A5062226829- Traumatic Brain Injury and Neurovascular Disturbances
- Neuroinflammation and Neurodegeneration Mechanisms
- Mesenchymal stem cell research
- S100 Proteins and Annexins
- Intensive Care Unit Cognitive Disorders
- Trauma, Hemostasis, Coagulopathy, Resuscitation
- Cardiac Arrest and Resuscitation
- Acute Ischemic Stroke Management
- Anesthesia and Neurotoxicity Research
- Immune Response and Inflammation
- Trauma and Emergency Care Studies
- Cerebrospinal fluid and hydrocephalus
- Tissue Engineering and Regenerative Medicine
- Glioma Diagnosis and Treatment
- CAR-T cell therapy research
- Platelet Disorders and Treatments
- Diverticular Disease and Complications
- Blood properties and coagulation
- Blood groups and transfusion
- Spinal Dysraphism and Malformations
- Cleft Lip and Palate Research
- Immune Cell Function and Interaction
- Cerebral Palsy and Movement Disorders
- Cell Adhesion Molecules Research
- Neonatal and fetal brain pathology
The University of Texas Health Science Center at Houston
2014-2024
University of Houston
2024
StemCells (United States)
2021
Forest Institute
2020
John Wiley & Sons (United States)
2020
The University of Texas Health Science Center at San Antonio
2020
Wake Forest University
2020
Charlottesville Medical Research
2020
Abstract Autologous bone marrow mononuclear cells (BMMNCs) infused after severe traumatic brain injury have shown promise for treating the injury. We evaluated their impact in children, particularly hypothesized ability to preserve blood–brain barrier and diminish neuroinflammation, leading structural CNS preservation with improved outcomes. performed a randomized, double-blind, placebo-sham-controlled Bayesian dose-escalation clinical trial at two children's hospitals Houston, TX Phoenix,...
Traumatic brain injury (TBI) is a major cause of death and disability. TBI results in prolonged secondary central neuro-inflammatory response. Previously, we have demonstrated that multiple doses (2 24 h after TBI) multipotent adult progenitor cells (MAPC) delivered intravenously preserve the blood-brain barrier (BBB), improve spatial learning, decrease activated microglia/macrophages dentate gyrus hippocampus. In order to determine if there an optimum treatment window BBB, cognitive...
Abstract Traumatic brain injury (TBI) causes a profound inflammatory response within the central nervous system and peripheral immune system, which contributes to secondary further morbidity mortality. Preclinical investigations have demonstrated that treatments downregulate microglia activation polarize them toward reparative/anti-inflammatory phenotype improved outcomes in preclinical models. However, no therapy date has translated into proven benefits human patients. Regulatory T cells...
Abstract Traumatic brain injury (TBI) results in a cascade of cellular responses, which produce neuroinflammation, partly due to microglial activation. Transforming from surveying primed phenotypes, microglia undergo considerable molecular changes. However, specific profiles rat remain elusive tedious methodology and limited availability reagents. Here, we present flow cytometry-based analysis 24 h after TBI using the controlled cortical impact model, validated with bioinformatics approach....
Abstract Traumatic brain injury (TBI) results in a cascade of cellular responses, which produce neuroinflammation, partly due to the activation microglia. Accurate identification microglial populations is key understanding therapeutic approaches that modify responses TBI and improve long-term outcome measures. Notably, previous studies often utilized an outdated convention describe phenotypes. We conducted temporal analysis response controlled cortical impact (CCI) rat microglia between...
Abstract The inflammatory response after traumatic brain injury (TBI) can lead to significant secondary and chronic inflammation within the central nervous system. Cell therapies, including mesenchymal stromal cells (MSC), have led improvements in animal models of TBI are under investigation human trials. One potential mechanism for therapeutic MSC is their ability augment endogenous immune suppressive regulatory T (Treg). We recently shown that infusion cord blood Treg decreased...
Traumatic brain injury (TBI) disrupts the complex arrangement of glia and neuronal cells in central nervous system. Microglia, resident immune cells, survey cellular milieu under homeostatic conditions play a neuroprotective role via clearance dead debris such as axons myelin. Resting (ramified) microglia possess distinct morphology—small rod-shaped somata with thin processes. After TBI, are activated transition into an amoeboid morphology. To delineate spatiotemporal morphological response...
We examined an autologous mononuclear-cell-therapy-based approach to treat cerebral palsy using umbilical cord blood or bone-marrow-derived mononuclear cells. The primary objective was determine if cells are safe administer in children with palsy. secondary objectives were there improvement motor function of patients 12 months after infusion the Gross Motor Function Measure and evaluate impact treatment on corticospinal tract microstructure as determined by radial diffusivity measurement....
Traumatic brain injury (TBI) causes both physical disruption of the blood barrier (BBB) and altered immune responses that can lead to significant secondary chronic inflammation within central nervous system (CNS). Cell therapies, including mesenchymal stromal cells (MSC), have been shown restore BBB integrity augment endogenous splenic regulatory T (Treg), a subset CD4+ function regulate prevent autoimmunity. We recently infusion human cord blood-derived Treg decreased neuroinflammation...
Traumatic brain injury (TBI) results in activated microglia. Activated microglia can be measured vivo by using positron emission topography (PET) ligand peripheral benzodiazepine receptor standardized uptake values (PBR28suv). Cell based therapies have utilized autologous bone marrow mononuclear cells (BMMNCs) to attenuate after TBI. This study aims utilize PBR28suv assess the efficacy of BMMNCs therapy Seventy-two hours CCI injury, were harvested from tibia and injected via tail-vein at 74...
Myosin Light Chain (MLC) regulates platelet contraction through its phosphorylation by Kinase (MLCK) or dephosphorylation Phosphatase (MLCP). The correlation between force and levels of MLC is unknown. We investigate the relationship using a novel microelectromechanical (MEMS) based clot sensor (CCS). MLCK MLCP pair were interrogated inhibitors activators function. CCS was fabricated from silicon photolithography techniques validated over range deflection for different chip spring constants....
Abstract Background : Traumatic brain injury (TBI) is a systemic that disrupts complex arrangement of interacting cells in the and gastrointestinal tract (GI). Disruption results neuroinflammation, which microglia are central component along with cytokines other soluble factors [pro anti-inflammatory (M1:M2)]. GI due to TBI inflammation dependent upon gut microbiome (GM). Gut can influence via gut-brain axis. In order determine if microbiome-microglia connections axis be modulated, we used...
Abstract Background: Traumatic brain injury (TBI) disrupts the complex arrangement of neuronal and glial cells. As a result TBI there is activation microglia. Activated microglia after can be measured in vivo by using positron emission topography (PET) ligand peripheral benzodiazepine receptor (PBR28) their phenotypes (activated vs resting) assessed ( ex ) morphology. This study aims to utilize (morphology) assess changes controlled cortical impact (CCI), rodent model for TBI. Methods: Male...