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"O'Neill, Robert John"
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War, Strategy and History
This is a collection of essays in honour of eminent Professor Robert O’Neill. Each chapter was written by prominent academics and practitioners who have had a professional connection with Professor O’Neill during his long and distinguished career. The overarching themes running throughout the book are war, strategy and history. All the essays are shaped by the role that Professor O’Neill has played over the last 50 years in the debates in Australia, Europe and the US. This book covers not only Professor O’Neill’s impressive career, but also the evolution of strategy in practice, and of strategic studies as an internationally recognised academic discipline.
eBook
World War II : the Eastern Front 1941-1945
This book details the blow-by-blow of one of the greatest turning points of World War II: The Eastern Front. In 1940, Hilter set his sights on the East and the Soviet Union. The battle, which Hitler thought would be swift, came at a cost of 27 million lives. It, however, would eventually lead to Russia becoming one of the world's capitalist superpowers.
BOOK
Strategies to identify novel therapeutic targets for oesophageal adenocarcinoma
Oesophageal adenocarcinoma (OAC) is a leading cause of cancer death in the UK and current systemic therapies are ineffective for the majority of patients. The central aim of this work was to explore strategies to identify novel therapeutic targets. Research has failed, thus far, to identify a dominant oncogene in OAC, although the tumour suppressor p53 is frequently mutated. Inhibiting the mitotic kinase, polo-like kinase 1 (PLK-1), was proposed as a synthetic lethal strategy. PLK-1 was demonstrated to be over-expressed in both verified OAC cell lines and human OAC tissue compared to non-transformed cells and epithelium. Mutation of p53 was associated with over-expression of PLK-1 in both OAC and ovarian cancer tissue. Using a carefully validated viability assay, both an established and novel PLK-1 inhibitor were demonstrated to induce a G2/M arrest and reduce OAC cell proliferation. Relative selectivity was demonstrated for OAC compared to non-transformed cells. This therapeutic window could be enhanced with the induction of cancer cell cytotoxicity by pulsed administration of a short half-life inhibitor. Immunotherapeutics offer potential tumour-selectivity but no OAC-specific proteins have been defined. A comparative proteomic approach was employed to identify OAC-specific proteins as potential therapeutic targets. A tissue resource was established and methods to lyse fresh frozen biopsies optimised. An isobaric quantitative proteomic workflow was applied to OAC and matched normal biopsies and quantitative accuracy confirmed for 6 candidate proteins by immunohistochemistry. Proteome coverage and quantitative dynamic range were compared between isobaric and label-free systematic sequencing proteomic strategies applied to further patients’ tissues. The challenges of combining incomplete datasets were approached with a Bayesian framework to estimate the probability that a protein was missed during an experiment compared to not being present in the sample. This method was applied to generate a complete set of protein identifications and relative tissue expression. To gain insight into the dysregulated cellular processes in human OAC tissue, a network analysis was applied to the quantitative proteomic data. Enriched functional clusters were identified suggesting deranged glucose metabolism, potentially due to the Warburg effect. These findings were duplicated and candidate tumour-specific proteins identified in a further set of biopsies using the optimised quantitative proteomic method. The combined quantitative oesophageal proteomic dataset represents the largest in OAC to date. This thesis demonstrates a hypothesis-driven, synthetic lethal approach can yield cancer-selective therapeutic effects. Novel candidate therapeutic targets are also revealed through the development of quantitative proteomic methods and the application of network analysis.
Dissertation
The forgotten Anzacs
Investigates the battle fought by Australian and New Zealand troops in the same gorges as the heroes of ancient Greece. Describes the 21 Battalion's defence and rearguard action at the Vale of Tempe in Greece, on April 18, 1941. Indicates Tempe was an engagement that delayed the Germans long enough for most of the 55,000 strong Allied forces to escape south through Larissa a few miles south. Quotes extensively from the 21st battalion's historian J.F. Cody. Source: National Library of New Zealand Te Puna Matauranga o Aotearoa, licensed by the Department of Internal Affairs for re-use under the Creative Commons Attribution 3.0 New Zealand Licence.
Newspaper Article
Glioma Groups Based on 1p/19q, IDH, and TERT Promoter Mutations in Tumors
Genetic analysis of 1087 gliomas shows that the genetic status of these tumors is associated with overall survival in patients with grade II or III tumors, as well as with specific germline variants.
The past 25 years of research into glioma biology have led to the discovery of hundreds of molecular alterations in grade II, III, and IV gliomas (grade II and III gliomas are sometimes described as lower-grade gliomas, and grade IV gliomas are commonly described as glioblastoma multiforme).
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Among these molecular alterations, three are particularly noteworthy, because they occur early during glioma formation, are prevalent in glioma, or are strongly associated with overall survival. The first alteration to be identified was the codeletion of chromosome arms 1p and 19q (1p/19q codeletion), which is associated with the oligodendroglial histologic type and . . .
Journal Article
Influenza A virus causes maternal and fetal pathology via innate and adaptive vascular inflammation in mice
Influenza A virus (IAV) infection during pregnancy causes severe maternal and perinatal complications, despite a lack of vertical transmission of IAV across the placenta. Here, we demonstrate a significant alteration in the maternal vascular landscape that underpins the maternal and downstream fetal pathology to IAV infection in mice. In IAV infection of nonpregnant mice, the local lung inflammatory response was contained to the lungs and was self-resolving, whereas in pregnant mice, virus dissemination to major maternal blood vessels, including the aorta, resulted in a peripheral \"vascular storm,\" with elevated proinflammatory and antiviral mediators and the influx of Ly6Clow and Ly6Chigh monocytes, plus neutrophils and T cells. This vascular storm was associated with elevated levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profound vascular dysfunction. The sequalae of this IAV-driven vascular storm included placental growth retardation and intrauterine growth restriction, evidence of placental and fetal brain hypoxia, and increased circulating cell free fetal DNA and soluble Flt1. In contrast, IAV infection in nonpregnant mice caused no obvious alterations in endothelial function or vascular inflammation. Therefore, IAV infection during pregnancy drives a significant systemic vascular alteration in pregnant dams, which likely suppresses critical blood flow to the placenta and fetus. This study in mice provides a fundamental mechanistic insight and a paradigm into how an immune response to a respiratory virus, such as IAV, is likely to specifically drive maternal and fetal pathologies during pregnancy.
Journal Article