This comprehensive review explores the broad landscape of brain–computer interface (BCI) technology and its potential use in intensive care units (ICUs), particularly for patients with motor impairments such as quadriplegia or severe brain injury. By employing brain signals from various sensing techniques, BCIs offer enhanced communication and motor rehabilitation strategies for patients. This review underscores the concept and efficacy of noninvasive, electroencephalogram-based BCIs in facilitating both communicative interactions and motor function recovery. Additionally, it highlights the current research gap in intuitive “stop” mechanisms within motor rehabilitation protocols, emphasizing the need for advancements that prioritize patient safety and individualized responsiveness. Furthermore, it advocates for more focused research that considers the unique requirements of ICU environments to address the challenges arising from patient variability, fatigue, and limited applicability of current BCI systems outside of experimental settings.

This comprehensive review explores the broad landscape of brain–computer interface (BCI) technology and its potential use in intensive care units (ICUs), particularly for patients with motor impairments such as quadriplegia or severe brain injury. By employing brain signals from various sensing techniques, BCIs offer enhanced communication and motor rehabilitation strategies for patients. This review underscores the concept and efficacy of noninvasive, electroencephalogram-based BCIs in facilitating both communicative interactions and motor function recovery. Additionally, it highlights the current research gap in intuitive “stop” mechanisms within motor rehabilitation protocols, emphasizing the need for advancements that prioritize patient safety and individualized responsiveness. Furthermore, it advocates for more focused research that considers the unique requirements of ICU environments to address the challenges arising from patient variability, fatigue, and limited applicability of current BCI systems outside of experimental settings.

This comprehensive review explores the broad landscape of brain–computer interface (BCI) technology and its potential use in intensive care units (ICUs), particularly for patients with motor impairments such as quadriplegia or severe brain injury. By employing brain signals from various sensing techniques, BCIs offer enhanced communication and motor rehabilitation strategies for patients. This review underscores the concept and efficacy of noninvasive, electroencephalogram-based BCIs in facilitating both communicative interactions and motor function recovery. Additionally, it highlights the current research gap in intuitive “stop” mechanisms within motor rehabilitation protocols, emphasizing the need for advancements that prioritize patient safety and individualized responsiveness. Furthermore, it advocates for more focused research that considers the unique requirements of ICU environments to address the challenges arising from patient variability, fatigue, and limited applicability of current BCI systems outside of experimental settings.

This comprehensive review explores the broad landscape of brain–computer interface (BCI) technology and its potential use in intensive care units (ICUs), particularly for patients with motor impairments such as quadriplegia or severe brain injury. By employing brain signals from various sensing techniques, BCIs offer enhanced communication and motor rehabilitation strategies for patients. This review underscores the concept and efficacy of noninvasive, electroencephalogram-based BCIs in facilitating both communicative interactions and motor function recovery. Additionally, it highlights the current research gap in intuitive “stop” mechanisms within motor rehabilitation protocols, emphasizing the need for advancements that prioritize patient safety and individualized responsiveness. Furthermore, it advocates for more focused research that considers the unique requirements of ICU environments to address the challenges arising from patient variability, fatigue, and limited applicability of current BCI systems outside of experimental settings.

When mouse bone marrow-derived macrophages were stimulated with serum amyloid A (SAA), which is a major acute-phase protein, there was strong inhibition of osteoclast formation induced by the receptor activator of nuclear factor kappaB ligand. SAA not only markedly blocked the expression of several osteoclast-associated genes (TNF receptor-associated factor 6 and osteoclast-associated receptor) but also strongly induced the expression of negative regulators (MafB and interferon regulatory factor 8). Moreover, SAA decreased c-fms expression on the cell surface via shedding of the c-fms extracellular domain. SAA also restrained the fusion of osteoclast precursors by blocking intracellular ATP release. This inhibitory response of SAA is not mediated by the well-known SAA receptors (formyl peptide receptor 2, Toll-like receptor 2 (TLR2) or TLR4). These findings provide insight into a novel inhibitory role of SAA in osteoclastogenesis and suggest that SAA is an important endogenous modulator that regulates bone homeostasis.
Adenosine Triphosphate/metabolism ; Animals ; Cell Differentiation ; Cell Line ; Gene Expression Regulation, Developmental ; Humans ; Macrophages/*cytology/metabolism ; Mice ; Osteoclasts/*cytology/metabolism ; RANK Ligand/*metabolism ; Receptor, Macrophage Colony-Stimulating Factor/genetics ; Receptors, Formyl Peptide/metabolism ; Serum Amyloid A Protein/*metabolism ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/metabolism