A Short Window Granger Causality Approach to Identify Brain Functional Pattern Associated with Changes of Performance Induced by Sleep Deprivation

The comprehensive effect of sleep deprivation on biological and behavioral functions largely remains unknown. There is evidence to support that human sleep must be of sufficient duration and physiological continuity to ensure neurocognitive performance while we are waking. Insufficient sleep would lead to high risk of human-error related to accidents, injuries or even fatal outcomes. However, in modern society, more and more people suffer from sleep deprivation because of the increasing social, academic or occupational demand. It is important to study the effect of sleep deprivation, not only on task performance, but also on neurocognitive functions. Recent research that has explored brain effective connectivity has demonstrated the directed inference interaction among pairs of brain areas, which may bring important insight to understand how brain works to support neurocognitive function. This research aimed to identify the brain effective connectivity pattern associated with changes of a task performance, response time, following sleep deprivation. Experiments were conducted by colleagues at Neuroergonomics Department at Jagiellonian University, Krakow, Poland. Ten healthy young women, with an average age of 23-year-old, performed visual spatial sustained-attention tasks under two conditions: (1) the rest-wakeful (RW) condition, where participants had their usual sleep and (2) the sleep-deprived (SD) condition, where participants had 3 hours less sleep than their usual sleep, for 7 nights (amounting to 21 h of sleep debt). Measures included eye tracking performance and functional magnetic resonance imaging (fMRI). In each condition, each subject*s eye-position was monitored through 13 sessions, each with 46 trials, while fMRI data was recorded. There were two task performance measures, accuracy and response time. Accuracy measured the proportion of correct responses of all trials in each session. Response time measured the average amount of milliseconds until participants gazed at the target stimuli in each session. An experimental session could be treated as a short window. By splitting long trials of fMRI data into consecutive windows, Granger causality was applied based on short trials of fMRI data. This procedure helped to calculate pairwise causal influences with respect to time-varying property in brain causal interaction. Causal influence results were then averaged across sessions to create one matrix for each participant. This matrix was averaged within each condition to formulate a model of brain effective connectivity, which also served as a basis of comparison. In conclusion, significant effect of sleep deprivation was found on response time and brain effective connectivity. In addition, the change of brain effective connectivity after sleep deprivation was linked to the change of response time. First, an analysis of variance (ANOVA) showed significant difference for response time between the RW condition and the SD condition. No significant changes for accuracy were found. A paired t-test showed that response time was significantly shorter in sleep deprivation for the visual spatial sustained-attention task. Second, Granger causality analysis demonstrated a reduction of bidirectional connectivity and an increase of directed influences from low-level brain areas to high-level brain areas after sleep deprivation. This observation suggested that sleep deprivation provoked the effective connectivity engaged in salient stimuli processing, but inhibited the effective connectivity in biasing selection of attention on task and in maintaining self-awareness in day time. Furthermore, in the SD condition, attention at the visual spatial task seemed to be driven by a bottom-up modulation mechanism. Third, a relationship was found between brain effective connectivity with response time. Decreases of Granger causal influences in two directions, from medial frontal lobe to sub cortical gray nuclei and from medial parietal lobe to sub cortical gray nuclei, were associated with shorter response time in the SD condition. Additionally, an increase of Granger causal influence from medial parietal lobe to cerebellum was associated with longer response time in the SD condition

2-D Compass Codes

The compass model on a square lattice provides a natural template for building subsystem stabilizer codes. The surface code and the Bacon-Shor code represent two extremes of possible codes depending on how many gauge qubits are fixed. We explore threshold behavior in this broad class of local codes by trading locality for asymmetry and gauge degrees of freedom for stabilizer syndrome information. We analyze these codes with asymmetric and spatially inhomogeneous Pauli noise in the code capacity and phenomenological models. In these idealized settings, we observe considerably higher thresholds against asymmetric noise. At the circuit level, these codes inherit the bare-ancilla fault-tolerance of the Bacon-Shor code.Comment: 10 pages, 7 figures, added discussion on fault-toleranc

Regulating Cytoplasmic Calcium Homeostasis Can Reduce Aluminum Toxicity in Yeast

Our previous study suggested that increased cytoplasmic calcium (Ca) signals may mediate aluminum (Al) toxicity in yeast (Saccharomyces cerevisiae). In this report, we found that a yeast mutant, pmc1, lacking the vacuolar calcium ion (Ca2+) pump Ca2+-ATPase (Pmc1p), was more sensitive to Al treatment than the wild-type strain. Overexpression of either PMC1 or an anti-apoptotic factor, such as Bcl-2, Ced-9 or PpBI-1, decreased cytoplasmic Ca2+ levels and rescued yeast from Al sensitivity in both the wild-type and pmc1 mutant. Moreover, pretreatment with the Ca2+ chelator BAPTA-AM sustained cytoplasmic Ca2+ at low levels in the presence of Al, effectively making the cells more tolerant to Al exposure. Quantitative RT-PCR revealed that the expression of calmodulin (CaM) and phospholipase C (PLC), which are in the Ca2+ signaling pathway, was down-regulated under Al stress. This effect was largely counteracted when cells overexpressed anti-apoptotic Ced-9 or were pretreated with BAPTA-AM. Taken together, our results suggest that the negative regulation of Al-induced cytoplasmic Ca signaling is a novel mechanism underlying internal resistance to Al toxicity