Works matching AU Raghupathi, Ramesh
Results: 39
In situ DNA fragmentation occurs in white matter up to 12 months after head injury in man.
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- Acta Neuropathologica, 2001, v. 102, n. 6, p. 581, doi. 10.1007/s004010100410
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TUNEL-positive staining of surface contusions after fatal head injury in man.
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- Acta Neuropathologica, 2000, v. 100, n. 5, p. 537, doi. 10.1007/s004010000222
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- Article
Age-Related Differences in Acute Physiologic Response to Focal Traumatic Brain Injury in Piglets.
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- Pediatric Neurosurgery, 2000, v. 33, n. 2, p. 76, doi. 10.1159/000028980
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Sedation and Analgesia in Children with Developmental Disabilities and Neurologic Disorders.
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- International Journal of Pediatrics, 2010, p. 1, doi. 10.1155/2010/189142
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REVIEW ■ : Calcium and the Pathogenesis of Traumatic CNS Injury: Cellular and Molecular Mechanisms.
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- Neuroscientist, 1997, v. 3, n. 3, p. 169, doi. 10.1177/107385849700300310
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Deletion of the p53 tumor suppressor gene improves neuromotor function but does not attenuate regional neuronal cell loss following experimental brain trauma in mice.
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- Journal of Neuroscience Research, 2010, v. 88, n. 15, p. 3414, doi. 10.1002/jnr.22491
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Concurrent loss and proliferation of astrocytes following lateral fluid percussion brain injury in the adult rat.
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- Journal of Neuroscience Research, 1999, v. 57, n. 2, p. 271, doi. 10.1002/(SICI)1097-4547(19990715)57:2<271::AID-JNR13>3.0.CO;2-Z
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Riluzole attenuates cortical lesion size, but not hippocampal neuronal loss, following traumatic brain injury in the rat.
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- Journal of Neuroscience Research, 1998, v. 52, n. 3, p. 342, doi. 10.1002/(SICI)1097-4547(19980501)52:3<342::AID-JNR10>3.0.CO;2-8
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A Role for the Amygdala in Impairments of Affective Behaviors Following Mild Traumatic Brain Injury.
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- Frontiers in Behavioral Neuroscience, 2021, v. 14, p. N.PAG, doi. 10.3389/fnbeh.2021.601275
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Neuron-Specific mRNA Complexity Responses during Hippocampal Apoptosis after Traumatic Brain Injury.
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- Journal of Neuroscience, 2004, v. 24, n. 12, p. 2866, doi. 10.1523/JNEUROSCI.5051-03.2004
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DNase I disinhibition is predominantly associated with actin hyperpolymerization after traumatic brain injury.
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- Journal of Neurochemistry, 2001, v. 77, n. 1, p. 173, doi. 10.1046/j.1471-4159.2001.00215.x
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Regional and Temporal Alterations in DNA Fragmentation Factor (DFF)-Like Proteins Following Experimental Brain Trauma in the Rat.
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- Journal of Neurochemistry, 1999, v. 73, n. 4, p. 1650, doi. 10.1046/j.1471-4159.1999.0731650.x
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Temporal Patterns of Poly(ADP-Ribose) Polymerase Activation in the Cortex Following Experimental Brain Injury in the Rat.
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- Journal of Neurochemistry, 1999, v. 73, n. 1, p. 205, doi. 10.1046/j.1471-4159.1999.0730205.x
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Preface.
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- Developmental Neuroscience, 2013, v. 35, n. 2/3, p. 87, doi. 10.1159/000353264
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Regionally Distinct Patterns of Calpain Activation and Traumatic Axonal Injury following Contusive Brain Injury in Immature Rats.
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- Developmental Neuroscience, 2006, v. 28, n. 4/5, p. 466, doi. 10.1159/000094172
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Mild head injury increasing the brain's vulnerability to a second concussive impact.
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- Journal of Neurosurgery, 2001, v. 95, n. 5, p. 859
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Is Gulf War Illness a prolonged early phase tauopathy?
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- Cytoskeleton, 2024, v. 81, n. 1, p. 41, doi. 10.1002/cm.21786
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Intranasal Administration of Oxytocin Attenuates Social Recognition Deficits and Increases Prefrontal Cortex Inhibitory Postsynaptic Currents following Traumatic Brain Injury.
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- eNeuro, 2021, v. 8, n. 3, p. 1, doi. 10.1523/ENEURO.0061-21.2021
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Cortical Fluoro-Jade staining and blunted adrenomedullary response to hypoglycemia after noncoma hypoglycemia in rats.
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- Journal of Cerebral Blood Flow & Metabolism, 2005, v. 25, n. 12, p. 1645, doi. 10.1038/sj.jcbfm.9600152
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Structural and Functional Damage Sustained by Mitochondria After Traumatic Brain Injury in the Rat: Evidence for Differentially Sensitive Populations in the Cortex and Hippocampus.
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- Journal of Cerebral Blood Flow & Metabolism, 2003, v. 23, n. 2, p. 219, doi. 10.1097/01.WCB.0000040581.43808.03
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A Review and Rationale for the Use of Genetically Engineered Animals in the Study of Traumatic Brain Injury.
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- Journal of Cerebral Blood Flow & Metabolism, 2001, v. 21, n. 11, p. 1241, doi. 10.1097/00004647-200111000-00001
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The Maxi-K Channel Opener BMS-204352 Attenuates Regional Cerebral Edema and Neurologic Motor Impairment After Experimental Brain Injury.
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- Journal of Cerebral Blood Flow & Metabolism, 2001, v. 21, n. 4, p. 396, doi. 10.1097/00004647-200104000-00008
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Interleukin-1 Receptor Antagonist Attenuates Regional Neuronal Cell Death and Cognitive Dysfunction After Experimental Brain Injury.
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- Journal of Cerebral Blood Flow & Metabolism, 1999, v. 19, n. 10, p. 1118, doi. 10.1097/00004647-199910000-00008
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Increased Vulnerability of NFH-LacZ Transgenic Mouse to Traumatic Brain Injury-Induced Behavioral Deficits and Cortical Damage.
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- Journal of Cerebral Blood Flow & Metabolism, 1999, v. 19, n. 7, p. 762, doi. 10.1097/00004647-199907000-00006
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BCL-2 Overexpression Attenuates Cortical Cell Loss After Traumatic Brain Injury in Transgenic Mice.
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- Journal of Cerebral Blood Flow & Metabolism, 1998, v. 18, n. 11, p. 1259, doi. 10.1097/00004647-199811000-00013
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Regional Induction of c-fos and Heat Shock Protein-72 mRNA Following Fluid-Percussion Brain Injury in the Rat.
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- Journal of Cerebral Blood Flow & Metabolism, 1995, v. 15, n. 3, p. 467, doi. 10.1038/jcbfm.1995.58
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Endothelin and the neurovascular unit in pediatric traumatic brain injury.
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- Neurological Research, 2011, v. 33, n. 2, p. 127, doi. 10.1179/016164111X12881719352138
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Bilateral growth-related protein expression suggests a transient increase in regenerative potential following brain trauma.
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- Journal of Comparative Neurology, 2000, v. 424, n. 3, p. 521, doi. 10.1002/1096-9861(20000828)424:3<521::AID-CNE9>3.0.CO;2-8
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Overexpression of Bcl-2 is neuroprotective after experimental brain injury in transgenic mice.
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- Journal of Comparative Neurology, 1999, v. 412, n. 4, p. 681, doi. 10.1002/(SICI)1096-9861(19991004)412:4<681::AID-CNE9>3.0.CO;2-F
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Traumatic brain injury in young, amyloid-β peptide overexpressing transgenic mice induces marked ipsilateral hippocampal atrophy and diminished Aβ deposition during aging.
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- Journal of Comparative Neurology, 1999, v. 411, n. 3, p. 390, doi. 10.1002/(SICI)1096-9861(19990830)411:3<390::AID-CNE3>3.0.CO;2-#
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Trajectory of Long-Term Outcome in Severe Pediatric Diffuse Axonal Injury: An Exploratory Study.
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- Frontiers in Neurology, 2021, v. 12, p. 1, doi. 10.3389/fneur.2021.704576
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A Pro-social Pill? The Potential of Pharmacological Treatments to Improve Social Outcomes After Pediatric Traumatic Brain Injury.
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- Frontiers in Neurology, 2021, v. 12, p. 1, doi. 10.3389/fneur.2021.714253
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Stem Cell Therapy for Pediatric Traumatic Brain Injury.
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- Frontiers in Neurology, 2020, v. 11, p. N.PAG, doi. 10.3389/fneur.2020.601286
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Twofold overexpression of human β-amyloid precursor proteins in transgenic mice does not affect the neuromotor, cognitive, or neurodegenerative sequelae following experimental brain injury.
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- Journal of Comparative Neurology, 1998, v. 392, n. 4, p. 428, doi. 10.1002/(SICI)1096-9861(19980323)392:4<428::AID-CNE2>3.0.CO;2-2
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Temporal Profiles of Cytoskeletal Protein Loss following Traumatic Axonal Injury in Mice.
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- Neurochemical Research, 2007, v. 32, n. 12, p. 2006, doi. 10.1007/s11064-007-9318-9
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Cell Death Mechanisms Following Traumatic Brain Injury.
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- Brain Pathology, 2004, v. 14, n. 2, p. 215, doi. 10.1111/j.1750-3639.2004.tb00056.x
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Cellular Responses to Experimental Brain Injury.
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- Brain Pathology, 1995, v. 5, n. 4, p. 437, doi. 10.1111/j.1750-3639.1995.tb00622.x
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Editorial: Long-term consequences of pediatric traumatic brain injury: Improved understanding to help young patients survive and thrive.
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- Frontiers in Neurology, 2022, v. 13, p. 1, doi. 10.3389/fneur.2022.1011998
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Sex and estrous‐phase dependent alterations in depression‐like behavior following mild traumatic brain injury in adolescent rats.
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- Journal of Neuroscience Research, 2022, v. 100, n. 2, p. 490, doi. 10.1002/jnr.24989
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