Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 551-560 of 1,773 results
Scientific Reports, 2024 • February 20, 2024
This study explores the optimal voltage for high-voltage pulsed radiofrequency (HVPRF) to treat neuropathic pain (NeP) in spared nerve injury (SNI) rats, focusing on pain reduction and underlying mech...
KEY FINDING: HVPRF application on the DRG significantly reduced mechanical allodynia, cold allodynia, and spontaneous pain induced by SNI in rats, with 85VPRF showing the best therapeutic efficacy.
Front. Genet., 2024 • February 13, 2024
Genetic analyses have transformed medicine, leading to personalized treatments and enhanced patient outcomes. Rehabilitation medicine is now incorporating genetics, with initial successes in stroke an...
KEY FINDING: Lack of significant progress in clinical SCI genetics studies is due to inadequate genetic data and lack of uniform endpoints.
Scientific Reports, 2024 • March 9, 2024
This study identified 129 autophagy-related genes that might play a role in SCI, providing new targets for future research and offering new perspectives on the pathogenesis of SCI. The results of the ...
KEY FINDING: A total of 129 autophagy-related DEGs were identified, including 126 up-regulated and 3 down-regulated genes.
J Cell Mol Med, 2024 • January 1, 2024
This study demonstrates the remarkable efficacy of EA intervention in ameliorating pain hypersensitivities induced by CCI and protecting neurons against injury and loss in NP rats. Moreover, EA effect...
KEY FINDING: EA treatment effectively attenuated CCI-induced pain hypersensitivity and mitigated neuron damage and loss in the spinal cord of NP rats.
Frontiers in Immunology, 2024 • March 13, 2024
Spinal cord injury results in tissue debris and an inflammatory microenvironment that inhibits nerve regeneration; macrophages, the primary cells for debris removal, can become foam cells, worsening i...
KEY FINDING: Foam cells persist in the lesion site after SCI and mediate chronic inflammation, which hampers nerve repair.
Drug Design, Development and Therapy, 2024 • April 29, 2024
This paper provides a comprehensive review of the potential molecular biology mechanisms of hydrogen therapy and its application in treating SCI. Hydrogen has been proven to possess anti-inflammatory,...
KEY FINDING: Hydrogen exhibits selective antioxidant action by eliminating excessive harmful free radicals and alleviating cellular damage, thereby promoting recovery from conditions such as cerebral ischemia.
J. Clin. Med., 2024 • May 8, 2024
Spinal cord injuries lead to debilitating neurological impairments. Microglia play a critical role in both inflammation and repair processes following SCI. Numerous therapeutic strategies targeting mi...
KEY FINDING: Microglia play a crucial role in the posttraumatic phenomena, particularly in neuroinflammation following spinal cord injury.
Cell Proliferation, 2024 • October 1, 2024
This study investigates the role of Syvn1 in spinal cord injury (SCI) and its impact on neuronal ferroptosis. It finds that Syvn1 suppresses ferroptosis and promotes functional recovery from SCI in vi...
KEY FINDING: Syvn1 suppresses ferroptosis and promotes functional recovery from SCI in vitro and in vivo.
Frontiers in Cellular Neuroscience, 2024 • May 22, 2024
This study compared the effects of BMP4 alone and a bFGF/BMP4 combination on neural stem cells (NSCs) in vitro, using RNA sequencing to analyze transcriptome profiles and immunofluorescence to validat...
KEY FINDING: Both BMP4 alone and bFGF/BMP4 combination induce a quiescent state in neural stem cells (qNSCs), but they result in different levels of quiescence.
Neurospine, 2024 • June 1, 2024
This study demonstrates that MSC-Exo treatment can effectively inhibit ferroptosis in BV2 cells and promote neurological recovery in SCI rats. The Nrf2/GCH1/BH4 signaling pathway plays a crucial role ...
KEY FINDING: MSC-Exo effectively inhibited the production of ferrous iron, lipid peroxidation products, and ferroptosis-promoting factor prostaglandin-endoperoxide synthase 2.