The effect of visual detail on cybersickness:predicting symptom severity using spatial velocity

Abstract. In this work, we examine the effect of visual realism on the severity of cybersickness symptoms experienced by users of virtual environments. We also seek to validate a metric called spatial velocity as a predictor of cybersickness. The proposed metric combines the visual complexity of a virtual scene with the amount of movement within the scene. To achieve this, we prepared two virtual scenes depicting the same environment with a variable level of detail. We recruited volunteers who were exposed to both scenes in two separate sessions. We obtained the sickness ratings after both sessions and saved the data required for spatial velocity calculations. After comparing the sickness ratings between the two scenes, we found no evidence of the visual realism playing any significant role in the generation of cybersickness symptoms. The spatial velocity also proved inadequate in characterizing the difference in visual complexity and correlated poorly with all the observed sickness scores.Visuaalisen yksityiskohtaisuuden vaikutus VR-pahoinvointiin : oireiden vakavuuden ennustaminen käyttäen SV-metriikkaa. Tiivistelmä. Tässä työssä tutkimme sitä, millainen vaikutus virtuaalisten ympäristöjen graafisella yksityiskohtaisuudella on VR-pahoinvointiin. Pyrimme myös validoimaan "spatial velocity" -nimisen mittasuureen kyvyn ennustaa VR-pahoinvoinnin oireiden vakavuutta. Kyseisen mittasuureen etuna on, että se yhdistää visuaalisen kompleksisuuden ja ympäristössä koetun liikkeen yhdeksi suureeksi. Tutkimusta varten valmistimme kaksi virtuaaliympäristöä, joissa mallinnettiin Oulun yliopiston kampusaluetta. Toinen ympäristö pyrki mahdollisimman realistiseen esitystapaan, kun taas toisessa yksityiskohtien määrä minimoitiin. Koetta varten värväsimme 18 vapaaehtoista. Vapaaehtoiset altistettiin kummallekin ympäristölle kahdessa noin kymmenen minuutin mittaisessa kokeessa. Vapaaehtoisten kokeman VR-pahoinvoinnin vakavuutta arvioitiin kunkin kokeen jälkeen täytetyillä kyselylomakkeilla. Kokeiden aikana tallensimme myös SV laskentaan tarvittavat tiedot. Verrattuamme koeolosuhteiden tuloksia, emme löytäneet todisteita siitä, että ympäristön graafisten yksityiskohtien määrällä olisi merkittävää vaikutusta koettuun pahoinvointiin. Käytetty SV metriikka ei myöskään kyennyt erottelemaan ympäristöjä oletetulla tavalla, eivätkä lasketut arvot korreloineet merkittävästi minkään mitatun pahoinvointisuureen kanssa

Genetic and Epigenetic Characteristics of Inflammatory Bowel Disease–Associated Colorectal Cancer

doi: 10.1053/j.gastro.2021.04.042Background & Aims Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder associated with an elevated risk of colorectal cancer (CRC). IBD-associated CRC (IBD-CRC) may represent a distinct pathway of tumorigenesis compared to sporadic CRC (sCRC). Our aim was to comprehensively characterize IBD-associated tumorigenesis integrating multiple high-throughput approaches, and to compare the results with in-house data sets from sCRCs. Methods Whole-genome sequencing, single nucleotide polymorphism arrays, RNA sequencing, genome-wide methylation analysis, and immunohistochemistry were performed using fresh-frozen and formalin-fixed tissue samples of tumor and corresponding normal tissues from 31 patients with IBD-CRC. Results Transcriptome-based tumor subtyping revealed the complete absence of canonical epithelial tumor subtype associated with WNT signaling in IBD-CRCs, dominated instead by mesenchymal stroma-rich subtype. Negative WNT regulators AXIN2 and RNF43 were strongly down-regulated in IBD-CRCs and chromosomal gains at HNF4A, a negative regulator of WNT-induced epithelial–mesenchymal transition (EMT), were less frequent compared to sCRCs. Enrichment of hypomethylation at HNF4α binding sites was detected solely in sCRC genomes. PIGR and OSMR involved in mucosal immunity were dysregulated via epigenetic modifications in IBD-CRCs. Genome-wide analysis showed significant enrichment of noncoding mutations to 5′untranslated region of TP53 in IBD-CRCs. As reported previously, somatic mutations in APC and KRAS were less frequent in IBD-CRCs compared to sCRCs. Conclusions Distinct mechanisms of WNT pathway dysregulation skew IBD-CRCs toward mesenchymal tumor subtype, which may affect prognosis and treatment options. Increased OSMR signaling may favor the establishment of mesenchymal tumors in patients with IBD.BACKGROUND & AIMS: Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder associated with an elevated risk of colorectal cancer (CRC). IBD-associated CRC (IBD-CRC) may represent a distinct pathway of tumorigenesis compared to sporadic CRC (sCRC). Our aim was to comprehensively characterize IBD-associated tumorigenesis integrating multiple high-throughput approaches, and to compare the results with in-house data sets from sCRCs. METHODS: Whole-genome sequencing, single nucleotide polymorphism arrays, RNA sequencing, genome-wide methylation analysis, and immunohistochemistry were performed using fresh-frozen and formalin-fixed tissue samples of tumor and corresponding normal tissues from 31 patients with IBD-CRC. RESULTS: Transcriptome-based tumor subtyping revealed the complete absence of canonical epithelial tumor subtype associated with WNT signaling in IBD-CRCs, dominated instead by mesenchymal stroma-rich subtype. Negative WNT regulators AXIN2 and RNF43 were strongly down-regulated in IBD-CRCs and chromosomal gains at HNF4A, a negative regulator of WNTinduced epithelial-mesenchymal transition (EMT), were less frequent compared to sCRCs. Enrichment of hypomethylation at HNF4 alpha binding sites was detected solely in sCRC genomes. PIGR and OSMR involved in mucosal immunity were dysregulated via epigenetic modifications in IBD-CRCs. Genome-wide analysis showed significant enrichment of noncoding mutations to 50 untranslated region of TP53 in IBD-CRCs. As reported previously, somatic mutations in APC and KRAS were less frequent in IBD-CRCs compared to sCRCs. CONCLUSIONS: Distinct mechanisms of WNT pathway dysregulation skew IBD-CRCs toward mesenchymal tumor subtype, which may affect prognosis and treatment options. Increased OSMR signaling may favor the establishment of mesenchymal tumors in patients with IBD.Peer reviewe