Gender differences in videoed accounts of victim blaming for revenge porn for self-taken and stealth-taken sexually explicit images and videos

© 2021 The Authors. Published by Masaryk University, Faculty of Social Studies. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.5817/CP2021-4-3Using video recounts from revenge porn victims, this study explores whether levels of victim blaming differs for the sharing of self- and stealth-taken sexually explicit images and videos. Building on previous work which has demonstrated victim blame for both self- and stealth generated images in occurrences of revenge porn (Zvi & Schechory-Bitton, 2020), the reported study presents an original and ecologically valid methodological approach whereby 342 (76 male, 266 female) participants (Mage = 39.27, SD = 11.70) from the UK watched videoed accounts of real experiences of falling victim to revenge porn, rather than using text based, often fictional, vignettes to attribute blame which dominate studies in this area. All data was collected in 2019. The results demonstrated that significantly more blame was assigned to victims when participants were indirectly rather than directly asked who was to blame for the occurrence of revenge porn, supporting the notion of an unconscious processing bias in attributing blame. More blame was also assigned to those victims who themselves generated the material compared to when it had been acquired without their awareness by a perpetrator, suggesting the cognitive bias to be in line with a just world hypothesis. Male participants were more likely to blame a victim than were female participants, although sex of victim and mode of shared sexually-explicit material (video or image) did not appear to affect levels of victim-blame. Findings are considered in terms of extant research and the need for future work in the area of victim blame and revenge pornography.Published onlin

Truncating SRCAP variants outside the Floating-Harbor syndrome locus cause a distinct neurodevelopmental disorder with a specific DNA methylation signature

Truncating variants in exons 33 and 34 of the SNF2-related CREBBP activator protein (SRCAP) gene cause the neurodevelopmental disorder (NDD) Floating-Harbor syndrome (FLHS), characterized by short stature, speech delay, and facial dysmorphism. Here, we present a cohort of 33 individuals with clinical features distinct from FLHS and truncating (mostly de novo) SRCAP variants either proximal (n = 28) or distal (n = 5) to the FLHS locus. Detailed clinical characterization of the proximal SRCAP individuals identified shared characteristics: developmental delay with or without intellectual disability, behavioral and psychiatric problems, non-specific facial features, musculoskeletal issues, and hypotonia. Because FLHS is known to be associated with a unique set of DNA methylation (DNAm) changes in blood, a DNAm signature, we investigated whether there was a distinct signature associated with our affected individuals. A machine-learning model, based on the FLHS DNAm signature, negatively classified all our tested subjects. Comparing proximal variants with typically developing controls, we identified a DNAm signature distinct from the FLHS signature. Based on the DNAm and clinical data, we refer to the condition as "non-FLHS SRCAP-related NDD.'' All five distal variants classified negatively using the FLHS DNAm model while two classified positively using the proximal model. This suggests divergent pathogenicity of these variants, though clinically the distal group presented with NDD, similar to the proximal SRCAP group. In summary, for SRCAP, there is a clear relationship between variant location, DNAm profile, and clinical phenotype. These results highlight the power of combined epigenetic, molecular, and clinical studies to identify and characterize genotype-epigenotype-phenotype correlations

Gender differences in videoed accounts of victim blaming for revenge porn for self-taken and stealth-taken sexually explicit images and videos

Using video recounts from revenge porn victims, this study explores whether levels of victim blaming differs for the sharing of self- and stealth-taken sexually explicit images and videos. Building on previous work which has demonstrated victim blame for both self- and stealth generated images in occurrences of revenge porn (Zvi & Schechory-Bitton, 2020), the reported study presents an original and ecologically valid methodological approach whereby 342 (76 male, 266 female) participants (Mage = 39.27, SD = 11.70) from the UK watched videoed accounts of real experiences of falling victim to revenge porn, rather than using text based, often fictional, vignettes to attribute blame which dominate studies in this area. All data was collected in 2019. The results demonstrated that significantly more blame was assigned to victims when participants were indirectly rather than directly asked who was to blame for the occurrence of revenge porn, supporting the notion of an unconscious processing bias in attributing blame. More blame was also assigned to those victims who themselves generated the material compared to when it had been acquired without their awareness by a perpetrator, suggesting the cognitive bias to be in line with a just world hypothesis. Male participants were more likely to blame a victim than were female participants, although sex of victim and mode of shared sexually-explicit material (video or image) did not appear to affect levels of victim-blame. Findings are considered in terms of extant research and the need for future work in the area of victim blame and revenge pornography

Obsessive-compulsive disorder and attention-deficit/hyperactivity disorder: distinct associations with DNA methylation and genetic variation

Abstract Background A growing body of research has demonstrated associations between specific neurodevelopmental disorders and variation in DNA methylation (DNAm), implicating this molecular mark as a possible contributor to the molecular etiology of these disorders and/or as a novel disease biomarker. Furthermore, genetic risk variants of neurodevelopmental disorders have been found to be enriched at loci associated with DNAm patterns, referred to as methylation quantitative trait loci (mQTLs). Methods We conducted two epigenome-wide association studies in individuals with attention-deficit/hyperactivity disorder (ADHD) or obsessive-compulsive disorder (OCD) (aged 4–18 years) using DNA extracted from saliva. DNAm data generated on the Illumina Human Methylation 450 K array were used to examine the interaction between genetic variation and DNAm patterns associated with these disorders. Results Using linear regression followed by principal component analysis, individuals with the most endorsed symptoms of ADHD or OCD were found to have significantly more distinct DNAm patterns from controls, as compared to all cases. This suggested that the phenotypic heterogeneity of these disorders is reflected in altered DNAm at specific sites. Further investigations of the DNAm sites associated with each disorder revealed that despite little overlap of these DNAm sites across the two disorders, both disorders were significantly enriched for mQTLs within our sample. Conclusions Our DNAm data provide insights into the regulatory changes associated with genetic variation, highlighting their potential utility both in directing GWAS and in elucidating the pathophysiology of neurodevelopmental disorders

Obsessive-compulsive disorder and attention-deficit/hyperactivity disorder: distinct associations with DNA methylation and genetic variation

Abstract Background A growing body of research has demonstrated associations between specific neurodevelopmental disorders and variation in DNA methylation (DNAm), implicating this molecular mark as a possible contributor to the molecular etiology of these disorders and/or as a novel disease biomarker. Furthermore, genetic risk variants of neurodevelopmental disorders have been found to be enriched at loci associated with DNAm patterns, referred to as methylation quantitative trait loci (mQTLs). Methods We conducted two epigenome-wide association studies in individuals with attention-deficit/hyperactivity disorder (ADHD) or obsessive-compulsive disorder (OCD) (aged 4–18 years) using DNA extracted from saliva. DNAm data generated on the Illumina Human Methylation 450 K array were used to examine the interaction between genetic variation and DNAm patterns associated with these disorders. Results Using linear regression followed by principal component analysis, individuals with the most endorsed symptoms of ADHD or OCD were found to have significantly more distinct DNAm patterns from controls, as compared to all cases. This suggested that the phenotypic heterogeneity of these disorders is reflected in altered DNAm at specific sites. Further investigations of the DNAm sites associated with each disorder revealed that despite little overlap of these DNAm sites across the two disorders, both disorders were significantly enriched for mQTLs within our sample. Conclusions Our DNAm data provide insights into the regulatory changes associated with genetic variation, highlighting their potential utility both in directing GWAS and in elucidating the pathophysiology of neurodevelopmental disorders.http://deepblue.lib.umich.edu/bitstream/2027.42/173262/1/11689_2020_Article_9324.pd