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Aleš Linhart

Researcher at First Faculty of Medicine, Charles University in Prague

Publications -  371
Citations -  36568

Aleš Linhart is an academic researcher from First Faculty of Medicine, Charles University in Prague. The author has contributed to research in topics: Fabry disease & Medicine. The author has an hindex of 50, co-authored 333 publications receiving 30467 citations. Previous affiliations of Aleš Linhart include University Hospital of Wales & Charles University in Prague.

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Plasma osteopontin levels, but not its myocardial expression, reflect heart failure severity in recently diagnosed dilated cardiomyopathy

TL;DR: Plasma OPN levels reflect heart failure severity in patients with recent-onset DCM (Ro-DCM), and myocardial OPN expression is not associated with either plasma OPN Levels or markers of heart failure in these individuals.
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Narrative review on Morbus Fabry: diagnosis and management of cardiac manifestations.

TL;DR: The objective of this review is to summarize the current knowledge on cardiac manifestations of FD and effects of targeted therapy, which recently became available for patients carrying amenable pathogenic GLA variants.
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Uric Acid as a Marker of Mortality and Morbidity in Fabry Disease.

TL;DR: Increased serum UA levels may represent an independent risk factor for adverse clinical outcomes in Fabry patients and are associated with all-cause mortality and morbidity in FD.
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Serum Bilirubin and Markers of Oxidative Stress and Inflammation in a Healthy Population and in Patients with Various Forms of Atherosclerosis

TL;DR: In this paper , Bilirubin and the markers of oxidative stress and inflammation in both healthy subjects and patients with various forms of atherosclerosis were assessed, and it was shown that elevated serum bilirubins are positively correlated with TAS, and negatively related to inflammatory markers.
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Serum Bilirubin Levels and Promoter Variations in HMOX1 and UGT1A1 Genes in Patients with Fabry Disease

TL;DR: Markedly lower serum bilirUBin levels in FD patients seem to be due to bilirubin consumption during increased oxidative stress, although UGT1A1 promoter gene polymorphism may modify the manifestation of FD as well.