377 research outputs found

    Structures and Conflicts: Ohio's Collective Bargaining Law for Public Employees

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    Wing Defects in Drosophila xenicid Mutant Clones Are Caused by C-Terminal Deletion of Additional Sex Combs (Asx)

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    Background: The coordinated action of genes that control patterning, cell fate determination, cell size, and cell adhesion is required for proper wing formation in Drosophila. Defects in any of these basic processes can lead to wing aberrations, including blisters. The xenicid mutation was originally identified in a screen designed to uncover regulators of adhesion between wing surfaces [1]. Principal Findings: Here, we demonstrate that expression of the bPS integrin or the patterning protein Engrailed are not affected in developing wing imaginal discs in xenicid mutants. Instead, expression of the homeotic protein Ultrabithorax (Ubx) is strongly increased in xenicid mutant cells. Conclusion: Our results suggest that upregulation of Ubx transforms cells from a wing blade fate to a haltere fate, and that the presence of haltere cells within the wing blade is the primary defect leading to the adult wing phenotypes observed

    Testing the neurodevelopmental, trauma and developmental risk factor models of psychosis using a naturalistic experiment

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    Background: The neurodevelopmental and trauma theories are two widely cited models of psychosis. A third – the developmental risk factor model (DRFM) – recognises the combined role of neurodevelopmental risks and trauma. Our objective was to test these theories using preterm populations as a natural experiment, given the high prevalence of neurodevelopmental deficits and exposure to trauma. Methods: Two population-based preterm birth cohorts, the Bavarian Longitudinal Study (BLS; N = 399) and EPICure Study (N = 184), were included with term-born controls. Peer victimisation in childhood was assessed by parent and child report and psychotic experiences (PE) were assessed in early adulthood. Different models of psychosis were tested using regression and mediation analyses. Results: There was support for the trauma and DRFM in the BLS. Peer victimisation increased the risk of PE for preterm and term-born participants equally [odds ratio = 4.87, 95% confidence interval (CI) 1.96–12.08]. There was an indirect effect where preterm children were more likely to be victimised, which subsequently increased risk of PE [β = 1.12 (s.e. = 0.61), 95% CI 0.11–2.48]. The results were replicated in EPICure. Conclusions: Exposure to trauma which is experienced more often by neurodevelopmental risk children rather than neurodevelopmental risk per se increases the risk of PE. The findings are consistent with the trauma model and DRFM. Interventions focused on reducing trauma may reduce the development of PE

    Deaf moths employ acoustic Müllerian mimicry against bats using wingbeat-powered tymbals

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    Abstract Emitting ultrasound upon hearing an attacking bat is an effective defence strategy used by several moth taxa. Here we reveal how Yponomeuta moths acquire sophisticated acoustic protection despite being deaf themselves and hence unable to respond to bat attacks. Instead, flying Yponomeuta produce bursts of ultrasonic clicks perpetually; a striated patch in their hind wing clicks as the beating wing rotates and bends. This wing structure is strikingly similar to the thorax tymbals with which arctiine moths produce their anti-bat sounds. And indeed, Yponomeuta sounds closely mimic such arctiine signals, revealing convergence in form and function. Because both moth taxa contain noxious compounds, we conclude they are mutual Müllerian acoustic mimics. Yponomeuta’s perpetual clicking would however also attract bat predators. In response, their click amplitude is reduced and affords acoustic protection just as far as required, matching the distance over which bat biosonar would pick up Yponomeuta echoes anyway – advanced acoustic defences for a deaf moth

    Is Long-Term Exposure to Ambient Air Pollution a Risk Factor for Parkinson’s Disease.

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    Objectives This paper links prescriptions data for the Northern Ireland population with data from the Northern Ireland Longitudinal Study and localized ambient air pollution data from 2002 onwards to estimate the association between long-term exposure to ambient air pollutant from fine particulates (PM2.5) and Parkinson’s Disease (PD). Approach Cox Proportional Hazards models are used to examine the impact of air pollution on PD, first unconditionally, and then conditioning on a rich set of observable individual, family and contextual characteristics. Long-term exposure to PM2.5 is defined as exposure averaged over the previous 5 years. Onset of PD is proxied by first receipt of a prescription for PD medication.  Estimates are presented in the form of hazard ratios for the effect of long-term PM2.5 exposure on the risk of PD onset. Results There is a non-trivial magnitude and statistically significant unconditional association between long-term exposure to ambient PM2.5 pollution and receiving a prescription for PD, with those exposed to higher levels of pollution more likely to receive a prescription for PD. This estimated association disappears (becomes insignificantly different from zero), however, when the model accounts for confounding variables at household, individual and geographical levels. Conclusions This study contributes to an emerging literature examining the association between ambient PM2.5 pollution and onset of PD. Despite finding an unconditional association, we find no evidence for an association once individual, family and contextual characteristics are controlled for, at least in the relatively low-pollution context of Northern Ireland

    Exposure to PM 2.5 and Birth Outcomes: Evidence from a Population-wide Database.

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    This paper links localised annual average ambient air pollution data to a population database of births in Northern Ireland between 2011 and 2017 to investigate the relationship between particulate matter (PM) 2.5 exposure during pregnancy and a range of birth outcomes, with a focus on birth weight. Linear regression analysis is used to estimate the effect of exposure to PM 2.5 during pregnancy on commonly studied markers of infant health (birth weight, preterm birth), less commonly studied markers such as Apgar scores, and markers of placental health which potentially represent a mechanism through which pollution might negatively affect newborns. In addition to maternal characteristics and weather conditions, detailed adjustment is made for area of residence. Moreover, comparisons of birth outcomes are drawn amongst siblings born at different times and subject to different levels of in utero exposure, permitting adjustment for mother-specific factors common to siblings. Most birth outcomes exhibit a strong unadjusted association with PM 2.5 exposure that conforms with expectations. For birth weight, the negative effect of PM 2.5 weakens slightly after adjusting for differences in maternal characteristics and weather, but weakens much further after adjusting additionally for area of residence. After adjustment, being born to mothers in the middling (6-10 micrograms per cubic metre) and highest (10-16 micrograms per cubic metre) categories of exposure is associated with a 12 gram and 32 gram reduction in mean birth weight, respectively, compared to being born into the lowest (3-6 micrograms per cubic metre) category. However, after adjusting additionally for mother-specific factors, these effects become statistically no different from zero. This holds for other outcomes, including measures of placental health. We find little evidence that exposure to PM 2.5 is related to worse infant health once we adjust as fully as possible for omitted variable bias. We conclude that the association between PM 2.5 and birth outcomes in this population at least partly reflects unmeasured characteristics of families

    Long-term Exposure to Ambient PM2.5 and Self-Reported Health: Evidence from Longitudinally-linked Census Data.

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    Objectives This paper estimates associations between long-term exposure to ambient particulate air pollution and 13 self-reported health outcomes including poor general health, chronic illness, experiencing long-running difficulties with breathing, and experiencing frequent periods of confusion or memory loss. It examines the extent to which these associations are explained by confounding factors. Approach Longitudinally-linked Census data from the Northern Ireland Longitudinal Study linked to data on annual average particulate (PM2.5) concentrations at the 1km grid-square level over the period 2002-2010, exploiting complete residential histories, are used. The paper controls for potentially confounding factors at the neighbourhood, household and individual level, including for prior health, in a multivariate regression framework. Robustness to the presence of remaining unobserved confounders is assessed in two extensions, first by assuming selection on unobservables is proportional to selection on observables, and second through inclusion of an extensive set of fixed effects in the model. Results There are strong statistical associations between long-term exposure to ambient particulate pollution and all 13 health outcomes measured by the 2011 Northern Ireland Census. Most of these estimated associations survive conditioning on an extensive set of observable controls. Of these, however, only two associations – with chronic illness and with long-running breathing difficulties, where we might expect the strongest causal effects – survive further analysis designed to elicit robustness to selection on unobservables. The estimated magnitudes of these remaining effects are non-trivial. For example, a 5 µg/m3 difference in particulate exposure averaged over 9 years has a similar magnitude effect on the probability of reporting long-running breathing difficulties as the difference between those aged in their 20s and those in their 40s. Conclusions This study provides evidence of substantial effects of long-term exposure to ambient particulates on the probabilities of experiencing chronic illness and long-running breathing difficulties. These are qualitatively robust to both observed and unobserved confounders. Associations between particulate exposure and other health outcomes in the study are shown to reflect confounders

    A new approach to high resolution, high contrast electron microscopy of macromolecular block copolymer assemblies

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    Determining the structure of macromolecular samples is vital for understanding and adapting their function. Transmission electron microscopy (TEM) is widely used to achieve this, but, owing to the weak electron scattering cross-section of carbon, TEM images of macromolecular samples are generally low contrast and low resolution. Here we implement a fast and practically simple routine to achieve high-contrast imaging of macromolecular samples using exit wave reconstruction (EWR), revealing a new level of structural detail. This is only possible using ultra-low contrast supports such as the graphene oxide (GO) used here and as such represents a novel application of these substrates. We apply EWR on GO membranes to study self-assembled block copolymer structures, distinguishing not only the general morphology or nanostructure, but also evidence for the substructure (i.e. the polymer chains) which gives insight into their formation mechanisms and functional properties

    Hand Preference Develops Across Childhood and Adolescence in Extremely Preterm Children: The EPICure Study.

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    AIM: To determine how handedness changes with age and its relation to brain injury and cognition following birth before 26 weeks of gestation. METHODS: We used data from the EPICure study of health and development following birth in the British Isles in 1995. Handedness was determined by direct observation during standardized testing at age 2.5, six, and 11 years and by self-report using the Edinburgh Handedness Inventory at 19 years. Control data from term births were included at six, 11, and 19 years. RESULTS: In extremely preterm children left handedness increased from 9% to 27% between 2.5 and 19 years, with a progressive reduction in mixed handedness from 59% to 13%. Although individual handedness scores varied over childhood, the between-group effects were consistent through 19 years, with greatest differences in females. In extremely preterm participants, neonatal brain injury was associated with lower right handedness scores at each age and left-handed participants had lower cognitive scores at 19 years after controlling for confounders, but not at other ages. CONCLUSION: Increasing hand lateralization is seen over childhood in extremely preterm survivors, but consistently more have non-right preferences at each age than controls
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