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Per Ladenvall

Researcher at University of Gothenburg

Publications -  20
Citations -  1262

Per Ladenvall is an academic researcher from University of Gothenburg. The author has contributed to research in topics: Stroke & T-plasminogen activator. The author has an hindex of 13, co-authored 19 publications receiving 1156 citations. Previous affiliations of Per Ladenvall include Sahlgrenska University Hospital.

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Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data

G. Eiriksdottir, +137 more
TL;DR: Human genetic data indicate that C reactive protein concentration itself is unlikely to be even a modest causal factor in coronary heart disease.
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Serum C-Reactive Protein Concentration and Genotype in Relation to Ischemic Stroke Subtype

TL;DR: 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, and Genetic variants at the CRP locus showed significant associations with CRP levels, however, neither CRP genotypes nor haplotypes showed an association to overall isChemic stroke.
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Fibrinolytic Gene Polymorphism and Ischemic Stroke

TL;DR: Neither the tPA −7351C>T nor the PAI-1 to 675 4G >5G polymorphism showed significant association with ischemic stroke, consistent with a more complex role for tPA and PAi-1 in the brain as compared with the heart.
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Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction.

TL;DR: Testing the hypothesis that the tPA -7,351C/T polymorphism is associated with myocardial infarction suggests that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.
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Gene Polymorphism of t-PA is Associated With Forearm Vascular Release Rate of t-PA

TL;DR: Results provide the first evidence of an association between a common genetic variation at the t-PA locus and interindividual differences in net release rates of t- PA in vivo, not reflected by circulating steady-state plasma levels and can thus not be disclosed by conventional venous plasma sampling.