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Up‐Regulation of Connexin45 in Heart Failure
- Kathryn A. Yamada, J. Rogers, R. Sundset, T. Steinberg, J. Saffitz
- Biology, MedicineJournal of cardiovascular electrophysiology
- 1 November 2003
Heart failure is associated with reduced expression of the major gap junction protein connexin43 (Cx43), which may contribute to arrhythmias and sudden cardiac death in this patient population, and the number, size, or distribution of Cx45 gap junctions is altered in the failing heart.
Ischemia Induces Closure of Gap Junctional Channels and Opening of Hemichannels in Heart-derived Cells and Tissue
- D. Johansen, V. Cruciani, R. Sundset, K. Ytrehus, S. Mikalsen
- Biology, MedicineCellular Physiology and Biochemistry
- 1 August 2011
Connexin 43 is most likely responsible for both closure of gap junction channels and opening of hemichannels during simulated ischemia in neonatal rat heart myofibroblasts, and the infarct size becomes significantly reduced by preventing the opening of these channels during early ischemic injury in the heart.
Overexpression of cardiac connexin45 increases susceptibility to ventricular tachyarrhythmias in vivo.
- T. Betsuyaku, Nkiruka S Nnebe, R. Sundset, S. Patibandla, C. M. Krueger, Kathryn A. Yamada
- Biology, MedicineAmerican journal of physiology. Heart and…
Increased myocardial expression of Cx45 results in remodeling of intercellular coupling and greater susceptibility to ventricular arrhythmias in vivo.
Injury coding in a national trauma registry: a one-year validation audit in a level 1 trauma centre
Concordance between the codes registered in the trauma registry and the reference standard was moderate, influencing individual patients’ injury codes validity and ISS/NISS reliability, and aggregated median group ISS/ NISS reliability was acceptable.
Ischemic Preconditioning Protects Against Gap Junctional Uncoupling in Cardiac Myofibroblasts
The role of gap junction communication in simulated preconditioning in cultured neonatal rat cardiac myofibroblasts was investigated to preserve gap junctional communication required for enhanced functional recovery during subsequent reperfusion.
Quantitative PET/MR imaging of lung cancer in the presence of artifacts in the MR-based attenuation correction maps
- Samuel Kuttner, M. Lassen, Silje Kjærnes Øen, R. Sundset, T. Beyer, L. Eikenes
- Medicine, PhysicsActa radiologica
- 1 January 2020
The absence of bone and truncation artifacts have limited effect on the PET quantification of lung lesions, while susceptibility artifacts caused significant and inconsistent underestimations of the lung tumor SUVs, between test–retest scans.
PET-CT in the sub-arctic region of Norway 2010–2013. At the edge of what is possible?
PET-CT was not similarly available within the region, and except for malignant melanoma, this finding was observed in all major cancer subgroups.
Mechanism of hypoxic preconditionin in guinea pig papillary muscles
- T. Ravingerová, Jan Eirik Loekeboe, J. Munch-Ellingsen, R. Sundset, P. Tande, K. Ytrehus
- Biology, MedicineMolecular and Cellular Biochemistry
- 1 September 1998
Guinea pig papillary muscle can be preconditioned with a brief hypoxic challenge against contractile dysfunction upon long-lasting hypoxia/reoxygenation and shows significantly better recovery of function.
Mechanism of hypoxic preconditioning in guinea pig papillary muscles.
- T. Ravingerová, J. E. Løkebø, J. Munch-Ellingsen, R. Sundset, P. Tande, K. Ytrehus
- Biology, MedicineMolecular and cellular biochemistry
- 1 September 1998
Guinea pig papillary muscle can be preconditioned with a brief hypoxic challenge against contractile dysfunction upon long-lasting hypoxia/reoxygenation, and possible mechanisms might involve facilitated opening of K(ATP)-dependent channels.
The role of glycolysis in myocardial calcium control.
- E. Aasum, D. A. Lathrop, T. Henden, R. Sundset, T. Larsen
- BiologyJournal of molecular and cellular cardiology
- 1 September 1998
It is concluded that glycolysis plays an essential role in the maintenance of intracellular calcium homeostasis during severe calcium overload, and was also essential for signalling the inotropic effect that accompanied elevation in extracellular calcium.