Sustaining democracy in the era of dependent financialization: Karl Polanyi's perspectives on the politics of finance

With the contemporary crisis of liberal democracy and the rise of illiberalism in the aftermath of the global financial crisis we need a theoretical framework that links modernization, crises and the fate of democracy. In my paper I attempt to show that Polanyi’s thinking represents such a framework. I focus on Polanyi’s historically informed political economic analysis of the tensions between liberal finance and liberal democracy. In the first section I reconstruct Polanyi’s political stance regarding democracy, socialism and the market. Based on this I will bring to the fore his often neglected views regarding the commodification of money and the tensions between international finance and democracy. Polanyi shows that monetary policy is not a technical but a deeply political question with major social implications. In the final section of my paper I conclude that Polanyi’s theory of the double movement and fictitious commodification can only be understood once we strip it of its excessive functionalism and bring it into dialogue with his political views. Polanyi urges to preserve the market by protecting the economy and society from the damages of excessive commodification: markets need to be protected from themselves.This is the final version of the article. It first appeared from the Centre for Social Sciences of the Hungarian Academy of Sciences via http://dx.doi.org/10.17356/ieejsp.v2i2.18

The wounds of post-socialism: a systematic review of the social determinants of mortality in Hungary

Eastern Europe underwent one of the most dramatic economic and demographic changes in recent history with skyrocketing mortality rates in some countries during the 1990s. The case of Hungary among the post-socialist transition countries is puzzling for several reasons. Although the Hungarian transition has been often characterised as smooth and successful, a look at the human dimension of the transformation reveals large costs and a slow improvement. Based on the analysis of 29 articles we provide a systematic review of the empirical evidence about the social determinants of mortality in post-socialist Hungary establishing a hierarchy of causes. Socioeconomic position, mental health, social capital, alcohol consumption, stress, and social integration are the most important explanatory variables that received attention by the researchers. Although economic policies might have played a central role in the rise of mortality there is no empirical research on the political economy of health in Hungary. No critical analysis of post-socialism can be complete without assessing the human costs of economic transformation. Social scientists have much to learn from social epidemiologists who have designed robust methodologies and complex theoretical frameworks to analyse the political economic determinants of health

The effect of rapid privatisation on mortality in mono-industrial towns in post-Soviet Russia: a retrospective cohort study

Background Population-level data suggest that economic disruptions in the early 1990s increased working-age male mortality in post-Soviet countries. This study uses individual-level data, using an indirect estimation method, to test the hypothesis that fast privatisation increased mortality in Russia. Methods In this retrospective cohort study, we surveyed surviving relatives of individuals who lived through the post-communist transition to retrieve demographic and socioeconomic characteristics of their parents, siblings, and male partners. The survey was done within the framework of the European Research Council (ERC) project PrivMort (The Impact of Privatization on the Mortality Crisis in Eastern Europe). We surveyed relatives in 20 mono-industrial towns in the European part of Russia (ie, the landmass to the west of the Urals). We compared ten fast-privatised and ten slow-privatised towns selected using propensity score matching. In the selected towns, population surveys were done in which respondents provided information about vital status, sociodemographic and socioeconomic characteristics and health-related behaviours of their parents, two eldest siblings (if eligible), and first husbands or long-term partners. We calculated indirect age-standardised mortality rates in fast and slow privatised towns and then, in multivariate analyses, calculated Poisson proportional incidence rate ratios to estimate the effect of rapid privatisation on all-cause mortality risk. Findings Between November, 2014, and March, 2015, 21 494 households were identified in 20 towns. Overall, 13 932 valid interviews were done (with information collected for 38 339 relatives [21 634 men and 16 705 women]). Fast privatisation was strongly associated with higher working-age male mortality rates both between 1992 and 1998 (age-standardised mortality ratio in men aged 20–69 years in fast vs slow privatised towns: 1·13, SMR 0·83, 95% CI 0·77–0·88 vs 0·73, 0·69–0·77, respectively) and from 1999 to 2006 (1·15, 0·91, 0·86–0·97 vs 0·79, 0·75–0·84). After adjusting for age, marital status, material deprivation history, smoking, drinking and socioeconomic status, working-age men in fast-privatised towns experienced 13% higher mortality than in slow-privatised towns (95% CI 1–26). Interpretation The rapid pace of privatisation was a significant factor in the marked increase in working-age male mortality in post-Soviet Russia. By providing compelling evidence in support of the health benefits of a slower pace of privatisation, this study can assist policy makers in making informed decisions about the speed and scope of government interventions.All authors acknowledge financial support from the European Research Council (ERC). DStu is funded by a Wellcome Trust Investigator Award

Advances in our understanding of the pathogenesis of glomerular thrombotic microangiopathy

Glomerular thrombotic microangiopathy is a hallmark feature of haemolytic uraemic syndrome, the leading cause of acute renal failure in childhood. This paper is a review of the different mechanistic pathways that lead to this histological picture in the kidney. It will focus on atypical HUS and complement dysregulation, but will also highlight some other recent advances in our understanding of this condition, including the potential role of the molecule vascular endothelial growth factor- A (VEGF-A)

Shiga Toxin Binding to Glycolipids and Glycans

Background: Immunologically distinct forms of Shiga toxin (Stx1 and Stx2) display different potencies and disease outcomes, likely due to differences in host cell binding. The glycolipid globotriaosylceramide (Gb3) has been reported to be the receptor for both toxins. While there is considerable data to suggest that Gb3 can bind Stx1, binding of Stx2 to Gb3 is variable. Methodology: We used isothermal titration calorimetry (ITC) and enzyme-linked immunosorbent assay (ELISA) to examine binding of Stx1 and Stx2 to various glycans, glycosphingolipids, and glycosphingolipid mixtures in the presence or absence of membrane components, phosphatidylcholine, and cholesterol. We have also assessed the ability of glycolipids mixtures to neutralize Stx-mediated inhibition of protein synthesis in Vero kidney cells. Results: By ITC, Stx1 bound both Pk (the trisaccharide on Gb3) and P (the tetrasaccharide on globotetraosylceramide, Gb4), while Stx2 did not bind to either glycan. Binding to neutral glycolipids individually and in combination was assessed by ELISA. Stx1 bound to glycolipids Gb3 and Gb4, and Gb3 mixed with other neural glycolipids, while Stx2 only bound to Gb3 mixtures. In the presence of phosphatidylcholine and cholesterol, both Stx1 and Stx2 bound well to Gb3 or Gb4 alone or mixed with other neutral glycolipids. Pre-incubation with Gb3 in the presence of phosphatidylcholine and cholesterol neutralized Stx1, but not Stx2 toxicity to Vero cells

Acute kidney injury in children

Acute kidney injury (AKI) (previously called acute renal failure) is characterized by a reversible increase in the blood concentration of creatinine and nitrogenous waste products and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately. The incidence of AKI in children appears to be increasing, and the etiology of AKI over the past decades has shifted from primary renal disease to multifactorial causes, particularly in hospitalized children. Genetic factors may predispose some children to AKI. Renal injury can be divided into pre-renal failure, intrinsic renal disease including vascular insults, and obstructive uropathies. The pathophysiology of hypoxia/ischemia-induced AKI is not well understood, but significant progress in elucidating the cellular, biochemical and molecular events has been made over the past several years. The history, physical examination, and laboratory studies, including urinalysis and radiographic studies, can establish the likely cause(s) of AKI. Many interventions such as ‘renal-dose dopamine’ and diuretic therapy have been shown not to alter the course of AKI. The prognosis of AKI is highly dependent on the underlying etiology of the AKI. Children who have suffered AKI from any cause are at risk for late development of kidney disease several years after the initial insult. Therapeutic interventions in AKI have been largely disappointing, likely due to the complex nature of the pathophysiology of AKI, the fact that the serum creatinine concentration is an insensitive measure of kidney function, and because of co-morbid factors in treated patients. Improved understanding of the pathophysiology of AKI, early biomarkers of AKI, and better classification of AKI are needed for the development of successful therapeutic strategies for the treatment of AKI