A5071674873- Traumatic Brain Injury and Neurovascular Disturbances
- S100 Proteins and Annexins
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune Response and Inflammation
- Anesthesia and Neurotoxicity Research
- Neonatal and fetal brain pathology
- Traumatic Brain Injury Research
- Acute Ischemic Stroke Management
- Neurogenesis and neuroplasticity mechanisms
- Trauma and Emergency Care Studies
- Cardiac Arrest and Resuscitation
- Intracerebral and Subarachnoid Hemorrhage Research
- Thermal Regulation in Medicine
- Barrier Structure and Function Studies
- Stress Responses and Cortisol
- Heme Oxygenase-1 and Carbon Monoxide
- Bone Metabolism and Diseases
- Intensive Care Unit Cognitive Disorders
- Erythropoietin and Anemia Treatment
- Epilepsy research and treatment
- Cerebrospinal fluid and hydrocephalus
- Cell Adhesion Molecules Research
- Chemokine receptors and signaling
- Spinal Fractures and Fixation Techniques
- HIV Research and Treatment
Barrow Neurological Institute
2013-2024
University of Arizona
2013-2024
Phoenix Children's Hospital
2014-2024
National Trauma Research Institute
2009-2023
The Alfred Hospital
2008-2023
Monash University
2012-2022
Australian and New Zealand Intensive Care Society
2013-2020
Karolinska Institutet
2016-2017
Yarra Valley Water (Australia)
2013
Bridge University
2013
Within minutes of a traumatic impact, robust inflammatory response is elicited in the injured brain. The complexity this post-traumatic squeal involves cellular component, comprising activation resident glial cells, microglia, and astrocytes, infiltration blood leukocytes. second component regards secretion immune mediators, which can be divided into following sub-groups: archetypal pro-inflammatory cytokines (Interleukin-1, Tumor Necrosis Factor, Interleukin-6), anti-inflammatory (IL-4,...
Cerebral inflammation involves molecular cascades contributing to progressive damage after traumatic brain injury (TBI). The chemokine CC ligand-2 (CCL2) (formerly monocyte chemoattractant protein-1, MCP-1) is implicated in macrophage recruitment into damaged parenchyma TBI. This study analyzed the presence of CCL2 human TBI, and further investigated role physiological cellular mechanisms secondary Sustained elevation was detected cerebrospinal fluid (CSF) severe TBI patients for 10 days...
The multifunctional cytokine, transforming growth factor beta (TGF-beta), was identified by immunocytochemistry in the brain tissues of four patients with acquired immune deficiency syndrome (AIDS), but not control tissue. TGF-beta staining localized to cells monocytic lineage as well astrocytes, especially areas pathology. In addition, from AIDS contained transcripts for human immunodeficiency virus 1 (HIV-1) situ hybridization, suggesting a correlation between presence HIV-1 and expression...
Patients with severe traumatic brain injury (TBI) show a profound acute-phase response. Because interleukin-6 (IL-6) is an important mediator of these pathophysiological changes, IL-6 levels were monitored in the cerebrospinal fluid (CSF) and serum 20 patients isolated TBI. All received indwelling ventricular catheters for intracranial pressure monitoring release CSF when exceeded 15 mmHg. blood samples drawn daily up to 14 days. The CSF/serum albumin ratio (QA) served as parameter barrier...
Cytokines are important mediators of intracranial inflammation following traumatic brain injury (TBI). In the present study, neurological impairment and mortality, blood-brain barrier (BBB) function, polymorphonuclear leukocyte (PMN) accumulation, posttraumatic neuronal cell death were monitored in mice lacking genes for tumor necrosis factor (TNF)/lymphotoxin-alpha (LT-alpha) (TNF/LT-alpha-/-) interleukin-6 (IL-6) wild-type (WT) littermates subjected to experimental closed head (total n =...
Interleukin (IL) 8 was measured in CSF of 14 patients with severe traumatic brain injury. IL-8 levels were significantly higher (up to 8,000 pg/ml) than serum 2,400 (p < 0.05), suggesting intrathecal production. Maximal values correlated a dysfunction the blood–brain barrier. Nerve growth factor (NGF) detected 7 (range maximal NGF: 62–12,130 pg/ml). concentrations these those without NGF 0.01). containing high (3,800–7,900 induced greater production cultured astrocytes (202–434 samples...
Little is known about the molecular events following severe traumatic brain injury (TBI) in humans and to date there are no efficient therapies for treatment of patients. In this study, first its kind human tissue, a total 21 post mortem trauma samples were analyzed. The inflammatory response within tissue was explored by measuring expression various cytokines at mRNA protein levels. These mediators interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha,...
Abstract The entry of therapeutic compounds into the brain and spinal cord is normally restricted by barrier mechanisms in cerebral blood vessels (blood–brain barrier) choroid plexuses (blood–CSF barrier). In injured brain, ruptured circumvent these allowing contents to escape directly parenchyma. This process may contribute secondary damage that follows initial primary injury. However, this localized compromise function also provide a ‘window opportunity’ through which drugs do not cross...
It has been hypothesized that immunoactivation may contribute to brain damage and affect outcome after traumatic injury (TBI). In order determine the role of inflammation TBI, we studied interrelationship immune mediators sICAM-1 IL-6 with levels S-100beta neuronal specific enolase (NSE), both recognized markers damage. addition, extent type cerebral neurological were related these measured injury. An evident elevation (range means: 2.7-81.4 ng/mL) NSE 2.0-81.3 was observed in CSF all 13...
Brain microglial morphology relates to function, with ramified microglia surveying the micro-environment and amoeboid engulfing debris. One subgroup of microglia, rod have been observed in a number pathological conditions, however neither function nor specific has defined. Historically, described intermittently as cells sausage-shaped soma long, thin processes, which align adjacent neurons. More recently, our group aligning end-to-end one another form trains neuronal processes. Confusion...
Traumatic brain injury (TBI) resulting in poor neurological outcome is predominantly associated with diffuse damage and secondary hypoxic insults. Post-traumatic hypoxia known to exacerbate primary injury; however, the underlying pathological mechanisms require further elucidation. Using a rat model of traumatic axonal (TAI) followed by post-traumatic insult, we characterized pathology, macrophage/microglia accumulation, astrocyte responses over 14 days. Rats underwent TAI alone, 30 min (TAI...