OB/GYN boot cAMP using high-fidelity human simulators: enhancing residents' perceived competency, confidence in taking a leadership role, and stress hardiness.

OBJECTIVES: To evaluate the effectiveness of an obstetrical and gynecologic (Ob/Gyn) Boot Camp simulation training on perceived technical competency, confidence in a leadership role, and stress hardiness of resident training. METHODS: We conducted a prospective pilot study on the effectiveness of an Ob/Gyn Boot Camp on resident training. Residents participated in an intensive immersion in clinical simulation of common obstetrical emergencies including shoulder dystocia, neonatal resuscitation, postpartum hemorrhage, and ruptured ectopic pregnancy. After the training, residents completed a Web-based survey on their perceptions of how the Ob/Gyn Boot Camp affected their 1) technical competency in the assessment and management of their patients, 2) confidence in taking a leadership role, and 3) stress hardiness. Residents rated their perceptions on a Likert scale of 1 to 5, 1 = poor to 5 = excellent. RESULTS: Twenty-three (14 Ob/Gyn and 9 family medicine) residents participated in this pilot study. Eighteen (78%) residents completed the online survey; 4 Ob/Gyn and 1 family medicine resident did not complete the survey. The residents reported that the simulation training stimulated an interest in learning key skills for obstetrical and gynecologic emergencies. Ob/Gyn residents reported significant improvement in their perceived technical competence and stress hardiness after the Boot Camp. However both Ob/Gyn and family medicine residents reported no significant improvement of confidence in their leadership abilities during obstetrical emergencies after the Boot Camp. CONCLUSION: Boot Camp simulation training early in the curriculum has the potential for enhancing residents' self-assessments of confidence, competency, and stress hardiness in managing obstetrical emergencies.

Using simulation to orient code blue teams to a new hospital facility.

OBJECTIVES: Prompt and successful cardiopulmonary resuscitation during a sudden cardiac arrest can be hindered by multiple variables, ie, ineffective communication, stress, lack of training, and an unfamiliar environment, such as a new hospital facility. The main objective of the study was to use high-fidelity simulations to orient Code Blue Teams (CBTs) to critical events in a new hospital facility. A secondary objective was to elucidate factors that may have contributed to responses by debriefing teams. METHODS: Mock Code Blue exercises using high-fidelity simulation were implemented in real workplace settings to orient CBTs to critical events. We measured arrival time of first responder, crash cart to code site, first six CBT responders, first chest compression, and first electrical shock. After each mock code, participants were debriefed to assess any barriers to effective response and decision making. RESULTS: Twelve mock codes were conducted at different locations of the new facility. Sixty-nine percent of the participants reported that the training was beneficial. The median time of arrival of the first responders was 42 seconds and the first CBT member was 66 seconds. The median time to initiation of chest compressions was 80 seconds, crash cart arrival was 68 seconds, and first electrical shock was 341 seconds. An additional outcome of the study was the identification of facility and systems issues that had the potential to impact patient safety. CONCLUSIONS: Clinical simulation can be effectively used to orient CBTs and identify critical safety issues in a newly constructed healthcare facility.

Recombinant prostate-specific antigen proaerolysin shows selective protease sensitivity and cell cytotoxicity.

Native proaerolysin is a channel-forming bacterial protoxin that binds to cell-surface receptors and then is activated by furin or furin-like proteases. We genetically engineered proaerolysin by replacing the furin-cleavage sequence with a prostate-specific antigen-selective sequence. The recombinant modified proaerolysin was expressed and purified from Aeromonas salmonicida in good yields and purity. Recombinant modified proaerolysin had no furin sensitivity and markedly increased prostate-specific antigen sensitivity relative to wild-type proaerolysin. Human prostate cancer cells were significantly more sensitive to recombinant modified proaerolysin in the presence of active prostate-specific antigen when compared with the absence of prostate-specific antigen or the presence of potent prostate-specific antigen inhibitors. Most normal human cells with the exception of prostate and renal epithelial cells showed very low sensitivity to recombinant modified proaerolysin. Our results suggest that recombinant modified proaerolysin is a potent prostate-specific antigen-sensitive protoxin that deserves further development for regional therapy of benign and malignant prostate growths.

Clozapine and the mitogen-activated protein kinase signal transduction pathway: implications for antipsychotic actions.

BACKGROUND: Mitogen-activated protein kinase (MAPK) signaling pathways respond to dopaminergic and serotonergic agents and mediate short- and long-term effects of intracellular signaling in neurons. Here we show that the antipsychotic agent, clozapine, selectively activates the MEK/ERK MAPK pathway, and inhibition of this pathway reverses clozapine's actions in the conditioned avoidance response (CAR) paradigm, a rodent behavioral assay of antipsychotic activity. METHODS: Phosphorylation patterns of MAPK pathway enzymes were determined by quantitative immunoblot analysis and immunohistochemistry of rat prefrontal cortex. Kinase inhibitors were used to assess the role of MAPK signaling pathways in mediating clozapine-induced suppression of CAR. RESULTS: Clozapine administration selectively increased phosphorylation of MEK1/2 but had no effect on p38 or JNK phosphorylation. Pretreatment with the 5-HT2A agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrochloride blocked the clozapine-induced increase in MEK1/2 phosphorylation. Immunohistochemistry revealed that clozapine treatment elevated the number of cells in the prefrontal cortex positive for phosphoERK, the downstream substrate of MEK1/2. Prior administration of MEK1/2 inhibitors U0126 or Sl327, or ERK inhibitor 5-iodotubercidin, reversed suppression of CAR induced by clozapine, whereas administration of vehicle, JNK or p38 inhibitors (L-JNK-1 and SB203580, respectively) had no effect. Inhibition of kinases upstream to MEK1/2 (PI-3K, PKC, and CaMKII) by administration of LY294002, bisindolylmaleimide, or KN-62, respectively, also reversed clozapine-induced suppression of CAR. CONCLUSIONS: These data support the hypothesis that the MEK/ERK signal transduction cascade participates in clozapine's antipsychotic actions.