The political economy of competitiveness and social mobility

Social mobility has become a mainstream political and media issue in recent years in the United Kingdom. This article suggests that part of the reason for this is that it can serve as a mechanism to discuss policy concerns that appear to be about social justice without questioning important aspects of neo-liberal political economy. The article charts the policy rhetoric on social mobility under both New Labour and the current Coalition Government. It is argued first that under New Labour the apparent commitment to social mobility was in fact subsumed beneath the pursuit of neo-liberal competitiveness, albeit imperfectly realised in policy. Second, the article suggests that under the Coalition Government the commitment to raising levels of social mobility has been retained and the recently published Strategy for Social Mobility promises that social mobility is what the Coalition means when it argues that the austerity programme is balanced with ‘fairness’. Third, however, the Strategy makes clear that the Coalition define social mobility in narrower terms than the previous government. It is argued here that in narrowing the definition the connection with the idea of competitiveness, while still clearly desirable for the Coalition, is weakened. Fourth, a brief analysis of the Coalition's main policy announcements provides little evidence to suggest that even the narrow definition set out in the Strategy is being seriously pursued. Fifth, the international comparative evidence suggests that any strategy aimed at genuinely raising the level of social mobility would need to give much more serious consideration to narrowing levels of inequality. Finally, it is concluded that when considered in the light of the arguments above, the Strategy for Social Mobility – and therefore ‘Fairness’ itself – is merely a discursive legitimation of the wider political economy programme of austerity

Assessment of β-amyloid deposits in human brain: a study of the BrainNet Europe Consortium

β-Amyloid (Aβ) related pathology shows a range of lesions which differ both qualitatively and quantitatively. Pathologists, to date, mainly focused on the assessment of both of these aspects but attempts to correlate the findings with clinical phenotypes are not convincing. It has been recently proposed in the same way as ι and α synuclein related lesions, also Aβ related pathology may follow a temporal evolution, i.e. distinct phases, characterized by a step-wise involvement of different brain-regions. Twenty-six independent observers reached an 81% absolute agreement while assessing the phase of Aβ, i.e. phase 1 = deposition of Aβ exclusively in neocortex, phase 2 = additionally in allocortex, phase 3 = additionally in diencephalon, phase 4 = additionally in brainstem, and phase 5 = additionally in cerebellum. These high agreement rates were reached when at least six brain regions were evaluated. Likewise, a high agreement (93%) was reached while assessing the absence/presence of cerebral amyloid angiopathy (CAA) and the type of CAA (74%) while examining the six brain regions. Of note, most of observers failed to detect capillary CAA when it was only mild and focal and thus instead of type 1, type 2 CAA was diagnosed. In conclusion, a reliable assessment of Aβ phase and presence/absence of CAA was achieved by a total of 26 observers who examined a standardized set of blocks taken from only six anatomical regions, applying commercially available reagents and by assessing them as instructed. Thus, one may consider rating of Aβ-phases as a diagnostic tool while analyzing subjects with suspected Alzheimer’s disease (AD). Because most of these blocks are currently routinely sampled by the majority of laboratories, assessment of the Aβ phase in AD is feasible even in large scale retrospective studies

SNP-SNP interactions in breast cancer susceptibility

BACKGROUND: Breast cancer predisposition genes identified to date (e.g., BRCA1 and BRCA2) are responsible for less than 5% of all breast cancer cases. Many studies have shown that the cancer risks associated with individual commonly occurring single nucleotide polymorphisms (SNPs) are incremental. However, polygenic models suggest that multiple commonly occurring low to modestly penetrant SNPs of cancer related genes might have a greater effect on a disease when considered in combination. METHODS: In an attempt to identify the breast cancer risk conferred by SNP interactions, we have studied 19 SNPs from genes involved in major cancer related pathways. All SNPs were genotyped by TaqMan 5'nuclease assay. The association between the case-control status and each individual SNP, measured by the odds ratio and its corresponding 95% confidence interval, was estimated using unconditional logistic regression models. At the second stage, two-way interactions were investigated using multivariate logistic models. The robustness of the interactions, which were observed among SNPs with stronger functional evidence, was assessed using a bootstrap approach, and correction for multiple testing based on the false discovery rate (FDR) principle. RESULTS: None of these SNPs contributed to breast cancer risk individually. However, we have demonstrated evidence for gene-gene (SNP-SNP) interaction among these SNPs, which were associated with increased breast cancer risk. Our study suggests cross talk between the SNPs of the DNA repair and immune system (XPD-[Lys751Gln] and IL10-[G(-1082)A]), cell cycle and estrogen metabolism (CCND1-[Pro241Pro] and COMT-[Met108/158Val]), cell cycle and DNA repair (BARD1-[Pro24Ser] and XPD-[Lys751Gln]), and within carcinogen metabolism (GSTP1-[Ile105Val] and COMT-[Met108/158Val]) pathways. CONCLUSION: The importance of these pathways and their communication in breast cancer predisposition has been emphasized previously, but their biological interactions through SNPs have not been described. The strategy used here has the potential to identify complex biological links among breast cancer genes and processes. This will provide novel biological information, which will ultimately improve breast cancer risk management

The financialisation of rental housing: A comparative analysis of New York City and Berlin

This paper compares how recent waves of private equity real estate investment have reshaped the rental housing markets in New York and Berlin. Through secondary analysis of separate primary research projects, we explore financialisation’s impact on tenants, neighbourhoods, and urban space. Despite their contrasting market contexts and investor strategies, financialisation heightened existing inequalities in housing affordability and stability, and rearranged spaces of abandonment and gentrification in both cities. Conversely cities themselves also shaped the process of financialisation, with weakened rental protections providing an opening to transform affordable housing into a new global asset class. We also show how financialisation’s adaptability in the face of changing market conditions entails ongoing, but shifting processes of uneven development. Comparative studies of financialisation can help highlight geographically disparate, but similar exposures to this global process, thus contributing to a critical urban politics of finance that crosses boundaries of space, sector and scale

Social patterning of chronic disease risk factors in a Latin American city

Most studies of socioeconomic status (SES) and chronic disease risk factors have been conducted in high-income countries, and most show inverse social gradients. Few studies examine these patterns in lower- or middle-income countries. Using cross-sectional data from a 2005 national risk factor survey in Argentina (a middle-income country), we investigated the associations of individual- and area-level SES with chronic disease risk factors (body mass index [BMI], hypertension, and diabetes) among residents of Buenos Aires. Associations of risk factors with income and education were estimated after adjusting for age, sex (except in sex-stratified models), and the other socioeconomic indicators. BMI and obesity were inversely associated with education and income for women, but not for men (e.g., mean differences in BMI for lowest versus highest education level were 1.55 kg/m2, 95%CI = 0.72-2.37 in women and 0.17 kg/m2, 95%CI = -0.72-1.06 in men). Low education and income were also associated with increased odds of hypertension diagnosis in all adults (adjusted odds ratio [AOR] = 1.48, 95%CI = 0.99-2.20 and AOR = 1.50, 95%CI = 0.99-2.26 for the lowest compared to the highest education and income categories, respectively). Lower education was strongly associated with increased odds of diabetes diagnosis (AOR = 4.12, 95%CI = 1.85-9.18 and AOR = 2.43, 95%CI = 1.14-5.20 for the lowest and middle education categories compared to highest, respectively). Area-level education also showed an inverse relationship with BMI and obesity; these results did not vary by sex as they did at the individual level. This cross-sectional study of a major urban area provides some insight into the global transition with a trend toward concentrations of risk factors in poorer populations.http://deepblue.lib.umich.edu/bitstream/2027.42/78528/1/FleischerDiezRoux2008_JUrbanHealth.pd

Influence of the MDM2 single nucleotide polymorphism SNP309 on tumour development in BRCA1 mutation carriers

BackgroundThe MDM2 gene encodes a negative regulator of the p53 tumour suppressor protein. A single nucleotide polymorphism (SNP) in the MDM2 promoter (a T to G exchange at nucleotide 309) has been reported to produce accelerated tumour formation in individuals with inherited p53 mutations. We have investigated the effect of the MDM2 SNP309 on clinical outcome in a cohort of patients with germline mutations of BRCA1.MethodsGenomic DNA was obtained for 102 healthy controls and 116 patients with established pathogenic mutations of BRCA1 and Pyrosequencing technology™ was used to determine the genotype at the MDM2 SNP309 locus.ResultsThe polymorphism was present in 52.9% of the controls (G/T in 37.3% and G/G in 15.6%) and 58.6% of the BRCA1 mutation carriers (47.4% G/T and 11.2% G/G). Incidence of malignancy in female BRCA1 carriers was not significantly higher in SNP309 carriers than in wildtype (T/T) individuals (72.7% vs. 75.6%, p = 1.00). Mean age of diagnosis of first breast cancer was 41.2 years in the SNP309 G/G genotype carriers, 38.6 years in those with the SNP309 G/T genotype and 39.0 years in wildtype subjects (p = 0.80).ConclusionWe found no evidence that the MDM2 SNP309 accelerates tumour development in carriers of known pathogenic germline mutations of BRCA1