan - PhD (Monash) Jane Honeyman - PhD (Melbourne) BmediSci, MBBS, PhD Professional & Technical Staff Database & Donor Liason Officer Professional & Technical Staff John Huynh - PhD (Monash) Visiting Scientists Molecular Hypertension Laboratory Willissa D’Souza Vivian Talbot - Experimental Cardiology Gavin Langmaid Gabrielle Callander - Marieke Kuut - Administration Planning & Giving Officer Phillip Koh- BSc (Hons), PhD Head of Laboratory Hons (Melbourne) Academic Medical Center, Univeristy Jeannette Bourke - Operational, Head of Laboratory Sandra Miljavec - DipApplSci Associate Professor Allison Bourne - Hons (Monash) of Amsterdam, The Netherlands Personal Assistant Administrative & Support Staff Building Infrastructure Dr Xiao-Jun Du - MBBS, M Med, PhD Belinda Davis - BSc (Hons), PhD Dr Zygmunt Krozowski - Fleur Kleijwegt - Steve Droste - Adenovirus Facility Human Neurotransmitter Chief Operating Officer Senior Scientific Adele Prestinenzi BSc (Hons), PhD Academic Medical Center, Univeristy Building Infrastructure Manager David Lloyd Shirley Moore - Head of Amsterdam, The Netherlands Head of Laboratory Blaze Gomes - Electronic Technician Students Cardiac Surgery Laboratory MBBS, Grad Dip Med Sc, PhD Walter Thomas - BSc (Hons), PhD Dr Gavin Lambert - PhD Administration Anna Calkin - PhD (Monash) Kidney Disease in Commercialisation Xiao-Ming Gao - Head of Metabolic Cardiology Gabrielle Doye - Professional & Technical Staff Diabetic Complications Professional & Technical Staff Chris Nave -Director MBBS, MD, MUNZ Fellowship Visiting Scienist Dr Salvatore Pepe - Executive Assistant Nicole Sevigny - MSc Ling Guo Julia Hill - Helen Kiriazis - BSc (Hons) PhD Audrey Koitka - PhD, BSc (Hons), Pgrad Dip Head of Laboratory Simon Neil - Jacqueline Hastings - BSc, PhD Head of Commercialisation Qi Xu - MBBS, PhD University of Anaers, France Health Counsel DNA Sequencing Dr Karin Jandeleit-Dahm Scientific Projects Officer Elisabeth Lambert - PhD Renee Dutton - Ourania Sideropoulos - Business Development Manager Professional & Technical Staff Proliferation & Fibrosis in Professional & Technical Staff Head Professional & Technical Staff Flora Soratous - BSc, PhD Receptionist Yidan Su - MBBS, PhD Diabetic Complications Laboratory Irumini Jayakody Walter Thomas - Sara Guinti Glen Wiesner - PhD Barbara Spaccatore - Subsidiaries Ziqiuo Ming BSc (Hons), PhD Nora Straznicky - Students Receptionist Head of Laboratory Students Bpharm, PhD, MPH Nucleus Network Students Dr Zhonglin Chai Catherine Huggins - Professional & Technical Staff Georgia Soldatos - PhD (Monash) Nina Eikelis - BSc (Hons) Finance Andrew Giddy - Karen Fang Lu - PhD (Melbourne) PhD (Melbourne) Michelle Cinel -Cert Vet Nursing, Chief Executive Officer Professional & Technical Staff Biochemistry of Kazuko Masuo - MD, PhD Anita Furnell - Director Freya Sheeran - PhD (Monash) AssDipAppSci (Animal Tech) Craig Rogers - Visiting Scientists Tieqiao Wu - Student Diabetic Complications Elodie Hotchkin - BSc (Hons) Bcomm, ACA Wendy Ip - PhD (Melbourne) Chief Operating Officer Jin Wang - Yugang Tu Molecular Celia Brenchley Ron Mak - Senior Accountant Head of Laboratory Lisa Nelson Department of Cardiology, People’s Cardiac Surgery Pharmacology Laboratory BBS, CA, MIMS Associate Professor Students Hospital, Wuhan University, PRC Precinct Animal Centre Gary Loetsch - Accountant General Manager Head Head of Laboratory Merlin Thomas Tye Dawood - PhD (Monash) Zhizhen Lu - Beijing University, Animal Services Manager Bec (Acc), CPA, DipOD Professional & Technical Staff Associate Professor Donald Esmore Dr Rebecca Ritchie Institute of Vascular Medicine Debra Ramsey - Professional & Technical Staff Visiting Scientist Helen Green - Viccy Wootton Katarzyna Bialkowski - BSc (Hons) Josefin Forsstrom - Accounts Payable/rec Officer Human Epigenetics Laboratory AppSc (Animal Tech), BHIT Surgeons Professional & Technical Staff Cameron Johnson Adrian Pick Anh Cao - BSc (Hons) Chris Tikellis - BSCc (Hons), PhD The Sahlgrenska Academy at Dale Hince - Jacqui Tomkins Operations Manager Head of Laboratory Frank Rosenfeldt Goteborg Universoty, Sweden Accounts Clerk Jacqueline Waterkeyn David Spiteri - Students Visiting Scientist Dr Assam El-Osta - BSc, BAppSci Justin Negri Johanna Johansson - Lisa Skigopoulos - Maeaghan Read AppSc (Animal Tech), BHIT Sarah Gamboni - Hons (Melbourne) Hongyan Liu - Renmin Hospital of Michael Rowland The Sahlgrenska Academy at Payroll Officer Bianca Scott Professional & Technical Staff Eliane Lin - Hons (Monash) Wuhan University, P.R.C Silvana Marasco Goteborg Universoty, Sweden Maria Chiam Harikrishnan Kaipananickal - Administration Information Systems Rajani Jasti - MSc (Animal Sci) JDRF Diabetes Glycation in Diabetic David Cannon MSc, PhD Applied Cardiovascular Neuropharmacology James Howard - & Metabolism Division Complications Laboratory Robyn Lichter Emma Baker - PhD Research Laboratory Laboratory Information Systems Manager Professional & Technical Staff Florence Merg Michael Yarski Samantha Hulme - Head Head of Laboratory Head of Laboratory Head of Laboratory Occupational Health & Safety Fiona Kennelly AppSci (Animal Tech) Professor Mark Cooper - Dr Josephine Forbes - BSc, PhD Students Dr John Power - BVSc (Hons), PhD Associate Professor Adrian Quintarelli - OH&S Manager Jenny Pyke Lynda Bonning - BVSC (Hons) MBBS, FRACP, PhD, FAHA, FASN Maggie Chow - PhD (Melbourne) Professional & Technical Staff Geoffrey Head - BSc (Hons), PhD Noel Tresider - Ming Pham Daniella Brasacchio - PhD (Monash) John Crawford - Professional & Technical Staff OH&S Chemical Project Officer Brian Motz Administration Melinda Coughlan - Senior Scientific AppSci (Animal Tech) Anka Smolic - BScHons, BAppSc Tracey Oakes - OH&S Project Officer Laurel Ring - Personal Assistant BSc (Hons), PhD Meg Kaegi Visiting Scientists Xin Du Adam Bilney - BE (Hons) Dmitri Mayorov - BSc (Hons), PhD Maryann Arnstein Liang Du - Shandong Provincial Claire Doran - AppSci (Animal Tech) Melissa Byrne Information Technology Senior Scientific Vicki Bonke - BAppSci Professional & Technical Staff Hospital, Japan Ian Briggs - Mia Ibrahim Laura Beaumont - Zemin Cao - MB BS, MD Sandra Burke - BSc (Hons), MSc Anna Gasser Information Technology Manager Emma Hickingbotham DippAppSc (Animal Technology) Luisa La Grecia - BBiol Sci (Hons) Damian Lee - Support Officer Kenny Scicluna Hayley Aisbett Pamela Davern Pierre Ithier - Support Officer Abby Padget Melinda Carrington Richard Lee - Web Administrator Emma Lanera James Armitage Scott Maxwell Lihong Kong Monthly Baker Donors Science Awards
66 Monthly Baker Research Prize Winners for 2005 The Institute is grateful for major Perpetual Endowments Silver Club Members - Dr Victor Kalff 67 contributions from: - Hazel & Pip Appel Fund - Mr Martin P Bade - Mr Rob Kerr Annual Report 2005 Report Annual Institute Research Heart Baker Month Winner Article - Atherosclerosis Research Trust of the UK - The Baker Foundation - Mr Geoff Bade - Mr John W Leslie Dec-04 Alex Bobik Kalinina N, Agrotis A, Antropova Y, DiVitto G, Kanellakis P, Kostolias G, Ilyinskaya O, Tararak E, Bobik A. - Australian Rotary Health Research Fund - Estate Lindsay J Baldy - Mr & Mrs L & E Berkowitz - Mrs C D Lewis Increased expression of the DNA-binding cytokine HMGB1 in human atherosclerotic lesions: role of activated - The Baker Foundation - Bell Charitable Trust - Mr Jeff Blutman - Mr & Mrs M W Ling - Diabetes Australia - William Buckland Foundation - Miss Mavis Bowskill - Mrs Clarissa A Linton-Smith macrophages and cytokines. - Juvenile Diabetes Research Foundation - Thomas, Annie & Doris Burgess - Mrs Lilian (Betty) Curtis - Mrs Margery Little
Annual Report 2005 Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):2320-5. - National Heart Foundation - Leslie Dickson Charitable Trust - Mrs J Ferrarin - Ms Joy A Macdonald Jan-05 David Kaye (1) (1) Schlaich MP, Parnell MM, Ahlers BA, Finch S, Marshall T, Zhang WZ, Kaye DM. - National Health & Medical Research Council - Grace & Herbert Foulkes Charitable Trust - Miss D J Gillies - Mr Howard Macmillan Murray Esler (2) - National Institutes of Health (USA) - Estate Kenneth W Hesse - Mrs Jane Gorman - Mrs Phyllis L Maggs Impaired L-arginine transport and endothelial function in hypertensive and genetically predisposed - Victorian Government - Estate George F Little Settlement - Mrs Joan Grimwade - Mr & Mrs W A & T A Matthews
Baker Heart Research Institute normotensive subjects. - M A & V L Perry Foundation - Mr & Mrs L & Y Harrison - Miss R O McIntyre Circulation. 2004 Dec 14;110(24):3680-6. Baker Research Foundation - George Thomas & Lockyer Potter Trust - Mrs W Keir - Mr Neil S McLaren (Founding Members) - Estate of Emily Elsie Elizabeth Stewart - Emerit Prof P I Korner AO & Mrs J Korner - Mrs G J McPhee - GSA Group Pty Ltd - Mr & Mrs S & M Marks - Mr Donald Michell (2) Campbell DJ, Krum H, Esler MD. - Mr William P Gurry AO Scholarships, Fellowships - Mr Robert G Miller - Miss Anne Miller Losartan increases bradykinin levels in hypertensive humans. - Kodak (Australasia) Pty Ltd - William Angliss (Vic.) Charitable Fund - Mr A R Moran - Mr John Dewar Milne - Mr Norman J O’Bryan - Besen Family Foundation Scholarship Circulation. 2005 Jan 25;111(3):315-20. - Mr Louis W Partos - Mrs Mary Minogue - Mrs Margaret S Ross - Henry Cooper Fellowship - Mr Ronald G Pitcher - Mr D Bruce Moore Feb-05 Karin Jandeleit-Dahm Lassila M, Jandeleit-Dahm K, Seah KK, Smith CM, Calkin AC, Allen TJ, Cooper ME. - The Cybec Foundation Scholarships - Mrs Denzil Smith - Mr Frederick Moore Major Gift Donations - Danar Scholarship - Mrs C Y Sullivan - Lt Gen (Rtd.) D M Mueller AO Imatinib attenuates diabetic nephropathy in apolipoprotein e-knockout mice. - Nancy Ainsworth - Heartbeat Alfred & Baker Scholarship - Mr Peter Swindells OAM & Mrs G Mueller J Am Soc Nephrol. 2005 Feb;16(2):363-73. - Anonymous - Lyonel & Joanna Middows Fellowship - Mr & Mrs L L Thompson - Mr & Mrs N & M Myers - Australia Foundation Mar-05 Sam El-Osta Harikrishnan KN, Chow MZ, Baker EK, Pal S, Bassal S, Brasacchio D, Wang L, - L & S Morgan Scholarship - Mr H E Vivian - Miss E A Nihill - Casella Wines - Munz Family Fellowship - Mr & Mrs A C Weber - Miss V H Notley Craig JM, Jones PL, Sif S, El-Osta A. - Centenary Foundation - Dame Elisabeth Murdoch Fellowship - Mr E P Oldham Brahma links the SWI/SNF chromatin-remodeling complex with MeCP2-dependent - Stephen J Cook - O’Bryan Family Scholarships Bronze Club Members - Mrs Carmel Opray - Albert & Barbara Edwards transcriptional silencing. - John T Reid Fellowship - Mr Alan K Abbey - Mr D L Palm - Goldman Sachs JB Were - Schwartz Family Scholarship - Mrs B Allison - Mr G J Paruit Nat Genet. 2005 Mar;37(3):254-64. - Harbig Charitable Foundation - Sportscolour Scholarship - Mr Lawrence Armstrong - Ms Diana Peatt Apr-05 No entries - GP & SK Johnston - Stewart Family Scholarship - Mr & Mrs S E & M L Barker - Mr & Mrs R I Pender - A S Leslie May-05 Dmitry Mayorov Mayorov DN. - VEADA Scholarship - Miss Paula N Barry - Mr & Mrs D & D Plant - Robert & Jan Lyng - Ruth Webster Scholarship - Mr Robert W Bell - Mr Mark Plunkett Selective sensitization by nitric oxide of sympathetic baroreflex in rostral ventrolateral medulla of conscious - Miller Foundation - Anonymous - Mr & Mrs L G & L M Bentley - Mrs M G Pollock rabbits. - Mingara Services P/L - Mr & Mrs D L Birch - Mrs Joan Ray - J Gordon Moffatt AM Perpetual Scholarships & Travel Bursaries Hypertension. 2005 May;45(5):901-6. - Mr & Mrs I G Bird - Mr E G Reid - Elisabeth Murdoch Trust - Hazel & Pip Appel Fellowship - Mrs L Bitterfeld - Mr & Mrs N & G Reid Jun-05 Anna Ahimastos Ahimastos AA, Natoli AK, Lawler A, Blombery PA, Kingwell BA. - Northryrie P/L - Ethel Mary Baillieu Memorial Trust - Mr James M Bland - Ms Bobbie Renard Ramipril reduces large-artery stiffness in peripheral arterial disease and - NH Peck AM - Bertalli Family Scholarship Fund - Mrs Gwendoline Bowman - Mr & Mrs Ralph M Renard - Emily & Herbert Perry Memorial Gift - Noel Dickson Scholarship Fund promotes elastogenic remodeling in cell culture. - Miss J Bromley - Mrs J A Repper - Reece Australia Limited - Robbie Eisner Scholarship Fund - Mrs B L Butcher - Mrs Patricia Roath Hypertension. 2005 Jun;45(6):1194-9. - BBS & Rosemary Robertson - Lang Research Fund - Mr P F Canobio - Mrs Patricia Robertson Jul-05 No entries - Margaret Ross AM - Edgar Rouse Memorial Fund - Ms Fiona Carmody - Mr William M Rooney - The Rotary Club of Melbourne - Ruby Wallace Travel Bursary Aug-05 Josephine Forbes Forbes JM, Thorpe SR, Thallas-Bonke V, Pete J, Thomas MC, Deemer ER, Bassal S, El-Osta A, Long DM, - Mrs D Carter - Mr Peter W Ryall - Pauline Row - Mrs L G Cheary Panagiotopoulos S, Jerums G, Osicka TM, Cooper ME. Bequests received - Dr & Mrs Stan & Joan Salamy - Snowy Nominees - Mr & Mrs J R Cheney - Esate Wilma E Dimsey - Mr Keith J Scott Modulation of soluble receptor for advanced glycation end products by - UBS Wealth Management Australia - Miss Pamela R Christensen - Estate Gwendoline M Dodgshun - Miss Patricia Singleton Angiotensin-converting enzyme-1 inhibition in diabetic nephropathy. - Lloyd & Sue Williams - Mr Stuart Cohen - Estate Robert A Dwyer - Dr W J Smith - Miss Verna A Cook J Am Soc Nephrol. 2005 Aug;16(8):2363-72. Trusts & Foundations - Estate Edith C Ley - Garry & Warren Smith Group - Mr & Mrs G F & M Cormack - Janina & Bill Amiet Foundation - Estate Daniel J Menhennitt - Mr & Mrs I H & B Y Smith Sep-05 Anna Calkin Calkin AC, Forbes JM, Smith CM, Lassila M, Cooper ME, Jandeleit-Dahm KA, Allen TJ. - Dame Joyce Daws - The Bennelong Foundation - Estate Mavis A Parry - Mr G C Snell Rosiglitazone attenuates atherosclerosis in a model of insulin insufficiency independent of its metabolic - Mr & Mrs M P de Jong - James & Elsie Borrowman Trust - Estate Klaus Singer - Mr & Mrs C J & E D Soutar - Mr & Mrs E A & M P Dodd effects. - L E W Carty Charitable Fund - Mr Philip Spry-Bailey AO - Mr & Mrs D & A Doig Arterioscler Thromb Vasc Biol. 2005 Sep;25(9):1903-9. - Rebecca L Cooper Med Research Foundation Gold Club Members - Miss J W Stephens - Mrs Heather Eather - Marian & E H Flack Trust - Mr E V Carroll - Mr Harold F Stevens RFM Oct-05 Merlin Thomas Thomas MC, Tikellis C, Burns WM, Bialkowski K, Cao Z, Coughlan MT, Jandeleit-Dahm K, Cooper ME, Forbes JM. - Mrs M I Euhus - Helen Macpherson Smith Trust - Construction Engineering Australia - Mrs Edna J Stock - Mrs K L Fairweather Interactions between renin angiotensin system and advanced glycation in the kidney. - Mazda Foundation - Mr Stephen J Cook - Miss B F Sutton - Mr Greg J Farmer J Am Soc Nephrol. 2005 Oct;16(10):2976-84. - Sarah & Baillieu Myer Family Foundation - Mrs Edna Davis - Mr & Mrs R & J Taylor - Mr & Mrs J & B Filgate - Pierce Armstrong Foundation - Mr & Mrs Albert & Barbara Edwards - Mr Ron Thomas Nov-05 Bronwyn Kingwell (1) (1) Natoli AK, Medley TL, Ahimastos AA, Drew BG, Thearle DJ, Dilley RJ, Kingwell BA. - Dr J M Gardiner - Ramaciotti Foundations - Mr Robbie Eisner - Mrs Jean Thomas - Mr & Mrs V M & E Gawne Jeremy Jowett (2) Sex steroids modulate human aortic smooth muscle cell matrix protein deposition and matrix - Jack & Robert Smorgon Families Foundation - Mr E L Garner AM & Mrs N Garner - Miss J L Thompson - Mrs J M Gibson metalloproteinase expression. - Sunshine Foundation - Miss Helen Glascodine - Mr John W Thompson - Mr Richard P Harbig - Mr & Mrs John & Kathleen Godfrey Hypertension. 2005 Nov;46(5):1129-34. - Joe White Bequest - Mrs Stella Thomson - Mr Malcolm Kemp - Mr John Griffiths OAM & Mrs Joan Griffiths - Mr & Mrs Ken & Sue Trezise - Mr N Lees - Dr James S Guest AM - Miss J A Turnbull (2) Curran JE, Jowett JB, Elliott KS, Gao Y, Gluschenko K, Wang J, Azim DM, Cai G, Mahaney MC, Comuzzie AG, - Mr & Mrs Denys McCullough - Mrs L K Hancock - Mr J L Vuillemain - Dr John K Harcourt OAM Dyer TD, Walder KR, Zimmet P, Maccluer JW, Collier GR, Kissebah AH, Blangero J. - Mr Frank A Roberts - Mrs J E Watkins - Mr & Mrs E & J Ross - Mr R J Harden - Dr W G Wicks Genetic variation in selenoprotein S influences inflammatory response. - Mrs Pauline Row - Mr & Mrs F & S Hawkins - Mrs Gwen Williams Nat Genet. 2005 Nov;37(11):1234-41. - Mrs Alison H Rowland - Mrs Ida L Hicks - Mr Kenneth Woolfe - Dr A David Hore Dec-05 Emma Baker Baker EK, Johnstone RW, Zalcberg JR, El-Osta A. - Mr & Mrs John & Helene Sutherland - Ms Jennifer Tatchell - Mr Robert Hudson Epigenetic changes to the MDR1 locus in response to chemotherapeutic drugs. - Miss G Jones Oncogene. 2005 Dec 1;24(54):8061-75. - Dr & Mrs F C Jones Development
68 the Baker could not do what it The Baker’s Wine Lovers’ Dinner Although it gives a level of A talent for creative thought Friends of Baker Comittee The Development team serves 69 does to combat cardiovascular has become a popular event on satisfaction to review the past and a mindset of continuous Mrs Bernadette Brodribb 2005 Report Annual Institute Research Heart Baker disease without the support of the Melbourne social calendar. year, we are always excited and improvement throughout the Baker Ms Catherine Collier to support the scientific and its many donors and benefactors. The 2005 event was once again a eager to look to the future. This results in constant progression Mr Stephen Cook The many generous donations, huge success and we thank Ian office was previously known as and innovation in our research. Mrs Miriam Greenfield clinical mission of the Baker. bequests and contributions of time Loftus for sourcing the magnificent the Foundation, but in 2005 we Diversity of skills, specialisation Mr Robert Lyng Annual Report 2005 and support we receive through wines from the following generous decided that it should be called and cultures provides the basis for Mrs Joy Mein Our activities are designed the year are vital, and the job wine makers -: the Development Department. robust, multi-disciplinary teams Sir Laurence Muir (Chair) of the Development team is to We believe this better reflects who collaborate to explore ideas Mrs Yvonne Oeser to align with the direction of
Baker Heart Research Institute › Casella Estate ensure that those who provide the work that we undertake. and methods to ensure unique and Mrs Marian Poynter › Delatite Winery this support to the Institute are Foundations are often defined valuable research findings. Mrs Vivienne Ritchie the organisation to ensure our › Majella Wines Pty Ltd themselves supported in the as philanthropic organisations These findings will ultimately save Mrs Margaret Ross › Morris Wines efforts assist the Institute in partnership they have that distribute funds. We see lives and improve the quality of Mr & Mrs Eric & June Ross › Peter Lehmann Wines chosen to establish with our our role as raising funds and life for many. Our donors play Mr Philip Ross › Plunkett’s Winery achieving its goals. scientific community. resources for the Baker, by building a major role in this process. By Mr Michael Stillwell › Taltarni Vineyards relationships and promoting the supporting innovation donors In 2005, the department was › Tuck’s Ridge science to a broad audience. provide us with the flexibility to involved in a broad range of › Westend 3 Bridges Estate Development is associated build on our successes and attract activities geared to increasing & the Milawa Cheese Company for with an act of improving, by research ‘stars’. awareness of the valuable their award winning cheeses. expanding or enlarging or refining and innovative research being We sincerely thank all those who Also on our event calendar was - characteristics that we closely undertaken at the Baker, and have contributed to the Baker in the Great Debate - ”Does a healthy identify with our efforts. raising funds to support that 2005, particularly our loyal base of lifestyle really mean a a longer research. The contribution of The Development department volunteers who worked over 1000 life?”, hosted by Mark Mitchell. donors was substantial, and as serves to support the scientific hours this year – a huge saving in The creative idea behind this event we progress we will build on and clinical mission of the Baker. man-hours, and a truly delightful was for guests to come and learn the achievements to ensure a Our activities are designed to group of people we have come to interesting facts about their health sustainable funding and align with the direction of the know very well. We look forward in an entertaining way. The tone support base. organisation to ensure our efforts to continuing these rewarding of the debate was informative yet assist the Institute in achieving relationships, as well as new ones Integral to our success is, of course, light-hearted. We did not realise its goals. into the future. our loyal supporter base. We the talent for comedy our scientific have approximately 60 volunteers researchers possess. This made In reflecting on the attributes assisting in wide ranging tasks. for an inspiring learning of the Baker, there is much We have established ‘Friends of experience as well as a most that is unique and much that Baker’. This enthusiastic, lively entertaining evening. we can promote to the broader group are committed to organising community. The organisation is Keverne Pearson had a near fatal events for us that will expose our extremely successful in the arena heart attack and underwent organisation to a broader audience of prevention, treatment and cure heart surgery in 2004. Kev’s and provide much needed funds. of cardiovascular disease. Less Relay Ride for Life was his obvious perhaps, is the exceptional Financial and resource support inspirational way to say thank skills and culture within, that comes from a number of sectors, you to the team that saved him makes the organisation a great including individuals, trusts, - a state-wide relay bike ride, success. Our capacity to mentor foundations, the business with six participants. Over six and nurture students and early community and from people who weeks the team rode around career scientists provides a wealth have kindly remembered us in Victoria, holding approximately 30 of scientific ‘stars’ for our own their wills. seminars in regional towns. The facility workforce, and those seminars presented information of international and national on Cardiovascular disease and the organisations. We are fortunate innovative work of the Baker. that in this particular area, Once again we were indebted to we are well supported by donors Maestro Vladimir Vais, legendary who specifically contribute to our conductor of the Bolshoi Theatre, scholars’ program. This program Moscow, for arranging an evening enhances our ability to attract soirée with opera’s rising stars ‘the best of the best’. Emily Wang, Lynlee Williams, Cosimo Ciccone and Matthew Davine. The acoustics of Christ Church South Yarra ensured a memorable evening of arias from our favourite classics. L-R: Bobbie Renard, Elizabeth Veal, Margherita Boemo, Lyn Brodie Baker Medical Baker Medical Research Institute Research Institute › Income Statement for the year › Balance Sheet as at ended 31 December 2005 31 December 2005
70 Consolidated Parent Consolidated Parent 71 2005 2004 2005 2004 2005 2004 2005 2004 2005 Report Annual Institute Research Heart Baker $ $ $ $ $ $ $ $ Revenue from ordinary activities 29,920,164 22,301,699 25,795,069 22,301,699 ASSETS Annual Report 2005 Expenses for building works - (1,895,018) - (1,895,018) Current assets Employee benefits expense (15,608,148) (12,474,984) (13,714,482) (12,474,984) Cash assets 4,888,886 2,746,574 3,200,150 2,746,574
Baker Heart Research Institute Laboratory consumables (5,322,948) (3,380,071) (4,314,372) (3,380,071) Trade and other receivables 2,372,365 3,367,728 1,471,801 3,367,728 Depreciation and Intercompany loan - - 226,463 - amortisation expenses (1,280,559) (1,148,452) (1,227,237) (1,148,452) Available-for-sale Share of loss in associate (93,040) - (93,040) - financial assets 13,306,474 6,901,515 13,306,484 6,901,515 Fixed assets written off (664,062) - (502,178) - Investment in associate 21,961 - 21,961 - Building overheads (431,101) (360,950) (372,029) (360,950) Other 107,464 90,754 67,057 90,754 Borrowing costs expense (114) (35,552) - (35,552) Total current assets 20,697,150 13,106,571 18,293,916 13,106,571 Laboratory support expenses (2,528,279) (1,313,078) (1,795,787) (1,313,078) Research and development (211,982) - - - Non-current assets Other expenses from Plant & equipment 4,453,638 4,538,053 4,216,899 4,538,053 ordinary activities (1,229,063) (1,612,781) (1,194,448) (1,612,781) Intangible assets 65,140 45,338 65,140 45,338 Total non-current assets 4,518,778 4,583,391 4,282,039 4,583,391 Surplus from ordinary TOTAL ASSETS 25,215,928 17,689,962 22,575,955 17,689,962 activities before income tax expense 2,550,868 80,813 2,581,496 80,813 LIABILITIES Current liabilities Income tax expense (70,877) - - - Trade and other payables 3,892,621 4,369,671 2,824,497 4,369,671 Prepaid income 1,663,136 - 179,441 - Surplus from ordinary activities Provisions 2,246,750 1,733,477 2,134,188 1,733,477 after income tax expense 2,479,991 80,813 2,581,496 80,813 Income tax payable 70,877 - - - Total current liabilities 7,873,384 6,103,148 5,138,126 6,103,148 TOTAL CHANGE IN FUNDS 2,479,991 80,813 2,581,496 80,813 Non-current liabilities Provisions 133,831 241,123 133,831 241,123 Other 6,220 - - - Total non-current liabilities 140,051 241,123 133,831 241,123 TOTAL LIABILITIES 8,013,435 6,344,271 5,271,957 6,344,271
NET ASSETS 17,202,493 11,345,691 17,303,998 11,345,691
FUNDS Accumulated funds Operating fund (7,372,845) (7,329,085) (7,271,340) (7,329,085) Capital fund 19,326,017 18,138,457 19,326,017 18,138,457 Specific purpose fund 1,872,510 536,319 1,872,510 536,319 Fair value reserve 3,376,811 - 3,376,811 -
TOTAL FUNDS 17,202,493 11,345,691 17,303,998 11,345,691 Baker Medical Journal Articles Research Institute 2005 › Cash Flow Statement for the year ended 31 December 2005
72 Agrotis A. The genetic basis for altered blood Burrell LM, Risvanis J, Kubota E, Dean RG, Duffy SJ, Biegelsen ES, Eberhardt RT, Kahn DF, Giunti S, Cooper M. Does the metabolic 73 Consolidated Parent vessel function in disease: large artery MacDonald PS, Lu S, Tikellis C, Grant SL, Lew RA, Kingwell BA, Vita JA. Low renin activity and syndrome make blood pressure control 2005 2004 2005 2004 stiffening. Vasc Health Risk Management Smith AI, Cooper ME, Johnston CI. Myocardial relative aldosterone excess are associated more difficult in diabetes? J Hypertens 2005 Report Annual Institute Research Heart Baker 2005;1(4):333-344. infarction increases ACE2 expression in rat with impaired nitric oxide-mediated 2005;23(12):2155-6. $ $ $ $ and humans. Eur Heart J 2005;26(4):369-75 resistance vessel vasodilation in hypertension. Agrotis A, Kalinina N, Bobik A. Transforming (discussion 322-4). Hypertension 2005;46(4):707-13. Gold PW, Wong ML, Goldstein DS, Gold HK, CASH FLOWS FROM ORDINARY ACTIVITIES growth factor-beta, cell signaling and Ronsaville DS, Esler M, Alesci S, Masood A, Receipts from granting bodies 12,279,185 9,947,993 12,147,321 9,947,993 cardiovascular disorders. Curr Vasc Pharmacol Calkin AC, Forbes JM, Smith CM, Lassila M, Eikelis N, Esler MD. The neurobiology of human Licinio J, Geracioti TD Jr, Perini G, DeBellis MD,
Annual Report 2005 2005;3(1):55-61. Cooper ME, Jandeleit-Dahm KA, Allen TJ. obesity. Exp Physiol 2005;90(5):673-82. Holmes C, Vgontzas AN, Charney DS, Chrousos Donations and bequests 4,141,020 3,193,181 4,141,020 3,193,181 Rosiglitazone Attenuates Atherosclerosis in a GP, McCann SM, Kling MA. Cardiac implications Ahimastos AA, Natoli AK, Lawler A, Blombery Model of insulin insufficiency independent of Escher G, Hoang A, Georges S, Tchoua U, El-Osta of increased arterial entry and reversible Receipts for building works - 450,000 - 450,000 PA, Kingwell BA. Ramipril Reduces Large- its metabolic effects. Arterioscler Thromb Vasc A, Krozowski Z, Sviridov D. Demethylation 24-h central and peripheral norepinephrine Artery Stiffness in Peripheral Arterial Disease Biol 2005;25(9):1903-9. using the epigenetic modifier, 5-azacytidine, levels in melancholia. Proc Natl Acad Sci USA
Baker Heart Research Institute Payments to suppliers & employees (22,965,869) (19,808,796) (20,715,924) (19,808,796) and Promotes Elastogenic Remodeling in Cell increases the efficiency of transient 2005;102(23):8303-8. Culture. Hypertension 2005;45(6):1194-9. Campbell DJ, Krum H, Esler MD. Losartan transfection of macrophages. J Lipid Res Dividends received 696,885 288,629 696,885 288,629 increases bradykinin levels in hypertensive 2005;46(2):356-65. Gould PA, Yii M, Esler MD, Power JM, Kaye DM. Interest received 197,244 191,645 186,178 191,645 Ahmed N, Oliva KT, Barker G, Hoffmann humans. Circulation 2005;111(3):315-20. Atrial fibrillation impairs cardiac sympathetic P, Reeve S, Smith IA, Quinn MA, Rice GE. Esler M, Dawood T. Is “cardiovascular response to baroreceptor unloading Rent received – Proteomic tracking of serum protein isoforms Chan CK, Burke SL, Zhu H, Piletz JE, Head protection” by estrogens due to inhibition of in congestive heart failure. Eur Heart J as screening biomarkers of ovarian cancer. GA. Imidazoline receptors associated with the sympathetic nervous system? Clin Auton 2005;26(23):2562-7. Baker and Burnet buildings 1,260,148 1,003,311 1,260,148 1,003,311 Proteomics 2005;5(17):4625-36. noradrenergic terminals in the rostral Res 2005;15(3):186-8. ventrolateral medulla mediate the hypotensive Groop PH, Forsblom C, Thomas MC. Selective Commercial Income 9,676,405 6,578,703 5,930,932 6,578,703 Ahmed N, Rice GE. Strategies for revealing responses of moxonidine but not clonidine. Esmore DS, Kaye D, Salamonsen R, Buckland insulin resistance and microvascular disease. General income 454,156 407,471 454,156 407,471 lower abundance proteins in two-dimensional Neuroscience 2005;132(4):991-1007. M, Rowland M, Negri J, Rowley Y, Woodward Nat Clin Pract Endo & Metab 2005;1(2):100-10. protein maps. J Chromatogr B 2005; J, Begg JR, Ayre P, Rosenfeldt FL. First clinical 815(1-2):39-50. Chin-Dusting J, Mizrahi J, Jennings G, Fitzgerald implant of the VentrAssist left ventricular Groop PH, Thomas MC. Brain Natriuretic Peptide D. Outlook: Finding improved medicines: the assist system as destination therapy for end- (BNP): the microalbuminuria of cardiac disease NET CASH INFLOW FROM Ahmed N, Riley C, Oliva K, Rice G, Quinn M. role of academic-industrial collaboration. stage heart failure. J Heart Lung Transplant and diabetes? Diabetologia 2005;48(1):3-5. ORDINARY ACTIVITIES Ascites induces modulation of alpha6beta1 Nat Rev Drug Discov 2005;4(11):891-7. 2005;24(8):150-4. 5,739,174 2,252,137 4,100,716 2,252,137 integrin and urokinase plasminogen Ha T, Li Y, Gao X, McMullen JR, Shioi T, Izumo activator receptor expression and associated Cooper ME, Jandeleit-Dahm K, Thomas MC. Fang L, Wei HM, Chowdhury SH, Gong NL, Song S, Kelley JL, Zhao A, Haddad GE, Williams DL, functions in ovarian carcinoma. Br J Cancer Targets to retard the progression of diabetic J, Xiong ZW, Mak KH, Wang D, Lim YL, Chatterjee Browder IW, Kao RL, Li C. Attenuation of cardiac CASH FLOWS FROM INVESTING ACTIVITIES 2005;92(8):1475-85. nephropathy. Kidney Int 2005;68(4):1439-45. S. Association of Leu125Val polymorphism of hypertrophy by inhibiting both mTOR and platelet endothelial cell adhesion molecule-1 NFkappaB activation in vivo. Free Radic Biol Payment for available-for-sale Ahmed N, Riley C, Rice G, Quinn M. Role of Cooper ME, Jandeleit-Dahm KA. Lipids (PECAM-1) gene & soluble level of PECAM-1 Med 2005;39(12):1570-80. financial assets (6,654,451) (5,856,551) (6,654,381) (5,856,551) Integrin Receptors for Fibronectin, Collagen and diabetic renal disease. Curr Diab Rep with coronary artery disease in Asian Indians. and Laminin in the Regulation of Ovarian 2005;5(6):445-8. Indian J Med Res 2005;121(2):92-9. Harikrishnan KN, Chow MZ, Baker EK, Pal S, Proceeds from sale of available- Carcinoma Functions in Response to a Matrix Bassal S, Brasacchio D, Wang L, Craig JM, Jones Microenvironment. Clin Exp Metastasis Corstius HB, Zimanyi MA, Maka N, Herath T, Forbes JM, Soldatos G, Thomas MC. Below PL, Sif S, El-Osta A. Brahma links the SWI/SNF for-sale financial assets 4,100,035 2,575,918 4,100,035 2,575,918 2005;22(5):391-402. Thomas W, van der Laarse A, Wreford NG, Black the radar: advanced glycation end products chromatin-remodeling complex with MeCP2- MJ. Effect of Intrauterine Growth Restriction on which detour “around the side”. Is HbA1c not dependent transcriptional silencing. Nat Genet Payment for plant & equipment (1,297,875) (1,258,376) (1,092,724) (1,258,376) Allen TJ, Jandeleit-Dahm KAM. Preventing the Number of Cardiomyocytes in Rat Hearts. an accurate enough predictor of long term 2005;37(3):254-264. Proceeds from related party loan 226,463 - - - Atherosclerosis with Angiotensin-Converting Pediatr Res 2005;57(6):796-800. progression and glycaemic control in diabetes? Enzyme Inhibitors: Emphasis on Diabetic Clin Biochem Rev 2005;26(4):123-34. Hashimura K, Sudhir K, Nigro J, Ling S, Cash transfer from subsidiary 29,036 - - - Atherosclerosis. Curr Drug Targets - Cardiovasc Coughlan MT, Cooper ME, Forbes JM. Can Williams MR, Komesaroff PA, Little PJ. Hematol Disorders 2005;5(6):503-12. advanced glycation end product inhibitors Forbes JM, Thorpe SR, Thallas-Bonke V, Pete Androgens stimulate human vascular smooth modulate more than one pathway to enhance J, Thomas MC, Deemer ER, Bassal S, El-Osta muscle cell proteoglycan biosynthesis and Bach LA, Gallicchio MA, McRobert EA, Tikoo A, renoprotection in diabetes? Ann N Y Acad Sci A, Long DM, Panagiotopoulos S, Jerums G, increase lipoprotein binding. Endocrinology NET CASH OUTFLOW FROM Cooper ME. Effects of advanced glycation end 2005;1043:750-8. Osicka TM, Cooper ME. Modulation of soluble 2005;146(4):2085-90. INVESTING ACTIVITIES (3,596,792) (4,539,009) (3,647,070) (4,539,009) products on ezrin-dependent functions in receptor for advanced glycation end products LLC-PK1 proximal tubule cells. Ann N Y Acad Sci D’Amore A, Black MJ, Thomas WG. The by angiotensin converting enzyme-1 inhibition Head GA, Reid CM, Lukoshkova EV. 2005;1043:609-16. angiotensin II type 2 receptor causes in diabetic nephropathy. J Am Soc Nephrol Nonsymmetrical double logistic analysis of constitutive growth of cardiomyocytes and 2005;16(8):2363-72. ambulatory blood pressure recordings. J Appl NET CASH INCREASE IN CASH HELD Baker EK, Johnstone RW, Zalcberg JR, El-Osta does not antagonize angiotensin II type 1 Physiol 2005;98(4):1511-8. A. Epigenetic changes to the MDR1 locus in receptor-mediated hypertrophy. Hypertension Fröjdö S, Sjölind S, Parkkonen M, Mäkinen response to chemotherapeutic drugs. Oncogene 2005;46(6):1347-54. V-P, Kilpikari R, Pettersson-Fernholm K, Henstridge DC, Kingwell BA, Formosa MF, Drew Cash at beginning of the 2005;24(54):8061-75. Forsblom C, Fagerudd J, Tikellis C, Cooper ME, BG, McConell GK, Duffy SJ. Effects of the nitric Dawood T, Williams MR, Fullerton MJ, Myles K, Wessman M; Per-Henrik Groop on behalf of oxide donor, sodium nitroprusside, on resting financial year 2,746,574 4,998,710 2,746,574 4,998,710 Ballinger ML, Thomas MC, Nigro J, Ivey ME, Schuijers J, Funder JW, Sudhir K, Komesaroff PA. the FinnDiane Study Group. Polymorphisms leg glucose uptake in patients with type 2 Dilley RJ, Little PJ. Glycated and carboxy- Glucocorticoid responses to stress in castrate Effects of exchange rate changes on in the angiotensin-converting enzyme 2 diabetes. Diabetologia 2005;48(12):2602-8. methylated proteins do not directly activate and testosterone-replaced rams. Regul Pept gene and diabetic nephropathy. Diabetologia cash held in foreign currencies (70) 34,736 (70) 34,736 human vascular smooth muscle cells. Kidney 2005;125(1-3):47-53. 2005;48(11):2278-81. Huber R, Nauck M, Basler N, Haas B, Mattern Int 2005;68(6):2756-65. M, Ludtke R, Peter K. Effects of subtotal fasting de Haan JB, Stefanovic N, Nikolic-Paterson Fukami K, Cooper ME, Forbes JM. Agents in on plasmatic coagulation, fibrinolytic status Bassal S, El-Osta A. DNA damage detection D, Scurr LL, Croft KD, Mori TA, Hertzog P, Kola development for the treatment of diabetic and platelet activation: a controlled pilot study CASH AT THE END OF THE and repair, and the involvement of epigenetic I, Atkins RC, Tesch GH. Kidney expression of nephropathy. Expert Opin Investig Drugs in healthy subjects. Nutr Metab Cardiovasc Dis FINANCIAL YEAR 4,888,886 2,746,574 3,200,150 2,746,574 states. Hum Mutat 2005;25(2):101-9. glutathione peroxidase-1 is not protective 2005;14(3):279-94. 2005;15(3):212-8. against streptozotocin-induced diabetic Boak LM, Dart AM, Duffy SJ, Chin-Dusting nephropathy. Am J Physiol Renal Physiol Fukushima K, Funayama Y, Yonezawa H, Jandeleit-Dahm K, Lassila M, Davis BJ, Candido JP. Responses to neither exogenous nor 2005;289(3):F544-51. Takahashi K, Haneda S, Suzuki T, Sasano H, R, Johnston CI, Allen TJ, Burrell LM, Cooper The summary financial information provided above and in the preceding two pages, being an income endogenous endothelin-1 are altered in Naito H, Shibata C, Krozowski ZS, Sasaki I. ME. Anti-atherosclerotic and renoprotective statement, balance sheet and cash flow statement, has been extracted from the audited special purpose patients with hypercholesterolemia. J Lipid Res Dean RG, Balding LC, Candido R, Burns WC, Aldosterone enhances 11beta-hydroxysteroid effects of combined angiotensin-converting 2005;46(12):2667-72. Cao Z, Twigg SM, Burrell LM. Connective dehydrogenase type 2 expression in colonic enzyme and neutral endopeptidase inhibition financial statements of the Baker Medical Research Institute and its controlled entities. The summary tissue growth factor and cardiac fibrosis after epithelial cells in vivo. Scand J Gastroenterol in diabetic apolipoprotein E-knockout mice. J Bobik A. The structural basis of hypertension: financial information does not include all the information and notes normally included in a statutory set myocardial infarction. J Histochem Cytochem 2005;240(7):850-7. Hypertens 2005;23(11):2071-82. vascular remodelling, rarefaction and 2005;53(10):1245-56. of financial statements. A full set of audited special purpose financial statements can be obtained from our angiogenesis/arteriogenesis. J Hypertens Gao XM, Kiriazis H, Moore XL, Feng XH, Jandeleit-Dahm KA, Tikellis C, Reid CM, website at http://www.baker.edu.au 2005;23(8):1473-5. Dilley RJ, Farrelly CA, Allen TJ, Jandeleit-Dahm Sheppard K, Dart A, Du XJ. Regression of Johnston CI, Cooper ME. Why blockade of J, Cooper ME, Morahan G, Little PJ. Diabetes Pressure-Overload Induced Left Ventricular the renin-angiotensin system reduces the Brown R, Wiesner G, Ur E, Wilkinson induces Na/H exchange activity and hypertrophy Hypertrophy in Mice. Am J Physiol Heart Circul incidence of new-onset diabetes. J Hypertens M. Pituitary resistin gene expression The statutory financial statements (from which the summary financial information has been extracted) have of rat mesenteric but not basilar arteries. Physiol 2005;288(6):2702-7. 2005;23(3):463-73. is upregulated in vitro and in vivo by Diabetes Res Clin Pract 2005;70(3):201-8. been prepared with Australian Accounting Standards, which include Australian equivalents to International dexamethasone but is unaffected by Gao XM, Xu Q, Kiriazis H, Dart AM, Du XJ. Mouse Jandeleit-Dahm KAM, Lassila M, Allen TJ. Financial Reporting Standard (‘AIFRS’). The statutory financial statements were qualified by the auditors Ernst rosiglitazone. Neuroendocrinology Dinh DT, Qian H, Seeber R, Lim E, Pfleger K, model of post-infarct ventricular rupture: Advanced glycation end products in diabetes 2005;81(1):41-8. Eidne KA, Thomas WG. Helix I of beta-arrestin & Young Australia in respect to the Institute’s policy to expense capital works undertaken on the buildings, time course, strain- and gender-dependency, associated atherosclerosis and renal disease: is involved in postendocytic trafficking but tensile strength, and histopathology. interventional studies. Ann N Y Acad Sci which the Institute utilises. Full details of the audit qualification are contained within the audit opinion in is not required for membrane translocation, Cardiovasc Res 2005;65(2):469-77. 2005;1043:759-66. receptor binding, and internalization. Mol the statutory financial statements. Pharmacol 2005;67(2):375-82. Publications Listing 2005 › Continued
74 Januszewski AS, Thomas MC, Chung SJ, Lassila M, Jandeleit-Dahm K, Seah KK, Calkin Mookerjee I, Unemori EN, Du XJ, Tregear GW, Parving HH, Mogensen CE, Thomas MC, Brenner Sato S, Fukushima K, Naito H, Funayama Y, Thomas M, Blennerhassett J, Walker R. Relapse Wei HM, Fang L, Song J, Chatterjee S. Statin- Zhang L, Cheng J, Ma Y, Thomas W, Zhang 75 Karschimkus CS, Rowley KG, Nelson C, O’Neal AC, Allen TJ, Cooper ME. Imatinib attenuates Samuel CS. Relaxin modulates fibroblast BM, Cooper ME. Poor prognosis in proteinuric Suzuki T, Sasano H, Krozowski Z, Shibata C, with transformation of lupus nephritis in a inhibited endothelial permeability could J, Du J. Dual pathways for nuclear factor D, Wang Z, Best JD, Jenkins AJ. Plasma diabetic nephropathy in apolipoprotein function, collagen production, and matrix type 2 diabetic patients with retinopathy: Sasaki I. Induction of 11beta-hydroxysteroid transplant kidney. Lupus 2005;14(7):554-6. be associated with its effect on PECAM-1 in kappaB activation by angiotensin II in vascular 2005 Report Annual Institute Research Heart Baker low-molecular weight fluorescence in E Knockout mice. J Am Soc Nephrol metalloproteinase-2 expression by cardiac insights from the RENAAL study. QJM-Int J Med dehydrogenase type 2 and hyperaldosteronism endothelial cells. FEBS Lett 2005;579(5):1272-8. smooth muscle: phosphorylation of p65 by Type 1 diabetes mellitus. Ann N Y Acad Sci 2005;16(2):367-73. fibroblasts. Ann N Y Acad Sci 2005;1041:190-3. 2005;98(2):119-26. are essential for enhanced sodium absorption Thomas MC, Burns WC, Cooper ME. Tubular IkappaB kinase and ribosomal kinase. Circ Res 2005;1043:655-61. after total colectomy in rats. Surgery changes in early diabetic nephropathy. Adv Wei HM, Fang L, Song J, Li GD, Chatterjee S. 2005;97(10):975-82. Lekgabe ED, Kiriazis H, Zhao C, Xu Q, Moore Morris JB, Kenney B, Huynh H, Woodcock EA. Pepe S. Effect of dietary polyunsaturated 2005;137(1):75-84. Chronic Kidney Dis 2005;12(2):177-86. Lovastatin compromises C-reactive protein Jennings G. Arterial pulse waveforms: defined XL, Su Y, Bathgate RA, Du XJ, Samuel CS. Regulation of the proapoptotic factor FOXO1 fatty acids on age-related changes in cardiac induced endothelial dysfunction including Zhang W-Z. Age-associated increase in creatine Thomas MC, Cooper ME. Facing the music:
Annual Report 2005 at birth or barking up the wrong arterial tree? Relaxin reverses cardiac and renal fibrosis in (FKHR) in cardiomyocytes by growth factors mitochondrial membranes. Exp Gerontol Schlaich MP, Kaye DM, Lambert E, Hastings J, altered expression of cell adhesion molecules kinase-MB-Specific Activity in Human Serum J Hypertens 2005;23(7):1337-9. spontaneously hypertensive rats. Hypertension and alpha1-adrenergic agonists. Endocrinology 2005;40(5):369-76. Campbell DJ, Lambert G, Esler MD. Angiotensin managing kidney disease in diabetes. Aust J and increased monocyte recruitment. Confounds its use as an Injury Marker. Heart 2005;46(2):412-8. 2005;146(10):4370-6. II and norepinephrine release: interaction Gen Pract 2005;5(2):1-5. Atherosclerosis 2005;178(2):399-401. Lung Circ 2005;14(2):104-6. Kamimori H, Unabia S, Thomas WG, Aguilar Pepe S, Lakatta EG. Aging hearts and vessels: and effects on the heart. J Hypertens MI. Evaluation of the membrane-binding Levidiotis V, Freeman C, Tikellis C, Cooper ME, Natoli AK, Medley TL, Ahimastos AA, Drew BG, masters of adaptation and survival. Cardiovasc 2005;23(5):1077-82. Thomas MC, Cooper ME, Forbes JM. Advanced Widlansky ME, Duffy SJ, Hamburg NM, Gokce Book Chapters
Baker Heart Research Institute properties of the proximal region of the Power DA. Heparanase inhibition reduces Thearle D, Dilley RJ, Kingwell BA. Sex steroids Res 2005;66(2):190-3. glycation end products and diabetic N, Warden BA, Wiseman S, Keaney JF Jr, Frei angiotensin II receptor (AT1A) carboxyl terminus proteinuria in a model of accelerated anti- modulate human aortic smooth muscle Sheehan PM, Rice GE, Moses EK, Brennecke nephropathy. Am J Ther 2005;12(6):562-72. B, Vita JA. Effects of black tea consumption on Ahrens I, Bode C, Peter K. Inhibition of platelet by surface plasmon resonance. Anal Sci glomerular basement membrane antibody cell matrix protein deposition and matrix Petersson M, Friberg P, Eisenhofer G, Lambert SP. 5 Beta-dihydroprogesterone and steroid 5 plasma catechins and markers of oxidative activation and aggregation. In: Handbooks of 2005;21(2):171-4. disease. Nephrology 2005;10(2):167-73. metalloproteinase expression. Hypertension G, Rundqvist B. Long-term outcome in relation beta-reductase decrease in association with Thomas MC, Cooper ME, Forbes JM. Interactions stress and inflammation in patients with Experimental Pharmacology; Atherosclerosis: 2005;46(5):1129-34. to renal sympathetic activity in patients with human parturition at term. Mol Hum Reprod between the Renin Angiotensin System and coronary artery disease. Free Radic Biol Med Diet and Drugs. Ed: von Eckardstein A. Springer Karagiannis TC, El-Osta A. RNA interference Luo J, McMullen JR, Sobkiw CL, Zhang L, chronic heart failure. Eur Heart 2005;11(7):495-501. Advanced Glycation in Diabetic Nephropathy. 2005;38(4):499-506. 2005;XII:443-65. and potential therapeutic applications of Dorfman AL, Sherwood MC, Logsdon MN, Horner Nelson MR, Ryan P, Willson K, Reid CM, Beilin J 2005;26(9):906-13. Ann N Y Acad Sci 2005;1043:927. short interfering RNAs. Cancer Gene Ther JW, DePinho RA, Izumo S, Cantley LC. Class IA LJ, Jennings GL, Johnston CI, Macdonald GJ, Shweta A, Denton KM, Kett MM, Bertram Wilkinson M, Wilkinson D, Wiesner G, Morash B, Jennings G. Exercise and Hypertension. In: 2005;12(10):787-95. phosphoinositide 3-kinase regulates heart size Marley JE, McNeil JJ, Morgan TO, West MJ, Wing Petersson M, Friberg P, Lambert G, Rundqvist JF, Lambert GW, Anderson WP. Paradoxical Thomas MC, Cooper ME, Tsalamandris C, Ur E. Hypothalamic resistin immunoreactivity Hypertension – Companion to Brenner & and physiological cardiac hypertrophy. Mol Cell LM. Predictors of failure to initiate randomized B. Decreased renal sympathetic activity structural effects in the unilaterally denervated MacIsaac R, Jerums G. Anemia with impaired is reduced by obesity in the mouse: co- Rector’s The Kidney, Second Edition. Eds: Oparil Karagiannis TC, Kn H, El-Osta A. The Histone Biol 2005;25(21):9491-502. treatment in a large trial of antihypertensive in response to cardiac unloading with spontaneously hypertensive rat kidney. erythropoietin response in diabetic patients. localization with alpha-melanostimulating S, Weber MA. Elsevier Saunders, Philadelphia Deacetylase Inhibitor, Trichostatin A, Enhances drug therapy in the aged. Am J Hypertens nitroglycerin in patients with heart failure. J Hypertens 2005;23(4):851-9. Arch Intern Med 2005;165(4):466-9. hormone. Neuroendocrinology 2005;81(1):19-30. 2005;496-506. Radiation Sensitivity and Accumulation of Masuo K, Katsuya T, Fu Y, Rakugi H, Ogihara T, 2005;18(6):885-8. Eur J Heart Fail 2005;7(6):1003-10. gammaH2A.X. Cancer Biol Ther 2005;4(7):787-93. Tuck ML. Beta2-adrenoceptor polymorphisms Soldatos G, Cooper ME. Dialysis and Diabetes. Thomas MC, Forbes JM, Cooper ME. Advanced Williams C. Australian attitudes to DNA sample Marasco S, Rosenfeldt FL, Pepe S. Coenzyme relate to insulin resistance and sympathetic Nestel PJ. Dietary factors that affect high Potter SM, Mitchell AJ, Simasathiansophon S, Diabetes Management 2005;35:20-1. glycation end products and diabetic banks and genetic screening. Curr Med Res Q10 treatment for heart disease: mechanism Kaye D, Esler M. Sympathetic neuronal overactivity as early markers of metabolic density lipoprotein concentration. Curr Med Cowden W, Sanni LA, Dinauer M, de Haan JB, nephropathy. Am J Ther 2005;12(6):562-72. Opin 2005;21(11):1773-5. of action and clinical results. In: Functional regulation of the heart in aging and heart disease in nonobese, normotensive Chem - IEMA 2005;5(4):361-5. Hunt N. Phagocyte-derived reactive oxygen Soldatos G, Cooper ME, Jandeleit-Dahm KA. Polyphenols and Carotenes with Antioxidative Thomas MC, Forbes JM, MacIsaac R, Jerums G, failure. Cardiovasc Res 2005;66(2):256-64. individuals. Am J Hypertens 2005;18(7):1009-14. species do not influence the progression of Advanced-glycation end products in insulin- Williams C, Kingwell BA, Burke K, McPherson Action. Chemical & Pharmaceutical Sciences Nestel PJ, Baghurst K, Colquhoun DM, Simes murine blood-stage malaria infections. Infect resistant states. Curr Hypertens Cooper ME. Low-molecular weight advanced J, Dart AM. Folic acid supplementation for 3 Review Series. Ed: Motohashi N. Research Kiriazis H, Du XJ, Feng X, Hotchkin E, Marshall Masuo K, Katsuya T, Fu Y, Rakugi H, Ogihara RJ, Mehalski K, White HD, Tonkin AM, Kirby Immun 2005;73(8):4941-7. Rep 2005;7(2):96-102. glycation end products: markers of tissue AGE wk reduces pulse pressure and large artery Signpost Publishing, India 2005;43-62. T, Finch S, Gao XM, Lambert G, Choate JK, Kaye T, Tuck ML. Lys418Asn polymorphism of the A, Pollicino C; Long-Term Intervention accumulation and more? Ann N Y Acad Sci stiffness independent of MTHFR genotype. Am DM. Preserved left ventricular structure and alpha2-adrenoceptor gene relates to serum with Pravastatin in Ischaemic Disease Power JM, Raman J, Byrne MJ, Alferness CA. Stewart RA, White HD, Kirby AC, Heritier SR, Simes 2005;1043:644-54. J Clin Nutr 2005;82(1):26-31. McMullen JR, Sadoshima J, Izumo S. function in mice with cardiac sympathetic uric acid levels but not to insulin sensitivity. Study Investigators. Relation of diet to Efficacy of the acorn cardiac support device in RJ, Nestel PJ, West MJ, Colquhoun DM, Tonkin Physiological versus Pathological Cardiac Thomas MC, Jerums G, Tsalamandris C, Macisaac hyperinnervation. Am J Physiol Heart Circul Hypertension 2005;46(1):144-50. cardiovascular disease risk factors in subjects animals with heart failure secondary to high AM; Long-Term Intervention With Pravastatin Winkle K, Tibballs J, Coles P, Ross-Smith M, Hypertrophy. In: Molecular Mechanisms for R, Panagiotopoulos S, Cooper ME; the MDNSG Physiol 2005;289(4):H1359-65. with cardiovascular disease in Australia and rate pacing. Heart Fail Rev 2005;10(2):117-23. in Ischemic Disease (LIPID) Study Investigators. Molenaar P, Lambert G, Wiltshire C, Fenner Cardiac Hypertrophy and Failure. Ed: Walsh RA. Study Group. Increased tubular organic ion Masuo K, Katsuya T, Fu Y, Rakugi H, Ogihara T, New Zealand: analysis of the Long-Term White blood cell count predicts reduction PJ, Gershwin L-A, Hawdon GM, Angus JA. The Parthenon Press, Lancaster 2005;117-36. clearance following chronic ACE inhibition Knight R, Rice GE, Permezel MP. Are alterations Tuck ML. Beta2- and beta3-adrenergic receptor Intervention with Pravastatin in Ischaemic Reid CM, Ryan P, Miles H, Willson K, Beilin in coronary heart disease mortality with cardiovascular actions of the Irukandji (Carukia in patients with type 1 diabetes. Kidney Int in plasma protease concentrations during polymorphisms are related to the onset of Disease trial. Am J Clin Nutr 2005;81(6):1322-9. LJ, Brown MA, Jennings GL, Johnston CI, pravastatin. Circulation 2005;111(14):1756-62. barnesi) jellyfish. Clin Exp Pharmacol Physiol Nestel P. Managing hyperlipidaemia: criteria for labour associated with obstetric outcomes? Am weight gain and blood pressure elevation over Macdonald GJ, Marley JE, McNeil JJ, Morgan TO, 2005;67(6):2494-9. 2005;32(9):777-88. investigating. In: Abnormal Laboratory Results, J Obstet Gynecol 2005;193(1):283-8. 5 years. Circulation 2005;111(25):3429-34. Nestel PJ, Chronopulos A, Cehun M. Dairy fat West MJ, Wing LM. Who’s really hypertensive?- Straznicky NE, Lambert EA, Lambert GW, 2nd edn. Ed: Kellerman G. McGraw-Hill, Sydney Thomas MC, Thorpe S, Baynes J, Cooper ME. in cheese raises LDL cholesterol less than that -Quality control issues in the assessment of Masuo K, Esler MD, Nestel PJ. Effects of Woodcock EA, Matkovich SJ. Ins(1,4,5)P(3) 2005;103-10. The role of AGEs and AGE inhibitors in diabetic Kooptiwut S, Kebede M, Zraika S, Favoloro Masuo K, Katsuya T, Kawaguchi H, Fu Y, Rakugi in butter in mildly hypercholesterolaemic blood pressure for randomized trials. Blood dietary weight loss on sympathetic activity receptors and inositol phosphates in the cardiovascular disease. Curr Drug Targets J, Tikellis C, Thomas MC, Forbes JM, Cooper H, Ogihara T, Tuck ML. Rebound weight gain as subjects. Eur J Clin Nutr 2005;59(9):1059-63. Press 2005;14(3):133-8. and cardiac risk factors associated with the heart-evolutionary artefacts or active signal Nestel PJ. Optimal macronutrient consumption ME, Dunlop M, Proietto J, Andrikopoulos S. associated with high plasma norepinephrine metabolic syndrome. J Clin Endocrinol Metab 2005;6(4):453-74. transducers? Pharmacol Ther 2005;107(2):240-51. for cardiovascular disease prevention. In: High glucose-induced impairment in insulin levels that are mediated through Nigro J, Ballinger M, Osman N, Dart AM, Little Reid CM, Thrift AG. Hypertension 2020: 2005;90(11):5998-6005. Dialogues in Cardiovascular Medicine. Eds: Thomas MC, Tikellis C. ACE-2; an ace up the secretion is associated with reduction in islet polymorphisms in the beta2-adrenoceptor. PJ. Anti-atherogenic role of Peroxisome confronting tomorrow’s problem today. Clin Woodcock EA, Matkovich SJ. Cardiomyocytes Hearse DJ, Ferrari R. 2005;10:89-95. sleeve. Curr Enz Inhib 2005;1(1):51-63. glucokinase in a mouse model of susceptibility Am J Hypertens 2005;18(11):1508-16. Proliferator Activated Receptor ligands. Curr Exp Pharmacol Physiol 2005;32(5-6):374-6. Sudhir K, Nigro J, Osman N, Little PJ. structure, function and associated pathologies. to islet dysfunction. J Mol Endocrinol Androgens: new effects on proteoglycan Int J Biochem Cell Biol 2005;37(9):1746-51. Peter K. Antiplatelet agents. In: Principles of Cardiol Rev 2005;1(2):89-102. Thomas MC, Tikellis C, Burns WM, Bialkowski K, 2005;35(1):39-48. Masuo K, Katsuya T, Ogihara T, Tuck ML. Acute Ritchie RH, Gordon JM, Woodman OL, Cao AH, biosynthesis and its consequences for Molecular Cardiology. Eds: Patterson C, Runge Cao Z, Coughlan MT, Jandeleit-Dahm K, Cooper hyperinsulinemia reduces plasma leptin levels Nigro J, Ballinger ML, Survase S, Osman N, Little Dusting GJ. Annexin-1 peptide Anx-1(2-26) atherosclerosis. ScientificWorldJournal Woodman RJ, Kingwell BA, Beilin LJ, Hamilton M. Humana Press 2005;203-18. ME, Forbes JM. Interactions between renin Kotschet E, Aggarwal A, Esmore D, Kaye D. in insulin-sensitive Japanese men. PJ. New approaches to regulating the CS/DS protects adult rat cardiac myocytes from 2005;5:521-6. SE, Dart AM, Watts GF. Assessment of central angiotensin system and advanced glycation in Left ventricular apical infection and rupture Am J Hypertens 2005;18(2 Pt 1):235-43. glycosaminoglycan component of the vascular cellular injury induced by simulated ischaemia. and peripheral arterial stiffness: studies Peter K. Platelet integrins and signalling. In: the kidney. J Am Soc Nephrol 2005;16(10):2976-84. complicating left ventricular assist device extracellular matrix. ScientificWorldJournal Br J Pharmacol 2005;145(4):495-502. Survase S, Ivey ME, Nigro J, Osman N, Little indicating the need to use a combination of Platelet Function: Assessment, Diagnosis and explantation in 2 women with postpartum Mayorov DN. Selective sensitization by nitric PJ. Actions of calcium channel blockers on techniques. Am J Hypertens 2005; Treatment. Eds: Quinn M, Fitzgerald D. Humana 2005;5:515-20. Thomas MC, Tsalamandris C, MacIssaac R, cardiomyopathy. J Heart Lung Transplant oxide of sympathetic baroreflex in rostral Rizkalla B, Forbes JM, Cao Z, Boner G, Cooper ME. vascular proteoglycan synthesis: relationship to 18(2 Pt 1):249-60. Press 2005;21-42. Jerums G. Anemia in diabetes; an emerging 2005;24(3):350-4. ventrolateral medulla of conscious rabbits. Oto T, Rabinov M, Rosenfeldt F, Esmore Temporal renal expression of angiogenic growth atherosclerosis. Vasc Health Risk Management complication of microvascular disease. Curr Hypertension 2005;45(5):901-6. DS. Extended pericardiotomy avoids factors and their receptors in experimental 2005;1(3):199-208. Woollard KJ. Soluble bio-markers in vascular Thomas MC, Cooper ME. Diabetic nephropathy. Diab Rev 2005;1(1):107-26. Lappas M, Permezel M, Rice GE. Leptin cardiopulmonary bypass during bilateral diabetes: role of the renin-angiotensin system. disease: much more than gauges of disease? In: The Year in Renal Medicine 2005, Ed. Levy J. and adiponectin stimulate the release of Meikle L, McMullen JR, Sherwood MC, Lader AS, J Hypertens 2005;23(1):153-64. Suzuki S, Tsubochi H, Ishibashi H, Matsuda Clin Exp Pharmacol Physiol 2005;32(4):233-40. Clinical Publishing, Oxford 2005;1:3-22. sequential lung transplantation. J Thorac Thomas WG. Double trouble for type 1 proinflammatory cytokines and prostaglandins Walker V, Chan JA, Kwiatkowski DJ. A mouse Y, Suzuki T, Krozowski ZS, Sasano H, Kondo Cardiovasc Surg 2005;129(2):466-7. angiotensin receptors in atherosclerosis. New from human placenta and maternal adipose model of cardiac rhabdomyoma generated by Rosenfeldt F, Marasco S, Lyon W, Wowk M, T. Inflammatory mediators down-regulate Woollard KJ, Fisch C, Newby R, Griffiths HR. Thomas MC, Groop PH. Diabetic Dyslipdaemia. Engl J Med 2005;352(5):506-8. tissue via nuclear factor-kappaB, PPAR-gamma loss of Tsc1 in ventricular myocytes. Hum Mol Paizis G, Tikellis C, Cooper ME, Schembri JM, Sheeran F, Bailey M, Esmore D, Davis B, Pick 11beta-hydroxysteroid dehydrogenase C-reactive protein mediates CD11b expression in In: Case Studies in Lipid Management. Ed: A, Rabinov M, Smith J, Nagley P, Pepe S. monocytes through the non-receptor tyrosine Betteridge J. Taylor & Francis 2005;127-42. and ERK 1/2. Endocrinology 2005;146(8):3334-42. Genet 2005;14(3):429-35. Lew RA, Smith AI, Shaw T, Warner FJ, Zulli A, type 2 in a human lung epithelial cell line Thorn LM, Forsblom C, Fagerudd J, Thomas MC, Coenzyme Q10 therapy before cardiac surgery kinase, Syk, and calcium mobilization but Burrell LM, Angus PW. Chronic liver injury in BEAS-2B and the rat lung. Tohoku J Exp Med Pettersson-Fernholm K, Saraheimo M, Waden J, Lappas M, Yee K, Permezel M, Rice GE. Mifune M, Ohtsu H, Suzuki H, Nakashima improves mitochondrial function and in vitro not through cytosolic peroxides. Inflamm Res Tikellis C, Johnston CI. Angiotensin-Converting rat and man upregulates the novel enzyme 2005;207(4):293-301. Ronnback M, Rosengard-Barlund M, Bjorkesten Release and regulation of leptin, resistin H, Brailoiu E, Dun NJ, Frank GD, Inagami contractility of myocardial tissue. J Thorac 2005;54(12):485-92. Enzymes: Properties and Function. In: angiotensin converting enzyme II. CG, Taskinen MR, Groop PH; FinnDiane Study and adiponectin from human placenta, fetal T, Higashiyama S, Thomas WG, Eckhart AD, Cardiovasc Surg 2005;129(1):25-32. Sviridov, D. The Hitch-Hiker’s guide for Hypertension – Companion to Brenner & Gut 2005;54(12):1790-6. Group. Metabolic syndrome in type 1 diabetes: membranes, and maternal adipose tissue and Dempsey PJ, Eguchi S. G Protein Coupling raising HDL cholesterol. Curr Med Chem - IEMA Younes A, Pepe S, Yoshishige D, Caffrey J, Rector’s The Kidney, Second Edition. Eds: Oparil association with diabetic nephropathy and skeletal muscle from normal and gestational and Second Messenger Generation Are Palliser HK, Hirst JJ, Ooi GT, Rice GE, Dellios Rosenfeldt FL, Mijch A, McCrystal G, Sweeney 2005;5(4):297-8. Lakatta EG. Ischemic preconditioning increases S, Weber MA. Elsevier Saunders, Philadelphia glycemic control (the FinnDiane study). diabetes mellitus-complicated pregnancies. Indispensable for Metalloprotease-dependent, NL, Escalona RM, Parkington HC, Young IR. C, Pepe S, Nicholls M, Dennett X. Skeletal the bioavailability of cardiac enkephalins. 2005;95. Diabetes Care 2005;28(8):2019-24. J Endocrinol 2005;186(3):457-65. Heparin-binding Epidermal Growth Factor Prostaglandin e and f receptor expression and myopathy associated with nucleoside reverse Sviridov, D. Therapeutic Targeting of HDL and Am J Physiol Heart Circul Physiol 2005;289(4): transcriptase inhibitor therapy: potential Reverse Cholesterol Transport. Curr Med Chem H1652-61. Shedding through Angiotensin II Type-1 myometrial sensitivity at labor onset in the Vozarova de Courten B, Hanson RL, Funahashi Lappas M, Yee K, Permezel M, Rice GE. benefit of coenzyme Q10 therapy. Int J STD AIDS - IEMA 2005;5(4):299-309. Receptor. J Biol Chem 2005;280(28):26592-9. sheep. Biol Reprod 2005;72(4):937-43. T, Lindsay RS, Matsuzawa Y, Tanaka S, Thameem Sulfasalazine and BAY 11-7082 interfere with 2005;16(12):827-9. Zhang GY, Ahmed N, Riley C, Oliva K, Barker F, Gruber JD, Froguel P, Wolford JK. Common the nuclear factor-kappa B and I kappa B Mix TC, Brenner RM, Cooper ME, de Zeeuw D, Parnell MM, Holst DP, Kaye DM. Augmentation Swarbrick JD, Buyya S, Gunawardana D, G, Quinn MA, Rice GE. Enhanced expression polymorphisms in the adiponectin gene ACDC kinase pathway to regulate the release of Ivanovich P, Levey AS, McGill JB, McMurray JJ, of endothelial function following exercise Samuel CS, Zhao C, Bathgate RA, Du XJ, Fletcher JI, Branson K, Smith B, Pepe S, of peroxisome proliferator-activated receptor are not associated with diabetes in Pima proinflammatory cytokines from human Parfrey PS, Parving HH, Pereira BJ, Remuzzi training is associated with increased L-arginine Summers RJ, Amento EP, Walker LL, McBurnie McLennan AG, Gayler KR, Gooley PR. 1H, 13C, gamma in epithelial ovarian carcinoma. Indians. Diabetes 2005;54(1):284-9. adipose tissue and skeletal muscle in vitro. G, Singh AK, Solomon SD, Stehman-Breen transport in human heart failure. Clin Sci M, Zhao L, Tregear GW. 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