Spinal Cord Injury (SCI) alters the excitability of neurons below the lesion, contributing to sensorimotor impairments. Less commonly acknowledged is SCI-related neuropathic pain (SCI-NP) that develops during the chronic phase of SCI, whose neural mechanisms are not yet fully understood. Previous work has demonstrated that electrical intraspinal microstimulation (ISMS) delivered amidst the spinal motor pools inside the ventral spinal gray matter causes an unexpected depression of sensory neuron responsiveness to nociceptive transmissions [1]. Given the lack of efficacious therapeutics for SCI-NP, we explored whether ISMS delivered in the sensory-dominant dorsal horn of the spinal cord could drive more robust depressive effects on pain-related transmission. Preliminary outcomes looked at population-level and single neuron-level modulatory actions of ISMS on neural transmission throughout the gray matter of a single segment of the lumbar enlargement in vivo in rats. Our preliminary results suggest dorsal ISMS may be less efficacious than motor-targeted ISMS at reducing spinal responsiveness to nociceptive sensory feedback. Future work will be required to determine the consistency of this finding and, if warranted, to optimize the stimulation parameters for multi-modal and/or pain-related applications.
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http://dx.doi.org/10.1109/EMBC53108.2024.10781916 | DOI Listing |
Front Immunol
March 2025
Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Background: Osteosarcoma, an aggressive bone malignancy predominantly affecting children and adolescents, presents significant therapeutic challenges with a 5-year survival rate below 30% in metastatic cases. T-cell exhaustion, characterized by the overexpression of immune checkpoint molecules, contributes to osteosarcoma progression and immune evasion. Although targeting these inhibitory pathways has shown potential in restoring T-cell activity, the molecular regulators of T-cell depletion in osteosarcoma are poorly understood.
View Article and Find Full Text PDFFront Neurol
February 2025
Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, China.
Background: Varicella-zoster virus (VZV) central nervous system infection is typically observed in immunocompromised patients, and there is a lack of studies involving large samples of non-immunocompromised individuals. In this study, we retrospectively analyzed 108 non-immunocompromised patients diagnosed with VZV central nervous system infection.
Methods: This retrospective study was conducted in the Department of Neurology, Affiliated Nanjing Brain Hospital, Nanjing Medical University, China.
Front Cell Dev Biol
February 2025
Wayne State University, Detroit, MI, United States.
Fluids Barriers CNS
March 2025
School of Veterinary Medicine, University of Surrey, Guildford, GU2 7XH, UK.
Cerebrospinal fluid (CSF) plays a crucial role in maintaining brain homeostasis by facilitating the clearance of metabolic waste and regulating intracranial pressure. Dysregulation of CSF flow can lead to conditions like syringomyelia, and hydrocephalus. This review details the anatomy of CSF flow, examining its contribution to waste clearance within the brain and spinal cord.
View Article and Find Full Text PDFJ Neuroinflammation
March 2025
Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Spinal cord injury (SCI) can cause permanent dysfunction proceeding from multifaceted neuroinflammatory processes that contribute to damage and repair. Fidgetin-like 2 (FL2), a microtubule-severing enzyme that negatively regulates axon growth, microglial functions, and wound healing, has emerged as a potential therapeutic target for central nervous system injuries and neuroinflammation. To test the hypothesis that FL2 knockdown increases acute neuroinflammation and improves recovery after SCI, we examined the effects of nanoparticle-encapsulated FL2 siRNA treatment after a moderate contusion SCI in rats.
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