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Problem-based learning (PBL) offers advantages for teaching anatomy and physiology for physical therapy students as clinical cases provide a scaffold for a comprehensive review of body systems. Although the utilization of interactive anatomy software greatly contributes to an active learning environment and efficient use of time, simply providing textbook readings, access to anatomy software, and models is not enough to engage students to become active in reaching their learning goals. Time constraints, meaningful technology implementation, resource abundance, and unfamiliarity are challenges that decrease the effectiveness of both facilitating and learning anatomy. The present study investigated the use of three supplemental learning tools to support anatomy instruction in a self-regulated manner. Friedman test results demonstrated significant differences for perceived engagement [X[subscript 2](2) = 15.74, P < 0.001, W = 0.23] but not for perceived learning. Survey responses demonstrated that perceived engagement was greatest with the nondigital supplemental learning tool compared with the two technology-enhanced learning tools (iBooks Author + SoftChalk and SoftChalk alone). Multivariate regression analyses demonstrated statistically significant relationships between the nondigital supplemental learning tool and anatomy practical scores (P < 0.001). The technology-enhanced supplemental learning tools did not further increase learning outcomes as measured by practical scores compared with nondigital learning tools. Incorporation of instructor-created instructional materials independent of technology is an efficient method to drive self-regulated learning, enhance engagement, and improve anatomy course outcomes and may overcome barriers associated with a purely self-directed PBL model.

First-year Doctor of Physical Therapy (DPT) students entering a problem-based learning (PBL) program are faced with a number of pedagogical challenges, including the development of self-directed learning skills, resource unfamiliarity, and group dynamics. These challenges can make learning anatomy in a self-directed manner less efficient. Prematriculation introduction of strategies to improve anatomy learning may help prepare students for a rigorous DPT program and improve anatomy learning efficiency. The present study describes a 2-day anatomy workshop offered to incoming students before a DPT program was initiated. Knowledge acquired during both days of the workshop resulted in statistically significant improvements in anatomy postquiz scores for each corresponding prequiz (P[less than] 0.001 for lower and upper limb quizzes). Workshop participants survey responses demonstrated that anatomy confidence and PBL preparedness increased at distinct intervals following the workshop and was significantly higher than controls after the first semester (P[less than]0.01 for anatomy confidence and PBL preparedness). Multivariate regression analyses demonstrated statistically significant relationships between semester anatomy practical scores and workshop participation (P=0.03 for practical 1 and P= 0.049 for practical 2) and undergraduate grade point average (P[less than] 0.001 for practical 1 and P= 0.03 for practical 2). First-year DPT students reported the anatomy workshop to be a valuable experience for learning strategies to improve anatomy self-efficacy. An introductory anatomy workshop is an effective strategy to improve self-directed anatomy learning efficiency before the start of a rigorous DPT program.

Mutations in parkin, an E3 ubiquitin ligase, are the most common cause of autosomal-recessive Parkinson's disease (PD). Here, we show that the stress-signaling non-receptor tyrosine kinase c-Abl links parkin to sporadic forms of PD via tyrosine phosphorylation. Under oxidative and dopaminergic stress, c-Abl was activated in cultured neuronal cells and in striatum of adult C57BL/6 mice. Activated c-Abl was found in the striatum of PD patients. Concomitantly, parkin was tyrosine-phosphorylated, causing loss of its ubiquitin ligase and cytoprotective activities, and the accumulation of parkin substrates,AIMP2 (aminoacyl tRNA synthetase complex-interacting multifunctional protein 2) (p38/JTV-1) and FBP-1.STI-571, a selective c-Abl inhibitor, prevented tyrosine phosphorylation of parkin and restored its E3 ligase activity and cytoprotective function both in vitro and in vivo. Our results suggest that tyrosine phosphorylation of parkin by c-Abl is a major post-translational modification that leads to loss of parkin function and disease progression in sporadic PD. Moreover, inhibition of c-Abl offers new therapeutic opportunities for blocking PD progression. [ABSTRACT FROM AUTHOR]

Abstract: Estrogen involvement in neuroprotection is now widely accepted, although the specific molecular and cellular mechanisms of estrogen action in neuroprotection remain unclear. This study examines estrogenic effects in a mixed population of cells in attempts to identify the contributing cells that result in estrogen-mediated neuroprotection. Utilizing primary mesencephalic neurons, we found expression of both estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) with a predominance of ERα on both dopamine neurons and astrocytes. We also found that 17β-estradiol protects dopamine neurons from injury induced by the complex I inhibitor, 1-methyl-4-phenyl pyridinium (MPP+) in a time- and ER-dependent manner. At least 4 h of estrogen pre-treatment was required to elicit protection, an effect that was blocked by the ER antagonist, ICI 182,780. Moreover, ERα mediated the protection afforded by estrogen since only the ERα agonist, HPTE, but not the ERβ agonist, DPN, protected against dopamine cell loss. Since glial cells were shown to express significant levels of ERα, we investigated a possible indirect mechanism of estrogen-mediated neuroprotection through glial cell interaction. Removal of glial cells from the cultures by application of the mitotic inhibitor, 5-fluoro-2′-deoxyuridine, significantly reduced the neuroprotective effects of estrogen. These data indicate that neuroprotection provided by estrogen against MPP+ toxicity is mediated by ERα and involves an interplay among at least two cell types. [Copyright &y& Elsevier]

This mixed method study assessed the perceptions of health professional graduate students on a sense of belonging and evaluated the engagement experiences valued most in a graduate program across three domains of belonging, academics and diversity, equity and inclusion. Hispanic students valued building professional relationships with faculty and mentors more than non-Hispanic students while non-Hispanic students valued opportunities to discuss race relations outside the classroom. Belonging at the graduate level in health professional programs is distinct from undergraduate programs because of new expectations of developing into entry level clinicians. This study showed that Hispanic students significantly valued building connections with mentors, faculty and staff, identifying a need of continued supportive mentoring relationships within this population at the graduate level. Implications of these findings across the available literature are discussed. [ABSTRACT FROM AUTHOR]

Ethnic-racial under-represented students (URM) exhibit greater attrition rates from physical therapy (PT) doctoral programs. Most predictive analytics in PT education are based on predictors of success in passing the licensure examination. However, data predicting the reasons why these groups of URM students withdraw from PT school are scarce. Admissions variables and academic perform¬ance of seven entry-level Doctor of Physical Therapy (DPT) cohorts (n = 191) from a US university were analyzed from their application and admission through graduation or withdrawal from the program. Through a binary logistic regression, it was found that the main predictors of with¬drawal from the DPT program were URM status (X2 = 8.77; p = 0.004; OR = 21.4) and failing the first practical exam (X2 = 12.30; p < 0.001; OR = 14.2). Those from URM back¬grounds were more than 20 times more likely to withdraw from PT school, while failing the first clinical practical exam increased 14 times the odds of withdrawing from PT school. Admission criteria and targeted retention strategies need to be addressed to ensure the success of URM students to ensure a more diverse PT workforce.

The discovery that impaired autophagy is linked to a wide variety of prominent diseases including cancer and neurodegeneration has led to an explosion of research in this area. Methodologies that allow investigators to observe and quantify the autophagic process will clearly advance knowledge of how this process contributes to the pathophysiology of many clinical disorders. The recent identification of essential autophagy genes in higher eukaryotes has made it possible to analyze autophagy in mammalian cells that express autophagy proteins tagged with fluorescent markers. This chapter describes such methods using primary cultured neurons that undergo up-regulation of autophagy when trophic factors are removed from their medium. The prolonged up-regulated autophagy, in turn, contributes to the death of these neurons, thus providing a model to examine the relationship between enhanced autophagy and cell death. Neurons are isolated from the cerebellum of postnatal day 7 rat pups and cultured in the presence of trophic factors and depolarizing concentrations of potassium. Once established, the neurons are transfected with an adeno-viral vector expressing MAP1-LC3 with red fluorescent protein (RFP). MAP1-LC3 is the mammalian homolog of the yeast autophagosomal marker Atg8 and when tagged to GFP or RFP, it is the most widely used marker for autophagosomes. Once expression is stable, autophagy is induced by removing trophic factors. At various time points after inducing autophagy, the neurons are stained with LysoSensor Green (a pH-dependent lysosome marker) and Hoechst (a DNA marker) and subjected to live-cell imaging. In some cases, time-lapse imaging is used to examine the stepwise process of autophagy in live neurons.