University of Tasmania, Australia

Location

AIS, Canberra

Background

A unique and exciting opportunity exists for a high achieving Exercise Science graduate with a passion for sport science research to complete a PhD with the Australian Institute of Sport (AIS) Performance Research Centre and the University of Tasmania. The co-funded scholarship will provide a unique opportunity for a graduate with research experience and Class 1 Honours degree or equivalent to carry out high quality applied sports science research focussing on the use of compression garments for performance and recovery.

The successful applicant will be primarily based at the AIS in Canberra and will have supervisors from both the AIS and the University of Tasmania. The scholarship provides a stipend of approximately $25,000 for three years. In addition to the stipend, there will be an operating budget for research projects.

Applicants must be able to demonstrate well-developed knowledge and research skills in exercise physiology, general physiology, biology or other academic fields relevant to elite sporting performance.

Preference will be given to Australian residents who would be competitive applicants for an APA PhD scholarship.

Read the brochure (pdf, 260.1 KB)

Closing Date for Applications

29 February 2012

Start Date

April 2012

Contacts

For more information please contact Dr James Fell on 03 6324 5485 or James.Fell@utas.edu.au.

Application Form

http://www.studentcentre.utas.edu.au/scholarships/Default.aspx

Location

Based at the School of Human Life Sciences, University of Tasmania, Launceston

Background

Ulcerative colitis and Crohn's disease are collectively called inflammatory bowel diseases (IBD). The causes for these devastating intestinal diseases are unknown. Recent studies have indicated a strong role for inflammasomes (mediated through two cytokines namely IL-1 beta and IL-18) in IBD. These controversial  investigations were mainly from the mouse system and not validated in human IBD.  

Project

The project aims to characterise the role of different components of the inflammasome in IBD. In particular, a number of mouse models (deficient in inflammasomes) along with our recently described spontaneous colitis model Winnie ( Eri et al., 2011, Heazelwood, Eri et al., 2008; McGuckin, Eri et al., 2009, 2010, 2011) will be used in conjunction with human studies to correlate the link between  inflammasomes and the pathogenesis of  colitis.

Facilities

The Mucosal Immunology lab (Dr Raj Eri)  located  at the School of Human Life Sciences, UTAS has excellent facilities for conducting both in vitro (cell lines, , human tissue) and in vivo (animal models) investigations. Due to strong links with the clinical gastroenterologists, human clinical studies can be done. The research laboratories at the School of Human Life Sciences are located on a dedicated floor space of about 450m² shared by 8 different research groups. Research facilities include the latest in cell culture (4 laminar flow hoods, liquid nitrogen storage, cold rooms/freezers), Molecular/cell Biology (normal and qPCR machines, western blot equipment, gel documentation, dedicated RNA room, PCR prep room, cold centrifuges) Immunology, Animal holding facilities, histology and microscopy.

Funding arrangements

We are seeking highly organized, enthusiastic, motivated and organised PhD scholars interested in working within a team environment with highly experienced supervisors. We have 2-3 scholarships available. There will be substantial research assistant support and there is a large cohort of senior PhD students already in our group. Funding is available through UTAS Elite Scholarship- around ~30,000 per annum.

The student

This project would suit a student with a strong molecular biology/immunology/physiology background and an interest in studying gut immunology. Although based at UTAS,Launceston, the collaboration with Mater Medical Research Institute, Brisbane will involve the student working in Brisbane occasionally.

Candidates for this scholarship must have first-class BSc Honours or Master's degree by research with research publications.

Contacts

Please contact Dr Raj Eri (rderi@utas.edu.au 03-63245467 or 0430 029 656) in the School of Human Life Sciences.

Tasmannia lanceolata (Native Pepper, NP) has high antioxidant capacity in both hydrophilic and lipophilic fractions, which may protect against oxidative damage. Oxidative damage and stress such as oxidation of low density lipoprotein and chronic inflammation contribute to the development and progression of atherosclerosis and oxidative DNA damage may contribute to the development of cancer. Aqueous extracts of whole NP berry, leaf and post-oil extracted NP leaf material (called marc) will be tested for their capacity to suppress oxidative lipid and DNA damage and a range of anti-inflammatory properties.

Methods include the Single-Cell Gel (Comet) assay, measurement of lipoprotein oxidation, high-sensitivity C - reactive protein and cytokine biomarkers for inflammation.

There are no published human trials in which the potential health benefits of NP have been investigated. We propose to investigate the potential of both whole NP whole leaf and the NP marc, which is a waste product of the essential oil manufacture. This project will conduct controlled clinical trials for the first time.

Another aim is to produce and test a prototype beverage including NP aqueous extract which can be commercialised through the Tasmanian Centre for Food Innovation (a joint collaboration between the University of Tasmania, CSIRO and DSTO).

Recent international commercial trends suggest that the development of such a novel beverage is timely.

Contacts

Please contact contact Professor Madeleine Ball, on (03) 6324 5480 or email Madeleine.Ball@utas.edu.au in the School of Human Life Sciences.

Background

Primary open-angle glaucoma (POAG) is a degenerative condition that is the world's leading cause of irreversible blindness.  In Australia, 1 in 10 people over the age of 80 have glaucoma, with the annual financial cost of glaucoma predicted to be more the $4 billion by 2025¹.  Genetic association studies have suggested that endoplasmic reticulum (ER) and oxidative stress are involved in the pathogenesis of POAG, due to the finding of disease-associated mutations in myocilin² (MYOC) and optineurin³ (OPTN) which can lead to ER^4,5 and oxidative⁶ stresses respectively.  Recent advances in POAG research have documented alleviation of ER stress in Myoc mutant mice produces a complete phenotype reversal⁵.  However, there is a dearth of cell biological-orientated research using clinical tissues into this disease.  We are well placed to study molecular aspects of both ER and oxidative stress in human cell lineages in vivo and in vitro, and have current ongoing collaborative projects in these areas in other disease models.

Project Outline

1. Spectrum of mutations in glaucoma-associated genes within the Tasmanian population
   We are proposing to obtain background genetic information on the frequency of mutations within two glaucoma-associated genes, MYOC and OPTN.  Our focus on these genes is due to the existing and complementary research interests of Dr Cook (oxidative stress, autophagy) and Dr Eri (ER stress).
2. Cell stress in the trabecular meshwork
   The trabecular meshwork (TM) is a tissue of interest in studying the cell biology of glaucoma.  Compromised TM function may lead to blockage of the meshwork and hence prevent efficient drainage of the aqueous humor from the eye with a concomitant increase in intraocular pressure, a well-established risk factor for glaucoma⁷.  Many of the genes associated with glaucoma, including myocilin and optineurin, are expressed by TM cells. 

We propose to determine the extent of oxidative and ER stress within TM cells using two complimentary approaches: clinically obtained TM samples from glaucoma patients, and cultured TM cells in which specific glaucoma-associated mutations in the myocilin and/or optineurin genes have been introduced.  Clinical specimens will be obtained via collaboration with ophthalmologists at the Launceston Eye Institute.  The cell culture-based studies will also involve screening of several pharmacologically active compounds for efficacy in alleviating the oxidative and ER stresses.  We anticipate that these studies will segue into experiments in rodent models and subsequent clinical trials.

Facilities

This research will be conducted with the School of Human Life Sciences at the University of Tasmania as part of the Cell Stress Cluster. You will have access to facilities for cell culture and other common molecular methodologies such as real-time PCR, western blotting, recombinant DNA vector construction and microplate reading using luminescence/fluorescence/spectroscopy.

We are seeking a self-motivated and highly organised PhD candidate with experience in molecular biology and/or cell biology.  You must have a B. Science degree (with First Class Honours), or a Masters degree with previous relevant publications.

References

1. Dirani, M. et al. Clin Experiment Ophthalmol (2011).
2. Stone, E. M. et al. Science 275, 668 (1997).
3. Rezaie, T. et al. Science 295, 1077 (2002).
4. Yam, G. H. et al. Invest Ophthalmol Vis Sci 48, 1683 (2007).
5. Zode, G. S. et al. J Clin Invest 121, 3542 (2011).
6. Chalasani, M. L. et al. Invest Ophthalmol Vis Sci 48, 1607 (2007).
7. Kwon, Y. H. et al. N Engl J Med 360, 1113 (2009).

For more information

Dr Anthony Cook	Dr Raj Eri
anthony.cook@utas.edu.au	Rajaraman.eri@utas.edu.au
Phone +61 3 6324 5465	Phone +61 3 6324 5467

Background

Parkinson’s disease is a complex neurological condition affecting 75,000 Australians. It has significant societal impact, on the patient and their family, and the healthcare system (in 2005, Parkinson’s disease was estimated to cost Australia $6.8 billion per year)¹.  A recurrent finding in Parkinson’s disease pathology is the presence of protein aggregations known as Lewy bodies, which impact on the metabolism and viability of the cells in which they occur.  Such inclusions can be removed via a catabolic process known as autophagy (literally means “self-eating”), a cellular process that recognises protein aggregates and facilitates their degradation in lysosomes, and which can cause neurodegeneration when disrupted in mice²,³ .  Autophagy is regulated by the mTOR signal transduction pathway⁴, which can be experimentally manipulated in cultured cells to monitor protein aggregation and removal.

Project Outline

This project will use a Parkinson’s disease Patient derived cell model⁵,⁶ , established by Dr Cook as part of a larger collaborative research program involving researchers at the National Centre for Adult Stem Cell Research at Griffith University in Brisbane.  This cell model is derived from the olfactory mucosa, the tissue within our nose responsible for the sense of smell.  Loss of this sense is as frequent in Parkinson’s disease as movement dysregulation, including the characteristic resting tremor.
We have preliminary data documenting the presence of protein inclusions in cells from Parkinson’s disease Patients, but not in cell from healthy Control donors.  We will investigate the functioning of mTOR signalling in this cell model, and directly quantify the ability of Patient cells to degrade protein aggregations relative to Control donor cells.  We will also investigate the activity of the mTOR pathway in this cellular model in response to (i) neurotoxic chemicals (which typically produce oxidative stress), and (ii) neuroprotective antioxidant molecules.

Facilities

This research will be conducted with the School of Human Life Sciences at the University of Tasmania as part of the Cell Stress Cluster. You will have access to facilities for cell culture and other common molecular methodologies such as real-time PCR, western blotting, recombinant DNA vector construction and microplate reading using luminescence/fluorescence/spectroscopy.

We are seeking a self-motivated and highly organised PhD candidate with experience in molecular biology and/or cell biology.  You must have a B. Science degree (with First Class Honours), or a Masters degree with previous relevant publications.

References

1. Access Economics.  (2007).
2. Klionsky, D. J. et al. Autophagy 4, 151 (2008).
3. Komatsu, M. et al. Autophagy 2, 315 (2006).
4. Jung, C. H. et al. FEBS Lett 584, 1287 (2010).
5. Cook, A. L. et al. PLoS One 6, e21907 (2011).
6. Matigian, N. et al. Dis Model Mech 3, 785 (2010).

For more information

Dr Anthony Cook
anthony.cook@utas.edu.au
Phone +61 3 6324 5465