Justice Beyond Borders? Australia and the International Criminal Court

The International Criminal Court (ICC) came into being on 1 July 2002. A four-person team opened an office in The Hague and will collect reports and allegations of genocide, war crimes and crimes against humanity until judges and a prosecutor are appointed towards the end of 2003. Although the court was heralded by many states and international lawyers as the most important positive development in international law since the formation of the United Nations, it did not get off to an auspicious start. The Bush administration was concerned that US military forces operating overseas would be particularly vulnerable to what it described as 'politicised' prosecutions. It therefore insisted that not only would it not be a part of the ICC, but also that it would not sanction the continuation of UN peacekeeping operations. Closer to home, the Australian Senate only ratified the ICC's founding treaty, the Rome Statute, after a bitter debate that split both the Liberal and National parties. This was the case even though the Howard government-and Foreign Minister Alexander Downer in particular-had been a leading advocate of the court and ratification of the Rome Statute had been a Liberal Party election promise in 2001. The cost that Downer, and pro-ICC Attorney-General Daryl Williams had to pay in order to appease restive conservative backbenchers, the National Party, and an increasingly reluctant (and pro-US) Prime Minister and secure the ratification was a declaration that reaffirmed the primacy of the Australian judicial system over the ICC. The declaration insisted that no Australian would be prosecuted by the court without the consent of the Attomey-General, and asserted Australia's right to define what is meant by the crimes of genocide, war crimes, and crimes against humanity. We argue that although Downer and Williams should be commended for their commitment to international justice, the declaration attached to Australia's ratification was unnecessary and unhelpful. The first and third aspects of the declaration were unnecessary: the principle of complementarity enshrined in the Rome Statute means that the ICC already recognises the primacy of domestic jurisdiction, and the crimes covered are already considered to fall under universal jurisdiction, as the Nuremberg, Tokyo and more recent Pinochet trials showed (see Weller 1999). The second is unhelpful because it contravenes both the letter and the spirit of the Rome Statute. We will begin, then, by tracing the development of the ICC debate in Australian politics. In 1998, the government was an enthusiastic advocate of the court but by 2002 an alliance of an ardently pro-US Prime Minister, vocal right-wing parliamentarians and their supporters, and The Australian (and its foreign affairs editor Greg Sheridan in particular) combined to put ratification in doubt. Contrary to Prime Minister John Howard's claims, this debate was not well informed. Instead, it was characterised by hearsay, inaccuracy and scare-mongering. The subsequent section of the article demonstrates this by focusing on the background to, and creation of, the Rome Statute

The Oxygen Paradox, the French Paradox, and age-related diseases

open46openDavies, Joanna M. S.; Cillard, Josiane; Friguet, Bertrand; Cadenas, Enrique; Cadet, Jean; Cayce, Rachael; Fishmann, Andrew; Liao, David; Bulteau, Anne-Laure; Derbré, Frédéric; Rébillard, Amélie; Burstein, Steven; Hirsch, Etienne; Kloner, Robert A.; Jakowec, Michael; Petzinger, Giselle; Sauce, Delphine; Sennlaub, Florian; Limon, Isabelle; Ursini, Fulvio; Maiorino, Matilde; Economides, Christina; Pike, Christian J.; Cohen, Pinchas; Salvayre, Anne Negre; Halliday, Matthew R.; Lundquist, Adam J.; Jakowec, Nicolaus A.; Mechta-Grigoriou, Fatima; Mericskay, Mathias; Mariani, Jean; Li, Zhenlin; Huang, David; Grant, Ellsworth; Forman, Henry J.; Finch, Caleb E.; Sun, Patrick Y.; Pomatto, Laura C. D.; Agbulut, Onnik; Warburton, David; Neri, Christian; Rouis, Mustapha; Cillard, Pierre; Capeau, Jacqueline; Rosenbaum, Jean; Davies, Kelvin J. A.Davies, Joanna M. S.; Cillard, Josiane; Friguet, Bertrand; Cadenas, Enrique; Cadet, Jean; Cayce, Rachael; Fishmann, Andrew; Liao, David; Bulteau, Anne-Laure; Derbré, Frédéric; Rébillard, Amélie; Burstein, Steven; Hirsch, Etienne; Kloner, Robert A.; Jakowec, Michael; Petzinger, Giselle; Sauce, Delphine; Sennlaub, Florian; Limon, Isabelle; Ursini, Fulvio; Maiorino, Matilde; Economides, Christina; Pike, Christian J.; Cohen, Pinchas; Salvayre, Anne Negre; Halliday, Matthew R.; Lundquist, Adam J.; Jakowec, Nicolaus A.; Mechta-Grigoriou, Fatima; Mericskay, Mathias; Mariani, Jean; Li, Zhenlin; Huang, David; Grant, Ellsworth; Forman, HENRY J.; Finch, Caleb E.; Sun, Patrick Y.; Pomatto, Laura C. D.; Agbulut, Onnik; Warburton, David; Neri, Christian; Rouis, Mustapha; Cillard, Pierre; Capeau, Jacqueline; Rosenbaum, Jean; Davies, Kelvin J. A

Binding and neutralization of vascular endothelial growth factor (VEGF) and related ligands by VEGF Trap, ranibizumab and bevacizumab

Pharmacological inhibition of VEGF-A has proven to be effective in inhibiting angiogenesis and vascular leak associated with cancers and various eye diseases. However, little information is currently available on the binding kinetics and relative biological activity of various VEGF inhibitors. Therefore, we have evaluated the binding kinetics of two anti-VEGF antibodies, ranibizumab and bevacizumab, and VEGF Trap (also known as aflibercept), a novel type of soluble decoy receptor, with substantially higher affinity than conventional soluble VEGF receptors. VEGF Trap bound to all isoforms of human VEGF-A tested with subpicomolar affinity. Ranibizumab and bevacizumab also bound human VEGF-A, but with markedly lower affinity. The association rate for VEGF Trap binding to VEGF-A was orders of magnitude faster than that measured for bevacizumab and ranibizumab. Similarly, in cell-based bioassays, VEGF Trap inhibited the activation of VEGFR1 and VEGFR2, as well as VEGF-A induced calcium mobilization and migration in human endothelial cells more potently than ranibizumab or bevacizumab. Only VEGF Trap bound human PlGF and VEGF-B, and inhibited VEGFR1 activation and HUVEC migration induced by PlGF. These data differentiate VEGF Trap from ranibizumab and bevacizumab in terms of its markedly higher affinity for VEGF-A, as well as its ability to bind VEGF-B and PlGF

The mammalian gene function resource: the International Knockout Mouse Consortium.

In 2007, the International Knockout Mouse Consortium (IKMC) made the ambitious promise to generate mutations in virtually every protein-coding gene of the mouse genome in a concerted worldwide action. Now, 5 years later, the IKMC members have developed high-throughput gene trapping and, in particular, gene-targeting pipelines and generated more than 17,400 mutant murine embryonic stem (ES) cell clones and more than 1,700 mutant mouse strains, most of them conditional. A common IKMC web portal (www.knockoutmouse.org) has been established, allowing easy access to this unparalleled biological resource. The IKMC materials considerably enhance functional gene annotation of the mammalian genome and will have a major impact on future biomedical research

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies