Whereabouts you are

•‘Whereabouts you are’ was an exhibition of work by ten Glasgow School of Art PhD Researchers, curated by Allyson Keehan (Glasgow School of Art) and guest curator Viviana Checchia (Centre for Contemporary Arts) • The exhibition ran from Saturday 15th October to Thursday 10th November in The Reid Gallery, Glasgow School of Art ‘Whereabouts you are’ explored the diverse research practices of the Glasgow School of Art PhD cohort. Bringing together researchers from disciplines across the fields of Fine Art and Design, the exhibition posed a number of questions about the role of arts practice in academic research, its unique character, and its particular challenges. For the exhibiting researchers, pinpointing whereabouts you are is about marking a particular moment in the research process, pausing to reflect and take stock of their individual journey so far and to consider the next steps. In that spirit, rather than deferring the questions posed by the exhibition, they tackled them head-on through accompanying events organised in collaboration with the Centre for Contemporary Arts. By bringing their work out of the studio, the group hoped to not only shed light on the thought-provoking and innovative research undertaken at Glasgow School of Art, but to enliven the research through conversation with its new audience. The exhibiting researchers were: • Eszter Biró (School of Fine Art) • Jacqueline Butler (School of Fine Art) • Mirian Calvo (Institute for Design Innovation) • Inês Bento Coelho (School of Fine Art) • Allyson Keehan (School of Fine Art) • Fiona Jane MacLellan (Institute for Design Innovation) • Catherine M. Weir (School of Fine Art) • Dawn Worsley (School of Fine Art) • Hanan Makki Zakari (School of Simulation and Visualisation) • Polina Zioga (School of Simulation and Visualisation). Curated by Allyson Keehan (Glasgow School of Art) and guest curator Viviana Checchia (Centre for Contemporary Arts)

Whereabouts you are

'Whereabouts you are' was an exhibition of work by ten Glasgow School of Art Ph.D. Researchers, curated by Allyson Keehan (Glasgow School of Art) and guest curator Viviana Checchia (Centre for Contemporary Arts Glasgow). The exhibition ran from Saturday 15th October to Thursday 10th November 2016 in The Reid Gallery, Glasgow School of Art. 'Whereabouts you are' explored the diverse research practices of the Glasgow School of Art Ph.D. cohort. Bringing together researchers from disciplines across the fields of Fine Art and Design, the exhibition posed a number of questions about the role of arts practice in academic research, its unique character, and its particular challenges. For the exhibiting researchers, pinpointing 'whereabouts you are' is about marking a particular moment in the research process, pausing to reflect and take stock of their individual journey so far and to consider the next steps. In that spirit, rather than deferring the questions posed by the exhibition, they tackled them head-on through accompanying events organised in collaboration with the Centre for Contemporary Arts Glasgow. By bringing their work out of the studio, the group hoped to not only shed light on the thought-provoking and innovative research undertaken at Glasgow School of Art, but to enliven the research through conversation with its new audience. The exhibiting researchers were: • Eszter Biró (School of Fine Art) • Jacqueline Butler (School of Fine Art) • Mirian Calvo (Institute for Design Innovation) • Inês Bento Coelho (School of Fine Art) • Allyson Keehan (School of Fine Art) • Fiona Jane MacLellan (Institute for Design Innovation) • Catherine M. Weir (School of Fine Art) • Dawn Worsley (School of Fine Art) • Hanan Makki Zakari (School of Simulation and Visualisation) • Polina Zioga (School of Simulation and Visualisation)

The global burden of cancer attributable to risk factors, 2010-19 : a systematic analysis for the Global Burden of Disease Study 2019

Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe

A serious game for children with Autism Spectrum Disorder and Auditory Hypersensitivity

Research in Serious Games (SGs) for children with Autism Spectrum Disorder (ASD) has become of higher interest throughout the last decade. The positive impact for children with ASD of playing SGs, more particularly on tablets, has been highlighted, facilitating improvements of communication skills, social interactions and understanding emotions. Autistic individuals have a limited range of interests,and often struggle to communicate with those around them. In addition, they often have to live with Moderating Sensory Hypersensitivity (MSH), leading them to experience increased sensitivity to sound, sight and/or touch. For these reasons, it is crucial to identify effective ways able to help them to relate to the society more easily, with a view to improving their quality of life. The research presented in this thesis describes a methodology for the creation of effective SG dedicated to children with ASD and auditory hypersensitivity, aiming at improving tolerance to critical sounds. The game, Sinbad and the Magic Cure was developed for Android devices and is intended for children aged 8-11, building upon interdisciplinary inputs from the fields of psychology, software engineering and design disciplines. This research first explores a collection of sounds to identify the most critical sounds for children with ASD, and then assesses the effectiveness of the game Sinbad and the Magic Cure to familiarise to these critical sounds. Overall, results suggest that playing SGs in the long-term can be an effective instrument for managing auditory hypersensitivity in autistic children. Finally, this thesis discusses and concludes the trend of utilising SGs for ASD, as well as a proposed future work

Neuroprotective effects of dexmedetomidine against hyperoxia-induced injury in the developing rat brain

<div><p>Dexmedetomidine (DEX) is a highly selective agonist of α2-receptors with sedative, anxiolytic, and analgesic properties. Neuroprotective effects of dexmedetomidine have been reported in various brain injury models. In the present study, we investigated the effects of dexmedetomidine on hippocampal neurogenesis, specifically the proliferation capacity and maturation of neurons and neuronal plasticity following the induction of hyperoxia in neonatal rats. Six-day old sex-matched Wistar rats were exposed to 80% oxygen or room air for 24 h and treated with 1, 5 or 10 μg/kg of dexmedetomidine or normal saline. A single pretreatment with DEX attenuated the hyperoxia-induced injury in terms of neurogenesis and plasticity. In detail, both the proliferation capacity (PCNA+ cells) as well as the expression of neuronal markers (Nestin+, PSA-NCAM+, NeuN+ cells) and transcription factors (SOX2, Tbr1/2, Prox1) were significantly reduced under hyperoxia compared to control. Furthermore, regulators of neuronal plasticity (Nrp1, Nrg1, Syp, and Sema3a/f) were also drastically decreased. A single administration of dexmedetomidine prior to oxygen exposure resulted in a significant up-regulation of expression-profiles compared to hyperoxia. Our results suggest that dexmedetomidine may have neuroprotective effects in an acute hyperoxic model of the neonatal rat.</p></div

Paraffin sections of the hippocampus at postnatal day (P)7 of Wistar rats stained with A/B) proliferating cell nuclear antigen (PCNA)/DAPI; double immunofluorescence staining with C/D) Nestin/PCNA/DAPI; E/F) polysialylated neuronal cell adhesion molecule (PSA-NCAM)/PCNA/DAPI; G/H) neuronal nuclei (NeuN)/PCNA/DAPI.

<p>Hyperoxia in neonatal rats decreased the proliferation positive cells (PCNA+, green, <b>A/B</b>) and the expression of neuronal marker for neuronal progenitor cells (Nestin+, red, <b>C/D</b>), immature neurons (PSA-NCAM+, red, <b>E/F</b>), and mature postmitotic neurons (NeuN+, red, <b>G/H</b>). Application of DEX1 and/or DEX5 under hyperoxic exposure resulted in improved expression of neuronal markers and increase of proliferation in granular cell layer and polymorphic layer of DG. DEX10 led to a reduction of cell counts of NeuN in hyperoxic animals. Under normoxic conditions DEX1 and/or DEX5 upregulated PCNA and the differentiation marker and DEX10 showed negative effects on PNCA and NeuN expression. All images were taken at identical magnification (original magnification 200 x).</p

Quantitation of A) PCNA+, B) Nestin+, C) PSA-NCAM+, and D) NeuN+ cell counts in sum of the granular cell layer and polymorphic layer with DEX (1, 5, and 10 μg/kg) under hyperoxia (hatched grey bars), hyperoxia alone (black bars), DEX under normoxic conditions (plain grey bars), and in comparison to normoxia control group (100%, white bars).

<p>Data are expressed relative to the normoxia-exposed control group as mean ± SEM of n = 5. The 100% values are for PCNA 258.9, for Nestin 354.1, for PSA-NCAM 209.3, and for NeuN 333.3. * p<0.05, ** p<0.01, and *** p<0.001 <i>versus</i> control; ^### p<0.001 <i>versus</i> hyperoxia (t-test, Bonferroni post hoc test after one-way ANOVA).</p

Sequences of oligonucleotides and gene locus.

<p>Sequences of oligonucleotides and gene locus.</p

Expression of mediators of transcriptional network is decreased in neonatal rats after hyperoxic injury and upregulated with DEX.

<p>The relative mRNA expressions of transcription factors were measured in rat brain homogenates with DEX (1, 5, and 10 μg/kg) under hyperoxia (hatched grey bars), hyperoxia alone (black bars), DEX under normoxic conditions (plain grey bars), and in comparison to normoxia control group (100%, white bars) by quantitative realtime PCR. <b>A)</b> There are no changes under normoxia/hyperoxia with or without DEX for Pax6. <b>B)</b> Note the significant reduction of SOX2 under hyperoxia and the increase with a single dose of DEX. Under normoxic conditions with DEX1 and DEX10 the mRNA expression of SOX2 was increased significantly. <b>C)</b> Tbr2 mRNA expression was reduced under hyperoxia and upregulated at DEX5. <b>D)</b> Hyperoxia has no influence on the mRNA expression of Tbr1, but DEX5 and DEX10 triggered the expression above the normoxia level. The same effect was detected for DEX10 under normoxia. <b>E)</b> There was a significant decrease for Prox1 mRNA expression under hyperoxia alone and with DEX1 and DEX5, but also a significant up-regulation with DEX10. Data shown as mean ± SEM, n = 5 per group. * p<0.05, ** p<0.01, and *** p<0.001 <i>versus</i> control; ^## p<0.01 and ^### p<0.001 <i>versus</i> hyperoxia (t-test, Bonferroni post hoc test after one-way ANOVA).</p