scispace - formally typeset
A

Adam Pleister

Researcher at Ohio State University

Publications -  20
Citations -  863

Adam Pleister is an academic researcher from Ohio State University. The author has contributed to research in topics: Heart failure & Chromosome 21. The author has an hindex of 11, co-authored 20 publications receiving 749 citations.

Papers
More filters
Journal ArticleDOI

Sleep disordered breathing and post-discharge mortality in patients with acute heart failure

TL;DR: This is the largest study to date to evaluate the effect of SDB on post-discharge mortality in patients with AHF and it shows that newly diagnosed CSA and OSA during AHF hospitalization are independently associated with post- disordered breathing mortality.
Journal ArticleDOI

Human chromosome 21-derived miRNAs are overexpressed in down syndrome brains and hearts.

TL;DR: It is hypothesized that trisomic 21 gene dosage overexpression of Hsa21-derived miRNAs results in the decreased expression of specific target proteins and contribute, in part, to features of the neuronal and cardiac DS phenotype.
Journal Article

Cardiomyopathy: an overview.

TL;DR: Although cardiomyopathy is asymptomatic in the early stages, symptoms are the same as those characteristically seen in any type of heart failure and may include shortness of breath, fatigue, cough, orthopnea, paroxysmal nocturnal dyspnea, and edema.
Journal ArticleDOI

Chromosome 21-derived MicroRNAs Provide an Etiological Basis for Aberrant Protein Expression in Human Down Syndrome Brains

TL;DR: This study demonstrates by luciferase/target mRNA 3′-untranslated region reporter assays that miR-155 and -802 can regulate the expression of the predicted mRNA target, the methyl-CpG-binding protein (MeCP2), and demonstrates that selective inactivation of Hsa21-derived miRNAs may provide a novel therapeutic tool in the treatment of DS.
Journal ArticleDOI

Endothelial nitric oxide synthase uncoupling: A novel pathway in OSA induced vascular endothelial dysfunction

TL;DR: It is found that eNOS is dysfunctional in OSA patients pre-treatment, and is a source of endothelial O2(•-) overproduction, and a potentially targetable pathway for treatment of cardiovascular risk in Osa.