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  • Synapse  (2)
  • Area postrema  (1)
  • CO oxidation  (1)
  • 1
    ISSN: 1572-879X
    Keywords: Au/Fe2O3 catalyst ; structural study ; CO oxidation ; mechanism of the structural changes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract 1 wt% Au/Fe2O3 catalyst was prepared by a co‐precipitation method. The structure of the sample in the as prepared, oxidized and reduced states was investigated by means of X‐ray photoelectron spectroscopy (XPS), transition electron microscopy (TEM), electron diffraction (ED) and X‐ray diffraction (XRD). The structure of the samples after various treatments and their activity in the CO oxidation were compared. The results show the stability of the gold particle size during the treatments. However, after oxidation, a slight shift in the Au 4f binding energy towards lower values points to the formation of an electron‐rich state of the metallic gold particles compared to that revealed in the as prepared sample. Simultaneously, a goethite phase in the Fe2O3 support is present, which is not observed in the “as prepared” and reduced samples. In the reduced sample the presence of a crystalline maghemite‐c phase indicates a change in the support morphology. In the CO oxidation the oxidized sample shows the highest activity and it might be the result of the cooperative effect of goethite, FeO and the electron‐rich metallic gold nanoparticles. We suggest that a structural transformation occurs along the gold/support perimeter during the treatments and we propose a possible mechanism for the effect of the oxidation treatment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Glia ; Motoneuron ; Ribosome ; Spinal cord injury ; Synapse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Structural changes in lumbosacral ventral horn neurons and their synaptic input were studied at 3, 10, 21, 42, and 90 days following low thoracic cord hemisection in adult rats by light microscopic examination of synaptophysin immunoreactivity (SYN-IR) and by electron microscopy. There was an ipsilateral transient decrease in SYN-IR at the somal and proximal dendritic surfaces of anterior horn neurons which extended caudally from the site of injury over a postoperative (p.o.) period of 42 days. Concomitantly, at 21 days p.o., perineuronal SYN-IR started to recover in upper lumbar segments. By 90 days p.o., a normal staining pattern of SYN was noted in upper and mid lumbar segments, but the perineuronal SYN-IR was still slightly below normal levels in low lumbar and sacral segments. Electron microscopy revealed ultrastructural changes coincident with the alterations in SYN-IR. At 3 days p.o., phagocytosis of degenerating axon terminals by activated microglial cells was observed at the somal and proximal dendritic surfaces of ventral horn neurons. These changes were most prominent up to two segments caudal to the lesion. At 10 days p.o., advanced stages of bouton phagocytosis were still detectable in all lumbosacral motor nuclei. Additionally, abnormal axon terminals, with a few dispersed synaptic vesicles and accumulations of large mitochondria, appeared at the scalloped somal surfaces of anterior horn neurons. At 21 days p.o., several large lumbosacral motoneurons had developed chromatolysis-like ultrastructural alterations and motoneuronal cell bodies had become partially covered by astrocytic lamellae. At 42 days p.o., there was a transient appearance of polyribosomes in some M-type boutons. In addition, at 42 and 90 days p.o., a few degenerating motoneurons were detected in all lumbosacral segments, but most displayed normal neuronal cell bodies contacted by numerous intact synapses as well as by astrocytic processes. In contrast to these striking alterations of synaptic input at somal and proximal dendritic surfaces of motoneurons, relatively few degenerating boutons were detected in the neuropil of motor nuclei at all the p.o. times studied. We suggest that the preferential disturbance of the predominantly inhibitory axosomatic synapses on ventral horn neurons may be involved in the mechanisms which influence the well-established increase in motoneuronal excitability after spinal cord injury.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Glia ; Motoneuron ; Ribosome ; Spinal cord injury ; Synapse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Structural changes in lumbosacral ventral horn neurons and their synaptic input were studied at 3, 10, 21, 42, and 90 days following low thoracic cord hemisection in adult rats by light microscopic examination of synaptophysin immunoreactivity (SYN-IR) and by electron microscopy. There was an ipsilateral transient decrease in SYN-IR at the somal and proximal dendritic surfaces of anterior horn neurons which extended caudally from the site of injury over a postoperative (p.o.) period of 42 days. Concomitantly, at 21 days p.o., perineuronal SYN-IR started to recover in upper lumbar segments. By 90 days p.o., a normal staining pattern of SYN was noted in upper and mid lumbar segments, but the perineuronal SYN-IR was still slightly below normal levels in low lumbar and sacral segments. Electron microscopy revealed ultrastructural changes coincident with the alterations in SYN-IR. At 3 days p.o., phagocytosis of degenerating axon terminals by activated microglial cells was observed at the somal and proximal dendritic surfaces of ventral horn neurons. These changes were most prominent up to two segments caudal to the lesion. At 10 days p.o., advanced stages of bouton phagocytosis were still detectable in all lumbosacral motor nuclei. Additionally, abnormal axon terminals, with a few dispersed synaptic vesicles and accumulations of large mitochondria, appeared at the scalloped somal surfaces of anterior horn neurons. At 21 days p.o., several large lumbosacral motoneurons had developed chromatolysis-like ultrastructural alterations and motoneuronal cell bodies had become partially covered by astrocytic lamellae. At 42 days p.o., there was a transient appearance of polyribosomes in some M-type boutons. In addition, at 42 and 90 days p.o., a few degenerating motoneurons were detected in all lumbosacral segments, but most displayed normal neuronal cell bodies contacted by numerous intact synapses as well as by astrocytic processes. In contrast to these striking alterations of synaptic input at somal and proximal dendritic surfaces of motoneurons, relatively few degenerating boutons were detected in the neuropil of motor nuclei at all the p.o. times studied. We suggest that the preferential disturbance of the predominantly inhibitory axosomatic synapses on ventral horn neurons may be involved in the mechanisms which influence the well-established increase in motoneuronal excitability after spinal cord injury.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 75 (1987), S. 16-22 
    ISSN: 1432-0533
    Keywords: Monosodium-l-glutamate ; Neuronal death ; Area postrema ; Acetylcholinesterase ; Fetal rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Monosodium-l-glutamate given subcutaneously to pregnant rats caused acute necrosis of the acetylcholinesterase-positive neurons in the area postrema. The same effect has been observed in the area postrema of fetal rats. The process of neuronal cell death and the elimination of debris by microglia cells proved to be similar in pregnant animals and in their fetuses. However, embryonal neurons were more sensitive to glutamate as judged by the rapidity of the process and the dose-response relationship. These observations raise the possibility of transplacental poisoning in human fetuses after the consumption of glutamate-rich food by the mother.
    Type of Medium: Electronic Resource
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