Risk assessment framework for microplastic in marine environments.

Constantly raising microplastic (MP) contamination of water sources poses a direct threat to the gentle balance of the marine environment. This study focuses on a multifactor hazard evaluation of conventional (polyethylene - PE, polypropylene - PP, and polystyrene - PS) and alternative (polyethylene terephthalate with 25 % or 50 % recycled material and polylactic acid) plastics. The risk assessment framework explored included MP abundance, water acidification potential, surface oxidation, fragmentation, and bacterial growth inhibition. Based on MP monitoring campaigns worldwide, we conclude that PE-based plastics are the most abundant MPs in water samples (comprise up to 82 % the MP in those samples). A year-long weathering experiment showed that PS-based and PP-based plastics were oxidized to a higher extent, resulting in the highest water acidification with pH reduction of up to three orders of magnitude. Finally, our laboratory experiments showed that weathered PS was the most fragile plastic during mechanical degradation, while both PP- and PS-based plastic extracts showed a significant growth inhibition toward the marine microorganisms (Bacillus sp. and Pseudoaltermonas sp). Using the examined factors as weighted inputs into our framework, this holistic evaluation of hazards suggest that PP-based plastic products were the most hazardous compared to the other conventional and alternative plastic types.

The involvement of ZnT-1, a new modulator of cardiac L-type calcium channels, in [corrected] atrial tachycardia remodeling. [corrected].

Atrial fibrillation (AF), the highest occurring cardiac arrhythmia in the Western world, is associated with substantial morbidity and increased mortality. In spite of extensive research, the cause of atrial electrical remodeling, a major factor in the self-perpetuating nature of AF, is still unknown. Downregulation of L-type Ca2+ channel (LTCC) activity is the hallmark of atrial electrical remodeling. ZnT-1 is a ubiquitous membrane protein that was recently suggested to inhibit the LTCC. We have studied and shown that ZnT-1 expression inhibits LTCC function in an oocyte expression system as well as in isolated cardiomyocytes. Our data also show that rapid electrical pacing can augment ZnT-1 expression in culture as well as in the atria of rats in vivo. Finally, in a pilot study, ZnT-1 expression was found to be augmented in the atria of AF patients. These findings position ZnT-1 as a probable missing link in the mechanism underlying atrial tachycardia remodeling.