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  • 1
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 81 (1997), S. 5282-5282 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Pseudobinary systems of the type Fe(2−x)MxZr (M=transition metal) have been studied extensively for their typical magnetic properties.12 The common features of such systems are a breakdown of magnetic order and change in crystal structure from cubic C15 (Cu2Mg) type to hexagonal C14 (MgZn2 type) with a variation in concentration (x). The origin of the structural change is not very clear. The Fe moment is thought to be influenced by the near neighbor environment and variation in electronic structure. The present investigation involving the substitution of Fe with isoelectronic Ru assumes importance in light of this and complements the previous reported work. We find that for x〈0.5 the structure is C15. For x=0.6, a structural transition to C14 type takes place. The structural transition in the case of Ru occurs at x=0.5 as against values between 0.2 and 0.4 reported for similar studies with other transition metals like V, Cr, and Mn. There seems to be a clear indication of electronic influence on the structural change. In the case of V, which has five outer electrons, the structural change occurs at a relatively low substitution of x=0.2, whereas in the case of Ru, which has eight outer electrons, the structural change occurs at x=0.5. For x=0.1 to 0.3, the samples show a behavior similar to that of Fe2Zr, which is a ferromagnet with a saturation moment of 1.7 Bohr magnetron/Fe atom at 5 K. In the case of x=0.4, however, the saturation moment undergoes a sharp fall to 1.1 Bohr magnetron. Moreover, x=0.4 shows re-entrant behavior with a Tc of about 325 K and a spin freezing temperature of 130 K. © 1997 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Monatshefte für Chemie 126 (1995), S. 91-97 
    ISSN: 1434-4475
    Keywords: 2,6-Dihydroxypyrimidines ; Pyrimidinones ; Pyrimidine-2,6-diones ; Cytosine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Description / Table of Contents: Zusammenfassung Die Reaktion von 2-Formyl-3-dimethylamino-propennitril (1a) und 2-Ethoxycarbonyl-3-dimethylamino-propennitril (1b) mit substituierten Harnstoffen führte zur Bildung der 2-Cyan-3-ureidoacrlate2, welche unter alkalischen Bedingungen zu den 5-Formyl-, 5-Cyan- oder 5-Alkoxycarbonyl-2-oxopyrimidinen3,6 bzw.7 cyclisiert werden konnten. Reaktion von3 mit Isopentylnitrit ergab eine Mischung aus deaminiertem und zugleich oxidiertem Produkt4 sowie dem Oxoderivat5, welches während der Säulentrennung auf Kieselgel zusätzlich acetalisiert worden war. Die ähnliche Reaktion mit den Alkoxycarbonyl-Derivativen7 führte zur Bildung der 1-Alkyl-5-alkoxycarbonyl-pyrimidin-2,6-dione8a–d.
    Notes: Summary Treatment of 2-formyl-3-dimethylamino-propenenitrile (1a) and 2-ethoxycarbonyl-3-dimethylamino-propenenitrile (1b), resp., with substituted ureas led to the 2-cyano-3-ureidoacrylates2, which can be cyclized under alkaline conditions to give 5-formyl-5-cyano-, and 5-alkoxycarbonyl-2-oxopyrimidine derivatives3,6, and7. Reaction of3 with isopentylnitrite gave a mixture of the deaminated and oxidized product4 and the oxo derivative5, which was acetalized during the separation step. Similar reaction with the alkoxycarbonyl derivatives7 led to the formation of 1-alkyl-5-alkoxycarbonyl-pyrimidine-2,6-diones8a–d.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Apoptosis 3 (1998), S. 387-394 
    ISSN: 1573-675X
    Keywords: Alzheimer's disease ; apoptosis ; hypoxia-ischaemia ; neuronal death ; programmed cell death ; stroke.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The importance of caspases in developmental neuronal death is well-established. Recent data provide compelling evidence of caspase activation after ischaemic brain injury. Caspase inhibitors reduce cell death in several models of ischaemic injury. This review summarizes our current understanding of caspase function in ischaemic brain injury and examines the accumulating evidence of caspase participation in several neurodegenerative diseases. The therapeutic consequences of caspase inhibitor treatment in reducing cell death after such injury are also discussed.
    Type of Medium: Electronic Resource
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