824 research outputs found

    (G)hosting television: Ghostwatch and its medium

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    This article’s subject is Ghostwatch (BBC, 1992), a drama broadcast on Halloween night of 1992 which adopted the rhetoric of live non-fiction programming, and attracted controversy and ultimately censure from the Broadcasting Standards Council. In what follows, we argue that Ghostwatch must be understood as a televisually-specific artwork and artefact. We discuss the programme’s ludic relationship with some key features of television during what Ellis (2000) has termed its era of ‘availability’, principally liveness, mass simultaneous viewing, and the flow of the television super-text. We trace the programme’s television-specific historicity whilst acknowledging its allusions and debts to other media (most notably film and radio). We explore the sophisticated ways in which Ghostwatch’s visual grammar and vocabulary and deployment of ‘broadcast talk’ (Scannell 1991) variously ape, comment upon and subvert the rhetoric of factual programming, and the ends to which these strategies are put. We hope that these arguments collectively demonstrate the aesthetic and historical significance of Ghostwatch and identify its relationship to its medium and that medium’s history. We offer the programme as an historically-reflexive artefact, and as an exemplary instance of the work of art in television’s age of broadcasting, liveness and co-presence

    A human phospholipid phosphatase activated by a transmembrane control module

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    In voltage-sensitive phosphatases (VSPs), a transmembrane voltage sensor domain (VSD) controls an intracellular phosphoinositide phosphatase domain, thereby enabling immediate initiation of intracellular signals by membrane depolarization. The existence of such a mechanism in mammals has remained elusive, despite the presence of VSP-homologous proteins in mammalian cells, in particular in sperm precursor cells. Here we demonstrate activation of a human VSP (hVSP1/TPIP) by an intramolecular switch. By engineering a chimeric hVSP1 with enhanced plasma membrane targeting containing the VSD of a prototypic invertebrate VSP, we show that hVSP1 is a phosphoinositide-5-phosphatase whose predominant substrate is PI(4,5)P(2). In the chimera, enzymatic activity is controlled by membrane potential via hVSP1\u27s endogenous phosphoinositide binding motif. These findings suggest that the endogenous VSD of hVSP1 is a control module that initiates signaling through the phosphatase domain and indicate a role for VSP-mediated phosphoinositide signaling in mammals

    Second trimester inflammatory and metabolic markers in women delivering preterm with and without preeclampsia.

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    ObjectiveInflammatory and metabolic pathways are implicated in preterm birth and preeclampsia. However, studies rarely compare second trimester inflammatory and metabolic markers between women who deliver preterm with and without preeclampsia.Study designA sample of 129 women (43 with preeclampsia) with preterm delivery was obtained from an existing population-based birth cohort. Banked second trimester serum samples were assayed for 267 inflammatory and metabolic markers. Backwards-stepwise logistic regression models were used to calculate odds ratios.ResultsHigher 5-α-pregnan-3β,20α-diol disulfate, and lower 1-linoleoylglycerophosphoethanolamine and octadecanedioate, predicted increased odds of preeclampsia.ConclusionsAmong women with preterm births, those who developed preeclampsia differed with respect metabolic markers. These findings point to potential etiologic underpinnings for preeclampsia as a precursor to preterm birth

    Longitudinal changes in peripapillary atrophy in the ocular hypertension treatment study: A case-control assessment

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    To explore the association between peripapillary atrophy (PPA) area and conversion from ocular hypertension (OHT) to glaucoma

    Comparison Between Spectral-Domain and Swept-Source Optical Coherence Tomography Angiographic Imaging of Choroidal Neovascularization

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    PURPOSE. The purpose of this study was to compare imaging of choroidal neovascularization (CNV) using swept-source (SS) and spectral-domain (SD) optical coherence tomography angiography (OCTA). METHODS. Optical coherence tomography angiography was performed using a 100-kHz SS-OCT instrument and a 68-kHz SD-OCTA instrument (Carl Zeiss Meditec, Inc.). Both 3 x 3-and 6 x 6-mm(2) scans were obtained on both instruments. The 3 x 3-mm(2) SS-OCTA scans consisted of 300 A-scans per B-scan at 300 B-scan positions, and the SD-OCTA scans consisted of 245 A-scans at 245 B-scan positions. The 6 x 6-mm(2) SS-OCTA scans consisted of 420 A-scans per B-scan at 420 B-scan positions, and the SD-OCTA scans consisted of 350 A-scans and 350 B-scan positions. B-scans were repeated four times at each position in the 3 x 3-mm(2) scans and twice in the 6 x 6-mm(2) scans. Choroidal neovascularization was excluded if not fully contained within the 3 x 3-mm(2) scans. The same algorithm was used to detect CNV on both instruments. Two graders outlined the CNV, and the lesion areas were compared between instruments. RESULTS. Twenty-seven consecutive eyes from 23 patients were analyzed. For the 3 x 3-mm(2) scans, the mean lesion areas for the SS-OCTA and SD-OCTA instruments were 1.17 and 1.01 mm(2), respectively (P = 0.047). For the 6 x 6-mm(2) scans, the mean lesion areas for the SS-OCTA and SD-OCTA instruments were 1.24 and 0.74 mm(2) (P = 0.003). CONCLUSIONS. The areas of CNV tended to be larger when imaged with SS-OCTA than with SD-OCTA, and this difference was greater for the 6 x 6-mm(2) scans.Carl Zeiss Meditec, Inc.National Eye InstituteResearch to Prevent Blindness, Inc. (New York, NY)National Eye Institute Center Core GrantCAPES Foundation, Ministry of Education of Brazil (Brasilia, Brazil)German Research FoundationUniv Miami, Miller Sch Med, Bascom Palmer Eye Inst, Dept Ophthalmol, Miami, FL 33136 USAUniv Fed Sao Paulo, Dept Ophthalmol, Sao Paulo, BrazilUniv Washington, Dept Bioengn, Seattle, WA 98195 USACarl Zeiss Meditec Inc, Adv Dev, Dublin, CA USAUniv Fed Sao Paulo, Dept Ophthalmol, Sao Paulo, BrazilNational Eye Institute: R01EY024158National Eye Institute Center Core Grant: P30EY014801German Research Foundation: SCHA 1869/1-1Web of Scienc

    HTLV-1 propels thymic human T cell development in “human immune system” Rag2-/- IL-2R γc-/- Mice

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    Alteration of early haematopoietic development is thought to be responsible for the onset of immature leukemias and lymphomas. We have previously demonstrated that TaxHTLV-1 interferes with ß-selection, an important checkpoint of early thymopoiesis, indicating that human T-cell leukemia virus type 1 (HTLV-1) infection has the potential to perturb thymic human αβ T-cell development. To verify that inference and to clarify the impact of HTLV-1 infection on human T-cell development, we investigated the in vivo effects of HTLV-1 infection in a “Human Immune System” (HIS) Rag2-/-γc-/- mouse model. These mice were infected with HTLV-1, at a time when the three main subpopulations of human thymocytes have been detected. In all but two inoculated mice, the HTLV-1 provirus was found integrated in thymocytes; the proviral load increased with the length of the infection period. In the HTLV-1-infected mice we observed alterations in human T-cell development, the extent of which correlated with the proviral load. Thus, in the thymus of HTLV-1-infected HIS Rag2-/-γc-/- mice, mature single-positive (SP) CD4+ and CD8+ cells were most numerous, at the expense of immature and double-positive (DP) thymocytes. These SP cells also accumulated in the spleen. Human lymphocytes from thymus and spleen were activated, as shown by the expression of CD25: this activation was correlated with the presence of tax mRNA and with increased expression of NF-kB dependent genes such as bfl-1, an anti-apoptotic gene, in thymocytes. Finally, hepato-splenomegaly, lymphadenopathy and lymphoma/thymoma, in which Tax was detected, were observed in HTLV-1-infected mice, several months after HTLV-1 infection. These results demonstrate the potential of the HIS Rag2-/-γc-/- animal model to elucidate the initial steps of the leukemogenic process induced by HTLV-1
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