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1. Learning Environments and Evidence-Based Practices in Bioengineering and Biomedical Engineering

Author

Billiar, Kristen, Gaver, Donald P, Barbee, Kenneth, Singh, Anita, DesJardins, John D, Pruitt, Beth, Tranquillo, Joe, Gaudette, Glenn, Winkelstein, Beth, Makowski, Lee, Amos, Jennifer R, Saterbak, Ann, LeDoux, Joe, Helmke, Brian, Grimm, Michele, Benkeser, Paul, Segan, LeAnn Dourte, Pfister, Bryan, Meaney, David, Arinzeh, Treena, and Margulies, Susan

Subjects
Curriculum and Pedagogy, Education, Bioengineering, Quality Education, Experiential learning, Learning environments, Problem-basedlearning, Project-based learning, Team-based learning
Abstract

This paper provides a synopsis of discussions related to the Learning Environments track of the Fourth BME Education Summit held at Case Western Reserve University in Cleveland, Ohio in May 2019. This summit was organized by the Council of Chairs of Bioengineering and Biomedical Engineering, and participants included over 300 faculty members from 100+ accredited undergraduate programs. The Learning Environments track had six interactive workshops that provided facilitated discussion and provide recommendations in the areas of: (1) Authentic project/problem identification in clinical, industrial, and global settings, (2) Experiential problem/project-based learning within courses, (3) Experiential learning in co-curricular learning settings, (4) Team-based learning, (5) Teaching to reach a diverse classroom, and (6) innovative platforms and pedagogy. A summary of the findings, best practices and recommendations from each of the workshops is provided under separate headings below, and a list of resources is provided at the end of this paper.

Published
2022

3. Biomechanical Model of Low Back Pain

Author

Winkelstein, Beth, Jaumard, Nicolas, Migliore, Michele, Section editor, Linster, Christiane, Section editor, Cavarretta, Francesco, Section editor, Jaeger, Dieter, editor, and Jung, Ranu, editor

Published
2022
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6. Manual therapy and exercise effects on inflammatory cytokines: a narrative overview.

Author

Cook, Chad E., Keter, Damian, Cade, William Todd, Winkelstein, Beth A., and Reed, William R.

Subjects
FEAR, MUSCULOSKELETAL pain, IRRITABLE colon, MULTIPLE sclerosis, EXERCISE therapy, MANIPULATION therapy, TREATMENT effectiveness, ANXIETY, GRANULOCYTE-macrophage colony-stimulating factor, PSYCHOLOGICAL stress, CYTOKINES, INFLAMMATION, SLEEP quality, CHRONIC fatigue syndrome, INTERLEUKINS, TUMOR necrosis factors, DIET, MENTAL depression, ASTHMA, EVALUATION
Abstract

Background: Matching disease and treatment mechanisms is a goal of the Precision Medicine Initiative. Pro- and anti-inflammatory cytokines (e.g., Tumor Necrosis Factor-alpha, Transforming Growth Factor-beta, and Interleukin-2, 10, and 12) have gained a significant amount of interest in their potential role in persistent pain for musculoskeletal (MSK) conditions. Manual therapy (MT) and exercise are two guideline-recommended approaches for treating MSK conditions. The objective of this narrative overview was to investigate of the effects of MT and exercise on pro- and anti-inflammatory cytokines and determine the factors that lead to variability in results. Methods: Two reviewers evaluated the direction and variabilities of MT and exercise literature. A red, yellow, and green light scoring system was used to define consistencies. Results: Consistencies in responses were seen with acute and chronic exercise and both pro- and anti-inflammatory cytokines. Chronic exercise is associated with a consistent shift towards a more anti-inflammatory cytokine profile (Transforming Growth Factor-beta, and Interleukin-2 and 13, whereas acute bouts of intense exercise can transiently increase pro-inflammatory cytokine levels. The influence of MT on cytokines was less commonly studied and yielded more variable results. Conclusion: Variability in findings is likely related to the subject and their baseline condition or disease, when measurement occurs, and the exercise intensity, duration, and an individual's overall health and fitness. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury

Author

Crosby, Nathan D, Zaucke, Frank, Kras, Jeffrey V, Dong, Ling, Luo, Z David, and Winkelstein, Beth A

Subjects
Neurodegenerative, Neurosciences, Peripheral Neuropathy, Chronic Pain, Physical Injury - Accidents and Adverse Effects, Pain Research, 2.1 Biological and endogenous factors, Aetiology, Neurological, Action Potentials, Amines, Analgesics, Animals, Arthralgia, Cyclohexanecarboxylic Acids, Excitatory Postsynaptic Potentials, Gabapentin, Ganglia, Spinal, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Hyperalgesia, Joint Capsule, Male, Neurons, Pain Measurement, Rats, Spinal Cord, Synapses, Thrombospondins, Time Factors, Tubulin, Zygapophyseal Joint, gamma-Aminobutyric Acid, Clinical Sciences, Psychology, Neurology & Neurosurgery
Abstract

Facet joint injury induces persistent pain that may be maintained by structural plasticity in the spinal cord. Astrocyte-derived thrombospondins, especially thrombospondin-4 (TSP4), have been implicated in synaptogenesis and spinal sensitization in neuropathic pain, but the TSP4 response and its relationship to synaptic changes in the spinal cord have not been investigated for painful joint injury. This study investigates the role of TSP4 in the development and maintenance of persistent pain following injurious facet joint distraction in rats and tests the hypothesis that excitatory synaptogenesis contributes to such pain. Painful facet joint loading induces dorsal horn excitatory synaptogenesis along with decreased TSP4 in the DRG and increased astrocytic release of TSP4 in the spinal cord, all of which parallel the time course of sustained tactile allodynia. Blocking injury-induced spinal TSP4 expression with antisense oligonucleotides or reducing TSP4 activity at its neuronal receptor in the spinal cord with gabapentin treatment both attenuate the allodynia and dorsal horn synaptogenesis that develop after painful facet joint loading. Increased spinal TSP4 also facilitates the development of allodynia and spinal hyperexcitability, even after non-painful physiological loading of the facet joint. These results suggest that spinal TSP4 plays an important role in the development and maintenance of persistent joint-mediated pain by inducing excitatory synaptogenesis and facilitating the transduction of mechanical loading of the facet joint that leads to spinal hyperexcitability.

Published
2015

18. Pain Biomechanics

Author

Crosby, Nathan D., Smith, Jenell R., Winkelstein, Beth A., The Medical College of Wisconsin Inc on behalf of Narayan Yoganandan, Yoganandan, Narayan, editor, Nahum, Alan M., editor, and Melvin, John W., editor

Published
2015
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36. MMPs Regulate Neuronal Substance P After a Painful Equibiaxial Stretch in a Co-Culture Collagen Gel Model Simulating Injury of an Innervated Ligament

Author

Ita, Meagan E. and Winkelstein, Beth A.

Subjects
Mechanical Engineering, General Materials Science, Industrial and Manufacturing Engineering, Computer Science Applications
Abstract

Chronic joint pain is a major health problem that can result from abnormal loading of the innervated ligamentous capsule that surrounds synovial joints. The matrix metalloproteinases-1 (MMP-1) and MMP-9 are hypothesized pain mediators from stretch-induced injuries since they increase in pathologic joint tissues and are implicated in biomechanical and nociceptive pathways that underlay painful joint injuries. There is also emerging evidence that MMP-1 and MMP-9 have mechanistic interactions with the nociceptive neuropeptide substance P. Yet, how a ligament stretch induces painful responses during sub-failure loading and whether MMP-1 or MMP-9 modulates nociception via substance P are unknown. We used a neuron–fibroblast co-culture collagen gel model of the capsular ligament to test whether a sub-failure equibiaxial stretch above the magnitude for initiating nociceptive responses in neurons also regulates MMP-1 and MMP-9. Pre-stretch treatment with the MMP inhibitor ilomastat also tested whether inhibiting MMPs attenuates the stretch-induced nociceptive responses. Because of the role of MMPs in collagen remodeling, collagen microstructural kinematics were measured in all tests. Co-culture gels were incubated for one week in either normal conditions, with five days of ilomastat treatment, or with five days of a vehicle control solution before a planar equibiaxial stretch that imposed strains at magnitudes that induce pain in vivo and increase nociceptive modulators in vitro. Force, displacement, and strain were measured, and polarized light imaging captured collagen fiber kinematics during loading. At 24 h after stretch, immunolabeling quantified substance P, MMP-1, and MMP-9 protein expression. The same sub-failure equibiaxial stretch was imposed on all co-cultures, inducing a significant re-organization of collagen fibers (p ≤ 0.031) indicative of fiber realignment. Stretch induces a doubling of substance P expression in normal and vehicle-treated co-cultures (p = 0.038) that is prevented with ilomastat treatment (p = 0.114). Although MMP-1 and MMP-9 expression are unaffected by the stretch in all co-culture groups, ilomastat treatment abolishes the correlative relationships between MMP-1 and substance P (p = 0.002; R2 = 0.13) and between MMP-1 and MMP-9 (p = 0.007; R2 = 0.11) that are detected without an inhibitor. Collectively, these findings implicate MMPs in a painful ligamentous injury and contribute to a growing body of work linking MMPs to nociceptive-related signaling pathways and/or pain.

Published
2022

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