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  • 2000-2004  (1)
  • 1980-1984  (1)
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  • 81.10.Dn  (1)
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  • Diffuse axonal ¶injury  (1)
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  • 2000-2004  (1)
  • 1980-1984  (1)
  • 1970-1974  (1)
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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Applied physics 26 (1981), S. 151-156 
    ISSN: 1432-0630
    Keywords: 78.60.Fi ; 73.40.Lq ; 81.10.Dn
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Abstract CdTep-n junction diodes were prepared by LPE using CdCl2 as a solvent. Excess cadmium was added to the CdCl2-CdTe solution. Capacitance-voltage characteristics show that the diode structure is ofp-i-n type. Injection electroluminescence spectra reveal that radiative transitions occur mainly in thep-type region; relevant recombination centers are discussed in connection with those in a previous paper on the photoluminescence of CdTe:P crystals. Temperature dependences of the electroluminescence spectra were explained taking into account a change in sites where electrons radiatively recombine.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 16 (1972), S. 161-183 
    ISSN: 1432-1106
    Keywords: Facial nucleus ; Topographical representation ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The facial nucleus (FN) of the cat was studied by electrophysiological method for (1) general characteristics of the FN neurons during antidromic activation, (2) topographical representation of the peripheral branches of the facial nerve and (3) synaptic activities induced in the FN neurons following peripheral facial nerve stimulation. Stimulation of either peripheral branches or the genu of the facial nerve produced negative field potential of 2–3 mV in the FN. The field potential had a latency of less than 1 msec, refractory period of 2–3 msec and a relatively short duration. During double shock testing of the antidromic field potentials, the test potentials were suppressed (after initial recovery from the refractory period) for a duration of up to 80–100 msec. Intracellular analysis revealed that antidromic firing of the FN neuron is composed of M, IS, SD spikes. The rise time of spike potentials ranged from 0.23 msec to 0.53 msec and fall time 0.73 msec to 4.7 msec. The duration of the spike after-hyperpolarization varied from 6 msec to 60 msec with latencies to peak of 1.5 msec to 14 msec. Double shock testing showed that the summation effect of the afterhyperpolarization was greater at shorter time intervals. The latencies of the spike potentials varied from 0.46 msec to 1.1 msec for peripheral nerve stimulation and 0.18 msec to 1 msec for genu stimulation. The conduction velocity of the facial nerve ranged from 25 m/sec to 75 m/sec. These results were compared with the known characteristics of other cranial and spinal motoneurons. Topographical representation of the peripheral branches of the facial nerve was that the PA was represented solely in the medial aspect, TZ mainly in the dorsal aspect of the intermediate portion and BL in the ventral aspect of the intermediate and mainly in the lateral aspect of the nucleus. Stimulation of peripheral facial nerve produced negative field potentials in the FN or induced EPSPs in the FN neurons with latencies of 4–7 msec. The synaptic inputs were found mainly in the medial aspect of the FN by PA stimulation. These synaptic inputs were discussed as being relayed through the trigeminal nucleus.
    Type of Medium: Electronic Resource
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