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The Core Facility for Advanced Light Microscopy, Ullevål is located at the Institute for Experimental Medical Research, 4th floor, building 7, Oslo University Hospital Ullevål.
We offer services with confocal laser scanning microscopy as well as whole cell fluorescence in combination with microelectrode techniques. We provide services to local Oslo University Hospital users as well as to regional Helse Sør-Øst users. More information about available techniques can be found under the Services tab at the top of the page.
For booking or technical questions, please contact:
Bill Louch, Core Facility Leader,
Michael Frisk, Core Facility Manager,
email: email@example.com, phone: 91545514
Organization and Funding
Our core facility is part of an Imaging platform at Oslo University Hospital, supported by Helse Sør-Øst in the ”Advanced Light Microscopy” platform, which includes two additional nodes located at:
Infrastructure included in the facility node at Ullevål has been purchased through grants from Helse Sør-Øst and the University of Oslo.
All users of the core facility services are charged an hourly fee. For Helse Sør-Øst users the fee is 100 NOK/hour for the use of a core facility microscope, and additionally, 400 NOK/hour for assistance from core facility staff. Academic users outside of Helse Sør-Øst are charged an additional 50% on the above fees, while non-academic users are charged an additional 100%.
Recent Publications from the Confocal Microscopy Core Facility, Ullevål
Louch WE, Frisk M, and Eggart B. High-Speed Recording of Cardiomyocyte Calcium and Contraction (2016) Optik & Photonik, 11:28-30.
Wanichawan P, Hodne K, Hafver TL, Lunde M, Martinsen M, Louch WE, Sejersted OM, and Carlson CR. Development of a high-affinity peptide that prevents phospholemman (PLM) inhibition of the sodium/calcium exchanger 1 (NCX1) (2016) Biochem J, 473:2413-2423.
Frisk M, Ruud, M, Espe EKS, Aronsen JM, Røe ÅT, Zhang, L, Norseng PA, Sejersted OM, Christensen G, Sjaastad I, and Louch WE. Elevated ventricular wall stress disrupts cardiomyocyte t-tubule structure and calcium homeostasis (2016) Cardiovasc Res, 112:443-451.
Gattoni S, Røe ÅT, Frisk M, Louch WE, Niederer SA, and Smith NP. The Calcium-Frequency Response in the Rat Ventricular Myocyte: An Experimental and Modeling Study (2016) J Physiol, 594:4193-4224.
Aronsen JM, Louch WE, and Sjaastad I. Cardiomyocyte Ca2+ dynamics: Clinical perspectives (2016) Scand Cardiovasc J, 50:65-77.
Hafver TL, Hodne K, Wanichawan P, Aronsen JM, Dalhus B, Lunde PK, Lunde M, Martinsen M, Enger UH, Fuller W, Sjaastad I, Louch WE, Sejersted OM, and Carlson CR. Protein Phosphatase 1c Associated with the Cardiac Sodium Calcium Exchanger1 Regulates its Activity by Dephosphorylating Serine 68 Phosphorylated Phospholemman (2016) J Biol Chem, 291:4561-4579.
Sadredini M, Danielsen TK, Aronsen JM, Manotheepan R, Hougen K, Sjaastad I, and Stokke MK. Beta-Adrenoceptor Stimulation Reveals Ca2+ Waves and Sarcoplasmic Reticulum Ca2+ Depletion in Left Ventricular Cardiomyocytes from Post-Infarction Rats with and without Heart Failure (2016) PLoS One, 11:e0153887.
Logantha SJ, Stokke MK, Atkinson AJ, Kharche SR, Parveen S, Saeed Y, Sjaastad I, Sejersted OM, and Dobrzynski H.Ca2+-Clock-Dependent Pacemaking in the Sinus Node Is Impaired in Mice with a Cardiac Specific Reduction in SERCA2 Abundance (2016) Front Physiol 7:197.
Manotheepan R, Danielsen TK, Sadredini M, Anderson ME, Carlson CR, Lehnart SE, Sjaastad I, and Stokke MK. Exercise training prevents ventricular tachycardia in CPVT1 due to reduced CaMKII-dependent arrhythmogenic Ca2+ release (2016) Cardiovasc Res 111:295-306.
Aronsen JM,Skogestad J,Lewalle A,Louch WE,Hougen K,Stokke MK,Swift F,Niederer S,Smith NP,Sejersted OM,Sjaastad I (2015). Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase a2 activity. J Physiol, 593:1509-1521.
Frisk M, Koivumäki JT, Norseng PA, Maleckar MM, Sejersted OM, and Louch WE (2014). Variable t-tubule organization and Ca2+ homeostasis across the atria. Am J Physiol – Heart Circ Physiol, 307:H609-20.
Misceoa D, Holmgrena A, Louch WE, Holmec PA, Mizobuchid M, Moralese RJ, De Paulaf AM, Stray-Pedersena A, Lylea R, Dalhusg B, Christensen G, Stormorken H, Tjønnfjord GE, and Frengen E. A dominant STIM1 mutation causes Stormorken syndrome (2014) Hum Mutat, 35:556-564.
Aronsen JM, Swift F, & Sejersted OM (2013). Cardiac sodium transport and excitation-contraction coupling. Journal of Molecular and Cellular Cardiology. 61, 11-19.
Herum KM, Lunde IG, Skrbic B, Florholmen G, Behmen D, Sjaastad I, Carlson CR, Gomez MF, & Christensen G (2013). Syndecan-4 signaling via NFAT regulates extracellular matrix production and cardiac myofibroblast differentiation in response to mechanical stress. J Mol Cell Cardiol 54, 73-81.
Land S, Louch WE, Niederer SA, Aronsen JM, Christensen G, Sjaastad I, Sejersted OM, & Smith NP (2013). Beta-adrenergic stimulation maintains cardiac function in serca2 knockout mice. Biophys J 104, 1349-1356.
Land S, Niederer S, Louch WE, Sejersted OM, & Smith NP (2013). Integrating multi-scale data to create a virtual physiological mouse heart. Interface Focus 3, 20120076.
Louch WE, Hake J, Mork HK, Hougen K, Skrbic B, Ursu D, Tonnessen T, Sjaastad I, & Sejersted OM (2013). Slow Ca2+ sparks de-synchronize Ca2+ release in failing cardiomyocytes: Evidence for altered configuration of Ca2+ release units? Journal of Molecular and Cellular Cardiology 58, 41-52.
Moltzau LR1, Aronsen JM, Meier S, Nguyen CH, Hougen K, Ørstavik Ø, Sjaastad I, Christensen G, Skomedal T, Osnes JB, Levy FO, & Qvigstad E (2013). SERCA2 activity is involved in the CNP-mediated functional responses in failing rat myocardium. Br J Pharmacol.;170:366-379.
Stokke MK, Tovsrud N, Louch WE, Øyehaug L, Hougen K, Sejersted OM, Swift F, & Sjaastad I (2013). ICaL inhibition prevents arrhythmogenic Ca2+waves caused by abnormal Ca2+ sensitivity of RyR or SR Ca2+accumulation. Cardiovasc Res 98, 315-325.
Øyehaug L, Loose KO, Jolle GF, Roe AT, Sjaastad I, Christensen G, Sejersted OM, & Louch WE (2013). Synchrony of Cardiomyocyte Ca2+Release is Controlled by t-tubule Organization, SR Ca2+ Content, and Ryanodine Receptor Ca2+ Sensitivity. Biophys J 104, 1685-1697.
Bjørnstad JL, Skrbic B, Marstein HS, Hasic A, Sjaastad I, Louch WE, Florholmen G, Christensen G, & Tønnessen T (2012). Inhibition of SMAD2 phosphorylation preserves cardiac function during pressure overload. Cardiovasc Res 93, 100-110.
Eidet JR, Utheim OA, Raeder S, Dartt DA, Lyberg T, Carreras E, Huynh TT, Messelt EB, Louch WE, Roald B, & Utheim TP (2012). Effects of serum-free storage on morphology, phenotype, and viability of ex vivo cultured human conjunctival epithelium. Exp Eye Res 94, 109-116.
Li L, Louch WE, Niederer SA, Aronsen JM, Christensen G, Sejersted OM, & Smith NP (2012). Sodium accumulation in SERCA KO induced HF. Biophys J 102, 2039-2049.
Louch WE, Stokke MK, Sjaastad I, Christensen G, & Sejersted OM (2012). No rest for the weary: Diastolic calcium homeostasis in the normal and failing myocardium. Physiology 27, 308-323.
Louch WE, Vangheluwe P, Bito V, Raeymaekers L, Wuytack F, & Sipido KR (2012). Phospholamban ablation in hearts expressing the high affinity SERCA2b isoform normalizes global Ca2+ homeostasis but not Ca2+-dependent hypertrophic signaling. Am J Physiol Heart Circ Physiol 302, H2574-H2582.
Swift F, Franzini-Armstrong C, Øyehaug L, Enger UH, Andersson KB, Christensen G, Sejersted OM, & Louch WE (2012). Extreme sarcoplasmic reticulum volume loss and compensatory T-tubule remodeling following Serca2 knockout. Proc Natl Acad Sci U S A 109, 3997-4001
Last updated 01.02.2017 by Bill Louch