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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    International journal of legal medicine 110 (1997), S. 305-311 
    ISSN: 1437-1596
    Keywords: Key words Traumatic head injury ; Tumor necrosis ; factor-α ; Blood-brain barrier ; Fluid percussion device ; Microglial cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Law
    Notes: Abstract To investigate the role of tumor necrosis factor-α (TNFα) after traumatic head injury in rats, moderate brain injury of 1000 mmHg was generated by an original fluid percussion injury device. TNFα levels in cerebrospinal fluid (CSF) gradually increased during the first 1 h, rose to a maximal elevation at 3 h and 6 h and returned to basal values by 24 h. Horseradish peroxidase tracer experiments revealed that primary microvascular damage appeared as early as 15 min after impact, but rapidly recovered and 1 h after impact secondary microvascular damage occurred in the hippocampus and parasagittal cortex. By immunoelectron microscopy, TNFα reactions were detected in the lysosomes of microglia accumulated at the impact site of the cortex 30 min after impact, and 1 h after impact these reactions were mainly detected at the glial cells (such as microglia and astrocytes) in the hippocampus and parasagittal cortex. Therefore the delayed microvascular damage observed in sites remote from the impact may be induced by TNFα which is synthesized mainly by glial cells. The present study suggests that TNFα conveyed from the microglial cells is one cofactor contributing to the fluid percussive brain edema formation after moderate brain injury.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    International journal of legal medicine 113 (2000), S. 221-228 
    ISSN: 1437-1596
    Keywords: Key words Traumatic head injury ; Diffuse axonal ¶injury ; Tumor necrosis factor-α ; β-Amyloid precursor ¶protein ; Fluid percussion device ; Glial cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Law
    Notes: Abstract The immunolocalization of tumor necrosis factor-α (TNFα) after diffuse axonal injury (DAI) is demonstrated using a midline fluid percussion rat model (moderate brain injury of 1000 mm Hg was generated) and the effects of TNFα on the axolemmal permeability using horseradish peroxidase as a tracer. In addition, the accumulation of β-amyloid precursor protein (β-APP) was investigated, which has recently been shown to be a reliable marker for the diagnosis of DAI in cases with fatal head injury. TNFα levels in brain tissues from the impact site and the cortex including the corpus callosum, gradually increased during the first 1 h, rose to a maximal elevation at 3 h, gradually decreased at 6 h and decreased further at 24 h. Horseradish peroxidase (HRP) tracer experiments revealed that primary axonal damage appeared as early as 15 min after impact but rapidly recovered and that 1 h after impact, secondary axonal damage occurred in the corpus callosum and the brain stem. By immunoelectron microscopy it was seen that β-APP accumulated in the axon from 1 h after impact demonstrating that there was functional axonal damage. TNFα reactions were detected in the lysosomes of microglia 30 min after impact and 1 h after impact these reactions were mainly detected in the glial cells (such as microglia, astrocytes and oligodendrocytes) in the corpus callosum and the brain stem. It is generally accepted that TNFα directly induces primary demyelination and oligodendrocyte apoptosis. Therefore, TNFα conveyed from the microglial cells is one cofactor contributing to the formation of the delayed axonal damage observed at these sites. The present study suggests that TNFα conveyed from the glial cells may contribute to the pathogenic mechanism of DAI formation following fluid percussive brain injury.
    Type of Medium: Electronic Resource
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