Graphic satire and public life in the age of terror

This paper investigates media representations of international insecurity through a selection of newspaper cartoons from some of the major daily Australian broadsheets. Since 2001, cartoonists such as Bruce Petty, John Spooner and Bill Leak (in The Age and The Australian) have provided an ongoing and vehement critique of the Australian government’s policies of ‘border protection’, the ‘war on terror’ and the words of mass distraction associated with Australia joining the war in Iraq. Cartoonists are often said to represent the ‘citizen’s perspective’ of public life through their graphic satire on the editorial pages of our daily newspapers. Increasingly, they can also be seen to be fulfilling the role of public intellectuals, defined by Richard A. Posner as ‘someone whose place it is publicly to raise embarrassing questions, to confront orthodoxy and dogma, to be someone who cannot easily be co-opted by governments and corporations’. Cartoonists enjoy an independence and freedom from censorship that is rarely extended to their journalistic colleagues in the print media and it is this independence that is the vital component in their being categorised as public intellectuals. Their role is to ‘question over and over again what is postulated as self-evident, to disturb people’s mental habits, to dissipate what is familiar and accepted, to re-examine rules and institutions’ (Posner, 2003: 31). With this useful — if generalised — definition in mind, the paper considers how cartoonists have contributed to debates concerning international insecurity in public life since 2001.

Lack of association between genetic markers on chromosome 16q22-Q24 and type 1 diabetes in Russian affected families

Aim To evaluate whether the T1D susceptibility locus on chromosome 16q contributes to the genetic susceptibility to T1D in Russian patients. Method Thirteen microsatellite markers, spanning a 47-centimorgan genomic region on 16q22-q24 were evaluated for linkage to T1D in 98 Russian multiplex families. Multipoint logarithm of odds (LOD) ratio (MLS) and nonparametric LOD (NPL) values were computed for each marker, using GENEHUNTER 2.1 software. Four microsatellites (D16S422, D16S504, D16S3037, and D16S3098) and 6 biallelic markers in 2 positional candidate genes, ICSBP1 and NQO1, were additionally tested for association with T1D in 114 simplex families, using transmission disequilibrium test (TDT). Results A peak of linkage (MLS = 1.35, NPL = 0.91) was shown for marker D16S750, but this was not significant (P = 0.18). The subsequent linkage analysis in the subset of 46 multiplex families carrying a common risk HLA-DR4 haplotype increased peak MLS and NPL values to 1.77 and 1.22, respectively, but showed no significant linkage (P = 0.11) to T1D in the 16q22-q24 genomic region. TDT analysis failed to find significant association between these markers and disease, even after the conditioning for the predisposing HLA-DR4 haplotype. Conclusion Our results did not support the evidence for the susceptibility locus to T1D on chromosome 16q22-24 in the Russian family data set. The lack of association could reflect genetic heterogeneity of type 1 diabetes in diverse ethnic groups.

The TAF5L gene on chromosome 1q42 is associated with type 1 diabetes in Russian affected patients

Type 1 diabetes (T1D) is a multifactorial autoimmune disease, with strong genetic component. Several susceptibility loci contribute to genetic predisposition to T1D. One of these loci have been mapped to chromosome 1q42 in UK and US joined affected family data sets but needs to be replicated in other populations. In this study, we evaluated sixteen microsatellites located on 1q42 for linkage with T1D in 97 Russian affected sibling pairs. A 2.7-cm region of suggestive linkage to T1D between markers D1S1644 and D1S225 was found by multipoint linkage analysis. The peak of linkage was shown for D1S2847 (P = 0.0005). Transmission disequilibrium test showed significant undertransmission of the 156-bp allele of D1S2847 from parents to diabetic children (28 transmissions vs. 68 nontransmissions, P = 0.043) in Russian affected families. A preferential transmission from parents to diabetic offspring was also shown for the T(-25) and T1362 alleles of the C/T(-25) and C/T1362 dimorphisms, both located at the TAF5L gene, which is situated 103 kb from D1S2847. Together with the A/C744 TAF5L SNP, these markers share common T(-25)/A744/T1362 and C(-25)/C744/T1362 haplotypes associated with higher and lower risk of diabetes (Odds Ratio = 2.15 and 0.62, respectively). Our results suggest that the TAF5L gene, encoding TAF5L-like RNA polymerase II p300/CBP associated factor (PCAF)-associated factor, could represent the susceptibility gene for T1D on chromosome 1q42 in Russian affected patients.

Evaluation of IDDM8 susceptibility locus in a Russian simplex family data set

Type 1 diabetes (TID) susceptibility locus, IDDM8, has been accurately mapped to 200 kilobases at the terminal end of chromosome 6q27. This is within the region which harbours a cluster of three genes encoding proteasome subunit beta 1 (PMSB1), TATA-box binding protein (TBP) and a homologue of mouse programming cell death activator 2 (PDCD2). In this study, we evaluated whether these genes contribute to TID susceptibility using the transmission disequilibrium test of the data set from 114 affected Russian simplex families. The A allele of the G/A1180 single nucleotide polymorphism (SNP) at the PDCD2 gene, which was significant in its preferential transfer from parents to diabetic children (75 transmissions vs. 47 non-transmissionS, x(2) = 12.85, P corrected = 0.0038), was found to be associated with T1D. G/A1180 dimorphism and two other SNPs, C/T771 TBP and G/T(-271) PDCD2, were shown to share three common haplotypes, two of which (A-T-G and A-T-T) have been associated with higher development risk of TID. The third haplotype (G-T-G) was related to having a lower risk of disease. These findings suggest that the PDCD2 gene is a likely susceptibility gene for TID within IDDM8. However, it was not possible to exclude the TBP gene from being another putative susceptibility gene in this region. (c) 2005 Elsevier Ltd. All rights reserved.

Television satire, decmocracy and the decay of public language: John Clarke's verbal caricature

This paper examines the contributions of John Clarke to the field of political satire through his interviews with straight-man Bryan Dawe on ABC TV’s The 7.30 Report. Clarke’s work represents one of the last vestiges of what was once a vigorous satiric tradition in TV comedy, specifically the practice of political caricature. There was The Mavis Bramston Show in the 1960s and The Naked Vicar Show in the 1970s, while The Gillies Report in the 1980s was probably the best example of sustained political caricature in television comedy. Even in later sketch-based shows such as Fast Forward and The Late Show in the early 1990s, political caricature was a significant component of the material, whereas it seems to have all but disappeared from current television comedy. The paper investigates the disappearance of this type of comedy from Australian television screens and also discusses why the longevity, consistency, not to mention accuracy, of Clarke’s satire is so important in the current political climate. Clarke’s political caricature is almost entirely language-based, expertly parodying the spin-doctored rhetoric of our elected representatives and business leaders. This leads to a secondary focus of the paper, which is a discussion of Clarke’s unique form of satire in the context of what an historian (and former satirist) identifies as ‘the decay of public language’.