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Nature Reviews Cardiology, ISSN 1759-5002, 12/2019, Volume 16, Issue 12, pp. 704 - 705
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 3/2018, Volume 113, Issue 2, pp. 1 - 6
Journal Article
Lancet, The, ISSN 0140-6736, 2015, Volume 385, Issue 9970, pp. 774 - 774
  Melatonin treatment helps to restore these human circadian rhythms, resulting in better cognition and less daytime fatigue.1 Experimental and clinical data... 
Internal Medicine | MEDICINE, GENERAL & INTERNAL | Central Nervous System Depressants - pharmacology | Cardiotonic Agents - pharmacology | Aspirin - adverse effects | Cardiotonic Agents - adverse effects | Melatonin - pharmacology | Humans | Aspirin | Melatonin | Heart attacks | Sleep | Rodents | Circadian rhythm | Preventive medicine
Journal Article
Frontiers in Physiology, ISSN 1664-042X, 05/2018, Volume 9, Issue MAY, p. 528
Journal Article
European Heart Journal – Cardiovascular Pharmacotherapy, ISSN 2055-6837, 10/2016, Volume 2, Issue 4, pp. 258 - 265
Journal Article
Cardiovascular Research, ISSN 0008-6363, 11/2009, Volume 84, Issue 2, pp. 201 - 208
Aims Ischaemic postconditioning (IPostC) is a powerful protective phenomenon that activates prosurvival intrinsic signalling cascades to limit reperfusion... 
Ischaemia | Infarction | Reperfusion | Postconditioning | Preconditioning | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | NECROSIS-FACTOR-ALPHA | CARDIAC MYOCYTE | MURINE MODEL | ISOLATED MOUSE HEARTS | INDUCED CARDIOPROTECTION | ACUTE MYOCARDIAL-INFARCTION | TNF-ALPHA | PROSURVIVAL KINASES | SIGNAL TRANSDUCER | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Tumor Necrosis Factor-alpha - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Tumor Necrosis Factor-alpha - deficiency | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Myocardial Infarction - pathology | Myocardium - metabolism | STAT3 Transcription Factor - deficiency | Flavonoids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Myocardium - pathology | Tyrphostins - pharmacology | Myocardial Infarction - metabolism | Glycogen Synthase Kinase 3 - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Myocardial Reperfusion Injury - metabolism | Animals | Androstadienes - pharmacology | Signal Transduction - drug effects | Mice | Myocardial Infarction - prevention & control | Protein Kinase Inhibitors - pharmacology | STAT3 Transcription Factor - antagonists & inhibitors | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Journal Article
Life Sciences, ISSN 0024-3205, 03/2018, Volume 196, p. 127
Aims: Acute heart failure (AHF) is a burden disease, with high mortality and re-hospitalisations. Using an ex-vivo model of AHF, we have previously reported... 
Heart failure | Phosphates | Pressure effects | Transcription | Stat3 protein | Recovery of function | Nuclei | Sphingosine 1-phosphate | Heart rate | Signal transduction | Lipoproteins | Materials recovery | Heart diseases
Journal Article
Journal Article