Helen M. Bramlett

ORCID: 0000-0002-8200-0973
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About
Contact & Profiles
Research Areas
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Cardiac Arrest and Resuscitation
  • Traumatic Brain Injury Research
  • Thermal Regulation in Medicine
  • S100 Proteins and Annexins
  • Inflammasome and immune disorders
  • Spinal Cord Injury Research
  • Anesthesia and Neurotoxicity Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Mitochondrial Function and Pathology
  • Estrogen and related hormone effects
  • Immune Response and Inflammation
  • Menopause: Health Impacts and Treatments
  • Neonatal and fetal brain pathology
  • Effects of Vibration on Health
  • Heme Oxygenase-1 and Carbon Monoxide
  • Neurogenesis and neuroplasticity mechanisms
  • Adipose Tissue and Metabolism
  • Neuroscience and Neuropharmacology Research
  • Extracellular vesicles in disease
  • Nerve injury and regeneration
  • Sepsis Diagnosis and Treatment
  • Epilepsy research and treatment
  • Neuroscience of respiration and sleep
  • Noise Effects and Management

University of Miami
2016-2025

Bruce W. Carter VA Medical Center
2015-2025

Neurological Surgery
2015-2024

United States Department of Veterans Affairs
2011-2015

Miami VA Healthcare System
2012

Ontario Neurotrauma Foundation
2000

Traumatic brain injury elicits acute inflammation that in turn exacerbates primary damage. A crucial part of innate immunity the immune privileged central nervous system involves production proinflammatory cytokines mediated by inflammasome signaling. Here, we show nucleotide-binding, leucine-rich repeat pyrin domain containing protein 1 (NLRP1) consisting NLRP1, caspase-1, caspase-11, apoptosis-associated speck-like a caspase recruitment (ASC), X-linked inhibitor apoptosis protein, and...

10.1038/jcbfm.2009.46 article EN Journal of Cerebral Blood Flow & Metabolism 2009-04-29

Diffuse axonal injury (DAI) is an important consequence of human head trauma. This experimental investigation utilized the immunocytochemical visualization beta-amyloid precursor protein (beta-APP) to document regional patterns after traumatic brain (TBI) and determine importance severity on magnitude damage. Rats underwent moderate (1.84–2.11 atm) or severe (2.38–2.52 parasagittal fluid-percussion (F-P) sham procedures. At 1, 3, 7 30 days TBI, rats were perfusion-fixed sections...

10.1097/00005072-199710000-00007 article EN other-oa Journal of Neuropathology & Experimental Neurology 1997-10-01

An important consideration in traumatic brain injury (TBI) females is the influence of hormones on recovery. Recent studies both cerebral ischemia and TBI have demonstrated an attenuation damage neurologic recovery following hormonal treatment. However, ability endogenous hormone levels to provide neuropathological protection after fluid percussion (FP) has not been studied. The purpose this experiment was determine whether circulating female rat could neuroprotection compared males...

10.1089/089771501750451811 article EN Journal of Neurotrauma 2001-09-01

We investigated the temporal and regional profile of blood-brain barrier (BBB) permeability to both large small molecules after moderate fluid percussion (FP) brain injury in rats determined effects post-traumatic modest hypothermia (33 degrees C/4 h) on these vascular perturbations. The visible tracers biotin-dextrin-amine 3000 (BDA-3K, 3 kDa) horseradish peroxidase (HRP, 44 were injected intravenously at 4 h or 7 days post-TBI. At 30 min tracer infusion, molecular weight detected contusion...

10.1089/neu.2008.0802 article EN Journal of Neurotrauma 2009-06-26

Members of the mammalian nucleotide binding domain, leucine-rich repeat (LRR)-containing receptor (NLR) family proteins are key modulators innate immunity regulating inflammation. Our previous work has shown that among members this family, NLRP1/NALP1, present in neurons, plays a crucial role inflammasome formation and production inflammatory cytokines interleukin (IL) -1β IL-18 after various types central nervous system injury.We investigated whether age-related cognitive decline may...

10.1186/1471-2202-12-123 article EN cc-by BMC Neuroscience 2011-12-01

The purpose of this study was to determine the degree sensorimotor and cognitive protection conferred by posttraumatic brain hypothermia. Baseline measurements were taken on tasks involving forelimb placing beam-walking, as well a spatial navigational task utilizing water maze. Twenty-four hours after last baseline measurements, normothermic (37°C) animals subjected fluid percussion pulse (1.9–2.4 atm) over right parietal cortex. Following trauma, temperature maintained for 3 h at either...

10.1089/neu.1995.12.289 article EN Journal of Neurotrauma 1995-06-01

A proliferation of stem/progenitor cells is observed after brain injury. We examined the regional and temporal profile mitotically active to determine whether traumatic injury (TBI) would increase neurogenesis in selective regions.Male Sprague-Dawley rats received injections (IP) 5-bromo-deoxyuridine (BrdU), a compound used detect mitotic cells, before fluid-percussion At 3 hr, 1, 2, 3, 7, 14 days moderate fluid percussion, brains were processed for immunocytochemical confocal analysis....

10.3233/rnn-2007-00369 article EN Restorative Neurology and Neuroscience 2007-01-01

Therapeutic hypothermia promotes protection after traumatic brain injury (TBI). The mechanisms underlying hypothermic are multifactorial and may include the modulation of microRNA (miRNA) expression trauma. We utilized microarrays to examine effects posttraumatic on 388 rat miRNAs. Animals were subjected sham or moderate fluid percussion injury, followed by 4 hours (33°C) normothermia (37°C) euthanized at 7 24 hours. At 7hours, 47 miRNAs significantly different ( P < 0.05) between TBI (15...

10.1038/jcbfm.2011.33 article EN Journal of Cerebral Blood Flow & Metabolism 2011-04-20

Abstract Cyclic AMP suppresses immune cell activation and inflammation. The positive feedback loop of proinflammatory cytokine production implies that cytokines may not only be regulated by cyclic but also conversely regulate AMP. This study examined the effects tumor necrosis factor (TNF)‐α interleukin (IL)‐1β on AMP‐phosphodiesterase (PDE) signaling in microglia vitro after spinal cord injury (SCI) or traumatic brain (TBI). TNF‐α IL‐1β stimulation produced a profound reduction (>90%)...

10.1002/glia.22401 article EN Glia 2012-08-02

Brain edema and associated increased intracranial pressure are major consequences of traumatic brain injury (TBI). While astrocyte swelling (cytotoxic edema) represents a component the in early phase TBI, its mechanisms unclear. One factor known to be activated by trauma is nuclear factor-κB (NF-κB). Because this has been implicated mechanism cell swelling/brain other neurological conditions, we examined whether NF-κB might also involved mediation post-traumatic edema. Here show an increase...

10.1089/neu.2013.3169 article EN Journal of Neurotrauma 2014-01-28

Traumatic brain injury (TBI) is characterized by histopathological damage and long-term sensorimotor cognitive dysfunction. Recent studies have reported the discovery of P7C3 class aminopropyl carbazole agents with potent neuroprotective properties for both newborn neural precursor cells in adult hippocampus mature neurons other regions central nervous system. This study tested, first time, whether highly active P7C3-A20 compound would be neuroprotective, promote hippocampal neurogenesis,...

10.1089/neu.2013.3135 article EN Journal of Neurotrauma 2013-09-26
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