RESUMEN
BACKGROUND: Communication with parents of sick premature and term infants in the NICU is complicated and challenging. Multiple efforts have been made to improve it, including the introduction of new electronic-based measures. AIM: We aimed to study the influence of implementation of a new communication technology on parents' satisfaction with care in the NICU during the COVID-19 pandemic. METHODS: Infants were video-recorded in their incubators or cots without being disturbed. These short films, with voice updates on the infant's condition, were sent on a daily basis to their parents via a WhatsApp application. RESULTS: Parents who chose to join the new communication project (study group) were older, and their infants were more premature. Parents were satisfied with this new communication modality. Satisfaction scores in both study and control groups were high, but not significantly different. CONCLUSIONS: Although the implementation of the new communication project was successful, we could not demonstrate significant improvement in satisfaction scores that were high in study and control groups, reflecting baseline high satisfaction. Further studies are needed employing other assessment tools in order to evaluate other aspects of parents' satisfaction with new modalities of communication introduced to the NICU, and their effects on parents' bonding with their infants.
RESUMEN
Parkin, which is mutated in most recessive Parkinsonism, is a key player in the selective removal of damaged mitochondria via mitophagy. Damaged mitochondria may carry mitochondrial DNA (mtDNA) mutations, thus creating a mixed mtDNA population within cells (heteroplasmy). It was previously shown that Parkin over-expression reduced the level of heteroplasmic mutations that alter mitochondrial membrane potential in human cytoplasmic hybrids. However, it remained unclear whether Parkin serves a similar role at the entire living organism, and whether this role is evolutionarily conserved. Here, we show that mutation in the Caenorhabditis elegans orthologue of Parkin (pdr-1) modulates the level of a large heteroplasmic mtDNA truncation. Massive parallel sequencing revealed that the mtDNAs of C. elegans wild type and pdr-1(gk448) mutant strains were virtually deprived of heteroplasmy, thus reflecting strong negative selection against dysfunctional mitochondria. Therefore, our findings show that the role of Parkin in the modulation of heteroplasmy is conserved between human and worm and raise the interesting possibility that mitophagy modulates the striking lack of heteroplasmy in C. elegans.
