Effectiveness of a comprehensive mental skills curriculum in enhancing surgical performance: Results of a randomized controlled trial

INTRODUCTION: We hypothesized that the implementation of a novel mental skills curriculum (MSC) during laparoscopic simulator training would improve mental skills and performance, and decrease stress. METHODS: Sixty volunteer novices were randomized into intervention and control groups. All participants received FLS training while the intervention group also participated in the MSC. Skill transfer and retention were assessed on a live porcine model after training and 2 months later, respectively. Performance was assessed using the Test of Performance Strategies-2 (TOPS-2) for mental skills, FLS metrics for laparoscopic performance, and the State Trait Anxiety Inventory (STAI-6) and heart rate (HR) for stress. RESULTS: Fifty-five participants (92%) completed training and the transfer test, and 46 (77%) the retention test. There were no significant differences between groups at baseline. Compared to controls the intervention group significantly improved their mental skill use, demonstrated higher laparoscopic skill improvement during retention, and reported less stress during the transfer test. CONCLUSIONS: The MSC implemented in this study effectively enhanced participants' mental skill use, reduced cognitive stress in the operating room with a small impact on laparoscopic performance

Stimulation of neural regeneration in the mouse retina

Müller glia can serve as a source of new neurons after retinal damage in both fish and birds. Investigations of regeneration in the mammalian retina in vitro have provided some evidence that Müller glia can proliferate after retinal damage and generate new rods; however, the evidence that this occurs in vivo is not conclusive. We have investigated whether Müller glia have the potential to generate neurons in the mouse retina in vivo by eliminating ganglion and amacrine cells with intraocular NMDA injections and stimulating Müller glial to re-enter the mitotic cycle by treatment with specific growth factors. The proliferating Müller glia dedifferentiate and a subset of these cells differentiated into amacrine cells, as defined by the expression of amacrine cell-specific markers Calretinin, NeuN, Prox1, and GAD67-GFP. These results show for the first time that the mammalian retina has the potential to regenerate inner retinal neurons in vivo

p38 MAPK signaling acts upstream of LIF-dependent neuroprotection during photoreceptor degeneration

In many blinding diseases of the retina, loss of function and thus severe visual impairment results from apoptotic cell death of damaged photoreceptors. In an attempt to survive, injured photoreceptors generate survival signals to induce intercellular protective mechanisms that eventually may rescue photoreceptors from entering an apoptotic death pathway. One such endogenous survival pathway is controlled by leukemia inhibitory factor (LIF), which is produced by a subset of Muller glia cells in response to photoreceptor injury. In the absence of LIF, survival components are not activated and photoreceptor degeneration is accelerated. Although LIF is a crucial factor for photoreceptor survival, the detailed mechanism of its induction in the retina has not been elucidated. Here, we show that administration of tumor necrosis factor-alpha (TNF) was sufficient to fully upregulate Lif expression in Muller cells in vitro and the retina in vivo. Increased Lif expression depended on p38 mitogen-activated protein kinase (MAPK) since inhibition of its activity abolished Lif expression in vitro and in vivo. Inhibition of p38 MAPK activity reduced the Lif expression also in the model of light-induced retinal degeneration and resulted in increased cell death in the light-exposed retina. Thus, expression of Lif in the injured retina and activation of the endogenous survival pathway involve signaling through p38 MAPK