Astrocyte Reactivity Following Blast Exposure Involves Aberrant Histone Acetylation

Astrocyte roles in traumatic brain injury

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Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury

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Histone acetylation in astrocytes suppresses GFAP and stimulates a reorganization of the intermediate filament network

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Hippocampal vulnerability and subacute response following varied blast magnitudes

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Can changes in histone acetylation contribute to memory formation?

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Corrigendum: Blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves

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Inflammation and white matter degeneration persist for years after a single traumatic brain injury

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Blockade of CXCR1/2 chemokine receptors protects against brain damage in ischemic stroke in mice: Ischemia and Reparixin

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Interplay of Hippocampus and Prefrontal Cortex in Memory

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Long-term consequences of single and multiple mild blast exposure on select physiological parameters and blood-based biomarkers

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Modeling clinically relevant blast parameters based on scaling principles produces functional & histological deficits in rats

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Induction of oxidative and nitrosative damage leads to cerebrovascular inflammation in an animal model of mild traumatic brain injury induced by primary blast

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Nuclear Factor  B-Dependent Histone Acetylation is Specifically Involved in Persistent Forms of Memory

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Blast induces oxidative stress, inflammation, neuronal loss and subsequent short-term memory impairment in rats

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Overpressure blast-wave induced brain injury elevates oxidative stress in the hypothalamus and catecholamine biosynthesis in the rat adrenal medulla

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Modulation of cholinergic pathways and inflammatory mediators in blast-induced traumatic brain injury

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Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation

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Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

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Involvement of the anterior cingulate cortex in formation, consolidation, and reconsolidation of recent and remote contextual fear memory

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The Role of Histone Acetylation in Memory Formation and Cognitive Impairments

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Neuro-glial and systemic mechanisms of pathological responses in rat models of primary blast overpressure compared to “composite” blast

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Ablation of CBP in Forebrain Principal Neurons Causes Modest Memory and Transcriptional Defects and a Dramatic Reduction of Histone Acetylation But Does Not Affect Cell Viability

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Tightly Coupled Repetitive Blast-Induced Traumatic Brain Injury: Development and Characterization in Mice

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Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression

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Activated microglia decrease histone acetylation and Nrf2-inducible anti-oxidant defence in astrocytes: Restoring effects of inhibitors of HDACs, p38 MAPK and GSK3β

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Increase in blood-brain barrier permeability, oxidative stress, and activated microglia in a rat model of blast-induced traumatic brain injury

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Valproate Administered after Traumatic Brain Injury Provides Neuroprotection and Improves Cognitive Function in Rats

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Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice

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Astrocytes: biology and pathology

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Inflammatory cytokines stimulate the chemokines CCL2/MCP-1 and CCL7/MCP-7 through NFκB and MAPK dependent pathways in rat astrocytes

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Ontogeny of Rat Recognition Memory measured by the novel object recognition task

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Combat Wounds in Operation Iraqi Freedom and Operation Enduring Freedom

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HDAC inhibitor increases histone H3 acetylation and reduces microglia inflammatory response following traumatic brain injury in rats

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Prefrontal cortex and hippocampus subserve different components of working memory in rats

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Histone deacetylase inhibitors improve learning consolidation in young and in KA-induced-neurodegeneration and SAMP-8-mutant mice

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Analyzing real-time PCR data by the comparative CT method

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Mild Traumatic Brain Injury in U.S. Soldiers Returning from Iraq

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