Hansjörg Schäfer

TL;DR: The utility of this system as a test bed for genetic manipulation was demonstrated by infecting the CMPMs with a recombinant β‐galactosidase‐carrying adenovirus, and transduction efficiency increased from about 5% (MOI 0.1) to about 50% ( MOI 100).

TL;DR: It is suggested that initial ischemia may cause loss of the ability of the heart muscle cells to regulate complement turnover at the membrane level, and resulting deposition of C5b-9 on the cell membranes may contribute to functional disturbance and irreversible damage of myocardial cells during the infarction process.

TL;DR: The short- and long-term outcomes after LRT and SLT did not differ significantly and LRT provides a solution for urgent cases in which a cadaveric graft cannot be found in time or if the choice of the optimal time point for transplantation is vital.

TL;DR: It is concluded that in the absence of reperfusion C5b-9 accumulation occurs as a late event when most of the jeopardized myocardium has probably already become necrotic, however, the complement system is activated rapidly and this could play a role in the pathogenesis of reperFusion injury.

TL;DR: Infarct size delineation by triphenyltetrazolium chloride (TTC) staining is dependent on sufficient reperfusion and the possibility of using propidium iodide (PI), a reagent conventionally used in flow cytometry to fluorescently stain dead cells, for infarct size analysis after short periods of reperfusions is evaluated.