367 research outputs found

    Qualitative network analysis for migration studies: beyond metaphors and epistemological pitfalls

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    In this introductory article, we as guest editors set out the key ambitions and arguments of the Special Issue and highlight our contribution to social network research within migration studies. We argue that social network analysis has the potential to address epistemological pitfalls in migration research especially in overcoming the metaphoric use of networks as well as nation‐state and ethnicity‐centred epistemologies. Moreover, we suggest that adopting a qualitative approach to social networks not only changes how we research networks but also what we understand them to be. While seeking to go beyond metaphors and delve into the tool box of SNA, in order to gain deeper understandings of social networks, we argue that this cannot mean purely quantitative research techniques. We draw upon the early roots of social network research, within anthropology, to find inspiration and consider the contribution of qualitative approaches to analysing dynamic social relationships and to including neglected aspects like meaning making and agency. Adopting a reflexive approach enables us to de‐migranticise our research turning the role of migration and ethnicity for social networks into an empirical question rather than taking them as an essentialist starting point for investigation. The Special Issue brings together an integrated set of articles drawn from a social networks and migration symposium. Using qualitative and mixed methods approaches, these articles focus on a diverse range of geographical and social contexts. In so doing, the authors offer new methodological and epistemological insights into migrants’ social networks

    Shared brain and genetic architectures between mental health and physical activity

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    Physical activity is correlated with, and effectively treats various forms of psychopathology. However, whether biological correlates of physical activity and psychopathology are shared remains unclear. Here, we examined the extent to which the neural and genetic architecture of physical activity and mental health are shared. Using data from the UK Biobank (N = 6389), we applied canonical correlation analysis to estimate associations between the amplitude and connectivity strength of subnetworks of three major neurocognitive networks (default mode, DMN; salience, SN; central executive networks, CEN) with accelerometer-derived measures of physical activity and self-reported mental health measures (primarily of depression, anxiety disorders, neuroticism, subjective well-being, and risk-taking behaviors). We estimated the genetic correlation between mental health and physical activity measures, as well as putative causal relationships by applying linkage disequilibrium score regression, genomic structural equational modeling, and latent causal variable analysis to genome-wide association summary statistics (GWAS N = 91,105-500,199). Physical activity and mental health were associated with connectivity strength and amplitude of the DMN, SN, and CEN (r\u27s ≥ 0.12, p\u27s \u3c 0.048). These neural correlates exhibited highly similar loading patterns across mental health and physical activity models even when accounting for their shared variance. This suggests a largely shared brain network architecture between mental health and physical activity. Mental health and physical activity (including sleep) were also genetically correlated (|rg| = 0.085-0.121), but we found no evidence for causal relationships between them. Collectively, our findings provide empirical evidence that mental health and physical activity have shared brain and genetic architectures and suggest potential candidate subnetworks for future studies on brain mechanisms underlying beneficial effects of physical activity on mental health

    Improvements in physical function and pain interference and changes in mental health among patients seeking musculoskeletal care

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    IMPORTANCE: Among patients seeking care for musculoskeletal conditions, there is mixed evidence regarding whether traditional, structure-based care is associated with improvement in patients\u27 mental health. OBJECTIVE: To determine whether improvements in physical function and pain interference are associated with meaningful improvements in anxiety and depression symptoms among patients seeking musculoskeletal care. DESIGN, SETTING, AND PARTICIPANTS: This cohort study included adult patients treated by an orthopedic department of a tertiary care US academic medical center from June 22, 2015, to February 9, 2022. Eligible participants presented between 4 and 6 times during the study period for 1 or more musculoskeletal conditions and completed Patient-Reported Outcomes Measurement Information System (PROMIS) measures as standard care at each visit. EXPOSURE: PROMIS Physical Function and Pain Interference scores. MAIN OUTCOMES AND MEASURES: Linear mixed effects models were used to determine whether improvements in PROMIS Anxiety and PROMIS Depression scores were associated with improved PROMIS Physical Function or Pain Interference scores after controlling for age, gender, race, and PROMIS Depression (for the anxiety model) or PROMIS Anxiety (for the depression model). Clinically meaningful improvement was defined as 3.0 points or more for PROMIS Anxiety and 3.2 points or more for PROMIS Depression. RESULTS: Among 11 236 patients (mean [SD] age, 57 [16] years), 7218 (64.2%) were women; 120 (1.1%) were Asian, 1288 (11.5%) were Black, and 9706 (86.4%) were White. Improvements in physical function (β = -0.14; 95% CI, -0.15 to -0.13; P \u3c .001) and pain interference (β = 0.26; 95% CI, 0.25 to 0.26; P \u3c .001) were each associated with improved anxiety symptoms. To reach a clinically meaningful improvement in anxiety symptoms, an improvement of 21 PROMIS points or more (95% CI, 20-23 points) on Physical Function or 12 points or more (95% CI, 12-12 points) on Pain Interference would be required. Improvements in physical function (β = -0.05; 95% CI, -0.06 to -0.04; P \u3c .001) and pain interference (β = 0.04; 95% CI, 0.04 to 0.05; P \u3c .001) were not associated with meaningfully improved depression symptoms. CONCLUSIONS AND RELEVANCE: In this cohort study, substantial improvements in physical function and pain interference were required for association with any clinically meaningful improvement in anxiety symptoms, and were not associated with any meaningful improvement in depression symptoms. Patients seeking musculoskeletal care clinicians providing treatment cannot assume that addressing physical health will result in improved symptoms of depression or potentially even sufficiently improved symptoms of anxiety

    Mapping prenatal predictors and neurobehavioral outcomes of an epigenetic marker of neonatal inflammation – A longitudinal population-based study

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    Background: DNA methylation levels at specific sites can be used to proxy C-reactive protein (CRP) levels, providing a potentially more stable and accurate indicator of sustained inflammation and associated health risk. However, its use has been primarily limited to adults or preterm infants, and little is known about determinants for − or offspring outcomes of − elevated levels of this epigenetic proxy in cord blood. The aim of this study was to comprehensively map prenatal predictors and long-term neurobehavioral outcomes of neonatal inflammation, as assessed with an epigenetic proxy of inflammation in cord blood, in the general pediatric population. Methods: Our study was embedded in the prospective population-based Generation R Study (n = 2,394). We created a methylation profile score of CRP (MPS-CRP) in cord blood as a marker of neonatal inflammation and validated it against serum CRP levels in mothers during pregnancy, as well as offspring at birth and in childhood. We then examined (i) which factors (previously associated with sustained inflammation) explain variability in MPS-CRP at birth, including a wide range of prenatal lifestyle and clinical conditions, pro-inflammatory exposures, as well as child genetic liability to elevated CRP levels; and (ii) whether MPS-CRP at birth associates with child neurobehavioral outcomes, including global structural MRI and DTI measures (child mean age 10 and 14 years) as well as psychiatric symptoms over time (Child Behavioral Checklist, at mean age 1.5, 3, 6, 10 and 14 years). Results: MPS-CRP at birth was validated with serum CRP in cord blood (cut-off &gt; 1 mg/L) (AUC = 0.72). Prenatal lifestyle pro-inflammatory factors explained a small part (i.e., &lt; 5%) of the variance in the MPS-CRP at birth. No other prenatal predictor or the polygenic score of CRP in the child explained significant variance in the MPS-CRP at birth. The MPS-CRP at birth prospectively associated with a reduction in global fractional anisotropy over time on mainly a nominal threshold (β = -0.014, SE = 0.007, p = 0.032), as well as showing nominal associations with structural differences (amygdala [(β = 0.016, SE = 0.006, p = 0.010], cerebellum [(β = -0.007, SE = 0.003, p = 0.036]). However, no associations with child psychiatric symptoms were observed. Conclusion: Prenatal exposure to lifestyle-related pro-inflammatory factors was the only prenatal predictor that accounted for some of the individual variability in MPS-CRP levels at birth. Further, while the MPS-CRP prospectively associated with white matter alterations over time, no associations were observed at the behavioral level. Thus, the relevance and potential utility of using epigenetic data as a marker of neonatal inflammation in the general population remain unclear. In the future, the use of epigenetic proxies for a wider range of immune markers may lend further insights into the relationship between neonatal inflammation and adverse neurodevelopment within the general pediatric population.</p

    Interventions to improve the appropriate use of polypharmacy in older people: a Cochrane systematic review

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    OBJECTIVE: To summarise the findings of an updated Cochrane review of interventions aimed at improving the appropriate use of polypharmacy in older people. DESIGN: Cochrane systematic review. Multiple electronic databases were searched including MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials (from inception to November 2013). Hand searching of references was also performed. Randomised controlled trials (RCTs), controlled clinical trials, controlled before-and-after studies and interrupted time series analyses reporting on interventions targeting appropriate polypharmacy in older people in any healthcare setting were included if they used a validated measure of prescribing appropriateness. Evidence quality was assessed using the Cochrane risk of bias tool and GRADE (Grades of Recommendation, Assessment, Development and Evaluation). SETTING: All healthcare settings. PARTICIPANTS: Older people (≥65 years) with ≥1 long-term condition who were receiving polypharmacy (≥4 regular medicines). PRIMARY AND SECONDARY OUTCOME MEASURES: Primary outcomes were the change in prevalence of appropriate polypharmacy and hospital admissions. Medication-related problems (eg, adverse drug reactions), medication adherence and quality of life were included as secondary outcomes. RESULTS: 12 studies were included: 8 RCTs, 2 cluster RCTs and 2 controlled before-and-after studies. 1 study involved computerised decision support and 11 comprised pharmaceutical care approaches across various settings. Appropriateness was measured using validated tools, including the Medication Appropriateness Index, Beers’ criteria and Screening Tool of Older Person's Prescriptions (STOPP)/ Screening Tool to Alert doctors to Right Treatment (START). The interventions demonstrated a reduction in inappropriate prescribing. Evidence of effect on hospital admissions and medication-related problems was conflicting. No differences in health-related quality of life were reported. CONCLUSIONS: The included interventions demonstrated improvements in appropriate polypharmacy based on reductions in inappropriate prescribing. However, it remains unclear if interventions resulted in clinically significant improvements (eg, in terms of hospital admissions). Future intervention studies would benefit from available guidance on intervention development, evaluation and reporting to facilitate replication in clinical practice

    Neuroinflammation in the amygdala is associated with recent depressive symptoms

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    BACKGROUND: Converging evidence suggests that elevated inflammation may contribute to depression. Yet, the link between peripheral inflammation and neuroinflammation in depression is unclear. Here, using data from the UK Biobank, we estimated associations among depression, C-reactive protein (CRP) as a measure of peripheral inflammation, and neuroinflammation as indexed by diffusion basis spectral imaging-based restricted fraction (DBSI-RF). METHODS: DBSI-RF was derived from diffusion-weighted imaging data (N = 11,512) for whole-brain gray matter (global-RF), and regions of interest in the bilateral amygdala (amygdala-RF) and hippocampus (hippocampus-RF), and CRP was estimated from blood (serum) samples. Self-reported recent depression symptoms were measured using a 4-item assessment. Linear regressions were used to estimate associations between CRP and DBSI-RFs with depression while adjusting for the following covariates: age, sex, body mass index, smoking, drinking, and medical conditions. RESULTS: Elevated CRP was associated with higher depression symptoms (β = 0.04, false discovery rate-corrected p \u3c .005) and reduced global-RF (β = -0.03, false discovery rate-corrected p \u3c .001). Higher amygdala-RF was associated with elevated depression-an effect resilient to added covariates and CRP (β = 0.02, false discovery rate-corrected p \u3c .05). Interestingly, this association was stronger in individuals with a lifetime history of depression (β = 0.07, p \u3c .005) than in those without (β = 0.03, p \u3c .05). Associations between global-RF or hippocampus-RF with depression were not significant, and no DBSI-RF indices indirectly linked CRP with depression (i.e., mediation effect). CONCLUSIONS: Peripheral inflammation and DBSI-RF neuroinflammation in the amygdala are independently associated with depression, consistent with animal studies suggesting distinct pathways of peripheral inflammation and neuroinflammation in the pathophysiology of depression and with investigations highlighting the role of the amygdala in stress-induced inflammation and depression

    Characteristics of patients making serious inhaler errors with a dry powder inhaler and association with asthma-related events in a primary care setting

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    Acknowledgements The iHARP database was funded by unrestricted grants from Mundipharma International Ltd and Research in Real-Life Ltd; these analyses were funded by an unrestricted grant from Teva Pharmaceuticals. Mundipharma and Teva played no role in study conduct or analysis and did not modify or approve the manuscript. The authors wish to direct a special appreciation to all the participants of the iHARP group who contributed data to this study and to Mundipharma, sponsors of the iHARP group. In addition, we thank Julie von Ziegenweidt for assistance with data extraction and Anna Gilchrist and Valerie L. Ashton, PhD, for editorial assistance. Elizabeth V. Hillyer, DVM, provided editorial and writing support, funded by Research in Real-Life, Ltd.Peer reviewedPublisher PD

    Anchoring genome sequence to chromosomes of the central bearded dragon (Pogona vitticeps) enables reconstruction of ancestral squamate macrochromosomes and identifies sequence content of the Z chromosome

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    We report here the first genome assembly and annotation of the human-pathogenic fungus Scedosporium aurantiacum, with a predicted 10,525 genes, and 11,661 transcripts. The strain WM 09.24 was isolated from the environment at Circular Quay, Sydney, New South Wales, Australi
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