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Functional Electrical Stimulation (FES): Clinical successes and failures to date

Published on: 2nd November, 2018

OCLC Number/Unique Identifier: 7929240992

Non-invasive electrical stimulation in the form of neuromuscular electrical stimulation (NMES) and functional electrical stimulation (FES) has been documented as an optional assessment and treatment technology for decades. In contrast, translation of the robust clinical evidence supporting the effectiveness of FES’ enhancement of muscle force generation and adding to the recovery of motor control following damage to the brain appears limited. Furthermore, enabling many patients to regain locomotion ability though utilization of FES as a standard care option in rehabilitation medicine remains unmet. This perspective evolved over years of collaborative experience in clinical research, teaching, and patient care having a common goal of advancing patients’ rehabilitation outcomes. The clinical successes are supported by repeated evidence of FES utilization across the life span, from toddlers to elders, from hospitals’ critical care units to the home environment. The utilization include managing multiple deficits associated with the musculo-skeletal, neurological, cardio-pulmonary, or peripheral vascular systems. These successes were achieved in no small part because of the technological advancement leading to today’s wearable wireless FES systems that are being used throughout the continuum of rehabilitation care. However, failures to benefit from FES utilization are likewise numerous, collectively depriving most patients from using the technology to maximize their rehabilitation gains. The most critical failures are both clinical and technological. Whereas numerous barriers to NMES and FES utilization have been published, the focus of this perspective is on barriers not considered to date.
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Neuroprotective Effect of 7,8-dihydroxyflavone in a Mouse Model of HIV-Associated Neurocognitive Disorder (HAND)

Published on: 18th September, 2024

Treatment for HIV-associated neurocognitive disorders (HAND) remains elusive. 7,8-dihydroxyflavone (DHF), an analog of brain-derived neurotrophic factor (BDNF) and a high-affinity TrkB agonist, has been proposed as a viable therapeutic alternative to BDNF in crossing the Blood-Brain Barrier (BBB) and promoting growth, differentiation, maintenance, and survival of neurons. Here, we expand on our previous study investigating the therapeutic role of DHF on the cortical and hippocampal brain regions of the Tg26 mice, an animal model of HAND. We detected increased immunoreactivity for ion channels (SUR1, TRPM4) and the water channel aquaporin-4 (AQP4), suggesting an ionic and osmotic imbalance in the brains of Tg26 mice. Tg26 mice also exhibited loss of synaptic stability (SYN, SYP) and nicotinamide metabolism (NAMPT, SIRT1) that were associated with astrogliosis. Furthermore, Tg26 mice demonstrated increased iNOS and reduced HO-1/NRF2 expressions, implicating increased ER and oxidative stress. DHF treatment in Tg26 mice reversed these pathological changes. These data suggest crosstalk among TrkB, Akt, and related transcription factors (NF-κB, STAT3, and NRF2) as an underlying mechanism of Tg26-associated pathology in the brain. Finally, taken together with our prior study, these results further highlight a therapeutic role of DHF in promoting neuroprotection in HAND that may be applied in conjunction with current antiviral therapies.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat
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