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J. Michael DiMaio

Researcher at University of Texas Southwestern Medical Center

Publications -  117
Citations -  7788

J. Michael DiMaio is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 32, co-authored 71 publications receiving 7113 citations. Previous affiliations of J. Michael DiMaio include Saint Paul University.

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Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis

TL;DR: It is concluded that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair

TL;DR: It is shown that the G-actin sequestering peptide thymosin β4 promotes myocardial and endothelial cell migration in the embryonic heart and retains this property in postnatal cardiomyocytes and that the pathway it regulates may be a new therapeutic target in the setting of acute myocardIAL damage.
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Immortalization of Human Bronchial Epithelial Cells in the Absence of Viral Oncoproteins

TL;DR: Cytogenetic analysis and array comparative genomic hybridization profiling show immortalized HBECs to have duplication of parts of chromosomes 5 and 20, and microarray gene expression profiling demonstrates that the Cdk4/hTERT-immortalized bronchial cell lines clustered together and with nonimmortalization bronchia cells, distinct from lung cancer cell lines.
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Reprogramming of human fibroblasts toward a cardiac fate

TL;DR: Findings indicate that human fibroblasts can be reprogrammed to cardiac-like myocytes by forced expression of cardiac transcription factors with muscle-specific microRNAs and represent a step toward possible therapeutic application of this reprogramming approach.
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Genetic Defects in Surfactant Protein A2 Are Associated with Pulmonary Fibrosis and Lung Cancer

TL;DR: A rare missense mutation in a candidate gene, SFTPA2, within the interval encoding surfactant protein A2 (SP-A2) was identified and another rare mutation in S FTPA2 was identified in another family with IPF and lung cancer.