Enhancing Pharmacy Faculty Well-Being and Productivity While Reducing Burnout.

Objective To explore methods that pharmacy programs can use to redefine their work environment to reduce stress, improve well-being, and increase faculty productivity.Findings To demonstrate a culture of support, organizations should consider a five-fold approach to enhancing and maintaining faculty well-being, including optimizing faculty and staff support, establishing a faculty development and mentoring program, permitting flexibility in work schedules, improving productivity of meetings, and managing communication tools. Individuals can also take measures to improve their well-being, including controlling email, giving attention to faculty citizenship, implementing stress reduction and coping techniques, and maintaining boundaries between work and home.Summary This article discusses approaches that have been shown to reduce burnout and provides strategies organizations and individuals can implement to improve productivity and faculty well-being. While certain areas, such as faculty wellness and productivity, have been well-studied in the pharmacy and health professions literature, significant gaps were identified in other areas, including alternate work arrangements. In some cases, data from the business sector can be extrapolated to pharmacy education; however, inferences from effective corporate strategies may not be transferable to the culture and expectations of academia. While there is significant overlap between institutional and individual strategies, a culture of communication, collaboration, support, and citizenship is foundational. There is no single strategy that will work for everyone, and flexibility is important to develop an individualized approach.

Determining Indicators of High-Quality Application Activities for Team-Based Learning.

Objective. To determine the indicators of quality for application activities in pharmacy team-based learning (TBL). Methods. A modified Delphi process was conducted with pharmacy TBL experts. Twenty-three experts met the inclusion criteria, including having at least four years of TBL experience, designing at least eight TBL sessions, training others to use TBL, and authoring a peer-reviewed TBL pharmacy paper. In round 1, panelists responded to five open-ended questions about their successful TBL applications activities, including satisfaction with the activity and methods for creating positive student outcomes. In round 2, panelists indicated their level of agreement with the round 1 quality indicators using a four-point Likert rating. Consensus was set at 80% strongly agree/agree. In an open comment period, panelists provided suggestions to help expand the indicator descriptions. Indicators were verified based on TBL and the education literature. Results. Twenty panelists (87% of those eligible) responded in round 1 and 17 (85% participation) in round 2. Sixteen quality indicators were identified in round 1, with 14 achieving consensus in round 2. "Uses authentic pharmacy challenges or situations" (88% strongly agree/agree) and "incorporates or provides effective feedback to groups" (88% strongly agree/agree) met consensus. However, "has multiple right answers" (76% strongly agree/agree) and "incorporates elements from school specific emphases (eg, faith, underserved)" (53% strongly agree/agree) did not reach consensus. Conclusions. These indicators can assist faculty members in designing application activities to provide high-quality TBL exercises that promote deep thinking and engaged classroom discussion. The indicators could also guide faculty development and quality improvement efforts, such as peer review of application activities.

Peer Evaluation Instrument Development, Administration, and Assessment in a Team-based Learning Curriculum.

Objective. To design and implement an instrument capable of providing students with valuable peer feedback on team behaviors and to provide results of the administration of the instrument. Methods. A three-part instrument was designed that requires teammate rankings with justification on attributes aligned with school outcomes and team functioning, reporting of student behaviors, and provision of feedback on the value of peer contributions to their team. Score results after three years of administration were analyzed. Results. Six evaluations per year were completed by members of four different professional classes over a three-year time period. Mean scores increased slightly as students progressed through the program. Students were able to differentially score peers on attributes and behaviors. Conclusion. The peer evaluation instrument presented here provides formative and summative feedback through qualitative and quantitative scores that allow students to acknowledge differential contributions of individual team members.

Orientating nonpharmacist faculty members to pharmacy practice.

OBJECTIVE: To design, implement, and evaluate a faculty development program intended to orient nonpharmacist faculty members to pharmacy practice. DESIGN: A multifaceted program was implemented in 2012 that included 4 shadowing experiences in which faculty members visited acute care, ambulatory care, hospital, and community pharmacy settings under the guidance of licensed preceptors. Itineraries for each visit were based on objective lists of anticipated practice experiences that define the role of the pharmacist in each setting. ASSESSMENT: The 4 shadowing experiences culminated with reflection and completion of a survey to assess the impact of the program. All of the faculty participants agreed that the experience improved their conceptual understanding of contemporary pharmacy practice and the role of the pharmacist in the healthcare setting. The experience also improved faculty comfort with creating practice-relevant classroom activities. CONCLUSIONS: A shadowing experience is an effective way of orienting nonpharmacist faculty members to the practice of pharmacy. This program inspired the creation of an experience to introduce pharmacy practice faculty to pharmaceutical science faculty research initiatives.

Alcohol use disorder: pathophysiology, effects, and pharmacologic options for treatment.

Alcohol use disorders (AUD) continue to be a concerning health issue worldwide. Harmful alcohol use leads to 2.5 million deaths annually worldwide. Multiple options exist for the management of dependence on alcohol, not all of which are approved by drug-regulating agencies. Current practice in treating AUD does not reflect the diversity of pharmacologic options that have potential to provide benefit, and guidance for clinicians is limited. Few medications are approved for treatment of AUD, and these have exhibited small and/or inconsistent effects in broad patient populations with diverse drinking patterns. The need for continued research into the treatment of this disease is evident in order to provide patients with more specific and effective options. This review describes the neurobiological mechanisms of AUD that are amenable to treatment and drug therapies that target pathophysiological conditions of AUD to reduce drinking. In addition, current literature on pharmacologic (both approved and non-approved) treatment options for AUD offered in the United States and elsewhere are reviewed. The aim is to inform clinicians regarding the options for alcohol abuse treatment, keeping in mind that not all treatments are completely successful in reducing craving or heavy drinking or increasing abstinence.

Genetic markers of comorbid depression and alcoholism in women.

BACKGROUND: Alcohol dependence (AD) is often accompanied by comorbid depression. Recent clinical evidence supports the benefit of subtype-specific pharmacotherapy in treating the population of alcohol-dependent subjects with comorbid major depressive disorder (MDD). However, in many alcohol-dependent subjects, depression is a reactive response to chronic alcohol use and withdrawal and abates with a period of abstinence. Genetic markers may distinguish alcohol-dependent subjects with MDD not tied chronologically and etiologically to their alcohol consumption. In this work, we investigated the association of adenylyl cyclase genes (ADCY1-9), which are implicated in both AD and mood disorders, with alcoholism and comorbid depression. METHODS: Subjects from Vienna, Austria (n = 323) were genotyped, and single nucleotide polymorphisms (1,152) encompassing the genetic locations of the 9 ADCY genes were examined. The Vienna cohort contained alcohol-dependent subjects differentiated using the Lesch Alcoholism Typology. In this typology, subjects are segregated into 4 types. Type III alcoholism is distinguished by co-occurrence of symptoms of depression and by affecting predominantly females. RESULTS: We identified 4 haplotypes associated with the phenotype of Type III alcoholism in females. One haplotype was in a genomic area in proximity to ADCY2, but actually within a lincRNA gene, 2 haplotypes were within ADCY5, and 1 haplotype was within the coding region of ADCY8. Three of the 4 haplotypes contributed independently to Type III alcoholism and together generated a positive predictive value of 72% and a negative predictive value of 78% for distinguishing women with a Lesch Type III diagnosis versus women designated as Type I or II alcoholics. CONCLUSIONS: Polymorphisms in ADCY8 and ADCY5 and within a lincRNA are associated with an alcohol-dependent phenotype in females, which is distinguished by comorbid signs of depression. Each of these genetic locations can rationally contribute to the polygenic etiology of the alcoholism/depression phenotype, and the use of these genetic markers may aid in choosing appropriate and beneficial treatment strategies.

Current progress in pharmacologic treatment strategies for alcohol dependence.

Alcoholism is a progressive neurological disorder that represents one of the leading preventable causes of morbidity and mortality in the USA. Individuals with alcohol dependence may exhibit differences in their sensitivity to intoxication, the age at which they begin heavy drinking or the presentation of comorbid psychiatric illness. The heterogeneous nature of the disorder has complicated efforts to predict treatment outcomes, indicating a need for improved diagnostic and therapeutic approaches. Pharmaceutical development has focused on treating the symptoms of alcohol withdrawal, reducing consumption of and craving for alcohol, preventing relapse and treating associated psychiatric problems. Current therapies may be optimized by combining psychosocial and pharmacologic approaches to treat alcoholic patients with the most appropriate regimen to achieve the desired therapeutic outcome. This article will describe the neurobiological mechanisms of dependence on alcohol in brief and review major medications approved for the treatment of alcoholism with regard to recent clinical evidence for the therapeutic efficacy of each agent. Investigations on the use of drugs with other indications (e.g., antidepressants and anticonvulsants) to target alcohol-dependent subtypes will also be discussed.

Phosphorylation regulates removal of synaptic N-methyl-D-aspartate receptors after withdrawal from chronic ethanol exposure.

Alterations in N-methyl-d-aspartate receptor (NMDAR) protein levels or subcellular localization in brain after chronic ethanol exposure may contribute to withdrawal-associated seizures and neurotoxicity. We have investigated synaptic localization of NMDARs in cultured hippocampal pyramidal neurons after prolonged (7 days) exposure to, and acute withdrawal from, 80 mM ethanol using fluorescence immunocytochemistry techniques. After chronic ethanol exposure, there was a significant increase in the clustering of NR1 and NR2B subunits and their colocalization with the synaptic proteins synaptophysin and postsynaptic density protein 95, respectively. There was also increased expression of NR1 variants containing the C2' cassette after chronic ethanol exposure. The ethanol-induced synaptic clustering and colocalization were rapidly reversed within 4 h after ethanol withdrawal. Surface labeling of NR2B subunits suggested that this rapid reversal involved lateral receptor movement to extrasynaptic sites rather than internalization of receptors. Receptor removal from the synapse during ethanol withdrawal was associated with changes in the phosphorylation state of NR2B Ser1480, controlled by the protein kinase CK2. The redistribution of NMDAR to synapses produced by long-term ethanol exposure, as well as the rapid removal during withdrawal, may not only affect neuronal withdrawal hyperexcitability but also may sensitize the system to subsequent synaptic plasticity.

How adaptation of the brain to alcohol leads to dependence: a pharmacological perspective.

The development of alcohol dependence is posited to involve numerous changes in brain chemistry (i.e., neurotransmission) that lead to physiological signs of withdrawal upon abstinence from alcohol as well as promote vulnerability to relapse in dependent people. These neuroadaptive changes often occur in those brain neurotransmission systems that are most sensitive to the acute, initial effects of alcohol and/or contribute to a person's initial alcohol consumption. Studies of these neuroadaptive changes have been aided by the development of animal models of alcohol dependence, withdrawal, and relapse behavior. These animal models, as well as findings obtained in humans, have shed light on the effects that acute and chronic alcohol exposure have on signaling systems involving the neurotransmitters glutamate, γaminobutyric acid (GABA), dopamine, and serotonin, as well as on other signaling molecules, including endogenous opioids and corticotrophin-releasing factor (CRF). Adaptation to chronic alcohol exposure by these systems has been associated with behavioral effects, such as changes in reinforcement, enhanced anxiety, and increased sensitivity to stress, all of which may contribute to relapse to drinking in abstinent alcoholics. Moreover, some of these systems are targets of currently available therapeutic agents for alcohol dependence.

Genetic selection of regulatory mutants of mammalian adenylyl cyclases.

Initial steps in the identification of the Gs alpha-binding site present in mammalian adenylyl cyclases can be achieved with the use of the yeast genetic system described. It must be stressed that this system serves as a means to identify mutants that are candidates; biochemical analysis of these mutants is a next and necessary step in the confirmation of these phenotypes. The system described can be readily adapted for the isolation of additional classes of mammalian adenylyl cyclase mutants including mutants with altered regulation toward forskolin, catalytic abnormalities, or enhanced sensitivities toward activators. In addition, this system can be employed for the isolation of constitutively active adenylyl cyclase mutants, or by coexpressing other adenylyl cyclase isoforms and their known regulators, mutations in the binding sites for these molecules can be elucidated.