476 research outputs found

    The paradox of the clumps mathematically explained

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    The lumpy distribution of species along a continuous one-dimensional niche axis recently found by Scheffer and van Nes (Scheffer and van Ness 2006) is explained mathematically. We show that it emerges simply from the eigenvalue and eigenvectors of the community matrix. Both the transient patterns—lumps and gaps between them—as well as the asymptotic equilibrium are explained. If the species are evenly distributed along the niche axis, the emergence of these patterns can be demonstrated analytically. The more general case, of randomly distributed species, shows only slight deviations and is illustrated by numerical simulation. This is a robust result whenever the finiteness of the niche is taken into account: it can be extended to different analytic dependence of the interaction coefficients with the distance on the niche axis (i.e., different kernel interactions), different boundary conditions, etc. We also found that there is a critical value both for the width of the species distribution s and the number of species n below which the clusterization disappear

    Letter from Lilian Scheffer to Dear Author, September 12, 1973

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    Letter regarding notifying Mr. Allen of the termination of contract for the book Black History

    The sit room ::in the theater of war and peace /

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    'The Sit Room' brings you into the secretive Situation Room of the White House, the most important deliberative room in the world, during the early 1990s when the author was one of the policymakers who framed the Clinton administration's policy toward the bloody Balkans War. With newly declassified documents and his own notes to draw upon, David Scheffer, who later became America's first Ambassador at Large for War Crimes Issues, weaves the true story of how policy options were debated in the Situation Room among the highest national security officials

    The Dispersive Art Gallery Problem

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    We introduce a new variant of the art gallery problem that comes from safety issues. In this variant we are not interested in guard sets of smallest cardinality, but in guard sets with largest possible distances between these guards. To the best of our knowledge, this variant has not been considered before. We call it the Dispersive Art Gallery Problem. In particular, in the dispersive art gallery problem we are given a polygon P\mathcal{P} and a real number \ell, and want to decide whether P\mathcal{P} has a guard set such that every pair of guards in this set is at least a distance of \ell apart. In this paper, we study the vertex guard variant of this problem for the class of polyominoes. We consider rectangular visibility and distances as geodesics in the L1L_1-metric. Our results are as follows. We give a (simple) thin polyomino such that every guard set has minimum pairwise distances of at most 33. On the positive side, we describe an algorithm that computes guard sets for simple polyominoes that match this upper bound, i.e., the algorithm constructs worst-case optimal solutions. We also study the computational complexity of computing guard sets that maximize the smallest distance between all pairs of guards within the guard sets. We prove that deciding whether there exists a guard set realizing a minimum pairwise distance for all pairs of guards of at least 55 in a given polyomino is NP-complete. We were also able to find an optimal dynamic programming approach that computes a guard set that maximizes the minimum pairwise distance between guards in tree-shaped polyominoes, i.e., computes optimal solutions. Because the shapes constructed in the NP-hardness reduction are thin as well (but have holes), this result completes the case for thin polyominoes.Comment: 21 pages, 17 figures, full version of an extended abstract that appeared in the proceedings of the 33rd International Symposium on Algorithms and Computation (ISAAC 2022); revised versio

    Chasing Impunity : A War Crimes Ambassador\u27s Memoir

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    The masterminds of atrocity crimes in modern times are facing fewer choices as war crimes tribunals and outraged citizens seek both justice and political upheaval. David Scheffer, America’s first Ambassador at Large for War Crimes Issues and author of All the Missing Souls: A Personal History of the War Crimes Tribunals, discusses atrocity crimes past, present, and future and how the fate of indicted leaders will be an international trial or vengeful retribution. The choice is no longer peace or justice to bring genocide or crimes against humanity to an end. The days of impunity are ending in the 21st century

    A New Locus For Generalized Epilepsy With Febrile Seizures Plus Maps To Chromosome 2

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    Generalized epilepsy with febrile seizures plus (GEFS+) is a recently recognized but relatively common form of inherited childhood-onset epilepsy with heterogeneous epilepsy phenotypes. We genotyped 41 family members, including 21 affected individuals, to localize the gene causing epilepsy in a large family segregating an autosomal dominant form of GEFS+. A genomewide search examining 197 markers identified linkage of GEFS+ to chromosome 2, on the basis of an initial positive LOD score for marker D2S294 (Z = 4.4, recombination fraction [θ] = 0). A total of 24 markers were tested on chromosome 2q, to define the smallest candidate region for GEFS+. The highest two-point LOD score (Z(max) = 5.29; θ = 0) was obtained with marker D2S324. Critical recombination events mapped the GEFS+ gene to a 29-cM region flanked by markers D2S156 and D2S311, with the idiopathic generalized epilepsy locus thereby assigned to chromosome 2q23-q31. The existence of the heterogeneous epilepsy phenotypes in this kindred suggests that seizure predisposition determined by the GEFS+ gene on chromosome 2q could be modified by other genes and/or by environmental factors, to produce the different seizure types observed.662698701Blair, L.A., Levitan, E.S., Marshall, J., Dionne, V.E., Barnard, E.A., Single sub-units of the GABAA receptor form ion channels with properties of the native receptor (1988) Science, 242, pp. 577-579Baulac, S., Gourfinkel-An, I., Picard, F., Rosenberg-Bourgin, M., Prud'homme, J.-F., Baulac, M., Brice, A., A second locus for familial generalized epilepsy with febrile seizures plus maps to chromosome 2q21-q33 (1999) Am J Hum Genet, 65, pp. 1078-1085Berkovic, S.F., Scheffer, I.E., Genetics of the epilepsies (1999) Curr Opin Neurol, 12, pp. 177-182Bievert, C., Schoeder, B.C., Kubisch, C., Berkovic, S.F., Propping, P., Jentsch, T.J., Steinlein, O.K., A potassium channel mutation in neonatal human epilepsy (1998) Science, 279, pp. 403-406Bu, D.F., Tobin, A.J., The exon-intron organization of the genes (GAD1 and GAD2) encoding two human glutamate decarboxylases (GAD67 and GAD65) suggests that they derive from a common ancestral GAD (1994) Genomics, 21, pp. 222-228Proposal for revised clinical and electroencephalographic classification of epileptic seizures (1981) Epilepsia, 22, pp. 489-501Gyapay, G., Morissette, J., Vignal, A., Dib, C., Fizames, C., Millasseau, P., Marc, S., The 1993-94 Généthon human genetic linkage map (1994) Nat Genet, 7, pp. 246-339Hauser, W.A., Annegers, J.F., Kurland, L.T., Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota: 1935-1984 (1993) Epilepsia, 34, pp. 453-468Lathrop, G.M., Lalouel, J.M., Easy calculations of LOD scores and genetic risks on small computers (1984) Am J Hum Genet, 36, pp. 460-465Lopes-Cendes, I., Scheffer, I.E., Berkovic, S.F., Rousseau, M., Andermann, E., Rouleau, G.A., Mapping a locus for idiopathic generalized epilepsy in a large multiplex family (1996) Epilepsia, 37 (SUPPL. 5), p. 127Moulard, B., Guipponi, M., Chaigne, D., Mouthon, D., Buresi, C., Malafosse, A., Identification of a new locus for generalized epilepsy with febrile seizures plus (GEFS+) on chromosome 2q24-q33 (1999) Am J Hum Genet, 65, pp. 1396-1400Peiffer, A., Thompson, J., Charlier, C., Otterud, B., Varvil, T., Pappas, C., Barnitz, C., A locus for febrile seizures (FEB3) maps to chromosome 2q23-24 (1999) Ann Neurol, 46, pp. 671-678Sambrook, J., Fritsch, E.F., Maniatis, T., (1989) Molecular Cloning: A Laboratory Manual, 2d Ed., pp. E3-E4. , Cold Spring Harbor Laboratory, Cold Spring Harbor, NYScheffer, I.E., Berkovic, S.F., Generalized epilepsy with febrile seizures plus: A genetic disorder with heterogeneous clinical phenotypes (1997) Brain, 120, pp. 479-490Singh, N.A., Charlier, C., Stauffer, D., DuPont, B.R., Leach, R.J., Melis, R., Ronen, G.M., A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns (1998) Nat Genet, 18, pp. 25-29Singh, R., Scheffer, I.E., Crossland, K., Berkovic, S.F., Generalized epilepsy with febrile seizures plus (GEFS+): A common, childhood-onset, genetic epilepsy syndrome (1999) Ann Neurol, 45, pp. 75-81Steinlein, O.K., Mulley, J.C., Propping, P., Wallace, R.H., Phillips, H.A., Sutherland, G.R., Scheffer, I.E., A missense mutation in the neuronal nicotinic acetylcholine receptor α4 subunit is associated with autosomal dominant nocturnal frontal lobe epilepsy (1995) Nat Genet, 11, pp. 201-203Wallace, R.H., Wang, D.W., Sing, R., Scheffer, I.E., George A.I., Jr., Phillips, H.A., Saar, K., Febrile seizures and generalized epilepsy associated with a mutation in the Na +-channel β1 subunit gene SCN1B (1998) Nat Genet, 19, pp. 366-37

    Missense mutations in the sodium-gated potassium channel gene KCNT1 cause severe autosomal dominant nocturnal frontal lobe epilepsy

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    Data source: Supplementary information, http://www.nature.com/ng/journal/v44/n11/full/ng.2440.html#supplementary-informationWe performed genomic mapping of a family with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) and intellectual and psychiatric problems, identifying a disease-associated region on chromosome 9q34.3. Whole-exome sequencing identified a mutation in KCNT1, encoding a sodium-gated potassium channel subunit. KCNT1 mutations were identified in two additional families and a sporadic case with severe ADNFLE and psychiatric features. These findings implicate the sodium-gated potassium channel complex in ADNFLE and, more broadly, in the pathogenesis of focal epilepsies.Sarah E Heron, Katherine R Smith, Melanie Bahlo, Lino Nobili, Esther Kahana, Laura Licchetta, Karen L Oliver, Aziz Mazarib, Zaid Afawi, Amos Korczyn, Giuseppe Plazzi, Steven Petrou, Samuel F Berkovic, Ingrid E Scheffer, Leanne M Dibben

    Author Correction: Towards the automatic detection of social biomarkers in autism spectrum disorder: introducing the simulated interaction task (SIT)

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    Drimalla H, Scheffer T, Landwehr N, et al. Author Correction: Towards the automatic detection of social biomarkers in autism spectrum disorder: introducing the simulated interaction task (SIT). npj Digital Medicine. 2022;5(1): 20.Correction to: npj Digital Medicine https://doi.org/10.1038/s41746-020-0227-5, published online 28 February 2020 The original version of the published Article included a power calculation that was unrelated to the main analysis performed in this study. The second sentence of the second paragraph of the methods section referred to this power analysis. To improve clarity and reproducibility, the sentence has been removed from the methods. Additionally, the original version of the Supplementary Information contained typographical errors in the Supplementary Tables, which have been corrected. The HTML and PDF versions of the Article have been corrected

    Covering Rectangles by Disks: The Video (Media Exposition)

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    In this video, we motivate and visualize a fundamental result for covering a rectangle by a set of non-uniform circles: For any λ ≥ 1, the critical covering area A^*(λ) is the minimum value for which any set of disks with total area at least A^*(λ) can cover a rectangle of dimensions λ× 1. We show that there is a threshold value λ₂ = √(√7/2 - 1/4) ≈ 1.035797…, such that for λ < λ₂ the critical covering area A^*(λ) is A^*(λ) = 3π(λ²/16 + 5/32 + 9/256λ²), and for λ ≥ λ₂, the critical area is A^*(λ) = π(λ²+2)/4; these values are tight. For the special case λ=1, i.e., for covering a unit square, the critical covering area is 195π/256 ≈ 2.39301…. We describe the structure of the proof, and show animations of some of the main components

    The paradox of the clumps mathematically explained

    No full text
    The lumpy distribution of species along a continuous one-dimensional niche axis recently found by Scheffer and van Nes (Scheffer and van Ness 2006) is explained mathematically. We show that it emerges simply from the eigenvalue and eigenvectors of the community matrix. Both the transient patterns—lumps and gaps between them—as well as the asymptotic equilibrium are explained. If the species are evenly distributed along the niche axis, the emergence of these patterns can be demonstrated analytically. The more general case, of randomly distributed species, shows only slight deviations and is illustrated by numerical simulation. This is a robust result whenever the finiteness of the niche is taken into account: it can be extended to different analytic dependence of the interaction coefficients with the distance on the niche axis (i.e., different kernel interactions), different boundary conditions, etc. We also found that there is a critical value both for the width of the species distribution s and the number of species n below which the clusterization disappear
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