Effect of ventricular fibrillation on infarct size after myocardial infarction: a translational study.

Ventricular fibrillation (VF)-induced cardiac arrest frequently complicates ST-segment elevation myocardial infarction (STEMI). Although larger infarct sizes (IS) correlate with a higher risk of VF, the influence of VF itself on IS has remained poorly investigated. To address this knowledge gap, we analyzed the effect of VF on IS in patients and two experimental models.

Zooming in the plastisphere: the ecological interface for phytoplankton-plastic interactions in aquatic ecosystems.

Phytoplankton is an essential resource in aquatic ecosystems, situated at the base of aquatic food webs. Plastic pollution can impact these organisms, potentially affecting the functioning of aquatic ecosystems. The interaction between plastics and phytoplankton is multifaceted: while microplastics can exert toxic effects on phytoplankton, plastics can also act as a substrate for colonisation.

Evaluating the Feasibility of a Telescreening Program for Retinopathy of Prematurity (ROP) in Denmark.

: This study investigates the feasibility of implementing telescreening for retinopathy of prematurity (ROP) using the ICON GO widefield camera operated by a non-physician healthcare professional (NPHP). We hypothesized that images captured by an NPHP are adequate to evaluate ROP changes without further examinations. Secondly, the level of agreement between independent ROP graders were evaluated based on the fundus photographs.

Interplay between the SAFE and the sphingolipid pathway for cardioprotection.

Aim: Activation of both the Survivor Activating Factor Enhancement (SAFE) pathway (including Tumor Necrosis Factor-alpha (TNF-α) and Signal Transducer and Activator of Transcription-3 (STAT-3)) and the sphingolipid signalling pathway (including sphingosine kinase-1 (SK1) and sphingosine-1 phosphate (S1P)) play a key role in promoting cardioprotection against ischemia-reperfusion injury (IRI). We investigated whether the activation of the SAFE pathway by exogenous S1P is dependent on the activation of SK1 for cardioprotection.

Materials And Methods: Isolated cardiomyocytes from TNF-α knockout (KO) mice, cardiomyocyte-specific STAT-3 KO mice and their wild-type (WT) littermates were exposed to simulated ischemia in the presence of a trigger of the SAFE pathway (S1P) and SK1 inhibitor (SK1-I).