Heart attack

Hot water immersion therapy for Myocardial Infarction:  Hot water immersion inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 20/November/2018, 11.17 pm
Hot water immersion therapy for Myocardial Infarction:  Hot water immersion inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 20/November/2018, 11.17 pm 960 720 Dr Boomi's Genom-2-Discovery Center

What they say:  A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac ageing and function.” This study was published, in the 7 March  2013 issue of of the journal Nature,  by Prof Dimmler,…

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Molecular therapy for Myocardial Infarction: Empagliflozin (trade name Jardiance), used in the treatment of TIIDM, inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 15/November/2018, 11.48 pm
Molecular therapy for Myocardial Infarction: Empagliflozin (trade name Jardiance), used in the treatment of TIIDM, inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 15/November/2018, 11.48 pm 960 720 Dr Boomi's Genom-2-Discovery Center

What they say:  A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac ageing and function.” This study was published, in the 7 March  2013 issue of of the journal Nature,  by Prof Dimmler,…

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Molecular therapy for cardiac dysfunction: Empagliflozin (trade name: Jardiance), used in the treatment of TIIDM, decreases Mir-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function, via upregulation of its target gene, 15/November/2018, 11.22 pm
Molecular therapy for cardiac dysfunction: Empagliflozin (trade name: Jardiance), used in the treatment of TIIDM, decreases Mir-29 expression, activates Wnt- signaling and its components GSK3B, ICAT/CTNNBIP1, HBP1, and GLIS2, attenuates pathologic hypertrophy, inhibits fibrosis of the heart tissue, and improves cardiac function, via upregulation of its target gene, 15/November/2018, 11.22 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say:   A recent study from the Institute of Pharmacology and Toxicology, Technical University Munich (TUM), 80802, Munich, Germany; DZHK (German Center for Cardiovascular Research), partner site Munich…

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Molecular therapy for safeguarding your heart against cardiac dysfunction: Canagliflozin (trade name: Invokana or Sulisent), a drug used in the treatment of TIIDM,  decreases tumor suppressor Mir-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up-regulation of its target gene, 15/November/2018, 10.02 pm
Molecular therapy for safeguarding your heart against cardiac dysfunction: Canagliflozin (trade name: Invokana or Sulisent), a drug used in the treatment of TIIDM,  decreases tumor suppressor Mir-128 and cyclin-dependent kinase inhibitor p27 expression, increases SUZ12 expression, increases Cyclin E and CDK2 expression, promotes proliferation/re-entry of postnatal/adult cardiomyocytes, attenuates fibrosis, ameliorates cardiac dysfunction, and promotes heart repair in response to myocardial infarction, via up-regulation of its target gene, 15/November/2018, 10.02 pm 960 720 Dr Boomi's Genom-2-Discovery Center

Introduction: What they say: A recent study from Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA; Key Laboratory of Molecular Target and…

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Molecular therapy for Myocardial Infarction: XBP-1, a regulator of mammalian ER stress response, inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 14/November/2018, 12.45 am
Molecular therapy for Myocardial Infarction: XBP-1, a regulator of mammalian ER stress response, inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 14/November/2018, 12.45 am 960 720 Dr Boomi's Genom-2-Discovery Center

What they say:  A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac aging and function.” This study was published, in the 7 March  2013 issue of the journal Nature,  by Prof Dimmler, Boon, and…

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Molecular therapy for Myocardial Infarction: AP-1 (Activator protein-1) inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 13/November/2018, 11.28 pm
Molecular therapy for Myocardial Infarction: AP-1 (Activator protein-1) inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte survival after myocardial infarction, via up-regulation of PNUTS, 13/November/2018, 11.28 pm 960 720 Dr Boomi's Genom-2-Discovery Center

What they say:  A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac ageing and function.” This study was published, in the 7 March  2013 issue of of the journal Nature,  by Prof Dimmler,…

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