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  • 2000-2004  (1)
  • 1980-1984  (2)
  • 1970-1974
  • 1965-1969
  • 81.10.Dn  (1)
  • Atypical PKU  (1)
  • Diffuse axonal ¶injury  (1)
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  • 2000-2004  (1)
  • 1980-1984  (2)
  • 1970-1974
  • 1965-1969
Year
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    The role of tumor necrosis factor-α in diffuse axonal injury following fluid-percussive brain injury in rats (2000)
    Springer
    International journal of legal medicine 113 (2000), S. 221-228 
    Details
    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
    URL: http://dx.doi.org/10.1007/s004149900095
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Injection electroluminescence from CdTe p-n junctions prepared by LPE (1981)
    Springer
    Applied physics 26 (1981), S. 151-156 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00614749
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Hyperphenylalaninemia due to impaired dihydrobiopterin biosynthesis (1981)
    Springer
    European journal of pediatrics 136 (1981), S. 275-280 
    Details
    ISSN: 1432-1076
    Keywords: Atypical PKU ; Deficiency of dihydrobiopterin ; Neurotransmitter treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A fourteen month-old boy with atypical phenylketonuria was treated with 5-hydroxytryptophan, L-dopa and peripheral aromatic amino acid decarboxylase inhibitor (Ro 4-4602:benserazide). Despite the good control of plasma phenylalanine on a low phenylalanine diet, he had shown no improvement in his development but progressive neurological symptoms, such asiirritability, convulsions and decrease voluntary movement. After beginning neurotransmitter therapy, his irritability disappeared promptly and the other symptoms diminished. He gradually reached his developmental milestones. At two and a half years of age, he had recovered sufficiently to be able to walk freely on treatment with 13 mg/kg/day of 5-hydroxytryptophan, 11 mg/kg/day of L-dopa and 2.7 mg/kg/day of benserazide in combination with slight restriction of phenylalanine intake (100 mg/kg/day). Levels of serotonin and 5-hydroxyindoleacetic acid were low in the patient's CSF. His urinary biopterin (Crithidia factor) excretion was low. An increase in serum biopterin following L-phenylalanine loading was not found. Dihydropteridine reductase activity in his skin fibroblasts was normal. He excreated large amounts of erythro- and threo-neopterins (but only a trace of biopterin) in his urine. After loading with phenylalanine the urinary excretion of neopterins was even more enhanced, but biopterin remained at low levels. These findings indicated that the patient has a dihydrobiopterin synthetase deficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442994
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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