Ideas for Free
On the following dates, ideas posted at http://genomediscovery.org will be available to the use of Scientists/Professors/Physicians/Researchers for free:
National Science day-28th February
Genome-2-Bio-Medicine Discovery center founder’s father’s (teacher) death anniversary day-26th May
National Teacher’s day-5th September
Mahatma Gandhi Birth Anniversary–2nd October
There will be no terms and conditions for the ideas posted on the above mentioned dates. Each idea posted will be served first come, first served basis.Write to info@genomediscovery.org for more details
LncRNA-based regenerative cardiovascular therapy: Sirtuin 5 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 14/December/2021, 6.38 am
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
Molecular therapy for safeguarding your heart against cardiac dysfunction: MiR-488-5p-based therapy for cardiomyocyte proliferation and heart regeneration: MiR-488-5p 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, 22/October/2021, 12.07 pm
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
LncRNA-based regenerative cardiovascular therapy: LncRNA RMRP inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 1/November/2021, 5.23 pm
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
LncRNA-based regenerative cardiovascular therapy: LncRNA βFaar inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 22/October/2021, 11.33 am
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
MiRNA-488-5p inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 14/December/2021, 7.07 am
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
Molecular therapy for safeguarding your heart against cardiac dysfunction: lncRNA βFaar-based therapy for cardiomyocyte proliferation and heart regeneration: lncRNA βFaar 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, 22/October/2021, 11.33 am
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
Molecular therapy for safeguarding your heart against cardiac dysfunction: Enoxacin-based therapy for cardiomyocyte proliferation and heart regeneration: Enoxacin, commonly used in the treatment of UTI and gonorrhea, 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, 26/June/2021, 7.17 pm
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
Molecular therapy for safeguarding your heart against cardiac dysfunction: Bergenin-based therapy for cardiomyocyte proliferation and heart regeneration: Bergenin 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, 26/June/2021, 7.01 pm
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
Little RNA can save you from cardiac hypertrophy and fibrosis: Intracardiac injection of LncRNA NEAT1 protects against cardiac hypertrophy and fibrosis: Intracardiac injection of LncRNA NEAT1 (Nuclear Paraspeckle Assembly Transcript 1) 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, 31/March/2021, 12.11 am
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
LncRNA-based regenerative cardiovascular therapy: LncRNA FLVCR1-AS1 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 29/March/2021, 11.55 pm
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
LncRNA-based regenerative cardiovascular therapy: LncRNA METRNL inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 29/March/2021, 11.51 pm
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
LncRNA-based regenerative cardiovascular therapy: LncRNA BCAR4 inhibits DNA damage responses, induces telomerase expression, inhibits telomere shortening, and promotes cardiomyocyte proliferation, regeneration, and survival after myocardial infarction, via up-regulation of its target gene, 17/March/2021, 5.40 pm
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
