The evaluation of Education Maintenance Allowance Pilots: three years' evidence: a quantitative evaluation

This is the third report of the longitudinal quantitative evaluation of Education Maintenance Allowance (EMA) pilots and the first since the government announced that EMA is to be rolled out nationally from 2004. The evaluation was commissioned in 1999, by the Department for Education and Skills (DfES) from a consortium of research organisations, led by the Centre for Research in Social Policy (CRSP) and including the National Centre for Social Research, the Institute for Fiscal Studies (IFS) and the National Institute for Careers Education and Counselling (NICEC). The statistical evaluation design is a longitudinal cohort study involving large random sample surveys of young people (and their parents) in 10 EMA pilot areas and eleven control areas. Two cohorts of young people were selected from Child Benefit records. The first cohort of young people left compulsory schooling in the summer of 1999 and they, and their parents, were interviewed between October 1999 and April 2000 (Year 12 interview). A second interview was carried out with these young people between October 2000 and April 2001 (Year 13 interview). The second cohort left compulsory education the following summer of 2000 and young people, and their parents, were first interviewed between October 2000 and April 2001. The report uses both propensity score matching (PSM) and descriptive techniques, each of which brings their own particular strengths to the analysis

Measurements of total alkalinity and inorganic dissolved carbon in the Atlantic Ocean and adjacent Southern Ocean between 2008 and 2010

Water column dissolved inorganic carbon and total alkalinity were measured during five hydrographic sections in the Atlantic Ocean and Drake Passage. The work was funded through the Strategic Funding Initiative of the UK's Oceans2025 programme, which ran from 2007 to 2012. The aims of this programme were to establish the regional budgets of natural and anthropogenic carbon in the North Atlantic, the South Atlantic, and the Atlantic sector of the Southern Ocean, as well as the rates of change of these budgets. This paper describes in detail the dissolved inorganic carbon and total alkalinity data collected along east–west sections at 47° N to 60° N, 24.5° N, and 24° S in the Atlantic and across two Drake Passage sections. Other hydrographic and biogeochemical parameters were measured during these sections, and relevant standard operating procedures are mentioned here. Over 95% of dissolved inorganic carbon and total alkalinity samples taken during the 24.5° N, 24° S, and the Drake Passage sections were analysed onboard and subjected to a first-level quality control addressing technical and analytical issues. Samples taken along 47° N to 60° N were analysed and subjected to quality control back in the laboratory. Complete post-cruise second-level quality control was performed using cross-over analysis with historical data in the vicinity of measurements, and data were submitted to the CLIVAR and Carbon Hydrographic Data Office (CCHDO), the Carbon Dioxide Information Analysis Center (CDIAC) and and will be included in the Global Ocean Data Analyses Project, version 2 (GLODAP 2), the upcoming update of Key et al. (2004)

Slow stress relaxation in randomly disordered nematic elastomers and gels

Randomly disordered (polydomain) liquid crystalline elastomers align under stress. We study the dynamics of stress relaxation before, during and after the Polydomain-Monodomain transition. The results for different materials show the universal ultra-slow logarithmic behaviour, especially pronounced in the region of the transition. The data is approximated very well by an equation Sigma(t) ~ Sigma_{eq} + A/(1+ Alpha Log[t]). We propose a theoretical model based on the concept of cooperative mechanical resistance for the re-orientation of each domain, attempting to follow the soft-deformation pathway. The exact model solution can be approximated by compact analytical expressions valid at short and at long times of relaxation, with two model parameters determined from the data.Comment: 4 pages (two-column), 5 EPS figures (included via epsfig

Reconstructing mechanisms of extinctions to guide mammal conservation biogeography

First published: 07 April 2023. OnlinePublAn emerging research program on population and geographic range dynamics of Australia's mammals illustrates an approach to better understand and respond to geographic range collapses of threatened wildlife in general. In 1788, Europeans colonized an Australia with a diverse and largely endemic mammal fauna, where many species that are now extinct or threatened were common and widespread. Subsequent population declines, range collapses and extinctions were caused by introduced predators and herbivores, altered land use, modified fire regimes and the synergies between these threats. Declines in population and range size continue for many Australian mammals despite legislative protection and conservation interventions. Here, we propose an approach that integrates museum data and other historical records into process-explicit macroecological models to better resolve mammal distributions and abundances as they were at European arrival. We then illustrate how this integrative approach can identify the likely synergistic mechanisms causing mammal population declines across these and other landscapes. This emerging research approach, undertaken with fine temporal and spatial resolution, but at large geographic scales, will provide valuable insights into the different pathways to, and drivers of extinction. Such insights may, in turn, underpin conservation strategies based on a process-explicit understanding of population decline and range collapse under alternative scenarios of impending climate and environmental change. Given that similar information is available for other regional biotas, the approach we describe here can be adapted to conserve threatened wildlife in other regions across the globe.Sean Tomlinson, Mark V. Lomolino, John C. Z. Woinarski, Brett P. Murphy, Elizabeth Reed, Chris N. Johnson, Sarah Legge, Kristofer M. Helgen, Stuart C. Brown, Damien A. Fordha

Lack of Support for the Genes by Early Environment Interaction Hypothesis in the Pathogenesis of Schizophrenia

Ursini et al reported recently that the liability of schizophrenia explained by a polygenic risk score (PRS) derived from the variants most associated with schizophrenia was increased 5-fold in individuals who experienced complications during pregnancy or birth. Follow-up gene expression analysis showed that the genes mapping to the most associated genetic variants are highly expressed in placental tissues. If confirmed, these findings will have major implications in our understanding of the joint effect of genes and environment in the pathogenesis of schizophrenia. We examined the interplay between PRS and obstetric complications (OCs) in 5 independent samples (effective N = 2110). OCs were assessed with the full or modified Lewis-Murray scale, or with birth weight < 2.5 kg as a proxy. In a large cohort we tested whether the pathways from placenta-relevant variants in the original report were associated with case-control status. Unlike in the original study, we did not find significant effect of PRS on the presence of OCs in cases, nor a substantial difference in the association of PRS with case-control status in samples stratified by the presence of OCs. Furthermore, none of the PRS by OCs interactions were significant, nor were any of the biological pathways, examined in the Swedish cohort. Our study could not support the hypothesis of a mediating effect of placenta biology in the pathway from genes to schizophrenia. Methodology differences, in particular the different scales measuring OCs, as well as power constraints for interaction analyses in both studies, may explain this discrepancy

Predicting prescribed magnification

Aim: To determine the best method of estimating the optimum magnification needed by visually impaired patients. Methods: The magnification of low vision aids prescribed to 187 presbyopic visually impaired patients for reading newspapers or books was compared with logMAR distance and near acuity (at 25 cm) and magnification predicted by +4 D step near additions. Results: Distance letter (r = 0.58) and near word visual acuity (r = 0.67) were strongly correlated to the prescribed magnification as were predictive formulae based on these measures. Prediction using the effect of proximal magnification resulted in a similar correlation (r = 0.67) and prediction was poorer in those who did not benefit from proximal magnification. The difference between prescribed and predicted magnification was found to be unrelated to the condition causing visual impairment (F = 2.57, p = 0.08), the central visual field status (F = 0.57, p = 0.57) and patient psychology (F = 0.44, p = 0.51), but was higher in those prescribed stand magnifiers than high near additions (F = 5.99, p < 0.01). Conclusions: The magnification necessary to perform normal visual tasks can be predicted in the majority of cases using visual acuity measures, although measuring the effect of proximal magnification demonstrates the effect of stronger glasses and identifies those in whom prescribed magnification is more difficult to predict

Modulatory effects of brain-derived neurotrophic factor Val66Met polymorphism on prefrontal regions in major depressive disorder

Background: Brain derived neurotrophic factor (BDNF) Val66Met polymorphism contributes to development of depression (MDD), but it is unclear whether neural effects observed in healthy individuals are sustained in MDD Aims: To investigate BDNF Val66Met effects on key regions in MDD neurocircuitry: amygdala, anterior cingulate, middle frontal and orbitofrontal regions. Method: MRI scans were acquired in 79 MDD (mean age 49 years) and 74 healthy volunteers (HV) (mean 50 years). Effects on surface area and cortical thickness were examined with multiple comparison correction. Results: Met allele carriers showed reduced caudal middle frontal thickness in both MDD and HV. Significant interaction effects were found in the anterior cingulate and rostral middle frontal regions in which Met MDD carriers showed the greatest reduction in surface area. Conclusions: Modulatory effects of the BDNF Val66Met polymorphism on distinct subregions in the prefrontal cortex in MDD support the neurotrophin model of depression

Using genetic variants to evaluate the causal effect of cholesterol lowering on head and neck cancer risk: A Mendelian randomization study

Head and neck squamous cell carcinoma (HNSCC), which includes cancers of the oral cavity and oropharynx, is a cause of substantial global morbidity and mortality. Strategies to reduce disease burden include discovery of novel therapies and repurposing of existing drugs. Statins are commonly prescribed for lowering circulating cholesterol by inhibiting HMG-CoA reductase (HMGCR). Results from some observational studies suggest that statin use may reduce HNSCC risk. We appraised the relationship of genetically-proxied cholesterol-lowering drug targets and other circulating lipid traits with oral (OC) and oropharyngeal (OPC) cancer risk using two-sample Mendelian randomization (MR). For the primary analysis, germline genetic variants in HMGCR, NPC1L1, CETP, PCSK9 and LDLR were used to proxy the effect of low-density lipoprotein cholesterol (LDL-C) lowering therapies. In secondary analyses, variants were used to proxy circulating levels of other lipid traits in a genome-wide association study (GWAS) meta-analysis of 188,578 individuals. Both primary and secondary analyses aimed to estimate the downstream causal effect of cholesterol lowering therapies on OC and OPC risk. The second sample for MR was taken from a GWAS of 6,034 OC and OPC cases and 6,585 controls (GAME-ON). Analyses were replicated in UK Biobank, using 839 OC and OPC cases and 372,016 controls and the results of the GAME-ON and UK Biobank analyses combined in a fixed-effects meta-analysis. We found limited evidence of a causal effect of genetically-proxied LDL-C lowering using HMGCR, NPC1L1, CETP or other circulating lipid traits on either OC or OPC risk. Genetically-proxied PCSK9 inhibition equivalent to a 1 mmol/L (38.7 mg/dL) reduction in LDL-C was associated with an increased risk of OC and OPC combined (OR 1.8 95%CI 1.2, 2.8, p = 9.31 x10-05), with good concordance between GAME-ON and UK Biobank (I2 = 22%). Effects for PCSK9 appeared stronger in relation to OPC (OR 2.6 95%CI 1.4, 4.9) than OC (OR 1.4 95%CI 0.8, 2.4). LDLR variants, resulting in genetically-proxied reduction in LDL-C equivalent to a 1 mmol/L (38.7 mg/dL), reduced the risk of OC and OPC combined (OR 0.7, 95%CI 0.5, 1.0, p = 0.006). A series of pleiotropy-robust and outlier detection methods showed that pleiotropy did not bias our findings. We found limited evidence for a role of cholesterol-lowering in OC and OPC risk, suggesting previous observational results may have been confounded. There was some evidence that genetically-proxied inhibition of PCSK9 increased risk, while lipid-lowering variants in LDLR, reduced risk of combined OC and OPC. This result suggests that the mechanisms of action of PCSK9 on OC and OPC risk may be independent of its cholesterol lowering effects; however, this was not supported uniformly across all sensitivity analyses and further replication of this finding is required