Legal aid and access to legal representation : re-defining the right to a fair trial

The unmet demand for legal aid generally and for criminal law matters in particular, has grown with the expansion of crime control and restrictions on funding for publicly funded welfare and support services. This article examines the connection between legal aid, legal representation and the right to a fair trial. It presents an in-depth case study of Victorian case law and policy development to illuminate dilemmas in the prioritised allocation of legal aid resources in serious criminal trials. It then compares the Victorian courts’ approach to a fair trial, with the tenets of current European Court of Human Rights jurisprudence regarding the scope and timing of an accused person’s right to access a lawyer. The comparison underlines the narrow definition of fair trial under Victorian common law, relative to Europe, where a fair trial is interpreted more broadly to include the right to legal representation during police and pre-trial investigations. The article questions whether international developments in access to legal aid for criminal trials and the extension of legal aid and representation to pre-trial procedures, most notably through the Salduz case (heard in the European Court of Human Rights), may inspire change in Victoria

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

`Counter-terrorism`, human security and globalisation - from welfare to warfare state?

The continuing erosion of civil liberties in Western democracies, and in particular Australia, as a response to the threat of terrorist attack - the position taken that laws eroding civil liberties will ultimately fail in its attempt to combat terrorist activity while adding to human insecurity and violence - counter-terrorism measures resulting in the militarisation of law enforcement and provoking terrorism - linking counter-terrorism with globalisation.<br /

Blue murder: press coverage of fatal shootings of and by police in Victoria

© 1994 Jude McCullochThis study is a qualitative content analysis of two newspapers' coverage of three fatal shootings in Victoria in October 1988. The shootings are those of Graeme Jensen, killed by the Armed Robbery Squad on 11 October 1988, and Constables Steven Tynan and Damian Eyre who were killed by offender/s unknown the following day. Qualitative content analysis consists of a detailed reading of a text in order to provide an interpretation by drawing out the latent meaning of the text. In conducting the analysis the overriding concern is not with whether the reports are true or false, but how meaning is created and to what effect. The newspapers studied represent the killing of Graeme Jensen as unproblematic, depicting it as lawful and necessary. Graeme Jensen is represented as a dangerous criminal living outside the community; his death is presented not as a tragedy but as the fulfilment of his life's destiny. Other ways of viewing the shooting, that are at least as well supported by the evidence, are given little space. In contrast, the killing of the two police officers is represented as a terrible crime. The great emphasis given to the brutality of the killings and killers, and the innocence of the police victims, constructs the officers as martyrs whose dead bodies provide the rhetorical base for police demands for greater powers, resources, and harsher punishments. The press coverage of the shootings supports the organisational legitimacy and interests of the police; there is little evidence of competition for meaning within the reports, and alternative viewpoints are only included to give the illusion of a contest