| 111. |
- Moshontz, Hannah, et al.
(författare)
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The Psychological Science Accelerator: Advancing Psychology Through a Distributed Collaborative Network
- 2018
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Ingår i: Advances in Methods and Practices in Psychological Science. - : SAGE Publications. - 2515-2459 .- 2515-2467. ; 1:4, s. 501-515
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Tidskriftsartikel (refereegranskat)abstract
- Concerns about the veracity of psychological research have been growing. Many findings in psychological science are based on studies with insufficient statistical power and nonrepresentative samples, or may otherwise be limited to specific, ungeneralizable settings or populations. Crowdsourced research, a type of large-scale collaboration in which one or more research projects are conducted across multiple lab sites, offers a pragmatic solution to these and other current methodological challenges. The Psychological Science Accelerator (PSA) is a distributed network of laboratories designed to enable and support crowdsourced research projects. These projects can focus on novel research questions or replicate prior research in large, diverse samples. The PSA’s mission is to accelerate the accumulation of reliable and generalizable evidence in psychological science. Here, we describe the background, structure, principles, procedures, benefits, and challenges of the PSA. In contrast to other crowdsourced research networks, the PSA is ongoing (as opposed to time limited), efficient (in that structures and principles are reused for different projects), decentralized, diverse (in both subjects and researchers), and inclusive (of proposals, contributions, and other relevant input from anyone inside or outside the network). The PSA and other approaches to crowdsourced psychological science will advance understanding of mental processes and behaviors by enabling rigorous research and systematic examination of its generalizability.
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| 112. |
- Nielsen, Mette L., et al.
(författare)
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One-hour glucose value as a long-term predictor of cardiovascular morbidity and mortality : the Malmö Preventive Project
- 2018
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Ingår i: European Journal of Endocrinology. - 1479-683X. ; 178:3, s. 225-236
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine the predictive capability of a 1-h vs 2-h postload glucose value for cardiovascular morbidity and mortality.DESIGN: Prospective, population-based cohort study (Malmö Preventive Project) with subject inclusion 1974-1992.RESULTS: Median age was 48 (25th-75th percentile: 48-49) years and mean FBG 4.6 ± 0.6 mmol/L. FBG and 2-h postload BG did not independently predict cardiovascular events or death. Conversely, 1-h postload BG predicted cardiovascular morbidity and mortality and remained an independent predictor of cardiovascular death (HR: 1.09, 95% CI: 1.01-1.17, P = 0.02) and all-cause mortality (HR: 1.10, 95% CI: 1.05-1.16, P < 0.0001) after adjusting for various traditional risk factors. Clinical risk factors with added 1-h postload BG performed better than clinical risk factors alone, in predicting cardiovascular death (likelihood-ratio test, P = 0.02) and all-cause mortality (likelihood-ratio test, P = 0.0001; significant IDI, P = 0.0003).METHODS: 4934 men without known diabetes and cardiovascular disease, who had blood glucose (BG) measured at 0, 20, 40, 60, 90 and 120 min during an OGTT (30 g glucose per m2 body surface area), were followed for 27 years. Data on cardiovascular events and death were obtained through national and local registries. Predictive capabilities of fasting BG (FBG) and glucose values obtained during OGTT alone and added to a clinical prediction model comprising traditional cardiovascular risk factors were assessed using Harrell's concordance index (C-index) and integrated discrimination improvement (IDI).CONCLUSION: Among men without known diabetes, addition of 1-h BG, but not FBG or 2-h BG, to clinical risk factors provided incremental prognostic yield for prediction of cardiovascular death and all-cause mortality.
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| 113. |
- Nielsen, Olav W., et al.
(författare)
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Assessing Optimal Blood Pressure in Patients With Asymptomatic Aortic Valve Stenosis The Simvastatin Ezetimibe in Aortic Stenosis Study (SEAS)
- 2016
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Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 134:6, s. 455-468
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Tidskriftsartikel (refereegranskat)abstract
- Background: Evidence for treating hypertension in patients with asymptomatic aortic valve stenosis is scarce. We used data from the SEAS trial (Simvastatin Ezetimibe in Aortic Stenosis) to assess what blood pressure (BP) would be optimal. METHODS: A total of 1767 patients with asymptomatic aortic stenosis and no manifest atherosclerotic disease were analyzed. Outcomes were all-cause mortality, cardiovascular death, heart failure, stroke, myocardial infarction, and aortic valve replacement. BP was analyzed in Cox models as the cumulative average of serially measured BP and a time-varying covariate. RESULTS: The incidence of all-cause mortality was highest for average follow-up systolic BP >= 160 mm Hg (4.3 per 100 person-years; 95% confidence interval [CI], 3.1-6.0) and lowest for average systolic BP of 120 to 139 mm Hg (2.0 per 100 person-years; 95% CI, 1.6-2.6). In multivariable analysis, all-cause mortality was associated with average systolic BP < 120 mm Hg (hazard ratio [HR], 3.4; 95% CI, 1.9-6.1), diastolic BP >= 90 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), and pulse pressure < 50 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), with systolic BP of 120 to 139 mm Hg, diastolic BP of 70 to 79 mm Hg, and pulse pressure of 60 to 69 mm Hg taken as reference. Low systolic and diastolic BPs increased risk in patients with moderate aortic stenosis. With a time-varying systolic BP from 130 to 139 mm Hg used as reference, mortality was increased for systolic BP >= 160 mm Hg (HR, 1.7; P=0.033) and BP of 120 to 129 mm Hg (HR, 1.6; P= 0.039). CONCLUSIONS: Optimal BP seems to be systolic BP of 130 to 139 mm Hg and diastolic BP of 70 to 90 mm Hg in these patients with asymptomatic aortic stenosis and no manifest atherosclerotic disease or diabetes mellitus.
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| 114. |
- Nilsson, Jan, et al.
(författare)
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Chronic Inflammation and Atherosclerosis
- 2015
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Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763 ; , s. 157-167
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Bokkapitel (refereegranskat)abstract
- Inflammation is a vital response and necessary for maintaining homeostasis. Inflammation protects against tissue damage and pathogens-but is also one of the main driving forces of the atherosclerotic plaque progression. How and why the inflammatory response is initiated in the atherosclerotic disease is not fully known, but evidence suggests modified lipids as potential antigens activating the immune response, according to the response-to-retention theory. The inflammatory response is an intricate interplay between the innate and adaptive immune system, tightly regulated by pro-inflammatory and anti-inflammatory mechanisms. Besides its role in the formation of the atherosclerotic plaque many studies also point toward inflammation as a driving force of plaque vulnerability and eventually plaque rupture.
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| 115. |
- Nilsson, Peter M., et al.
(författare)
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Early Vascular Aging in the Young : Influence of Birth Weight and Prematurity
- 2015
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Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763 ; , s. 129-136
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Bokkapitel (refereegranskat)abstract
- Longitudinal data from cohort studies show that early life factors such as low birth weight are associated with the development of hypertension, coronary heart disease, and type 2 diabetes in adulthood. Moreover, the majority of published studies concur that blood pressure is higher in adolescents and young adults with a history of low birth weight. Although the precise mechanisms linking early life factors with increased future cardiovascular risk are unclear, the architecture of the vascular system is programmed in utero and the majority of elastin, the major structural component underlying arterial wall elasticity, is synthesized and deposited during this time. Therefore, the arterial system has been a major focus of investigations aimed toward improving our understanding of the natural history of hypertension and future cardiovascular risk. A number of studies have now described properties relating to arterial structure and function in children, adolescents, and young adults, with a history of low birth weight, due to being either small for gestational age or premature. While the combination of prematurity and intrauterine growth retardation resulting in a small for gestational age phenotype appears to be associated with the most marked impairments in vascular structure and function, the small for gestational age phenotype, followed by a rapid "catch-up" growth also appears harmful. Further studies are needed to understand the long-term consequences of cardiovascular health of being born under adverse conditions, especially when post-natal growth trajectories are taken into account.
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| 116. |
- Nilsson, Peter M., et al.
(författare)
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Preface
- 2015
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Ingår i: Early Vascular Aging (EVA) : New Directions in Cardiovascular Protection - New Directions in Cardiovascular Protection. - 9780128013878 - 9780128016763
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 117. |
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| 118. |
- Olsen, Michael H., et al.
(författare)
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Changes in subclinical organ damage vs. in Framingham risk score for assessing cardiovascular risk reduction during continued antihypertensive treatment : a LIFE substudy
- 2011
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 29:5, s. 997-1004
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Tidskriftsartikel (refereegranskat)abstract
- Aim: To investigate whether in-treatment measurements of subclinical organ damage (SOD) assessed by elevated urine albumin/creatinine ratio (UACR) or electrocardiographic left ventricular hypertrophy improved the prediction of the composite cardiovascular endpoint of cardiovascular death, nonfatal myocardial infarction and stroke beyond in-treatment Framingham risk score (FRS).Methods: Excluding patients with a composite cardiovascular endpoint within the first year of treatment, 598 endpoints occurred in 6460 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study with baseline and 1 year values for UACR, left ventricular hypertrophy by electrocardiography and FRS available.Results: Using Cox-regression analyses, FRS1year [hazard ratio = 1.006 (0.98-1.04)] did not predict the endpoint independently of history of cardiovascular disease [hazard ratio = 1.76 (1.49-2.08)], FRSbaseline [hazard ratio = 1.07 (1.04-1.11)], UACR(baseline) [hazard ratio = 1.15 (1.07-1.23), all three P < 0.001], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.006-1.02), P < 0.01] and treatment allocation, whereas Cornell product(1yea)r [hazard ratio = 1.01 (1.006-1.02), P < 0.001] and to some degree UACR(1year) [hazard ratio = 1.05 (0.99-1.10), P = 0.09] predicted the endpoint independently of history of cardiovascular disease [hazard ratio = 1.71 (1.44-2.02)], FRSbaseline [hazard ratio = 1.08 (1.06-1.10)], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.007-1.02), both P < 0.001], UACR(baseline) [hazard ratio = 1.11 (1.03-1.20), P < 0.01] and treatment allocation decreasing -2 Log likelihood significantly (P < 0.01).Presence of left ventricular hypertrophy by Cornell product1year or UACR(1year) at least 1 mmol/l [hazard ratio = 1.40 (1.15-1.70), P = 0.001] but not FRS1year above the median baseline value of 20 [hazard ratio = 1.22 (0.94-1.57), not significant] was associated with higher risk of subsequent endpoint after adjustment for history of cardiovascular disease [hazard ratio = 1.82 (1.54-2.15)], FRSbaseline at least 20 [hazard ratio = 1.67 (1.30-2.16)], left ventricular hypertrophy by Sokolow-Lyonbaseline or UACR(baseline) at least 1 mmol/l [hazard ratio = 1.61 (1.33-1.94), all P < 0.001] and treatment allocation [hazard ratio = 0.93 (0.79-1.09), not significant]. In contrast to FRS1year at least 20 decreased, SOD1year decreased -2Log likelihood significantly (P < 0.01).Conclusion: Cornell product(1year) and UACR(1year) improved in contrast to FRS1year risk prediction based on FRSbaseline, Sokolow-Lyon(baseline) and UACR(baseline) significantly in LIFE patients during antihypertensive treatment.
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| 119. |
- Olsen, Michael Hecht, et al.
(författare)
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Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy : the losartan intervention for endpoint reduction in hypertension (LIFE) study
- 2009
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 27:3, s. 567-574
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Beta-blockers and angiotensin II receptor blockers have different effects on lipids. Methods: We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke. We measured total and high-density lipoprotein cholesterol at baseline and annually during 4.8 years of losartan-based compared with atenolol-based treatment in 8611 patients with hypertension and left ventricular hypertrophy. Results: Patients randomized to losartan-based or atenolol-based treatment had similar baseline total (6.04 ± 1.12 vs. 6.05 ± 1.13 mmol/l, NS) and high-density lipoprotein (HDL) cholesterol (1.50 ± 0.44 vs. 1.49 ± 0.44 mmol/l, NS). Total cholesterol decreased significantly but equally (-0.37 ± 1.05 vs. -0.34 ± 1.09 mmol/l, NS), whereas HDL cholesterol decreased less during the first 2 years in patients randomized to losartan compared with atenolol (-0.13 ± 0.24 vs. -0.19 ± 0.25 mmol/l) and remained higher each year (1.38, 1.37, 1.42, 1.47, and 1.48 mmol/l vs. 1.32, 1.30, 1.36, 1.40, and 1.42 mmol/l, all P < 0.001) independent of hydrochlorothiazide or statin treatment. In Cox regression analysis, baseline total cholesterol [hazard ratio (HR) = 1.08 (1.02–1.14) per mmol/l, P < 0.01], HDL cholesterol [HR = 0.56 (0.48–0.66) per mmol/l, P < 0.001], and treatment allocation [HR = 0.86 (0.76–0.98), P < 0.05] predicted composite endpoint independently. Using time-varying analyses, the predictive strength of HDL cholesterol was increased [HR = 0.36 (0.30–0.44) per mmol/l, P < 0.001], whereas that of total cholesterol [HR = 1.03 (0.97–1.09) per mmol/l, NS] and treatment allocation [HR = 0.91 (0.80–1.03), NS] were reduced. Conclusion: Losartan blunted the decrease in HDL cholesterol during antihypertensive treatment in the LIFE study. Higher intreatment HDL cholesterol was associated with fewer composite endpoints and may partly explain the better outcome of losartan-based treatment.
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