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The research carried out within the Division and its associated programs has been enhanced by the establishment of the Medical Genome Centre. The mutant mice generated in the Centre will provide a range of animal models for the detailed study of the many biological processes under investigation within the School.
The groups within the Division continuously review their research findings to identify those aspects with potential clinical applications. In most cases, the groups have well established collaborations with hospital based researchers to facilitate the transfer, to the clinic, of advances made in fundamental research.
Professor Philip Board, Head of Division
In relation to transplant rejection, our aims are to understand the mechanisms by which xenogeneic (cross-species) and allogeneic (between genetically disparate members of the same species) islet grafts are rejected and then target intervention therapy to either the activation or expression of the immune response.Although xenograft and allograft rejection correlate with Th2 and Th1 cytokine responses respectively, our recent studies have shown that rejection is not regulated by switching intragraft cytokine profiles from a Th2- to Th1-type, and vice versa. These findings suggest that immunotherapy designed to polarise inflammatory cytokine responses probably would not be suitable as an anti-graft rejection strategy for clinical islet transplantation. Current studies are examining whether the intragraft expression of other immunoregulatory, anti-inflammatory cytokines (e.g. TGFbeta) correlates with the induction of xenograft and/or allograft tolerance in immunosuppressed recipient mice. Gene therapy technologies are being evaluated for facilitating the local expression of such immunoregulatory cytokines at the transplant site e.g. gene delivery directly to islet tissue using recombinant non-replicating virus vectors. Proislets transduced with recombinant avipox virus engineered to express a reporter gene have demonstrated reporter gene expression pre- and post- transplant. Based on this evidence, avipox virus represents a feasible gene delivery vector for proislet allografts and xenografts. Recombinant avipox virus will be constructed to determine whether production of immunoregulatory cytokines at the graft site can prevent graft rejection (in conventional mouse strains) as well as recurrence of autoimmune disease in diabetic NOD hosts; such inhibition could occur via the selective development of regulatory T cells. In relation to susceptibility to autoimmune damage, the immunopathology associated with the destruction of pig proislet xenografts in diabetic NOD mice has suggested that pig proislet tissue may be resistant to autoimmune injury; whereas autoimmune islet damage in NOD mice correlates with an intense CD8 T cell response, the destruction of pig proislet xenografts is characterised by a weak CD8 T cell reaction. Retransplant studies have clarified that this pathology is not related to the undifferentiated state of the fetal proislet tissue. Our findings suggest that the autoimmune disease in NOD mice is species-specific;immunotherapy for clinical islet xenotransplantation may therefore need to target only the graft rejection process.
| It is known that the susceptibility to some bowel cancer is inherited. In about 5% of cases it can be said with some certainty that a faulty gene is responsible. One of the cancer syndromes where susceptibility to develop tumours is clearly inherited is Hereditary Nonpolyposis Colorectal Cancer (HNPCC). Six different susceptibility genes have been identified for HNPCC If a person is found to have inherited one of the genes, preventative measures can be taken to greatly reduce the risk of contracting cancer, or to identify and treat it at an early and relatively harmless stage. A research project is being conducted involving 60 families in Melbourne, Sydney and Canberra, who have a family history of bowel cancer. |
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For the great majority of bowel cancer sufferers however, the cause of their cancer is much more obscure. Probably in about a quarter of cases, there is some family history of bowel cancer or pre-malignant polyps, but in the remaining cases there is no family history. To what extent the cancer is caused by unknown inherited faulty genes, or by environmental factors such as diet, or a poor diet exacerbating inherited susceptibility, is still a mystery. This presents the next challenge for research and the answers are likely to be found using experimental mouse models.
We are studying knockout mice deficient for the Msh2 gene, the homolog of one of the susceptibility genes involved in human HNPCC The cancers that develop in this mouse model resemble the cancers in HNPCC patients. Our aim is to determine how factors such as dietary carcinogens or chronic inflammation may interact with the susceptibility genes and trigger cancer development.
| An elevated LDL (low density lipoprotein) is at the core of atherogenesis, but the mechanisms whereby LDL initiates and promotes atherosclerosis remain unknown. Furthermore, the measurement of LDL cholesterol alone is generally useless for predicting risk of CHD This stems from the fact that the standard measurement of LDL cholesterol comprises a number of separate components which are not atherogenic. The number of small dense LDL particles is much more predictive of CHD risk than are levels of total cholesterol. This finding is being exploited to obtain a greater understanding of atherogenesis, and to develop new diagnostic tests for detection of coronary disease.
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In summary, major aims are to identify and characterise modified LDL particles involved in atheroma development, investigate metabolic factors linked to LDL modification, determine how LDL particles cause atheroma, and develop new diagnostic approaches to CHD
Several of our projects focus on interaction between the precursor cells destined to provide the basis for blood cell formation and immune responses and the gastrointestinal system. One project concerns the generation, by somatic hypermutation, of B lymphocytes specifically reactive against a variety of antigens, followed by the elimination of those cells potentially reactive against self. In the normal fetal lamb, these processes seem to occur sequentially in the spleen and then in the lymphoid tissue in the wall of the intestine. The location and cellular kinetics of these processes have been deliberately disrupted by surgical removal of the spleen, which is normally involved, with the aim of disclosing any compensatory mechanisms. Our preliminary results suggest that the destruction of anti-self reactive B lymphocytes is relocated from the spleen to abdominal lymph nodes after early splenectomy.
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A second project which also seeks to find out more about the development and early functioning of the immune system in the gut wall is specifically directed to discovering how the epithelial cells lining the gut cavity organize the formation of lymphoid structures in the underlying tissues of the gut wall during fetal development. This induction process has been mimicked in vitro by allowing combinations of different fetal tissues to interact with each other.
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Apart from study of fetal gastrointestinal and immune systems, another current project is examining the development of the fetal lungs and the role of thyroid hormones in lung maturation. . The longer term aim of this project is to test the possibility that these hormones may be of value in accelerating lung maturation in premature infants with the respiratory distress syndrome. At present, the treatment of this condition is not entirely satisfactory and some clinical trials have suggested a potential use for thyroid hormones.
 Click to enlarge photo | Research in the Human Genetics Group is aimed at understanding the nature of genetic variation in humans and how it relates to disease. We take a broad view, recognising the importance of the evolutionary forces that have shaped the structure of the human genome and the nature of human genetic diversity. |
Gene and genome evolution
In mammals genetic novelty may arise through a diversity of genetic and evolutionary processes, such as mutation, gene duplication, gene conversion, genetic drift and natural selection, occurring in large and structurally complex genomes. Information relating to genome and protein function, the processes by which functional novelty has arisen and patterns of species evolution are contained within DNA and protein sequences. We use a comparative approach to the interpretation of this information, investigating differences in genomes, genes and the proteins they encode, among related species, particularly humans and other primates. Work is focussed on the mitochondrial genome, the MHC complex and a number of other multigene families.
Human genetic and genomic variation
Medical genetics has largely been focussed in recent years on understanding single gene defects. Less attention has been given to genetic disorders that have a polygenic basis, such as mental illness, cardiovascular disease and diabetes. Although these are more important from a public health point of view, they are technically more difficult to investigate. This situation is changing largely through the technological advances of the human genome project. Associated with this change is an increased recognition of the importance of the normal range of human genetic variation, and its importance in relation to disease prevention. Furthermore, understanding the relationship between molecular genotypes and disease phenotypes becomes more dependent on population-based rather than family-based investigations and an understanding of the genetic structure of human populations is needed. Our research is directed at understanding the basis of a number of genetic disorders, and of the patterns of normal genetic variation in human populations.
One particular focus is the genetic basis of personality variation, which is associated with a predisposition to common forms of mental illness involving depression and anxiety. This work is done in collaboration with the NH&MRC Social Psychiatry Research Unit. We also investigate the pattern of genetic variation among human groups particularly in relation to HLA loci, mitochondrial genes, and microsatellite loci. Our work on HLA variation includes analysis of structure and function and, in addition to its significance to medical genetics, it has important implications with respect to organ transplant programs and to the rational design of peptide-based vaccines. Variation at mitochondrial genes and microsatellite loci have important forensic implications and the work has an overall goal of understanding the origin and evolution of humans and of human groups.
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The GSTs are a large family of enzymes which our previous studies have shown can be subdivided into a number of different classes that have characteristic structural variations, substrate preferences and sites of expression. The GSTs function by conjugating glutathione to the target chemical thereby making it more water soluble and making it recognisable by an export pump that expels glutathione conjugates from cells.
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Parkinson's disease, a neuro degenerative disorder, is thought to be secondary to neurotoxin exposure and pesticides have been implicated as possible causitive agents. Since GSTs are known to metabolize some pesticides, we recently investigated the role of genetically variant GSTs in the pathogenesis of Parkinson's disease. We found that a variant form of GSTP1 was associated with the occurrence of Parkinson's disease in patients who had been exposed to pesticides. This study confirms the significant interaction between genetics and response to environmental toxins.
Critical steps in the control of complex processes such as cell growth, development, and gene expression, are controlled by proteins that are only required transiently and must be rapidly destroyed to control their activity. This is accomplished by attaching multiple ubiquitin proteins to the target, which "marks" it for destruction by a large proteolytic complex called the proteasome. Most of our research focuses on a family of enzymes called ubiquitin-specific proteases (USPs), that have the ability to cleave ubiquitin from such marked proteins, and thus slow or prevent their destruction. In this context, some USPs can be considered "proof-reading" components of the system, safeguarding a target from inappropriate ubiquitination (and thus destruction), and imposing a further level of regulation on the pathway.
We have previously identified a USP that functions as a proto-oncogene in mice; that is, it causes cancer when overproduced. Others have linked the human version of this USP with certain types of lung cancer. We have recently shown that this mouse USP interacts with the Retinoblastoma protein, which functions to prevent cell growth by keeping transcription factors (proteins that control gene expression) in check.
Interestingly, these very transcription factors are normally destroyed by the ubiquitin pathway. When we overproduce this mouse USP oncogene, the levels of these transcription factors rise, implying that too much of this USP stabilises them, presumably by preventing their ubiquitination. Our current efforts are aimed at elucidating this mechanism further. We have also recently identified a very close relative of this oncogenic USP in both mouse and human cells, and we are studying it further.
We also study USP enzymes using yeast as a model system, both because it is very amenable to genetic and biochemical studies, and also because the ubiquitin system is so highly conserved between yeast and humans, that insights we gain in yeast can be applied to our studies on mouse and human enzymes. Our current work centres on two of the family of 16 USPs in yeast, Ubp6 and Ubp15. Ubp6 is involved in regulating destruction of target proteins that share the unusual feature of containing a sequence related to ubiquitin itself. Interestingly, Ubp6 also contains a ubiquitin-like sequence, and we are studying its function in proteolysis. Ubp15 is involved in regulation of gene expression, but apparently by a different mechanism to the Retinoblastoma example above. We are currently seeking proteins that Ubp15 interacts with, to gain insight into its function. Human relatives of both Ubp6 and Ubp15 have been identified, the latter a target of herpes-virus infection, and we will extend our functional studies to the human enzymes.
Our results show that USPs can play important roles in regulating the ubiquitin pathway, and through this processes such as cell growth. Aberrations in these USPs may lead to cancer and disease.
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Our research aims to understand how immune cells make a fundamental decision: either to fight or to disarm. The process of deciding which immune cells should fight and which should disarm is key to our ability to resist infection and parasitism. Mistakes in this process result in autoimmune diseases, allergy, lymphoma leukemia. Moreover, drugs and other ways to alter fight or disarm decisions are sorely needed to improve the success of organ transplantation and treatment of autoimmune diseases and metastatic cancer. |
By chance, other lymphocytes carry receptors for self antigens, ie. parts of our own normal tissues and body fluids. When a lymphocyte binds a self antigen it normally receives a signal to disarm. Instead of multiplying and producing destructive compounds, the lymphocyte either commits cell suicide by apoptosis or the cell disarms itself by becoming functionally tolerant, ie. less responsive to antigens and less able to multiply or produce destructive compounds.
For a long time it was not possible to see how self-reactive lymphocytes disarm themselves. Our laboratory has developed ways to visualize this process in genetically modified laboratory mice called transgenic mice. By studying cells in the transgenic mice, we have discovered that each immune cell must run through a complex series of fight or disarm checkpoints before it can be fully launched into an immune response. In some ways, the process resembles the sequence of fight/disarm decisions in a military missile launch, which serve a similar purpose of preventing friendly fire.
Members of the laboratory are deciphering different fight/disarm checkpoint processes, using a combination of biochemistry, cellular immunology, genetic analysis, and transgenesis. At each of these checkpoints, we are focussing much of our work on elucidating how it is that antigen receptors on lymphocytes can trigger several different cell fates ranging from cell proliferation to cell death. Progress on this goal in the last year is summarized below.
Role of receptor crosslinking in determining lymphocyte fate. As part of her PhD studies, Jane Rayner has been analysing a new transgenic model to explore how intracellular signaling by a single class of antigen receptors on immature B cells promotes three alternative fates: survival in some cells, survival with diminished responsiveness in others (anergy), and inhibition of maturation and survival in other cells. We previously found that monomeric HEL antigen, when present in the blood as a self antigen, engaged the receptors on immature B cells in the bone marrow in a way that could trigger anergy responses in the cells, but was unable to abort the cells’ development and survival. By studying a new set of transgenic mice where HEL is present in the blood as a covalent dimer, Jane has found that this single change in the the antigen switches its effects so that it now aborts the cells in the bone marrow. The proportion of receptors engaged by the monomer and dimer antigens are the same, yet the responses elicited are strikingly different, indicating that small differences in the extent of receptor clustering play a key role in determining the cellular outcome. Using this model, we hope to illuminate the biochemical signaling pathways that underpin these different ways of controlling self-reactive lymphocytes.
Role of receptor location in determining lymphocyte fate. In B cells that have been made functionally tolerant (anergic) to self antigen, all of the known signaling molecules are present but the antigen receptor is somehow desensitized from triggering them (eg to activate NFkB and JNK) to promote cell growth and division. Interestingly, other signaling pathways (eg. ERK activation and NFATc/p nuclear translocation) are still activated efficiently. Our previous work identified a tyrosine phosphatase, SHP-1/PTP1C, as a key negative regulator of signaling by B cell antigen receptors, but biochemical studies of whole cell extracts have not revealed any change in SHP-1 activity that might account for the signaling block in anergic B cells. Studies by Dr Bennett Weintraub in the last year have revealed a novel, early step in signaling by B cell antigen receptors that appears to hold the key to how the receptor can be selectively uncoupled from mitogenic signaling pathways in anergic cells. He has found that when antigen binds, the receptor quickly moves into specialized domains on the cell surface that appear to correspond to cholesterol and src-kinase-rich rafts. Most of the induced receptor phosphorylation and downstream kinase activation appears to occur after the receptor moves into these domains. In anergic B cells, movement into the signaling domains is suppressed, presumably accounting for the uncoupling of key signaling pathways.
Gene expression changes underpinning different lymphocyte fates. To search for gene expression differences that bring about different cell fates in lymphocytes responding to antigen, Dr Richard Glynne has been cataloguing genes whose expression patterns collectively provide a signature for activation, anergy, or immunosuppression in mature B cells. Using Gene Chip arrays at Affymetrix, Inc to probe mRNA abundance for 6500 mouse genes, he has identified a set of 37 early response genes in activated cells, only a subset of which are inhibited by the immunosuppressive drug FK506. A much larger fraction of these genes are inhibited in anergic cells, while a distinct set of genes are increased or decreased selectively in anergic cells. Interestingly, many of the changes in anergic cells are in the range of 2-4 fold differences in mRNA abundance. An accumulation of 2-fold differences can culminate in very different cell fates if they affect successive steps in a common biochemical pathway, as illustrated by our recent findings in mice triply heterozygous for loss-of-function mutations in the Lyn-CD22-SHP1 pathway. The gene expression profile found by Dr Glynne raises the possibility that the striking signaling and response alterations seen in anergic cells reflect an accumulation of smaller changes in the expression of multiple genes - a quantitative trait - rather than a single molecular change as we might have anticipated.
Role of T cell activation-induced death versus anergy. A similar dichotomy of responses in CD4 T cells has been the focus of research by Dr Sarah Townsend and Dr Srini Akkaraju. Using TCR transgenic mice, they found that self antigen that was abundant in the circulation triggered self-reactive T cells into a transient phase of cell division followed by death and dissappearance of most of the cells. This fate did not appear to reflect the role of a specialized antigen-presenting cell, because B cells or other antigen-presenting cells had the same effect. By contrast, when the antigen was present in only trace amounts in the circulation but abundant in the pancreatic islets or thyroid gland, it triggers a distinct response characterized by loss of helper activity but no cell division or death. Our hypothesis is that antigen triggers these different ways of controlling self-reactive T cells by differences in the amount of antigen in lymphoid tissues and hence different amounts of receptor clustering, akin to the effects described above for B cells. Defining the molecular pathways underpinning these different cellular processes, and how they impact on tolerance and autoimmunity to specific organs, is a major goal for the lab.
Rapid advances in gene technology are bringing us to the point of visualizing the imbalance between our genetic code and lifestyle/environment. A worldwide effort has already given us a map and a "dictionary" of many of our genes -– collectively referred to as our genome. The epic challenge for the next decade is to decipher what these gene words mean. How are they combined into the genetic language that guides the cells in our body and determines how well we cope with different environmental stresses? Differences in the spelling of those gene words underly differences in susceptibility to modern diseases, and it is likely that technology will soon allow a list of spelling differences to be rapidly compiled from each person's unique genetic dictionary.
The Medical Genome Centre was officially opened in 1997 to promote research into the function of genes that underpin human health. To decipher the functional meaning of genes and their contextual interactions, laboratory mice represent a crucial Rosetta stone. A database of many of the genes in the mouse genome has recently been compiled by researchers in the US and almost all of the genes match a human counterpart with only small changes in their spelling. While surprising given the large differences in external appearance, the mouse and human genetic languages are in fact no more different than Chaucer's english and modern english. This underlying similarity makes it possible to define the function of genes in the mouse in a way that is impossible in humans.
In the last year, the Medical Genome Centre has successfully created the first of a series of libraries of laboratory mice in which single letters in the spelling of many of the genes in the mouse genetic dictionary have been changed by random chemical mutagenesis. This resource will be used by collaborating research groups to identify and study genes that are important in susceptibility, resistance or prevention of particular disease processes, by looking for subtle changes in the behaviour of cells and tissues, by transgenesis, and through DNA chip technology. State-of-the-art facilities for transgenic mouse production, sperm freezing, and database tracking of genetic and phenotypic data have been developed to support this resource and provide a service to researchers.
A two-way traffic between studies of mouse genes and their human counterparts is being developed in collaboration with the Human Genetics Group led by Dr Simon Easteal, and the other members of the Integrative Genetics Programme in the School. Human genetics advances are driving the search for better experimental models in the mouse, where information can be more clearly obtained about the way individual gene products link together into coordinated molecular pathways guiding the behaviour of cells. Molecular and cellular context for gene function yielded by the mouse, can in turn be quickly applied to human health by revealing the best targets for drug development, and by illuminating patterns of genetic variation between people that alter susceptibility to disease and response to treatments. To accelerate the process of deriving mouse strains with mutations in specific genes of interest, a collaborative MGC/Integrative Genetics Programme effort has started developing a library of mouse gene deletions. The deletion library will be archived as frozen sperm and DNA, and screened by gene-specific tests to identify individuals carrying deletions in these genes.
Two chief problems that are being addressed immediately by programmes using the Centre are the regulation of cell growth, death, migration and differentiation in cancer, and the regulation of immunity to infection or cancer and the dysregulation of immunity that occurs in autoimmune diseases and allergy. New mouse mutation models to study genes involved in lymphoma, blindness, cataracts, physical coordination, pigmentation, and dermatitis have already been identified in the early phases of library production. Programmes targetted to other disease areas will be developed and interested researchers are encouraged to contact Prof. Goodnow.
Genes that are important to cancer will be detected using the library of mouse mutations and strategies to detect subtle changes in cell growth, death, differentiation, migration, angiogenesis and immunity. The models that arise and the light that these shed on the human counterparts of these genes will be available to the research community to help in three key areas: 1. primary prevention, where illuminating patterns of inherited susceptibility will help to resolve environmental risk factors and target preventive measures; 2. early diagnosis, where alterations in gene spelling and expression pattern will help to distinguish cancer cells early and predict the best course for treatment; 3. therapy and prevention of secondary tumours, where the genes identified will provide new targets for drugs and new avenues for chemotherapeutic or immunological intervention.
ThromboTrace® is an injectable radiotracer derived from an inhalable agent Technegas discovered at the School in 1984 and now used as a routine imaging agent for lung ventilation studies in 34 countries. The Group is entirely funded by Tetley Medical Ltd with assistance this year from a Commonwealth Government START Grant. The Technegas website (http://jcsmr.anu.edu.au/technegas/) is receiving around 40 visits a day from all over the world.
The major achievement this year was to take the ThromboTrace® discovery from the laboratory bench and animal studies to a human trial at The Canberra Hospital. ThromboTrace® is the name given to an hydrophilic suspension of the graphitic nano-encapsulates of Technetium-99m in 5% glucose. These particles are found to have the capacity to bind specifically to fibrin, the structural matrix of blood clots, and being radioactive, they can highlight the position and size of the clot through standard Nuclear Medicine imaging processes.
Six normal volunteer subjects (two from our group and two others from within the JCSMR) showed there was no ill effect from an injection of the agent, and a single patient who was not on anti-coagulation therapy was shown by ThromboTrace® to have an extensive deep vein thrombosis, later proven by x-ray technology. Three other patients had blood clots that were not seen since they were all on high doses of anti-coagulants.
An extensive phase 2 clinical trial to explore the full potential of ThromboTrace® is planned to commence early in 1999. This should include another application, namely the detection of inflammation in the large bowel simply by swallowing the agent in a glass of water. Preliminary animal studies suggest this route of administration will label the sites without the tracer needing to circulate to the whole body.
School Technical Manager:
J Bateman, BSc (Syd)
Divisional Administrator:
M Goodisson
Administrative Assistants:
G Noble; M Tankosic
Cardiovascular Disease Group
Senior Fellow and Leader:
NG Ardlie, MB BS, MD (Adel), PhD (McMaster), FRACP
Postdoctoral Fellow:
IA Popov, MD, PhD, BSc (Crimean Medical University, Simferepol, Ukraine)
Laboratory Technician
M Yang (from December)
Visiting Fellows:
JE Dahlstrom, MB BS(Hons) (Syd), PhD
DP Dhall, MB ChB (Manchester), PhD (Aberdeen), MIBiol, MRCS, LRCP, FRACS
DA McGill,BSc(Hons) (UNSW) BS&M (UNSW), PhD (ANU) FRACP, DipDU(ASUM)
CH Nair, BSc (Hons) (Aberdeen), PhD (ANU)
SG Nogrady, MB BS (Syd), FRACP
Developmental Physiology Group
Senior Fellow and Leader:
PJ McCullagh, MD BS (Melb), DPhil (Oxon), MRCP
School Visitors:
W Whitten, BVSc, DSc (Syd), FAA
M Peek, MB, BS, BSc (Med) (Hons) PhD, FRACOG, MRCOG
HA McKenzie, MSc, PhD (Syd) FRACI
Technical Officers:
B Barancewicz, BRTC, AIST
K King, BAppSc, MedLabSci (Canberra)
Goodnow Laboratory
Professor and Leader:
CC Goodnow, BVSc (Hons) Syd, BScVet (Hons) Syd, PhD (Syd)
Postdoctoral Fellows (externally funded):
B Weintraub, BS (MIT), PhD (UCSD)
S Townsend, BS (Cornell), PhD (UC Berkeley)
S Hartley, BSc (Hons) ANU, PhD (Syd)
Laboratory Technicians:
L Wilson, Dipl.Biol. Science (CIT)
C White (part time)
Medical Genome Centre
Facility Manager:
A McKenzie,BSc (Hons) Monash
Animal Technicians:
J Carter, City & Guilds 244 Marine Craft Fitter (BCA, UK)
S Chaudhry,Assoc.Dip.App.Sci (Animal Science)
L De Wit,Animal Care Certificate Course, (CIT)
S Ewing,Biological Research Techicians’s Certificate, (CIT)
K Sullivan, Assoc.Dip.App.Sci. (Animal Science), Adv. Cert.Vet.Nursing
Material Support Technicians:
S Gregory, (Until Nov)
J Webster
A Wright
Diabetes Research Program
Professor and Leader:
K Lafferty, BSc(Melb), PhD (ANU) (until July)
Visiting Fellow (from November)
Postdoctoral Fellow:
RS Schmidli, MB(Otago), ChB(Otago), PhD(Wehai), MRCP, FRACP
Senior Technical Officer:
L Croft, BSc (Glasgow) (until August)
Technical Officers:
D Newington, BSc (ANU)
K Sutton, BSc (ANU)
Laboratory Technicians:
M Crammond
S Dilts
L Starkey
Autoimmunity/Genetic Manipulation Laboratory
Fellow:
B Charlton, MB Bs, PhD (UNSW)
Technical Officer:
K Currie, BSc
Laboratory Technician:
J Kofler,DipApp.Animal.Sc
Transplant Immunology Laboratory
Fellow:
CJ Simeonovic, BSc (Hons), PhD (ANU) (Convenor of Diabetes Research Program from July)
Visiting Fellow:
JD Wilson, BSc (Hons), MB BCh, BAO (Hons), MD (Queens, Belfast), MRCP (UK), FRACP
Senior Technical Officer:
MJ Townsend, Ass. Dip. App. Path. (Bruce TAFE)
Technical Officer:
KUS McKenzie, Ass. Dip. App. Sci., Animal Sci. (Bruce TAFE)
Laboratory Technicians:
K De Bono, (from May)
M Yang (from March until December)
JC Zarb
R McMurray, (Part-time)
Molecular Genetics Group
Professor and Leader:
PG Board, BSc (Hons), PhD (UNE)
Post Doctoral Fellows:
L Whitbread, BSc (Hons), PhD (Adel) (until September)
A Blackburn, BSc (Hons) (UNSW), PhD
Visiting Fellows:
D Liu, PhD (Syd)
M Webb, MB BS, FRACP (UWA), FRCPA
D Le Couteur, MB BS (Hons) (Syd), FRACP, PhD (UQLD)
Senior Technical Officer:
MA Coggan, BSc (Hons)
Laboratory Technicians:
L Langton, Ass Dip Sci (Pathology) (CIT)
Research Assistant:
M Taylor, BSc (from April)
Ubiquitin Laboratory
Fellow (RFT) and Leader:
RT Baker, BSc (Hons) (UNSW), PhD
Post Doctoral Fellow:
G McGurk, BSc (Hons), PhD (Edinburgh) (from August)
Visiting Scholars:
J Hehl, Vordiplom (Stuttgart) (from August)
M Vogel, Vordiplom (Stuttgart) (from August)
Technical Officer:
X-W Wang, BSc (Fudan, Shanghai, China), MSc (Melb)
Human Genetics Group
Senior Fellow and Leader:
S Easteal, BSc (St Andrews), PhD (Griffith)
Research Fellows:
X Gao, BM (Beijing), MMedSc (Beijing Lung Tumour and Tuberculosis Institute), PhD (until June)
G Chelvanayagam, BSc (UWA), PhD (UWA/EMBL)
LS Jermiin, Cand. Scient. (Århus), PhD (LaTrobe) (until September)
Postdoctoral Fellows:
G Huttley, BSc (Hons I) (Macquarie); PhD (Univ California, Riverside, USA)
Visiting Fellows:
LS Jermiin, Cand. Scient. (Århus), PhD (LaTrobe) (from September)
SW Serjeantson, BSc (NSW), PhD (Hawaii)
N Saha, BSc (Calcutta), MBBS (Calcutta), MD (Punjab), PhD (Med) (Calcutta) (from February)
Senior Technical Officer:
X Tan, BSc, (Shandong University, Jinan), MSc (China Pharmaceutical Univ, Nanjing)
Technical Officers:
B Whittle, BSc (Hons)
Y Zhang, MSc (Xinjing, China) (from May)
G Herbert, BSc (Hons) (Leics UK) (from October)
Mucosal Inflammation and Cancer Group
Professor and Leader:
WF Doe, MB BS (Syd), MSc, FRCP (Lond), FRACP (Until February)
Cancer Genetics Laboratory (From March)
Research Fellow and Leader:
M Kohonen-Corish, BSc, MSc (Helsinki) PhD
Visiting Fellows:
ML Bassett, MB ChB (Otago), MD (Qld), FRACP
G Buffinton, BSc (Hons), PhD
WM Burch, MSc (Melb), PhD (Lond), MIE (Aust)
J Cavanaugh, BSc (ANU) MS (North Carolina State University), PhD (ANU)
PB Herdson, BMedSci, MB BS, PhD, FRCPA
F Lomas, MB BS (Hons) (Syd), FRACP,DDU,FRACR
P Pavli, MB BS (Hons) (Syd), PhD FRACP
Y Wang, MS (Nanjing), PhD
Senior Technical Officers:
J Olsen, BSc (until March)
J Hornby, BSc (Hons) (Queens, Belfast)
Laboratory Technician:
A Janssen, BSc (ANU)