• Exosome
• Extra-cellular vesicle
• Inflammation
• Stem cell therapy
• TBI
• Trauma

• Humans
• Brain Injuries, Traumatic/therapy
• Brain Injuries, Traumatic/physiopathology
• Brain Injuries, Traumatic/immunology
• Mesenchymal Stem Cell Transplantation/methods
• Animals
• Mesenchymal Stem Cells
• Brain

• low back pain
• lumbar spine
• manual therapy
• nerve mobilization
• physical therapy

• Humans
• Low Back Pain/therapy
• Movement

• biomembrane
• chronic wound healing
• hydrogels
• microstructures
• nanostructures

Traumatic brain injury (TBI) places a heavy load on healthcare systems worldwide. Despite significant advancements in care, the TBI-related mortality is 30–50% and in most cases involves adolescents or young adults. Previous literature has suggested that neutrophil-to-lymphocyte ratio (NLR) may serve as a sensitive biomarker in predicting clinical outcomes following TBI. With conclusive evidence in this regard lacking, this study aimed to systematically review all original studies reporting the effectiveness of NLR as a predictor of TBI outcomes. A systematic search of eight databases was conducted according to the Preferred Reporting Items for Systematic Review and Meta-Analyses statement (PRISMA) recommendations. The risk of bias was assessed using the Quality in Prognostic Studies (QUIPS) tool. Eight studies were ultimately included in the study. In most of the studies interrogated, severity outcomes were successfully predicted by NLR in both univariate and multivariate prediction models, in different follow-up durations up to 6 months. A high NLR at 24 and 48 h after TBI in pediatric patients was associated with worse clinical outcomes. On pooling the NLR values within studies assessing its association with the outcome severity (favorable or not), patients with favorable outcomes had 37% lower NLR values than those with unfavorable ones (RoM= 0.63; 95% CI = 0.44–0.88; p = 0.007). However, there were considerable heterogeneity in effect estimates (I² = 99%; p < 0.001). Moreover, NLR was a useful indicator of mortality at both 6-month and 1-year intervals. In conjunction with clinical and radiographic parameters, NLR might be a useful, inexpensive marker in predicting clinical outcomes in patients with TBI. However, the considerable heterogeneity in current literature keeps it under investigation with further studies are warranted to confirm the reliability of NLR in predicting TBI outcomes.

• King Abdulaziz University

• Ageing
• Immunomodulation
• Mesenchymal stromal cells
• Secretome
• Traumatic brain injury

• CCR2
• Neuroinflammation
• Novel ligands
• Traumatic brain injury

• Dihydrotestosterone
• Endocrine disruption
• Inflammation
• Mitochondria
• Neuroprotection
• Traumatic brain injury

• animal models
• cell culture models
• in vitro models
• mechanical assay
• traumatic brain injury

• Animals
• Brain Injuries, Traumatic/etiology
• Brain Injuries, Traumatic/pathology
• Brain Injuries, Traumatic/therapy
• Humans
• In Vitro Techniques
• Models, Biological

Emerging evidence suggests that the spread of glioma to the subventricular zone (SVZ) is closely related to glioma recurrence and patient survival. Neural stem cells (NSCs) are the main cell type in the SVZ region and exhibit tumor-homing ability.

To evaluate the effects of conditioned medium (CM) derived from SVZ NSCs on the cancer-related behaviors of glioma cells.

The characteristics of SVZ hNSCs were identified by immunofluorescence. The normoxic-hNSC-CM and hypoxic-hNSC-CM (3% O₂, oxygen-glucose deprived [OGD] culturing) were collected from 80%-90% confluent SVZ NSCs in sterile conditions. The CCK8 and Transwell assays were used to compare and evaluate the effects of normoxic-CM and hypoxic-CM on glioma proliferation and invasion. Then proteins secreted from SVZ NSCs into the CM were investigated by mass spectrometry, and the potential effects of candidate protein NCAN in the regulation of glioma progression were examined by CCK8 and Transwell assays.

The CM from SVZ NSCs significantly increased the proliferation and invasion of glioma cells, particularly the CM from OGD NSCs induced under hypoxic conditions. Furthermore, the secreted protein neurocan (NCAN) in CM from OGD NSCs was identified by proteomic analysis. NCAN was expressed in glioma cells and played regulatory roles in mediating the progression of glioma cells mainly via the Rho/Rho-associated protein kinase pathway.

Our study identified a potential interactive mechanism between SVZ NSCs and glioma cells, in which SVZ NSCs promote glioma progression via the secreted protein NCAN. These findings suggested that exploring the CM derived from cells could be a novel strategy for optimizing treatments and that NCAN derived from SVZ NSCs may be a potential new target in glioma progression.

• Neural stem cells
• Glioma
• Conditioned medium
• NCAN
• Hypoxia
• Protein

• CNS trauma
• ex vivo injury model
• in vitro injury model
• spinal cord injury
• traumatic brain injury

• P41 RR012408 NCRR NIH HHS
• T32 GM008339 NIGMS NIH HHS

• HPL
• human platelet lysates
• neurorestoration
• neurotrophins

• Central nervous system
• Exosome
• Neurodegenerative diseases
• Neuroprotection
• Regeneration
• Stem cell

• Animals
• Exosomes/transplantation
• Humans
• Mesenchymal Stem Cell Transplantation/methods
• Mesenchymal Stem Cell Transplantation/trends
• Mesenchymal Stem Cells/physiology
• Neurodegenerative Diseases/diagnosis
• Neurodegenerative Diseases/therapy

Preserving the integrity of the blood-brain barrier (BBB) is beneficial to avoid further brain damage after acute ischemic stroke (AIS). Astrocytes, an important component of the BBB, promote BBB breakdown in subjects with AIS by secreting inflammatory factors. The glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 (Ex-4) protects the BBB and reduces brain inflammation from cerebral ischemia, and GLP-1R is expressed on astrocytes. However, the effect of Ex-4 on astrocytes in subjects with AIS remains unclear.

In the present study, we investigated the effect of Ex-4 on astrocytes cultured under oxygen-glucose deprivation (OGD) plus reoxygenation conditions and determined whether the effect influences bEnd.3 cells. We used various methods, including permeability assays, western blotting, immunofluorescence staining, and gelatin zymography, in vitro and in vivo.

Ex-4 reduced OGD-induced astrocyte-derived vascular endothelial growth factor (VEGF-A), matrix metalloproteinase-9 (MMP-9), chemokine monocyte chemoattractant protein-1 (MCP-1), and chemokine C-X-C motif ligand 1 (CXCL-1). The reduction in astrocyte-derived VEGF-A and MMP-9 was related to the increased expression of tight junction proteins (TJPs) in bEnd.3 cells. Ex-4 improved neurologic deficit scores, reduced the infarct area, and ameliorated BBB breakdown as well as decreased astrocyte-derived VEGF-A, MMP-9, CXCL-1, and MCP-1 levels in ischemic brain tissues from rats subjected to middle cerebral artery occlusion. Ex-4 reduced the activation of the JAK2/STAT3 signaling pathway in astrocytes following OGD.

Based on these findings, ischemia-induced inflammation and BBB breakdown can be improved by Ex-4 through an astrocyte-dependent manner.

• Astrocyte
• Blood-brain barrier
• Exendin-4
• Ischemic stroke
• Oxygen-glucose deprivation

• Brain
• Mesenchymal stem cells
• Paracrine factors
• Pathologies
• Secretome
• Therapeutics

• Adherent culture
• adipose tissue extract
• potency metrics
• repeatability
• stirred suspension culture

• Astrocytes
• Conditioned medium
• Inflammation
• Mesenchymal stem cells
• Neuroglobin
• Scratch assay

• Alzheimer’s disease
• Mitochondria
• Mitochondrial dynamics
• Neurodegenerative diseases
• Oxidative stress
• Parkinson’s disease

• Alzheimer disease
• UPR (unfolded protein response)
• aging
• endoplasmic reticulum stress (ER)
• neurodegenerative diseases

Alzheimer's disease (AD) is a slowly progressive, neurodegenerative disorder of uncertain etiology. According to the amyloid cascade hypothesis, accumulation of non-soluble amyloid β peptides (Aβ) in the Central Nervous System (CNS) is the primary cause initiating a pathogenic cascade leading to the complex multilayered pathology and clinical manifestation of the disease. It is, therefore, not surprising that the search for mechanisms underlying cognitive changes observed in AD has focused exclusively on the brain and Aβ-inducing synaptic and dendritic loss, oxidative stress, and neuronal death. However, since Aβ depositions were found in normal non-demented elderly people and in many other pathological conditions, the amyloid cascade hypothesis was modified to claim that intraneuronal accumulation of soluble Aβ oligomers, rather than monomer or insoluble amyloid fibrils, is the first step of a fatal cascade in AD. Since a characteristic reduction of cerebral perfusion and energy metabolism occurs in patients with AD it is suggested that capillary distortions commonly found in AD brain elicit hemodynamic changes that alter the delivery and transport of essential nutrients, particularly glucose and oxygen to neuronal and glial cells. Another important factor in tissue oxygenation is the ability of erythrocytes (red blood cells, RBC) to transport and deliver oxygen to tissues, which are first of all dependent on the RBC antioxidant and energy metabolism, which finally regulates the oxygen affinity of hemoglobin. In the present review, we consider the possibility that metabolic and antioxidant defense alterations in the circulating erythrocyte population can influence oxygen delivery to the brain, and that these changes might be a primary mechanism triggering the glucose metabolism disturbance resulting in neurobiological changes observed in the AD brain, possibly related to impaired cognitive function. We also discuss the possibility of using erythrocyte biochemical aberrations as potential tools that will help identify a risk factor for AD.

• Alzheimer's disease
• amyloid β
• clinical manifestation
• erythrocytes
• metabolic dysfunction
• multilayered pathology