970 research outputs found

    Pemahaman Identitas dan Toleransi Keberagaman Budaya Mahasiswa Sastra Inggris UAI melalui Puisi Multikultural Kesusasteraan Inggris: sebuah Kajian Multikulturalisme

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    - Penelitian ini dilakukan untuk melihat respon mahasiswa Sastra Inggris UAI dalam memahami konflik keberagaman dan pemahaman identitas budaya terkait dengan ideologi multikulturalisme melalui puisi multikultural kesusasteraan Inggris. Penelitian ini merupakan penelitian kualitatif dengan menggunakan metode reader-response (respon pembaca) dengan subjek penelitian yaitu mahasiswa Sastra Inggris UAI yang mengambil mata kuliah Pengkajian Puisi sebanyak 26 orang. Dengan menggunakan teori Identitas oleh Stuart Hall sebagai kajian multikulturalisme dan teori intrinsik puisi, penelitian ini diharapkan dapat memberikan gambaran jelas mengenai respon mahasiswa Sastra Inggris terhadap teks-teks sastra bertema multikultural dan juga gambaran jelas sejauh mana pemahaman lintas budaya mereka. Pada akhirnya hasil ini secara garis besar menunjukkan bahwa pemahaman keberagaman, kepedulian sosial dan toleransi di kalangan mahasiswa sastra Inggris UAI belum baik karena sebanyak 53.86% responden terlihat mengalami kesulitan untuk memahami dan menginterpretasikan isi puisi serta tidak bisa mengaitkan tema puisi dengan kondisi keberagaman di kehidupan mereka sehari-hari. Kata Kunci – Multikulturalisme, Identitas Budaya, Identitas Budaya, Tanggapan Pembac

    Periods for flat algebraic connections

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    In previous work, we established a duality between the algebraic de Rham cohomology of a flat algebraic connection on a smooth quasi-projective surface over the complex numbers and the rapid decay homology of the dual connection relying on a conjecture by C. Sabbah, which has been proved recently by T. Mochizuki for algebraic connections in any dimension. In the present article, we verify that Mochizuki's results allow to generalize these duality results to arbitrary dimensions also

    Analytic continuation of residue currents

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    Let XX be a complex manifold and f\colon X\to \C^p a holomorphic mapping defining a complete intersection. We prove that the iterated Mellin transform of the residue integral associated to ff has an analytic continuation to a neighborhood of the origin in \C^p

    Verdier specialization via weak factorization

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    Let X in V be a closed embedding, with V - X nonsingular. We define a constructible function on X, agreeing with Verdier's specialization of the constant function 1 when X is the zero-locus of a function on V. Our definition is given in terms of an embedded resolution of X; the independence on the choice of resolution is obtained as a consequence of the weak factorization theorem of Abramovich et al. The main property of the specialization function is a compatibility with the specialization of the Chern class of the complement V-X. With the definition adopted here, this is an easy consequence of standard intersection theory. It recovers Verdier's result when X is the zero-locus of a function on V. Our definition has a straightforward counterpart in a motivic group. The specialization function and the corresponding Chern class and motivic aspect all have natural `monodromy' decompositions, for for any X in V as above. The definition also yields an expression for Kai Behrend's constructible function when applied to (the singularity subscheme of) the zero-locus of a function on V.Comment: Minor revision. To appear in Arkiv f\"or Matemati

    Cosmic ray short burst observed with the Global Muon Detector Network (GMDN) on June 22, 2015

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    We analyze the short cosmic ray intensity increase ("cosmic ray burst": CRB) on June 22, 2015 utilizing a global network of muon detectors and derive the global anisotropy of cosmic ray intensity and the density (i.e. the omnidirectional intensity) with 10-minute time resolution. We find that the CRB was caused by a local density maximum and an enhanced anisotropy of cosmic rays both of which appeared in association with Earth's crossing of the heliospheric current sheet (HCS). This enhanced anisotropy was normal to the HCS and consistent with a diamagnetic drift arising from the spatial gradient of cosmic ray density, which indicates that cosmic rays were drifting along the HCS from the north of Earth. We also find a significant anisotropy along the HCS, lasting a few hours after the HCS crossing, indicating that cosmic rays penetrated into the inner heliosphere along the HCS. Based on the latest geomagnetic field model, we quantitatively evaluate the reduction of the geomagnetic cut-off rigidity and the variation of the asymptotic viewing direction of cosmic rays due to a major geomagnetic storm which occurred during the CRB and conclude that the CRB is not caused by the geomagnetic storm, but by a rapid change in the cosmic ray anisotropy and density outside the magnetosphere.Comment: accepted for the publication in the Astrophysical Journa

    Retinoic acid inducible gene I Activates innate antiviral response against human parainfluenza virus type 3

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    Human parainfluenza virus type 3 (HPIV3) is a respiratory paramyxovirus that infects lung epithelial cells to cause high morbidity among infants and children. To date, no effective vaccine or antiviral therapy exists for HPIV3 and therefore, it is important to study innate immune antiviral response induced by this virus in infected cells. Type-I interferons (IFN, interferon-α/β) and tumor necrosis factor-α (TNFα activated by NFκB) are potent antiviral cytokines that play an important role during innate immune antiviral response. A wide-spectrum of viruses utilizes pattern recognition receptors (PRRs) like toll-like receptors (TLRs) and RLH (RIG like helicases) receptors such as RIGI (retinoic acid inducible gene -I) and Mda5 to induce innate antiviral response. Previously it was shown that both TNFα and IFNβ are produced from HPIV3 infected cells. However, the mechanism by which infected cells activated innate response following HPIV3 infection was not known. In the current study, we demonstrated that RIGI serves as a PRR in HPIV3 infected cells to induce innate antiviral response by expressing IFNβ (via activation of interferon regulatory factor-3 or IRF3) and TNFα (via activation of NF-κB)
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