4,347 research outputs found

    The Economic Roots of Anti-immigrant Prejudice in the Global South: Evidence from South Africa

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    Most research in developed countries on prejudice toward foreign-born minorities suggests that cultural rather than economic threat motivates xenophobia. Prior studies leave unanswered questions about the origins of anti-immigrant prejudice in developing countries, where one-third of worldwide immigration occurs. Alternatively, developing-country research simply assumes that economic threat drives prejudice in the global South but has not presented credible empirical evidence. In this study, we seek to reliably measure anti-immigrant prejudice and examine possible determinants of prejudice and prejudice-based voting behavior. Through a list experiment conducted on a random sample of South Africans (N = 1,088), we investigate the predictive power of economic threat theory in explaining prejudice toward immigrants in South Africa. The results show that significant prejudice toward immigrants exists among South Africans and that such prejudice is higher among the unemployed, but these sentiments do not seem to influence vote choice. The evidence suggests that the determinants of anti-immigrant sentiments due to South-South migration are distinct from South-North migration

    Opioid-related deaths during hospital admissions or shortly after discharge in the United Kingdom: A thematic framework analysis of coroner reports

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    BACKGROUND: People who use heroin and other illicit opioids are at high risk of fatal overdose in the days after hospital discharge, but the reasons for this risk have not been studied. METHODS: We used the National Programme on Substance Abuse Deaths, a database of coroner reports for deaths following psychoactive drug use in England, Wales, and Northern Ireland. We selected reports where the death occurred between 2010 and 2021, an opioid was detected in toxicology testing, the death was related to nonmedical opioid use, and death was either during an acute medical or psychiatric hospital admission or within 14 days after discharge. We used thematic framework analysis of factors that may contribute to the risk of death during hospital admission or after discharge. RESULTS: We identified 121 coroners’ reports; 42 where a patient died after using drugs during hospital admission, and 79 where death occurred shortly after discharge. The median age at death was 40 (IQR 34–46); 88 (73%) were male; and sedatives additional to opioids were detected at postmortem in 88 cases (73%), most commonly benzodiazepines. In thematic framework analysis, we categorised potential causes of fatal opioid overdose into three areas: (a) hospital policies and actions. Zero-tolerance policies mean that patients conceal drug use and use drugs in unsafe places such as locked bathrooms. Patients may be discharged to locations such as temporary hostels or the street while recovering. Some patients bring their own medicines or illicit opioids due to expectations of low-quality care, including undertreated withdrawal or pain; (b) high-risk use of sedatives. People may increase sedative use to manage symptoms of acute illness or a mental health crisis, and some may lose tolerance to opioids during a hospital admission; (c) declining health. Physical health and mobility problems posed barriers to post-discharge treatment for substance use, and some patients had sudden deteriorations in health that may have contributed to respiratory depression. CONCLUSION: Hospital admissions are associated with acute health crises that increase the risk of fatal overdose for patients who use illicit opioids. Hospitals need guidance to help them care for this patient group, particularly in relation to withdrawal management, harm reduction interventions such as take-home naloxone, discharge planning including continuation of opioid agonist therapy during recovery, management of poly-sedative use, and access to palliative care

    Technology versus tradition: a non-inferiority trial comparing video to face-to-face consultations with a physiotherapist for people with knee osteoarthritis. Protocol for the PEAK randomised controlled trial.

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    BACKGROUND: Knee osteoarthritis (OA) is a global problem that causes significant pain and physical dysfunction, substantially impacting on quality of life and imposing enormous cost to the healthcare system. Exercise is pivotal to OA management, yet uptake by people with knee OA is inadequate. Limited access to appropriately skilled health professionals, such as physiotherapists, for prescription of an exercise program and support with exercise is a major barrier to optimal care. Internet-enabled video consultations permit widespread reach. However, services offering video consultations with physiotherapists for musculoskeletal conditions are scant in Australia where there is typically no Government or private health insurer funding for such services. The paucity of robust evidence demonstrating video consultations with physiotherapists are clinically effective, safe and cost-effective for knee OA is hampering implementation of, and willingness of healthcare policymakers to pay for, these services. METHODS: This is an assessor- and participant-blinded, two-arm, pragmatic, comparative effectiveness non-inferiority randomised controlled trial (RCT) conducted in Australia. We are recruiting 394 people from the community with chronic knee pain consistent with a clinical diagnosis of knee OA. Participants are randomly allocated to receive physiotherapy care via i) video-conferencing or; ii) face-to-face consultations. Participants are provided five consultations (30-45 min each) with a physiotherapist over 3 months for prescription of a home-based strengthening exercise program (to be conducted independently at home) and physical activity plan, as well as OA education. Participants in both groups are provided with educational booklets and simple exercise equipment via post. The co-primary outcomes are change in self-reported i) knee pain on walking; and ii) physical function, with a primary end-point of 3 months and a secondary end-point of 9 months. Secondary outcomes include changes in other clinical outcomes (health-related quality of life; therapeutic relationship; global ratings of change; satisfaction with care; self-efficacy; physical activity levels), time and financial costs of attending consultations, healthcare usage and convenience. Non-inferiority will be assessed using the per-protocol dataset. DISCUSSION: Findings will determine if video consultations with physiotherapists are non-inferior to traditional face-to-face consultations for management of people with knee OA. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry, ACTRN12619001240134. http://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=377672&isReview=true

    A systematic review and meta-analysis of the relationship between flow states and performance

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    This is the final version. Available on open access from Routledge via the DOI in this recordData availability: All relevant data and code is available online from https://osf.io/3hfcu/Flow is an optimal experience that has received particular interest within sport because of a possible relationship with enhanced athletic performances. Yet, the strength and direction of the putative flow–performance relationship remain unclear. Consequently, a PRISMA guided systematic review was conducted in May 2020 to examine the empirical evidence for a flow–performance relationship, to examine potential mechanisms, and to assess the quality of current evidence. Peer-reviewed articles that examined the relationship between flow and performance in sport or computer gaming tasks were searched for using five online databases. The results were collated into a narrative synthesis and a meta-analysis. Twenty articles met the inclusion criteria, featuring 22 studies that were appropriate for meta-analysis. The overall quality of the studies was fairly good, with a mean quality assessment score of 76.5% (SD = 9.7). The pooled effect size (r = 0.31, 95% CI [0.24; 0.38]) indicated that across a range of sport and gaming tasks there was a medium-sized flow–performance relationship. However, current evidence is unable to determine the causal direction of this relationship or the mechanisms that mediate it. A number of conceptual and methodological challenges facing the study of flow are discussed and recommendations for future work are outlined.Royal Academy of Engineering (RAE

    Effect of Cyclooxygenase(COX)-1 and COX-2 inhibition on furosemide-induced renal responses and isoform immunolocalization in the healthy cat kidney

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    BACKGROUND: The role of cyclooxygenase(COX)-1 and COX-2 in the saluretic and renin-angiotensin responses to loop diuretics in the cat is unknown. We propose in vivo characterisation of isoform roles in a furosemide model by administering non-steroidal anti-inflammatory drugs (NSAIDs) with differing selectivity profiles: robenacoxib (COX-2 selective) and ketoprofen (COX-1 selective). RESULTS: In this four period crossover study, we compared the effect of four treatments: placebo, robenacoxib once or twice daily and ketoprofen once daily concomitantly with furosemide in seven healthy cats. For each period, urine and blood samples were collected at baseline and within 48 h of treatment starting. Plasma renin activity (PRA), plasma and urinary aldosterone concentrations, glomerular filtration rate (GFR) and 24 h urinary volumes, electrolytes and eicosanoids (PGE(2), 6-keto-PGF1(α,) TxB(2)), renal injury biomarker excretions [N-acetyl-beta-D-glucosaminidase (NAG) and Gamma-Glutamyltransferase] were measured. Urine volume (24 h) and urinary sodium, chloride and calcium excretions increased from baseline with all treatments. Plasma creatinine increased with all treatments except placebo, whereas GFR was significantly decreased from baseline only with ketoprofen. PRA increased significantly with placebo and once daily robenacoxib and the increase was significantly higher with placebo compared to ketoprofen (10.5 ± 4.4 vs 4.9 ± 5.0 ng ml(−1) h(−1)). Urinary aldosterone excretion increased with all treatments but this increase was inhibited by 75 % with ketoprofen and 65 % with once daily robenacoxib compared to placebo. Urinary PGE(2) excretion decreased with all treatments and excretion was significantly lower with ketoprofen compared to placebo. Urinary TxB(2) excretion was significantly increased from baseline only with placebo. NAG increased from baseline with all treatments. Immunohistochemistry on post-mortem renal specimens, obtained from a different group of cats that died naturally of non-renal causes, suggested constitutive COX-1 and COX-2 co-localization in many renal structures including the macula densa (MD). CONCLUSIONS: These data suggest that both COX-1 and COX-2 could generate the signal from the MD to the renin secreting cells in cats exposed to furosemide. Co-localization of COX isoenzymes in MD cells supports the functional data reported here. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12917-015-0598-z) contains supplementary material, which is available to authorized users

    After the Ice Age: The Impact of Post-Glacial Dispersal on the Phylogeography of a Small Mammal, Muscardinus avellanarius

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    We used genetic tools to assess phylogeographic structure of the common dormouse (Muscardinus avellenarius) since the end of the last glacial maximum, to identify post-glacial dispersal routes and to describe population units for conservation. Comparative analysis of mitochondrial genes (Cytochrome b, 704 bp, D-loop, 506 bp) and one nuclear gene (Beta-Fibrinogen, 550 bp) was conducted to reconstruct the recent demographic history within and between UK and continental European populations. Our analysis indicated phylogeographic variation in the UK is similar in magnitude to that found in other regions of continental Europe and suggests a recent population expansion. We present evidence which supports a single post-glacial colonization into the UK. Dispersal time calculations, calibrated with geophysical events, are coincident with the start of the Holocene period, 7.5–11 kya, a time when geological evidence suggests temperatures were stable, woodland habitat was prevalent and a land bridge was present to allow the dispersal of small mammals into the UK. We discuss our findings in the context of the extant geographical genetic structure described here and in relation to conservation management of this threatened species

    Associations between alcohol use and accelerated biological ageing

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    Harmful alcohol use is a leading cause of premature death and is associated with age-related disease. Biological ageing is highly variable between individuals and may deviate from chronological ageing, suggesting that biomarkers of biological ageing (derived from DNA methylation or brain structural measures) may be clinically relevant. Here, we investigated the relationships between alcohol phenotypes and both brain and DNA methylation age estimates. First, using data from UK Biobank and Generation Scotland, we tested the association between alcohol consumption (units/week) or hazardous use (Alcohol Use Disorders Identification Test [AUDIT] scores) and accelerated brain and epigenetic ageing in 20,258 and 8051 individuals, respectively. Second, we used Mendelian randomisation (MR) to test for a causal effect of alcohol consumption levels and alcohol use disorder (AUD) on biological ageing. Alcohol use showed a consistent positive association with higher predicted brain age (AUDIT-C: β = 0.053, p = 3.16 × 10−13; AUDIT-P: β = 0.052, p = 1.6 × 10−13; total AUDIT score: β = 0.062, p = 5.52 × 10−16; units/week: β = 0.078, p = 2.20 × 10−16), and two DNA methylation-based estimates of ageing, GrimAge (units/week: β = 0.053, p = 1.48 × 10−7) and PhenoAge (units/week: β = 0.077, p = 2.18x10−10). MR analyses revealed limited evidence for a causal effect of AUD on accelerated brain ageing (β = 0.118, p = 0.044). However, this result should be interpreted cautiously as the significant effect was driven by a single genetic variant. We found no evidence for a causal effect of alcohol consumption levels on accelerated biological ageing. Future studies investigating the mechanisms associating alcohol use with accelerated biological ageing are warranted
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