Reducing Wasted Time Prior To Starting Thoracic Surgical Operations.

To design and implement multidisciplinary interventions to decrease the interval between when a patient entered the operating room and when skin incision was made during thoracic surgical operations. Thirty-eight steps that occurred during the pre-incision time were identified during meetings with surgery, anesthesia, and nursing teams. Using a critical path method and Pareto analysis, standardization of intubation and positioning techniques as well as establishing strict guidelines to avoid unnecessary urinary catheter and arterial line placement were identified as high-value interventions. The duration of every step, and the total pre-incision time, was recorded during four phases of this project: (1) a pre-intervention period; (2) a run-in period; (3) a post-intervention period; and (4) a follow-up period five months later. 101 cases were analyzed. The median (IQR) pre-incision time dropped from 42.5(36-61) min prior to intervention to 34.5(29-39.5). This improvement persisted at five months (33 (28-41) min). Median positioning time decreased from 9(7-11) min to 4(3-5) min, with improvement persistent at late analysis 5(3.5-6) min. Median intubation times decreased from 7.5(5-15.5) min to 6(5-8) min post-intervention, with persistent improvement at five months 6(4-8). Engagement of a multidisciplinary team to design interventions to streamline pre-incision steps reduced the pre-incision time by 19%. Persistence of this improvement likely reflects the investment each teams' members had in achieving efficiency. Decreasing variability in the processes helped to achieve these benefits.

Protecting axonal degeneration by increasing nicotinamide adenine dinucleotide levels in experimental autoimmune encephalomyelitis models.

Axonal damage is a major morphological alteration in the CNS of patients with multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanism for the axonal damage associated with MS/EAE and its contribution to the clinical symptoms remain unclear. The expression of a fusion protein, named "Wallerian degeneration slow" (Wld(S)), can protect axons from degeneration, likely through a beta-nicotinamide adenine dinucleotide (NAD)-dependent mechanism. In this study, we find that, when induced with EAE, Wld(S) mice showed a modest attenuation of behavioral deficits and axon loss, suggesting that EAE-associated axon damage may occur by a mechanism similar to Wallerian degeneration. Furthermore, nicotinamide (NAm), an NAD biosynthesis precursor, profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits in EAE models. Finally, we demonstrate that delayed NAm treatment is also beneficial to EAE models, pointing to the therapeutic potential of NAm as a protective agent for EAE and perhaps MS patients.