Ethics Beyond the Horizon: Why Regulate the Global Practice of Law?

This Article explores whether global self-regulation of the legal profession is desirable. The Author explains that as global law practice has grown over the past decade, so has the desire to formulate global rules of professional responsibility. The Article focuses on large law firms offering transnational legal services in many countries. The Author addresses whether and for whom the aspiration to deliver core values at the global level is desirable. He does so by comparing the rhetoric of global self-regulation with the reality of global law practice. In reality, the global law practice has undermined the power of nation states because large law firm clients are powerful enough to manipulate nation states; lawyers are not capable of independent professional judgment because competition for profits puts loyalty to clients at a premium; and lawyers are capable of manipulating the rule of law to their clients\u27 advantage. The Author concludes that global rules of professional responsibility based on core values will add value to private clients, but they will add little to the public interest

Is It Time for Global Justice? International Human Rights and Wrongs in the 21st Century

Human rights are controversial, yet the question posed in this Article – “is it time for Global Justice?” – begs several, critical, questions which must be addressed first. If humans disagree on which rights should be universal; if human rights are “little more than thistledown, springing up at random and blowing away as time’s whirligig spins,” then how on earth can there be international human rights

Industrialisation, Class Formation and Social Mobility in Ireland. ESRI Working Paper No. 30, October 1991

No Abstrac

Work-Poor Households: the Welfare Implications of Changing Household Employment Patterns. ESRI Policy Series No. 52. March 2004

In the following report we consider how the employment situation of working-age Irish households has changed over a period of remarkable economic growth between 1994 and 2000. High levels of household joblessness became a matter of public concern in Ireland and elsewhere during the late 1980s and early 1990s. The concentration of unemployment and non-employment within households meant that many of the unemployed did not have access to the protection and support afforded by living with someone in employment. Therefore, household joblessness has serious implications for the financial situation of households and consequently for the psychological well-being of their members. It also has important implications for the scale of public support necessary to prevent poverty. For a given level of unemployment, a concentration of joblessness within households will require greater financing because there is no other source of household income

HIV-2/SIV Vpx antagonises NF-κB activation by targeting p65

BACKGROUND: The NF-κB family of transcription factors and associated signalling pathways are abundant and ubiquitous in human immune responses. Activation of NF-κB transcription factors by viral pathogen-associated molecular patterns, such as viral RNA and DNA, is fundamental to anti-viral innate immune defences and pro-inflammatory cytokine production that steers adaptive immune responses. Diverse non-viral stimuli, such as lipopolysaccharide and cytokines, also activate NF-κB and the same anti-pathogen gene networks. Viruses adapted to human cells often encode multiple proteins targeting the NF-κB pathway to mitigate the anti-viral effects of NF-κB-dependent host immunity. RESULTS: In this study we have demonstrated using a variety of assays, in a number of different cell types including primary cells, that plasmid-encoded or virus-delivered simian immunodeficiency virus (SIV) accessory protein Vpx is a broad antagonist of NF-κB signalling active against diverse innate NF-κB agonists. Using targeted Vpx mutagenesis, we showed that this novel Vpx phenotype is independent of known Vpx cofactor DCAF1 and other cellular binding partners, including SAMHD1, STING and the HUSH complex. We found that Vpx co-immunoprecipitated with canonical NF-κB transcription factor p65, but not NF-κB family members p50 or p100, preventing nuclear translocation of p65. We found that broad antagonism of NF-κB activation by Vpx was conserved across distantly related lentiviruses as well as for Vpr from SIV Mona monkey (SIVmon), which has Vpx-like SAMHD1-degradation activity. CONCLUSIONS: We have discovered a novel mechanism by which lentiviruses antagonise NF-κB activation by targeting p65. These findings extend our knowledge of how lentiviruses manipulate universal regulators of immunity to avoid the anti-viral sequelae of pro-inflammatory gene expression stimulated by both viral and extra-viral agonists. Importantly our findings are also relevant to the gene therapy field where virus-like particle associated Vpx is routinely used to enhance vector transduction through antagonism of SAMHD1, and perhaps also through manipulation of NF-κB