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John H Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Rodent neonatal germinal matrix hemorrhage mimics the human brain injury, neurological consequences, and post-hemorrhagic hydrocephalus.
    Experimental neurology, 2012
    Co-Authors: Tim Lekic, Anatol Manaenko, Jiping Tang, William B. Rolland, Richard E. Hartman, Paul R. Krafft, Regina Peters, Orhan Altay, John H Zhang
    Abstract:

    Germinal matrix hemorrhage (GMH) is the most common neurological disease of premature newborns. GMH causes neurological sequelae such as cerebral palsy, post-hemorrhagic hydrocephalus, and mental retardation. Despite this, there is no standardized animal model of spontaneous GMH using newborn rats to depict the condition. We asked whether stereotactic injection of collagenase type VII (0.3 U) into the ganglionic eminence of neonatal rats would reproduce the acute brain injury, gliosis, hydrocephalus, periventricular leukomalacia, and attendant neurological consequences found in humans. To test this hypothesis, we used our neonatal rat model of collagenase-induced GMH in P7 pups, and found that the levels of free-radical adducts (nitrotyrosine and 4-hyroxynonenal), proliferation (mammalian target of rapamycin), inflammation (COX-2), blood components (hemoglobin and thrombin), and gliosis (vitronectin and GFAP) were higher in the forebrain of GMH pups, than in controls. Neurobehavioral Testing showed that pups with GMH had developmental delay, and the juvenile animals had significant cognitive and motor disability, suggesting clinical relevance of the model. There was also evidence of white-matter reduction, ventricular dilation, and brain atrophy in the GMH animals. This study highlights an instructive animal model of the neurological consequences after germinal matrix hemorrhage, with evidence of brain injuries that can be used to evaluate strategies in the prevention and treatment of post-hemorrhagic complications.

  • arginine vasopressin v1a receptor inhibition improves neurologic outcomes following an intracerebral hemorrhagic brain injury
    Neurochemistry International, 2011
    Co-Authors: Anatol Manaenko, Nancy Fathali, Nikan H Khatibi, Tim Lekic, Yu Hasegawa, Robert D Martin, Jiping Tang, John H Zhang
    Abstract:

    Abstract Cerebral edema is a devastating consequence of brain injury leading to cerebral blood flow compromise and worsening parenchyma damage. In the present study, we investigated the effects of arginine-vasopressin (AVP) V 1a receptor inhibition following an intracerebral hemorrhagic (ICH) brain injury in mice and closely assessed the role it played in cerebral edema formation, Neurobehavioral functioning, and blood–brain-barrier (BBB) disruption. To support our investigation, SR49059, an AVP V 1a receptor competitive antagonist, and NC1900, an arginine-vasopressin analogue, were used. Male CD1 mice ( n  = 205) were randomly assigned to the following groups: naive, sham, ICH, ICH with SR49059 at 0.5 mg/kg, ICH with SR49059 at 2 mg/kg, ICH with NC1900 at 1 ng/kg, ICH with NC1900 at 10 ng/kg, and ICH with a combination of SR49059 at 2 mg/kg and NC1900 at 10 ng/kg. ICH was induced by using the collagenase injection model and treatment was given 1 h after surgery. Post assessment was conducted at 6, 12, 24, and 72 h after surgery and included brain water content, Neurobehavioral Testing, Evans Blue assay, western blotting, and hemoglobin assay. The study found that inhibition of the AVP V 1a receptor significantly reduced cerebral edema at 24 and 72 h post-ICH injury and improved Neurobehavioral function while reducing BBB disruption at 72 h. Western blot analysis demonstrated increased protein expression of aquaporin 4 (AQP4) in vehicle, which was reduced with AVP V 1a receptor inhibition. Our study suggests that blockage of the AVP V 1a receptor, is a promising treatment target for improving ICH-induced brain injury. Further studies will be needed to confirm this relationship and determine future clinical direction.

Susan P Proctor - One of the best experts on this subject based on the ideXlab platform.

  • magnetic resonance imaging mri Neurobehavioral Testing and toxic encephalopathy two cases1
    Neurobehavioral Methods and Effects in Occupational and Environmental Health, 1994
    Co-Authors: Roberta F White, Robert G Feldman, Mark B Moss, Susan P Proctor
    Abstract:

    The objective of this investigation was to examine cerebral magnetic resonance imaging (MRI) pathology and functional deficits demonstrated by neuropsychological Testing in cases of toxic encephalopathy. Two subjects, occupationally exposed to toxic chemicals, were studied. As part of their neurological assessment, MRI was done and each underwent a neuropsychological battery for patients with toxic exposures (White et al. Clin. Neuropharmacol.13(5), 392–412, 1990). In Case 1, who was exposed to inorganic mercury, MRI showed mild central and cortical atrophy. Punctiform foci (T2) were noted in both frontal regions underlying the precentral gyri and in the subcortical myelin. Neuropsychological Testing showed problems in cognitive flexibility, cognitive tracking, inhibiting perseveration, fine manual motor coordination, visuospatial analysis and organization, memory, and affect and personality. In Case 2, who was exposed to 2,6-dimethyl-4-heptanone, MRI showed multiple small foci in the white matter and pons. Neuropsychological Testing indicated affective changes, deficits in manual motor speed, verbal fluency, visuospatial organization, and short-term memory. Lack of aphasia in patients with toxic encephalopathy indicates that neurotoxins probably affect subcortical and mesial temporal structures more than cortical gray matter. These MRI studies show subcortical sites of pathology. © 1993 Academic Press, Inc.

  • magnetic resonance imaging mri Neurobehavioral Testing and toxic encephalopathy two cases
    Environmental Research, 1993
    Co-Authors: Roberta F White, Robert G Feldman, Mark B Moss, Susan P Proctor
    Abstract:

    The objective of this investigation was to examine cerebral magnetic resonance imaging (MRI) pathology and functional deficits demonstrated by neuropsychological Testing in cases of toxic encephalopathy. Two subjects, occupationally exposed to toxic chemicals, were studied. As part of their neurological assessment, MRI was done and each underwent a neuropsychological battery for patients with toxic exposures (White et al. Clin. Neuropharmacol. 13(5), 392-412, 1990). In Case 1, who was exposed to inorganic mercury, MRI showed mild central and cortical atrophy. Punctiform foci (T2) were noted in both frontal regions underlying the precentral gyri and in the subcortical myelin. Neuropsychological Testing showed problems in cognitive flexibility, cognitive tracking, inhibiting perseveration, fine manual motor coordination, visuospatial analysis and organization, memory, and affect and personality. In Case 2, who was exposed to 2.6-dimethyl-4-heptanone, MRI showed multiple small foci in the white matter and pons. Neuropsychological Testing indicated affective changes, deficits in manual motor speed, verbal fluency, visuospatial organization, and short-term memory. Lack of aphasia in patients with toxic encephalopathy indicates that neurotoxins probably affect subcortical and mesial temporal structures more than cortical gray matter. These MRI studies show subcortical sites of pathology.

Camila M Batoreu - One of the best experts on this subject based on the ideXlab platform.

  • evidence of zinc protection against 2 5 hexanedione neurotoxicity correlation of Neurobehavioral Testing with biomarkers of excretion
    Neurotoxicology, 2002
    Co-Authors: Luisa M Mateus, Ana Paula Dos Santos, Camila M Batoreu
    Abstract:

    Risk prevention of human exposure against n-hexane neurotoxicity is relevant towards the protective measures to be proposed in occupational toxicology. Metabolic studies have identified 2,5-hexanedione (2,5-HD) as the main neurotoxic metabolite of n-hexane, which reacts with amino groups of lysine in axonal neurofilaments forming 2,5-dimethylpyrrole adducts, which are responsible for n-hexane neurotoxicity. In the present study, we have investigated the interaction of zinc with 2,5-HD, by correlating the decrease of pyrrole derivatives excretion with changes of Neurobehavioral effects. Two subchronic experiments (11 and 8 weeks of exposure) were performed in Wistar rats exposed to different doses of 2,5-HD (200, 400 mg/kg per day) and to the mixture of 2,5-HD + zinc acetate (200 + 300 mg/kg per day) and (400 + 500 mg/kg per day). The results obtained show a significant increase in the excretion of pyrroles in the groups exposed to 2,5-HD alone as compared to controls, and a significant decrease in the excretion of pyrrole derivatives in the groups of rats co-exposed to 2,5-HD + zinc acetate when compared to the rats exposed to 2,5-HD alone. These biochemical changes were immediately evident after the first day of exposure. Simultaneously, Neurobehavioral Testing (rearing and ambulation in open field) was performed weekly in the same groups of rats. The results demonstrated a significant decrease in Neurobehavioral dysfunction in rats co-exposed to 2,5-HD and zinc acetate. At the end of the exposure period, pyrroles levels returned to control values progressively, and the recovery of the neurotoxic effects was gradually established depending on the dose of exposure. The results suggest that zinc is a potential chemo-protector against 2,5-HD neurotoxicity which was identified by Neurobehavioral Testing. Moreover, pyrrole derivatives are good predictive biochemical biomarkers of 2,5-HD exposure and could be used as a complementary tool to characterize its neurotoxic effects.

Praveen Ballabh - One of the best experts on this subject based on the ideXlab platform.

  • characterization of acute brain injuries and Neurobehavioral profiles in a rabbit model of germinal matrix hemorrhage
    Stroke, 2008
    Co-Authors: Paraskevi Georgiadis, Edmund F. Lagamma, Caroline Chua, Lee Collins, Chau Huynh, Praveen Ballabh
    Abstract:

    Background and Purpose— Germinal matrix hemorrhage-intraventricular hemorrhage (GMH-IVH) is the most common neurological problem of premature infants and has enormous financial and social impact. Despite this, there is no standardized animal model of IVH depicting acute brain injuries. Methods— We delivered rabbit-pups prematurely at 29-day gestation by C-section, administered intraperitoneal glycerol to the pups at 3-hour postnatal age to induce IVH, and evaluated the brain for evidence of injuries. Results— About 80% of glycerol-treated pups developed gross IVH. We found greater neutrophil and microglia infiltration around the ventricles (periventricular zone) in pups with IVH than in controls. We noted more apoptosis and neuronal degeneration in the periventricular zone than in the neocortex in pups with IVH, but not in controls. There was evidence of axonal damage revealed by β-amyloid precursor protein and neurofilament immunolabeling. Neurobehavioral Testing showed that pups with IVH were more wobbl...

Roberta F White - One of the best experts on this subject based on the ideXlab platform.

  • magnetic resonance imaging mri Neurobehavioral Testing and toxic encephalopathy two cases1
    Neurobehavioral Methods and Effects in Occupational and Environmental Health, 1994
    Co-Authors: Roberta F White, Robert G Feldman, Mark B Moss, Susan P Proctor
    Abstract:

    The objective of this investigation was to examine cerebral magnetic resonance imaging (MRI) pathology and functional deficits demonstrated by neuropsychological Testing in cases of toxic encephalopathy. Two subjects, occupationally exposed to toxic chemicals, were studied. As part of their neurological assessment, MRI was done and each underwent a neuropsychological battery for patients with toxic exposures (White et al. Clin. Neuropharmacol.13(5), 392–412, 1990). In Case 1, who was exposed to inorganic mercury, MRI showed mild central and cortical atrophy. Punctiform foci (T2) were noted in both frontal regions underlying the precentral gyri and in the subcortical myelin. Neuropsychological Testing showed problems in cognitive flexibility, cognitive tracking, inhibiting perseveration, fine manual motor coordination, visuospatial analysis and organization, memory, and affect and personality. In Case 2, who was exposed to 2,6-dimethyl-4-heptanone, MRI showed multiple small foci in the white matter and pons. Neuropsychological Testing indicated affective changes, deficits in manual motor speed, verbal fluency, visuospatial organization, and short-term memory. Lack of aphasia in patients with toxic encephalopathy indicates that neurotoxins probably affect subcortical and mesial temporal structures more than cortical gray matter. These MRI studies show subcortical sites of pathology. © 1993 Academic Press, Inc.

  • magnetic resonance imaging mri Neurobehavioral Testing and toxic encephalopathy two cases
    Environmental Research, 1993
    Co-Authors: Roberta F White, Robert G Feldman, Mark B Moss, Susan P Proctor
    Abstract:

    The objective of this investigation was to examine cerebral magnetic resonance imaging (MRI) pathology and functional deficits demonstrated by neuropsychological Testing in cases of toxic encephalopathy. Two subjects, occupationally exposed to toxic chemicals, were studied. As part of their neurological assessment, MRI was done and each underwent a neuropsychological battery for patients with toxic exposures (White et al. Clin. Neuropharmacol. 13(5), 392-412, 1990). In Case 1, who was exposed to inorganic mercury, MRI showed mild central and cortical atrophy. Punctiform foci (T2) were noted in both frontal regions underlying the precentral gyri and in the subcortical myelin. Neuropsychological Testing showed problems in cognitive flexibility, cognitive tracking, inhibiting perseveration, fine manual motor coordination, visuospatial analysis and organization, memory, and affect and personality. In Case 2, who was exposed to 2.6-dimethyl-4-heptanone, MRI showed multiple small foci in the white matter and pons. Neuropsychological Testing indicated affective changes, deficits in manual motor speed, verbal fluency, visuospatial organization, and short-term memory. Lack of aphasia in patients with toxic encephalopathy indicates that neurotoxins probably affect subcortical and mesial temporal structures more than cortical gray matter. These MRI studies show subcortical sites of pathology.