Public Policy to Reduce Inequalities across Europe

There is a broad consensus across European states and the EU that social and economic inequality is a problem that needs to be addressed. Yet inequality policy is notoriously complex and contested. This book approaches the issue from two linked perspectives. First, a focus on functional requirements highlights what policymakers think they need to deliver policy successfully, and the gap between their requirements and reality. We identify this gap in relation to the theory and practice of policy learning, and to multiple sectors, to show how it manifests in health, education, and gender equity policies. Second, a focus on territorial politics highlights how the problem is interpreted at different scales, subject to competing demands to take responsibility. This contestation and spread of responsibilities contributes to different policy approaches across spatial scales. We conclude that governments promote many separate equity initiatives, across territories and sectors, without knowing if they are complementary or contradictory. This outcome could reflect the fact that ambiguous policy problems and complex policymaking processes are beyond the full knowledge or control of governments. It could also be part of a strategy to make a rhetorically radical case while knowing that they will translate into safer policies. It allows them to replace debates on values, regarding whose definition of equity matters and which inequalities to tolerate, with more technical discussions of policy processes. Governments may be offering new perspectives on spatial justice or new ways to reduce political attention to inequalities

Public Policy to Reduce Inequalities across Europe

There is a broad consensus across European states and the EU that social and economic inequality is a problem that needs to be addressed. Yet inequality policy is notoriously complex and contested. This book approaches the issue from two linked perspectives. First, a focus on functional requirements highlights what policymakers think they need to deliver policy successfully, and the gap between their requirements and reality. We identify this gap in relation to the theory and practice of policy learning, and to multiple sectors, to show how it manifests in health, education, and gender equity policies. Second, a focus on territorial politics highlights how the problem is interpreted at different scales, subject to competing demands to take responsibility. This contestation and spread of responsibilities contributes to different policy approaches across spatial scales. We conclude that governments promote many separate equity initiatives, across territories and sectors, without knowing if they are complementary or contradictory. This outcome could reflect the fact that ambiguous policy problems and complex policymaking processes are beyond the full knowledge or control of governments. It could also be part of a strategy to make a rhetorically radical case while knowing that they will translate into safer policies. It allows them to replace debates on values, regarding whose definition of equity matters and which inequalities to tolerate, with more technical discussions of policy processes. Governments may be offering new perspectives on spatial justice or new ways to reduce political attention to inequalities

The trouble with NHS psychiatry in England

In ‘Wake-up call for British psychiatry’ Craddock et al explained how recent attempts to improve psychosocial care for people with mental illness focus on non-specific psychosocial support. This has been at the expense of proper diagnostic assessment and prescription of treatment by psychiatrists aimed at treatment of specific disorders and recovery. They describe a creeping devaluation of psychiatry which is caricatured as narrow, biological, reductionist, oppressive, discriminatory and stigmatising. Some trusts have implemented ‘New Ways of Working for Psychiatrists’ in a way that undermines the central importance of psychiatrists in mental healthcare. Consequently, patients may be treated in secondary care without ever being seen by a psychiatrist. We consider a number of different changes that have interacted in unforeseen ways, with unintended adverse consequences for psychiatric services in England. We aim to continue the debate here

Relationship between red blood cell lifespan and endogenous carbon monoxide in the common bottlenose dolphin and beluga

Certain deep-diving marine mammals (i.e., northern elephant seal (Mirounga angustirosis), Weddell seal (Leptonychotes weddellii)) have blood carbon monoxide (CO) levels that are comparable to those of chronic cigarette smokers. Most CO produced in humans is a by-product of heme degradation, which is released when red blood cells (RBC) are destroyed. Elevated CO can occur in humans when RBC lifespan decreases. The contribution of RBC turnover to CO concentrations in marine mammals is unknown. Here, we report the first RBC lifespans in two healthy, marine mammal species with different diving capacities and heme stores, the shallow diving bottlenose dolphin (Tursiops truncatus) and deep-diving beluga (Delphinapterus leucas) and relate the lifespans to the levels of CO in blood and breath. The belugas, with high blood heme stores, had the longest mean RBC lifespan compared to humans and bottlenose dolphins. Both cetacean species were found to have three times higher blood CO content compared to humans. The estimated CO production rate from heme degradation indicates some marine mammals may have additional mechanisms for CO production, or delay CO removal from the body, potentially from long duration breath-holds

Dysregulation of ErbB4 Signaling Pathway in the Dorsal Hippocampus after Neonatal Hypoxia-Ischemia and Late Deficits in PV+ Interneurons, Synaptic Plasticity and Working Memory

Neonatal hypoxic-ischemic (HI) injury leads to deficits in hippocampal parvalbumin (PV)+ interneurons (INs) and working memory. Therapeutic hypothermia (TH) does not prevent these deficits. ErbB4 supports maturation and maintenance of PV+ IN. Thus, we hypothesized that neonatal HI leads to persistent deficits in PV+ INs, working memory and synaptic plasticity associated with ErbB4 dysregulation despite TH. P10 HI-injured mice were randomized to normothermia (NT, 36 °C) or TH (31 °C) for 4 h and compared to sham. Hippocampi were studied for α-fodrin, glial fibrillary acidic protein (GFAP), and neuroregulin (Nrg) 1 levels; erb-b2 receptor tyrosine kinase 4 (ErbB4)/ Ak strain transforming (Akt) activation; and PV, synaptotagmin (Syt) 2, vesicular-glutamate transporter (VGlut) 2, Nrg1, and ErbB4 expression in coronal sections. Extracellular field potentials and behavioral testing were performed. At P40, deficits in PV+ INs correlated with impaired memory and coincided with blunted long-term depression (LTD), heightened long-term potentiation (LTP) and increased Vglut2/Syt2 ratio, supporting excitatory-inhibitory (E/I) imbalance. Hippocampal Nrg1 levels were increased in the hippocampus 24 h after neonatal HI, delaying the decline documented in shams. Paradoxically ErbB4 activation decreased 24 h and again 30 days after HI. Neonatal HI leads to persistent deficits in hippocampal PV+ INs, memory, and synaptic plasticity. While acute decreased ErbB4 activation supports impaired maturation and survival after HI, late deficit reemergence may impair PV+ INs maintenance after HI

Plants for planting ; indirect evidence for the movement of a serious forest pathogen, Teratosphaeria destructans, in Asia

Fungal diseases caused by native pathogens and pathogens introduced with planting stock have a significant impact on exotic plantation forestry in the tropics. Teratosphaeria destructans (formerly Kirramyces destructans) is a serious pathogen causing leaf, bud and shoot blight diseases of Eucalyptus spp. in plantations in the sub-tropics and tropics of south-east Asia. This pathogen was first discovered in Indonesia in 1995 and has subsequently spread to Thailand, China, Vietnam and East Timor. The biology, ecology and genetics of this important pathogen have not been explored yet. The objective of this study was, thus, to determine the genetic diversity and movement of T. destructans throughout south-east Asia using multi-gene phylogenies and microsatellite markers. Out of nine gene regions only two microsatellite markers detected a very low nucleotide polymorphism between isolates; seven other gene regions, ITS, β-tubulin, EF1-α, CHS, ATP6 and two microsatellite loci, reflected genetic uniformity. The two polymorphic molecular markers resolved six haplotypes among isolates from Indonesia and only a single haplotype elsewhere in Asia. The low diversity observed among isolates in the region of the first outbreak is as expected for a small founder population. The spread of a single clone over large distances throughout the region supports the hypothesis of spread via the human-mediated movement of germplasm.Murdoch University Doctoral Research Scholarship, University of Pretoria