The production and reproduction of inequality in the UK in times of austerity

Inequality appears to be back on the intellectual and political agenda. This paper provides a commentary on this renewed interest, drawing on an empirical discussion of inequality in the UK. The paper argues that inequality should be seen as produced in the inherently unequal social relations of production, drawing attention to the role of social struggle in shaping dynamics of inequality. However, inequality is not just produced in dynamic class struggle in the formal economy, but also through the social reproduction of labour power on a day-to-day and inter-generational basis. As such, inequalities of household resources at any point in time may be reproductive of greater future inequality. It is argued that inequality has risen in the UK over recent decades because of changes in the social relations of production in the formal economy and social reproduction in the domestic sector, both of which have witnessed significant state interventions that have increased structural inequalities. It is argued that, absent of significant change, the underpinning structural dynamics in the UK will lead to further increases in inequality over the short and longer-term. Given this, we might expect to see an already emergent ‘New Politics of Inequality’ intensifying in the coming decades.n/

QT dispersion in patients with systemic lupus erythematosus: the impact of disease activity

<p>Abstract</p> <p>Background</p> <p>Patients with systemic lupus erythematosus (SLE) have increased cardiovascular morbidity and mortality. Although autopsy studies have documented that the heart is affected in most SLE patients, clinical manifestations occur in less than 10%. QT dispersion is a new parameter that can be used to assess homogeneity of cardiac repolarization and autonomic function. We compared the increase in QT dispersion in SLE patients with high disease activity and mild or moderate disease activity.</p> <p>Methods and Results</p> <p>One hundred twenty-four patients with SLE were enrolled in the study. Complete history and physical exam, ECG, echocardiography, exercise test and SLE disease activity index (SLEDAI) were recorded. Twenty patients were excluded on the basis of our exclusion criteria. The patients were divided to two groups based on SLEDAI: 54 in the high-score group (SLEDAI > 10) and 50 in the low-score group (SLEDAI < 10).</p> <p>QT dispersion was significantly higher in high-score group (58.31 ± 18.66 vs. 47.90 ± 17.41 respectively; <it>P </it>< 0.004). QT dispersion was not significantly higher in patients who had received hydroxychloroquine (54.17 ± 19.36 vs. 50.82 ± 15.96, <it>P </it>= 0.45) or corticosteroids (53.58 ± 19.16 vs. 50.40 + 11.59, <it>P </it>= 0.47). There was a statistically significant correlation between abnormal echocardiographic findings (abnormalities of pericardial effusion, pericarditis, pulmonary hypertension and Libman-Sacks endocarditis) and SLEADI (<it>P </it>< 0.004).</p> <p>Conclusions</p> <p>QT dispersion can be a useful, simple noninvasive method for the early detection of cardiac involvement in SLE patients with active disease. Concerning high chance of cardiac involvement, cardiovascular evaluation for every SLE patient with a SLEDAI higher than 10 may be recommended.</p> <p>Trial registration</p> <p>Clinicaltrial.gov registration <a href="http://www.clinicaltrials.gov/ct2/show/NCT01031797">NCT01031797</a></p

Does the aldosterone: renin ratio predict the efficacy of spironolactone over bendroflumethiazide in hypertension? A clinical trial protocol for RENALDO (RENin-ALDOsterone) study

&lt;p&gt;Background: High blood pressure is an important determinant of cardiovascular disease risk. Treated hypertensives do not attain a risk level equivalent to normotensives. This may be a consequence of suboptimal blood pressure control to which indiscriminate use of antihypertensive drugs may contribute. Indeed the recent ALLHAT[1]study suggests that thiazides should be given first to virtually all hypertensives. Whether this is correct or whether different antihypertensive therapies should be targeted towards different patients is a major unresolved issue, which we address in this study.&lt;/p&gt; &lt;p&gt;The measurement of the ratio of aldosterone: renin is used to identify hypertensive subjects who may respond well to treatment with the aldosterone antagonist spironolactone. It is not known if subjects with a high ratio have aldosteronism or aldosterone-sensitive hypertension is debated but it is important to know whether spironolactone is superior to other diuretics such as bendroflumethiazide in this setting.&lt;/p&gt; &lt;p&gt;Methods/design: The study is a double-blind, randomised, crossover, controlled trial that will randomise 120 hypertensive subjects to 12 weeks treatment with spironolactone 50 mg once daily and 12 weeks treatment with bendroflumethiazide 2.5 mg once daily. The 2 treatment periods are separated by a 2-week washout period. Randomisation is stratified by aldosterone: renin ratio to include equal numbers of subjects with high and low aldosterone: renin ratios.&lt;/p&gt; &lt;p&gt;Primary Objective – To test the hypothesis that the aldosterone: renin ratio predicts the antihypertensive response to spironolactone, specifically that the effect of spironolactone 50 mg is greater than that of bendroflumethiazide 2.5 mg in hypertensive subjects with high aldosterone: renin ratios.&lt;/p&gt; &lt;p&gt;Secondary Objectives – To determine whether bendroflumethiazide induces adverse metabolic abnormalities, especially in subjects with high aldosterone: renin ratios and if baseline renin measurement predicts the antihypertensive response to spironolactone and/or bendrofluazide.&lt;/p&gt; &lt;p&gt;Discussion: The numerous deleterious effects of hypertension dictate the need for a systematic approach for its treatment. In spite of various therapies, resistant hypertension is widely prevalent. Among various factors, primary aldosteronism is an important cause of resistant hypertension and is now more commonly recognised. More significantly, hypertensives with primary aldosteronism are also exposed to various other deleterious effects of excess aldosterone. Hence treating hypertension with specific aldosterone antagonists may be a better approach in this group of patients. It may lead on to better blood pressures with fewer medications.&lt;/p&gt

Pre-clinical studies investigating the combination of hypofractionated radiation with hyperthermia in a murine tumor and normal skin

Introduction This preclinical study evaluated the effects of combining hypofractionated radiation (HFRT), either as X-ray photons or protons, with hyperthermia on tumor response and normal tissue damage in mice.Methods The tumors were C3H mammary carcinomas implanted in the right rear foot of male CDF1 mice, while non-tumor-bearing mice were used to assess normal foot skin. HFRT was delivered in three fractions (5, 10, or 15 Gy) at 3 to 4-day intervals. Hyperthermia (40.5–42.5 °C) was applied once for 60 min, either 30, 90, or 180 min after the final radiation dose. Endpoints included tumor growth delay and moist skin desquamation. Mechanistic studies assessed DNA damage (γ-H2AX foci) 24 h after 3 × 10 Gy, with or without hyperthermia (42.5 °C for 1 h, administered 30 min post-RT), and tumor hypoxia (pimonidazole staining) measured 1 h after the last radiation fraction.Results Animals responded similarly to X-ray photons and protons in the tumor and skin. Hyperthermia enhanced the response to X-ray photons in both tissues, with temperature and time-interval dependency, showing the greatest effects at higher temperatures and shorter intervals. Protons combined with hyperthermia showed similar results, although with less decay in time-interval effects at 42.5 °C. DNA damage assessments revealed no significant difference between radiation types, but a significant enhancement was seen when tumors were heated at 42.5 °C. Tumor hypoxia was reduced after 3 × 10 Gy irradiation with either radiation type.Conclusions Combining HFRT with hyperthermia yielded effects comparable to single-dose studies for both tumors and normal tissues. These responses were similar for both X-rays and protons

P4533Duration of heart failure and effect of defibrillator implantation in patients with non-ischemic systolic heart failure

Abstract Introduction Patients with non-ischemic systolic heart failure have increased risk of sudden cardiac death (SCD) and death from progressive pump failure. Whether the risk of SCD changes over time is unknown. We seek to investigate the relationship between duration of heart failure, mode of death, and effect of implantable cardioverter defibrillator (ICD) implantation. Methods We examined the risk of all-cause death and SCD according to the duration of heart failure among patients with non-ischemic systolic heart failure enrolled in the Danish Study to Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heart Failure on Mortality (DANISH) trial. Patients were divided according to quartiles of heart failure duration (Q1 ≤8 months, Q2 9 ≤18 months, Q3 19 ≤65 months, Q4 ≥66 months). Results A total number of 1116 patients were included. Patients with the longest duration of heart failure were older, more often men, had more comorbidity, and more often received cardiac resynchronizing therapy device. Doubling of heart failure duration was an independent predictor of both all-cause mortality (HR 1.26 95% CI 1.17–1.37, p&lt;0.0001), and SCD (HR 1.29 95% CI 1.11–1.49, p=0.0009). The proportion of deaths caused by SCD was not different between heart failure quartiles (p=0.91), and the effect of ICD implantation on all-cause mortality was not modified by the duration of heart failure (p=0.59). Duration of heart failure and death Conclusions Duration of heart failure predicted both all-cause mortality and risk of SCD independently of other risk indicators. However, the proportion of death caused by SCD did not change with longer duration of heart failure and the effect of ICD was not modified by the duration of heart failure. Acknowledgement/Funding The work was sponsored by The Danish Heart Foundation (Hjerteforeningen) and the Lundbeck Foundation (Lundbeckfonden). The DANISH trial was supported </jats:sec