Browse the latest research summaries in the field of genetics for spinal cord injury patients and caregivers.
Showing 711-720 of 1,773 results
CNS Neuroscience & Therapeutics, 2025 • March 11, 2025
This study investigates the role of ferritinophagy-mediated ferroptosis in spinal cord ischemia-reperfusion injury (SCIRI) and the potential therapeutic effects of hydrogen sulfide (H2S). The results ...
KEY FINDING: SCIRI induces autophagic ferritin degradation, leading to iron-dependent ferroptosis.
Military Med Res, 2021 • May 12, 2021
This is a correction article addressing errors in figures in a previous publication regarding the conversion of astrocytes to motor neuron-like cells using small molecules. The corrected figures and s...
KEY FINDING: Small molecules can induce morphological changes in human astrocytes, converting them into neuron-like cells.
Cell Bioscience, 2021 • March 24, 2021
This study investigates the evolutionary divergence in tail regeneration between Xenopus laevis and Xenopus tropicalis. The researchers found that Xenopus tropicalis lacks the refractory period observ...
KEY FINDING: Xenopus laevis tadpoles exhibit a refractory period (stages 45-47) during which they cannot regenerate their tails after amputation.
Cell and Tissue Research, 2022 • November 25, 2021
Rodent studies tracing endogenous NSCs in injuries and disease have revealed diversified roles for these cells depending on the model system. In SCI-based models, many endogenous NSCs have been found ...
KEY FINDING: Endogenous NSCs can contribute to reactive gliosis by differentiating into reactive astrocytes, while in other models, they can provide new myelination and neural replacement.
J Comp Neurol, 2016 • February 1, 2016
We examined whether there were changes in the number of different types of synapses during the development of chronic orofacial pain after CCI-ION. Our data indicate that trigeminal nerve injury leads...
KEY FINDING: Trigeminal nerve injury leads to an increase in R-synaptic profiles (presumably excitatory synapses) in lamina I of Vc/C2.
Neuroimmunol Neuroinflamm, 2019 • January 1, 2019
This review explores the roles of microRNAs (miRNAs) in spinal cord injury (SCI) pathophysiology, focusing on how miRNAs modulate key molecular processes such as neuroplasticity, astrogliosis, neuropa...
KEY FINDING: miRNAs are deregulated after SCI and impact inflammation, oxidative stress, and apoptosis, which are crucial for progressive pathogenesis in SCI, suggesting that abnormal miRNA expression may contribute to SCI pathogenesis.
Neurochemical Research, 2023 • September 12, 2022
This study investigates the context-dependent effects of the complement peptide C3a on primary mouse astrocytes under different conditions: naive, after chemical ischemia, and after exposure to lipopo...
KEY FINDING: C3a down-regulated the expression of Gfap, C3 and Nes in astrocytes after ischemia, suggesting a reduction in reactive astrocyte markers in this context.
Frontiers in Cellular and Infection Microbiology, 2023 • May 5, 2023
This study investigates the pathogenic mechanisms of Prototheca wickerhamii by integrating transcriptomics, proteomics, and metabolomics data from different strains. The researchers identified that do...
KEY FINDING: Mannan endo-1,4-b-mannosidase was significantly downregulated in the mucous strain (S1) of P. wickerhamii, contributing to a thinner cell wall.
ASSAY and Drug Development Technologies, 2015 • September 1, 2015
The study developed two HCA assays to investigate reactive-like changes in astrocytes: one measuring the stellation index (GFAP+ process area/cell body area) and another monitoring the expression of g...
KEY FINDING: The GFAP morphology assay is suitable for counter-screening with a Z-factor of 0.44 – 0.03.
American Journal of Pathology, 2015 • September 1, 2015
This study investigates the role of astrocyte activation, specifically via Stat3 signaling, in determining whether oligodendrocytes or Schwann cells are responsible for remyelination in the CNS after ...
KEY FINDING: Ablation of astrocyte activation leads to decreased oligodendrocyte-mediated remyelination.