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Lei Tian

Researcher at Stanford University

Publications -  81
Citations -  2125

Lei Tian is an academic researcher from Stanford University. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 18, co-authored 59 publications receiving 1070 citations. Previous affiliations of Lei Tian include Cardiovascular Institute of the South & Chinese Academy of Sciences.

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Single-cell RNA sequencing in cardiovascular development, disease and medicine.

TL;DR: The currently available scRNA-seq technologies and analytical tools are summarized and the latest findings using sc RNA-seq that have substantially improved knowledge on the development of the cardiovascular system and the mechanisms underlying cardiovascular diseases are discussed.
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Single-Cell RNA Sequencing Unveils Unique Transcriptomic Signatures of Organ-Specific Endothelial Cells

TL;DR: This work uses scRNA-seq data generated by the Tabula Muris consortium to uncover transcriptional networks that maintain tissue-specific EC identity and to identify novel angiocrine and functional relationships between tissue- specific ECs.
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Human-Induced Pluripotent Stem Cell Model of Trastuzumab-Induced Cardiac Dysfunction in Patients With Breast Cancer.

TL;DR: It is found that clinically relevant doses of trastuzumab significantly impaired the contractile and calcium-handling properties of iPSC-CMs without inducing cardiomyocyte death or sarcomeric disorganization, and targeting the altered metabolism may be a promising therapeutic approach for trastzumab-induced cardiac dysfunction.
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Large-Scale Single-Cell RNA-Seq Reveals Molecular Signatures of Heterogeneous Populations of Human Induced Pluripotent Stem Cell-Derived Endothelial Cells.

TL;DR: Massively parallel, droplet-based scRNA-seq allowed meticulous analysis of thousands of human iPSCs subjected to iPSC-EC differentiation, which showed inefficiency of the differentiation technique, which can be improved with further studies based on identification of molecular signatures that inhibit expansion of nonendothelial cell types.