BACKGROUND Despite the fact that weaning from mechanical ventilation (MV) is one of the main rehabilitation goals in patients with spinal cord injury (SCI), controversies are still open about the optimal rehabilitation approach.

Moderate acute intermittent hypoxia (mAIH) elicits a form of phrenic motor plasticity known as phrenic long-term facilitation (pLTF), which requires spinal 5-HT2 receptor activation, ERK/MAP kinase signaling, and new brain-derived neurotrophic factor (BDNF) synthesis.

This finding has important experimental, biological, and translational implications, particularly since BDNF-dependent spinal plasticity is being translated to restore breathing and nonrespiratory movements in diverse clinical disorders, such as spinal cord injury (SCI) and amyotrophic lateral sclerosis (ALS).

Congeneric confirmatory factor analyses (CFA) were employed to investigate structural validity.

At the molecular level, KLF2 overexpression alleviated the TJ proteins degradation and the endothelial permeability by tuning the ALP dysfunction caused by SCI and oxygen glucose deprivation (OGD).

Rechargeable implantable pulse generators (r-IPGs) have been available for spinal cord stimulation (SCS) claiming to offer a longer service life but demanding continuous monitoring and regular recharging by the patients.

Central post-stroke pain (CPSP) is a highly refractory form of central neuropathic pain that has been poorly studied mechanistically.

Results: In SCI, autophagy flux disruption in endothelial cells contributes to TJ proteins degradation, leading to blood-spinal cord barrier (BSCB) impairment.

Aim: To highlight the role of secondary aeromedical services and required knowledge of Critical Care Flight Nurses (CCFN), in facilitating the safe inter-hospital transfer of patients with acute Spinal Cord Impairment (SCI) from a Major Trauma Centre (MTC) to a specialist SCI centre.

In this study, rats were subjected to thalamic hemorrhage to investigate the role of spinal monocyte chemoattractant protein-1 (MCP-1) and C-C motif chemokine receptor 2 (CCR2) in the development of CPSP.