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Sökning: WFRF:(Jood Katarina) > Chalmers tekniska högskola

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  • Hanson, Ellen, et al. (författare)
  • Genetic Variants of Coagulation Factor XI Show Association with Ischemic Stroke Up to 70 Years of Age
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Coagulation factor XI (FXI) has an important role in the propagation and stabilization of a thrombus upon vessel injury. High FXI levels have been implicated in thrombotic diseases including ischemic stroke. The aim of our study was to investigate whether FXI gene (F11) variants are associated with ischemic stroke. The discovery sample, the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), included 844 patients with ischemic stroke and 668 controls, all aged 18-70 years. Replication was performed in the Lund Stroke Register (LSR) and Malmö Diet and Cancer study (MDC), together including 1213 patients and 788 controls up to 70 years of age, and in total 3145 patients and 1793 controls (18-102 years). Seven F11 single-nucleotide polymorphisms (SNPs) were selected using a tagging approach. The SNPs rs3733403, rs925451, and rs1593 showed independent associations with overall ischemic stroke in SAHLSIS, ORs of 0.74 (95% CI 0.59-0.94), 1.24 (95% CI 1.06-1.46), and 0.70 (95% CI 0.55-0.90), respectively. The association for rs925451 was replicated in the LSR and MDC sample in a pre-specified analysis of subjects aged 70 years or younger, OR of 1.16 (95% CI 1.00-1.34), whereas no SNP was replicated when all ages were included. In line with this, one F11 haplotype was associated with overall ischemic stroke in the discovery sample and in the replication sample ≤70 years. We found significant associations between F11 variation and overall ischemic stroke up to 70 years of age. These findings motivate further studies on the role of F11 in ischemic stroke, especially in younger individuals.
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  • Hanson, Ellen, et al. (författare)
  • No evidence for an association between ABO blood group and overall ischemic stroke or any of the major etiologic subtypes
  • 2012
  • Ingår i: Thrombosis Research. - : Elsevier BV. - 0049-3848 .- 1879-2472. ; 130:3, s. 339-342
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The ABO blood group system is encoded by one gene, ABO. Previous studies have reported an association between blood group non-O (i.e. phenotype A, B or AB) and myocardial infarction. Studies on stroke and ABO are, however, more scarce. Therefore, we aimed to investigate whether ABO phenotype or genotype is associated with ischemic stroke and/or etiologic subtypes of ischemic stroke. Materials and methods: The study was performed in the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), which comprises 600 patients with ischemic stroke before the age of 70 years, and 600 matched controls. Patients were classified according to the TOAST criteria. Results: There was no significant association between ABO phenotype (blood group O vs. non-O) and overall ischemic stroke (multivariable odds ratio of 0.9, 95% confidence interval 0.7-1.2). This was also true for blood group O vs. A and O vs. B. Furthermore, no association between ABO genotypes and ischemic stroke was detected. The ischemic stroke subtype analysis was confined to large-vessel disease, small-vessel disease, cardioembolic stroke and cryptogenic stroke. In this analysis, there was no significant association between any ischemic stroke subtype and ABO phenotype or genotype. Conclusions: The findings in this study suggest that ABO phenotype or genotype does not have a major impact in the pathophysiology of ischemic stroke or any of the ischemic stroke subtypes.
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  • Hanson, Ellen, et al. (författare)
  • Plasma factor VII-activating protease antigen levels and activity are increased in ischemic stroke.
  • 2012
  • Ingår i: Journal of thrombosis and haemostasis : JTH. - : Elsevier BV. - 1538-7836 .- 1538-7933. ; 10:5, s. 848-56
  • Tidskriftsartikel (refereegranskat)abstract
    • Factor VII-activating protease (FSAP) is a recently discovered plasma protease with a role in the regulation of hemostasis and vascular remodeling processes. Higher levels and activity of FSAP have been reported in patients with deep vein thrombosis, but there are no data on plasma FSAP in ischemic stroke (IS).
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  • Hanson, Ellen, et al. (författare)
  • Plasma levels of von Willebrand factor in the etiologic subtypes of ischemic stroke
  • 2011
  • Ingår i: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 9:2, s. 275-281
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Compared with coronary artery disease, there are few studies on von Willebrand factor (VWF) in ischemic stroke (IS). Moreover, there is little information on VWF in the etiologic subtypes of IS. Objectives: The aim of the present study was to investigate VWF in IS and in the etiologic subtypes of IS. Patients/methods: The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) is a case-control study comprising 600 patients and 600 matched controls. Etiologic IS subtype was defined according to the TOAST criteria. Blood sampling was performed in the acute phase and after 3 months. Results: The levels of VWF were increased in overall IS, at both time-points. The 3-month VWF levels were increased in the subtypes of large-vessel disease (LVD), cardioembolic (CE) stroke and cryptogenic stroke, but not in the subtype of small-vessel disease (SVD), as compared with the controls. The acute phase VWF levels were significantly increased in all four subtypes. In the multivariate regression analysis, with vascular risk factors as covariates, the 3-month VWF levels were associated with CE stroke and cryptogenic stroke, and the acute phase VWF levels with all subtypes. There were significant subtype-specific differences in VWF, with the highest levels in LVD and CE stroke. Conclusions: The present results show that VWF levels are increased in patients with IS. Furthermore, the VWF levels differ between etiologic IS subtypes and thus, it is important to consider etiologic subtypes in future studies of VWF in patients with IS.
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  • Jalo, Hoor, 1994, et al. (författare)
  • Early identification and characterisation of stroke to support prehospital decision-making using artificial intelligence : A scoping review protocol
  • 2023
  • Ingår i: BMJ Open. - : BMJ Publishing Group. - 2044-6055. ; 13:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction Stroke is a time-critical condition and one of the leading causes of mortality and disability worldwide. To decrease mortality and improve patient outcome by improving access to optimal treatment, there is an emerging need to improve the accuracy of the methods used to identify and characterise stroke in prehospital settings and emergency departments (EDs). This might be accomplished by developing computerised decision support systems (CDSSs) that are based on artificial intelligence (AI) and potential new data sources such as vital signs, biomarkers and image and video analysis. This scoping review aims to summarise literature on existing methods for early characterisation of stroke by using AI. Methods and analysis The review will be performed with respect to the Arksey and O'Malley's model. Peer-reviewed articles about AI-based CDSSs for the characterisation of stroke or new potential data sources for stroke CDSSs, published between January 1995 and April 2023 and written in English, will be included. Studies reporting methods that depend on mobile CT scanning or with no focus on prehospital or ED care will be excluded. Screening will be done in two steps: title and abstract screening followed by full-text screening. Two reviewers will perform the screening process independently, and a third reviewer will be involved in case of disagreement. Final decision will be made based on majority vote. Results will be reported using a descriptive summary and thematic analysis. Ethics and dissemination The methodology used in the protocol is based on information publicly available and does not need ethical approval. The results from the review will be submitted for publication in a peer-reviewed journal. The findings will be shared at relevant national and international conferences and meetings in the field of digital health and neurology. © 2023 BMJ Publishing Group. All rights reserved.
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  • Jood, Katarina, 1966, et al. (författare)
  • Fibrinolytic gene polymorphism and ischemic stroke
  • 2005
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 36:10, s. 2077-81
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. METHODS: In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. RESULTS: There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. CONCLUSIONS: Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart.
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  • Ladenvall, Claes, 1974, et al. (författare)
  • Serum C-reactive protein concentration and genotype in relation to ischemic stroke subtype
  • 2006
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 37:8, s. 2018-23
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: C-reactive protein (CRP) has evolved as an inflammatory risk marker of cardiovascular disease. Several single-nucleotide polymorphisms at the CRP locus have been found to be associated with CRP levels. The aim of the present study was to investigate CRP levels and genetic variants in etiological subtypes of ischemic stroke. METHODS: The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) comprises 600 consecutive ischemic stroke cases (18 to 69 years) and 600 matched controls from western Sweden. Stroke subtypes were defined by the TOAST classification. Serum CRP levels were determined by a high-sensitivity immunometric assay. RESULTS: CRP levels were significantly higher for all ischemic stroke subtypes compared with controls, both in the acute phase and at the 3-month follow-up. After adjustment for traditional risk factors, CRP at follow-up was related to higher odds ratios (ORs) of overall ischemic stroke (OR, 1.25; 95% CI, 1.09 to 1.43) and large-vessel disease (OR, 1.48; 95% CI, 1.09 to 2.00). The CRP -286C>T>A, 1059G>C, and 1444C>T single-nucleotide polymorphisms showed significant associations with CRP levels. However, neither CRP genotypes nor haplotypes showed an association to overall ischemic stroke. CONCLUSIONS: This is the first large study on CRP in different TOAST subtypes in a young ischemic stroke population. CRP levels differed between etiological subtypes of ischemic stroke both in the acute phase and at the 3-month follow-up. CRP at follow-up was associated with overall ischemic stroke and the large-vessel disease subtype. Genetic variants at the CRP locus were associated with CRP levels, but no association was detected for overall ischemic stroke.
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  • Ladenvall, Per, 1972, et al. (författare)
  • Genetic variation at the human tissue-type plasminogen activator (tPA) locus: haplotypes and analysis of association to plasma levels of tPA.
  • 2003
  • Ingår i: European journal of human genetics : EJHG. - : Springer Science and Business Media LLC. - 1018-4813 .- 1476-5438. ; 11:8, s. 603-10
  • Tidskriftsartikel (refereegranskat)abstract
    • Tissue-type plasminogen activator (tPA) plays a key role in thrombus dissolution and plasma levels of tPA have been associated with cardiovascular disease. We have previously resequenced regulatory and coding regions of the human tPA gene (PLAT) and identified eight single-nucleotide polymorphisms (SNPs). In a small experimental study, four common variants were associated with invasively determined vascular tPA release rates. The aim of the present study was to investigate whether there is an association between genetic variants at this locus and plasma levels of tPA. To this end, 240 Swedish individuals without cardiovascular disease were typed for the eight SNPs and an Alu insertion polymorphism at the PLAT locus, as well as for a polymorphism in the plasminogen activator inhibitor type 1 (PAI-1) promoter (PAI-1 -675 4G>5G). Stepwise regression analysis, with established predictors of plasma tPA including plasma PAI-1 and genetic variants, showed that neither genotypes nor haplotypes were major contributors to plasma tPA. The results also showed that the level of linkage disequilibrium was high at the PLAT locus, as demonstrated by the fact that only three haplotypes had a frequency above 5%. In conclusion, in the present study neither genetic variation at the PLAT locus nor the PAI-1 -675 4G>5G polymorphism was strong predictors of plasma tPA levels, which suggests that variations in other genes contribute to the heritability of this phenotype. The results also show that three haplotypes at the PLAT locus accounted for nearly 90% of the chromosomes and that they could be defined by typing only two SNPs.
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