Selective auditory attention detection based on effective connectivity by single-trial EEG.
Focusing attention on one speaker in an environment with lots of speakers is one of the important abilities of the human auditory system. The temporal dynamics of the attention process and how the brain precisely performs this task are yet unknown. This paper proposes a new method for the selective auditory attention detection (SAAD) from single-trial EEG signals using the brain effective connectivity and complex network analysis for two groups of listeners attending to the left or right ear.Here, the connectivity matrices of all subjects obtained from the Granger causality method are used to extract different features. Then, by employing the processes of feature selection and optimization, an optimized feature set is determined for the train of a classifier.
Among different measures of brain connectivity (i.e., segregation, integration, and centrality), the evaluation results show that the optimized feature set obtained by the combination of the centrality measures contain the most discriminative features for the classification process. The proposed SAAD method as compared with state-of-the-art attention detection approaches from the literature yields the best performance in terms of various measures.The new SAAD approach is advantageous, in the sense that the detection of attention is performed from single-trial EEG signals of each subject, without reconstructing the speech stimuli. This means that the proposed method could be employed for real-time applications such as smart hearing aid devices or brain-computer interface (BCI) systems.
The protective effect of metformin on mitochondrial dysfunction and endoplasmic reticulum stress in diabetic mice brain.
Diabetes is a metabolic disorder associated with mitochondrial (mt) dysfunction and oxidative stress. The molecular mechanisms involved in diabetes-associated neurological complications remain elusive. This study aims to investigate the protective effect of metformin (MF) on regulatory networks and integrated stress responses in brain tissue of Streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice were treated with MF (20 mg/kg BW), and whole brain tissue was harvested for further analysis. Protein carbonylation was measured as a marker of neuronal oxidative stress.
Protein expression of mt chaperones, maintenance proteins, and regulators of the unfolded protein response (UPR) were measured by Western blot. Transcript levels of antioxidant enzyme GSTA4; mt biogenesis markers, ER stress regulators, and miR-132 and miR-148a were analysed using qPCR. The results showed that MF efficiently reduced protein carbonylation and oxidation. Mt function was improved by MF-treatment through upregulation of chaperone proteins (HSP60, HSP70 and LonP1). MF elicits the UPR to attenuate ER stress through a miR-132 repression mechanism. Additionally, MF was found to elevate deacetylases- Sirt1, Sirt3; and mt biogenesis marker PGC-1α through miR-148a repression.
This is the first study to demonstrate the epigenetic regulation of mt maintenance by MF in diabetic C57BL/6 mouse whole brain tissue. We thus conclude that MF, beyond its anti-hyperglycaemic role, mediates neuroprotection through epigenomic and integrated stress responses in diabetic mice.
Oral glutathione administration inhibits the oxidative stress and the inflammatory responses in AppNL-G-F/NL-G-F knock-in mice.
Alzheimer’s disease (AD) is the most common neurodegenerative disease characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles. Reduced antioxidants and increased oxidative stress and inflammation are responsible for the pathological features characteristic of an AD brain. We observed decreased levels of the reduced form of glutathione (GSH), the most abundant brain antioxidant, and decreased GSH/glutathione disulfide (GSSG) ratios in AppNL-G-F/NL-G-F knock-in (NL-G-F) mouse brains. Repeated oral GSH administration for 3 weeks dose-dependently increased GSH levels and restored the GSH/GSSH ratio. Consistent with the restoration of GSH levels, the levels of 4-hydroxy-2-nonenal (4-HNE), a marker of oxidative stress, were significantly decreased in the hippocampus of NL-G-F mice.
Additionally, inflammatory responses, such as microgliosis and increased mRNA expression of inflammatory cytokines, were also inhibited. Moreover, behavioral deficits including cognitive decline, depressive-like behaviors, and anxiety-related behaviors observed in NL-G-F mice were significantly improved by oral and chronic GSH administration. Taken together, our data suggest that oral GSH administration is an attractive therapeutic strategy to reduce the excessive oxidative stress and inflammatory responses in the AD brain.
Screening and Treatment of Obstetric Anemia: A Review of Clinical Effectiveness, Cost-Effectiveness, and Guidelines
Iron deficiency is a major cause of anemia.1 Other causes of anemia include deficiency in nutrients (e.g., vitamin B12 and folate), inflammation, parasitic infections and disorders in hemoglobin (Hb) synthesis or red blood cell production and survival (e.g., hemoglobinopathies).
1 Iron deficiency anemia is defined as blood Hb concentrations of less than 110 g/L in the first trimester, less than 105 g/L in the second and third trimesters of pregnancy, and less than 100 g/L postpartum.
2 The serum ferritin level provides information about the capacity of the body to reserve iron and its concentration of less than 15 µg/L (a cut off that is associated with higher specificity) during pregnancy is diagnostic of iron deficiency anemia.
2,3 A level of less than 30 µg/L of ferritin (a cut off that is associated with higher sensitivity) should prompt treatment.
2,3 However, serum ferritin measurement may not be accurate during infection or inflammation, as it can be normal or elevated despite a low Hb concentration.
1 Iron deficiency in pregnancy has significant negative effects on both maternal and fetal outcomes, including low birthweight, prematurity, perinatal mortality, increased risk of maternal infections and lowered tolerance to blood loss and infection.1 It also affects immediate and long term neurodevelopment of infants.
4 It was found that low maternal iron intake is associated with increased risk of autism, schizophrenia and abnormal brain structure in the offspring.
4 A review reported that findings from several cross-sectional studies suggested that the prevalence of iron deficiency among pregnant Canadians and pregnant adolescents ranged from 3% to 66%.5 Given the negative impacts of iron deficiency on maternal and child health, there is still uncertainty as whether screening of iron deficiency anemia in pregnancy should be part of routine care, and which type of testing (e.g., Hb or ferritin) is more effective to improve maternal and infant health outcomes. The aim of this report is to evaluate the clinical effectiveness and cost-effectiveness of screening obstetric iron deficiency in the first or second trimester using ferritin testing, and to review evidence-based guidelines for assessing and treating obstetric iron deficiency.
In this report, gender-neutral language has been used where possible in order to be inclusive of all gender identities. When reporting results from the published manuscript, gender-neutral language was not used in order to be consistent with the terms used in the source material. The Architecture of the Human Fovea
We summarize the development, structure, different neural types and neural circuitry in the human fovea. The foveal pit is devoid of rod photoreceptors and of secondary and tertiary neurons, allowing light to directly stimulate cones and give us maximal visual acuity. The circuitry underlying the transmission to the brain occurs at the rim of the fovea. The predominant circuitry is concerned with the ‘private’ cone to midget bipolar cell and midget ganglion cell pathways.
Every cone drives two midget bipolar cells and two midget ganglion cells so that the message from a single cone is provided to the brain as a contrast between lighter signals (ON pathways) or darker signals (OFF pathways). The sharpening of this contrast message is provided by horizontal-cell feedback circuits and, in some pathways by amacrine circuitry. These midget pathways carry a concentric color and spatially opponent message from red and green cones. Blue cones are sparse, even largely missing in the foveal center while occurring at somewhat higher density than elsewhere in the cone mosaic of the foveal slope. Signals from blue cones have different pathways to ganglion cells. The best understood is through an ON-type blue-cone-selecting bipolar cell to a non-midget, small bistratified ganglion cell.
An OFF-center blue midget bipolar is known to be present in the fovea and connects to a blue OFF midget ganglion cell. Another OFF blue message is sent to a giant melanopsin ganglion cell that is present in the foveal rim area, but the circuitry driving that is less certain and possibly involves an intermediate amacrine cell. The H2 horizontal cells are thought to be feedback neurons primarily of the blue cone system.
Amacrine cells of the fovea are mostly small-field and glycinergic. The larger field GABAergic amacrines are present but more typically surround the fovea in a ring of processes, with little or no penetration into the foveal center. Thus, the small field glycinergic amacrines are important in some sort of interplay with the midget bipolar–midget ganglion cell channels. We have anatomical descriptions of their synaptology but only a few have been recorded from physiologically. Both OFF pathway and ON pathway amacrines are present in the fovea.
Measuring water exchange across the blood-brain barrier using MRI.
The blood-brain barrier (BBB) regulates the transfer of solutes and essential nutrients into the brain. Growing evidence supports BBB dysfunction in a range of acute and chronic brain diseases, justifying the need for novel research and clinical tools that can non-invasively detect, characterize, and quantify BBB dysfunction in-vivo.
Many approaches already exist for measuring BBB dysfunction in man using positron emission tomography and magnetic resonance imaging (e.g. dynamic contrast-enhanced MRI measurements of gadolinium leakage).