37 research outputs found

    SAFECAR: A Brain–Computer Interface and intelligent framework to detect drivers’ distractions

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    As recently reported by the World Health Organization (WHO), the high use of intelligent devices such as smartphones, multimedia systems, or billboards causes an increase in distraction and, consequently, fatal accidents while driving. The use of EEG-based Brain–Computer Interfaces (BCIs) has been proposed as a promising way to detect distractions. However, existing solutions are not well suited for driving scenarios. They do not consider complementary data sources, such as contextual data, nor guarantee realistic scenarios with real-time communications between components. This work proposes an automatic framework for detecting distractions using BCIs and a realistic driving simulator. The framework employs different supervised Machine Learning (ML)-based models on classifying the different types of distractions using Electroencephalography (EEG) and contextual driving data collected by car sensors, such as line crossings or objects detection. This framework has been evaluated using a driving scenario without distractions and a similar one where visual and cognitive distractions are generated for ten subjects. The proposed framework achieved 83.9% -score with a binary model and 73% with a multiclass model using EEG, improving 7% in binary classification and 8% in multi-class classification by incorporating contextual driving into the training dataset. Finally, the results were confirmed by a neurophysiological study, which revealed significantly higher voltage in selective attention and multitasking

    Decentralized Federated Learning: Fundamentals, State-of-the-art, Frameworks, Trends, and Challenges

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    In the last decade, Federated Learning (FL) has gained relevance in training collaborative models without sharing sensitive data. Since its birth, Centralized FL (CFL) has been the most common approach in the literature, where a central entity creates a global model. However, a centralized approach leads to increased latency due to bottlenecks, heightened vulnerability to system failures, and trustworthiness concerns affecting the entity responsible for the global model creation. Decentralized Federated Learning (DFL) emerged to address these concerns by promoting decentralized model aggregation and minimizing reliance on centralized architectures. However, despite the work done in DFL, the literature has not (i) studied the main aspects differentiating DFL and CFL; (ii) analyzed DFL frameworks to create and evaluate new solutions; and (iii) reviewed application scenarios using DFL. Thus, this article identifies and analyzes the main fundamentals of DFL in terms of federation architectures, topologies, communication mechanisms, security approaches, and key performance indicators. Additionally, the paper at hand explores existing mechanisms to optimize critical DFL fundamentals. Then, the most relevant features of the current DFL frameworks are reviewed and compared. After that, it analyzes the most used DFL application scenarios, identifying solutions based on the fundamentals and frameworks previously defined. Finally, the evolution of existing DFL solutions is studied to provide a list of trends, lessons learned, and open challenges

    L-arginine ameliorates defective autophagy in GM2 gangliosidoses by mTOR modulation

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    Aims: Tay–Sachs and Sandhoff diseases (GM2 gangliosidosis) are autosomal recessive disorders of lysosomal function that cause progressive neurodegeneration in infants and young children. Impaired hydrolysis catalysed by β-hexosaminidase A (HexA) leads to the accumulation of GM2 ganglioside in neuronal lysosomes. Despite the storage phenotype, the role of autophagy and its regulation by mTOR has yet to be explored in the neuropathogenesis. Accordingly, we investigated the effects on autophagy and lysosomal integrity using skin fibroblasts obtained from patients with Tay–Sachs and Sandhoff diseases. Results: Pathological autophagosomes with impaired autophagic flux, an abnormality confirmed by electron microscopy and biochemical studies revealing the accelerated release of mature cathepsins and HexA into the cytosol, indicating increased lysosomal permeability. GM2 fibroblasts showed diminished mTOR signalling with reduced basal mTOR activity. Accordingly, provision of a positive nutrient signal by L-arginine supplementation partially restored mTOR activity and ameliorated the cytopathological abnormalities. Innovation: Our data provide a novel molecular mechanism underlying GM2 gangliosidosis. Impaired autophagy caused by insufficient lysosomal function might represent a new therapeutic target for these diseases. Conclusions: We contend that the expression of autophagy/lysosome/mTOR-associated molecules may prove useful peripheral biomarkers for facile monitoring of treatment of GM2 gangliosidosis and neurodegenerative disorders that affect the lysosomal function and disrupt autophagy

    Hydroxytyrosol Supplementation Modifies Plasma Levels of Tissue Inhibitor of Metallopeptidase 1 in Women with Breast Cancer

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    The etiology of breast cancer can be very different. Most antineoplastic drugs are not selective against tumor cells and also affect normal cells, leading to a wide variety of adverse reactions such as the production of free radicals by altering the redox state of the organisms. Therefore, the objective of this study was to elucidate if hydroxytyrosol (HT) (an antioxidant present in extra virgin olive oil) has a chemomodulatory effect when combined with the chemotherapeutic drugs epirubicin and cyclophosphamide followed by taxanes in breast cancer patients. Changes in plasma levels of matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinases 1 (TIMP-1) throughout the chemotherapy treatment were studied. Both molecules are involved in cell proliferation, apoptosis, neoangiogenesis, and metastasis in breast cancer patients. Women with breast cancer were divided into two groups: a group of patients receiving a dietary supplement of HT and a control group of patients receiving placebo. The results showed that the plasma levels of TIMP-1 in the group of patients receiving HT were significantly lower than those levels found in the control group after the epirubicin-cyclophosphamide chemotherapy.This research was funded by Junta de Andalucía, Spain, Servicio Andaluz de Salud: Subvenciones para la financiacion de la Investigación, Desarrollo, e Innovación Biomédica en Ciencias de la Salud en Biomedicina, Grant number PI-0695-2012

    L-Arginine Ameliorates Defective Autophagy in GM2 Gangliosidoses by mTOR Modulation.

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    AIMS: Tay-Sachs and Sandhoff diseases (GM2 gangliosidosis) are autosomal recessive disorders of lysosomal function that cause progressive neurodegeneration in infants and young children. Impaired hydrolysis catalysed by β-hexosaminidase A (HexA) leads to the accumulation of GM2 ganglioside in neuronal lysosomes. Despite the storage phenotype, the role of autophagy and its regulation by mTOR has yet to be explored in the neuropathogenesis. Accordingly, we investigated the effects on autophagy and lysosomal integrity using skin fibroblasts obtained from patients with Tay-Sachs and Sandhoff diseases. RESULTS: Pathological autophagosomes with impaired autophagic flux, an abnormality confirmed by electron microscopy and biochemical studies revealing the accelerated release of mature cathepsins and HexA into the cytosol, indicating increased lysosomal permeability. GM2 fibroblasts showed diminished mTOR signalling with reduced basal mTOR activity. Accordingly, provision of a positive nutrient signal by L-arginine supplementation partially restored mTOR activity and ameliorated the cytopathological abnormalities. INNOVATION: Our data provide a novel molecular mechanism underlying GM2 gangliosidosis. Impaired autophagy caused by insufficient lysosomal function might represent a new therapeutic target for these diseases. CONCLUSIONS: We contend that the expression of autophagy/lysosome/mTOR-associated molecules may prove useful peripheral biomarkers for facile monitoring of treatment of GM2 gangliosidosis and neurodegenerative disorders that affect the lysosomal function and disrupt autophagy

    NLRP3 inflammasome suppression improves longevity and prevents cardiac aging in male mice

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    While NLRP3‐inflammasome has been implicated in cardiovascular diseases, its role in physiological cardiac aging is largely unknown. During aging, many alterations occur in the organism, which are associated with progressive impairment of metabolic pathways related to insulin resistance, autophagy dysfunction, and inflammation. Here, we investigated the molecular mechanisms through which NLRP3 inhibition may attenuate cardiac aging. Ablation of NLRP3‐inflammasome protected mice from age‐related increased insulin sensitivity, reduced IGF‐1 and leptin/adiponectin ratio levels, and reduced cardiac damage with protection of the prolongation of the agedependent PR interval, which is associated with atrial fibrillation by cardiovascular aging and reduced telomere shortening. Furthermore, old NLRP3 KO mice showed an inhibition of the PI3K/AKT/mTOR pathway and autophagy improvement, compared with old wild mice and preserved Nampt‐mediated NAD+ levels with increased SIRT1 protein expression. These findings suggest that suppression of NLRP3 prevented many age‐associated changes in the heart, preserved cardiac function of aged mice and increased lifespan.Andalusian regional government; Consejería de Salud de la Junta de Andalucia, Grant/ Award Number: PI‐0036‐2014; Ministerio de economía y competitividad, Grant/Award Number: SAF2017‐84494‐C2‐1‐

    Measurement of the charge asymmetry in top-quark pair production in the lepton-plus-jets final state in pp collision data at s=8TeV\sqrt{s}=8\,\mathrm TeV{} with the ATLAS detector

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    ATLAS Run 1 searches for direct pair production of third-generation squarks at the Large Hadron Collider

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    Breaching Subjects’ Thoughts Privacy: A Study with Visual Stimuli and Brain-Computer Interfaces

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    Brain-computer interfaces (BCIs) started being used in clinical scenarios, reaching nowadays new fields such as entertainment or learning. Using BCIs, neuronal activity can be monitored for various purposes, with the study of the central nervous system response to certain stimuli being one of them, being the case of evoked potentials. However, due to the sensitivity of these data, the transmissions must be protected, with blockchain being an interesting approach to ensure the integrity of the data. This work focuses on the visual sense, and its relationship with the P300 evoked potential, where several open challenges related to the privacy of subjects’ information and thoughts appear when using BCI. The first and most important challenge is whether it would be possible to extract sensitive information from evoked potentials. This aspect becomes even more challenging and dangerous if the stimuli are generated when the subject is not aware or conscious that they have occurred. There is an important gap in this regard in the literature, with only one work existing dealing with subliminal stimuli and BCI and having an unclear methodology and experiment setup. As a contribution of this paper, a series of experiments, five in total, have been created to study the impact of visual stimuli on the brain tangibly. These experiments have been applied to a heterogeneous group of ten subjects. The experiments show familiar visual stimuli and gradually reduce the sampling time of known images, from supraliminal to subliminal. The study showed that supraliminal visual stimuli produced P300 potentials about 50% of the time on average across all subjects. Reducing the sample time between images degraded the attack, while the impact of subliminal stimuli was not confirmed. Additionally, younger subjects generally presented a shorter response latency. This work corroborates that subjects’ sensitive data can be extracted using visual stimuli and P300

    Noise-based cyberattacks generating fake P300 waves in brain–computer interfaces

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    Most of the current Brain–Computer Interfaces (BCIs) application scenarios use electroencephalographic signals (EEG) containing the subject’s information. It means that if EEG were maliciously manipulated, the proper functioning of BCI frameworks could be at risk. Unfortunately, it happens in frameworks sensitive to noise-based cyberattacks, and more efforts are needed to measure the impact of these attacks. This work presents and analyzes the impact of four noise-based cyberattacks attempting to generate fake P300 waves in two different phases of a BCI framework. A set of experiments show that the greater the attacker’s knowledge regarding the P300 waves, processes, and data of the BCI framework, the higher the attack impact. In this sense, the attacker with less knowledge impacts 1% in the acquisition phase and 4% in the processing phase, while the attacker with the most knowledge impacts 22% and 74%, respectively
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