41 research outputs found

    Refining Outreach to Woodland Owners in West Virginia--Preferred Topics and Assistance Methods

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    Four hundred and fourteen private forest landowners in West Virginia responded to a questionnaire assessing their forest management assistance topics and delivery methods of interest. Logistic regression was used to analyze 39 independent variables in relation to the dependent variables of wanting a specific topic of forestry assistance or not. Ownership of property for investment, cultivation of wildlife food crops, and receiving assistance from the West Virginia State Division of Forestry were recurrent significant variables characterizing landowners wanting a specific assistance topic. These results can be used to develop forestry assistance programs that achieve landowner objectives and good forest management

    Are interventions to promote healthy eating equally effective for all? Systematic review of socioeconomic inequalities in impact.

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    BACKGROUND: Interventions to promote healthy eating make a potentially powerful contribution to the primary prevention of non communicable diseases. It is not known whether healthy eating interventions are equally effective among all sections of the population, nor whether they narrow or widen the health gap between rich and poor. We undertook a systematic review of interventions to promote healthy eating to identify whether impacts differ by socioeconomic position (SEP). METHODS: We searched five bibliographic databases using a pre-piloted search strategy. Retrieved articles were screened independently by two reviewers. Healthier diets were defined as the reduced intake of salt, sugar, trans-fats, saturated fat, total fat, or total calories, or increased consumption of fruit, vegetables and wholegrain. Studies were only included if quantitative results were presented by a measure of SEP. Extracted data were categorised with a modified version of the "4Ps" marketing mix, expanded to 6 "Ps": "Price, Place, Product, Prescriptive, Promotion, and Person". RESULTS: Our search identified 31,887 articles. Following screening, 36 studies were included: 18 "Price" interventions, 6 "Place" interventions, 1 "Product" intervention, zero "Prescriptive" interventions, 4 "Promotion" interventions, and 18 "Person" interventions. "Price" interventions were most effective in groups with lower SEP, and may therefore appear likely to reduce inequalities. All interventions that combined taxes and subsidies consistently decreased inequalities. Conversely, interventions categorised as "Person" had a greater impact with increasing SEP, and may therefore appear likely to reduce inequalities. All four dietary counselling interventions appear likely to widen inequalities. We did not find any "Prescriptive" interventions and only one "Product" intervention that presented differential results and had no impact by SEP. More "Place" interventions were identified and none of these interventions were judged as likely to widen inequalities. CONCLUSIONS: Interventions categorised by a "6 Ps" framework show differential effects on healthy eating outcomes by SEP. "Upstream" interventions categorised as "Price" appeared to decrease inequalities, and "downstream" "Person" interventions, especially dietary counselling seemed to increase inequalities. However the vast majority of studies identified did not explore differential effects by SEP. Interventions aimed at improving population health should be routinely evaluated for differential socioeconomic impact

    Power, control, communities and health inequalities III: participatory spaces-an English case.

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    This article-third in a series of three-uses theoretical frameworks described in Part 1, and empirical markers reported in Part 2, to present evidence on how power dynamics shifted during the early years of a major English community empowerment initiative. We demonstrate how the capabilities disadvantaged communities require to exercise collective control over decisions/actions impacting on their lives and health (conceptualized as emancipatory power) and the exercise of power over these communities (conceptualized as limiting power) were shaped by the characteristics of participatory spaces created by and/or associated with this initiative. Two main types of participatory spaces were identified: governance and sense-making. Though all forms of emancipatory power emerged in all spaces, some were more evident in particular spaces. In governance spaces, the development and enactment of 'power to' emerged as residents made formal decisions on action, allocated resources and managed accountability. Capabilities for alliance building-power with-were more likely to emerge in these spaces, as was residents' resistance to the exercise of institutional power over them. In contrast, in sense-making spaces residents met informally and 'made sense' of local issues and their ability to influence these. These processes led to the development of power within capabilities and power to resist stigmatizing forms of productive power. The findings highlight the importance of designing community initiatives that: nurture diverse participatory spaces; attend to connectivity between spaces; and identify and act on existing power dynamics undermining capabilities for collective control in disadvantaged communities

    Correction:The Health Equity and Effectiveness of Policy Options to Reduce Dietary Salt Intake in England: Policy Forecast

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    There is information missing from funding section of this paper. The funding section should read: This article presents independent research funded by the National Institute for Health Research School for Public Health Research (NIHR SPHR) through a grant (SPHR-LIL-PH1-MCD) to the LiLaC collaboration between the University of Liverpool and Lancaster University. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health

    Enhanced axonal response of mitochondria to demyelination offers neuroprotection:implications for multiple sclerosis

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    Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises the possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show that upon demyelination mitochondria move from the neuronal cell body to the demyelinated axon, increasing axonal mitochondrial content, which we term the axonal response of mitochondria to demyelination (ARMD). However, following demyelination axons degenerate before the homeostatic ARMD reaches its peak. Enhancement of ARMD, by targeting mitochondrial biogenesis and mitochondrial transport from the cell body to axon, protects acutely demyelinated axons from degeneration. To determine the relevance of ARMD to disease state, we examined MS autopsy tissue and found a positive correlation between mitochondrial content in demyelinated dorsal column axons and cytochrome c oxidase (complex IV) deficiency in dorsal root ganglia (DRG) neuronal cell bodies. We experimentally demyelinated DRG neuron-specific complex IV deficient mice, as established disease models do not recapitulate complex IV deficiency in neurons, and found that these mice are able to demonstrate ARMD, despite the mitochondrial perturbation. Enhancement of mitochondrial dynamics in complex IV deficient neurons protects the axon upon demyelination. Consequently, increased mobilisation of mitochondria from the neuronal cell body to the axon is a novel neuroprotective strategy for the vulnerable, acutely demyelinated axon. We propose that promoting ARMD is likely to be a crucial preceding step for implementing potential regenerative strategies for demyelinating disorders.</p

    Enhanced axonal response of mitochondria to demyelination offers neuroprotection:implications for multiple sclerosis

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    Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises the possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show that upon demyelination mitochondria move from the neuronal cell body to the demyelinated axon, increasing axonal mitochondrial content, which we term the axonal response of mitochondria to demyelination (ARMD). However, following demyelination axons degenerate before the homeostatic ARMD reaches its peak. Enhancement of ARMD, by targeting mitochondrial biogenesis and mitochondrial transport from the cell body to axon, protects acutely demyelinated axons from degeneration. To determine the relevance of ARMD to disease state, we examined MS autopsy tissue and found a positive correlation between mitochondrial content in demyelinated dorsal column axons and cytochromecoxidase (complex IV) deficiency in dorsal root ganglia (DRG) neuronal cell bodies. We experimentally demyelinated DRG neuron-specific complex IV deficient mice, as established disease models do not recapitulate complex IV deficiency in neurons,and found that these mice are able to demonstrate ARMD, despite the mitochondrial perturbation.Enhancement of mitochondrial dynamics in complex IV deficient neurons protects the axon upon demyelination. Consequently, increased mobilisation of mitochondria from the neuronal cell body to the axon is a novel neuroprotective strategy for the vulnerable, acutely demyelinated axon. We propose that promoting ARMD is likely to be a crucial preceding step for implementing potential regenerative strategies for demyelinating disorders.</p

    A Prominent Role for DC-SIGN+ Dendritic Cells in Initiation and Dissemination of Measles Virus Infection in Non-Human Primates

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    Measles virus (MV) is a highly contagious virus that is transmitted by aerosols. During systemic infection, CD150+T and B lymphocytes in blood and lymphoid tissues are the main cells infected by pathogenic MV. However, it is unclear which cell types are the primary targets for MV in the lungs and how the virus reaches the lymphoid tissues. In vitro studies have shown that dendritic cell (DC) C-type lectin DC-SIGN captures MV, leading to infection of DCs as well as transmission to lymphocytes. However, evidence of DC-SIGN-mediated transmission in vivo has not been established. Here we identified DC-SIGNhiDCs as first target cells in vivo and demonstrate that macaque DC-SIGN functions as an attachment receptor for MV. Notably, DC-SIGNhicells from macaque broncho-alveolar lavage and lymph nodes transmit MV to B lymphocytes, providing in vivo support for an important role for DCs in both initiation and dissemination of MV infection

    The Health Equity and Effectiveness of Policy Options to Reduce Dietary Salt Intake in England: Policy Forecast

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    Background Public health action to reduce dietary salt intake has driven substantial reductions in coronary heart disease (CHD) over the past decade, but avoidable socio-economic differentials remain. We therefore forecast how further intervention to reduce dietary salt intake might affect the overall level and inequality of CHD mortality. Methods We considered English adults, with socio-economic circumstances (SEC) stratified by quintiles of the Index of Multiple Deprivation. We used IMPACTSEC, a validated CHD policy model, to link policy implementation to salt intake, systolic blood pressure and CHD mortality. We forecast the effects of mandatory and voluntary product reformulation, nutrition labelling and social marketing (e.g., health promotion, education). To inform our forecasts, we elicited experts’ predictions on further policy implementation up to 2020. We then modelled the effects on CHD mortality up to 2025 and simultaneously assessed the socio-economic differentials of effect. Results Mandatory reformulation might prevent or postpone 4,500 (2,900–6,100) CHD deaths in total, with the effect greater by 500 (300–700) deaths or 85% in the most deprived than in the most affluent. Further voluntary reformulation was predicted to be less effective and inequality-reducing, preventing or postponing 1,500 (200–5,000) CHD deaths in total, with the effect greater by 100 (−100–600) deaths or 49% in the most deprived than in the most affluent. Further social marketing and improvements to labelling might each prevent or postpone 400–500 CHD deaths, but minimally affect inequality. Conclusions Mandatory engagement with industry to limit salt in processed-foods appears a promising and inequality-reducing option. For other policy options, our expert-driven forecast warns that future policy implementation might reach more deprived individuals less well, limiting inequality reduction. We therefore encourage planners to prioritise equity
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