Plastblommor, torra blad och crazy plant ladies: En etnologisk studie av krukväxters funktion i subjektspositionering

This paper examines how our relationship with potted plants from a class perspective can reflect different subject positions. The aim is that through interviews with houseplant owners show the function of the plant in the owners´ subject positioning. The material consists of transcribed interviews with six informants in their home. To my help to interpret the material I have been using the French cultural sociologist Pierre Bourdieu´s theories about the social space, symbolic capital and distinction, but with the British sociologist Beverley Skeggs´ interpretation and development of the concepts. Her theories on respectability and disidentification also get a significant role in the interpretation of the material. I also used the cultural anthropologist Mary Douglas´ theory of dirt and cleanliness. The result shows how the potted plant can serve as a distinction over other people and that class can be made in the view of various characteristics of plants.Denna uppsats undersöker hur vårt förhållande till krukväxter utifrån ett klassperspektiv kan spegla olika subjektspositioner. Syftet är att genom intervjuer med krukväxtägare visa på krukväxtens funktion i deras subjektspositionering. Materialet består av transkriberade intervjuer med sex olika informanter i deras hem. Till min hjälp att tolka materialet har jag använt mig av den franske kultursociologen Pierre Bourdieus teorier om bland annat det sociala rummet, symboliskt kapital och distinktion, men med den brittiske sociologen Beverley Skeggs tolkning och utveckling av begreppen. Hennes teorier om respektabilitet och disidentifikation får också en betydande funktion i tolkningen av materialet. Jag har även använt mig av kulturantropologen Mary Douglas teori om smuts och renlighet. Resultatet visar på hur förhållandet till en krukväxt kan fungera som en distinktion gentemot andra människor och att klass kan göras i synen på olika växters egenskaper

Cardiorespiratory fitness and the metabolic syndrome:Roles of inflammation and abdominal obesity

Individuals with metabolic syndrome have increased risk of type 2 diabetes and cardiovascular disease. We aimed to test the hypothesis that a high level of cardiorespiratory fitness (CR-fitness), counteracts accumulation of visceral fat, decreases inflammation and lowers risk factors of the metabolic syndrome.The study sample included 1,293 Danes (age 49-52 years) who from 2009 to 2011 participated in the Copenhagen Aging and Midlife Biobank, including a questionnaire, physical tests, and blood samples. Multiple linear regression models were performed with CR-fitness as exposure and plasma levels of cytokines and high sensitive C-reactive protein as outcomes and measures of abdominal obesity were added to test if they explained the potential association. Similarly, multiple linear regression models were performed with CR-fitness as exposure and factors of the metabolic syndrome as outcomes and the potential explanation by inflammatory biomarkers were tested. All models were adjusted for the effect of age, sex, smoking, alcohol consumption, socio-economic status, and acute inflammatory events within the preceding two weeks.CR-fitness was inversely associated with high sensitive C-reactive protein, Interleukin (IL)-6, and IL-18, and directly associated with the anti-inflammatory cytokine IL-10, but not associated with tumor necrosis factor alpha, interferon gamma or IL-1β. Abdominal obesity could partly explain the significant associations. Moreover, CR-fitness was inversely associated with an overall metabolic syndrome score, as well as triglycerides, glycated haemoglobin A1c, systolic blood pressure, diastolic blood pressure and directly associated with high-density lipoprotein. Single inflammatory biomarkers and a combined inflammatory score partly explained these associations.Data suggest that CR-fitness has anti-inflammatory effects that are partly explained by a reduction in abdominal obesity and a decrease in the metabolic syndrome risk profile. The overall inflammatory load was mainly driven by high sensitive C-reactive protein and IL-6

Coronary artery disease-associated genetic variants and biomarkers of inflammation

Introduction: Genetic constitution and inflammation both contribute to development of coronary artery disease (CAD). Several CAD-associated single-nucleotide polymorphisms (SNPs) have recently been identified, but their functions are largely unknown. We investigated the associations between CAD-associated SNPs and five CAD-related inflammatory biomarkers. Methods: We genotyped 45 CAD-associated SNPs in 701 stable CAD patients in whom levels of high-sensitivity C-reactive protein (hsRCP), interleukin-6, calprotectin, fibrinogen and complement component 3 levels had previously been measured. A genetic risk score was calculated to assess the combined risk associated with all the genetic variants. A multiple linear regression model was used to assess associations between the genetic risk score, single SNPs, and the five inflammatory biomarkers. Results: The minor allele (G) (CAD risk allele) of rs2075650 (TOMM40/APOE) was associated with lower levels of high-sensitivity C-reactive protein (effect per risk allele: -0.37 mg/l [95%CI -0.56 to -0.18 mg/l]). The inflammatory markers tested showed no association with the remaining 44 SNPs or with the genetic risk score. Conclusions: In stable CAD patients, the risk allele of a common CAD-associated marker at the TOMM40/APOE locus was associated with lower hsCRP levels. No other genetic variants or the combined effect of all variants were associated with the five inflammatory biomarkers

Detailed statistical analysis plan for the Danish Palliative care trial (DanPaCT)

Acknowledgements We wish to thank the students who sent out the questionnaires, who entered and compared all data, help with data management, made material blind to the investigators, and were/will be outcome assessors of interventions given. They were: Nicla Rohde Christensen, Ellen Lundorff, Marc Klee Olsen, Charlotte Lund Rasmussen, and Nete Skjødt. This work was funded by the Tryg Foundation [journal number 7-10-0838A] and the Danish Cancer Society [journal number R16-A695]. Other than funding the trial, the funding body had no role in the design, conduct, analysis, or reporting of the present trial.Peer reviewedPublisher PD

Fibrin clot properties independently predict adverse clinical outcome following acute coronary syndrome: a PLATO substudy

Aims: To determine whether fibrin clot properties are associated with clinical outcomes following acute coronary syndrome (ACS). Methods and results: Plasma samples were collected at hospital discharge from 4354 ACS patients randomized to clopidogrel or ticagrelor in the PLATelet inhibition and patient Outcomes (PLATO) trial. A validated turbidimetric assay was employed to study plasma clot lysis time and maximum turbidity (a measure of clot density). One-year rates of cardiovascular (CV) death, spontaneous myocardial infarction (MI) and PLATO-defined major bleeding events were assessed after sample collection. Hazard ratios (HRs) were estimated using Cox proportional hazards models. After adjusting for CV risk factors, each 50% increase in lysis time was associated with CV death/spontaneous MI [HR 1.17, 95% confidence interval (CI) 1.05-1.31; P  0.05). Neither lysis time nor maximum turbidity was associated with major bleeding events. Conclusion: Fibrin clots that are resistant to lysis independently predict adverse outcome in ACS patients. Novel therapies targeting fibrin clot properties might be a new avenue for improving prognosis in patients with ACS

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition

Thrombosis and Vascular Inflammation in Diabetes: Mechanisms and Potential Therapeutic Targets

Cardiovascular disease remains the main cause of morbidity and mortality in patients with diabetes. The risk of vascular ischemia is increased in this population and outcome following an event is inferior compared to individuals with normal glucose metabolism. The reasons for the adverse vascular profile in diabetes are related to a combination of more extensive atherosclerotic disease coupled with an enhanced thrombotic environment. Long-term measures to halt the accelerated atherosclerotic process in diabetes have only partially addressed vascular pathology, while long-term antithrombotic management remains largely similar to individuals without diabetes. We address in this review the pathophysiological mechanisms responsible for atherosclerosis with special emphasis on diabetes-related pathways. We also cover the enhanced thrombotic milieu, characterized by increased platelet activation, raised activity of procoagulant proteins together with compromised function of the fibrinolytic system. Potential new therapeutic targets to reduce the risk of atherothrombosis in diabetes are explored, including alternative use of existing therapies. Special emphasis is placed on diabetes-specific therapeutic targets that have the potential to reduce vascular risk while keeping an acceptable clinical side effect profile. It is now generally acknowledged that diabetes is not a single clinical entity but a continuum of various stages of the condition with each having a different vascular risk. Therefore, we propose that future therapies aiming to reduce vascular risk in diabetes require a stratified approach with each group having a “stage-specific” vascular management strategy. This “individualized care” in diabetes may prove to be essential to improve vascular outcome in this high risk population

The benefits of strength training on musculoskeletal system health: practical applications for interdisciplinary care

Global health organizations have provided recommendations regarding exercise for the general population. Strength training has been included in several position statements due to its multi-systemic benefits. In this narrative review, we examine the available literature, first explaining how specific mechanical loading is converted into positive cellular responses. Secondly, benefits related to specific musculoskeletal tissues are discussed, with practical applications and training programmes clearly outlined for both common musculoskeletal disorders and primary prevention strategies