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1.
  • Olofsson, P, et al. (författare)
  • Genetic variants of TNFSF4 and risk for carotid artery disease and stroke
  • 2008
  • Ingår i: Journal of Molecular Medicine. - New York : Springer. - 0946-2716 .- 1432-1440. ; 87:4, s. 337-346
  • Tidskriftsartikel (refereegranskat)abstract
    • In two independent human cohorts, the minor allele of SNP rs3850641 in TNFSF4 was significantly more frequent in individuals with myocardial infarction than in controls. In mice, Tnfsf4 expression is associated with increased atherosclerosis. The expression of TNFSF4 in human atherosclerosis and the association between genotype and cerebrovascular disease have not yet been investigated. TNFSF4 messenger RNA (mRNA) levels were significantly higher in human atherosclerotic lesions compared with controls (730 +/- 30 vs 330 +/- 65 arbitrary units, p < 0.01). TNFSF4 was mainly expressed by macrophages in atherosclerotic lesions. In cell culture, endothelial cells upregulated TNFSF4 in response to tumor necrosis factor alpha (TNF-alpha; 460 +/- 110 vs 133 +/- 8 arbitrary units, p < 0.001 after 6 h of stimulation). We analyzed the TNFSF4 gene in 239 patients who had undergone carotid endarterectomy and 138 matching controls from The Biobank of Karolinska Carotid Endarterectomies and Stockholm Heart Epidemiology Program cohorts and 929 patients and 1,382 matching controls from the Sahlgrenska Academy Study on Ischemic Stroke and Case Control Study of Stroke cohorts, limiting inclusion to patients with ischemic stroke. Participants were genotyped for the rs3850641 SNP in TNFSF4. Genotype associations were neither found with TNFSF4 mRNA levels nor with atherosclerosis associated systemic factors or risk for stroke. This study shows that TNFSF4 is expressed on antigen-presenting cells in human carotid atherosclerotic lesions but provides no evidence for an association of TNFSF4 gene variation with the risk for ischemic stroke.
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2.
  • Andersson, Malin E, 1978, et al. (författare)
  • Kinesin gene variability may affect tau phosphorylation in early Alzheimer's disease.
  • 2007
  • Ingår i: International journal of molecular medicine. - : D.A. Spandidos. - 1107-3756 .- 1791-244X. ; 20:2, s. 233-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Kinesin is a microtubule-associated motor protein that transports Alzheimer-associated amyloid precursor protein (APP) in neurons. In animal models, impaired kinesin-mediated APP transport seems to enhance formation of the neurotoxic 42 amino acid fragment of beta-amyloid (A beta 42). In man, one study suggests that a polymorphism (rs8702, 56,836G>C) in the kinesin light chain 1 gene (KNS2) may affect the risk of Alzheimer's disease (AD). To further assess KNS2 as a susceptibility gene for AD we analyzed 802 patients with sporadic AD and 286 controls, 134 longitudinally followed patients with mild cognitive impairment (MCI) and 39 cognitively stable controls for the rs8702 polymorphism. The rs8702 polymorphism did not influence risk of AD (p=0.46). However, rs8702 interacted with APOE epsilon 4 carrier status in AD (p=0.006) and influenced cerebrospinal fluid levels of hyperphosphorylated tau in MCI patients who converted to AD during follow-up (p=0.018). These findings support earlier indications that genetic variability in the KNS2 gene may play a role during early stages of AD pathogenesis.
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3.
  • Björkman, Jan-Arne, et al. (författare)
  • Cardiac sympathetic nerve stimulation triggers coronary t-PA release.
  • 2003
  • Ingår i: Arteriosclerosis, thrombosis, and vascular biology. - 1524-4636. ; 23:6, s. 1091-7
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: This study was undertaken to determine whether stimulation of sympathetic cardiac nerves induces release of the thrombolytic enzyme tissue-type plasminogen activator (t-PA) in the coronary vascular bed. METHODS AND RESULTS: Anesthetized pigs were studied in an open chest model. Bilateral vagotomy was performed, and sympathetic cardiac nerves were activated by electrical stimulation (1 and 8 Hz). To evaluate possible mediating effects of increased heart rate and enhanced local blood flow, tachycardia was induced by pacing and hyperemia by local infusion of sodium nitroprusside and clevedipine. Furthermore, to study the effects of alpha- and beta-adrenergic receptor stimulation, phenylephrine and isoprenaline were infused locally. In response to low- and high-frequency sympathetic stimulation, mean coronary net release of total t-PA increased approximately 6- and 25-fold, respectively. Active t-PA showed a similar response pattern. Neither tachycardia nor coronary hyperemia stimulated t-PA release. In contrast, beta-adrenergic stimulation by isoprenaline induced an approximately 6-fold increase in coronary t-PA release, whereas no significant change in release rates occurred in response to alpha-adrenergic stimulation by phenylephrine. CONCLUSIONS: Stimulation of cardiac sympathetic nerves induces a marked coronary release of t-PA, and part of this response may be mediated through stimulation of beta-adrenergic receptors.
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4.
  • Chauhan, G., et al. (författare)
  • Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting
  • 2019
  • Ingår i: Neurology. - : American Academy of Neurology. - 0028-3878 .- 1526-632X. ; 92:5, s. E486-E503
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveTo explore genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts.MethodsWe performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely, small subcortical BI (SSBI), in 18 population-based cohorts (n = 20,949) from 5 ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in 7 population-based cohorts (n = 6,862; 1,483 with BI, 630 with SBBI), and we tested associations with related phenotypes including ischemic stroke and pathologically defined BI.ResultsThe mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, p = 1.77 x 10(-8); and LINC00539/ZDHHC20, p = 5.82 x 10(-9). Both have been associated with blood pressure (BP)-related phenotypes, but did not replicate in the smaller follow-up sample or show associations with related phenotypes. Age- and sex-adjusted associations with BI and SSBI were observed for BP traits (p value for BI, p([BI]) = 9.38 x 10(-25); p([SSBI]) = 5.23 x 10(-14) for hypertension), smoking (p([BI]) = 4.4 x 10(-10); p([SSBI]) = 1.2 x 10(-4)), diabetes (p([BI]) = 1.7 x 10(-8); p([SSBI]) = 2.8 x 10(-3)), previous cardiovascular disease (p([BI]) = 1.0 x 10(-18); p([SSBI]) = 2.3 x 10(-7)), stroke (p([BI]) = 3.9 x 10(-69); p([SSBI]) = 3.2 x 10(-24)), and MRI-defined white matter hyperintensity burden (p([BI]) = 1.43 x 10(-157); p([SSBI]) = 3.16 x 10(-106)), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p 0.0022), without indication of directional pleiotropy.ConclusionIn this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI.
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5.
  • Cole, John W, et al. (författare)
  • Genetics of the thrombomodulin-endothelial cell protein C receptor system and the risk of early-onset ischemic stroke.
  • 2018
  • Ingår i: PloS one. - : Public Library of Science. - 1932-6203. ; 13:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Polymorphisms in coagulation genes have been associated with early-onset ischemic stroke. Here we pursue an a priori hypothesis that genetic variation in the endothelial-based receptors of the thrombomodulin-protein C system (THBD and PROCR) may similarly be associated with early-onset ischemic stroke. We explored this hypothesis utilizing a multi-stage design of discovery and replication.Discovery was performed in the Genetics-of-Early-Onset Stroke (GEOS) Study, a biracial population-based case-control study of ischemic stroke among men and women aged 15-49 including 829 cases of first ischemic stroke (42.2% African-American) and 850 age-comparable stroke-free controls (38.1% African-American). Twenty-four single-nucleotide-polymorphisms (SNPs) in THBD and 22 SNPs in PROCR were evaluated. Following LD pruning (r2≥0.8), we advanced uncorrelated SNPs forward for association analyses. Associated SNPs were evaluated for replication in an early-onset ischemic stroke population (onset-age<60 years) consisting of 3676 cases and 21118 non-stroke controls from 6 case-control studies. Lastly, we determined if the replicated SNPs also associated with older-onset ischemic stroke in the METASTROKE data-base.Among GEOS Caucasians, PROCR rs9574, which was in strong LD with 8 other SNPs, and one additional independent SNP rs2069951, were significantly associated with ischemic stroke (rs9574, OR = 1.33, p = 0.003; rs2069951, OR = 1.80, p = 0.006) using an additive-model adjusting for age, gender and population-structure. Adjusting for risk factors did not change the associations; however, associations were strengthened among those without risk factors. PROCR rs9574 also associated with early-onset ischemic stroke in the replication sample (OR = 1.08, p = 0.015), but not older-onset stroke. There were no PROCR associations in African-Americans, nor were there any THBD associations in either ethnicity.PROCR polymorphisms are associated with early-onset ischemic stroke in Caucasians.
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6.
  • Ekblom, Maria M., et al. (författare)
  • Device-measured sedentary behavior, physical activity and aerobic fitness are independent correlates of cognitive performance in healthy middle-aged adults—results from the SCAPIS pilot study
  • 2019
  • Ingår i: International Journal of Environmental Research and Public Health. - : MDPI. - 1661-7827 .- 1660-4601. ; 16:24
  • Tidskriftsartikel (refereegranskat)abstract
    • © 2019 by the authors. Licensee MDPI, Basel, Switzerland. High aerobic fitness, more moderate to vigorous physical activity (MVPA) and less sedentary behavior (SED) have all been suggested to promote cognitive functions, but it is unclear whether they are independent predictors of specific cognitive domains. This study aimed to investigate to what extent aerobic fitness MVPA and SED are independently associated with cognitive performance among middle-aged Swedish adults. We acquired device-based measures of aerobic fitness, cognitive performance and percent daily time spent in MVPA and SED in Swedish adults (n = 216; 54–66 years old). Aerobic fitness was associated with better performance at one out of two tests of speed/attention and one out of four tests of executive attention, and with worse performance at one of seven tests of memory. Increasing %MVPA was associated with better performance at one out of seven tests of memory and two out of three tests of verbal ability, whereas increasing %SED was associated with better performance at all four tests of executive attention and four out of seven tests of memory. These findings suggest that aerobic fitness, %MVPA and %SED are partly independent correlates of cognitive performance. To fully understand the association between SED and performance at several tests of cognitive function, future investigations might attempt to investigate intellectually engaging SED (such as reading books) separately from mentally undemanding SED (such as watching TV).
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7.
  • Franceschini, N., et al. (författare)
  • GWAS and colocalization analyses implicate carotid intima-media thickness and carotid plaque loci in cardiovascular outcomes
  • 2018
  • Ingår i: Nature Communications. - : NATURE PUBLISHING GROUP. - 2041-1723. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Carotid artery intima media thickness (cIMT) and carotid plaque are measures of subclinical atherosclerosis associated with ischemic stroke and coronary heart disease (CHD). Here, we undertake meta-analyses of genome-wide association studies (GWAS) in 71,128 individuals for cIMT, and 48,434 individuals for carotid plaque traits. We identify eight novel susceptibility loci for cIMT, one independent association at the previously-identified PINX1 locus, and one novel locus for carotid plaque. Colocalization analysis with nearby vascular expression quantitative loci (cis-eQTLs) derived from arterial wall and metabolic tissues obtained from patients with CHD identifies candidate genes at two potentially additional loci, ADAMTS9 and LOXL4. LD score regression reveals significant genetic correlations between cIMT and plaque traits, and both cIMT and plaque with CHD, any stroke subtype and ischemic stroke. Our study provides insights into genes and tissue-specific regulatory mechanisms linking atherosclerosis both to its functional genomic origins and its clinical consequences in humans. © 2018, The Author(s).
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8.
  • Gerafi, Joel, et al. (författare)
  • Neglect and aphasia in the acute phase as predictors of functional outcome 7 years after ischemic stroke
  • 2017
  • Ingår i: European Journal of Neurology. - : Wiley-Blackwell Publishing Inc.. - 1351-5101 .- 1468-1331. ; 24:11, s. 1407-1415
  • Tidskriftsartikel (refereegranskat)abstract
    • © 2017 EAN Background and purpose: Visuospatial inattention (VSI) and language impairment (LI) are often present early after stroke and associations with an unfavorable short-term functional outcome have been reported. The purpose of this study was to investigate whether a screening of VSI and LI as indicators of cortical symptoms early after stroke could predict long-term functional outcomes. Methods: A consecutive cohort of 375 patients with ischemic stroke was assessed for the occurrence of VSI at a median of 7 days after admission (interquartile range, 1–5 days) using the Star Cancellation Test and for LI (within the first 7 days) with the language item in the Scandinavian Stroke Scale. Seven years later, functional outcomes were assessed by the modified Rankin scale and Frenchay Activities Index in 235 survivors without recurrent stroke. Relationships between baseline predictors and functional outcome at 7 years were analyzed with bivariate correlations and multiple categorical regressions with optimal scaling. Results: The regression model significantly explained variance in the modified Rankin scale (R 2 = 0.435, P < 0.001) and identified VSI (P = 0.001) and neurological deficits (P < 0.001; Scandinavian Stroke Scale score without the language item) as the significant independent predictors. The model for Frenchay Activities Index was also significant (R 2 = 0.269, P < 0.001) with VSI (P = 0.035) and neurological deficits (P < 0.001) as significant independent predictors. Conclusions: Visuospatial inattention at acute stroke has an independent impact on long-term functional outcomes. Early recognition may enable targeted rehabilitative interventions.
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9.
  • Giang, Kok Wai, 1984, et al. (författare)
  • Long-term trends in the prevalence of patients hospitalized with ischemic stroke from 1995 to 2010 in Sweden
  • 2017
  • Ingår i: Plos One. - 1932-6203. ; 12:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective The prevalence of stroke is expected to increase partly because of prolonged life expectancy in the general population. The objective of this study was to investigate trends in the prevalence of patients hospitalized with ischemic stroke (IS) in Sweden from 1995-2010. The Swedish inpatient and cause-specific death registries were used to estimate the absolute numbers and prevalence of patients who were hospitalized with and survived an IS from 1995-2010. The overall number of IS increased from 129,418 in 1995 to 148,778 in 2010. In 1995, the prevalence of IS was 189 patients per 10,000 population. An increase in overall prevalence was observed until 2000, and then it remained stable, followed by a decline with an annual percentage change of (APC)-0.8% (95% CI -1.0 to 0.6) and with a final prevalence of 199 patients per 10,000 population in 2010. The prevalence of IS in people aged <45 years increased from 6.4 in 1995 to 7.6 patients per 10,000 population in 2010, with an APC of 2.1% (95% CI 0.9 to 3.4) from 1995-1998 and 0.7% (95% CI 0.6-0.9) from 1998-2010. Among those aged 45-54 years, the prevalence rose through the mid to late 1990s, followed by a slight decrease (APC:-0.7%, 95% CI -1.1 to -0.4) until 2006 and then remained stable with a prevalence of 43.8 patients per 10,000 population in 2010. Among >= 85 years, there was a minor decrease (APC: -0.3%, 95% CI -0.5 to -0.1) in overall prevalence after 2002 from 1481 to 1453 patients per 10,000 population in 2010. The overall prevalence of IS increased until 2000, but then remained stable followed by a slight decline. However, the prevalence of IS in the young increased through the study period. The absolute number of IS survivors has markedly increased, mainly because of demographic changes.
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10.
  • Giang, Kok Wai, 1984, et al. (författare)
  • Trends in risk of recurrence after the first ischemic stroke in adults younger than 55 years of age in Sweden
  • 2016
  • Ingår i: International Journal of Stroke. - 1747-4930. ; 11:1, s. 52-61
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Previous studies on stroke recurrence in younger adults often contain small sample size which makes it difficult to study trends in stroke recurrence over a long period of time. Aims: The aim of the present study was to investigate temporal trends in the risk of recurrence in younger patients with a first ischemic stroke. Methods: All men and women aged 18-54 years who had survived at least 28 days after a first ischemic stroke from 1987 to 2006 were identified in the Swedish Inpatient Register. The patients were stratified into four 5-year periods according to their admission period and were followed up for a total of four years after the index event with regard to recurrent ischemic stroke. A Cox regression model was used to analyze the risk of recurrent ischemic stroke. Results: Of the 17,149 ischemic stroke patients who were identified, 2432 (14.2%) had a recurrent ischemic stroke event within four years. From the first to the last periods (1987-1991 versus 2002-2006), the four-year risk of recurrent ischemic stroke decreased by 55% (hazard ratio 0.45, 95% confidence interval 0.39-0.53) in men and 59% (hazard ratio 0.41, 95% confidence interval, 0.33-0.50) in women. The cumulative four-year risk was 11.8% (95% CI 10.55-13.25) in men and 9.8% (95% CI 8.40-11.46) in women during the last five-year period (2002-2006). Conclusions: The risk of recurrence among younger ischemic stroke patients has decreased over the past 20 years. Despite these improvements, younger patients are still at a high risk for recurrent ischemic stroke.
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