72 research outputs found

    A Damage Assessment of Iraq’s Past: Archaeological Heritage Management on the Rania Plain in Iraqi Kurdistan

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    This paper advocates an increasing focus on damage assessment, monitoring and adaptation to the impact of urban development on archaeologically rich regions.As a case-study of the wider Middle East, this discussion focuses on archaeological strategies for damage assessment, monitoring and handling archaeological cultural resources on the Rania plain in the Kurdistan autonomous region of northeast Iraq. The pressures of modern development, with extensive infrastructure development, rapid expansion of population settlements and a hydro-electric dam, whose waters inundate a substantial proportion of the plain, make the recording of valuable cultural heritage a demanding task

    April 10, 1986

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    https://scholarlycommons.obu.edu/arbn_85-89/1126/thumbnail.jp

    Circ-ZNF609 regulates G1-S progression in rhabdomyosarcoma

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    Circular RNAs (circRNAs) represent a class of covalently closed RNAs, derived from non-canonical splicing events, which are expressed in all eukaryotes and often conserved among different species. We previously showed that the circRNA originating from the ZNF609 locus (circ-ZNF609) acts as a crucial regulator of human primary myoblast growth: indeed, the downregulation of the circRNA, and not of its linear counterpart, strongly reduced the proliferation rate of in vitro cultured myoblasts. To deepen our knowledge about circ-ZNF609 role in cell cycle regulation, we studied its expression and function in rhabdomyosarcoma (RMS), a pediatric skeletal muscle malignancy. We found that circ-ZNF609 is upregulated in biopsies from the two major RMS subtypes, embryonal (ERMS) and alveolar (ARMS). Moreover, we discovered that in an ERMS-derived cell line circ-ZNF609 knock-down induced a specific block at the G1-S transition, a strong decrease of p-Akt protein level and an alteration of the pRb/Rb ratio. Regarding p-Akt, we were able to show that circ-ZNF609 acts by counteracting p-Akt proteasome-dependent degradation, thus working as a new regulator of cell proliferation-related pathways. As opposed to ERMS-derived cells, the circRNA depletion had no cell cycle effects in ARMS-derived cells. Since in these cells the p53 gene resulted downregulated, with a concomitant upregulation of its cell cycle-related target genes, we suggest that this could account for the lack of circ-ZNF609 effect in ARMS

    Further work at Kilise Tepe, 2007-11: refining the Bronze to Iron Age transition

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    The excavations at Kilise Tepe in the 1990s inevitably left a range of research questions unanswered, and our second spell of work at the site from 2007 to 2011 sought to address some of these, relating to the later second and early first millennia. This article gathers the architectural and stratigraphie results of the renewed excavations, presenting the fresh information about the layout and character of the Late Bronze Age North-West Building and the initial phases of the Stele Building which succeeded it, including probable symbolic practices, and describing the complex stratigraphic sequence in the Central Strip sounding which covers the lapse of time from the 12th down to the seventh century. There follow short reports on the analyses of the botanical and faunal materials recovered, a summary of the results from the relevant radiocarbon dating samples and separate studies addressing issues resulting from the continuing study of the ceramics from the different contexts. Taken together, a complex picture emerges of changes in settlement layout, archi¬tectural traditions, use of external space, artefact production and subsistence strategies during the centuries which separate the Level III Late Bronze Age settlement from the latest Iron Age occupation around 700 BC

    Trans-generational epigenetic regulation associated with the amelioration of Duchenne Muscular Dystrophy

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    Exon skipping is an effective strategy for the treatment of many Duchenne Muscular Dystrophy (DMD) mutations. Natural exon skipping observed in several DMD cases can help in identifying novel therapeutic tools. Here, we show a DMD study case where the lack of a splicing factor (Celf2a), which results in exon skipping and dystrophin rescue, is due to a maternally inherited trans-generational epigenetic silencing. We found that the study case and his mother express a repressive long non-coding RNA, DUXAP8, whose presence correlates with silencing of the Celf2a coding region. We also demonstrate that DUXAP8 expression is lost upon cell reprogramming and that, upon induction of iPSCs into myoblasts, Celf2a expression is recovered leading to the loss of exon skipping and loss of dystrophin synthesis. Finally, CRISPR/Cas9 inactivation of the splicing factor Celf2a was proven to ameliorate the pathological state in other DMD backgrounds establishing Celf2a ablation or inactivation as a novel therapeutic approach for the treatment of Duchenne Muscular Dystrophy
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