22 research outputs found

    Film remakes, the black sheep of translation

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    Film remakes have often been neglected by translation studies in favour of other forms of audiovisual translation such as subtitling and dubbing. Yet, as this article will argue, remakes are also a form of cinematic translation. Beginning with a survey of previous, ambivalent approaches to the status of remakes, it proposes that remakes are multimodal, adaptive translations: they translate the many modes of the film being remade and offer a reworking of that source text. The multimodal nature of remakes is explored through a reading of Breathless, Jim McBride's 1983 remake of Jean-Luc Godard's À bout de souffle (1959), which shows how remade films may repeat the narrative of, but differ on multiple levels from, their source films. Due to the collaborative nature of film production, remakes involve multiple agents of translation. As such, remakes offer an expanded understanding of audiovisual translation

    Active Oxygen Species Accumulation in the Immunization and Manifestation Stages of Systemic Acquired Resistance During an Arabidopsis Thaliana-pseudomonas Syringae pv Tomato Interaction

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    grantor: University of TorontoActive oxygen species (AOS) accumulation was studied in the signalling and manifestation stages of the systemic acquired resistance (SAR) response in the Arabidopsis thaliana-Pseudomonas syringae pv tomato pathosystem. During the manifestation of SAR, AOS do not accumulate to a magnitude comparable to that observed following inoculation with avirulent Pst. Immunization of plants with the glucose/glucose oxidase (G/GO) AOS generating system resulted in the establishment of SAR, but did not result in cell death, suggesting an involvement of AOS, but not necessarily of cell death, in SAR signalling. In response to avirulent bacteria, the SAR mutants npr1 and dir1 demonstrated AOS accumulation comparable to that observed in wild type Arabidopsis, but salicylic acid (SA) deficient NahG Arabidopsis did not. Immunization of NahG plants with G/GO or avirulent Pst did not result in the induction of pathogenesis-related proteins, nor did it result in cell death, suggesting a dependence in both of these processes on SA.M.Sc

    Polyploid genome of Camelina sativa revealed by isolation of fatty acid synthesis genes

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    <p>Abstract</p> <p>Background</p> <p><it>Camelina sativa</it>, an oilseed crop in the Brassicaceae family, has inspired renewed interest due to its potential for biofuels applications. Little is understood of the nature of the <it>C. sativa </it>genome, however. A study was undertaken to characterize two genes in the fatty acid biosynthesis pathway, <it>fatty acid desaturase (FAD) 2 </it>and <it>fatty acid elongase (FAE) 1</it>, which revealed unexpected complexity in the <it>C. sativa </it>genome.</p> <p>Results</p> <p>In <it>C. sativa</it>, Southern analysis indicates the presence of three copies of both <it>FAD2 </it>and <it>FAE1 </it>as well as <it>LFY</it>, a known single copy gene in other species. All three copies of both <it>CsFAD2 </it>and <it>CsFAE1 </it>are expressed in developing seeds, and sequence alignments show that previously described conserved sites are present, suggesting that all three copies of both genes could be functional. The regions downstream of <it>CsFAD2 </it>and upstream of <it>CsFAE1 </it>demonstrate co-linearity with the Arabidopsis genome. In addition, three expressed haplotypes were observed for six predicted single-copy genes in 454 sequencing analysis and results from flow cytometry indicate that the DNA content of <it>C. sativa </it>is approximately three-fold that of diploid <it>Camelina </it>relatives. Phylogenetic analyses further support a history of duplication and indicate that <it>C. sativa </it>and <it>C. microcarpa </it>might share a parental genome.</p> <p>Conclusions</p> <p>There is compelling evidence for triplication of the <it>C. sativa </it>genome, including a larger chromosome number and three-fold larger measured genome size than other <it>Camelina </it>relatives, three isolated copies of <it>FAD2</it>, <it>FAE1</it>, and the <it>KCS17-FAE1 </it>intergenic region, and three expressed haplotypes observed for six predicted single-copy genes. Based on these results, we propose that <it>C. sativa </it>be considered an allohexaploid. The characterization of fatty acid synthesis pathway genes will allow for the future manipulation of oil composition of this emerging biofuel crop; however, targeted manipulations of oil composition and general development of <it>C. sativa </it>should consider and, when possible take advantage of, the implications of polyploidy.</p

    Alberta Incidence Study of Reported Child Abuse and Neglect-2008 (AIS-2008): Major Findings

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    The Alberta Incidence Study of Reported Child Abuse and Neglect‑2008 (AIS‑2008) is the second province‑wide study to examine the incidence of reported child maltreatment and the characteristics of the children and families investigated by Alberta child intervention offices. The AIS‑2008 tracked 2,239 child maltreatment investigations conducted in a representative sample of 14 Child Intervention Service offices across Alberta in the fall of 2008.The AIS‑2008 research was funded by: Government of Alberta Children and Youth Services, and the Injury and Child Maltreatment Section, Public Health Agency of Canada. Additional support was provided by the University of Calgary, Faculty of Social Work

    A small sustained increase in NOD1 abundance promotes ligand-independent inflammatory and oncogene transcriptional responses.

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    Small, genetically determined differences in transcription [expression quantitative trait loci (eQTLs)] are implicated in complex diseases through unknown molecular mechanisms. Here, we showed that a small, persistent increase in the abundance of the innate pathogen sensor NOD1 precipitated large changes in the transcriptional state of monocytes. A ~1.2- to 1.3-fold increase in NOD1 protein abundance resulting from loss of regulation by the microRNA cluster miR-15b/16 lowered the threshold for ligand-induced activation of the transcription factor NF-ÎşB and the MAPK p38. An additional sustained increase in NOD1 abundance to 1.5-fold over basal amounts bypassed this low ligand concentration requirement, resulting in robust ligand-independent induction of proinflammatory genes and oncogenes. These findings reveal that tight regulation of NOD1 abundance prevents this sensor from exceeding a physiological switching checkpoint that promotes persistent inflammation and oncogene expression. Furthermore, our data provide insight into how a quantitatively small change in protein abundance can produce marked changes in cell state that can serve as the initiator of disease

    British Columbia Incidence Study of Reported Child Abuse and Neglect - 2008 (BCIS-2008)

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    Non‑commercial reproduction of this report in whole or in part is permitted, provided the authors are acknowledged as the source of all copies.The Public Health Agency of Canada provided core funding for the British Columbia Incidence Study of Reported Child Abuse and Neglect‑2008 (BCIS‑2008). Additional provincial oversampling funds were provided by the Government of British Columbia, Ministry of Children and Family Development

    Saskatchewan Incidence Study of Reported Child Abuse and Neglect-2008 (SIS‑2008): Major Findings

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    Non‑commercial reproduction of this report in whole or in part is permitted, provided the authors are acknowledged as the source of all copies.The following report presents the major descriptive findings from the Saskatchewan Incidence Study of Reported Child Abuse and Neglect (SIS‑2008). The SIS‑2008 is the first province-wide study to examine the incidence of reported child maltreatment and the characteristics of the children and families investigated by child welfare services in Saskatchewan. The estimates presented in this report are primarily based on information collected from child welfare investigators on a representative sample of 8,933 child welfare investigations conducted across Saskatchewan.The SIS‑2008 research was funded by: Government of Saskatchewan Ministry of Social Services, and the Injury and Child Maltreatment Section, Public Health Agency of Canada. Additional support was provided by the University of Calgary, Faculty of Social Work
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