Object substitution masking and it's relationship with visual crowding

Object substitution masking (OSM) occurs when the perceptibility of a brief target is reduced by a trailing surround mask typically composed of four dots. Camp et al. (Journal of Experimental Psychology: Human Perception and Performance, 41, 940–957, 2015) found that crowding a target by adding adjacent flankers, in addition to OSM, had a more deleterious effect on performance than expected based on the combined individual effects of crowding and masking alone. The current experiments test why OSM and crowding interact in this way. In three experiments, target-flanker distance is manipulated whilst also varying mask duration in a digit identification task. The OSM effect—as indexed by the performance difference between unmasked and masked conditions—had a quadratic function with respect to target-flanker distance. Results suggest it is OSM affecting crowding rather than the converse: Masking seems to amplify crowding at intermediate target-distractor distances at the edge of the crowding interference zone. These results indicate that OSM and crowding share common mechanisms. The effect of OSM is possibly a consequence of changes to the types of feature detectors which are pooled together for target identification when that target must compete for processing with a trailing mask in addition to competition from adjacent flankers

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

British Animation Awards: Public Choice Award screenings, 2016

Screening 1: 27th JANUARY 2016 Screening 2: 03rd FEBRUARY 2016 Screening 3: 10th FEBRUARY 2016 Screening programme curated by BAA. Chaired and hosted by Stuart Messinger and Laura Weston with collaboration of current Students. Ticketed event to open to staff, students, Alumni and General Public

Stromal myofibroblasts are drivers of invasive cancer growth.

Tissue integrity is maintained by the stroma in physiology. In cancer, however, tissue invasion is driven by the stroma. Myofibroblasts and cancer-associated fibroblasts are important components of the tumor stroma. The origin of myofibroblasts remains controversial, although fibroblasts and bone marrow-derived precursors are considered to be the main progenitor cells. Myofibroblast reactions also occur in fibrosis. Therefore, we wonder whether nontumorous myofibroblasts have different characteristics and different origins as compared to tumor-associated myofibroblasts. The mutual interaction between cancer cells and myofibroblasts is dependent on multiple invasive growth-promoting factors, through direct cell-cell contacts and paracrine signals. Since fibrosis is a major side effect of radiotherapy, we address the question how the main methods of cancer management, including chemotherapy, hormonotherapy and surgery affect myofibroblasts and by inference the surrogate endpoints invasion and metastasis.Journal ArticleResearch Support, Non-U.S. Gov'tReviewSCOPUS: sh.jFLWINinfo:eu-repo/semantics/publishe