PharmaCORE: Optimizing medical pharmacology education with an innovative instructional dashboard.

WHAT WAS THE EDUCATIONAL CHALLENGE?: Diminishing emphasis on pharmacology education in medical schools has resulted in a concerning lack of prescribing knowledge among physician graduates. These concerns mirror our graduates' expressed dissatisfaction with the structure and quality of pharmacology educational experiences over the past 5 years. WHAT WAS THE SOLUTION?: PharmaCORE, a web-based instructional dashboard, was developed as an interactive faculty development tool to enhance integration and instruction of pharmacology content in pre-clinical curriculum at a US medical school. HOW WAS THE SOLUTION IMPLEMENTED?: PharmaCORE was introduced in Spring 2022 for instructors teaching pharmacology in the pre-clinical curriculum. Instructors used the dashboard to assess coverage of specific drug topics throughout the curriculum and to apply tailored, learner-centered teaching strategies to optimize learner engagement and comprehension. WHAT LESSONS WERE LEARNED THAT ARE RELEVANT TO A WIDER GLOBAL AUDIENCE?: The initial assessment indicated that the dashboard was user-friendly and positively influenced instructor awareness of pharmacology content and learner-centered teaching. This faculty development approach underscores the importance of skill-based mapping and maintaining learner-centered teaching standards to address other integrated subjects and broader curricular challenges. WHAT ARE THE NEXT STEPS?: This study lays the foundation for the broader applicability of instructional dashboards in tracking and addressing curricular challenges across pharmacology and other science subjects. Future steps include more personalized feedback for instructors, creating a student-accessible version, and ongoing monitoring of maintenance measures like milestone exams.

Pharmacy students' perceptions of clinical reasoning development through a foundational thinking application framework.

BACKGROUND AND PURPOSE: Pharmacy students must learn to integrate the foundational and clinical sciences to make therapeutic decisions. There is a need for a developmental framework and scaffolding tools to bridge foundational knowledge with clinical reasoning among novice learners in pharmacy education. Our purpose is to describe the development and student perceptions of a framework designed to integrate foundational knowledge and clinical reasoning in second-year pharmacy students. EDUCATIONAL ACTIVITY AND SETTING: Using script theory as a conceptual model, a Foundational Thinking Application Framework (FTAF) was designed around a four-credit Pharmacotherapy of Nervous Systems Disorders course at the beginning of the second year of the doctor of pharmacy curriculum. The framework was implemented as two structured learning guides known as a unit plan and a pharmacologically based therapeutic evaluation. A total of 71 students in the course were asked to complete a 15-question online survey assessing perceptions towards specific components of the FTAF. FINDINGS: Of 39 survey respondents, 37 (95%) described the unit plan as a useful organizer for the course. Thirty-five (80%) students agreed or strongly agreed that the unit plan helped organize instructional material for a given topic. Students (n = 32, 82%) preferred the pharmacologically based therapeutic evaluation format, with text comments highlighting that it provided good practice for clinical experiences and helped to organize critical thinking. SUMMARY: Our study found that students had positive perceptions of FTAF's implementation within a pharmacotherapy course. Pharmacy education can benefit by adapting script-based strategies that have been successful in other health professions.

Assessment for Deeper Understanding using Concept Maps: Lessons Learned from Flipped Teaching of Pharmacology.

To foster a deeper understanding of pharmacology concepts among physician assistant students, we integrated concept mapping into our flipped teaching to provide assessment for learning. Different mapping-based assessment strategies were adopted based on learner feedback, including in-person collaborative mapping, an individual computerized mapping-based quiz with automated feedback, and a collaborative computerized mapping-based quiz enhanced by the jigsaw strategy. Each mapping activity also leveraged the strength of a specific technology platform. Based on the findings from comparing learner ratings of these mapping activities and thematic analysis of learner feedback, we engaged in critical reflection and share our lessons learned.

A flexible, group-based assessment strategy for Historically Black College and University pharmacy students.

BACKGROUND AND PURPOSE: Historically Black College and University (HBCU) students often have diverse educational backgrounds and learning needs. We describe the implementation of a group-based assessment (GBA) strategy within a pharmacotherapy course at a HBCU. EDUCATIONAL ACTIVITY AND SETTING: Ninety second-year pharmacy students participated in the study, completing eight formative GBAs, two summative exams, and a demographic questionnaire. In this study, GBAs were administered as post-assessments after each topic and prior to an exam. Our pilot study sought to describe mean GBA scores in relation to summative exam performance. Data analysis employed descriptive statistics. FINDINGS: The majority of students were female (61%), identified as either African American (37.8%) or East Asian (35.5%) descent, and claimed English as a second language. The preliminary analysis described student performance levels on Exam 1 and Exam 2 and means of each corresponding GBA. There was a general upward trend in GBA mean scores across the majority of exam performance levels with the exception of GBA 6. GBAs 1 through 4 had the lowest mean scores across all Exam 1 performance levels. SUMMARY: This pilot study described a flexible group-based assessment format that encouraged student-paced learning among HBCU students. Frequent GBA may act as an early-warning system for these students and can engage students earlier in the course to improve academic performance on major exams. Future studies with a larger number of subjects are needed to validate the use of this GBA strategy in similar settings.

Correction to: Comparison of the Effect of Exercise on Late-Phase LTP of the Dentate Gyrus and CA1 of Alzheimer's Disease Model.

The original version of this article unfortunately does not include the second affiliating institution of Dr. Munder A. Zagaar. "Department of Pharmacy Pracce and Clinical Health Sciences, Texas Southern University, Houston, TX 77004" should have been included on the paper.

Correction to: Moderate Treadmill Exercise Protects Synaptic Plasticity of the Dentate Gyrus and Related Signaling Cascade in a Rat Model of Alzheimer's Disease.

The original version of this article unfortunately does not include the second affiliating institution of Dr. Munder A. Zagaar. "Department of Pharmacy Pracce and Clinical Health Sciences, Texas Southern University, Houston, TX 77004" should have been included on the paper.

Correction to: Prevention by Regular Exercise of Acute Sleep Deprivation-Induced Impairment of Late Phase LTP and Related Signaling Molecules in the Dentate Gyrus.

The original version of this article unfortunately does not include the second affiliating institution of Dr. Munder A. Zagaar. "Department of Pharmacy Pracce and Clinical Health Sciences, Texas Southern University, Houston, TX 77004" should have been included on the paper.

Case-based studies in teaching medicinal chemistry in PharmD curriculum: Perspectives of students, faculty, and pharmacists from academia.

BACKGROUND AND PURPOSE: Pharmacy practice has evolved tremendously over the years to meet the demands of the growing healthcare system. Foundational sciences like, medicinal chemistry can enhance the critical-thinking and therapeutic decision-making skills of today's professional pharmacists. The importance of medicinal chemistry for the doctor of pharmacy (PharmD) curriculum has been discussed from the perspectives of medicinal chemistry and practicing clinical faculty whose focused practices vary from infectious diseases to geriatrics. EDUCATIONAL ACTIVITY AND SETTING: An Institutional Review Board (IRB)-approved perception survey and a year-end course evaluation were given to the second and third professional year students. FINDINGS: Eighty-eight percent of the participating second-year students and 92% of the participating third-year students thought that the introduction of case studies in the medicinal chemistry curriculum enhanced their learning and appreciation for the subject. DISCUSSION AND SUMMARY: The Pharmacy Curriculum Outcomes Assessment (PCOA) exams, given at the University of Houston College of Pharmacy during the years of 2013-2015, were briefly discussed. Since the requirement to administer the PCOA went into effect in early 2016, the authors felt that not enough time existed to establish meaningful controls to conduct a correlation study with the student perspective survey results obtained and PCOA data provided in 2015. This study, therefore, highlights the importance of integrated approaches to pharmacy teaching at the University of Houston.

Comparison of the Effect of Exercise on Late-Phase LTP of the Dentate Gyrus and CA1 of Alzheimer's Disease Model.

We investigated the neuroprotective effect of regular treadmill exercise training on long-term memory and its correlate: the late-phase long-term potentiation (L-LTP) and plasticity- and memory-related signaling molecules in the DG and CA1 areas of a rat model of Alzheimer's disease (AD) (i.c.v. infusion of Aß1-42 peptides, 2 weeks, 250 pmol/day). Testing in the radial arm water maze revealed severe impairment of spatial long-term memory in Aß-infused sedentary rats but not in exercised Aß-infused rats. The L-LTP, measured as changes in the field (f)EPSP and in the amplitude of population spike (pspike), was induced by multiple high-frequency stimulation in the CA1 and DG areas of anesthetized rats. The L-LTP of fEPSP in both areas was severely impaired in the sedentary Aß rats but not in exercised Aß rats. However, L-LTP of the pspike was severely suppressed in the CA1 area but not in the DG of sedentary Aß rats. Immunoblot analysis revealed no increase in the levels of phosphorylated (p)-CREB, CaMKIV, and brain-derived neurotrophic factor (BDNF) in both CA1 and DG areas of sedentary Aß rats during L-LTP, whereas the levels of these molecules were robustly increased in exercised Aß rats. Impairment of synaptic function may be due to deleterious changes in the molecular signaling cascades that mediate synaptic structural and functional changes. The protective effect of regular exercise can be a promising therapeutic measure for countering or delaying the AD-like pathology.

Prevention by Regular Exercise of Acute Sleep Deprivation-Induced Impairment of Late Phase LTP and Related Signaling Molecules in the Dentate Gyrus.

The dentate gyrus (DG) and CA1 regions of the hippocampus are intimately related physically and functionally, yet they react differently to insults. The purpose of this study was to determine the protective effects of regular treadmill exercise on late phase long-term potentiation (L-LTP) and its signaling cascade in the DG region of the hippocampus of rapid eye movement (REM) sleep-deprived rats. Adult Wistar rats ran on treadmills for 4 weeks then were acutely sleep deprived for 24 h using the modified multiple platform method. After sleep deprivation, the rats were anesthetized and L-LTP was induced in the DG region. Extracellular field potentials from the DG were recorded in vivo, and levels of L-LTP-related signaling proteins were assessed both before and after L-LTP expression using immunoblot analysis. Sleep deprivation reduced the basal levels of phosphorylated cAMP response element-binding protein (P-CREB) as well as other upstream modulators including calcium/calmodulin kinase IV (CaMKIV) and brain-derived neurotrophic factor (BDNF) in the DG of the hippocampus. Regular exercise prevented impairment of the basal levels of P-CREB and total CREB as well as those of CaMKIV in sleep-deprived animals. Furthermore, regular exercise prevented sleep deprivation-induced inhibition of L-LTP and post-L-LTP downregulation of P-CREB and BDNF levels in the DG. The current findings show that our exercise regimen prevents sleep deprivation-induced deficits in L-LTP as well as the basal and poststimulation levels of key signaling molecules.

Moderate Treadmill Exercise Protects Synaptic Plasticity of the Dentate Gyrus and Related Signaling Cascade in a Rat Model of Alzheimer's Disease.

The dentate gyrus (DG) of the hippocampus is known to be more resistant to the effects of various external factors than other hippocampal areas. This study investigated the neuroprotective effects of moderate treadmill exercise on early-phase long-term potentiation (E-LTP) and its molecular signaling pathways in the DG of amyloid ß rat model of sporadic Alzheimer's disease (AD). Animals were preconditioned to run on treadmill for 4 weeks and concurrently received ICV infusion of Aß1₋42 peptides (250 pmol/day) during the third and fourth weeks of exercise training. We utilized in vivo electrophysiological recordings to assess the effect of exercise and/or AD pathology on basal synaptic transmission and E-LTP magnitude of the perforant pathway synapses in urethane-anesthetized rats. Immunoblotting analysis was used to quantify changes in the levels of learning and memory-related key signaling molecules. The AD-impaired basal synaptic transmission and suppression of E-LTP in the DG were prevented by prior moderate treadmill exercise. In addition, exercise normalized the basal levels of memory and E-LTP-related signaling molecules including Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), calcineurin (PP2B), and brain-derived neurotrophic factor (BDNF). Exercise also prevented the reduction of phosphorylated CaMKII and aberrant increase of PP2B seen after E-LTP induction in amyloid-infused rats. Our data suggests that by restoring the balance of kinase-phosphatase, 4 weeks of moderate treadmill exercise prevents DG synaptic deficits and deleterious alterations in signaling pathways associated with AD.

Regular exercise prevents non-cognitive disturbances in a rat model of Alzheimer's disease.

Previously, we reported that in a rat model of sporadic Alzheimer's disease (AD) generated by exogenous administration of Aß1₋42 (250 pmol/d for 2 wk) via mini-osmotic pump, the animals exhibited learning and memory impairment, which could be attributed to the deleterious alterations in the levels of cognition-related signalling molecules. We showed that 4 wk of treadmill exercise totally prevented these impairments. Here, we evaluated the effect of exercise on non-cognitive function and basal synaptic transmission in the Cornu Ammonis 1 (CA1) area using the same AD model. Our results indicated that the anxiety behaviour of Aß-treated rats was prevented by 4 wk of treadmill exercise. Exercised/Aß-infused rats spent a longer time in the centre area of the open field (OF), elevated plus maze (EPM) paradigms and the light area of the light-dark (LD) box, which were similar to those of control and exercise rats. Furthermore, under basal conditions the aberrant up-regulation of calcineurin (PP2B) and reduction of phosphorylated Ca²âº/calmodulin dependent protein kinase II (p-CaMKII) levels induced by AD-like pathology were normalised by the exercise regimen. We conclude that regular exercise may exert beneficial effects on both cognitive and non-cognitive functions in this AD model.

Neurobiological consequences of sleep deprivation.

Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed.

Regular treadmill exercise prevents sleep deprivation-induced disruption of synaptic plasticity and associated signaling cascade in the dentate gyrus.

STUDY OBJECTIVES: Evidence suggests that regular exercise can protect against learning and memory impairment in the presence of insults such as sleep deprivation. The dentate gyrus (DG) area of the hippocampus is a key staging area for learning and memory processes and is particularly sensitive to sleep deprivation. The purpose of this study was to determine the effect of regular exercise on early-phase long-term potentiation (E-LTP) and its signaling cascade in the presence of sleep deprivation. EXPERIMENTAL DESIGN: Rats were exposed to 4 weeks of regular treadmill exercise then subsequently sleep-deprived for 24h using the modified multiple platform model before experimentation. We tested the effects of exercise and/or sleep deprivation using electrophysiological recording in the DG to measure synaptic plasticity; and Western blot analysis to quantify the levels of key signaling proteins related to E-LTP. MEASUREMENTS AND RESULTS: Regular exercise prevented the sleep deprivation-induced impairment of E-LTP in the DG area as well as the sleep deprivation-associated decrease in basal protein levels of phosphorylated and total α calcium/calmodulin-dependent protein kinase II (P/total-CaMKII) and brain-derived neurotrophic factor (BDNF). High frequency stimulation (HFS) to the DG area was used to model learning stimuli and increased the P-CaMKII and BDNF levels in normal animals: yet failed to change these levels in sleep-deprived rats. However, HFS in control and sleep-deprived rats increased the levels of the phosphatase calcineurin. In contrast, exercise increased BDNF and P-CaMKII levels in exercised/sleep-deprived rats. CONCLUSIONS: Regular exercise appears to exert a protective effect against sleep deprivation-induced spatial memory impairment by inducing hippocampal signaling cascades that positively modulate basal and stimulated levels of key effectors such as P-CaMKII and BDNF, while attenuating increases in the protein phosphatase calcineurin.

Treadmill exercise prevents learning and memory impairment in Alzheimer's disease-like pathology.

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by progressive memory loss. In contrast, accumulating evidence suggests a neuroprotective role of regular exercise in aging associated memory impairment. In this study, we investigated the ability of regular exercise to prevent impairments of short-term memory (STM) and early long-term potentiation (E-LTP) in area CA1 of the hippocampus in a rat model of AD (i.c.v. infusion of 250 pmol/day Aß1-42 peptides). We utilized behavioral assessment, in vivo electrophysiological recording, and immunoblotting in 4 groups of adult Wistar rats: control, treadmill exercise (Ex), ß-amyloid-infused (Aß), and amyloid-infused/treadmill exercised (Ex/Aß). Our findings indicated that Aß rats made significantly more errors in the radial arm water maze (RAWM) compared to all other groups and exhibited suppressed E-LTP in area CA1, which correlated with deleterious alterations in the levels of memory and E-LTP-related signaling molecules including calcineurin (PP2B), brain derivedneurotrophic factor (BDNF) and phosphorylated CaMKII (p-CaMKII). Compared to controls, Ex and Ex/Aß rats showed a similar behavioral performance and a normal E-LTP with no detrimental changes in the levels of PP2B, BDNF, and p- CaMKII. We conclude that treadmill exercise maybe able to prevent cognitive impairment associated with AD pathology.

Regular exercise prevents sleep deprivation associated impairment of long-term memory and synaptic plasticity in the CA1 area of the hippocampus.

STUDY OBJECTIVES: The present study aimed to investigate the effects of treadmill exercise on sleep deprivation (S-D)-induced impairment of hippocampal dependent long-term memory, late phase long-term potentiation (L-LTP) and its signaling cascade in the cornu ammonis 1 (CA1) area. EXPERIMENTAL DESIGN: Animals were conditioned to run on treadmills for 4 weeks then deprived of sleep for 24 h using the columns-in-water method. We tested the effect of exercise and/or S-D on behavioral performance using a post-learning paradigm in the radial arm water maze (RAWM) and in vivo extracellular recording in the CA1 area. The levels of L-LTP-related molecules in the CA1 area were then assessed both before and after L-LTP induction. MEASUREMENTS AND RESULTS: After 24 h of S-D, spatial long-term memory impairment in the RAWM and L-LTP suppression was prevented by 4 weeks of regular exercise. Regular exercise also restored the S-D-associated decreases in the basal levels of key signaling molecules such as: calcium/calmodulin kinase IV (CaMKIV), mitogen-activated protein kinase (MAPK/ERK), phosphorylated cAMP response element-binding protein (P-CREB) and brain derived neurotrophic factor (BDNF), in the CA1 area. After L-LTP induction, regular exercise also prevented the S-D-induced down regulation of BDNF and P-CREB protein levels. CONCLUSIONS: The results suggest that our exercise protocol may prevent 24-h S-D-induced impairments in long-term memory and LTP by preventing deleterious changes in the basal and post-stimulation levels of P-CREB and BDNF associated with S-D.

The beneficial effects of regular exercise on cognition in REM sleep deprivation: behavioral, electrophysiological and molecular evidence.

Inadequate sleep is prevalent in modern societies and is known to profoundly impair cognitive function. We examined the impact of 4 weeks of regular treadmill exercise on sleep deprivation induced spatial learning and memory, synaptic plasticity and related signaling molecules in area CA1 of the rat hippocampus. Rats were exercised on a treadmill and subsequently sleep-deprived for 24h using the modified multiple platform technique. Testing of learning and short-term memory performance in the radial arm water maze showed that although sedentary sleep deprived rats were severely impaired, exercised sleep deprived rats' performance was normal. Extracellular recording from area CA1 of anesthetized rats revealed that early phase LTP (E-LTP) was markedly impaired in the sedentary sleep deprived animals, but was normal in the exercised sleep deprived group. Additionally, immunoblot analysis of CA1 area before (basal) and after expression of E-LTP indicated that the significant down-regulation of the brain derived neurotrophic factor (BDNF) and phosphorylated calcium-calmodulin dependent protein kinase II (P-CaMKII) levels in sleep deprived animals was prevented by the regular exercise regimen. The results suggest that the regular exercise protocol prevents the sleep deprivation induced impairments in short-term memory and E-LTP by preventing deleterious changes in the basal and post-stimulation levels of P-CaMKII and BDNF associated with sleep deprivation.

Exercise prevents sleep deprivation-associated anxiety-like behavior in rats: potential role of oxidative stress mechanisms.

Our previous work suggests that pharmacological induction of oxidative stress causes anxiety-like behavior in rats. Interestingly, sleep deprivation is reported to cause oxidative damage in the brain and is also reported to be anxiogenic. Minimal mechanistic insights are available. In this study, using a behavioral and biochemical approach, we investigated involvement of oxidative stress mechanisms in sleep deprivation-induced anxiety-like behavior of rats and the protective role of treadmill exercise in this process. We report that acute sleep deprivation (SD) increases oxidative stress in the cortex, hippocampus and amygdala while prior treadmill exercise prevents this increase. Serum corticosterones also increase with SD but its levels are normalized in exercised sleep-deprived rats. Also, anxiety-like behavior of rats significantly increases with SD while prior treadmill exercise prevents this increase. Protein expression of two enzymes involved in antioxidant defense, glyoxalase (GLO)-1 and glutathione reductase (GSR)-1 increased after 24h SD in the hippocampus, cortex and amygdala while their levels were normalized in exercised sleep-deprived rats. It is plausible that oxidative stress via regulation of GLO1 and GSR1 is involved in sleep deprivation-induced anxiety-like behavior of rats.