Conferencing otherwise: a feminist new materialist writing experiment

This paper attempts to reconfigure hegemonic framings of ‘the academic conference’ and thereby offer a means to (re-)encounter the spatial, temporal and affective forces that conferences generate, differently. We are a geographically dispersed but multiply entangled group of academic researchers united by theoretical fault lines within our work that seek to ask what if (Haraway, 2016) and what else (Manning, 2016). This ‘what if’ and ‘what else’ thinking has manifested in experimental and subversive doings otherwise at a series of academic conferences. The storying practices presented in this paper were made possible by the vital materialism (Bennett, 2010) of a shared google.doc. It was within this virtual environment that we attempted to weave diffractive accounts of what conferencing otherwise produces. This writing experiment offers a series of speculative provocations and counter-provocations to ask what else does conferencing make possible. This article is an invitation to the reader to plunge in and wallow (Taylor, 2016) within the speculative accounts which ensue and to contemplate the possibilities of breaking free from sedimented ways of neoliberal conferencing

Associations between resting state brain activity and A1 adenosine receptor availability in the healthy brain: Effects of acute sleep deprivation

Introduction: Previous resting-state fMRI (Rs-fMRI) and positron emission tomography (PET) studies have shown that sleep deprivation (SD) affects both spontaneous brain activity and A1 adenosine receptor (A1AR) availability. Nevertheless, the hypothesis that the neuromodulatory adenosinergic system acts as regulator of the individual neuronal activity remains unexplored. Methods: Therefore, fourteen young men underwent Rs-fMRI, A1AR PET scans, and neuropsychological tests after 52 h of SD and after 14 h of recovery sleep. Results: Our findings suggested higher oscillations or regional homogeneity in multiple temporal and visual cortices, whereas decreased oscillations in cerebellum after sleep loss. At the same time, we found that connectivity strengths increased in sensorimotor areas and decreased in subcortical areas and cerebellum. Discussion: Moreover, negative correlations between A1AR availability and rs- fMRI metrics of BOLD activity in the left superior/middle temporal gyrus and left postcentral gyrus of the human brain provide new insights into the molecular basis of neuronal responses induced by high homeostatic sleep pressure

Impact of acute sleep deprivation on dynamic functional connectivity states

Sleep deprivation (SD) could amplify the temporal fluctuation of spontaneous brain activities that reflect different arousal levels using a dynamic functional connectivity (dFC) approach. Therefore, we intended to evaluate the test–retest reliability of dFC characteristics during rested wakefulness (RW), and to explore how the properties of these dynamic connectivity states were affected by extended durations of acute sleep loss (28/52 hr). We acquired resting-state fMRI and neuropsychological datasets in two independent studies: (a) twice during RW and once after 28 hr of SD (n = 15) and (b) after 52 hr of SD and after 14 hr of recovery sleep (RS; n = 14). Sliding-window correlations approach was applied to estimate their covariance matrices and corresponding three connectivity states were generated. The test–retest reliability of dFC properties demonstrated mean dwell time and fraction of connectivity states were reliable. After SD, the mean dwell time of a specific state, featured by strong subcortical–cortical anticorrelations, was significantly increased. Conversely, another globally hypoconnected state was significantly decreased. Subjective sleepiness and objective performances were separately positive and negative correlated with the increased and decreased state. Two brain connectivity states and their alterations might be sufficiently sensitive to reflect changes in the dynamics of brain mental activities after sleep loss

Reliability and validity of a 3-min psychomotor vigilance task in assessing sensitivity to sleep loss and alcohol: fitness for duty in aviation and transportation

Study Objectives: The psychomotor vigilance task (PVT) is a widely used objective method to measure sustained attention, but the standard 10-min version is often impractical in operational settings. We investigated the reliability and validity of a 3-min PVT administered on a portable handheld device assessing sensitivity to sleep loss and alcohol in relation to a 10-min PVT and to applied tasks. Methods: A total of 47 healthy volunteers underwent a 12 consecutive days sleep lab protocol. A cross-over design was adopted including total sleep deprivation (38 h awake), sleep restriction (SR, 4 h sleep opportunity), acute alcohol consumption, and SR after alcohol intake (SR/Alc 4 h sleep opportunity). Participants performed a 10-min and 3-min PVT and operationally relevant tasks related to demands in aviation and transportation. Results: Sleep loss resulted in significant performance impairments compared with baseline measurements detected by both PVT versions—particularly for mean speed (both p < 0.001)—and the operationally relevant tasks. Similar effects were observed due to alcohol intake (speed: both p < 0.001). The 3-min and 10-min PVT results were highly correlated (speed: between r = 0.72 and r = 0.89). Three of four aviation-related tasks showed robust correlations with the 3-min PVT. Correlations with the parameters of the task related to transportation were lower, but mainly significant. Conclusion: The 3-min PVT showed a high reliability and validity in assessing sleep loss and alcohol-induced impairments in cognitive performance. Thus, our results underline its usefulness as potential fitness for duty self-monitoring tool in applied settings

Total Sleep Deprivation Increases Brain Age Prediction Reversibly in Multisite Samples of Young Healthy Adults

Sleep loss pervasively affects the human brain at multiple levels. Age-related changes in several sleep characteristics indicate that reduced sleep quality is a frequent characteristic of aging. Conversely, sleep disruption may accelerate the aging process, yet it is not known what will happen to the age status of the brain if we can manipulate sleep conditions. To tackle this question, we used an approach of brain age to investigate whether sleep loss would cause age-related changes in the brain. We included MRI data of 134 healthy volunteers (mean chronological age of 25.3 between the age of 19 and 39 years, 42 females/92 males) from five datasets with different sleep conditions. Across three datasets with the condition of total sleep deprivation (>24 h of prolonged wakefulness), we consistently observed that total sleep deprivation increased brain age by 1–2 years regarding the group mean difference with the baseline. Interestingly, after one night of recovery sleep, brain age was not different from baseline. We also demonstrated the associations between the change in brain age after total sleep deprivation and the sleep variables measured during the recovery night. By contrast, brain age was not significantly changed by either acute (3 h time-in-bed for one night) or chronic partial sleep restriction (5 h time-in-bed for five continuous nights). Together, the convergent findings indicate that acute total sleep loss changes brain morphology in an aging-like direction in young participants and that these changes are reversible by recovery sleep

ADORA2A variation and adenosine A 1 receptor availability in the human brain with a focus on anxiety-related brain regions: modulation by ADORA1 variation

Adenosine, its interacting A1 and A2A receptors, and particularly the variant rs5751876 in the A2A gene ADORA2A have been shown to modulate anxiety, arousal, and sleep. In a pilot positron emission tomography (PET) study in healthy male subjects, we suggested an effect of rs5751876 on in vivo brain A1 receptor (A1AR) availability. As female sex and adenosinergic/dopaminergic interaction partners might have an impact on this rs5751876 effect on A1AR availability, we aimed to (1) further investigate the pilot male-based findings in an independent, newly recruited cohort including women and (2) analyze potential modulation of this rs5751876 effect by additional adenosinergic/dopaminergic gene variation. Healthy volunteers (32/11 males/females) underwent phenotypic characterization including self-reported sleep and A1AR-specific quantitative PET. Rs5751876 and 31 gene variants of adenosine A1, A2A, A2B, and A3 receptors, adenosine deaminase, and dopamine D2 receptor were genotyped. Multivariate analysis revealed an rs5751876 effect on A1AR availability (P = 0.047), post hoc confirmed in 30 of 31 brain regions (false discovery rate (FDR) corrected P values < 0.05), but statistically stronger in anxiety-related regions (e.g., amygdala, hippocampus). Additional effects of ADORA1 rs1874142 were identified; under its influence rs5751876 and rs5751876 × sleep had strengthened effects on A1AR availability (Pboth < 0.02; post hoc FDR-corrected Ps < 0.05 for 29/30 regions, respectively). Our results support the relationship between rs5751876 and A1AR availability. Additional impact of rs1874142, together with rs5751876 and sleep, might be involved in regulating arousal and thus the development of mental disorders like anxiety disorders. The interplay of further detected suggestive ADORA2A × DRD2 interaction, however, necessitates larger future samples more comparable to magnetic resonance imaging (MRI)-based samples

Effect of aging on cerebral A1 adenosine receptors: A [18F]CPFPX study in humans

Cerebral A(1) adenosine receptors (A(1)AR) fulfill important neuromodulatory and homeostatic functions. The present study examines possible age-related A(1)AR changes in living humans by positron emission tomography (PET) and the A(1)AR ligand [(18)F]CPFPX. Thirty-six healthy volunteers aged 22-74 years were included. The apparent binding potential (BP'2) of [(18)F]CPFPX in various cerebral regions was calculated non-invasively using the cerebellum as reference region. In addition, the total distribution volume (DV't) was assessed in 10 subjects undergoing arterial blood sampling. There was no significant association between regional DV't and age, gender, caffeine consumption or sleep duration. BP'2 showed a significant age-dependent decrease in all regions except cingulate gyrus (p=0.062). The BP'2 decline ranged from -17% (striatum) to -34% (postcentral gyrus), the average cortical decline being -23%. There was no significant effect of gender, caffeine consumption and sleep duration on BP'2. In line with in vitro animal studies, the present in vivo PET study detected an age-dependent A(1)AR loss in humans that may be of pathophysiological importance in various neurological diseases associated with aging. Because of the discrepant results of the invasive (DV't) and the non-invasive (BP'2) analyses the present study needs further validation