A standardized curriculum to introduce novice health professional students to practice-based learning and improvement: a multi-institutional pilot study.

BACKGROUND: Practice-based learning and improvement (PBLI) combines the science of continuous quality improvement with the pragmatics of day-to-day clinical care delivery. PBLI is a core-learning domain in nursing and medical education. We developed a workbook-based, project-focused curriculum to teach PBLI to novice health professional students. PURPOSE: Evaluate the efficacy of a standardized curriculum to teach PBLI. DESIGN: Nonrandomized, controlled trial with medical and nursing students from 3 institutions. METHODS: Faculty used the workbook to facilitate completion of an improvement project with 16 participants. Both participants and controls (N = 15) completed instruments to measure PBLI knowledge and self-efficacy. Participants also completed a satisfaction survey and presented project posters at a national conference. RESULTS: There was no significant difference in PBLI knowledge between groups. Self-efficacy of participants was higher than that of controls in identifying best practice, identifying measures, identifying successful local improvement work, implementing a structured change plan, and using Plan-Do-Study-Act methodology. Participant satisfaction with the curriculum was high. CONCLUSION: Although PBLI knowledge was similar between groups, participants had higher self-efficacy and confidently disseminated their findings via formal poster presentation. This pilot study suggests that using a workbook-based, project-focused approach may be effective in teaching PBLI to novice health professional students.

What Do I Do When Something Goes Wrong? Teaching Medical Students to Identify, Understand, and Engage in Reporting Medical Errors.

PROBLEM: Identifying and processing medical errors are overlooked components of undergraduate medical education. Organizations and leaders advocate teaching medical students about patient safety and medical error, yet few feasible examples demonstrate how this teaching should occur. To provide students with familiarity in identifying, reporting, and analyzing medical errors, the authors developed the interactive patient safety reporting curriculum (PSRC), requiring clinical students to engage intellectually and emotionally with personally experienced events in which the safety of one of their patients was compromised. APPROACH: In 2015, the authors incorporated the PSRC into the third-year internal medicine clerkship. Students completed a structured written report, analyzing a patient safety incident they experienced. The report focused on severity of outcome, root cause(s) analysis, system-based prevention, and personal reflection. The report was bookended by 2 interactive, case-based sessions led by faculty with expertise in patient safety, quality improvement, and medical errors. OUTCOMES: Students accurately analyzed the severity of the outcome, and their reports directly led to 2 formal root cause analyses and 4 system-based improvements. NEXT STEPS: The time- and resource-efficient PSRC allows students to apply patient safety knowledge to a medical error they experienced in a way that can directly affect care delivery. This model-interactive learning sessions coupled with engaging in a personally experienced case-can be implemented in various settings. Educators seeking to use student-experienced events for learning should not discount the emotional effects of those events on medical students.

Learning to Overcome Hierarchical Pressures to Achieve Safer Patient Care: An Interprofessional Simulation for Nursing, Medical, and Physician Assistant Students.

To positively impact patient safety, the Institute of Medicine, as well as the Quality and Safety Education for Nurses initiative, has recommended clinician training in structured communication techniques. Such techniques are particularly useful in overcoming hierarchical barriers in health care settings. This article describes an interprofessional simulation program to teach structured communication techniques to preprofessional nursing, medical, and physician assistant students. The teaching and evaluation plans are described to aid replication.

Regulation of matrix metalloproteinase gene expression by a retinoid X receptor-specific ligand.

OBJECTIVE: To evaluate the effects of LG100268 (LG268), a synthetic ligand for the nuclear hormone receptor retinoid X receptor, on the expression of matrix metalloproteinase 1 (MMP-1) and MMP-13 induced by proinflammatory cytokines in a chondrocyte model. METHODS: SW-1353 human chondrosarcoma cells were used to study the effects of LG268 on interleukin-1beta (IL-1beta)-stimulated MMP production and collagen degradation. Gene expression was determined by quantitative real-time reverse transcription-polymerase chain reaction, and protein levels were determined by Western blot analysis. Collagen degradation was determined by an in vitro matrix destruction assay. The effects of LG268 on nuclear protein binding and histone acetylation were determined by electrophoretic mobility shift assay and chromatin immunoprecipitation assay, respectively. RESULTS: LG268 treatment specifically antagonized the IL-1beta-mediated induction of MMP-1 and MMP-13 heterogeneous nuclear RNA, messenger RNA, and protein. The inhibitory effect of LG268 was found to be due to a decrease in the rate of MMP-1 and MMP-13 transcription. LG268 treatment also prevented the in vitro degradation of a type I collagen matrix by IL-1beta-treated SW-1353 cells. The inhibitory effect of LG268 on MMP-1 and MMP-13 transcription appears to be mediated, at least in part, through modulation of histone modification in regions of the MMP-1 and MMP-13 promoters that contain binding sites for activator protein 1 transcription factors. CONCLUSION: These data indicate that LG268 treatment selectively inhibits inflammatory cytokine-induced production of MMP-1 and MMP-13 at the level of gene transcription and blocks collagen destruction by proinflammatory cytokine-stimulated chondrocytic cells. This study is among the first to describe how rexinoids affect gene expression, and the findings suggest that the rexinoid class of compounds may have a future role in preventing the irreversible collagen destruction seen in the arthritides.

Overexpression of collagenase 1 (MMP-1) is mediated by the ERK pathway in invasive melanoma cells: role of BRAF mutation and fibroblast growth factor signaling.

Melanoma progresses as a multistep process where the thickness of the lesion and depth of tumor invasion are the best prognostic indicators of clinical outcome. Degradation of the interstitial collagens in the extracellular matrix is an integral component of tumor invasion and metastasis, and much of this degradation is mediated by collagenase-1 (MMP-1), a member of the matrix metalloproteinase (MMP) family. MMP-1 levels increase during melanoma progression where they are associated with shorter disease-free survival. The Ras/Raf/MEK/ERK mitogen-activated protein kinase (MAPK) pathway is a major regulator of melanoma cell proliferation. Recently, BRAF has been identified as a common site of activating mutations, and, although many reports focus on its growth-promoting effects, this pathway has also been implicated in progression toward metastatic disease. In this study, we describe four melanoma cell lines that produce high levels of MMP-1 constitutively. In each cell line the Ras/Raf/MEK/ERK pathway is constitutively active and is the dominant pathway driving the production of MMP-1. Activation of this pathway arises due to either an activating mutation in BRAF (three cell lines) or autocrine fibroblast growth factor signaling (one cell line). Furthermore, blocking MEK/ERK activity inhibits melanoma cell proliferation and abrogates collagen degradation, thus decreasing their metastatic potential. Importantly, this inhibition of invasive behavior can occur in the absence of any detectable changes in cell proliferation and survival. Thus, constitutive activation of this MAPK pathway not only promotes the increased proliferation of melanoma cells but is also important for the acquisition of an invasive phenotype.