Pediatic code blue event anaylsis: Performance of non-acute health-care providers.

In-hospital pediatric cardiopulmonary arrest is rare. With more than 50% of patients not surviving to discharge following cardiopulmonary arrest, it is important that health-care providers (HCPs) respond appropriately to deteriorating patients. Our study evaluated the performance of basic life support skills using non-acute HCPs during pediatric inpatient resuscitation events. We conducted a retrospective chart review of all code blue team (CBT) activations in non-acute care areas of a tertiary care children's hospital from 2008 to 2017. The main outcomes were frequency of life support algorithmic assessments and interventions (critical actions) performed by non-acute HCPs prior to the arrival of CBT. CBT activation and outcome data were summarized descriptively. Logistic regression was used to assess for an association of outcomes with the presence of established leadership. A total of 60 CBT activations were retrieved, 48 of which had data available on isolated non-acute HCP performance. Most children (93%) survived to discharge. Critical action performance review revealed that an airway, breathing and pulse assessment was documented to have occurred in 33%, 69% and 29% of cases, respectively. A full primary assessment was documented in 6% of cases. The presence of established leadership was associated with the performance of a partial ABC assessment. Our results suggest that resuscitation performance of pediatric inpatient non-acute HCPs often does not adhere to standard life support guidelines. These results highlight the need to reconsider the current approaches used for non-acute HCP resuscitation training.

Targeted delivery of doxorubicin to mitochondria.

Several families of highly effective anticancer drugs are selectively toxic to cancer cells because they disrupt nucleic acid synthesis in the nucleus. Much less is known, however, about whether interfering with nucleic acid synthesis in the mitochondria would have significant cellular effects. In this study, we explore this with a mitochondrially targeted form of the anticancer drug doxorubicin, which inhibits DNA topoisomerase II, an enzyme that is both in mitochondria and nuclei of human cells. When doxorubicin is attached to a peptide that targets mitochondria, it exhibits significant toxicity. However, when challenged with a cell line that overexpresses a common efflux pump, it does not exhibit the reduced activity of the nuclear-localized parent drug and resists being removed from the cell. These results indicate that targeting drugs to the mitochondria provides a means to limit drug efflux and provide evidence that a mitochondrially targeted DNA topoisomerase poison is active within the organelle.