Biometrics

Biometrics uses methods for unique recognition of humans based upon one or more intrinsic physical or behavioral traits. In computer science, particularly, biometrics is used as a form of identity access management and access control. It is also used to identify individuals in groups that are under surveillance. The book consists of 13 chapters, each focusing on a certain aspect of the problem. The book chapters are divided into three sections: physical biometrics, behavioral biometrics and medical biometrics. The key objective of the book is to provide comprehensive reference and text on human authentication and people identity verification from both physiological, behavioural and other points of view. It aims to publish new insights into current innovations in computer systems and technology for biometrics development and its applications. The book was reviewed by the editor Dr. Jucheng Yang, and many of the guest editors, such as Dr. Girija Chetty, Dr. Norman Poh, Dr. Loris Nanni, Dr. Jianjiang Feng, Dr. Dongsun Park, Dr. Sook Yoon and so on, who also made a significant contribution to the book

Rôle du TRPV1 dans la régulation cardio-protectrices des voies de signalisation locale et distale

L'insuffisance cardiaque (IC) est l'une des principales causes de décès dans le monde. Les maladies cardiovasculaires sont devenues une préoccupation majeure de santé publique et le resteront probablement à l'avenir avec le vieillissement de la population et l'augmentation du taux de survie des patients atteints de maladies cardiovasculaires. L'infarctus du myocarde (IM) est le principal facteur de risque favorisant le développement de l’IC. L'une des principales caractéristiques de l'IC est une dérégulation du fonctionnement du système nerveux autonome (SNA), en particulier une hyperactivité du système nerveux sympathique (SNS) qui contribue largement à la progression de la maladie et à l'augmentation de la morbidité. Le mécanisme de l'hyperactivité du SNS n'est que partiellement connu. En ce qui concerne la progression de l'IM à l'IC, des études suggèrent un engagement concerté du cerveau (médulla), du nerf vague et des nerfs sympathiques, en plus du tissu cardiaque qui serait à l'origine de la maladie systémique. En plus des altérations du SNA, des exemples de comorbidités de l'IC comprennent des troubles cognitifs tel que l’anxiété et la dépression ainsi que des modifications atrophiques des régions cérébrales chez les patients atteints d'IC. L’ensemble, de ces données montrent l'importance du système nerveux central et périphérique dans l'IC. En plus du système nerveux cardiaque intrinsèque, qui comprend un réseau de ganglions intracardiaques et de neurones interconnectés, le coeur, en particulier l'épicarde, possède des milliers de neurones intégrés, dont beaucoup expriment le récepteur vanilloïde 1 (TRPV1). Au cours des dernières années, des études scientifiques ont montré que l'application épicardique de résinifératoxine (RTX), un agoniste spécifique de TRPV1, au moment de l'IM induit, conduit à une réduction de la fibrose cardiaque, prévient l'hyperactivation du SNS et améliore la fonction cardiaque dans plusieurs modèles. La thèse visait à mieux caractériser la fonction de ces fibres exprimant TRPV1 dans l'IM et l'IC qui en découle. Les principaux objectifs de présente étude sont les suivants : 1) Identifier si les fibres épicardiques exprimant TRPV1 entraînent des modifications des fonctions cérébrales. 2) Élucider les mécanismes moléculaires sous-jacents dans les tissus du système nerveux en aval des traitements IM et RTX en utilisant la protéomique ; et 3) Déterminer si les stimuli nociceptifs dans un modèle alternatif, C. elegans, via la modulation des récepteurs vanilloïdes orthologues par RTX, peuvent entraîner une modification du comportement et des mécanismes moléculaires associés aux effets induits par l'exposition à RTX. Pour répondre à ces 4 objectifs, nous avons combiné la dénervation des afférences sympathiques cardiaques, via l'application épicardique de RTX, avec un modèle IM validé. Des études comportementales ont été menées pour évaluer la dépression et l'anxiété des animaux après le début de l’IC. L'analyse protéomique a été réalisée sur plusieurs tissus dont le cortex frontal, le ventricule gauche, le bulbe rachidien (médulla), la moelle épinière et le nerf vague. Les principaux résultats de cette thèse ont montré que la dénervation afférente cardiaque sympathique par RTX atténue le remodelage cardiaque et restaure la fonction cardiaque lors d’un IM dans un modèle murin. L'analyse comportementale a démontré que les souris IM sont déprimées et anxieuses et que le traitement RTX réduit significativement l'expression du phénotype anxieux. La protéomique réalisée sur des cortex frontaux isolés a identifié des signatures protéiques uniques pour chacun des groupes (IM, RTX et IM/RTX), indiquant des voies partagées et uniques attribuées par IM et RTX. Les analyses bio-informatiques ont montré un enrichissement significatif des voies métaboliques dans tous les tissus et traitements, et à tout moment, suggérant un rôle central de la fonction mitochondriale après les traitements IM et RTX. Des voies fonctionnelles enrichies dans ces tissus, y compris le cytosquelette, les vésicules et la transduction du signal, peuvent être en aval des réponses initiées par les mitochondries en raison de modifications du taux d'impulsion neuronale après un IM ou d'une altération de la communication coeur-cerveau après l'application de RTX. Certaines voies et molécules communes ont aussi été observées chez C. elegans, comme la voie de signalisation de Wnt, ce qui suggère des effets semblable de RTX. La thèse contribue à une meilleure compréhension des mécanismes physiologiques des nerfs exprimant TRPV1 et offre des informations clés pour comprendre les mécanismes sous-jacents aux troubles neurologiques d'origine cardiaque. Le modèle de C. elegans peut servir de futur modèle pour tester des molécules pharmacologiquement actives pour de futures thérapeutiques.Heart failure (HF) is one of the leading causes of death worldwide. Cardiovascular diseases are therefore becoming a major health problem and will probably continue to be so in the future with the aging of the population and the increase in the survival rate of patients with cardiovascular disease. Myocardial infarction (MI) is the main risk factor for developing HF. One of the prominent features of HF is a dysregulation in the functioning of the autonomic nervous system (ANS), in particular a sympathetic nervous system (SNS) hyperactivity that largely contributes to disease progression and increased morbidity. The mechanism for the SNS hyperactivity is only partially known. Regarding the progression from MI to HF, studies suggest a concerted engagement of the brain (medulla oblongata), the vagus nerve and the sympathetic nerves, in addition to cardiac tissue that are thought to instigate systemic disease. In addition to the alterations in the ANS, examples of HF comorbidities include cognitive impairment and atrophic changes in brain regions in HF patients. Together these data show the importance of the central and peripheral nervous system in HF. In addition to the intrinsic cardiac nervous system, which includes a network of intracardiac ganglia and interconnecting neurons, the heart, especially the epicardium, has thousands of embedded neurons, many of which express the transient receptor potential cation channel subfamily V member 1 (TRPV1). Over recent years studies have shown that the epicardial application of resiniferatoxin (RTX), a specific agonist of TRPV1, at the time of induced MI, leads to a reduction of cardiac fibrosis, prevents hyperactivation of the SNS and improves the heart function in several model systems. The thesis was aimed to better characterize the function of these TRPV1-positive fibers in MI and resulting HF. The main objectives of the current study were : 1) To identify whether the TRPV1 expressing epicardial fibers lead to changes in brain activity and function. 2) To elucidate the underlying molecular mechanisms in nervous system tissue downstream from MI and RTX treatments using proteomics; and 3) To determine if nociceptive stimuli in an alternate model, C. elegans, via the modulation of orthologous vanilloid receptors by RTX, can lead to altered behavior and molecular mechanisms associated with RTX exposureinduced effects. To meet these objectives, we combined denervation of cardiac sympathetic afferents, via epicardial application of RTX, with a validated MI model. Behavioral studies were carried out to evaluate the depression and anxiety of the animals after the onset of HFt. Proteomic 6 analysis was carried out on several tissues including the frontal cortex, left ventricle, medulla oblangata, spinal cord, and vagus nerve. The major findings of this thesis are that sympathetic cardiac afferent denervation by RTX attenuates cardiac remodeling and restores cardiac function during MI in a mouse model. Behavioral analysis demonstrated that MI mice are depressed and anxious and that RTX treatment significantly reduced the expression of the anxious phenotype. Proteomics performed on isolated frontal cortices identified unique protein signatures for each of the groups (MI, RTX and MI/RTX), indicating shared and unique pathways attributed by MI and RTX. Bioinformatic analyses showed a significant enrichment for metabolic pathways in all tissues and treatments, and at all time points, suggesting a central role of mitochondria function following MI and RTX treatments. Enriched functional pathways in these tissues, including cytoskeleton, vesicles, and signal transduction, may be downstream of mitochondria-initiated responses due to changes in neural impulse rate after MI or altered heart-brain communication following RTX application. Some common pathways and molecules were observed in C. elegans, such as the Wnt signaling pathway, suggesting similar effects of RTX. The current thesis contributes to a better understanding of the physiological mechanisms of the TRPV1 expressing nerves and offers key information to understand the mechanisms underlying neurological disorders of cardiac origin. The C. elegans model may serve as a future model for testing pharmacologically active molecules for future therapeutics

Quantifying Quality of Life

Describes technological methods and tools for objective and quantitative assessment of QoL Appraises technology-enabled methods for incorporating QoL measurements in medicine Highlights the success factors for adoption and scaling of technology-enabled methods This open access book presents the rise of technology-enabled methods and tools for objective, quantitative assessment of Quality of Life (QoL), while following the WHOQOL model. It is an in-depth resource describing and examining state-of-the-art, minimally obtrusive, ubiquitous technologies. Highlighting the required factors for adoption and scaling of technology-enabled methods and tools for QoL assessment, it also describes how these technologies can be leveraged for behavior change, disease prevention, health management and long-term QoL enhancement in populations at large. Quantifying Quality of Life: Incorporating Daily Life into Medicine fills a gap in the field of QoL by providing assessment methods, techniques and tools. These assessments differ from the current methods that are now mostly infrequent, subjective, qualitative, memory-based, context-poor and sparse. Therefore, it is an ideal resource for physicians, physicians in training, software and hardware developers, computer scientists, data scientists, behavioural scientists, entrepreneurs, healthcare leaders and administrators who are seeking an up-to-date resource on this subject

Quantifying Quality of Life

Describes technological methods and tools for objective and quantitative assessment of QoL Appraises technology-enabled methods for incorporating QoL measurements in medicine Highlights the success factors for adoption and scaling of technology-enabled methods This open access book presents the rise of technology-enabled methods and tools for objective, quantitative assessment of Quality of Life (QoL), while following the WHOQOL model. It is an in-depth resource describing and examining state-of-the-art, minimally obtrusive, ubiquitous technologies. Highlighting the required factors for adoption and scaling of technology-enabled methods and tools for QoL assessment, it also describes how these technologies can be leveraged for behavior change, disease prevention, health management and long-term QoL enhancement in populations at large. Quantifying Quality of Life: Incorporating Daily Life into Medicine fills a gap in the field of QoL by providing assessment methods, techniques and tools. These assessments differ from the current methods that are now mostly infrequent, subjective, qualitative, memory-based, context-poor and sparse. Therefore, it is an ideal resource for physicians, physicians in training, software and hardware developers, computer scientists, data scientists, behavioural scientists, entrepreneurs, healthcare leaders and administrators who are seeking an up-to-date resource on this subject

New insights on the multidimensionality of fatigue and on its relationship with cognitive impairments in multiple sclerosis

Multiple Sclerosis (MS) is an inflammatory disease of the central nervous system (CNS), and it represents the most common cause of irreversible impairment in young adults, affecting about 2.5 million individuals worldwide. In MS, acute attacks of inflammation, leading to demyelination and axonal loss, determine the accumulation of disabilities, varying in number, nature, and severity. Indeed, motor, sensory, cognitive, and behavioral symptoms may manifest at different times during the disease's variable clinical course. Fatigue is a complex and multifaceted phenomenon and one of the most prevalent and disabling symptoms of MS, affecting 75%–90% of patients. Despite its prevalence, MS- related fatigue is still poorly understood. The absence of a well-validated definition and of clear insights into its pathophysiological causes makes fatigue a hybrid symptom, approached within the context of different disciplines, each with their own methods and tools. As a result, the scientific literature abounds with irreconcilable data, leaving fatigue in a dark shadow zone, at the expense of MS patients still lacking adequate therapies and strategies of management. The main topic of this thesis relates to the multidimensional nature of fatigue, to its variability, and its effects on attentional processes, most commonly affected in MS patients. Specifically, studies presented in the current thesis address four research issues: (i) are physical and mental fatigue two distinct constructs? (ii) how do physical and mental fatigue vary within a short (within a day) and long (within a year) period? (iii) how do induced physical and mental fatigue impact the attentional functions of alerting, orienting, and conflict resolution in MS? The main results of the studies are reported: a) A clear distinction between physical and mental fatigue has been psychometrically documented in MS patients. b) MS patients reported experiencing more overall fatigue than Controls. c) A gradual increase in overall fatigue from the morning to the evening was reported by MS participants. d) Across experiments physical fatigue was significantly more pronounced in MS patients as compared to Controls. e) Both MS patients and Controls reported having experienced more overall fatigue in the past (one year ago) than in the present (the last 24 hours). f) MS patients were slower as compared to Controls in performing attentional tasks; however, inconclusive results have emerged regarding the effects of physical and mental fatigue on attentional processes. g) Sleep quality and depression were both associated with fatigue across the experiments. The relationship between self-efficacy, general cognitive functioning, functional deterioration, and physical and mental fatigue is fragmented, thus preventing a clear conclusion

Research and technology operating plan: A summary Fiscal Year 1974

A compilation is presented of the summary portions of RTOPs used for management review and control of research. Citations and abstracts of RTOPs are included. A list is presented of RTOPs which have been changed, completed, or terminated since the last summary. Indexes presented include: subject, technical monitor, responsible NASA organization, and RTOP number

Foundations and applications of human-machine-interaction

Der vorliegende Tagungsband zur 10. Berliner Werkstatt Mensch-Maschine-Systeme gibt einen Einblick in die aktuelle Forschung im Bereich der Mensch-Maschine- Interaktion. Einen besonderen Fokus stellt das Wechselspiel von Grundlagenforschung und anwendungsbezogener Forschung dar, was sich im breiten Themenspektrum widerspiegelt, welches von theoretischen und methodischen Betrachtungen bis hin zu anwendungsnahen Fragestellungen reicht. Dabei finden Inhalte aus allen Phasen des Forschungsprozesses Beachtung, sodass auch im Rahmen der 10. Berliner Werkstatt MMS wieder sowohl neue Untersuchungskonzepte als auch abschließende Befunde diskutiert werden. Zentrale Themengebiete sind u. a. Fahrer-Fahrzeug-Interaktion, Assistenzsysteme, User Experience, Usability, Ubiquitous Computing, Mixed & Virtual Reality, Robotics & Automation, Wahrnehmungsspezifika sowie Psychophysiologie und Beanspruchung in der Mensch-Maschine-Interaktion.The proceedings of the 10th Berlin Workshop Human-Machine-Systems provide an insight into the current research in the field of human-machine-interaction. The main focus lies on the interplay between basic and applied research, which is reflected in the wide range of subjects: from theoretical and methodological issues to application oriented considerations. Again all stages of the research process are represented in the contributions of the 10th Berlin Workshop HMS. This means new research concepts as well as final results are subject of this volume. Central topics include driver-vehicleinteraction, assistance systems, user experience, usability, ubiquitous computing, mixed and virtual reality, robotics & automation, perception specifics, as well as psychophysiology and workload in human-machine-interaction