Assessing the benefits of an online prematriculation anatomy workshop on knowledge acquisition and anatomy competency in a Doctor of Physical Therapy program.

Preparing students for the transition to graduate-level education with greater learning demands in a condensed time frame is a challenging process for health professions educators and incoming students. Prematriculation programs offer a solution for exposing students to the foundational sciences in preparation for the academic rigor of a doctoral program. This retrospective study assessed whether incoming students enrolled across 3 yr of a 2-day online anatomy workshop, offered in July and August before the start of their first semester resulted in improved anatomy knowledge.

Association Between Ethnic-Racial Minority Status, Admissions Data, and Academic Performance in Student Retention from a Physical Therapy Program in a Minority-Serving Institution.

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.

Effect of self-regulated learning and technology-enhanced activities on anatomy learning, engagement, and course outcomes in a problem-based learning program.

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.

An anatomy workshop for improving anatomy self-efficacy and competency when transitioning into a problem-based learning, Doctor of Physical Therapy program.

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 Additive Effects of Creatine Supplementation and Exercise Training in an Aging Population: A Systematic Review of Randomized Controlled Trials.

Background And Purpose: The role of creatine supplementation in young athletes and bodybuilders is well established including ergogenic properties of muscular hypertrophy, strength, power, and endurance. Whether the benefits of creatine supplementation translate to an aging population with moderate training stimulus remains unclear especially in regard to gender, creatine dose, and duration. This systematic review assessed whether creatine supplementation combined with exercise results in additive improvements in indices of skeletal muscle, bone, and mental health over exercise alone in healthy older adults.

Estrogen protects against dopamine neuron toxicity in primary mesencephalic cultures through an indirect P13K/Akt mediated astrocyte pathway.

Astrocytes regulate neuronal homeostasis and have been implicated in affecting the viability and functioning of surrounding neurons under stressed and injured conditions. Previous data from our lab suggests indirect actions of estrogen through ERα in neighboring astroglia to protect dopamine neurons against 1-methyl-4-phenylpyridinium (MPP(+)) toxicity in mouse mesencephalic cultures. We further evaluate estrogen signaling in astrocytes and the mechanism of estrogen's indirect neuroprotective effects on dopamine neurons.

Pharmacological analysis of the cortical neuronal cytoskeletal protective efficacy of the calpain inhibitor SNJ-1945 in a mouse traumatic brain injury model.

The efficacy of the amphipathic ketoamide calpain inhibitor SNJ-1945 in attenuating calpain-mediated degradation of the neuronal cytoskeletal protein α-spectrin was examined in the controlled cortical impact (CCI) traumatic brain injury (TBI) model in male CF-1 mice. Using a single early (15 min after CCI-TBI) i.p.

Antioxidant therapies in traumatic brain and spinal cord injury.

Free radical formation and oxidative damage have been extensively investigated and validated as important contributors to the pathophysiology of acute central nervous system injury. The generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is an early event following injury occurring within minutes of mechanical impact. A key component in this event is peroxynitrite-induced lipid peroxidation.

Novel regulation of parkin function through c-Abl-mediated tyrosine phosphorylation: implications for Parkinson's disease.

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.

A pharmacological analysis of the neuroprotective efficacy of the brain- and cell-permeable calpain inhibitor MDL-28170 in the mouse controlled cortical impact traumatic brain injury model.

The cytoskeletal and neuronal protective effects of early treatment with the blood-brain barrier- and cell-permeable calpain inhibitor MDL-28170 was examined in the controlled cortical impact (CCI) traumatic brain injury (TBI) model in male CF-1 mice. This was preceded by a dose-response and pharmacodynamic evaluation of IV or IP doses of MDL-28170 with regard to ex vivo inhibition of calpain 2 activity in harvested brain homogenates. From these data, we tested the effects of an optimized MDL-28170 dosing regimen on calpain-mediated degradation of the neuronal cytoskeletal protein α-spectrin in cortical or hippocampal tissue of mice 24 h after CCI-TBI (1.

IGF-I stimulates Rab7-RILP interaction during neuronal autophagy.

Restoration of autophagy represents a potential therapeutic target for neurodegenerative disorders, but factors that regulate autophagic flux are largely unknown. When deprived of trophic factors, cultured Purkinje neurons die by an autophagy associated cell death mechanism. The accumulation of autophagic vesicles and cell death of Purkinje neurons is inhibited by insulin-like growth factor, by a mechanism that enhances autophagic vesicle turnover.

Insulin-like growth factor-I prevents the accumulation of autophagic vesicles and cell death in Purkinje neurons by increasing the rate of autophagosome-to-lysosome fusion and degradation.

Continuous macroautophagic activity is critical for the maintenance of neuronal homeostasis; however, unchecked or dysregulated autophagy can lead to cell death. Cultured Purkinje neurons die by an autophagy-associated cell death mechanism when deprived of trophic support. Here, we report that insulin-like growth factor-I (IGF-I) completely blocked the autophagy-associated cell death of Purkinje neurons.

Live-cell imaging of autophagy induction and autophagosome-lysosome fusion in primary cultured neurons.

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.

Neuroprotection by estrogen against MPP+-induced dopamine neuron death is mediated by ERalpha in primary cultures of mouse mesencephalon.

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 (ERalpha) and estrogen receptor beta (ERbeta) with a predominance of ERalpha on both dopamine neurons and astrocytes.