Medication use in hospitals is a complex process and is dependent on the successful interaction of health professionals functioning within different disciplines. Errors can occur at any one of the five main stages of prescribing, documenting, dispensing or preparation, administering and monitoring. The responsibility for the error is often placed on the nurse, as she or he is the last person in the drug administration chain whilst more pressing underlying causal factors remain unresolved.\ud \ud This paper demonstrates how hierarchical task analysis can be used to model drug administration and then uses the systematic human error reduction and prediction approach to predict which errors are likely to occur. The paper also puts forward design solutions to mitigate these errors
This study investigated whether exposures to butyltins (BTs), tributylin (TBT) and dibutyltin (DBT) were able to alter cytosolic calcium levels in human natural killer (NK) cells. Additionally, the effects of cytosolic calcium ion increases on the activation state of mitogen activated protein kinases (MAPKs) in NK cells were also investigated. NK cells are an intital immune defense against the development of tumors or viral infections. TBT and DBT are widespread environmental contaminants, due to their various industrial applications. Both TBT and DBT have been shown to decrease the ability of NK cells to lyse tumor cells (lytic function). TBT has also been shown to activate MAPKs in NK cells. The results of this study indicated that TBT increased cytosolic calcium levels by as much as 100% after a 60 min exposure to 500 nM TBT while DBT increased cytosolic calcium levels to a much smaller extent (and required higher concentrations). The results also indicated that increases in cytosolic calcium could activate MAPKs but only for a short period of time (5 min), while previous studies showed that activation of MAPKs by TBT last for at least 6 hours. Thus, it appears that TBT stimulated increases in cytosolic calcium may contribute to, but are not fully responsible for, TBT-induced activation of MAPKs.
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