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Although inequalities in health and socioeconomic status have an important influence on childhood educational performance, the interactions between these multiple factors relating to variation in educational outcomes at micro-level is unknown, and how to evaluate the many possible interactions of these factors is not well established. This paper aims to examine multi-dimensional deprivation factors and their impact on childhood educational outcomes at micro-level, focusing on geographic areas having widely different disparity patterns, in which each area is characterised by six deprivation domains (Income, Health, Geographical Access to Services, Housing, Physical Environment, and Community Safety). Traditional health statistical studies tend to use one global model to describe the whole population for macro-analysis. In this paper, we combine linked educational and deprivation data across small areas (median population of 1500), then use a local modelling technique, the Takagi-Sugeno fuzzy system, to predict area educational outcomes at ages 7 and 11. We define two new metrics, “Micro-impact of Domain” and “Contribution of Domain”, to quantify the variations of local impacts of multidimensional factors on educational outcomes across small areas. The two metrics highlight differing priorities. Our study reveals complex multi-way interactions between the deprivation domains, which could not be provided by traditional health statistical methods based on single global model. We demonstrate that although Income has an expected central role, all domains contribute, and in some areas Health, Environment, Access to Services, Housing and Community Safety each could be the dominant factor. Thus the relative importance of health and socioeconomic factors varies considerably for different areas, depending on the levels of each of the other factors, and therefore each component of deprivation must be considered as part of a wider system. Childhood educational achievement could benefit from policies and intervention strategies that are tailored to the local geographic areas' profiles. [ABSTRACT FROM AUTHOR]

Populations may potentially respond to climate change in various ways including moving to new areas or alternatively staying where they are and adapting as conditions shift. Traditional laboratory and mesocosm experiments last days to weeks and thus only give a limited picture of thermal adaptation, whereas ocean warming occurring over decades allows the potential for selection of new strains better adapted to warmer conditions. Evidence for adaptation in natural systems is equivocal. We used a 50-year time series comprising of 117 056 samples in the NE Atlantic, to quantify the abundance and distribution of two particularly important and abundant members of the ocean plankton (copepods of the genus Calanus) that play a key trophic role for fisheries. Abundance of C. finmarchicus, a cold-water species, and C. helgolandicus, a warm-water species, were negatively and positively related to sea surface temperature ( SST) respectively. However, the abundance vs. SST relationships for neither species changed over time in a manner consistent with thermal adaptation. Accompanying the lack of evidence for thermal adaptation there has been an unabated range contraction for C. finmarchicus and range expansion for C. helgolandicus. Our evidence suggests that thermal adaptation has not mitigated the impacts of ocean warming for dramatic range changes of these key species and points to continued dramatic climate induced changes in the biology of the oceans. [ABSTRACT FROM AUTHOR]

A recent shift by the scientific and regulatory community, towards accepting the existence of non-linear dose responses for certain DNA reactive genotoxic agents, has unveiled a myriad of questions regarding their biological basis. The mechanisms responsible for `genotoxic tolerance' at low doses are wide ranging but poorly understood, yet this information is essential when analysing non-linear dose responses for hazard and risk assessment. For DNA reactive genotoxins, non-linear dose responses can arise from many diŠerent biological mechanisms, including DNA repair. Recent work from our group explored the contributory role of DNA repair to nonlinear genotoxic dose responses, in human cells exposed alkylating agents. Here we discuss the involvement of the repair enzymes methylpurine DNA-glycosylase and methyl-guanine methyl-transferase in modulating the non-linear dose responses observed in human cells exposed to ethyl methanesulfonate (EMS) and N-methyl-N-nitrosourea, respectively. We also discuss the exposure of binary mixtures, and how combinations of the dissimilar acting agents Benomyl and EMS at their no observed genotoxic eŠect levels, induce a significant increase in micronuclei. [ABSTRACT FROM AUTHOR]