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  • 1
    Electronic Resource
    Electronic Resource
    Novel mutations of the peripheral myelin protein22 gene in two pedigrees with Dejerine-Sottas disease (1998)
    Springer
    Human genetics 〈Berlin〉 102 (1998), S. 294-298 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Peripheral myelin protein22 (PMP22), a membrane glycoprotein, plays a significant role in the formation and/or maintenance of compact myelin in the peripheral nervous system. We studied two pedigrees with Dejerine-Sottas disease and identified two novel mutations in the PMP22 gene: one a 2-bp deletional mutation at nucleotide positions426 and 427 of exon4 (this is predicted to alter the reading frame at leucine80 and thus to lead to frame-shifted translation), and the other a guanine to thymine substitution at nucleotide position636 leading to a cysteine substitution for glycine150. Both mutations were located in the putative transmembrane domains reported in many cases of Charcot-Marie-Tooth neuropathy, Dejerine-Sottas disease, and hereditary neuropathy with liability to pressure palsies. The results suggest an important role for the putative transmembrane domains of PMP22 in its function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004390050694
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Flow threshold for enhanced phorbol ester binding in the ischemic gerbil brain (1995)
    Springer
    Neurochemical research 20 (1995), S. 1007-1012 
    Details
    ISSN: 1573-6903
    Keywords: Cerebral ischemia ; second messenger ; phorbol ester ; protein kinase C ; autoradiography ; cerebral blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The correlation between regional phorbol ester binding and cerebral blood flow (CBF) was evaluated in the gerbil brain after 2-hour unilateral common carotid artery occlusion [3H]phorbol 12, 13-dibutyrate (PDBu) was used as a specific ligand for estimating the translocation of protein kinase C (PKC), and CBF was determined by the [14C]iodoantipyrine method. A quantitative autoradiographic method permitted concurrent measurement of these two parameters in the same brain. In the ischemia group of the animals, statistically significant, inverse correlations were noted between the CBF and PDBu binding in the hippocampus (CA1 and CA3 regions and dentate gyrus), the caudate-putamen and lateral nuclei of the thalamus. In these regions, the PDBu binding increased progressively as CBF fell below 35–40 ml/100 g/min. On the other hand, the PDBu binding in the cerebral cortices did not show any significant changes even when CBF was decreased to below 35 ml/100 g/min. The above data suggest that (1) the translocation of PKC to the cell membrane may be regionally specific in response to ischmia and may remain in the regions particularly vulnerable to ischemia such as the hippocampus, caudate-putamen and lateral nuclei of the thalamus in the early ischemic phase; (2) the threshold of CBF below which PKC begins to translocate to the cell membrane in the above regions, may be 35–40 ml/100 g/min in 2-hour ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00995553
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Role of the Ryanodine Receptor in Ischemic Brain Damage—Localized Reduction of Ryanodine Receptor Binding During Ischemia in Hippocampus CA1 (1999)
    Springer
    Cellular and molecular neurobiology 19 (1999), S. 119-131 
    Details
    ISSN: 1573-6830
    Keywords: ryanodine receptor ; cerebral ischemia ; second messenger ; Ca2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. The ryanodine receptor has recently been shown to play a pivotal role in the regulation of intracellular Ca2+ concentration via Ca2+-induced Ca2+ release (CICR). Effects of ischemia on CICR in the brain tissue, however, remain largely unknown since only a few reports have been published on this subject. In this paper we report on work in this area by our group and review related progress in this field. 2. We examined alterations of ryanodine receptor binding and local cerebral blood flow (LCBF) at 15 min, 30 min, and 2 hr after occlusion of the right common carotid artery in the gerbil brain. A quantitative autoradiographic method permitted simultaneous measurement of these parameters in the same brain. The LCBF was significantly reduced in most of the cerebral regions on the occluded side during each time period of ischemia. In contrast, only in the hippocampus CA1 on the occluded side was a significant reduction in ryanodine binding found at 15 min, 30 min and 2 hr after the occlusion. 3. These findings suggest that suppression of ryanodine binding in the hippocampus CA1 may be attributable to a regionally specific perturbation of CICR and that this perturbation may be closely associated with the pathophysiological mechanism that leads to the selective ischemic vulnerability of this region. 4. Other recent studies have also reported an important role for ryanodine receptors in neuronal injury such as the delayed neuronal death in the hippocampus CA1. These data suggest that derangement of CICR is likely to be involved in acute neuronal necrosis as well as in delayed neuronal death in ischemia. 5. Further studies on clarifying the role of CICR in ischemic brain damage are needed in order to develop new therapeutic strategies for stroke patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006924826572
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    Paper (German National Licenses)
    Fulltext
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