The analysis of injury-reactivated tectal radial glia in zebrafish reveals a stochastic cell-cycle entry and cell-state-dependent regulation of the balance between neurogenesis and gliogenesis.
Terren K Niethamer, Collin T Stabler ... Edward E Morrisey
Single-cell RNA sequencing reveals extensive endothelial cell (EC) heterogeneity throughout the lung vasculature and identifies two distinct populations, Car4-high ECs and proliferative ECs, that preferentially respond to lung injury.
Peripheral injury induces a programmed but reversible transformation of gene expression in somatosensory neurons providing a mechanism to regulate sensory input during wound healing.
In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.
Abel Torres-Espín, Jenny Haefeli ... The TRACK-SCI Investigators
The application of topological network analysis on multicenter high-frequency intra-operative physiology data discovers a precise range of blood pressure during surgery predicting poor recovery in spinal cord injury patients.
Nicole A Terpolilli, Reinhard Dolp ... Nikolaus Plesnila
High mortality following traumatic brain injury in mice carrying a human mutation for familial hemiplegic migraine type 1 (FHM1) is caused by a decreased threshold for cortical spreading depolarizations (CSDs) and subsequent brain edema formation.
Jordan W Squair, Seth Tigchelaar ... Michael A Skinnider
Integrating decades of small-scale experiments with human gene expression data provides a systems-level view of the coordinated molecular processes triggered by spinal cord injury, and their relationship to recovery.
Sequential introduction of transcription factors enables large-scale generation of induced motor neurons (iMNs) from human somatic cells, and transplantation of iMNs exhibit therapeutic effects in spinal cord injury model.
Single-cell analysis of injured mouse sciatic nerves reveals rapid reprogramming of macrophages toward a glycolytic, proinflammatory phenotype during the early repair process.
