2,448 research outputs found

    Integral constraints on the monodromy group of the hyperkahler resolution of a symmetric product of a K3 surface

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    Let M be a 2n-dimensional Kahler manifold deformation equivalent to the Hilbert scheme of length n subschemes of a K3 surface S. Let Mon be the group of automorphisms of the cohomology ring of M, which are induced by monodromy operators. The second integral cohomology of M is endowed with the Beauville-Bogomolov bilinear form. We prove that the restriction homomorphism from Mon to the isometry group O[H^2(M)] is injective, for infinitely many n, and its kernel has order at most 2, in the remaining cases. For all n, the image of Mon in O[H^2(M)] is the subgroup generated by reflections with respect to +2 and -2 classes. As a consequence, we get counter examples to a version of the weight 2 Torelli question, when n-1 is not a prime power.Comment: Version 3: Latex, 54 pages. Expository change

    Lagrangian fibrations of holomorphic-symplectic varieties of K3^[n]-type

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    Let X be a compact Kahler holomorphic-symplectic manifold, which is deformation equivalent to the Hilbert scheme of length n subschemes of a K3 surface. Let L be a nef line-bundle on X, such that the 2n-th power of c_1(L) vanishes and c_1(L) is primitive. Assume that the two dimensional subspace H^{2,0}(X) + H^{0,2}(X), of the second cohomology of X with complex coefficients, intersects trivially the integral cohomology. We prove that the linear system of L is base point free and it induces a Lagrangian fibration on X. In particular, the line-bundle L is effective. A determination of the semi-group of effective divisor classes on X follows, when X is projective. For a generic such pair (X,L), not necessarily projective, we show that X is bimeromorphic to a Tate-Shafarevich twist of a moduli space of stable torsion sheaves, each with pure one dimensional support, on a projective K3 surface.Comment: 34 pages. v3: Reference [Mat5] and Remark 1.8 added. Incorporated improvement to the exposition and corrected typos according to the referees suggestions. To appear in the proceedings of the conference Algebraic and Complex Geometry, Hannover 201

    Does Peer Ability Affect Student Achievement?

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    Empirical analysis of peer effects on student achievement has been open to question because of the difficulties of separating peer effects from other confounding influences. While most econometric attention has been directed at issues of simultaneous determination of peer interactions, we argue that issues of omitted and mismeasured variables are likely to be more important. We control for the most important determinants of achievement that will confound peer estimates by removing student and school-by-grade fixed effects in addition to observable family and school characteristics. The analysis also addresses the reciprocal nature of peer interactions and the interpretation of estimates based upon models using past achievement as the measure of peer group quality. The results indicate that peer achievement has a positive effect on achievement growth. Moreover, students throughout the school test score distribution appear to benefit from higher achieving schoolmates. On the other hand, the variance in achievement appears to have no systematic effect.

    The 1982 Amendments To The Voting Rights Act: A Legislative History

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    Treating cisplatin-resistant cancer: a systematic analysis of oxaliplatin or paclitaxel salvage chemotherapy

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    Objective: To examine the pre-clinical and clinical evidence for the use of oxaliplatin or paclitaxel salvage chemotherapy in patients with cisplatin-resistant cancer. Methods: Medline was searched for 1) Cell models of acquired resistance reporting cisplatin, oxaliplatin and paclitaxel sensitivities and 2) Clinical trials of single agent oxaliplatin or paclitaxel salvage therapy for cisplatin/carboplatin-resistant ovarian cancer. Results: Oxaliplatin - Oxaliplatin is widely regarded as being active in cisplatin-resistant cancer. In contrast, data in cell models suggests that there is cross-resistance between cisplatin and oxaliplatin in cellular models with resistance levels which reflect clinical resistance (<10 fold). Oxaliplatin as a single agent had a poor response rate in patients with cisplatin-resistant ovarian cancer (8%, n=91). Oxaliplatin performed better in combination with other agents for the treatment of platinum-resistant cancer suggesting that the benefit of oxaliplatin may lie in its more favourable toxicity and ability to be combined with other drugs rather than an underlying activity in cisplatin resistance. Oxaliplatin therefore should not be considered broadly active in cisplatin-resistant cancer. Paclitaxel – Cellular data suggests that paclitaxel is active in cisplatin-resistant cancer. 68.1% of cisplatin-resistant cells were sensitive to paclitaxel. Paclitaxel as a single agent had a response rate of 22% in patients with platinum-resistant ovarian cancer (n = 1918), a significant increase from the response of oxaliplatin (p<0.01). Paclitaxel-resistant cells were also sensitive to cisplatin, suggesting that alternating between agents may be beneficial. Studies of single agent paclitaxel in platinum-resistant ovarian cancer where patients had previously received paclitaxel had an improved response rate of 35.3% n=232 (p<0.01), suggesting that pre-treatment with paclitaxel improves the response of salvage paclitaxel therapy. Conclusions: Cellular models reflect the resistance observed in the clinic as the cross resistant agent oxaliplatin has a lower response rate compared to the non-cross resistant agent paclitaxel in cisplatin-resistant ovarian cancer. Alternating therapy with cisplatin and paclitaxel may therefore lead to an improved response rate in ovarian cancer

    Synchronous Presentation of a Primary Iliac Lymph Node Plasmacytoma and a Prostate Adenocarcinoma

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    Synchronous presentation of primary nodal plasmacytoma and prostate cancer is very rare and has not been described in the literature. Here, we report a case of a patient with nodal plasmacytoma whose clinical presentation was suggestive of metastatic prostate cancer in the setting of recently diagnosed prostate cancer. The workup and treatment of both malignancies as well as a possible underlying common pathologic mechanism (IL-6 gene mutation) are discussed
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