1,721 research outputs found

    Work restructuring and changing craft identity: the Tale of the Disaffected Weavers (or what happens when the rug is pulled from under your feet)

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    This article explores the changes in worker identity that can occur during manufacturing restructuring – specifically those linked to the declining status of craft work – through an in-depth case study of Weaveco, a UK carpet manufacturer. An analysis of changes in the labour process is followed by employee reactions centred on the demise of the traditional craft identity of male carpet weavers. The voices of the weavers dramatize the tensions involved in reconstructing their masculine identity, and we consider the implications this has for understanding gendered work relations

    Protocol for randomized personalized trial for stress management compared to standard of care

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    Stress is a significant public health burden in the United States, with most Americans reporting unhealthy levels of stress. Stress management techniques include various evidence-based treatments shown to be effective but with heterogeneous treatment responses, indicating a lack of uniform benefits for all individuals. Designed to assess a participant’s response to a specific intervention, personalized (N-of-1) trials provide guidance for which treatment (s) work (s) best for the individual. Prior studies examining the effects of mindfulness meditation, yoga, and walking for stress reduction found all three interventions to be associated with significant reductions in self-reported measures of stress. Delivering these treatments using a personalized trial approach has the potential to assist clinicians in identifying the best stress management techniques for individuals with persistently high stress while fostering treatment decisions that consider their personal condition/barriers. This trial will evaluate a personalized approach compared to standard of care for three interventions (guided mindfulness meditation; guided yoga; and guided brisk walking) to manage perceived stress. Participants will respond to daily surveys and wear a Fitbit device for 18 weeks. After a 2-week baseline period, participants in the personalized trial groups will receive 12 weeks of interventions in randomized order, while participants in the standard-of-care group will have access to all interventions for self-directed stress management. After intervention, all participants will undergo 2 weeks of observation, followed by two additional weeks of the stress management intervention of their choosing while continuing outcome measurement. At study completion, all participants will be sent a satisfaction survey. The primary analysis will compare perceived stress levels between the personalized and standard of care arms. The results of this trial will provide further support for the use of personalized designs for managing stress.Clinical Trial Registration: clinicaltrials.gov, NCT05408832.Protocol version: 9/14/2022, 21-0968-MRB

    The Harms of Constructing Addiction as a Chronic, Relapsing Brain Disease.

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    As an international network of historians and social scientists who study approaches to the management of drugs across time and place, we have noticed the effort to redefine addiction as a chronic, relapsing brain disease (CRBD). The CRBD model is promoted as a route to destigmatize addiction and to empower individuals to access treatment that works within that model’s terms.1 CRBD usefully recognizes that brain-based neural adaptations place individual brains in chronic states of readiness to relapse. But brains are housed inside of people. Substance use is biological, social, and political; our concepts and approaches to complex questions surrounding substance use must be, too.2,3 By overlooking the sociopolitical dynamics and inequalities bound up with substance use, the CRBD model can paradoxically further marginalize people who use drugs by positing them as neurobiologically incapable of agency or choice. We are concerned that the CRBD model paints drug users as individuals whose exclusion from social, economic, and political participation is justified by their biological flaws and damaged brains

    Evaluation of polygenic risk scores for breast and ovarian cancer risk prediction in BRCA1 and BRCA2 mutation carriers

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    Background: Genome-wide association studies (GWAS) have identified 94 common single-nucleotide polymorphisms (SNPs) associated with breast cancer (BC) risk and 18 associated with ovarian cancer (OC) risk. Several of these are also associated with risk of BC or OC for women who carry a pathogenic mutation in the high-risk BC and OC genes BRCA1 or BRCA2. The combined effects of these variants on BC or OC risk for BRCA1 and BRCA2 mutation carriers have not yet been assessed while their clinical management could benefit from improved personalized risk estimates. Methods: We constructed polygenic risk scores (PRS) using BC and OC susceptibility SNPs identified through population-based GWAS: for BC (overall, estrogen receptor [ER]-positive, and ER-negative) and for OC. Using data from 15 252 female BRCA1 and 8211 BRCA2 carriers, the association of each PRS with BC or OC risk was evaluated using a weighted cohort approach, with time to diagnosis as the outcome and estimation of the hazard ratios (HRs) per standard deviation increase in the PRS. Results: The PRS for ER-negative BC displayed the strongest association with BC risk in BRCA1 carriers (HR = 1.27, 95% confidence interval [CI] = 1.23 to 1.31, P = 8.2 x 10(53)). In BRCA2 carriers, the strongest association with BC risk was seen for the overall BC PRS (HR = 1.22, 95% CI = 1.17 to 1.28, P = 7.2 x 10(-20)). The OC PRS was strongly associated with OC risk for both BRCA1 and BRCA2 carriers. These translate to differences in absolute risks (more than 10% in each case) between the top and bottom deciles of the PRS distribution; for example, the OC risk was 6% by age 80 years for BRCA2 carriers at the 10th percentile of the OC PRS compared with 19% risk for those at the 90th percentile of PRS. Conclusions: BC and OC PRS are predictive of cancer risk in BRCA1 and BRCA2 carriers. Incorporation of the PRS into risk prediction models has promise to better inform decisions on cancer risk management

    BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

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    Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

    The Sloan Digital Sky Survey Reverberation Mapping Project: Key Results

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    We present the final data from the Sloan Digital Sky Survey Reverberation Mapping (SDSS-RM) project, a precursor to the SDSS-V Black Hole Mapper Reverberation Mapping program. This data set includes 11-year photometric and 7-year spectroscopic light curves for 849 broad-line quasars over a redshift range of 0.1<z<4.5 and a luminosity range of Lbol=1E44-47.5 erg/s, along with spectral and variability measurements. We report 23, 81, 125, and 110 reverberation mapping lags (relative to optical continuum variability) for broad Halpha, Hbeta, MgII and CIV using the SDSS-RM sample, spanning much of the luminosity and redshift ranges of the sample. Using 30 low-redshift RM AGNs with dynamical-modeling black hole masses, we derive a new estimate of the average virial factor of =0.62+-0.07 for the line dispersion measured from the RMS spectrum. The intrinsic scatter of individual virial factors is 0.31+-0.07 dex, indicating a factor of two systematic uncertainty in RM black hole masses. Our lag measurements reveal significant R-L relations for Hbeta and MgII at high redshift, consistent with the latest measurements based on heterogeneous samples. While we are unable to robustly constrain the slope of the R-L relation for CIV given the limited dynamical range in luminosity, we found substantially larger scatter in CIV lags at fixed L1350. Using the SDSS-RM lag sample, we derive improved single-epoch (SE) mass recipes for Hbeta, MgII and CIV, which are consistent with their respective RM masses as well as between the SE recipes from two different lines, over the luminosity range probed by our sample. The new Hbeta and MgII recipes are approximately unbiased estimators at given RM masses, but there are systematic biases in the CIV recipe. The intrinsic scatter of SE masses around RM masses is ~0.45 dex for Hbeta and MgII, increasing to ~0.58 dex for CIV.Comment: 33 pages. Data products available at ftp://quasar.astro.illinois.edu/public/sdssrm/final_result

    ĐŃŃĐŸŃ†ĐžĐ°Ń‚ĐžĐČĐœĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡Đ”ŃĐșая группа ĐșĐ°Đș ŃĐ·Ń‹ĐșĐŸĐČая ĐŸŃĐœĐŸĐČĐ° ĐșĐŸĐœŃ†Đ”ĐżŃ‚Đ°

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    Статья ĐżĐŸŃĐČŃŃ‰Đ”ĐœĐ° ĐŸĐżĐžŃĐ°ĐœĐžŃŽ ĐŸŃĐŸĐ±ĐŸĐč лДĐșсОĐșĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡Đ”ŃĐșĐŸĐč ĐżĐ°Ń€Đ°ĐŽĐžĐłĐŒŃ‹ Đ°ŃŃĐŸŃ†ĐžĐ°Ń‚ĐžĐČĐœĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡Đ”ŃĐșĐŸĐč группы, ĐșĐŸŃ‚ĐŸŃ€Đ°Ń яĐČĐ»ŃĐ”Ń‚ŃŃ частью Đ°ŃŃĐŸŃ†ĐžĐ°Ń‚ĐžĐČĐœĐŸ- ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡Đ”ŃĐșĐŸĐłĐŸ ĐșĐŸĐŒĐżĐ»Đ”Đșса Đž Ń€Đ°ŃŃĐŒĐ°Ń‚Ń€ĐžĐČĐ°Đ”Ń‚ŃŃ ĐșĐ°Đș ŃĐ·Ń‹ĐșĐŸĐČая ĐŸŃĐœĐŸĐČĐ° ĐșĐŸĐœŃ†Đ”ĐżŃ‚Đ°. Đ˜ŃŃĐ»Đ”ĐŽĐŸĐČĐ°ĐœĐžĐ” ĐżŃ€ĐŸĐČĐ”ĐŽĐ”ĐœĐŸ с ĐżŃ€ĐžĐŒĐ”ĐœĐ”ĐœĐžĐ”ĐŒ ĐŸĐżĐžŃĐ°Ń‚Đ”Đ»ŃŒĐœĐŸĐłĐŸ, струĐșŃ‚ŃƒŃ€ĐœĐŸĐłĐŸ Đž Ń„ŃƒĐœĐșŃ†ĐžĐŸĐœĐ°Đ»ŃŒĐœĐŸĐłĐŸ ĐŒĐ”Ń‚ĐŸĐŽĐŸĐČ.Статтю просĐČŃŃ‡Đ”ĐœĐŸ ĐŸĐżĐžŃŃƒ ĐŸŃĐŸĐ±Đ»ĐžĐČĐŸŃ— лДĐșсОĐșĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡ĐœĐŸŃ— ĐżĐ°Ń€Đ°ĐŽĐžĐłĐŒĐž Đ°ŃĐŸŃ†Ń–Đ°Ń‚ĐžĐČĐœĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡ĐœĐŸŃ— групо, яĐșĐ° є Ń‡Đ°ŃŃ‚ĐžĐœĐŸŃŽ Đ°ŃĐŸŃ†Ń–Đ°Ń‚ĐžĐČĐœĐŸ-ŃĐ”ĐŒĐ°ĐœŃ‚ĐžŃ‡ĐœĐŸĐłĐŸ ĐșĐŸĐŒĐżĐ»Đ”Đșсу і яĐČĐ»ŃŃ” ŃĐŸĐ±ĐŸŃŽ ĐŒĐŸĐČĐœŃƒ ĐŸŃĐœĐŸĐČу ĐșĐŸĐœŃ†Đ”ĐżŃ‚Ńƒ. Đ”ĐŸŃĐ»Ń–ĐŽĐ¶Đ”ĐœĐœŃ ĐżŃ€ĐŸĐČĐ”ĐŽĐ”ĐœĐŸ Ń–Đ· Đ·Đ°ŃŃ‚ĐŸŃŃƒĐČĐ°ĐœĐœŃĐŒ ĐŸĐżĐžŃĐŸĐČĐŸĐłĐŸ, струĐșŃ‚ŃƒŃ€ĐœĐŸĐłĐŸ та Ń„ŃƒĐœĐșŃ†Ń–ĐŸĐœĐ°Đ»ŃŒĐœĐŸĐłĐŸ ĐŒĐ”Ń‚ĐŸĐŽŃ–ĐČ.The particular lexico-semantic paradigm – associative-semantic group (ASG) which is the part of associative-semantic complex (ASC) – is investigated in the article as a linguistic base of concept. Descriptive, structural, and functional methods were used

    The BARRIERS scale -- the barriers to research utilization scale: A systematic review

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    <p>Abstract</p> <p>Background</p> <p>A commonly recommended strategy for increasing research use in clinical practice is to identify barriers to change and then tailor interventions to overcome the identified barriers. In nursing, the BARRIERS scale has been used extensively to identify barriers to research utilization.</p> <p>Aim and objectives</p> <p>The aim of this systematic review was to examine the state of knowledge resulting from use of the BARRIERS scale and to make recommendations about future use of the scale. The following objectives were addressed: To examine how the scale has been modified, to examine its psychometric properties, to determine the main barriers (and whether they varied over time and geographic locations), and to identify associations between nurses' reported barriers and reported research use.</p> <p>Methods</p> <p>Medline (1991 to September 2009) and CINHAL (1991 to September 2009) were searched for published research, and ProQuest<sup>Âź </sup>digital dissertations were searched for unpublished dissertations using the BARRIERS scale. Inclusion criteria were: studies using the BARRIERS scale in its entirety and where the sample was nurses. Two authors independently assessed the study quality and extracted the data. Descriptive and inferential statistics were used.</p> <p>Results</p> <p>Sixty-three studies were included, with most using a cross-sectional design. Not one study used the scale for tailoring interventions to overcome identified barriers. The main barriers reported were related to the setting, and the presentation of research findings. Overall, identified barriers were consistent over time and across geographic locations, despite varying sample size, response rate, study setting, and assessment of study quality. Few studies reported associations between reported research use and perceptions of barriers to research utilization.</p> <p>Conclusions</p> <p>The BARRIERS scale is a nonspecific tool for identifying general barriers to research utilization. The scale is reliable as reflected in assessments of internal consistency. The validity of the scale, however, is doubtful. There is no evidence that it is a useful tool for planning implementation interventions. We recommend that no further descriptive studies using the BARRIERS scale be undertaken. Barriers need to be measured specific to the particular context of implementation and the intended evidence to be implemented.</p

    Phenotypic Characterization of EIF2AK4 Mutation Carriers in a Large Cohort of Patients Diagnosed Clinically With Pulmonary Arterial Hypertension.

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    BACKGROUND: Pulmonary arterial hypertension (PAH) is a rare disease with an emerging genetic basis. Heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type 2 (BMPR2) are the commonest genetic cause of PAH, whereas biallelic mutations in the eukaryotic translation initiation factor 2 alpha kinase 4 gene (EIF2AK4) are described in pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis. Here, we determine the frequency of these mutations and define the genotype-phenotype characteristics in a large cohort of patients diagnosed clinically with PAH. METHODS: Whole-genome sequencing was performed on DNA from patients with idiopathic and heritable PAH and with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis recruited to the National Institute of Health Research BioResource-Rare Diseases study. Heterozygous variants in BMPR2 and biallelic EIF2AK4 variants with a minor allele frequency of <1:10 000 in control data sets and predicted to be deleterious (by combined annotation-dependent depletion, PolyPhen-2, and sorting intolerant from tolerant predictions) were identified as potentially causal. Phenotype data from the time of diagnosis were also captured. RESULTS: Eight hundred sixty-four patients with idiopathic or heritable PAH and 16 with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis were recruited. Mutations in BMPR2 were identified in 130 patients (14.8%). Biallelic mutations in EIF2AK4 were identified in 5 patients with a clinical diagnosis of pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis. Furthermore, 9 patients with a clinical diagnosis of PAH carried biallelic EIF2AK4 mutations. These patients had a reduced transfer coefficient for carbon monoxide (Kco; 33% [interquartile range, 30%-35%] predicted) and younger age at diagnosis (29 years; interquartile range, 23-38 years) and more interlobular septal thickening and mediastinal lymphadenopathy on computed tomography of the chest compared with patients with PAH without EIF2AK4 mutations. However, radiological assessment alone could not accurately identify biallelic EIF2AK4 mutation carriers. Patients with PAH with biallelic EIF2AK4 mutations had a shorter survival. CONCLUSIONS: Biallelic EIF2AK4 mutations are found in patients classified clinically as having idiopathic and heritable PAH. These patients cannot be identified reliably by computed tomography, but a low Kco and a young age at diagnosis suggests the underlying molecular diagnosis. Genetic testing can identify these misclassified patients, allowing appropriate management and early referral for lung transplantation
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