Rethinking the impact of regeneration on poverty: a (partial) defence of a 'failed' policy

For decades regeneration programmes in England targeted areas where spatial concentrations of poverty exist. These 'area-based initiatives' (ABIs) came under sustained attack, however, from the previous coalition government for being expensive and ineffective. This paper assesses this claim by re-evaluating past evidence on the impact of regeneration on poverty. It finds regeneration did relatively little to transform households' material circumstances but significantly ameliorated negative experiences of living in poverty in relation to housing, community safety and the physical environment. This partially undermines the rationale for the policy shift away from neighbourhood renewal interventions toward the current focus on 'local growth' as the sole remedy for spatial inequalities. It also suggests a need for more nuance in wider critical accounts of regeneration as a deepening form of neoliberalism

Ethnic minority customers of the Pensions, Disability and Carers Service: an evidence review.

The aim of this project was to review and synthesise available evidence that could throw light on: why Black and Minority Ethnic (BME) customers are less satisfied with the Pension, Disability and Carers Service (PDCS); why BME individuals eligible for the PDCS benefits are less likely to apply for them; what interventions might be successful at raising levels of take-up and satisfaction with PDCS services; and what important gaps exist in research evidence to answer these questions

Regeneration and poverty: evidence and policy review. Final report

First paragraph: This review assesses the impact of regeneration on poverty. It is one of a series of evidence reviews produced for the Joseph Rowntree Foundation (JRF) as part of a programme of work to develop an anti-poverty strategy for the UK

Hybrid Decay: A Transgenerational Epigenetic Decline in Vigor and Viability Triggered in Backcross Populations of Teosinte with Maize.

In the course of generating populations of maize with teosinte chromosomal introgressions, an unusual sickly plant phenotype was noted in individuals from crosses with two teosinte accessions collected near Valle de Bravo, Mexico. The plants of these Bravo teosinte accessions appear phenotypically normal themselves and the F1 plants appear similar to typical maize × teosinte F1s. However, upon backcrossing to maize, the BC1 and subsequent generations display a number of detrimental characteristics including shorter stature, reduced seed set, and abnormal floral structures. This phenomenon is observed in all BC individuals and there is no chromosomal segment linked to the sickly plant phenotype in advanced backcross generations. Once the sickly phenotype appears in a lineage, normal plants are never again recovered by continued backcrossing to the normal maize parent. Whole-genome shotgun sequencing reveals a small number of genomic sequences, some with homology to transposable elements, that have increased in copy number in the backcross populations. Transcriptome analysis of seedlings, which do not have striking phenotypic abnormalities, identified segments of 18 maize genes that exhibit increased expression in sickly plants. A de novo assembly of transcripts present in plants exhibiting the sickly phenotype identified a set of 59 upregulated novel transcripts. These transcripts include some examples with sequence similarity to transposable elements and other sequences present in the recurrent maize parent (W22) genome as well as novel sequences not present in the W22 genome. Genome-wide profiles of gene expression, DNA methylation, and small RNAs are similar between sickly plants and normal controls, although a few upregulated transcripts and transposable elements are associated with altered small RNA or methylation profiles. This study documents hybrid incompatibility and genome instability triggered by the backcrossing of Bravo teosinte with maize. We name this phenomenon "hybrid decay" and present ideas on the mechanism that may underlie it

Glycine receptor autoantibodies disrupt inhibitory neurotransmission

Chloride-permeable glycine receptors have an important role in fast inhibitory neurotransmission in the spinal cord and brainstem. Human immunoglobulin G (IgG) autoantibodies to glycine receptors are found in a substantial proportion of patients with progressive encephalomyelitis with rigidity and myoclonus, and less frequently in other variants of stiff person syndrome. Demonstrating a pathogenic role of glycine receptor autoantibodies would help justify the use of immunomodulatory therapies and provide insight into the mechanisms involved. Here purified IgGs from four patients with progressive encephalomyelitis with rigidity and myoclonus or stiff person syndrome and glycine receptor autoantibodies were observed to profoundly disrupt glycinergic neurotransmission. In whole cell patch clamp recordings from cultured rat spinal motoneurons, glycinergic synaptic currents were almost completely abolished following incubation in patient IgGs. Most human autoantibodies targeting other CNS neurotransmitter receptors, such as N-methyl-D-aspartate (NMDA) receptors, affect whole cell currents only after several hours’ incubation and this effect has been shown to be the result of antibody-mediated crosslinking and internalisation of receptors. By contrast, we observed substantial reductions in glycinergic currents with all four patient IgG preparations with 15 minutes of exposure to patient IgGs. Moreover, monovalent Fab fragments generated from the purified IgG of three of the four patients also profoundly reduced glycinergic currents compared with control Fab-IgG. We conclude that human glycine receptor autoantibodies disrupt glycinergic neurotransmission, and also suggest that the pathogenic mechanisms include direct antagonistic actions on glycine receptors.SJC is supported by from the Wellcome Trust (101696/Z/13/Z), the National Institute for Health Research (NIHR), BMA Foundation for Medical Research (Vera Down Award 2017) and the National Organisation for Rare Disorders (16006). CLD is supported by the Wellcome Trust. SRI is supported by the Wellcome Trust (104079/Z/14/Z), BMA Research Grants- Vera Down grant (2013) and Margaret Temple (2017), and by Epilepsy Research UK (P1201). The research was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC; The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health). LJ, MIL and AV received support from the Nuffield Department of Clinical Neurosciences. DMK is supported by the Wellcome Trust, Medical Research Council and Epilepsy Research UK

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy