Suchergebnisse

Although the body of research literature on prostitution is extensive, systematic research on why and how women break with prostitution is lacking. The purpose of this paper is to report some empirical findings from a Swedish study of women leaving a life in the sex trade. In a broader perspective the study ties into a social psychological research tradition which focuses on illuminating individuals' processes of change, turning points, role changes and exit behaviours.The study comprises life‐story interviews with 23 women who exited prostitution during the years 1981–1995. Half of the women were referred to us via a special social outreach operation within the social services in a major Swedish city, the other half were recruited via newspaper and tabloid announcements. The majority of the women had been active in the sex trade for more than five years, thus classifying them as "long‐term residents". The majority had experiences exclusively of street prostitution, the most common form in Sweden.Our analysis shows a number of different exit courses, ranging from breakaways that happened quickly and were executed primarily by women who were relatively loosely integrated in the milieu, to breakaways that were made by women who, after many years of being exploited in prostitution, had reached the limit of the existentially bearable. In our account, we also identify four main challenges which the women have been faced with after leaving the trade: (1) working through and understanding the experiences of a life in prostitution, (2) dealing with shame, (3) living in a marginal situation, and (4) dealing with intimate and close relationships. Finally, we present an integrated exit model which combines structural, situational, interpersonal and individual factors in explaining how and why women leave prostitution. The purpose of our model is to create a general understanding of why certain people not only survive a difficult life situation, but are able to grow and develop further during the course of the process.

Background and aims: Unstable carotid atherosclerosis causes stroke, but methods to identify patients and lesions at risk are lacking. We recently found enrichment of genes associated with calcification in carotid plaques from asymptomatic patients. Here, we hypothesized that calcification represents a stabilising feature of plaques and investigated how macro-calcification, as estimated by computed tomography (CT), correlates with gene expression profiles in lesions. Methods: Plaque calcification was measured in pre-operative CT angiographies. Plaques were sorted into high- and lowcalcified, profiled with microarrays, followed by bioinformatic analyses. Immunohistochemistry and qPCR were performed to evaluate the findings in plaques and arteries with medial calcification from chronic kidney disease patients. Results: Smooth muscle cell (SMC) markers were upregulated in high-calcified plaques and calcified plaques from symptomatic patients, whereas macrophage markers were downregulated. The most enriched processes in high-calcified plaques were related to SMCs and extracellular matrix (ECM) organization, while inflammation, lipid transport and chemokine signaling were repressed. These findings were confirmed in arteries with high medial calcification. Proteoglycan 4 (PRG4) was identified as the most upregulated gene in association with plaque calcification and found in the ECM, SMA+ and CD68+/TRAP + cells. Conclusions: Macro-calcification in carotid lesions correlated with a transcriptional profile typical for stable plaques, with altered SMC phenotype and ECM composition and repressed inflammation. PRG4, previously not described in atherosclerosis, was enriched in the calcified ECM and localized to activated macrophages and smooth muscle-like cells. This study strengthens the notion that assessment of calcification may aid evaluation of plaque phenotype and stroke risk. ; The European Union's Horizon 2020/Marie Sklodowska-Curie grant agreement No 722609 (INTRICARE); ; Swedish Heart and Lung Foundation ; Swedish Research Council (K2009-65X-2233-01-3, K2013- 65X-06816-30-4, 349-2007-8703) ; Uppdrag Besegra Stroke (P581/ 2011-123) ; Stockholm County Council (ALF2011-0260, ALF-2011- 0279) ; Swedish Society for Medical Research ; Tore Nilsson's Foundation ; Magnus Bergvall's Foundation ; Karolinska Institutet Foundation ; European Commission (722609) ; Published

The Data Supplement is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCGEN.118.002115 ; BACKGROUND: Atherosclerosis is a chronic inflammatory disease in part caused by lipid uptake in the vascular wall, but the exact underlying mechanisms leading to acute myocardial infarction and stroke remain poorly understood. Large consortia identified genetic susceptibility loci that associate with large artery ischemic stroke and coronary artery disease. However, deciphering their underlying mechanisms are challenging. Histological studies identified destabilizing characteristics in human atherosclerotic plaques that associate with clinical outcome. To what extent established susceptibility loci for large artery ischemic stroke and coronary artery disease relate to plaque characteristics is thus far unknown but may point to novel mechanisms. METHODS: We studied the associations of 61 established cardiovascular risk loci with 7 histological plaque characteristics assessed in 1443 carotid plaque specimens from the Athero-Express Biobank Study. We also assessed if the genotyped cardiovascular risk loci impact the tissue-specific gene expression in 2 independent biobanks, Biobank of Karolinska Endarterectomy and Stockholm Atherosclerosis Gene Expression. RESULTS: A total of 21 established risk variants (out of 61) nominally associated to a plaque characteristic. One variant (rs12539895, risk allele A) at 7q22 associated to a reduction of intraplaque fat, P=5.09×10-6 after correction for multiple testing. We further characterized this 7q22 Locus and show tissue-specific effects of rs12539895 on HBP1 expression in plaques and COG5 expression in whole blood and provide data from public resources showing an association with decreased LDL (low-density lipoprotein) and increase HDL (high-density lipoprotein) in the blood. CONCLUSIONS: Our study supports the view that cardiovascular susceptibility loci may exert their effect by influencing the atherosclerotic plaque characteristics. ; Dr van der Laan is funded through grants from the Netherlands CardioVascular Research Initiative of the Netherlands Heart Foundation (CVON 2011/B019 and CVON 2017-20: Generating the best evidence-based pharmaceutical targets for atherosclerosis [GENIUS I&II]) and the Interuniversity Cardiology Institute of the Netherlands (ICIN, 09.001). Drs van der Laan and Haitjema are both funded through the FP7 EU project CVgenes@target (HEALTH-F2-2013–601456). Dr Siemelink is funded by the European Union (BiomarCaRE, grant number: HEALTH-2011–278913), and the technology foundation Stichting voor de Technische Wetenschappen through the Danone partnership program (Project 11679). The UCL Hospitals NIHR Biomedical Research Centre and the Dutch Heart Foundation (Junior Staff Member 2014T001) supported by Dr Asselbergs. The BiKE study was conducted with support from the Swedish Heart and Lung Foundation, the Swedish Research Council (K2009-65X-2233-01-3, K2013-65X-06816-30-4, and 349-2007-8703), Uppdrag Besegra Stroke (P581/2011–123), the Strategic Cardiovascular Programs of Karolinska Institutet and Stockholm County Council, the Stockholm County Council (ALF2011-0260 and ALF-2011-0279), the Foundation for Strategic Research and the European Commission (CarTarDis). ; Peer-reviewed ; Publisher Version