256 research outputs found

    The Number of Hierarchical Orderings

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    An ordered set-partition (or preferential arrangement) of n labeled elements represents a single ``hierarchy''; these are enumerated by the ordered Bell numbers. In this note we determine the number of ``hierarchical orderings'' or ``societies'', where the n elements are first partitioned into m <= n subsets and a hierarchy is specified for each subset. We also consider the unlabeled case, where the ordered Bell numbers are replaced by the composition numbers. If there is only a single hierarchy, we show that the average rank of an element is asymptotic to n/(4 log 2) in the labeled case and to n/4 in the unlabeled case.Comment: 7 page

    Generation of All Possible Multiselections from a Multiset

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    The concept of a [k1, k2,..., kK]-selection applied on a multiset is introduced and an algorithm is outlined to generate all [k1, k2,..., kK]-selections from a given multiset. Key words: Multiselection; Mutiset; Contingency matrix; Combinatorie

    Christian Delage, Vincent Guigueno, L’Historien et le Film, Gallimard, coll. Folio Histoire, 362 p., 48 ill. NB, 2004.

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    L’Historien et le Film était un livre attendu: depuis les sorties concomitantes, en 1977, des ouvrages fondateurs de Marc Ferro (Cinéma et Histoire, Denoël-Gonthier) et de Pierre Sorlin (Sociologie du cinéma, Aubier-Montaigne), aucune synthèse réflexive, de nature à la fois épistémologique et théorique, n’avait été publiée sur l’apport du cinéma à la connaissance de l’histoire. Ce dont témoigne d’abord l’ouvrage de Christian Delage et Vincent Guigueno, respectivement maîtres de conférences à ..

    Pharmacophore Models Derived From Molecular Dynamics Simulations of Protein-Ligand Complexes: A Case Study.

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    A single, merged pharmacophore hypothesis is derived combining 2000 pharmacophore models obtained during a 20 ns molecular dynamics simulation of a protein-ligand complex with one pharmacophore model derived from the initial PDB structure. This merged pharmacophore model contains all features that are present during the simulation and statistical information about the dynamics of the pharmacophore features. Based on the dynamics of the pharmacophore features we derive two distinctive feature patterns resulting in two different pharmacophore models for the analyzed system – the first model consists of features that are obtained from the PDB structure and the second uses two features that can only be derived from the molecular dynamics simulation. Both models can distinguish between active and decoy molecules in virtual screening. Our approach represents an objective way to add/remove features in pharmacophore models and can be of interest for the investigation of any naturally occurring system that relies on ligand-receptor interactions for its biological activity

    Lectures géographiques d’un journaliste français à Berlin

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    Après des études à l’École Normale Supérieure de la rue d’Ulm et à Sciences Po Paris, titulaire d’une agrégation d’histoire puis d’une thèse en histoire contemporaine, Thomas Wieder devient journaliste au Monde dans le service politique, puis son correspondant en Allemagne à partir de 2016. Son témoignage montre quelle place a la géographie dans son métier et éclaire sur une géographie citadine qui mobilise au quotidien représentations héritées de la ville, analyses statistiques, espaces repè..

    Bcl-2 antagonizes apoptotic cell death induced by two new ceramide analogues

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    AbstractCeramides which arise in part from the breakdown of sphingomyelin comprise a class of antiproliferative lipids and have been implicated in the regulation of programmed cell death better known as apoptosis. In the present study, two new synthetic ceramide analogues, N-thioacetylsphingosine and FS-5, were used in Molt4 cells to induce cell death. Besides their cytotoxic effects at concentrations ≥14 μM the data obtained clearly show that both analogues induced apoptosis at concentrations below this critical concentration as assessed by trypan blue exclusion and cleavage of the death substrate poly-(ADP-ribose) polymerase (PARP). Additional experiments in bcl-2-transfected Molt4 cells revealed that the apoptotic but not the lytic effects of the analogues were antagonized by the apoptosis inhibitor Bcl-2. Furthermore, neither N-thio-acetylsphingosine nor FS-5 induced PARP cleavage in bcl-2-transfected Molt4 cells indicating that the induction of apoptotic cell death by cell permeable ceramides is not due to unspecific disturbance of the cell membrane

    The Bax/Bcl-2 Ratio Determines the Susceptibility of Human Melanoma Cells to CD95/Fas-Mediated Apoptosis

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    Defective cytochrome c release and the resulting loss of caspase-3 activation was recently shown to be essential for the susceptibility of human melanoma cells to CD95/Fas-induced apoptosis. Cytochrome c release from mitochondria is regulated by the relative amounts of apoptosis-promoting and apoptosis-inhibiting Bcl-2 proteins in the outer membrane of these organelles. The assignment of Bax/Bcl-2 ratios by quantitative Western blotting in 11 melanoma cell populations revealed a relation to the susceptibility to CD95-mediated apoptosis. We could show that a low Bax/Bcl-2 ratio was characteristic for resistant cells and a high Bax/Bcl-2 ratio was characteristic for sensitive cells. Low Bax expression was not a consequence of mutations in the p53 coding sequence. The Bax/Bcl-2 ratio was also in clear correlation with sensitivity to another cell death inducer, N-acetylsphingosine. Furthermore, Bcl-2 overexpression abolished apoptosis triggered by both apoptotic stimuli, confirming the critical role of the Bax/Bcl-2 ratio as a rheostat that determines the susceptibility to apoptosis in melanoma cells by regulating mitochondrial function. Interestingly, some chemotherapeutics lead to the activation of death pathways by CD95L upregulation, ceramide generation, direct activation of upstream caspases, or upregulation of proapoptotic genes. Taken together, these signals enter the apoptotic pathway upstream of mitochondria, resulting in activation of this central checkpoint. We therefore assumed that apoptosis deficiency of malignant melanoma can be circumvented by drugs directly influencing mitochondrial functions. For this purpose we used betulinic acid, a cytotoxic agent selective for melanoma, straightly perturbing mitochondrial functions. In fact, betulinic acid induced mitochondrial cytochrome c release and DNA fragmentation in both CD95-resistant and CD95-sensitive melanoma cell populations, independent of the Bax/Bcl-2 ratio
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