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  • 2000-2004  (3)
  • G2/M arrest  (1)
  • Immunocytochemistry  (1)
  • Lagrange interpolation polynomial  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Annals of the Institute of Statistical Mathematics 52 (2000), S. 557-573 
    ISSN: 1572-9052
    Keywords: Chebyshev polynomials ; convex combination ; extremal problems for polynomials ; Lagrange interpolation polynomial ; optimal discrimination designs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Notes: Abstract The extrapolation design problem for polynomial regression model on the design space [−1,1] is considered when the degree of the underlying polynomial model is with uncertainty. We investigate compound optimal extrapolation designs with two specific polynomial models, that is those with degrees |m, 2m}. We prove that to extrapolate at a point z, |z| 〉 1, the optimal convex combination of the two optimal extrapolation designs |ξ m * (z), ξ2m * (z)} for each model separately is a compound optimal extrapolation design to extrapolate at z. The results are applied to find the compound optimal discriminating designs for the two polynomial models with degree |m, 2m}, i.e., discriminating models by estimating the highest coefficient in each model. Finally, the relations between the compound optimal extrapolation design problem and certain nonlinear extremal problems for polynomials are worked out. It is shown that the solution of the compound optimal extrapolation design problem can be obtained by maximizing a (weighted) sum of two squared polynomials with degree m and 2m evaluated at the point z, |z| 〉 1, subject to the restriction that the sup-norm of the sum of squared polynomials is bounded.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0219-1032
    Keywords: Calcium-binding Protein ; Immunocytochemistry ; Localization ; Visual Cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The distribution and morphology of neurons containing three calcium-binding proteins, calbindin D28K, calretinin, and parvalbumin in the adult rabbit visual cortex were studied. The calcium-binding proteins were identified using antibody immunocytochemistry. Calbindin D28K-immunoreactive (IR) neurons were located throughout the cortical layers with the highest density in layer V. However, calbindin D28K-IR neurons were rarely encountered in layer I. Calretinin-IR neurons were mainly located in layers II and III. Considerably lower densities of calretinin-IR neurons were observed in the other layers. Parvalbumin-IR neurons were predominantly located in layers III, IV, V, and VI. In layers I and II, parvalbumin-IR neurons were only rarely seen. The majority of the calbindin D28K-IR neurons were stellate, round or oval cells with multipolar dendrites. The majority of calretinin-IR neurons were vertical fusiform cells with long processes traveling perpendicularly to the pial surface. The morphology of the majority of parvalbumin-IR neurons was similar to that of calbindin D28K: stellate, round or oval with multipolar dendrites. These results indicate that these three different calcium-binding proteins are contained in specific layers and cells in the rabbit visual cortex.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-675X
    Keywords: apoptosis ; cyclin B1/CDC 2 ; G2/M arrest ; MAD 2 ; paclitaxel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Paclitaxel (Taxol™) is a microtubule-interfering agent that induced persistent and transient G2/M arrest before apoptosis in human nasopharyngeal carcinoma (NPC) cells at high and low concentrations, respectively. In this study, we intended to explore the underlying molecular events and found that cellular cyclin B1/CDC 2 kinase activity was increased and persisted for 〉6 h upon paclitaxel treatment both at high and low concentrations. Furthermore, activation of MAD 2 checkprotein could account for the loss of cyclin B1 ubiquitination and the persistence of cyclin B1/CDC 2 activation in the cases. To investigate the involvement of cyclin B1 and MAD 2 activation in paclitaxel-induced apoptosis, we introduced affinity-purified anti-cyclin B1 and MAD 2 antibodies into NPC cells by electroporation before the further paclitaxel treatment. The antibodies against cyclin B1 and MAD 2 indeed attenuated paclitaxel-induced cytotoxicity and DNA fragmentation. Our study suggests that activation of cyclin B1/CDC 2 and MAD 2 were the M-phase events required for paclitaxel-induced apoptosis in NPC cells. The dys-regulated cyclin B1/CDC 2 activation could enhance the prometaphase progression, but activation of MAD 2 rendered cells inable to exit from the metaphase. Under this circumstance, cells were probably going to “mitotic catastrophe” and ultimately, destined to apoptosis.
    Type of Medium: Electronic Resource
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