Skills (87)
Research experience
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Oct 2012–
presentResearch: Visiting Fellow
Australian National University · John Curtin School of Medical Research · Molecular GeneticsAustralia · CanberraDiabetes and cancer research. -
Jan 2011
Research: University of Otago
University of Otago · Wakefield Biomedical Research UnitNew Zealand · Dunedin -
Jan 2007–
Dec 2009Research: University of Queensland
University of QueenslandAustralia · Brisbane -
Mar 2006–
presentResearch: Obesity and diabetes Research Program
Otago University · Pathology and Molecular Medicine · Wakefield Biomedical Research UnitNew Zealand · WellingtonInvestigation of the underlying mechanisms behind the rapid resolution of T2DM post RYGB surgery. -
Mar 2006–
presentResearch: Biomarker Discovery for Colorectal Cancer
The University of Otago · Pathology and Molecular Medicine · Wakefield Biomedical Research UnitNew Zealand · WellingtonIdentification of deferentially expressed proteins in colorectal cancer by the combination of laser dissection microscopy, 2DDIGE and Maldi TOF mass spectroscopy. Validation of prognostic utility with tissue micro-arrays. -
Mar 2000–
Dec 2006Research: FGFR3 mutations and craniosynostoses
University of Queensland · Pediatrics and Child Health · GeneticsAustralia · BrisbaneStudies of the mutation in FGFR3 and their effects on severity of Craniosynostoses. -
Jan 2000–
Dec 2006Research: Short Stature Homeobox Gene
University of Queensland · Pediatrics and Child Health · EndocrinologyAustralia · BrisbaneStudies of children with haploinsufficiency or mutations in the shox gene and its affects on phenotype -
Jan 2000–
Feb 2006Research: Burns and Wound Healing
University of Queensland · Pediatrics and Child Health · Burns GroupAustralia · BrisbaneInvestigation of why fetal wounds heal without scale while newborns scar. -
Feb 1998–
Dec 1999Research: Effect of IGF-1 on rate of apoptosis in hair follicle post exposure to chemotherapy drugs
University of Queensland · Pediatrics and Child Health · EndocrinologyAustralia · Brisbane -
Jan 1998
Research: Queensland Institute of Medical Research
Queensland Institute of Medical ResearchAustralia · Brisbane
Education
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Mar 1994–
Apr 2000Queensland Institute of Medical Research
Melanoma and Chemotherapy · PhDAustralia · Brisbane -
Mar 1989–
Jul 1990University of New England
Tertiary Education · Diploma of Education (Tertiary)Australia · Armidale -
Mar 1981–
Feb 1988University of Sydney
Agronomy · MScAustralia · Sydney -
Mar 1972–
Nov 1975University of Sydney
Biology/Chemistry · BScAustralia · Sydney
Other
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LanguagesEnglish
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Scientific MembershipsWellington Medical Research Foundation
Royal Society New Zealand
American Association for the Advancement of Science
American Society for Biochemistry and Molecular Biology
Questions and Answers (3) View all
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Answer added in Cell Culture7 Hormone content of FBS? Insulin depletion from FBS?If you are doing anything with glucose uptake you should not use FBS. Fetuin is nearly 50% of total protein in FBS and has independent effects on glu... [more]
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Question asked in ObesityOpen What is the best way to measure degree of central obesity in humans?I want to determine the relative amount of omental fat to abdominal fat accurately in human subjects and correlate these with a blood biomarkers. Wou... [more]
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Answer added in Diabetology22 Does anyone have experience of the type 2 diabetes rat model that uses a high fat diet in combination with a low dose of STZ?Zucker ZDF rats purchased directly from Charles River are reliably diabetic at 12 weeks with a sharp reduction in serum insulin levels from week 12. ... [more]
Publications (36) View all
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Article: TUFM is a potential new prognostic indicator for colorectal carcinoma.
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ABSTRACT: : Mitochondrial Tu translation elongation factor (TUFM) is a nuclear encoded protein that participates in mitochondrial polypeptide translation. TUFM has been reported to be over-expressed in many tumour types including colorectal carcinoma (CRC) by proteomics. The present study aims to examine the prognostic implication of TUFM in CRC. : Immunohistochemical staining was performed in tissue microarrays composed of 123 cases of CRC using a polyclonal anti-TUFM antibody. Immunoreactivity was quantified using Image-Pro plus software, and analysed in association with patients' clinicopathological parameters and survival time. : The immunoreactivity of TUFM was negative in 25%, weak in 50% and strong in 25% of CRC cases. TUFM immunoreactivity had no significant association with the clinicopathological parameters examined including TNM stage and grade. However, strong TUFM expression significantly correlated with a higher 5-year recurrence rate (p = 0.024). Kaplan-Meier analysis revealed that patients with strong TUFM expression had significantly shorter cancer-specific survival than patients with negative TUFM (log-rank test, p = 0.038). In multivariate analysis, strong TUFM expression remained a stage-independent unfavourable prognostic indicator (p = 0.024). : Increased expression of TUFM is a promising new prognostic indicator for CRC. Selective inhibition of TUFM in tumour cells may present a new avenue for the targeted therapy of this cancer.Pathology 07/2012; 44(6):506-12. · 2.38 Impact Factor -
Article: Cathepsin D Expression in Colorectal Cancer: From Proteomic Discovery through Validation Using Western Blotting, Immunohistochemistry, and Tissue Microarrays.
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ABSTRACT: Despite recent advances in surgical techniques and therapeutic treatments, survival from colorectal cancer (CRC) remains disappointing with some 40-50% of newly diagnosed patients ultimately dying of metastatic disease. Current staging by light microscopy alone is not sufficiently predictive of prognosis and would benefit from additional support from biomarkers in order to stratify patients appropriately for adjuvant therapy. We have identified that cathepsin D expression was significantly greater in cells from invasive front (IF) area and liver metastasis (LM) than those from main tumour body (MTB). Cathepsin D expression was subsequently examined by immunohistochemistry in tissue microarrays from 119 patients with CRC. Strong expression in tumour cells at the IF did not correlate significantly with any clinico-pathological parameters examined or patient survival. However, cathepsin D expression in cells from the MTB was highly elevated in late stage CRC and showed significant correlation with subsequent distant metastasis and shorter cancer-specific survival. We also found that macrophages surrounding tumour cells stained strongly for cathepsin D but there was no significant correlation found between cathepsin D in macrophages at IF and MTB of CRC patient with the clinic-pathological parameters examined.International journal of proteomics. 01/2012; 2012:245819. -
Article: Somatic and germline mosaicism for a R248C missense mutation in FGFR3, resulting in a skeletal dysplasia distinct from thanatophoric dysplasia.
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ABSTRACT: In this communication, we report the identification of a mosaic R248C missense mutation in the IgII-III linker region of the gene encoding the fibroblast growth factor receptor-3 (FGFR3), in an individual who manifests a skeletal dysplasia and epidermal hyperplasia. By means of Denaturing High Performance Liquid Chromatography (DHPLC), we determined that 25% of her lymphocytes are heterozygous for this particular missense mutation in FGFR3, and that 12.5% of her lymphocyte-derived genomic DNA encodes a cysteine residue at this position. The proposita has disproportionate short stature, radial head dislocation, coxa vara, and bowing of some of the long bones, associated with an S-shaped deformity of the humerus, accompanied by widespread acanthosis nigricans in the integument. These features do not match any previously described skeletal dysplasia. Further, the proposita's only pregnancy ended in the delivery of a fetus manifesting a lethal short-limbed dwarfism with pulmonary hypoplasia, strongly suggestive of an undiagnosed thanatophoric dysplasia. These findings confirm the proposita to be a somatic and germline mosaic for this particular missense mutation in FGFR3. Thus far, all reported FGFR3 R248C mutations have resulted in thanatophoric dysplasia type I (TDI).American Journal of Medical Genetics Part A 08/2003; 120A(2):157-68. · 2.39 Impact Factor -
Article: Vascular endothelial growth factor-B and retinal vascular development in the mouse.
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ABSTRACT: Vascular endothelial growth factor-A (VEGF-A) is crucial to retinal vascular growth, both normal and pathological. VEGF-B, recently characterized, is reported to be expressed in retinal tissues, but the importance of VEGF-B to retinal vascular development remained unknown. The aim of this study was to analyse retinal vascular growth in the Vegfb-/- knockout mouse. Retinal vascular growth was measured in Vegfb-/- knockout mice raised under normal conditions, and Vegfb-/- knockout mice with an oxygen-induced proliferative retinopathy. Wild type Vegfb+/+ mice served as controls. Vessels were perfused with ink and retinal flatmounts secondarily labelled with FITC-lectin (BS-1, Griffonia simplicifolia). Area and diameter of retinal growth and retinal vascular growth were recorded over days 0-20, and capillary density and mean diameter recorded from day 17 pups. A variety of techniques confirmed that Vegfb+/+ mice expressed VEGF-B and that VEGF-B expression was absent in Vegfb-/- mice. Vegfb-/- mice raised in room air showed no significant differences from Vegfb+/+ controls. No differences were found in oxygen-induced retinopathy between Vegfb-/- and Vegfb+/+ pups in either the extent of the initial oxygen-induced ablation, or in the regrowth of retinal vessels or vitreal (neovascular) sprouts; vitreal sprouts are important markers of the abnormal proliferative response, and are maximally expressed on day 17 in this model of oxygen-induced retinopathy. These results indicate that a lack of VEGF-B does not significantly affect development of the retinal vasculature under normal conditions, nor does it appear to affect the proliferative retinal responses seen in oxygen-induced retinopathy.Clinical and Experimental Ophthalmology 03/2003; 31(1):61-5. · 1.98 Impact Factor -
Article: Expression of SHOX in human fetal and childhood growth plate.
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ABSTRACT: Abnormalities in the growth plate may lead to short stature and skeletal deformity including Leri Weil syndrome, which has been shown to result from deletions or mutations in the SHOX gene, a homeobox gene located at the pseudoautosomal region of the X and Y chromosome. We studied the expression of SHOX protein, by immunohistochemistry, in human fetal and childhood growth plates and mRNA by in situ hybridization in childhood normal and Leri Weil growth plate. SHOX protein was found in reserve, proliferative, and hypertrophic zones of fetal growth plate from 12 wk to term and childhood control and Leri Weil growth plates. The pattern of immunostaining in the proliferative zone of childhood growth plate was patchy, with more intense uniform immunostaining in the hypertrophic zone. In situ hybridization studies of childhood growth plate demonstrated SHOX mRNA expression throughout the growth plate. No difference in the pattern of SHOX protein or mRNA expression was seen between the control and Leri Weil growth plate. These findings suggest that SHOX plays a role in chondrocyte function in the growth plate.Journal of Clinical Endocrinology & Metabolism 09/2004; 89(8):4130-5. · 6.50 Impact Factor
