Perils of development funding? The tale of EU Funds and grand corruption in Central and Eastern Europe

Given the unprecedented scale of intergovernmental development funding and the importance of institutional quality for human wellbeing, it is imperative to precisely understand the impact of development funds on corruption. In Europe, EU Funds provide a boost to public spending in recipient member states while introducing additional corruption controls. We investigate whether EU Funds increase high-level corruption in the Czech Republic and Hungary in 2009-2012. We analyse newly collected data from over 100,000 public procurement contracts to develop objective corruption risk indicators and link them to agency-level data of the public sector. Propensity score matching estimations suggest that EU funds increase corruption risks by up to 34%. The negative effects are largely attributable to overly formalistic compliance and EU Funds overriding domestic accountability mechanisms in public organisations entirely dependent on external funds. The policy implications are profound: governments should reduce barriers to market entry by lowering red tape and they should prevent excessive concentration of funds.The authors would like to thank the generous support of the European Union (FP7, grant agreement number: 290529) for financing much of the data collection efforts underpinning this research

Incarceration and mortality in the United States

The ongoing COVID-19 pandemic has spotlighted the role of America's overcrowded prisons as vectors of ill health, but robust analyses of the degree to which high rates of incarceration impact population-level health outcomes remain scarce. In this paper, we use county-level panel data from 2927 counties across 43 states between 1983 and 2014 and a novel instrumental variable technique to study the causal effect of penal expansion on age-standardised cause-specific and all-cause mortality rates. We find that higher rates of incarceration have substantively large effects on deaths from communicable, maternal, neonatal, and nutritional diseases in the short and medium term, whilst deaths from non-communicable disease and from all causes combined are impacted in the short, medium, and long run. These findings are further corroborated by a between-unit analysis using coarsened exact matching and a simulation-based regression approach to predicting geographically anchored mortality differences

IMF conditionality and development policy space, 1985–2014

In recent years, the International Monetary Fund (IMF) has re-emerged as a central actor in global economic governance. Its rhetoric and policies suggest that the organization has radically changed the ways in which it offers financial assistance to countries in economic trouble. We revisit two long-standing controversies: Has the policy content of IMF programmes evolved to allow for more policy space? Do these programmes now allow for the protection of labour and social policies? We collected relevant archival material on the IMF's lending operations and identified all policy conditionality in IMF loan agreements between 1985 and 2014, extracting 55,465 individual conditions across 131 countries in total. We find little evidence of a fundamental transformation of IMF conditionality. The organization's post-2008 programmes reincorporated many of the mandated reforms that the organization claims to no longer advocate and the number of conditions has been increasing. We also find that policies introduced to ameliorate the social consequences of IMF macroeconomic advice have been inadequately incorporated into programme design. Drawing on this evidence, we argue that multiple layers of rhetoric and ceremonial reforms have been designed to obscure the actual practice of adjustment programmes, revealing an escalating commitment to hypocrisy.The authors gratefully acknowledge funding by the Institute for New Economic Thinking (INET Grant INO13-00020: ‘The Political Economy of Structural Adjustment’), the Cambridge Political Economy Society Trust, and the Centre for Business Research at the University of Cambridge

An Objective Corruption Risk Index Using Public Procurement Data

In order to address the lack of reliable indicators of corruption, this article develops a composite indicator of high-level institutionalised corruption through a novel ‘Big Data’ approach. Using publicly available electronic public procurement records in Hungary, we identify “red flags” in the public procurement process and link them to restricted competition and recurrent contract award to the same company. We use this method to create a corruption indicator at contract level that can be aggregated to the level of individual organizations, sectors, regions and countries. Because electronic public procurement data is available in virtually all developed countries from about the mid-2000s, this method can generate a corruption index based on objective data that is consistent over time and across countries. We demonstrate the validity of the corruption risk index by showing that firms with higher corruption risk score had relatively higher profitability, higher ratio of contract value to initial estimated price, greater likelihood of politicians managing or owning them, and greater likelihood of registration in tax havens, than firms with lower scores on the index. In the conclusion we discuss the uses of this data for academic research, investigative journalists, civil society groups, and small and medium business.This is the author accepted manuscript. The final version is available from Springer at http://dx.doi.org/10.1007/s10610-016-9308-z

The association between income and life expectancy revisited: deindustrialization, incarceration and the widening health gap

BACKGROUND: The health gap between the top and the bottom of the income distribution is widening rapidly in the USA, but the lifespan of America’s poor depends substantially on where they live. We ask whether two major developments in American society, deindustrialization and incarceration, can explain variation among states in life expectancy of those in the lowest income quartile. METHODS: life expectancy estimates at age 40 of those in the bottom income quartile were used to fit panel data models examining the relationship with deindustrialization and incarceration between 2001 and 2014 for all US states. RESULTS: A one standard deviation (s.d.) increase in deindustrialization (mean = 11.2, s.d. = 3.5) reduces life expectancy for the poor by 0.255 years [95% confidence interval (CI): 0.090–0.419] and each additional prisoner per 1000 residents (mean = 4.0, s.d. = 1.5) is associated with a loss of 0.468 years (95% CI: 0.213–0.723). Our predictors explain over 20% of the state-level variation in life expectancy among the poor and virtually the entire increase in the life expectancy gap between the top and the bottom income quartiles since the turn of the century. CONCLUSIONS: In the USA between 2001 and 2014, deindustrialization and incarceration subtracted roughly 2.5 years from the lifespan of the poor, pointing to their role as major health determinants. Future research must remain conscious of the upstream determinants and the political economy of public health. If public policy responses to growing health inequalities are to be effective, they must consider strengthening industrial policy and ending hyper-incarceration

Historical Criminology and the Explanatory Power of the Past

To what extent can the past ‘explain’ the present? This deceptively simple question lies at the heart of historical criminology (research which incorporates historical primary sources while addressing present-day debates and practices in the criminal justice field). This article seeks first to categorise the ways in which criminologists have used historical data thus far, arguing that it is most commonly deployed to ‘problematize’ the contemporary rather than to ‘explain’ it. The article then interrogates the reticence of criminologists to attribute explicative power in relation to the present to historical data. Finally, it proposes the adoption of long time-frame historical research methods, outlining three advantages which would accrue from this: the identification and analysis of historical continuities; a more nuanced, shared understanding of micro/macro change over time in relation to criminal justice; and a method for identifying and analysing instances of historical recurrence, particularly in perceptions and discourses around crime and justice

Economic decline, incarceration, and mortality from drug use disorders in the USA between 1983 and 2014: an observational analysis

Background: Drug use disorders are an increasing cause of disability and early death in the USA, with substantial geographical variation. We aimed to investigate the associations between economic decline, incarceration rates, and age-standardised mortality from drug use disorders at the county level in the USA. // Methods: In this observational analysis, we examined age-standardised mortality data from the US National Vital Statistics System and the Institute for Health Metrics and Evaluation, household income data from the US Census Bureau, and county-level jail and prison incarceration data from the Vera Institute of Justice for 2640 US counties between 1983 and 2014. We also extracted data on county-level control variables from the US Census Bureau, the National Center for Health Statistics, and the US Centers for Disease Control and Prevention. We used a two-way fixed-effects panel regression to examine the association between reduced household income, incarceration, and mortality from drug use disorders within counties over time. To assess between-county variation, we used coarsened exact matching and a simulation-based modelling approach. // Findings: After adjusting for key confounders, each 1 SD decrease in median household income was associated with an increase of 12·8% (95% CI 11·0–14·6; p<0·0001) in drug-related deaths within counties. Each 1 SD increase in jail and prison incarceration rates was associated with an increase of 1·5% (95% CI 1·0–2·0; p<0·0001) and 2·6% (2·1–3·1; p<0·0001) in drug-related mortality, respectively. The association between drug-related mortality and income and incarceration persisted after controlling for local opioid prescription rates. Our model accounts for a large proportion of within-county variation in mortality from drug use disorders (R2=0·975). Between counties, high rates of incarceration were associated with a more than 50% increase in drug-related deaths. // Interpretation: Reduced household income and high incarceration rates are associated with poor health. The rapid expansion of the prison and jail population in the USA over the past four decades might have contributed to the increasing number of deaths from drug use disorders

Differential Regulation of the Period Genes in Striatal Regions following Cocaine Exposure

Several studies have suggested that disruptions in circadian rhythms contribute to the pathophysiology of multiple psychiatric diseases, including drug addiction. In fact, a number of the genes involved in the regulation of circadian rhythms are also involved in modulating the reward value for drugs of abuse, like cocaine. Thus, we wanted to determine the effects of chronic cocaine on the expression of several circadian genes in the Nucleus Accumbens (NAc) and Caudate Putamen (CP), regions of the brain known to be involved in the behavioral responses to drugs of abuse. Moreover, we wanted to explore the mechanism by which these genes are regulated following cocaine exposure. Here we find that after repeated cocaine exposure, expression of the Period (Per) genes and Neuronal PAS Domain Protein 2 (Npas2) are elevated, in a somewhat regionally selective fashion. Moreover, NPAS2 (but not CLOCK (Circadian Locomotor Output Cycles Kaput)) protein binding at Per gene promoters was enhanced following cocaine treatment. Mice lacking a functional Npas2 gene failed to exhibit any induction of Per gene expression after cocaine, suggesting that NPAS2 is necessary for this cocaine-induced regulation. Examination of Per gene and Npas2 expression over twenty-four hours identified changes in diurnal rhythmicity of these genes following chronic cocaine, which were regionally specific. Taken together, these studies point to selective disruptions in Per gene rhythmicity in striatial regions following chronic cocaine treatment, which are mediated primarily by NPAS2. © 2013 Falcon et al

Deficient and null variants of SERPINA1 are proteotoxic in a Caenorhabditis elegans model of α1-antitrypsin deficiency

α1-antitrypsin deficiency (ATD) predisposes patients to both loss-of-function (emphysema) and gain-of-function (liver cirrhosis) phenotypes depending on the type of mutation. Although the Z mutation (ATZ) is the most prevalent cause of ATD, >120 mutant alleles have been identified. In general, these mutations are classified as deficient (<20% normal plasma levels) or null (<1% normal levels) alleles. The deficient alleles, like ATZ, misfold in the ER where they accumulate as toxic monomers, oligomers and aggregates. Thus, deficient alleles may predispose to both gain- and loss-of-function phenotypes. Null variants, if translated, typically yield truncated proteins that are efficiently degraded after being transiently retained in the ER. Clinically, null alleles are only associated with the loss-of-function phenotype. We recently developed a C. elegans model of ATD in order to further elucidate the mechanisms of proteotoxicity (gain-of-function phenotype) induced by the aggregationprone deficient allele, ATZ. The goal of this study was to use this C. elegans model to determine whether different types of deficient and null alleles, which differentially affect polymerization and secretion rates, correlated to any extent with proteotoxicity. Animals expressing the deficient alleles, Mmalton, Siiyama and S (ATS), showed overall toxicity comparable to that observed in patients. Interestingly, Siiyama expressing animals had smaller intracellular inclusions than ATZ yet appeared to have a greater negative effect on animal fitness. Surprisingly, the null mutants, although efficiently degraded, showed a relatively mild gainoffunction proteotoxic phenotype. However, since null variant proteins are degraded differently and do not appear to accumulate, their mechanism of proteotoxicity is likely to be different to that of polymerizing, deficient mutants. Taken together, these studies showed that C. elegans is an inexpensive tool to assess the proteotoxicity of different AT variants using a transgenic approach