108 research outputs found

    ā€œPower, control, strainā€: Lay perceptions of health inequalities across England\u27s ā€˜North South divideā€™

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    \ua9 2024People in the North of England live shorter, less healthy lives than those in the South. Despite the significance of this ā€˜North South health divideā€™, regional health inequalities in England are under-researched qualitatively. Existing literature on geographical inequalities in health is largely confined to the neighbourhood level, is quantitative, and consists of very little lay knowledge. The current study is the first to examine lay perspectives of health inequalities on a regional level: exploring how people living in two urban areas of the North and South of England experience and perceive the North South health divide ā€“ including its causes and solutions. Using three focus group discussions with a total of 34 participants, and conducting participatory analysis, we identified three key themes: ā€˜inequalities of powerā€™, ā€˜lack of control over lived environmentā€™ and ā€˜communities under strainā€™. Findings align with existing research on lay perspectives of health inequalities at the neighbourhood level ā€“ identifying a network of material-structural and psychosocial factors. Participants across both regions discussed political and economic structures as central to understanding regional health inequalities, supporting calls to adopt a political economy approach in understanding health and place. Deindustrialisation, unemployment, loss of community facilities, and disengagement from politics were more present in Northern narratives than Southern. Findings add important ā€˜social meaningā€™ to emerging research on the North South health divide, reinforcing the urgency of public health professionals\u27 recommendations for fair redistribution of power, wealth and resources to reduce regional health inequalities. In the context of government policy which diverges from public health evidence, this study sparks questions of how health inequalities research can intersect with wider social and political movements organising for systemic change

    Community empowerment and mental wellbeing: longitudinal findings from a survey of people actively involved in the big local place-based initiative in England

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    Background: Community empowerment initiatives are receiving increased interest as ways of improving health and reducing health inequalities. Purpose: Longitudinally examine associations between collective control, social-cohesion and mental wellbeing amongst participants in the Big Local community empowerment initiative across 150 disadvantaged areas of England. Methods: As part of the independent Communities in Control study, we analysed nested cohort survey data on mental wellbeing (Short Warwick Edinburgh Mental Wellbeing Scaleā€”SWEMWBS) and perceptions of collective control and social-cohesion. Data were obtained in 2016, 2018 and 2020 for 217 residents involved in the 150 Big Local areas in England. Adjusted linear mixed effect models were utilized to examine changes in SWEMWBS over the three waves. Subgroup analysis by gender and educational level was conducted. Results: There was a significant 1.46 (0.14, 2.77) unit increase in mental wellbeing score at wave 2 (2018) but not in wave 3 (2020) (0.06 [āˆ’1.41, 1.53]). Across all waves, collective control was associated with a significantly higher mental wellbeing score (3.36 [1.51, 5.21]) as was social cohesion (1.09 [0.19, 2.00]). Higher educated participants (1.99 [0.14, 3.84]) and men (2.41 [0.55, 4.28]) experienced significant increases in mental wellbeing in 2018, but lower educated participants and women did not. Conclusion: Collective control and social cohesion are associated with better mental wellbeing amongst residents engaged with the Big Local initiative. These health benefits were greater amongst men and participants from higher educational backgrounds. This suggests that additional care must be taken in future interventions to ensure that benefits are distributed equally

    Long-term perspectives on terrestrial and aquatic carbon cycling from palaeolimnology

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    Lakes are active processors and collectors of carbon (C) and thus recognized as quantitatively important within the terrestrial C cycle. Better integration of palaeolimnology (lake sediment core analyses) with limnological C budgeting approaches has the potential to enhance understanding of lacustrine C processing and sequestration. Palaeolimnology simultaneously assimilates materials from across lake habitats, terrestrial watersheds, and airsheds to provide a uniquely broad overview of the terrestrial-atmospheric-aquatic linkages across different spatial scales. The examination of past changes over decadalā€“millennial timescales via palaeolimnology can inform understanding and prediction of future changes in C cycling. With a particular, but not exclusive, focus on northern latitudes we examine the methodological approaches of palaeolimnology, focusing on how relatively standard and well-tested techniques might be applied to address questions of relevance to the C cycle. We consider how palaeolimnology, limnology, and sedimentation studies might be linked to provide more quantitative and holistic estimates of lake C cycling and budgets. Finally, we use palaeolimnological examples to consider how changes such as terrestrial vegetation shifts, permafrost thaw, the formation of new lakes and reservoirs, hydrological modification of inorganic C processing, land use change, soil erosion and disruption to global nitrogen and phosphorus cycles might influence lake C cycling

    Regional variability in the atmospheric nitrogen deposition signal and its transfer to the sediment record in Greenland lakes

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    Disruption of the nitrogen cycle is a major component of global environmental change. Ī“15N in lake sediments is increasingly used as a measure of reactive nitrogen input but problematically, the characteristic depleted Ī“15N signal is not recorded at all sites. We used a regionally replicated sampling strategy along a precipitation and N-deposition gradient in SW Greenland to assess the factors determining the strength of Ī“15N signal in lake sediment cores. Analyses of snowpack N and Ī“15N-NO3 and water chemistry were coupled with bulk sediment Ī“15N. Study sites cover a gradient of snowpack Ī“15N (ice sheet: āˆ’6ā€°; coast āˆ’10ā€°), atmospheric N deposition (ice sheet margin: āˆ¼ 0.2 kg haāˆ’1 yrāˆ’1; coast: 0.4 kg haāˆ’1 yrāˆ’1) and limnology. Three 210Pb-dated sediment cores from coastal lakes showed a decline in Ī“15N of ca.āˆ’1ā€° from āˆ¼ 1860, reflecting the strongly depleted Ī“15N of snowpack N, lower in-lake total N (TN) concentration (āˆ¼ 300 Ī¼g N Lāˆ’1) and a higher TN-load. Coastal lakes have 3.7ā€“7.1Ɨ more snowpack input of nitrate than inland sites, while for total deposition the values are 1.7ā€“3.6Ɨ greater for lake and whole catchment deposition. At inland sites and lakes close to the ice-sheet margin, a lower atmospheric N deposition rate and larger in-lake TN pool resulted in greater reliance on N-fixation and recycling (mean sediment Ī“15N is 0.5ā€“2.5ā€° in most inland lakes; nā€‰=ā€‰6). The primary control of the transfer of the atmospheric Ī“15N deposition signal to lake sediments is the magnitude of external N inputs relative to the in-lake N-pool

    Dissolution dominating calcification process in polar pteropods close to the point of aragonite undersaturation

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    Thecosome pteropods are abundant upper-ocean zooplankton that build aragonite shells. Ocean acidification results in the lowering of aragonite saturation levels in the surface layers, and several incubation studies have shown that rates of calcification in these organisms decrease as a result. This study provides a weight-specific net calcification rate function for thecosome pteropods that includes both rates of dissolution and calcification over a range of plausible future aragonite saturation states (Omega_Ar). We measured gross dissolution in the pteropod Limacina helicina antarctica in the Scotia Sea (Southern Ocean) by incubating living specimens across a range of aragonite saturation states for a maximum of 14 days. Specimens started dissolving almost immediately upon exposure to undersaturated conditions (Omega_Ar,0.8), losing 1.4% of shell mass per day. The observed rate of gross dissolution was different from that predicted by rate law kinetics of aragonite dissolution, in being higher at Var levels slightly above 1 and lower at Omega_Ar levels of between 1 and 0.8. This indicates that shell mass is affected by even transitional levels of saturation, but there is, nevertheless, some partial means of protection for shells when in undersaturated conditions. A function for gross dissolution against Var derived from the present observations was compared to a function for gross calcification derived by a different study, and showed that dissolution became the dominating process even at Omega_Ar levels close to 1, with net shell growth ceasing at an Omega_Ar of 1.03. Gross dissolution increasingly dominated net change in shell mass as saturation levels decreased below 1. As well as influencing their viability, such dissolution of pteropod shells in the surface layers will result in slower sinking velocities and decreased carbon and carbonate fluxes to the deep ocean

    PDGF-RĪ± gene expression predicts proliferation, but PDGF-A suppresses transdifferentiation of neonatal mouse lung myofibroblasts

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    <p>Abstract</p> <p>Background</p> <p>Platelet-derived growth factor A (PDGF-A) signals solely through PDGF-RĪ±, and is required for fibroblast proliferation and transdifferentiation (fibroblast to myofibroblast conversion) during alveolar development, because <it>pdgfa</it>-null mice lack both myofibroblasts and alveoli. However, these PDGF-A-mediated mechanisms remain incompletely defined. At postnatal days 4 and 12 (P4 and P12), using mouse lung fibroblasts, we examined (a) how PDGF-RĪ± correlates with ki67 (proliferation marker) or alpha-smooth muscle actin (Ī±SMA, myofibroblast marker) expression, and (b) whether PDGF-A directly affects Ī±SMA or modifies stimulation by transforming growth factor beta (TGFĪ²).</p> <p>Methods</p> <p>Using flow cytometry we examined PDGF-RĪ±, Ī±SMA and Ki67 in mice which express green fluorescent protein (GFP) as a marker for PDGF-RĪ± expression. Using real-time RT-PCR we quantified Ī±SMA mRNA in cultured Mlg neonatal mouse lung fibroblasts after treatment with PDGF-A, and/or TGFĪ².</p> <p>Results</p> <p>The intensity of GFP-fluorescence enabled us to distinguish three groups of fibroblasts which exhibited absent, lower, or higher levels of PDGF-RĪ±. At P4, more of the higher than lower PDGF-RĪ± + fibroblasts contained Ki67 (Ki67+), and Ki67+ fibroblasts predominated in the Ī±SMA + but not the Ī±SMA- population. By P12, Ki67+ fibroblasts comprised a minority in both the PDGF-RĪ± + and Ī±SMA+ populations. At P4, most Ki67+ fibroblasts were PDGF-RĪ± + and Ī±SMA- whereas at P12, most Ki67+ fibroblasts were PDGF-RĪ±- and Ī±SMA-. More of the PDGF-RĪ± + than - fibroblasts contained Ī±SMA at both P4 and P12. In the lung, proximate Ī±SMA was more abundant around nuclei in cells expressing high than low levels of PDGF-RĪ± at both P4 and P12. Nuclear SMAD 2/3 declined from P4 to P12 in PDGF-RĪ±-, but not in PDGF-RĪ± + cells. In Mlg fibroblasts, Ī±SMA mRNA increased after exposure to TGFĪ², but declined after treatment with PDGF-A.</p> <p>Conclusion</p> <p>During both septal eruption (P4) and elongation (P12), alveolar PDGF-RĪ± may enhance the propensity of fibroblasts to transdifferentiate rather than directly stimulate Ī±SMA, which preferentially localizes to non-proliferating fibroblasts. In accordance, PDGF-RĪ± more dominantly influences fibroblast proliferation at P4 than at P12. In the lung, TGFĪ² may overshadow the antagonistic effects of PDGF-A/PDGF-RĪ± signaling, enhancing Ī±SMA-abundance in PDGF-RĪ±-expressing fibroblasts.</p

    Engendering harm: a critique of sex selection for 'family balancing'

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    The most benign rationale for sex-selection is deemed to be ā€œfamily balancing.ā€ On this view, provided the sex-distribution of an existing offspring group is ā€œunbalanced,ā€ one may legitimately use reproductive technologies to select the sex of the next child. I present four novel concerns with granting ā€œfamily balancingā€ as a justification for sex-selection: (a) families or family subsets should not be subject to medicalization; (b) sex selection for ā€œfamily balancingā€ entrenches heteronormativity, inflicting harm in at least three specific ways; (c) the logic of affirmative action is appropriated; (d) the moral mandate of reproductive autonomy is misused. I conclude that the harms caused by ā€œfamily balancingā€ are sufficiently substantive to over-ride any claim arising from a supposed right to sex selection as an instantiation of procreative autonomy

    Large Proteins Have a Great Tendency to Aggregate but a Low Propensity to Form Amyloid Fibrils

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    The assembly of soluble proteins into ordered fibrillar aggregates with cross-Ī² structure is an essential event of many human diseases. The polypeptides undergoing aggregation are generally small in size. To explore if the small size is a primary determinant for the formation of amyloids under pathological conditions we have created two databases of proteins, forming amyloid-related and non-amyloid deposits in human diseases, respectively. The size distributions of the two protein populations are well separated, with the systems forming non-amyloid deposits appearing significantly larger. We have then investigated the propensity of the 486-residue hexokinase-B from Saccharomyces cerevisiae (YHKB) to form amyloid-like fibrils in vitro. This size is intermediate between the size distributions of amyloid and non-amyloid forming proteins. Aggregation was induced under conditions known to be most effective for amyloid formation by normally globular proteins: (i) low pH with salts, (ii) pH 5.5 with trifluoroethanol. In both situations YHKB aggregated very rapidly into species with significant Ī²-sheet structure, as detected using circular dichroism and X-ray diffraction, but a weak Thioflavin T and Congo red binding. Moreover, atomic force microscopy indicated a morphology distinct from typical amyloid fibrils. Both types of aggregates were cytotoxic to human neuroblastoma cells, as indicated by the MTT assay. This analysis indicates that large proteins have a high tendency to form toxic aggregates, but low propensity to form regular amyloid in vivo and that such a behavior is intrinsically determined by the size of the protein, as suggested by the in vitro analysis of our sample protein

    Identification of modifiable factors associated with owner-reported equine laminitis in Britain using a web-based cohort study approach

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    Equine laminitis is a complex disease that manifests as pain and lameness in the feet, often with debilitating consequences. There is a paucity of data that accounts for the multifactorial nature of laminitis and considers time-varying covariates that may be associated with disease development; particularly those that are modifiable and present potential interventions. A previous case-control study identified a number of novel, modifiable factors associated with laminitis which warranted further investigation and corroboration. The aim of this study was to identify factors associated with equine laminitis in horses/ponies in Great Britain (GB) using a prospective, web-based cohort study design, with particular interest in evaluating modifiable factors previously identified in the case-control study
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