613 research outputs found

    Zirconia for protein stabilisation of wines

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    Backgrounds and Aims:  White wines are stabilised by removing the heat unstable proteins through adsorption by bentonite. Bentonite fining is not an efficient wine processing step and can also remove other wine components. Alternative absorbents are thus sought; zirconium dioxide (zirconia) is recognised as a promising candidate. The aim of this work was to assess the viability of zirconia treatments to stabilise white wines, with particular attention on process development. Methods and Results:  Effective treatment was achieved by enclosing zirconia pellets into a metallic cage submerged in the wine. With this method, the wine could be treated with the adsorbent for the time required for protein stabilisation, and then removed without further manipulation. Zirconia treatments of three unstable wines partially or fully stabilised them without detectable modifications of their physicochemical parameters and colours, apart from the removal of metals and some acids, particularly when wines were treated for long times and with high dosages of the adsorbent. A simple and inexpensive zirconia regeneration method was also developed. Conclusions:  The zirconia application to wine was very effective in removing proteins, and the proposed regeneration procedure could facilitate the uptake and development of zirconia-based solutions for the wine industry. Significance of the Study:  This study confirmed the effectiveness of zirconia in removing wine proteins and demonstrated that the proposed method of application has the potential to become a viable alternative to bentonite

    Battleground Texas: Gendered Media Framing of the 2014 Texas Gubernatorial Race

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    Feminist political theory is a sprawling theoretical field that intertwines sociological and philosophical perspectives and applies them to the study of campaigns, policy, voting, and the general structure of what Americans call politics. In Western democratic republics, the concept of participation has been hotly debated, specifically with regard to voting. Applying the critical lens of an intersectional feminist perspective introduces questions about the participation of different genders, races, classes, and cultural groups in political action, voting, and running for office. Before equal representation can be attained (if that is, indeed, desirable), it is important to understand how our politics are constructed. Feminism in the field of political communication is almost as old as the discipline itself. In this paper, the researchers explore a specific mixed-gender race in Texas, using the underlying assumptions of feminist political theory as a lens to examine how the race was rhetorically constructed in the media. By mixing methodologies and multiple analyses, both content-related and critical, these stories of mixed-gender campaigns may illuminate how gender is constructed in political races by the media and elucidate the potential constraints imposed on candidates seeking office

    The impact of behavioural screening on intervention outcomes in a randomised, controlled multiple behaviour intervention trial

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    Background: With an increasing research focus on multiple health behaviour change interventions, a methodological issue requiring further investigation is whether or not to employ pre-trial behavioural screening to exclude participants who are achieving a pre-specified level of one or more behaviours. Behavioural screening can be used to direct limited resources to participants most in need of a behaviour change intervention; but may reduce the representativeness of the sample and limit comparability with trials that do not employ pre-trial behavioural screening. Furthermore, the impact of this type of screening on intervention participation and intervention effects is unknown

    Apoptosis signal-regulating kinase-1 promotes inflammasome priming in macrophages

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    © 2019 the American Physiological Society. previously showed that mice deficient in apo-ptosis signal-regulating kinase-1 (ASK1) were partially protected against ventilator-induced lung injury. Because ASK1 can promote both cell death and inflammation, we hypothesized that ASK1 activation regulates inflammasome-mediated inflammation. Mice deficient in ASK1 expression (ASK1 +/+ ) exhibited significantly less inflammation and lung injury (as measured by neutrophil infiltration, IL-6, and IL-1β) in response to treatment with inhaled lipopolysaccharide (LPS) compared with wild-type (WT) mice. To determine whether this proinflammatory response was mediated by ASK1, we investigated inflammasome-mediated responses to LPS in primary macrophages and bone marrow-derived macrophages (BMDMs) from WT and ASK1 +/+ mice, as well as the mouse alveolar macrophage cell line MH-S. Cells were treated with LPS alone for priming or LPS followed by ATP for activation. When macrophages were stimulated with LPS followed by ATP to activate the inflammasome, we found a significant increase in secreted IL-1β from WT cells compared with ASK1-deficient cells. LPS priming stimulated an increase in NOD-like receptor 3 (NLRP3) and pro-IL-1β in WT BMDMs, but expression of NLRP3 was significantly decreased in ASK1 +/+ BMDMs. Subsequent ATP treatment stimulated an increase in cleaved caspase-1 and IL-1β in WT BMDMs compared with ASK1 +/+ BMDMs. Similarly, treatment of MH-S cells with LPS + ATP caused an increase in both cleaved caspase-1 and IL-1β that was diminished by the ASK-1 inhibitor NQDI1. These results demonstrate, for the first time, that ASK1 promotes inflammasome priming

    The World Health Organization’s Health Promoting Schools framework: a Cochrane systematic review and meta-analysis

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    BACKGROUND: Healthy children achieve better educational outcomes which, in turn, are associated with improved health later in life. The World Health Organization's Health Promoting Schools (HPS) framework is a holistic approach to promoting health and educational attainment in school. The effectiveness of this approach has not yet been rigorously reviewed. METHODS: We searched 20 health, education and social science databases, and trials registries and relevant websites in 2011 and 2013. We included cluster randomised controlled trials. Participants were children and young people aged four to 18 years attending schools/colleges. HPS interventions had to include the following three elements: input into the curriculum; changes to the school's ethos or environment; and engagement with families and/or local communities. Two reviewers identified relevant trials, extracted data and assessed risk of bias. We grouped studies according to the health topic(s) targeted. Where data permitted, we performed random-effects meta-analyses. RESULTS: We identified 67 eligible trials tackling a range of health issues. Few studies included any academic/attendance outcomes. We found positive average intervention effects for: body mass index (BMI), physical activity, physical fitness, fruit and vegetable intake, tobacco use, and being bullied. Intervention effects were generally small. On average across studies, we found little evidence of effectiveness for zBMI (BMI, standardized for age and gender), and no evidence for fat intake, alcohol use, drug use, mental health, violence and bullying others. It was not possible to meta-analyse data on other health outcomes due to lack of data. Methodological limitations were identified including reliance on self-reported data, lack of long-term follow-up, and high attrition rates. CONCLUSION: This Cochrane review has found the WHO HPS framework is effective at improving some aspects of student health. The effects are small but potentially important at a population level

    An exploratory cluster randomised controlled trial of knowledge translation strategies to support evidence-informed decision-making in local governments (The KT4LG study)

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    Background: Childhood overweight and obesity is the most prevalent and, arguably, politically complex child health problem internationally. Governments, communities and industry have important roles to play, and are increasingly expected to deliver an evidence-informed system-wide prevention program. However, efforts are impeded by a lack of organisational access to and use of research evidence. This study aims to identify feasible, acceptable and ideally, effective knowledge translation (KT) strategies to increase evidence-informed decision making in local governments, within the context of childhood obesity prevention as a national policy priority.Methods/Design: This paper describes the methods for KT4LG, a cluster randomised controlled trial which is exploratory in nature, given the limited evidence base and methodological advances. KT4LG aims to examine a program of KT strategies to increase the use of research evidence in informing public health decisions in local governments. KT4LG will also assess the feasibility and acceptability of the intervention. The intervention program comprises a facilitated program of evidence awareness, access to tailored research evidence, critical appraisal skills development, networking and evidence summaries and will be compared to provision of evidence summaries alone in the control program. 28 local governments were randomised to intervention or control, using computer generated numbers, stratified by budget tertile (high, medium or low). Questionnaires will be used to measure impact, costs, and outcomes, and key informant interviews will be used to examine processes, feasibility, and experiences. Policy tracer studies will be included to examine impact of intervention on policies within relevant government policy documents.Discussion: Knowledge translation intervention studies with a focus on public health and prevention are very few in number. Thus, this study will provide essential data on the experience of program implementation and evaluation of a system-integrated intervention program employed within the local government public health context. Standardised programs of system, organisational and individual KT strategies have not been described or rigorously evaluated. As such, the findings will make a significant contribution to understanding whether a facilitated program of KT strategies hold promise for facilitating evidence-informed public health decision making within complex multisectoral government organisations.<br /

    The Influences of Reproductive Status and Acute Stress on the Levels of Phosphorylated Mu Opioid Receptor Immunoreactivity in Rat Hippocampus

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    Opioids play a critical role in hippocampally dependent behavior and plasticity. In the hippocampal formation, mu opioid receptors (MOR) are prominent in parvalbumin (PARV) containing interneurons. Previously we found that gonadal hormones modulate the trafficking of MORs in PARV interneurons. Although sex differences in response to stress are well documented, the point at which opioids, sex, and stress interact to influence hippocampal function remains elusive. Thus, we used quantitative immunocytochemistry in combination with light and electron microscopy for the phosphorylated MOR (pMOR) at the SER375 carboxy-terminal residue in male and female rats to assess these interactions. In both sexes, pMOR-immunoreactivity (ir) was prominent in axons and terminals and in a few neuronal somata and dendrites, some of which contained PARV in the mossy fiber pathway region of the dentate gyrus (DG) hilus and CA3 stratum lucidum. In unstressed rats, the levels of pMOR-ir in the DG or CA3 were not affected by sex or estrous cycle stage. However, immediately following 30 min of acute immobilization stress (AIS), males had higher levels of pMOR-ir whereas females at proestrus and estrus (high estrogen stages) had lower levels of pMOR-ir within the DG. In contrast, the number and types of neuronal profiles with pMOR-ir were not altered by AIS in either males or proestrus females. These data demonstrate that although gonadal steroids do not affect pMOR levels at resting conditions, they are differentially activated both pre and postsynaptic MORs following stress. These interactions may contribute to the reported sex differences in hippocampally dependent behaviors in stressed animals

    Mortality among Workers Exposed to Polychlorinated Biphenyls (PCBs) in an Electrical Capacitor Manufacturing Plant in Indiana: An Update

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    An Indiana capacitor-manufacturing cohort (n = 3,569) was exposed to polychlorinated biphenyls (PCBs) from 1957 to 1977. The original study of mortality through 1984 found excess melanoma and brain cancer; other studies of PCB-exposed individuals have found excess non-Hodgkin lymphoma and rectal, liver, biliary tract, and gallbladder cancer. Mortality was updated through 1998. Analyses have included standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) using rates for Indiana and the United States, standardized rate ratios (SRRs), and Poisson regression rate ratios (RRs). Estimated cumulative exposure calculations used a new job–exposure matrix. Mortality overall was reduced (547 deaths; SMR, 0.81; 95% CI, 0.7–0.9). Non-Hodgkin lymphoma mortality was elevated (9 deaths; SMR, 1.23; 95% CI, 0.6–2.3). Melanoma remained in excess (9 deaths; SMR, 2.43; 95% CI, 1.1–4.6), especially in the lowest tertile of estimated cumulative exposure (5 deaths; SMR, 3.72; 95% CI, 1.2–8.7). Seven of the 12 brain cancer deaths (SMR, 1.91; 95% CI, 1.0–3.3) occurred after the original study. Brain cancer mortality increased with exposure (in the highest tertile, 5 deaths; SMR, 2.71; 95% CI, 0.9–6.3); the SRR dose–response trend was significant (p = 0.016). Among those working ≥90 days, both melanoma (8 deaths; SMR, 2.66; 95% CI, 1.1–5.2) and brain cancer (11 deaths; SMR, 2.12; 95% CI, 1.1–3.8) were elevated, especially for women: melanoma, 3 deaths (SMR, 5.99; 95% CI, 1.2–17.5); brain cancer, 3 deaths (SMR, 2.87; 95% CI, 0.6–8.4). These findings of excess melanoma and brain cancer mortality confirm results of the original study. Melanoma mortality was not associated with estimated cumulative exposure. Brain cancer mortality did not demonstrate a clear dose–response relationship with estimated cumulative exposure

    Deficiency of the two-pore-domain potassium channel TREK-1 promotes hyperoxia-induced lung injury

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    Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Objectives: We previously reported the expression of the twoporedomain K+ channel TREK-1 in lung epithelial cells and proposed a role for this channel in the regulation of alveolar epithelial cytokine secretion. In this study, we focused on investigating the role of TREK-1 in vivo in the development of hyperoxia-induced lung injury. Design: Laboratory animal experiments. Setting: University research laboratory. Subjects: Wild-type and TREK-1-deficient mice. Interventions: Mice were anesthetized and exposed to 1) room air, no mechanical ventilation, 2) 95% hyperoxia for 24 hours, and 3) 95% hyperoxia for 24 hours followed by mechanical ventilation for 4 hours. Measurements and Main Results: Hyperoxia exposure accentuated lung injury in TREK-1-deficient mice but not controls, resulting in increase in lung injury scores, bronchoalveolar lavage fluid cell numbers, and cellular apoptosis and a decrease in quasi-static lung compliance. Exposure to a combination of hyperoxia and injurious mechanical ventilation resulted in further morphological lung damage and increased lung injury scores and bronchoalveolar lavage fluid cell numbers in control but not TREK-1-deficient mice. At baseline and after hyperoxia exposure, bronchoalveolar lavage cytokine levels were unchanged in TREK-1-deficient mice compared with controls. Exposure to hyperoxia and mechanical ventilation resulted in an increase in bronchoalveolar lavage interleukin-6, monocyte chemotactic protein-1, and tumor necrosis factor-á levels in both mouse types, but the increase in interleukin-6 and monocyte chemotactic protein-1 levels was less prominent in TREK-1-deficient mice than in controls. Lung tissue macrophage inflammatory protein-2, keratinocytederived cytokine, and interleukin-1β gene expression was not altered by hyperoxia in TREK-1-deficient mice compared with controls. Furthermore, we show for the first time TREK-1 expression on alveolar macrophages and unimpaired tumor necrosis factor-á secretion from TREK-1-deficient macrophages. Conclusions: TREK-1 deficiency resulted in increased sensitivity of lungs to hyperoxia, but this effect is less prominent if overwhelming injury is induced by the combination of hyperoxia and injurious mechanical ventilation. TREK-1 may constitute a new potential target for the development of novel treatment strategies against hyperoxiainduced lung injury
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