ORCID Profile
0000-0002-8208-4054
Current Organisation
University of South Australia
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Publisher: Elsevier BV
Date: 02-2009
DOI: 10.1038/LABINVEST.2008.123
Abstract: T cells are in general tolerant of prostate-specific tumor antigens. That prostate tumor tissue makes transforming growth factor-beta (TGFbeta) is thought to play a role in the induction of T-cell tolerance within the host and to contribute to tumor progression itself. Here we sought to investigate the influence of TGFbeta signaling on prostate antigen-specific T-cell responses as well as prostate tumorogenesis in an autochthonous murine model of the disease. The response of naive and activated ovalbumin (OVA) antigen-specific T cells, which had been rendered incapable of responding to TGFbeta through T-cell-specific transgenic expression of a dominant-negative variant of the TGFbeta receptor II (dnTGFRII), was analyzed after adoptive transfer into prostate OVA-expressing transgenic (POET) mice. The role of TGFbeta signaling in endogenous T cells in mice, which spontaneously form tumors, was also assessed by monitoring prostate tumor formation and progression in F1 progeny of productive matings between transgenic adenocarcinoma of the mouse prostate (TRAMP) and dnTGFRII mice. TGFbeta-resistant CD8(+) T cells proliferated more and produced IFNgamma more readily after OVA stimulation in vitro. OVA-specific T cells did not damage the prostate gland of POET mice irrespective of TGFbeta responsiveness. However, ex vivo activation facilitated entry of TGFbeta-insensitive T cells into the prostate and was associated with prostate tissue damage. Early tumor progression was delayed in TRAMP mice that carried endogenous TGFbeta-insensitive T cells. Together, these results suggest that TGFbeta-signaling represses CD8(+) T-cell responses to a prostate-specific antigen. TGFbeta-mediated repression of T-cell function may include production of IFNgamma, which is known to contribute to tumor immunosurveillance.
Publisher: Wiley
Date: 11-2009
Abstract: There is contradictory published evidence on the potential efficacy of 'tongue ties' (TTs) for treatment of intermittent dorsal displacement of the soft palate (DDSP) in racehorses. To evaluate the effect of TTs on racing performance in Thoroughbred racehorses in the U.K. using a retrospective cohort study. Data on in idual horses' lifetime racing performance and TT use were retrieved from the Racing Post Online Database. Exposed cases were horses that ran with a TT in randomly chosen race meetings on one of 60 randomly chosen dates from 2001-2003. Unexposed (control) horses were matched to each exposed horse. Various measures of racing performance were analysed both within and between exposed and unexposed groups. Subsets of exposed horses that ran for 3 or 5 consecutive starts wearing TTs and their matched controls were analysed separately to examine the effect of repeated TT use. The inclusion criteria were fulfilled by 108 horses. The odds ratio for 'improvement' in race earnings between exposed and unexposed horses was 1.85 for horses that ran at least once with a TT, and 3.60 and 4.24, respectively, for horses that ran in 3 or 5 consecutive races wearing a TT. After instigation of TT use, horses that ran in 3 or 5 consecutive races wearing a TT had a significant increase in earnings when they ran wearing a TT compared to their pre-TT races. The use of a TT appears to have a beneficial effect on racing performance in a selected population of Thoroughbred racehorses.
Publisher: Elsevier
Date: 2019
Publisher: Wiley
Date: 16-03-2016
Publisher: Georg Thieme Verlag KG
Date: 2009
DOI: 10.1160/TH09-03-0162
Abstract: Trocarin D is a prothrombin activator from the Tropidechis carinatus venom. It is a functional and structural homologue to mammalian blood coagulation factor Xa.Trocarin D is hypothesised to have evolved from its factor X counterpart (TrFX) through gene duplication and recruitment.The genes of trocarin D and TrFX have significant sequence identities, except for insertions/deletions in their intron 1 and promoter regions. In trocarin D intron 1 region, there are three insertions and two deletions. In trocarin D promoter region, there is a novel 264 bp insertion which has potential cis-elements.This insertion is termed as Venom Recruitment/Switch Element (VERSE) and is hypothesised to account for switching the low-level constitutive expression of factor X in the liver to the high-level inducible expression of trocarin D in the venom gland. To understand the role of VERSE in the trocarin D expression,its cis-elements were characterised by luciferase assays in mammalian cell lines as well as snake venom gland cells. The ability of VERSE to drive luciferase expression is comparable to that of the trocarin D promoter. The predicted cis-elements are important in promoting expression as their mutagenesis resulted in lower luciferase expression.VERSE minimal core promoter and three novel cis-elements (two up-regulatory and one suppressor elements) were identified using deletion/site-directed mutagenesis studies. VERSE is primarily responsible for the increase of trocarin D expression. The insertions/deletions within trocarin D intron 1 need to be characterised for their role in tissue-specific and inducible expression of trocarin D.
Publisher: Hindawi Limited
Date: 2013
DOI: 10.1155/2013/816283
Abstract: Aim . The aim of this investigation was to examine the alterations in the peritoneum after cold dry CO 2 , heated dry CO 2 , and humidified heated CO 2 at pressures equivalent to intraperitoneal pressures used in human laparoscopy. Methods . Eighteen rats were ided into 4 treatment groups—group 1: untreated control group 2: insufflation with cold dry CO 2 group 3: insufflation with heated, dry CO 2 group 4: insufflation with heated and humidified CO 2 . The abdomen was insufflated to 5 mm/Hg (flow rate 50 mL/min) for 2 h. Twelve hours later, tissue s les were collected for analysis by light microscopy (LM) and scanning electron microscopy (SEM). Results . Group 1: no abnormalities were detected. Group 2: specimens revealed an inflammatory response with loss of mesothelium and mesothelial cell nuclei showing lytic change. Cells were rounded with some areas of cell flattening and separation. Group 3: some animals showed little or no alteration, while others had a mild inflammatory response. Mesothelial cells were rounded and showed crenation on the exposed surface. Group 4: specimens showed little change from the control group. Conclusions . The LM results indicate that insufflations with heated, humidified CO 2 are the least likely to induce mesothelial damage.
Publisher: Proceedings of the National Academy of Sciences
Date: 02-12-2013
Abstract: Snake venoms are toxic protein cocktails used for prey capture. To investigate the evolution of these complex biological weapon systems, we sequenced the genome of a venomous snake, the king cobra, and assessed the composition of venom gland expressed genes, small RNAs, and secreted venom proteins. We show that regulatory components of the venom secretory system may have evolved from a pancreatic origin and that venom toxin genes were co-opted by distinct genomic mechanisms. After co-option, toxin genes important for prey capture have massively expanded by gene duplication and evolved under positive selection, resulting in protein neofunctionalization. This erse and dramatic venom-related genomic response seemingly occurs in response to a coevolutionary arms race between venomous snakes and their prey.
Publisher: Elsevier
Date: 2019
Publisher: Springer Science and Business Media LLC
Date: 02-07-2021
DOI: 10.1186/S12885-021-08482-4
Abstract: The formation of blood vessels within solid tumors directly contributes to cancer growth and metastasis. Until recently, tumor vasculature was thought to occur exclusively via endothelial cell (EC) lined structures (i.e. angiogenesis), but a second source of tumor vasculature arises from the cancer cells themselves, a process known as vasculogenic mimicry (VM). While it is generally understood that the function of VM vessels is the same as that of EC-lined vessels (i.e. to supply oxygen and nutrients to the proliferating cancer cells), the molecular mechanisms underpinning VM are yet to be fully elucidated. Human VM-competent melanoma cell lines were examined for their VM potential using the in vitro angiogenesis assays (Matrigel), together with inhibition studies using small interfering RNA and blocking monoclonal antibodies. Invasion assays and adhesion assays were used to examine cancer cell function. Herein we demonstrate that CD36, a cell surface glycoprotein known to promote angiogenesis by ECs, also supports VM formation by human melanoma cancer cells. In silico analysis of CD36 expression within the melanoma cohort of The Cancer Genome Atlas suggests that melanoma patients with high expression of CD36 have a poorer clinical outcome. Using in vitro ‘angiogenesis’ assays and CD36-knockdown approaches, we reveal that CD36 supports VM formation by human melanoma cells as well as adhesion to, and invasion through, a cancer derived extracellular matrix substrate. Interestingly, thrombospondin-1 (TSP-1), a ligand for CD36 on ECs that inhibits angiogenesis, has no effect on VM formation. Further investigation revealed a role for laminin, but not collagen or fibronectin, as ligands for CD36 expressing melanoma cells. Taken together, this study suggests that CD36 is a novel regulator of VM by melanoma cancer cells that is facilitated, at least in part, via integrin-α 3 and laminin. Unlike angiogenesis, VM is not perturbed by the presence of TSP-1, thus providing new information on differences between these two processes of tumor vascularization which may be exploited to combat cancer progression.
Publisher: Elsevier BV
Date: 08-2021
No related grants have been discovered for Anthony Woods.