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  • 1
    Electronic Resource
    Electronic Resource
    Overexpression of the Neurotrophic Cytokine S100β in Human Temporal Lobe Epilepsy (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Neuritic sprouting and disturbances of calcium homeostasis are well described in epilepsy. S100β is an astrocyte-derived cytokine that promotes neurite growth and induces increases in levels of intracellular calcium in neurons. In sections of neocortex of surgically resected temporal lobe tissue from patients with intractable epilepsy, we found that the number of S100β-immunoreactive astrocytes was approximately threefold higher than that found in control patients (p 〈 0.001). These astrocytes were activated, i.e., enlarged, and had prominent processes. Temporal lobe tissue levels of S100β were shown by ELISA to be fivefold higher in 21 epileptics than in 12 controls (p 〈 0.001). The expression of the astrocyte intermediate filament protein, glial fibrillary acidic protein, was not significantly elevated in epileptics, suggesting a selective up-regulation of S100β expression. Our findings, together with established functions of S100β, suggest that this neurotrophic cytokine may be involved in the pathophysiology of epilepsy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.65010228.x
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  • 2
    Electronic Resource
    Electronic Resource
    Increased Neuronal β-Amyloid Precursor Protein Expression in Human Temporal Lobe Epilepsy: Association with Interleukin-1α Immunoreactivity (1994)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 63 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Levels of immunoreactive β-amyloid precursor protein and interleukin-1α were found to be elevated in surgically resected human temporal lobe tissue from patients with intractable epilepsy compared with postmortem tissue from neurologically unaffected patients (controls). In tissue from epileptics, the levels of the 135-kDa β-amyloid precursor protein isoform were elevated to fourfold (p 〈 0.05) those of controls and those of the 130-kDa isoform to threefold (p 〈 0.05), whereas those of the 120-kDa isoform (p 〉 0.05) were not different from control values. β-Amyloid precursor protein-immunoreactive neurons were 16 times more numerous, and their cytoplasm and proximal processes were more intensely immunoreactive in tissue sections from epileptics than controls (133 ± 12 vs. 8 ± 3/mm2; p 〈 0.001). However, neither β-amyloid precursor protein-immunoreactive dystrophic neurites nor β-amyloid deposits were found in this tissue. Interleukin-1α-immunoreactive cells (microglia) were three times more numerous in epileptics than in controls (80 ± 8 vs. 25 ± 5/mm2; p 〈 0.001), and these cells were often found adjacent to β-amyloid precursor protein-immunoreactive neuronal cell bodies. Our findings, together with functions established in vitro for interleukin-1, suggest that increased expression of this protein contributes to the increased levels of β-amyloid precursor protein in epileptics, thus indicating a potential role for both of these proteins in the neuronal dysfunctions, e.g., hyperexcitability, characteristic of epilepsy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.63051872.x
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  • 3
    Electronic Resource
    Electronic Resource
    S100β Induction of the Proinflammatory Cytokine Interleukin-6 in Neurons (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Levels of the neurotrophic cytokine S100β and the proinflammatory cytokine interleukin-6 (IL-6) are both elevated in Alzheimer’s brain, and both have been implicated in β-amyloid plaque formation and progression. We used RT-PCR and electrophoretic mobility shift assay to assess S100β induction of IL-6 expression and the role of κB-dependent transcription in this induction in neuron-enriched cultures and in neuron-glia mixed cultures from fetal rat cortex. S100β (10 or 100 ng/ml × 24 h) increased IL-6 mRNA levels two- and fivefold, respectively (p 〈 0.05 in each case), and S100β (100-1,000 ng/ml) induced increases in medium levels of biologically active IL-6 (30-80%). Combined in situ hybridization and immunohistochemistry preparations localized IL-6 mRNA to neurons in these cultures. S100β induction of IL-6 expression correlated with an increase in DNA binding activity specific for a κB element and was inhibited (75%) by suppression of κB binding with double-stranded “decoy” oligonucleotides. The low levels of S100β required to induce IL-6 overexpression in neurons, shown here, suggest that overexpression of S100β induces neuronal expression of IL-6 and of IL-6-induced neurodegenerative cascades in Alzheimer’s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0740143.x
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  • 4
    Electronic Resource
    Electronic Resource
    S100β Increases Levels of β-Amyloid Precursor Protein and Its Encoding mRNA in Rat Neuronal Cultures (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 71 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: S100β has been implicated in the formation of dystrophic neurites, overexpressing β-amyloid precursor protein (βAPP), in the β-amyloid plaques of Alzheimer's disease. We assessed the effects of S100β on cell viability of, neurite outgrowth from, and βAPP expression by neurons in primary cultures from fetal rat cortex. S100β (1–10 ng/ml) enhanced neuronal viability (as assessed by increased mitochondrial activity and decreased lactic acid dehydrogenase release) and promoted neurite outgrowth. Higher levels of S100β (100 ng/ml, but not 1 µg/ml) produced qualitatively similar, but less marked, effects. S100β also induced increased neuronal expression of the microtubule-associated protein MAP2, an effect that is consistent with trophic effects of S100β on neurite outgrowth. S100β (10 and 100 ng/ml) induced graded increases in neuronal expression of βAPP and of βAPP mRNA. These results support our previous suggestion that excessive expression of S100β by activated, plaque-associated astrocytes in Alzheimer's disease contributes to the appearance of dystrophic neurites overexpressing βAPP in diffuse amyloid deposits, and thus to the conversion of these deposits into the diagnostic neuritic β-amyloid plaques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.71041421.x
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  • 5
    Electronic Resource
    Electronic Resource
    Overexpression of the Neuritotrophic Cytokine S100β Precedes the Appearance of Neuritic β-Amyloid Plaques in APPV717F Mice (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Homozygous APPV717F transgenic mice overexpress a human β-amyloid precursor protein (βAPP) minigene encoding a familial Alzheimer’s disease mutation. These mice develop Alzheimer-type neuritic β-amyloid plaques surrounded by astrocytes. S100β is an astrocyte-derived cytokine that promotes neurite growth and promotes excessive expression of βAPP. S100β overexpression in Alzheimer’s disease correlates with the proliferation of βAPP-immunoreactive neurites in β-amyloid plaques. We found age-related increases in tissue levels of both βAPP and S100β mRNA in transgenic mice. Neuronal βAPP overexpression was found in cell somas in young mice, whereas older mice showed βAPP overexpression in dystrophic neurites in plaques. These age-related changes were accompanied by progressive increases in S100β expression, as determined by S100β load (percent immunoreactive area). These increases were evident as early as 1 and 2 months of age, months before the appearance of β-amyloid deposits in these mice. Such precocious astrocyte activation and S100β overexpression are similar to our earlier findings in Down’s syndrome. Accelerated age-related overexpression of S100β may interact with age-associated overexpression of mutant βAPP in transgenic mice to promote development of Alzheimer-like neuropathological changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.0740295.x
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  • 6
    Electronic Resource
    Electronic Resource
    S100B-induced microglial and neuronal IL-1 expression is mediated by cell type-specific transcription factors (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 92 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Both the astrocytic cytokine S100B and the pro-inflammatory interleukin-1 (IL-1) are elevated in Alzheimer's disease, and each has been implicated in Alzheimer-related neuropathology. We examined the gene-regulatory events through which S100B induces IL-1β expression. In primary microglia, S100B activated the transcription factors Sp1 and NFκB, followed by an increase in IL-1β mRNA levels. The latter was blocked by a peptide inhibitor of NFκB or by a double-stranded oligonucleotide containing a NFκB-binding site to serve as ‘decoy’ DNA and reduce available NFκB. But in primary cortical neurons, decoy and siRNA experiments indicated that the IL-1β induction by S100B was mediated by Sp1 without evidence of a role for NFκB. Our results suggest that the elevation of S100B and IL-1 in Alzheimer brain and consequent neurodegenerative events are mediated through cell-type specific gene-regulatory events, providing mechanistic insight into connections between glial activation and neuronal dysfunction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02909.x
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  • 7
    Electronic Resource
    Electronic Resource
    Timing of Late Neoproterozoic glaciation on Baltica constrained by detrital zircon geochronology in the Hedmark Group, south-east Norway (2005)
    Oxford, UK : Blackwell Science Ltd
    Terra nova 17 (2005), S. 0 
    Details
    ISSN: 1365-3121
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Geosciences
    Notes: The Moelv Tillite is the Late Neoproterozoic Varanger glacial deposit recorded in the Hedmark Group, SE Norway. Paired U–Pb and Lu–Hf data collected on detrital zircons in the Rendalen Formation underlying the Moelv Tillite have identified an uncommon 677 ± 15 to 620 ± 14 Ma population, that constrain the deposition of the Moelv Tillite to be younger than 620 ± 14 Ma. The youngest detrital zircons may be derived from granite magmatism related to the 616 ± 3 Ma Egersund dolerite magmatism, situated in the western part of the Sveconorwegian orogen. The Moelv Tillite, which is not overlain by a cap carbonate, possibly correlates with the c. 580 Ma Squantum-Gaskiers glacial deposits of Avalonia. Available palaeomagnetic data for the Late Neoproterozoic suggest that Baltica was located at intermediate to high latitude between 620 and 555 Ma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3121.2005.00609.x
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  • 8
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    Super-reduced mineral assemblages in "ophiolitic" chromitites and peridotites: the view from Mount Carmel (2017)
    Schweizerbart
    Details
    Publication Date: 2017-09-28
    Description: Ultrahigh-pressure ( UHP ) materials ( e.g ., diamond, high-pressure polymorph of chromite) and super-reduced (SuR) phases ( e.g ., carbides, nitrides, silicides and native metals) have been identified in chromitites and peridotites of the Tibetan and Polar-Urals ophiolites. These unusual assemblages suggest previously unrecognized fluid- or melt-related processes in the Earth’s mantle. However, the origin of the SuR phases, and in particular their relationships with the UHP materials in the ophiolites, are still enigmatic. Studies of a recently recognized SuR mineral system from Cretaceous volcanics on Mt Carmel, Israel, suggest an alternative genesis for the ophiolitic SuR phases. The Mt Carmel SuR mineral system (associated with Ti-rich corundum xenocrysts) appears to reflect the local interaction of mantle-derived CH 4 ± H 2 fluids with basaltic magmas in the shallow lithosphere (depths of ~30–100 km). These interactions produced desilication of the magma, supersaturation in Al 2 O 3 leading to rapid growth of corundum, and phase assemblages requiring local oxygen fugacity ( f O 2 ) gradually dropping to ~11 log units below the iron–wüstite (IW) buffer. The strong similarities between this system and the SuR phases and associated Ti-rich corundum in the Tibetan and Polar-Urals ophiolites suggest that the ophiolitic SuR suite probably formed by local influx of CH 4 ± H 2 fluids within previously subducted peridotites (and included chromitites) during their rapid exhumation from the deep upper mantle to lithospheric levels. In the final stages of their ascent, the recycled peridotites and chromitites were overprinted by a shallow magmatic system similar to that observed at Mt Carmel, producing most of the SuR phases and eventually preserving them within the Tibetan and Polar-Urals ophiolites.
    Print ISSN: 0935-1221
    Electronic ISSN: 1617-4011
    Topics: Geosciences
    Published by Schweizerbart
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