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EXECUTIVE SUMMARY. The 2021-22 Academic Affairs Committee was charged to 1) Update the Center for the Advancement of Pharmacy Education (CAPE) Outcomes and Entrustable Professional Activity (EPA) statements for new pharmacy graduates; 2) Nominate at least one person for an elected AACP or Council Office; and 3) Consider ways that AACP can improve its financial health. This report primarily focuses on the process undertaken by the committee to revise the CAPE Educational Outcomes and EPAs. Proposed changes to the current outcomes are discussed and the reasoning behind these revisions are described. AACP members will have the opportunity to provide feedback prior to the final document being approved and published later this year.

Background Guidelines for perioperative antibiotic prophylaxis in lung transplantation (LT) are limited; since Pseudomonas colonization has been linked to acute graft rejection and development of bronchiolitis obliterans syndrome, some centers utilize an anti-pseudomonal β-lactam as part of the surgical prophylaxis regimen. Internal data from our large academic medical center, a center that does not frequently transplant cystic fibrosis patients, identified low rates of Pseudomonascolonization and infection in LT patients. The surgical prophylaxis regimen was therefore narrowed from vancomycin/piperacillin–tazobactam (VPT) in 2013 to vancomycin/ceftriaxone (VCT). The purpose of this study was to examine the protocol change to on the incidence of Pseudomonas isolation in the post-operative period for lung transplant recipients. Methods This was a single-center, retrospective quasi-experimental before-after study of lung transplant recipients from July 2006 to February 2017 comparing patients who received VPT to VCT for surgical prophylaxis. Patients receiving other surgical prophylaxis regimens due to allergy or colonization history were excluded. Donor and recipient culture data from bronchoscopy samples were collected to determine the incidence of Pseudomonas in the 14-day post-transplant period. The secondary outcome was the incidence of post-transplant CDC-defined pneumonia. Statistical analysis was performed using SAS 9.4 (Cary, NC). Results One hundred patients were included in the pre-protocol group (VPT), and 65 in the post-protocol group (VCT). Pseudomonas was recovered in recipient BALs on post-op day 2–14 in 8 (8%) patients in the VPT group compared with 5 (7.7%) patients in the VCT group (P = 1.0). Mean time to Pseudomonas isolation was 8.4 days in the VPT group compared with 5.4 days in the VCT group. Incidence of pneumonia on post-op day 2–14 was 6% in the VPT group vs. 3% in the VCT group (P = 0.48). Surgical site infections were rare in the VCT group with an incidence of 1.5% (1/65). Conclusion Isolation of Pseudomonas was rare in both time periods and an increase was not detected when anti-pseudomonal coverage was removed from the surgical prophylaxis regimen. Safe deescalation of surgical prophylaxis regimens are an important antimicrobial stewardship initiative. Disclosures E. Heil, ALK-Abelló: Grant Investigator, Research grant.

Sphingosine 1-phosphate (S1P) is a lipid agonist that regulates smooth muscle cell (SMC) and endothelial cell functions by activating several members of the S1P subfamily of G-protein-coupled Edg receptors. We have shown previously that SMC differentiation is regulated by RhoA-dependent activation of serum response factor (SRF). Because S1P is a strong activator of RhoA, we hypothesized that S1P would stimulate SMC differentiation. Treatment of primary rat aortic SMC cells with S1P activated RhoA as measured by precipitation with a glutathione S-transferase-rhotekin fusion protein. In SMC and 10T1/2 cells, S1P treatment up-regulated the activities of several transiently transfected SMC-specific promoters, and these effects were inhibited by the Rho-kinase inhibitor, Y-27632. S1P also increased smooth muscle alpha-actin protein levels in SMC but had no effect on SRF binding to the smooth muscle alpha-actin CArG B element. Quantitative reverse transcriptase-PCR showed that S1P treatment of SMC or 10T1/2 cells did not increase the mRNA level of either of the recently identified SRF co-factors, myocardin or myocardin-related transcription factor-A (MRTF-A). MRTF-A protein was expressed highly in SMC and 10T1/2 cultures, and importantly the effects of S1P were inhibited by a dominant negative form of MRTF-A indicating that S1P may regulate the transcriptional activity of MRTF-A. Indeed, S1P treatment increased the nuclear localization of FLAG-MRTF-A, and the effect of MRTF-A overexpression on smooth muscle alpha-actin promoter activity was inhibited by dominant negative RhoA. S1P also stimulated SMC growth by activating the early growth response gene, c-fos. This effect was not attenuated by Y-27632 but could be inhibited by the MEK inhibitor, UO126. S1P enhanced SMC growth through ERK-mediated phosphorylation of the SRF co-factor, Elk-1, as measured by gel shift and Elk-1 activation assays. Taken together these results demonstrate that S1P activates multiple signaling pathways in SMC and regulates proliferation by ERK-dependent activation of Elk-1 and differentiation by RhoA-dependent activation of MRTF-A.