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We reported herein a case of isolated cerebral actinomycosis in a 54-year-old immunocompetent man. Brain MRI showed a left frontal intra-axial lesion and perilesional edema. We performed an open biopsy of the left frontal enhancing lesion.
View Article and Find Full Text PDFA Mild Traumatic Brain Injury in Mice Produces Lasting Deficits in Brain Metabolism.
J Neurotrauma
October 2018
1 Spinal Cord & Brain Injury Research Center, University of Kentucky, Lexington Kentucky.
Metabolic uncoupling has been well-characterized during the first minutes-to-days after a traumatic brain injury (TBI), yet mitochondrial bioenergetics during the weeks-to-months after a brain injury is poorly defined, particularly after a mild TBI. We hypothesized that a closed head injury (CHI) would be associated with deficits in mitochondrial bioenergetics at one month after the injury. A significant decrease in state-III (adenosine triphosphate production) and state-V (complex-I) driven mitochondrial respiration was found at one month post-injury in adult C57Bl/6J mice.
View Article and Find Full Text PDFMild elevation of N-acetylaspartic acid and macrocephaly: diagnostic problem.
J Child Neurol
November 2003
Department of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77555-0359, USA.
Patients with slightly increased excretion of N-acetylaspartic acid in urine, together with macrocephaly, present a dignostic dilemma for Canavan's disease. We describe a 13-year-old male patient with macrocephaly, mild developmental delay, increased signal intensity in the basal ganglia bilaterally, partial cortical blindness, and retinitis pigmentosa. Although the clinical course and magnetic resonance imaging findings did not resemble typical Canavan's disease, N-acetylaspartic acid excretion in the patient's urine was slightly elevated, 99.
View Article and Find Full Text PDFIdentification and distribution of aspartoacylase in the postnatal rat brain.
Neuroreport
October 2003
Department of Molecular Medicine and Pathology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. m.
Aspartoacylase metabolizes N-acetylaspartic acid to produce L-aspartate and acetate. An aspartoacylase deficiency in humans is responsible for Canavan disease, a lethal autosomal recessive leukodystrophy. The role of aspartoacylase in the mammalian brain is unclear.
View Article and Find Full Text PDFPurification and preliminary characterization of brain aspartoacylase.
Arch Biochem Biophys
May 2003
Department of Chemistry, University of Toledo, 2801 W. Bancroft Street, OH 43606, USA.
Aspartoacylase catalyzes the deacetylation of N-acetylaspartic acid (NAA) in the brain to produce acetate and L-aspartate. An aspartoacylase deficiency, with concomitant accumulation of NAA, is responsible for Canavan disease, a lethal autosomal recessive disorder. To examine the mechanism of this enzyme the genes encoding murine and human aspartoacylase were cloned and expressed in Escherichia coli.
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