How Does Religiosity Influence Gambling? A Cross-Cultural Study Between Portuguese and English Youth.

Research has shown that religion can play a protective role in diverse risky behaviors among young people. However, very little is known about the effect of religion in gambling, especially among young problem gamblers. A strong moral belief regarding gambling may prevent adolescents and young adults engaging in gambling and developing problems. Nevertheless, some evidence suggests that religion might have an influence on gambling cognitive distortions (i.e., some religious beliefs might influence the conceptions of chance and luck, which may contribute to an increase in gambling participation). The present study examined the different effects that religion can have on gambling behavior, in two different cultural contexts (i.e., Portugal and England), characterized by different religious affiliations. A sample (n = 725) comprising Portuguese (n = 312) and English (n = 413) adolescents and young adults completed an online survey. The findings indicated that Portuguese youth were more religious than their English counterparts. Moreover, religiosity was associated with lower gambling engagement among participants in both samples. Mediation analyses also showed that the cognitive distortion of illusion of control mediated the relationship between religiosity and problem gambling among the Portuguese participants, and the interpretative bias was a significant mediator in the English sample. The study's findings suggest that religion can have a protective role on gambling behaviors. However, further research is needed to explore the interactive role of religion and cognitive distortions.

The Multiple Object Avoidance (MOA) task measures attention for action: Evidence from driving and sport.

Performance in everyday tasks, such as driving and sport, requires allocation of attention to task-relevant information and the ability to inhibit task-irrelevant information. Yet there are individual differences in this attentional function ability. This research investigates a novel task for measuring attention for action, called the Multiple Object Avoidance task (MOA), in its relation to the everyday tasks of driving and sport. The aim in Study 1 was to explore the efficacy of the MOA task to predict simulated driving behaviour and hazard perception. Whilst also investigating its test-retest reliability and how it correlates to self-report driving measures. We found that superior performance in the MOA task predicted simulated driving performance in complex environments and was superior at predicting performance compared to the Useful Field of View task. We found a moderate test-retest reliability and a correlation between the attentional lapses subscale of the Driving Behaviour Questionnaire. Study 2 investigated the discriminative power of the MOA in sport by exploring performance differences in those that do and do not play sports. We also investigated if the MOA shared attentional elements with other measures of visual attention commonly attributed to sporting expertise: Multiple Object Tracking (MOT) and cognitive processing speed. We found that those that played sports exhibited superior MOA performance and found a positive relationship between MOA performance and Multiple Object Tracking performance and cognitive processing speed. Collectively, this research highlights the utility of the MOA when investigating visual attention in everyday contexts.

A comparison of cybersickness symptoms across 360-degree hazard perception and hazard prediction tests for drivers.

Hazard perception assessment may benefit from VR-presentation by removing field-of-view restrictions imposed by single-screen tests. One concern is whether VR-induced 'cybersickness' will offset any benefits. Self-reported cybersickness ratings were recorded from 77 participants viewing two variants of a 360-degree hazard test: hazard perception and hazard prediction. The latter was hypothesised to be particularly susceptible as clips abruptly cut to a probe question at hazard onset. Such sudden occlusions are thought to increase cybersickness. Overall cybersickness levels were low, with only four participants excluded for above-threshold sickness ratings. The remaining participants showed unexpectedly lower symptoms for the hazard prediction test and rated this test format as more comfortable and engaging. These findings mitigate concerns over the use of 360-degree videos in formative hazard assessments, even when clips involve sudden occlusions. Nonetheless, removal of any participants due to cybersickness raises problems for using VR for formal assessments of hazard perception skill.

Global gene expression profiling of a mouse model of ovarian clear cell carcinoma caused by ARID1A and PIK3CA mutations implicates a role for inflammatory cytokine signaling.

Ovarian clear-cell carcinoma (OCCC) is an aggressive form of epithelial ovarian cancer (EOC). OCCC represents 5-25% of all EOC incidences and is the second leading cause of death from ovarian cancer (Glasspool and McNeish, 2013) [1]. A recent publication by Chandler et al. reported the first mouse model of OCCC that resembles human OCCC both genetically and histologically by inducing a localized deletion of ARID1A and the expression of the PIK3CA(H1047R) substitution mutation (Chandler et al., 2015) [2]. We utilized Affymetrix Mouse Gene 2.1 ST arrays for the global gene expression profiling of mouse primary OCCC tumor samples and animal-matched normal ovaries to identify cancer-dependent gene expression. We describe the approach used to generate the differentially expressed genes from the publicly available data deposited at the Gene Expression Omnibus (GEO) database under the accession number GSE57380. These data were used in cross-species comparisons to publically available human OCCC gene expression data and allowed the identification of coordinately regulated genes in both mouse and human OCCC and supportive of a role for inflammatory cytokine signaling in OCCC pathogenesis (Chandler et al., 2015) [2].

Developmental and degenerative features in a complicated spastic paraplegia.

OBJECTIVE: We sought to explore the genetic and molecular causes of Troyer syndrome, one of several complicated hereditary spastic paraplegias (HSPs). Troyer syndrome had been thought to be restricted to the Amish; however, we identified 2 Omani families with HSP, short stature, dysarthria and developmental delay-core features of Troyer syndrome-and a novel mutation in the SPG20 gene, which is also mutated in the Amish. In addition, we analyzed SPG20 expression throughout development to infer how disruption of this gene might generate the constellation of developmental and degenerative Troyer syndrome phenotypes. METHODS: Clinical characterization of 2 non-Amish families with Troyer syndrome was followed by linkage and sequencing analysis. Quantitative polymerase chain reaction and in situ hybridization analysis of SPG20 expression were carried out in embryonic and adult human and mouse tissue. RESULTS: Two Omani families carrying a novel SPG20 mutation displayed clinical features remarkably similar to the Amish patients with Troyer syndrome. SPG20 mRNA is expressed broadly but at low relative levels in the adult brain; however, it is robustly and specifically expressed in the limbs, face, and brain during early morphogenesis. INTERPRETATION: Null mutations in SPG20 cause Troyer syndrome, a specific clinical entity with developmental and degenerative features. Maximal expression of SPG20 in the limb buds and forebrain during embryogenesis may explain the developmental origin of the skeletal and cognitive defects observed in this disorder.

Molecular specification and patterning of progenitor cells in the lateral and medial ganglionic eminences.

We characterized intrinsic and extrinsic specification of progenitors in the lateral and medial ganglionic eminences (LGE and MGE). We identified seven genes whose expression is enriched or restricted in either the LGE [biregional cell adhesion molecule-related/downregulated by oncogenes binding protein (Boc), Frizzled homolog 8 (Fzd8), Ankrd43 (ankyrin repeat domain-containing protein 43), and Ikzf1 (Ikaros family zinc finger 1)] or MGE [Map3k12 binding inhibitory protein 1 (Mbip); zinc-finger, SWIM domain containing 5 (Zswim5); and Adamts5 [a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5]]. Boc, Fzd8, Mbip, and Zswim5 are apparently expressed in LGE or MGE progenitors, whereas the remaining three are seen in the postmitotic mantle zone. Relative expression levels are altered and regional distinctions are lost for each gene in LGE or MGE cells propagated as neurospheres, indicating that these newly identified molecular characteristics of LGE or MGE progenitors depend on forebrain signals not available in the neurosphere assay. Analyses of Pax6(Sey/Sey), Shh(-/-), and Gli3(XtJ/XtJ) mutants suggests that LGE and MGE progenitor identity does not rely exclusively on previously established forebrain-intrinsic patterning mechanisms. Among a limited number of additional potential patterning mechanisms, we found that extrinsic signals from the frontonasal mesenchyme are essential for Shh- and Fgf8-dependent regulation of LGE and MGE genes. Thus, extrinsic and intrinsic forebrain patterning mechanisms cooperate to establish LGE and MGE progenitor identity, and presumably their capacities to generate distinct classes of neuronal progeny.