Increasing emphasis has been placed on improving clinician resilience and well-being due to concerning rates of burnout, depression, and suicide in healthcare professionals. Session participants will learn how multiple instiutions have created initiatives that promote a culture of health and well-being for students, staff, and faculty. Particpants will learn about practical strategies for performing an environmental scan of current culture and incorporating assessment tools, educational programs, and workplace wellness into their own organizational initiatives.

Presentation will describe the overarching recommendations put forth by the PMTF and apply findings from the PMTF report in the context of South Central Appalachia.

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Explain the concept of wellbeing and factors that influence it Describe downstream consequences of burnout and distress Analyze personal wellbeing across multiple domains Evaluate the extent to which wellbeing is supported across organization levels Describe interventions that could be implemented to foster a culture of wellbeing

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Objectives: Foster personal and professional development through implementing a 1st-professional year course focused on increasing student self-awareness related to themselves, their chosen profession, and their future careers. Method: Eighty-nine students enrolled in a required 2-credit hour Contemporary Practice of Pharmacy I course during the Fall 2013 semester. Course content aligned closely with the CAPE 2013 Self-Awareness subdomain. Topics included, but were not limited to: effective learning strategies, achievement motivation, finance and time management, professional communication and etiquette, career exploration, and professional history and visioning. Formative and summative evaluations, e-portfolio entries, and submitted assessments and reflections were used to evaluate inaugural course outcomes. Results: Early course self-reflections and self-assessments revealed students particularly appreciated increasing their self-awareness related to strengths, learning strategies, and financial management. However, mid-semester formative evaluations revealed that 75% of students perceived little benefit from the class secondary to previous exposure to course topics. Purposeful activities were used to stress differences between topic exposure and reflection upon and integration of content into one’s self-schema. Summative course evaluations were subsequently positive (median 4 or 5 on 5-point Likert scale for all items), and e-portfolio submissions and course self-reflections indicated self-reported professional and personal growth in multiple domains. Implications: Students benefitted from multiple, purposeful, authentic opportunities to develop personal and professional self-awareness through participation in the course. However, incorporation of perceivably familiar personal and professional development topics in pharmacy curricula may be met with student reservation. Integration of self-awareness opportunities throughout the curriculum may foster student buy-in regarding perceivably familiar topics.

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XXX Pharmacy is an independently-owned retail pharmacy in Johannesburg. Good Pharmacy Practice standards make it mandatory for pharmacists to provide “pharmaceutical care”, a highly patient-centred approach to providing pharmaceutical services. Since XXX Pharmacy has a high patient load, a shortage of dispensary staff and a strategic focus on operational efficiency, the question arose whether pharmacists comply fully with Good Pharmacy Practice standards for the provision of pharmaceutical care. Non-compliance poses operational risks that could undermine the business’s financial performance. The research statement was thus that the current performance management system undermines compliance with Good Pharmacy Practice standards for the provision of pharmaceutical care to patients. A triangulation approach was used. The quantitative research method, in which 200 patients completed a questionnaire, investigated two research objectives: (i) whether the pharmacy complies with Good Pharmacy Practice standards for pharmaceutical care; and (ii) whether there is a relationship between patients’ race or gender and their responses. The qualitative research method involved conducting individual semi-structured interviews with all four dispensary employees to achieve another two research objectives: (i) to determine whether the provision of pharmaceutical care is viewed as a key performance area by pharmacists; and (ii) to investigate what aspects of the implementation of the performance management system are viewed as enabling or undermining the provision of pharmaceutical care.

<div>The human ether-a-go-go-related gene (hERG, KCNH2) potassium channel has been implicated in diverse physiological and pathological processes. The KCNH2 gene encodes a rectifier voltage-gated potassium channel (Kv 11.1) that governs the chief repolarizing current, IKr, which is essential for normal electrical activity in excitable cells such as cardiomyocytes. It is also involved in cell growth and apoptosis regulation in non-excitable cells, such as tumor cells. Dysfunction of hERG is associated with potentially lethal complications, including diseases and sudden death under certain circumstances. While the mechanisms regulating KCNH2 expression remain unclear, recent data suggested that microRNAs (miRNAs) are involved, particularly in the context of several pathologic effects. </div><div>miRNA is a class of RNA defined by its conserved, short, non-coding nature. miRNAs are important regulators of gene expression at the post-transcriptional level that bind through complimentary annealing to the 3’ untranslated regions (3’ UTRs) of target mRNAs, resulting in mRNA destabilization and translational repression. The primary objectives of this research were to 1) identify miRNAs regulating KCNH2 expression in cancer, 2) investigate the potential association between miR-362-3p expression and risk of drug-induced QT interval lengthening, and 3) identify miRNAs potentially regulating KCNH2 expression and function in cardiac cells. </div><div>Through bioinformatics approaches, five miRNAs were identified to potentially regulate KCNH2 expression and function in breast cancer cells. The five identified miRNAs were validated through a Dual-Luciferase Assay using the KCNH2 3′ UTR. Only miR-362-3p was validated to bind to the KCNH2 3’ UTR, decreasing luciferase activity by 10% ± 2.3 (P < 0.001, n = 3) when compared to cells transfected with luciferase plasmid alone. miR-362-3p was also the only miRNA that its expression positively correlated with overall survival of patients with breast cancer from The Cancer Genome Atlas-Cancer Genome (TCGA) database by log-rank test (HR: 0.39, 95% CI: 0.18 to 0.82, P = 0.012). Cell proliferation was assessed by MTS assay (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) 48 hours following transfection in breast cancer cell lines, including SK-BR-3 and MCF-7. miR-362-3p significantly decreased proliferation of SK-BR-3 and MCF-7 cells by 23% ± 8.7 (P = 0.014, n = 3) and 11.7% ± 1.0 (P < 0.001, n = 3), respectively. Cell cycle phases in SK-BR-3 and MCF-7 cells were differentiated by flow cytometry 48 hours following transfection. miR-362-3p and hERG siRNA (positive control) significantly increased the accumulation of cells in G0/G1 phase in MCF-7 by 11.7% (from 51.1% ± 0.64 to 57.1 ± 0.96, P = 0.002, n = 3) and 10% (from 51.1% ± 0.64 to 56.8 ± 0.96, P < 0.001, n = 3), respectively. </div><div>The demonstrated ability of miR-362-3p to regulate hERG in breast cancer cells coupled with previously published data that indicated an alteration of miR-362-3p expression during HF and a potential association between its expression and QT interval prolongation suggesting an important role for this miRNA in regulation of hERG function during HF. Therefore, the contribution of miR-362-3p to hERG function was investigated in patients administered the QT prolonging drug ibutilide, known to inhibit hERG. A total of 22 patients completed a prospective, parallel-group comparative study during which they received subtherapeutic doses (0.003 mg/kg) of ibutilide. The study was originally designed to investigate the influence of heart failure with preserved ejection fraction (HFpEF) on response to drug-induced QT prolongation. Blood for determination of serum Ibutilide concentrations and miR-362-3p expression, along with electrocardiograms (ECGs) were serially collected over a span of 12 hours. ΔΔ-Fridericia-heart rate corrected QT (ΔΔ QTF) intervals were utilized for all analyses to account for baseline and diurnal variation. </div><div>To assess the ability of miR-362-3p to predict ibutilide QT-induced ΔΔQTF changes, nonlinear mixed effects pharmacokinetic/ pharmacodynamic (PKPD) modeling was performed to assess the contribution of miR-362-3p to drug-induced QT interval lengthening. The model that best fit serum ibutilide concentrations versus time was a 3-compartment model with first order elimination and proportional residual errors, while the model that best described the ibutilide concentration- ΔΔQTF relationship was an Emax model with an effect compartment. In addition to miR-362-3p expression, several demographic and clinical data were evaluated as potential covariates on PK and PD parameter estimates. Of tested covariates, heart failure (HF) status on Emax (ΔOFV = -4.1; P < 0.05), and miR-362-3p expression on EC50 (ΔOFV = -9.9; P < 0.05) were incorporated in the final PKPD model. The mean individual Emax was significantly higher in HF patients when compared to non-HF patients (P = 0.015), while EC50 was negatively correlated with miR-362-3p expression (P < 0.0001, R2 0.93). </div><div>Previous evidence indicates that miR-362-3p is altered in patients with HF. In addition, several miRNAs commonly regulate the same ion channel. Therefore, we have developed a large-scale high-throughput bioassay (HT-bioassay) to explore and identify other miRNAs potentially involved in KCNH2 expression and function in human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CM) during sustained β-adrenergic receptor (βAR) stimulation or overexpression of activated calcium/calmodulin-dependent protein kinase 2 (CaMKII), which are classical consequences of HF. </div><div>Through bioinformatic approaches, putative miRNA binding sites (n=327) were identified in the KCNH2 3′ UTR. Fragments containing these putative binding sites were synthesized, cloned into linearized plasmids, and amplified. The plasmid pool was transfected into hiPS-CM cells either treated with βAR stimulation or overexpressing CaMKII. Next-generation sequencing was performed to identify: 1) expression of putative miRNA binding sites and 2) endogenous miRNAs versus control. Eight predicted binding sites were found to be significantly downregulated in the CAMKII group (P <0.05, log fold change -0.287 to -0.59), and six significantly downregulated in the sustained βAR group (P <0.05, log fold change -0.29 to -0.72). Two binding sites were significantly reduced in both treatment groups (P < 0.05, log fold change between -0.38 and -0.61).</div><div>Thirty-one miRNAs were predicted to bind to the 16 binding sites identified from the bioassay. Of these, seven were selected for further screening using dual luciferase assays. None of the putative miRNAs reduced luciferase activity. However, hERG expression was assessed by immunoblot analysis following transfection of the seven miRNAs into HEK293 cells stably expressing hERG (HEK293-hERG). Six of the seven miRNA mimics reduced hERG protein expression. An additional validation step was performed by assessing hERG-related current density by whole cell electrophysiology, in which three of the six miRNAs inhibited hERG protein transfected into HEK293-hERG cells. Those same three miRNA mimics significantly decreased Ikr current (P <0.05). </div><div>Finally, expression of the miRNAs identified by HT-bioassay was examined in the patients enrolled in the clinical trial in which genome-wide next generation sequencing was performed on miRNAs extracted from whole blood samples. Of the 31 miRNAs identified from HT-bioassay, six were found to be expressed in patients (n = 12). A correlation analysis was performed between levels of the expressed miRNAs and corresponding QTF interval lengthening with ibutilide. Of the six miRNAs, only miR-4665-5p was significantly associated with QTF interval (P = 0.0379). </div><div>In summary, miR-362-3p was identified to regulate hERG, and reduces proliferation of breast cancer cells through a mechanism that may be partially mediated by hERG inhibition. While miR-362-3p may have modest effects in cancer, in Aim 2 we demonstrated that it along with HF status accounts for a significant amount of variability in QTF prolongation following ibutilide administration. However, it is common for several miRNAs to regulate a single ion channel. Therefore, an HT-bioassay was developed to identify all miRNAs that potentially regulate KCNH2 during HF. In addition to miR-362-3p, thirty-one miRNAs were predicted to regulate KCNH2; one miRNA (miR-4665-5p) was significantly associated with QTF prolongation. The potential for miR-362-3p and HT-bioassay-identified miRNAs to reduce hERG-related current and influence susceptibility to drug-induced QT interval prolongation warrants further investigation. </div><div><br></div>