Publications by authors named "Jenny Fortun"

Introduction: Sedating and anesthetic drugs are widely used in clinical practice; however, relevant teaching remains underrepresented in undergraduate medical education. We developed a 2-hour flipped classroom activity integrating foundational science topics, evidence-based medicine, and clinical reasoning on anesthetic pharmacology for preclinical medical students.

Methods: Presession, second-year medical students reviewed a study guide and completed a readiness assessment.

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Introduction and objective Interstitial lung disease (ILD) is a subject with which preclinical medical students often struggle. Because case-based learning (CBL) engages students in discussions centered around complex clinical scenarios, it may be effective for teaching ILD to preclinical medical students by fostering the development of critical thinking and clinical reasoning skills. Methods Lecture-based learning on ILD in the second-year Respiratory System course was replaced with a large group CBL session.

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When we reflect on medical education as a whole, novelty in structure and content promotes growth and enhances student outcomes. The teaching of neurology is no different and presents a more unique hurdle in its instruction considering the well-described phenomenon of . With the burden of neurological diseases on the rise, there is a heightened demand for medical educators to understand the possible causes of this educational misalignment and implement solutions necessary to ensure adequate education of students.

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Dysregulation of the autonomic nervous system is an important long-term consequence of spinal cord injury (SCI). Yet, there is a scarcity of teaching resources about this topic for preclinical medical students. Given the association of SCI sequelae with emergency complications and mortality, it is imperative to equip medical students with the ability to recognize them.

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Objective The coronavirus disease 2019 (COVID-19) pandemic has led to massive disruptions in medical education. In the fall of 2020, newly matriculated medical students around the country started medical school in a remote learning setting. The purpose of this study is to assess the impact of remote learning during the COVID-19 pandemic on academic performance and student satisfaction among first-year medical students.

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Here we propose the use of adeno-associated virus (AAV) vectors as a non-invasive vehicle for the nervous system to deliver genes to spinal motoneurons, based on their retrograde transport from muscle. Long-term protein expression in lower cervical motoneurons was achieved after injections of AAV into the triceps, independently of serotypes 1, 2, or 5. Muscle injections of AAV5-neurotrophin 3 (NT3) resulted in a significant increase in the levels of NT3 in the cervical enlargement, compared to those obtained after injections of AAV5-GFP.

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The accumulation of misfolded proteins is associated with various neurodegenerative conditions. Peripheral myelin protein 22 (PMP22) is a hereditary neuropathy-linked, short-lived molecule that forms aggresomes when the proteasome is inhibited or the protein is mutated. We previously showed that the removal of pre-existing PMP22 aggregates is assisted by autophagy.

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Charcot-Marie-Tooth disease type 1A (CMT1A) is commonly associated with duplication of the peripheral myelin protein 22 (PMP22) gene. Mice expressing seven copies of the human PMP22, termed C22, suffer from a demyelinating neuropathy and display phenotypic traits of CMT1A. In this article, we investigate whether protein aggregates play a role in the CMT1A-like pathology of C22 mice.

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A cDNA fragment originally identified in U-937 cells as a vitamin D(3)-regulated gene is here designated the glutamate-rich WD-repeat (GRWD1) gene. WD-repeat proteins are a class of functionally divergent molecules that cooperate with other proteins to regulate cellular processes. GRWD1 encodes a 446-amino-acid protein containing a glutamate-rich region followed by four WD repeats.

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Accumulation of misfolded proteins and alterations in the ubiquitin-proteasome pathway are associated with various neurodegenerative conditions of the CNS and PNS. Aggregates containing ubiquitin and peripheral myelin protein 22 (PMP22) have been observed in the Trembler J mouse model of Charcot-Marie-Tooth disease type 1A demyelinating neuropathy. In these nerves, the turnover rate of the newly synthesized PMP22 is reduced, suggesting proteasome impairment.

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The presence of protein aggregates in the nervous system is associated with various pathological conditions, yet their contribution to disease mechanisms is poorly understood. One type of aggregate, the aggresome, accumulates misfolded proteins destined for degradation by the ubiquitin-proteasome pathway. Peripheral myelin protein 22 (PMP22) is a short-lived Schwann cell (SC) protein that forms aggresomes when the proteasome is inhibited or the protein is overexpressed.

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