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Benjamin Meder

Researcher at Heidelberg University

Publications -  226
Citations -  9623

Benjamin Meder is an academic researcher from Heidelberg University. The author has contributed to research in topics: Dilated cardiomyopathy & Medicine. The author has an hindex of 49, co-authored 198 publications receiving 7530 citations. Previous affiliations of Benjamin Meder include University Hospital Heidelberg & Stanford University.

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Left ventricular long axis strain: a new prognosticator in non-ischemic dilated cardiomyopathy?

TL;DR: Assessment of long axis function with LAS offers significant incremental information for the prediction of cardiac events in NIDCM and improves risk stratification beyond established CMR parameters.
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Diagnosis and treatment of cardiac amyloidosis: position statement of the German Cardiac Society (DGK)

TL;DR: In this article, the main objective of the diagnostic algorithm outlined in this position statement is to detect cardiac amyloidosis as reliably and early as possible, to accurately determine its extent, and to reliably identify the underlying subtype of amyloids, thereby enabling subsequent targeted treatment.
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Next-Generation Sequencing: From Understanding Biology to Personalized Medicine

TL;DR: It is illustrated how next-generation sequencing technologies help to constantly improve the authors' understanding of genetic mechanisms in biological systems and summarize the progress made so far in the case of heritable heart muscle diseases.
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Paleoproteomic study of the Iceman's brain tissue.

TL;DR: The proteome of two distinct brain samples is studied using gel-based and liquid chromatography–mass spectrometry-based proteomics technologies together with a multiple-databases and -search algorithms-driven data-analysis approach, finding 41 proteins known to be highly abundant in brain tissue and 9 specifically expressed in the brain.
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Protein Kinase D2 Controls Cardiac Valve Formation in Zebrafish by Regulating Histone Deacetylase 5 Activity

TL;DR: In this article, a missense mutation in zebrafish protein kinase D2 (pkd2) was found to selectively perturb valve formation in the embryonic heart by abrogating endocardial Notch signaling in cardiac cushions.