The practice of going helps children to stop:The importance of context monitoring in inhibitory control

How do we stop ourselves during ongoing action? Recent work implies that stopping per se is easy given sufficient monitoring of contextual cues signaling the need to change action. We test key implications of this idea for improving inhibitory control. Seven- to 9-year old children practiced stopping an ongoing action, or monitoring for cues that signaled the need to go again. Both groups subsequently showed better response inhibition in a Stop-Signal task than active controls, and practice monitoring yielded a dose-response relationship. When monitoring practice was optimized to occur while children engaged in responding, the greatest benefits were observed – even greater than from practicing stopping itself. These findings demonstrate the importance of monitoring processes in developing response inhibition, and suggest promising new directions for interventions

Capturing the personal through the lens of the professional: The use of external data sources in autoethnography

This article shows how external data sources can be utilised in autoethnographic research. Beginning with an account of a critical incident that examines the incompatibility of private and professional identities, I show how, through the collection of data sources, I capture the impact of homophobic and heteronormative discursive practices on health, wellbeing and identity. In the critical incident, I explore how I prospered as a teacher at a British village school for almost 10 years by censoring my sexuality and carefully managing the intersection between my private and professional identities. However, when a malicious and homophobic neighbour and parent of children at the school exposed my sexuality to the Headteacher, I learned the extent to which the rural school community privileged and protected the heteronormative discourse. A poststructuralist theoretical framework underpins this article. My experience of being a subject is understood as the outcome of discursive practices. Sexual identity, teacher identity and autoethnographer identity are understood to be fluid, and constantly produced and reproduced in response to social, cultural and political influences. The article describes how email correspondence, medical records and notes from a course of cognitive behaviour therapy were deployed to augment my personal recollection and give a depth and richness to the narrative. As the critical incident became a police matter, examination takes place of how I sought to obtain and utilise data from the police national computer in the research. Attempts to collect data from the police and Crown Prosecution Service were problematic and provided an unexpected development in the research and offered additional insight into the nature of the British rural community and its police force

Between feminism and anorexia: An autoethnography

Critical feminist work on eating disorders has grown substantially since its establishment in the 1980s, and has increasingly incorporated the use of anorexic stories, voices and experiences. Yet rarely do such accounts offer the anorexic a space to respond to the now established feminist conceptions of the problem which structure the books or articles in which they appear. Anorexic, or recovered anorexic, voices are used by the researcher to interpret the role played by gender, even whilst the subjects are invited to respond to and critique, medical and popular discourses on the disorder. This lack of dialogue is all the more striking in the context of the feminist aim to fight ‘back against the tendency to silence anorexic women’s’ own interpretations of their starving, treatment and construction (Saukko, 2008: 34). As someone who suffered from anorexia for 20 years, this article offers an autoethnographic account of my experience of encountering the feminist literature on anorexia in a bid to speak back, or enter into a dialogue between feminist politics and eating disorder experience

Resting state EEG power spectrum and functional connectivity in autism: a cross-sectional analysis

BACKGROUND: Understanding the development of the neuronal circuitry underlying autism spectrum disorder (ASD) is critical to shed light into its etiology and for the development of treatment options. Resting state EEG provides a window into spontaneous local and long-range neuronal synchronization and has been investigated in many ASD studies, but results are inconsistent. Unbiased investigation in large and comprehensive samples focusing on replicability is needed. METHODS: We quantified resting state EEG alpha peak metrics, power spectrum (PS, 2-32 Hz) and functional connectivity (FC) in 411 children, adolescents and adults (n = 212 ASD, n = 199 neurotypicals [NT], all with IQ > 75). We performed analyses in source-space using individual head models derived from the participants' MRIs. We tested for differences in mean and variance between the ASD and NT groups for both PS and FC using linear mixed effects models accounting for age, sex, IQ and site effects. Then, we used machine learning to assess whether a multivariate combination of EEG features could better separate ASD and NT participants. All analyses were embedded within a train-validation approach (70%-30% split). RESULTS: In the training dataset, we found an interaction between age and group for the reactivity to eye opening (p = .042 uncorrected), and a significant but weak multivariate ASD vs. NT classification performance for PS and FC (sensitivity 0.52-0.62, specificity 0.59-0.73). None of these findings replicated significantly in the validation dataset, although the effect size in the validation dataset overlapped with the prediction interval from the training dataset. LIMITATIONS: The statistical power to detect weak effects-of the magnitude of those found in the training dataset-in the validation dataset is small, and we cannot fully conclude on the reproducibility of the training dataset's effects. CONCLUSIONS: This suggests that PS and FC values in ASD and NT have a strong overlap, and that differences between both groups (in both mean and variance) have, at best, a small effect size. Larger studies would be needed to investigate and replicate such potential effects

The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism

Increased intake of dietary carbohydrate that is fermented in the colon by the microbiota has been reported to decrease body weight, although the mechanism remains unclear. Here we use in vivo11C-acetate and PET-CT scanning to show that colonic acetate crosses the blood–brain barrier and is taken up by the brain. Intraperitoneal acetate results in appetite suppression and hypothalamic neuronal activation patterning. We also show that acetate administration is associated with activation of acetyl-CoA carboxylase and changes in the expression profiles of regulatory neuropeptides that favour appetite suppression. Furthermore, we demonstrate through 13C high-resolution magic-angle-spinning that 13C acetate from fermentation of 13C-labelled carbohydrate in the colon increases hypothalamic 13C acetate above baseline levels. Hypothalamic 13C acetate regionally increases the 13C labelling of the glutamate–glutamine and GABA neuroglial cycles, with hypothalamic 13C lactate reaching higher levels than the ‘remaining brain’. These observations suggest that acetate has a direct role in central appetite regulation

Being and doing anorexia nervosa: An autoethnography of diagnostic identity and performance of illness

This autoethnography examines my experience of the diagnosis and treatment of anorexia nervosa. Drawing on memory and personal and medical documents relating to inpatient admissions in an adult specialist eating disorder unit, I narrate and analyse my experience in terms of my relationship to the diagnosis of anorexia and the constructions of it I encountered. I show how I came to value an identity based on anorexia and how I learned ways of ‘doing’ the diagnosis in treatment. This involved me valuing medical markers of illness, including signs of poor health, which became crucial to how I performed my diagnosis and retained the diagnostically-informed sense of self that I valued. I suggest that, ultimately, these diagnostic-dynamics, alongside other effects of long-term inpatient treatment such as detachment from ‘normal life’, prolonged my struggles with self-starvation. The insights from this autoethnography shed light on potential iatrogenic impacts of diagnosis and treatment for anorexia

O-GlcNAc Modification of NFκB p65 Inhibits TNF-α-Induced Inflammatory Mediator Expression in Rat Aortic Smooth Muscle Cells

BACKGROUND: We have shown that glucosamine (GlcN) or O-(2-acetamido-2-deoxy-D-glucopyranosylidene)amino-N-phenylcarbamate (PUGNAc) treatment augments O-linked-N-acetylglucosamine (O-GlcNAc) protein modification and attenuates inflammatory mediator expression, leukocyte infiltration and neointima formation in balloon injured rat carotid arteries and have identified the arterial smooth muscle cell (SMC) as the target cell in the injury response. NFκB signaling has been shown to mediate the expression of inflammatory genes and neointima formation in injured arteries. Phosphorylation of the p65 subunit of NFκB is required for the transcriptional activation of NFκB. This study tested the hypothesis that GlcN or PUGNAc treatment protects vascular SMCs against tumor necrosis factor (TNF)-α induced inflammatory stress by enhancing O-GlcNAcylation and inhibiting TNF-α induced phosphorylation of NFκB p65, thus inhibiting NFκB signaling. METHODOLOGY/PRINCIPAL FINDINGS: Quiescent rat aortic SMCs were pretreated with GlcN (5 mM), PUGNAc (10(-4) M) or vehicle and then stimulated with TNF-α (10 ng/ml). Both treatments inhibited TNF-α-induced expression of chemokines [cytokine-induced neutrophil chemoattractant (CINC)-2β and monocyte chemotactic protein (MCP)-1] and adhesion molecules [vascular cell adhesion molecule (VCAM)-1 and P-Selectin]. Both treatments inhibited TNF-α induced NFκB p65 activation and promoter activity, increased NFκB p65 O-GlcNAcylation and inhibited NFκB p65 phosphorylation at Serine 536, thus promoting IκBα binding to NFκB p65. CONCLUSIONS: There is a reciprocal relationship between O-GlcNAcylation and phosphorylation of NFκB p65, such that increased NFκB p65 O-GlcNAc modification inhibits TNF-α-Induced expression of inflammatory mediators through inhibition of NFκB p65 signaling. These findings provide a mechanistic basis for our previous observations that GlcN and PUGNAc treatments inhibit inflammation and remodeling induced by acute endoluminal arterial injury