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  • Peripheral nerve  (3)
  • 23Na MRI  (2)
  • Calmodulin  (2)
  • 1
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    FEBS Letters 166 (1984), S. 373-377 
    ISSN: 0014-5793
    Schlagwort(e): Calmodulin ; Tetrahymena ; Trifluoperazine ; ^1^9F NMR
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie , Physik
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    FEBS Letters 160 (1983), S. 182-186 
    ISSN: 0014-5793
    Schlagwort(e): Calmodulin ; Circular dichroism ; Trifluoperazine ; ^1^9F NMR
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie , Physik
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    FEBS Letters 334 (1993), S. 281-285 
    ISSN: 0014-5793
    Schlagwort(e): Dp116 ; Dystroglycan ; Dystrophin ; Dystrophin-associated protein ; Peripheral nerve ; Utrophin
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie , Physik
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism 1214 (1994), S. 27-31 
    ISSN: 0005-2760
    Schlagwort(e): (Rabbit) ; Development ; Dorsal root ganglion ; Ganglioside ; Motor neuron ; Peripheral nerve ; Spinal cord
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Chemie und Pharmazie , Medizin , Physik
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 5
    Digitale Medien
    Digitale Medien
    Springer
    Neuroradiology 35 (1993), S. 416-419 
    ISSN: 1432-1920
    Schlagwort(e): 23Na MRI ; Cerebral infarction ; Cell viability ; Cerebral oedema
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract 23Na MRI changes from the acute to chronic phase were investigated in seven patients with cerebral in-farcts. They showed no signal increase during the first 13 h after the stroke and revealed a definite signal increase thereafter. This reached a maximum 45–82 h after stroke and became slightly less marked in the subactue and chronic phases, probably as a result of disappearance of cerebral oedema. In the early acute phase of stroke,23Na MRI appears to fail to demonstrate Na+ increases in the ischaemic area, due presumably to the invisibility on MRI of intracellular23Na in the intact brain. The increase more than 13 h after stroke, during which ischaemic cells are likely to die, is presumably because of increased visibility of intracellular23Na in the dead cells.23Na MRI is apparently insensitive to early ischaemic changes, but may be useful for assessing the cell viability in the ischaemic brain.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 6
    Digitale Medien
    Digitale Medien
    Springer
    Neuroradiology 34 (1992), S. 301-304 
    ISSN: 1432-1920
    Schlagwort(e): 23Na MRI ; 1H MRI ; Cerebral hemorrhage
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Four patients with cerebral hemorrhage were examined serially from the acute to chronic phase by1H magnetic resonance imaging (MRI),23Na MRI and computed tomography (CT). At 1–2 days after bleeding, the23Na image revealed no visible signal change in the area of hemorrhage, although CT and1H images clearly demonstrated the existence of a hematoma in the thalamus or putamen. At 4–7 days after the hemorrhage, the23Na images began to exhibit a small increase in signal intensity at the hematoma site, while at 2–3 weeks, a marked increase in23Na signal intensity was observed. These findings suggest that the hematoma consisted mainly of a corpuscular component, with a low Na+ concentration, with little serum component. Lack of signal from the corpuscular component on the23Na image was confirmed by an in vitro study. In the late acute phase, Na+ accumulation may occur in the corpuscular component due to failure of the Na+ pump. The intracellular23Na appears to be totally visible to MRI, resulting in an increase in signal intensity. In the subacute or chronic phase, the corpuscular component may be destroyed, leaving fluid in its place. A high Na+ concentration in this fluid may give markedly increased23Na signal intensity on MRI.23Na MRI appears to provide important information for understanding the evoluation of cerebral hemorrhage and for estimating the viability of cells, although its value for diagnosis may not be great.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 7
    ISSN: 1432-0533
    Schlagwort(e): Key words Dystrophin-associated protein ; Laminin ; Peripheral nerve ; Schwann cell ; Regeneration
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract In Schwann cells, the transmembrane glycoprotein β-dystroglycan composes the dystroglycan complex, together with the extracellular glycoprotein α-dystroglycan which binds laminin-2, a major component of the Schwann cell basal lamina. To provide clues to the biological functions of the interaction of the dystroglycan complex with laminin-2 in peripheral nerve, the expression of β-dystroglycan and laminin-α2 chain was studied in rat sciatic nerves undergoing axonal degeneration and regeneration as well as in normal condition. In normal sciatic nerve, immunoreactivity for the cytoplasmic domain of β-dystroglycan was consistently and selectively localized in the Schwann cell cytoplasm underlying the outer (abaxonal) membrane apposing the basal lamina. While β-dystroglycan expression was gradually down-regulated in Schwann cells losing contact with axons during axonal degeneration, it was progressively up-regulated as the regenerating process of ensheathment and myelination proceeded during regeneration. Interestingly, β-dystroglycan expression, when detectable, was always restricted to the Schwann cell cytoplasm beneath the outer membrane apposing the basal lamina during both axonal degeneration and regeneration. Furthermore, laminin-α2 immunoreactivity roughly paralleled that of β-dystroglycan during both axonal degeneration and regeneration, indicating that the expression of β-dystroglycan and laminin-α2 is induced and maintained by the Schwann cell contact with axons. Our results indicate that the dystroglycan complex is involved in the adhesion of the Schwann cell outer membrane with the basal lamina and suggest that the dystroglycan complex may play a role in the process of Schwann cell ensheathment and myelination through the interaction with laminin-2.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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