8 research outputs found
Censorship as Criticism: Performance Art and Fair Use in Virtual Territory
No full text The author discusses the removal of his machinima-based performance artwork from the popular online video sharing site Vimeo, based on the accusation that it violated the service’s terms of use. The artist challenged the validity of Vimeo’s administrators via a series of emails, without much success. By examining this particular case, the author raises a series of important questions related to copyright, e.g. who owns virtual space and who is responsible for policing it? Are multi-user games a territory or a tool? Can a creative act transform a videogame from private property into a public art site? And perhaps most appropriate in the author’s situation: can copyright censors distinguish their personal criticism of an artwork from that work’s legal status? </jats:p
Wrecking the Game: The Artist as Griefer
No full textThis paper aims at examining the anti-game practice of artists that assume a subverting behaviour inside video games. They hijack gameplay to turn it into a space for artistic intervention. The artists discussed in this paper are Kent Sheely, Marque Cornblatt, Justin Berry, and Alan Butler. Their practice shares similarities with the artistic interventions developed by Dada and International Situationist, two artistic movements that aimed at redefining the culture of their time thanks to subversive actions. The artists featured in this paper are defined griefers, deliberate hecklers. Their works are then analysed along with the concepts of counter-gaming and ludic mutation defined by Alexander Galloway and Anne-Marie Schleiner to better understand the characteristics of their subversive behaviour
Machinima! Teorie. Pratiche. Dialoghi
No full textMachinima! Teorie. Pratiche. Dialoghi esamina uno dei fenomeni di ibridazione mediale più interessanti degli ultimi vent’anni. Contrazione di machine e animation, il machinima si colloca all’intersezione tra videogioco e cinema, animazione elettronica e performance in tempo reale nei mondi virtuali. Opera derivata ma inaspettata, il machinima ha introdotto una nuova estetica, ma soprattutto, un nuovo modo di giocare con l’immagine. La sua storia è contraddistinta da innovazioni e imprevisti, alterazioni e alterchi, hacking e modding.
Il volume si articola in tre sezioni. La prima, TEORIE, inquadra il fenomeno sul piano concettuale, storico e legislativo, illuminando testi e contesti produttivi, distributivi, giuridici e commerciali. La seconda, PRATICHE, presenta i contributi di artisti e registi, producer e performer che hanno definito la natura del medium. Infine, DIALOGHI propone conversazioni su temi che spaziano dall’arte al mercato, dal disimpegno ludico all’attivismo politico. Il carattere interdisciplinare e l’eterogeneità degli approcci rendono Machinima! uno strumento ideale per comprendere le trasformazioni dei media e dell’arte contemporanea nell’era digitale.
Con contributi di Matteo Bittanti, Matteo Bonvicino, Alessandro Cavaleri, Marque Cornblatt, Frank R. Dellario, Joshua Diltz, Jun Faklenstein, Douglas Gayeton, Friedrich Kirschner, Kate Fosk, Kari Kraus, Mathias Jansson, Robert Jones, Clint Hackleman, Hugh Hancock, Tracy Harwood, Paul Marino, Mizuko Ito, Henry Lowood, Mark Methenitis, Michael Nitsche, Paolo Pedercini, Ilaria Ravarino, Dan O'Reilly Rowe, Valerio Sillari, Eddo Stern
Networks of blood proteins in the neuroimmunology of schizophrenia
No full text© 2018 The Author(s). Levels of certain circulating cytokines and related immune system molecules are consistently altered in schizophrenia and related disorders. In addition to absolute analyte levels, we sought analytes in correlation networks that could be prognostic. We analyzed baseline blood plasma samples with a Luminex platform from 72 subjects meeting criteria for a psychosis clinical high-risk syndrome; 32 subjects converted to a diagnosis of psychotic disorder within two years while 40 other subjects did not. Another comparison group included 35 unaffected subjects. Assays of 141 analytes passed early quality control. We then used an unweighted co-expression network analysis to identify highly correlated modules in each group. Overall, there was a striking loss of network complexity going from unaffected subjects to nonconverters and thence to converters (applying standard, graph-theoretic metrics). Graph differences were largely driven by proteins regulating tissue remodeling (e.g. blood-brain barrier). In more detail, certain sets of antithetical proteins were highly correlated in unaffected subjects (e.g. SERPINE1 vs MMP9), as expected in homeostasis. However, for particular protein pairs this trend was reversed in converters (e.g. SERPINE1 vs TIMP1, being synthetical inhibitors of remodeling of extracellular matrix and vasculature). Thus, some correlation signals strongly predict impending conversion to a psychotic disorder and directly suggest pharmaceutical targets
Generalized and specific cognitive performance in clinical high-risk cohorts: A review highlighting potential vulnerability markers for psychosis
No full textCognitive deficits are a core feature of established psychotic illnesses. However, the association between cognition and emerging psychosis is less understood. While there is some evidence that cognitive deficits are present prior to the onset of psychosis, findings are not consistent. In this article we provide an overview of the more general cognitive findings available from genetic high-risk studies, retrospective studies, and birth cohort studies. We then focus the review on neuropsychological performance in clinically "at-risk" groups. Overall, general cognitive ability as assessed by established batteries appears to remain relatively intact in these ultra-high risk cohorts and is a poor predictor close to illness onset relative to other vulnerability factors. Further decline may occur with illness progression, more consistent with state relative to trait factors. In addition, most established cognitive tasks involve several relatively discrete cognitive subprocesses, where findings from general batteries of subtests may mask specific deficits. In this context, our review suggests that relatively specific olfactory identification and spatial working memory deficits exist prior to illness onset and may be more potent trait markers for psychosis than cognitively dense tasks such as verbal memory. Suggestions for further research address the importance of standardization of inclusion criteria and the maintenance of basic neuropsychological assessment to allow better comparison of findings across centers. Further, in order to better understand the aetiopathology of cognitive dysfunction in psychosis, more experimental, hypothesis-driven measures of discrete cognitive processes are required. Delineation of the relationship between specific cognitive ability and symptoms from data-driven approaches may improve our understanding of the role of cognition during psychosis onset. © The Author 2006. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved
Altered brain activation during memory retrieval precedes and predicts conversion to psychosis in individuals at clinical high risk
No full text© The Author(s) 2018. Memory deficits are a hallmark of psychotic disorders such as schizophrenia. However, whether the neural dysfunction underlying these deficits is present before the onset of illness and potentially predicts conversion to psychosis is unclear. In this study, we investigated brain functional alterations during memory processing in a sample of 155 individuals at clinical high risk (including 18 subjects who later converted to full psychosis) and 108 healthy controls drawn from the second phase of the North American Prodrome Longitudinal Study (NAPLS-2). All participants underwent functional magnetic resonance imaging with a paired-associate memory paradigm at the point of recruitment and were clinically followed up for approximately 2 years. We found that at baseline, subjects at high risk showed significantly higher activation during memory retrieval in the prefrontal, parietal, and bilateral temporal cortices (PFWE \u3c .035). This effect was more pronounced in converters than nonconverters and was particularly manifested in unmedicated subjects (P \u3c .001). The hyperactivation was significantly correlated with retrieval reaction time during scan in converters (P = .009) but not in nonconverters and controls, suggesting an exaggerated retrieval effort. These findings suggest that hyperactivation during memory retrieval may mark processes associated with conversion to psychosis, and such measures have potential as biomarkers for psychosis prediction
Erratum: Specificity of incident diagnostic outcomes in patients at clinical high risk for psychosis (Schizophrenia Bulletin (2015) 41 (1066-1075) DOI: 10.1093/schbul/sbv091)
No full text© The Author(s) 2018. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. An error in statistical syntax defining baseline disorder led to misidentification of baseline anxiety disorder in five cases in one of the two reported samples (PREDICT). NAPLS-1 data and previous publications of PREDICT data were not affected. The error affected rows in Table 1 labeled \u27DSM-IV anxiety\u27 and \u27Any mood/anx disorder\u27 and rows in Table 3 labeled \u27Baseline Anxiety Excluded\u27 and \u27Any Baseline Mood/ Anxiety Excluded.\u27 Corrected Tables are shown below with corrected numbers in bold. Tables S1-S5 in the data supplement were also affected. Note that the online paper has also been replaced. The abstract is unchanged, and overall findings and conclusions are not affected. One paragraph in the Results describing supplementary tables 1 and 2 is slightly changed (changes in bold): Sensitivity analyses showed that the CHR vs HSC difference for incident psychosis continued to hold whether analyses included or excluded subjects with each or any baseline disorder from the model (all p\u27s = 0.001, Table S1). Similarly, the lack of CHR vs HSC differences for incident nonpsychotic disorders also continued to hold whether models included subjects with baseline disorder (as non-cases of emergent disorder) or excluded them (all p\u27s = 0.390, Table S2). We regret the error
The molecular genetics of bipolar affective disorder : South African populations, endophenotypes, and environmental influence
No full textIncludes bibliographical references.The identification of the genetic variants underpinning bipolar disorder (BPD) has been impeded by a complex pattern of inheritance that may include by genetic heterogeneity, genetic epistasis, gene-environment interactions, incomplete penetrance and variable expressivity. In this thesis three strategies were employed to ameliorate these confounding factors. The first strategy was to focus on a theoretically genetically-homogeneous population with BPD. A unique South African sample including 190 individuals of the relativity reproductively-isolated Afrikaner population yielded promising evidence of linkage to chromosome 1 q31-32 and weaker peaks at lOq23 and 13q32, regions previously implicated in the disorder. A family-based analysis suggested that the 3' variable number tandem repeat (VNTR) variant of the dopamine transporter gene (DAT) is associated with bipolar-spectrum illness in the 132-strong sample of British ancestry. The second strategy was to carry out genetic linkage and association analyses using quantitative traits (elldophenotypes) that were closely associated with BPD. As part of this process a variety of personality traits were evaluated in the cohort, and anxiety related, novelty-seeking, hyperthymic, and cyclothymic personality traits were found to aggregate in participants with BPD and to a lesser extent repeated unipolar illness (MDE-R). These traits were therefore used as quantitative markers or endophenotypes of BPD. The quantitative linkage analysis indicated that a variant in the region of 13q32 may influence the development of novelty-seeking-related traits in the largest Afrikaner pedigree, while the personality trait, ""Stability"", was weakly linked to 4p16 in the total sample. The catechol-o-methytransferase (COM1) Va1l58Mct and the Brain Derived Neurotrophic Factor (BDNF) Va1l66Met polymorphisms were associated with mood-labile-cyclothymic and hyperthymic·-novelty-seeking traits, respectively. the DA T VNTR and the Notch4 exonic repeat variants were associated with a broad range of ""pathological"" personality traits in the sa11lples of British and Afrikaner origin, respectively. The sample was also evaluated with a battery of neuropsychological tasks and the BPD 1 and MDE-R groups displayed both verbal and visual memory recall deficits while the BPD 1 sample also suffered from recognition memory deficits. The neurocognitive trait, ""Memory"" was therefore used as a second endophenotype generating potential linkage signals on IOq23 and 22q 11. The exonic 48bp VNTR polymorphism in the dopamine 4 receptor (DRD4) gene was associated with '""Memory"" performance. As a third strategy, a potentially important aetiological factor, childhood trauma, was measured, and used to test for gene-environment interactions between the various candidate genes and bipolar-illness or BPD-related endophenotypes in the cohort. BPD and M DE-R individuals displayed significantly higher levels of emotional and physical abuse, and the former variable was also associated with the development of anxiety-related and unstable personality traits. A functional variant of the COM1 gene was found to interact with abuse to predispose to anxiety-related, unstable cyclothymic and novelty-seeking related personality traits. The combination of childhood abuse and possession of low-activity MAO-A gene variants was also associated the development of more anxious and unstable personality traits. All interaction between sexual abuse and the B])NF gene modulated performance on verbal and visual memory tasks. A similar interaction between the ApoE gene and sexual abuse was observed. Although a number of theoretical obstacles remain to be resolved, the analyses of isolated populations coupled with the use of endophenotypes and the testing or gene environment interactions, holds out great promise for the eventual elucidation of the genetic basis of hi polar affective disorder
