OUTCOME MEASURES The primary outcome was the aggregate cost of vancomycin therapy, which included the cost associated with sample collection (i.e., supply cost and nursing time), sample analysis (i.e., assay cost and laboratory technician time), result interpretation (i.e., pharmacist time), and drug cost (i.e., cost of total administered vancomycin dose) during the hospital stay. RESULTS A total of 52 patients met inclusion criteria with 26 patients in each group. The median (interquartile range) total vancomycin drug and monitoring cost was $338.14 ($235.07-$601.05) for the AUCMIC-based group compared with $316.79 ($253.36-$520.96) for the trough-based group (P = 0.687). CONCLUSION Vancomycin monitoring using 2 steady-state serum concentrations and first-order PK equations to calculate AUCMIC was no more costly than a trough-based approach in patients with MRSA bacteremia at our institution. Women with antiphospholipid antibodies (aPL) have increased risks of pregnancy complications, including a ten-fold increased risk of preeclampsia, which is potentially triggered by the release of placental toxins. Previously, aPL were shown to enter the outer layer of the placenta, the syncytiotrophoblast, associate with mitochondria, and alter mitochondrial function. We hypothesised that aPL may also increase mitochondrial reactive oxygen species (ROS) production, leading to cellular dysfunction and release of toxins. First trimester placental explants were incubated with monoclonal aPL, ID2 and IIC5 (25, 50, and 100 μg/mL), for 3 h at 37 °C and ROS production followed using CellROX Deep Red. In addition, the candidate treatment compounds chloroquine, melatonin, and Mito-Q were tested at therapeutic concentrations for their ability to prevent ROS production. Mitochondria isolated from term placentae were incubated with fluorescently-labelled ID2, IIC5, or control IgG antibodies (2.5, 5, 10, or 20 μg/mL) for 30 min, and mitochondria with bound antibodies were quantified using flow cytometry. In addition, respirometry coupled with fluorimetry was used to interrogate explant mitochondrial respiration and ROS production following incubation with 25, 50, or 100 μg/mL ID2, IIC5, or control IgG for 3 h at 37 °C. ID2 increased explant ROS production in a manner that was completely prevented by the endocytosis inhibitor chloroquine, and partially prevented by the antioxidants melatonin and Mito-Q. Both ID2 and IIC5 displayed a greater ability to bind isolated mitochondria than control antibodies, and increased ROS production attributable to the mitochondrial enzyme glycerol 3-phosphate dehydrogenase (mGPDH). Our evidence supports the hypothesis that aPL interact with syncytiotrophoblast mitochondria, likely via the binding of cardiolipin and β2 glycoprotein I in mitochondrial membranes, and induce ROS production which contributes to overall oxidative stress and placental dysfunction. Neck muscle activation is increasingly important for accurate prediction of occupant response in automotive impact scenarios and occupant excursion resulting from active safety systems such as autonomous emergency braking. Muscle activation and optimization in frontal impact scenarios using computational Human Body Models have not been investigated over the broad range of accelerations relevant to these events. This study optimized the muscle activation of a contemporary finite element model of the human head and neck for human volunteer experiments over a range of frontal impact severities (2 g to 15 g). The neck muscles were grouped as flexors and extensors, and optimization was undertaken for each group based on muscle activation level and activation time. The boundaries for optimization were defined using data from the literature and a preliminary parametric study. A linear polynomial method was used to optimize the model head kinematics to the volunteer experiments for each impact severity. Eflornithine nmr The optimized models predicted muscle activation to increase with higher impact severities, and improved the average cross-correlation by 35% (0.561-0.755) relative to the Maximum Muscle Activation (MMA) scheme in the original model. Importantly, a newly proposed Cocontraction Muscle Activation (CMA) scheme for maintaining the head in a neutral posture provided a 23% on average improvement in correlation compared to the MMA scheme. In conclusion, this study identified a new scheme to obtain more accurate response kinematics across multiple impact severities in computational Human Body Models as well as contributing to the understanding of muscle influence during frontal impact scenarios. Tracheal stenosis is a health condition in which local narrowing of the upper trachea can cause breathing difficulties and increased incidence of infection, among other symptoms. Occurring most commonly due to intubation of infants, tracheal stenosis often requires corrective surgery. It is challenging to determine the most effective surgical strategy for a given patient as current clinical methods used to assess tracheal stenosis are simplistic and subjective, and are not rigorously based on aerodynamic considerations. This paper summarizes a non-invasive approach based on computational fluid dynamics (CFD) and medical imaging to establish relationships between trachea anatomy and inspiration performance. Though patient-specific CFD analysis has gained recent popularity, an objective of this study is to computationally formulate dimensionless analytical correlations between anatomy and performance that are applicable to any member of a class of patients and that can be interpreted within the context of the Myer-Cotton stenotic airway classification system. These correlations can provide aerodynamics-based insight for the development of more robust stenosis evaluation methods and may allow for time-efficient assessment of corrective surgical strategies. Mechanical adaptions of cells, including stiffness variation, cytoskeleton remodeling, motion coordination, and shape changing, are essential for tissue morphogenesis, wound healing, and malignant progression. In this paper, we take confluent monolayers of Madin-Darby canine kidney (MDCK) and mouse myoblast (C2C12) cells as model systems to probe how cells collectively adapt their mechanical features in response to a free tissue boundary. We show that the free boundary not only can trigger unjamming transition but also induces cell fluidization nearby the boundary. The Young’s moduli of cells near the boundary are found to be much lower than those of interior cells. We demonstrate that the stiffness of cells in monolayers with a free tissue boundary exhibits negative dependence on the projected cell area, in contrast to previous studies where cells were found to stiffen as cellular area increases in a confluent MDCK monolayer without boundary. In addition, the free tissue boundary may activate cell remodeling, rendering volume enlargement and cell-specified cytoskeleton organization.