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Bin Zhou

Researcher at Chinese Academy of Sciences

Publications -  469
Citations -  29938

Bin Zhou is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Medicine & Stem cell. The author has an hindex of 71, co-authored 394 publications receiving 21049 citations. Previous affiliations of Bin Zhou include Lawrence Berkeley National Laboratory & University of Oxford.

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Metascape provides a biologist-oriented resource for the analysis of systems-level datasets.

TL;DR: A biologist-oriented portal that provides a gene list annotation, enrichment and interactome resource and enables integrated analysis of multi-OMICs datasets, Metascape is an effective and efficient tool for experimental biologists to comprehensively analyze and interpret OMICs-based studies in the big data era.
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Epicardial progenitors contribute to the cardiomyocyte lineage in the developing heart

TL;DR: A novel cardiogenic precursor marked by expression of the transcription factor Wt1 and located within the epicardium—an epithelial sheet overlying the heart is identified and identified as previously unrecognized cardiomyocyte progenitors.
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De novo cardiomyocytes from within the activated adult heart after injury

TL;DR: It is demonstrated in mice that the adult heart contains a resident stem or progenitor cell population, which has the potential to contribute bona fide terminally differentiated cardiomyocytes after myocardial infarction and is shown to structurally and functionally integrate with resident muscle.
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A long noncoding RNA protects the heart from pathological hypertrophy

TL;DR: The role of long noncoding RNA (lncRNA) in adult heart is unknown; also unclear is how lncRNA modulates nucleosome remodelling as discussed by the authors. But they identify a cluster of LncRNA transcripts from myosin heavy chain 7 (Myh7) loci and demonstrate a new lnc RNA-chromatin mechanism for heart failure.
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Resident fibroblast lineages mediate pressure overload–induced cardiac fibrosis

TL;DR: Following pressure overload, fibroblasts were not derived from hematopoietic cells, EndoMT, or epicardial epithelial-to-mesenchymal transition; instead, pressure overload promoted comparable proliferation and activation of two resident fibroblast lineages, including a previously described epicardsial population and a population of endothelial origin.