Almira Hasic
Senior Engineer & Safety representative (VO)
Email: almira.hasic@medisin.uio.no
Phone: +47 472 54 747
Education
-Cand.mag, University of Oslo, The Faculty of Mathematics and Natural Sciences, Department of Biosciences (2003)
-Cand.scient, University of Oslo, The Faculty of Mathematics and Natural Sciences, Department of Biosciences (2006)
-Praktisk-pedagogisk utdanning, University of Oslo (2009)
Research area
- Heart failure
Latest publications
view all >Sasi A, Romaine A, Erusappan PM, Melleby AO, Hasic A, Dahl CP, Broch K, Almaas VM, Puertas RD, Roderick HL, Lunde IG, Sjaastad I, Vistnes M, Christensen G (2023)
Temporal expression and spatial distribution of the proteoglycan versican during cardiac fibrosis development
Matrix Biol Plus, 19-20, 100135
PubMed 38076279 DOI 10.1016/j.mbplus.2023.100135
Temporal expression and spatial distribution of the proteoglycan versican during cardiac fibrosis development
Matrix Biol Plus, 19-20, 100135
PubMed 38076279 DOI 10.1016/j.mbplus.2023.100135
Haugsten Hansen M, Sadredini M, Hasic A, Eriksen M, Stokke MK (2023)
Myocardial oxidative stress is increased in early reperfusion, but systemic antioxidative therapy does not prevent ischemia-reperfusion arrhythmias in pigs
Front Cardiovasc Med, 10, 1223496
PubMed 37823177 DOI 10.3389/fcvm.2023.1223496
Myocardial oxidative stress is increased in early reperfusion, but systemic antioxidative therapy does not prevent ischemia-reperfusion arrhythmias in pigs
Front Cardiovasc Med, 10, 1223496
PubMed 37823177 DOI 10.3389/fcvm.2023.1223496
Haugsten Hansen M, Sadredini M, Hasic A, Anderson ME, Sjaastad I, Korseberg Stokke M (2022)
CaMKII and reactive oxygen species contribute to early reperfusion arrhythmias, but oxidation of CaMKIIδ at methionines 281/282 is not a determining factor
J Mol Cell Cardiol, 175, 49-61
PubMed 36528076 DOI 10.1016/j.yjmcc.2022.12.002
CaMKII and reactive oxygen species contribute to early reperfusion arrhythmias, but oxidation of CaMKIIδ at methionines 281/282 is not a determining factor
J Mol Cell Cardiol, 175, 49-61
PubMed 36528076 DOI 10.1016/j.yjmcc.2022.12.002
Romaine A, Melleby AO, Alam J, Lobert VH, Lu N, Lockwood FE, Hasic A, Lunde IG, Sjaastad I, Stenmark H, Herum KM, Gullberg D, Christensen G (2022)
Integrin α11β1 and syndecan-4 dual receptor ablation attenuate cardiac hypertrophy in the pressure overloaded heart
Am J Physiol Heart Circ Physiol, 322 (6), H1057-H1071
PubMed 35522553 DOI 10.1152/ajpheart.00635.2021
Integrin α11β1 and syndecan-4 dual receptor ablation attenuate cardiac hypertrophy in the pressure overloaded heart
Am J Physiol Heart Circ Physiol, 322 (6), H1057-H1071
PubMed 35522553 DOI 10.1152/ajpheart.00635.2021
Nordén ES, Bendiksen BA, Andresen H, Bergo KK, Espe EK, Hasic A, Hauge-Iversen IM, Veras I, Hussain RI, Sjaastad I, Christensen G, Cataliotti A (2021)
Sacubitril/valsartan ameliorates cardiac hypertrophy and preserves diastolic function in cardiac pressure overload
ESC Heart Fail, 8 (2), 918-927
PubMed 33497525 DOI 10.1002/ehf2.13177
Sacubitril/valsartan ameliorates cardiac hypertrophy and preserves diastolic function in cardiac pressure overload
ESC Heart Fail, 8 (2), 918-927
PubMed 33497525 DOI 10.1002/ehf2.13177