\\n\\n
IntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\\n\\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\\n\\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\\n\\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\\n\\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\\n\\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\\n\\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\\n\\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\\n\\nFeel free to share this news on social media and help us mark this memorable moment!
\\n\\n\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/237"}},components:[{type:"htmlEditorComponent",content:'
After years of being acknowledged as the world's leading publisher of Open Access books, today, we are proud to announce we’ve successfully launched a portfolio of Open Science journals covering rapidly expanding areas of interdisciplinary research.
\n\n\n\nIntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\n\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\n\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\n\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\n\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\n\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\n\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\n\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\n\nFeel free to share this news on social media and help us mark this memorable moment!
\n\n\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"50",leadTitle:null,fullTitle:"Cancer Stem Cells Theories and Practice",title:"Cancer Stem Cells",subtitle:"Theories and Practice",reviewType:"peer-reviewed",abstract:"Cancer Stem Cells Theories and Practice does not 'boldly go where no one has gone before!' Rather, Cancer Stem Cells Theories and Practice boldly goes where the cutting edge of research theory meets the concrete challenges of clinical practice. Cancer Stem Cells Theories and Practice is firmly grounded in the latest results on cancer stem cells (CSCs) from world-class cancer research laboratories, but its twenty-two chapters also tease apart cancer's vulnerabilities and identify opportunities for early detection, targeted therapy, and reducing remission and resistance.",isbn:null,printIsbn:"978-953-307-225-8",pdfIsbn:"978-953-51-6426-5",doi:"10.5772/582",price:139,priceEur:155,priceUsd:179,slug:"cancer-stem-cells-theories-and-practice",numberOfPages:474,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"3407f8f3a110b5e2b9e11628c3dcfb18",bookSignature:"Stanley Shostak",publishedDate:"March 22nd 2011",coverURL:"https://cdn.intechopen.com/books/images_new/50.jpg",numberOfDownloads:82834,numberOfWosCitations:38,numberOfCrossrefCitations:14,numberOfCrossrefCitationsByBook:3,numberOfDimensionsCitations:34,numberOfDimensionsCitationsByBook:3,hasAltmetrics:0,numberOfTotalCitations:86,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 5th 2010",dateEndSecondStepPublish:"June 2nd 2010",dateEndThirdStepPublish:"September 7th 2010",dateEndFourthStepPublish:"November 6th 2010",dateEndFifthStepPublish:"January 20th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"28104",title:"Prof.",name:"Stanley",middleName:null,surname:"Shostak",slug:"stanley-shostak",fullName:"Stanley Shostak",profilePictureURL:"https://mts.intechopen.com/storage/users/28104/images/1561_n.jpg",biography:"For fifty years, I have studied the evolution of growth’s integration with form. Hydras’ ability to move excess cells into buds was my model for cancer’s ability to support metastasis (e.g., Vegetative reproduction by budding in Hydra: A perspective on tumors. Perspectives in Biology and Medicine, 20:545–68; 1977; “Hydra and cancer: Immortality and budding,” pp. 275-86 in C.J. Dawe, J.C. Harshbarger, S. Kondo, T. Sugimura, and S. Takayama, eds., Phyletic Approaches to Cancer. Tokyo: Sci. Soc. 1981). I have concentrated on the origins of stem cells (Symbiogenetic origins of cnidarian cnidocysts. Symbiosis, 19:1–29; 1995 [with V. Kolluri]; “Speculation on the Evolution of Stem Cells,” Breast Disease, 29:3–13; 2007–8) and have developed my ideas further in books (Evolution of Death: Why We Are Living Longer. Albany: SUNY Press; 2006; Becoming Immortal: Combining Cloning and Stem-Cell Therapy. Albany: SUNY Press; 2002; Evolution of Sameness and Difference: Perspectives on the Human Genome Project. Amsterdam: Harwood Academic Publishers, 1999; Death of Life: The Legacy of Molecular Biology. London: Macmillan, 1998).",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"2",institution:null}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1082",title:"Hemato-Oncology",slug:"medicine-oncology-hemato-oncology"}],chapters:[{id:"14457",title:"The Dark Side of Cellular Plasticity: Stem Cells in Development and Cancer",doi:"10.5772/13969",slug:"the-dark-side-of-cellular-plasticity-stem-cells-in-development-and-cancer",totalDownloads:4698,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:null,signatures:"Fernando Abollo-Jimenez, Elena Campos-Sanchez, Ana Sagrera, Maria Eugenia Muñoz, Ana Isabel Galan, Rafael Jimenez and Cesar Cobaleda",downloadPdfUrl:"/chapter/pdf-download/14457",previewPdfUrl:"/chapter/pdf-preview/14457",authors:[{id:"16416",title:"Dr.",name:"Cesar",surname:"Cobaleda",slug:"cesar-cobaleda",fullName:"Cesar Cobaleda"},{id:"17538",title:"BSc.",name:"Fernando",surname:"Abollo-Jimenez",slug:"fernando-abollo-jimenez",fullName:"Fernando Abollo-Jimenez"},{id:"17544",title:"Dr.",name:"Rafael",surname:"Jimenez",slug:"rafael-jimenez",fullName:"Rafael Jimenez"},{id:"17545",title:"Dr.",name:"Maria Eugenia",surname:"Muñoz",slug:"maria-eugenia-munoz",fullName:"Maria Eugenia Muñoz"},{id:"17546",title:"Dr.",name:"Ana Isabel",surname:"Galan",slug:"ana-isabel-galan",fullName:"Ana Isabel Galan"},{id:"17658",title:"Prof.",name:"Ana",surname:"Sagrera",slug:"ana-sagrera",fullName:"Ana Sagrera"},{id:"25494",title:"Prof.",name:"Elena",surname:"Campos-Sanchez",slug:"elena-campos-sanchez",fullName:"Elena Campos-Sanchez"}],corrections:null},{id:"14458",title:"From where do Cancer-Initiating Cells Originate?",doi:"10.5772/14903",slug:"from-where-do-cancer-initiating-cells-originate-",totalDownloads:2594,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:null,signatures:"Stéphane Ansieau, Anne-Pierre Morel and Alain Puisieux",downloadPdfUrl:"/chapter/pdf-download/14458",previewPdfUrl:"/chapter/pdf-preview/14458",authors:[{id:"19039",title:"Dr.",name:"Alain",surname:"Puisieux",slug:"alain-puisieux",fullName:"Alain Puisieux"},{id:"19041",title:"Dr.",name:"Stéphane",surname:"Ansieau",slug:"stephane-ansieau",fullName:"Stéphane Ansieau"}],corrections:null},{id:"14459",title:"Connections between Genomic Instability and Cancer Stem Cells",doi:"10.5772/14074",slug:"connections-between-genomic-instability-and-cancer-stem-cells",totalDownloads:3067,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Linda Li, Laura Borodyansky and Youxin Yang",downloadPdfUrl:"/chapter/pdf-download/14459",previewPdfUrl:"/chapter/pdf-preview/14459",authors:[{id:"16709",title:"Dr.",name:"Youxin",surname:"Yang",slug:"youxin-yang",fullName:"Youxin Yang"},{id:"19288",title:"Ms.",name:"Linda",surname:"Li",slug:"linda-li",fullName:"Linda Li"},{id:"19289",title:"Dr.",name:"Laura",surname:"Borodyansky",slug:"laura-borodyansky",fullName:"Laura Borodyansky"}],corrections:null},{id:"14460",title:"Cancer Stem Cells as a Result of a Reprogramming-Like Mechanism",doi:"10.5772/13761",slug:"cancer-stem-cells-as-a-result-of-a-reprogramming-like-mechanism",totalDownloads:2724,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Carolina Vicente-Dueñas, Isabel Romero-Camarero, Teresa Flores, Juan Jesús Cruz and Isidro Sanchez-Garcia",downloadPdfUrl:"/chapter/pdf-download/14460",previewPdfUrl:"/chapter/pdf-preview/14460",authors:[{id:"15832",title:"Dr.",name:"Isidro",surname:"Sanchez-Garcia",slug:"isidro-sanchez-garcia",fullName:"Isidro Sanchez-Garcia"},{id:"15836",title:"Dr.",name:"Carolina",surname:"Vincente-Dueñas",slug:"carolina-vincente-duenas",fullName:"Carolina Vincente-Dueñas"},{id:"15837",title:"Prof.",name:"Isabel",surname:"Romero-Camarero",slug:"isabel-romero-camarero",fullName:"Isabel Romero-Camarero"},{id:"15838",title:"Dr.",name:"Teresa",surname:"Flores",slug:"teresa-flores",fullName:"Teresa Flores"},{id:"15839",title:"Prof.",name:"Juan",surname:"Cruz Hernández",slug:"juan-cruz-hernandez",fullName:"Juan Cruz Hernández"}],corrections:null},{id:"14461",title:"Breast Cancer Stem Cells",doi:"10.5772/13977",slug:"breast-cancer-stem-cells",totalDownloads:3215,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:null,signatures:"Marco A. 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Boyd, Tony J. Svejcar and Jose J. Zamora",authors:[{id:"101539",title:"Dr.",name:"Chad",middleName:null,surname:"Boyd",fullName:"Chad Boyd",slug:"chad-boyd"},{id:"101568",title:"Dr.",name:"Tony",middleName:null,surname:"Svejcar",fullName:"Tony Svejcar",slug:"tony-svejcar"},{id:"136597",title:"Mr.",name:"Jose",middleName:null,surname:"Zamora",fullName:"Jose Zamora",slug:"jose-zamora"}]},{id:"36812",title:"Effects of Discharge Characteristics on Aqueous Pollutant Concentration at Jebel Ali Harbor, Dubai-UAE",slug:"effects-of-discharge-characteristics-on-aqueous-pollutant-concentration-at-jebel-ali-harbor-dubai-ua",signatures:"Munjed A. Maraqa, Ayub Ali, Hassan D. Imran, Waleed Hamza and Saed Al Awadi",authors:[{id:"93159",title:"Dr.",name:"Munjed",middleName:null,surname:"Maraqa",fullName:"Munjed Maraqa",slug:"munjed-maraqa"},{id:"128832",title:"Dr.",name:"Ayub",middleName:null,surname:"Ali",fullName:"Ayub Ali",slug:"ayub-ali"},{id:"128833",title:"Dr.",name:"Hassan",middleName:null,surname:"Imran",fullName:"Hassan Imran",slug:"hassan-imran"},{id:"128834",title:"Prof.",name:"Waleed",middleName:null,surname:"Hamza",fullName:"Waleed Hamza",slug:"waleed-hamza"},{id:"128839",title:"MSc.",name:"Saed",middleName:null,surname:"Al Awadi",fullName:"Saed Al Awadi",slug:"saed-al-awadi"}]},{id:"36813",title:"The Effect of Wastes Discharge on the Quality of Samaru Stream, Zaria, Nigeria",slug:"the-effect-of-wastes-discharge-on-the-quality-of-samaru-stream-zaria-nigeria",signatures:"Y.O. Yusuf and M.I. Shuaib",authors:[{id:"93194",title:"Ph.D.",name:"Yakubu",middleName:"Obadaki",surname:"Yusuf",fullName:"Yakubu Yusuf",slug:"yakubu-yusuf"},{id:"128357",title:"BSc.",name:"Maimuna",middleName:null,surname:"Shuaib",fullName:"Maimuna Shuaib",slug:"maimuna-shuaib"}]},{id:"36814",title:"Water Quality in Hydroelectric Sites",slug:"water-quality-in-hydroelectric-sites",signatures:"Florentina Bunea, Diana Maria Bucur, Gabriela Elena Dumitran and Gabriel Dan Ciocan",authors:[{id:"90061",title:"Dr.",name:"Florentina",middleName:null,surname:"Bunea",fullName:"Florentina Bunea",slug:"florentina-bunea"},{id:"100794",title:"Dr.",name:"Diana Maria",middleName:null,surname:"Bucur",fullName:"Diana Maria Bucur",slug:"diana-maria-bucur"},{id:"100801",title:"Dr.",name:"Gabriel Dan",middleName:null,surname:"Ciocan",fullName:"Gabriel Dan Ciocan",slug:"gabriel-dan-ciocan"},{id:"128309",title:"Dr.",name:"Gabriela Elena",middleName:null,surname:"Dumitran",fullName:"Gabriela Elena Dumitran",slug:"gabriela-elena-dumitran"}]},{id:"36815",title:"Removal Capability of Carbon-Soil-Aquifer Filtering System in Water Microbiological Pollutants",slug:"removal-capability-of-carbon-soil-aquifer-filtering-system-in-removing-water-microbiological-polluta",signatures:"W.B. Wan Nik, M.M. Rahman, M.F. Ahmad, J. Ahmad and A. M Yusof",authors:[{id:"91132",title:"Dr.",name:"Wan Sani",middleName:null,surname:"Wan Nik",fullName:"Wan Sani Wan Nik",slug:"wan-sani-wan-nik"},{id:"99367",title:"Dr.",name:"Muklesur",middleName:null,surname:"Rahman",fullName:"Muklesur Rahman",slug:"muklesur-rahman"},{id:"128481",title:"Dr.",name:"Mohd Fadhli",middleName:null,surname:"Ahmad",fullName:"Mohd Fadhli Ahmad",slug:"mohd-fadhli-ahmad"},{id:"128482",title:"Prof.",name:"Ahmad",middleName:null,surname:"Jusoh",fullName:"Ahmad Jusoh",slug:"ahmad-jusoh"}]},{id:"36816",title:"Impact of Agricultural Contaminants in Surface Water Quality: A Case Study from SW China",slug:"agricultural-contaminants",signatures:"Binghui He and Tian Guo",authors:[{id:"97281",title:"Prof.",name:"Binghui",middleName:null,surname:"He",fullName:"Binghui He",slug:"binghui-he"},{id:"100889",title:"Ms",name:"Tian",middleName:null,surname:"Guo",fullName:"Tian Guo",slug:"tian-guo"}]},{id:"36817",title:"Fluxes in Suspended Sediment Concentration and Total Dissolved Solids Upstream of the Galma Dam, Zaria, Nigeria",slug:"fluxes-in-suspended-sediment-concentration-and-total-dissolved-solids-upstream-of-the-galma-dam-zari",signatures:"Y.O. 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Dennis",slug:"gary-r.-dennis"}]}]}],publishedBooks:[{type:"book",id:"1998",title:"Water Quality",subtitle:"Monitoring and Assessment",isOpenForSubmission:!1,hash:"fd1b9d4bb120268c760014c263f7ef9f",slug:"water-quality-monitoring-and-assessment",bookSignature:"Kostas Voudouris and Dimitra Voutsa",coverURL:"https://cdn.intechopen.com/books/images_new/1998.jpg",editedByType:"Edited by",editors:[{id:"36891",title:"Prof.",name:"Konstantinos (Kostas)",surname:"Voudouris",slug:"konstantinos-(kostas)-voudouris",fullName:"Konstantinos (Kostas) Voudouris"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6644",title:"Emerging Pollutants",subtitle:"Some Strategies for the Quality Preservation of Our Environment",isOpenForSubmission:!1,hash:"9e03aeca8b09510ef11fcf3621a2a996",slug:"emerging-pollutants-some-strategies-for-the-quality-preservation-of-our-environment",bookSignature:"Sonia Soloneski and Marcelo L. 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A healthy interaction between wakefulness and sleep periods and a balance specific to the organism is necessary for the proper functioning of human physiology and specifically that of the central nervous system (CNS) to be maintained. Sleep is a physiological need, it is a behavior during which the response of the brain to environmental stimuli is reversibly diminished. The absence or diminishment of this need negatively impacts the interactions in the neuronal networks and pathways responsible for the wakefulness of the brain. Electrical activity changes that appear in the brain during NREM and REM periods with the help of neurohumoral factors gives way to different physiological mechanisms in the body. Motor networks are integrated during REM, and non-motor ones during NREM. Thus, diseases that affect bodily organs and systems as well as medications can change NREM and REM activities thereby changing the motor and sensory functions of the brain. We can easily claim that many basic and clinical neurophysiological incidents taking place when we are awake are in fact realized through physiological processes and pathophysiological mechanisms occurring during sleep. Anxiety disorders, depression and schizophrenia where neurotransmitter-receptor relationships are hindered, as well as motor and non-motor degenerative diseases (Amyotrophic Lateral Sclerosis, Parkinson’s disease) present with sleep disturbances and REM behavior changes years ahead of clinical symptoms. Sleep is as important a piece of life as wakefulness. As we continue to understand sleep, many of the causes of basic and clinical processes from pediatric age to geriatric years will be further demystified.
When we talk about brain, we think about cortex; when cortex is mentioned, we focus on somatosensory (senses) and somatomotor (movement) cortex activities; when we hear about hypothalamus, we then consider hypothalamopituitary hormones and feedback mechanisms. Yet, humans are not limited to biological functions. Behavior is what defines a human being. Physiological and social characteristics associated with behaviors and even habits can influence the diseases individuals develop and the treatment approaches that are used. The emergence of behavior is managed by the limbic system which in itself means limit. Hypothalamus is at the center of the limbic system; rather than primarily focusing on biological-feedback interactions, it plays a key role in the integration and control of behavior [1, 2, 3]. The most important element of sleep and wakefulness cycle is our behavior model. Sleep is the most basic physiological need and the most important electrical activity of the brain influencing wakefulness behaviors (thirst, hunger, satiety, emotional state, mood, social motivation, love, compassion, argument, fear, attention, concentration, learning, memory and many other cognitive, motor, sensory and autonomous functions) [2, 3, 4, 5]. Deep brain has hypothalamus at its center and it orchestrates affective sensations (like/dislike, satisfaction/revulsion, reward/punishment) together with surrounding limbic structures. As the main center of integration, hypothalamus uses parasympathetic and sympathetic fibers of the autonomous nervous system generating vegetative, emotional and motivational mechanisms. Amygdala is the main limbic structure for emotions: (1) it stimulates sympathetic activity, especially previously learned fear-related behavior. (2) Can be voluntary, when the cerebral cortex decides to recall frightful experiences it acts through amygdala. (3) Some people can regulate some autonomic activities by gaining extraordinary control over their emotions. (4) It is sensitive to sleep deprivation that is why you get cranky when you have not slept enough. Reticular formation of brain stem, regulation of pupil size, respiration, heart, blood pressure, swallowing etc. Sleep/wakefulness cycle is a complex blend of all these physiological and behavioral processes. There are two distinct stages during sleep: a stage where there are no rapid eye movements NREM (Non Rapid Eye Movement) and one where there are rapid eye movements REM (Rapid Eye Movement). These stages are separated from one another and from wakefulness with hard limits [4, 5, 6, 7, 8].
There are two main regions (mesopontine reticular activating system
“Glutamate, Acetylcholine, Histamine, Norepinephrine and GABA”.
Reticular activating system stimulates the cortex by utilizing glutamate while ponto-mesencephalic tegmental neurons do this by using acetylcholine. Neurons at locus coeruleus predominantly utilize norepinephrine, they extend from the brain stem to the cerebral cortex encompassing the forebrain; by activating the stimulation of the cortex, and they contribute to maintaining wakefulness.
It projects to laterodorsal tegmental and pedinculopontine tegmental nuclei, midline and intralaminar thalamic nuclei and to a lesser degree to lateral hypothalamus and basal forebrain.
Cholinergic neuron group starts from the basal forebrain with a widespread projection to cortex. This pontomesencephalic neuron group is a part of the ascending reticular activating system; they play a part in the activation during wakefulness and are actively involved in paradoxical sleep. Glutamate is another excitatory neurotransmitter acting as the primary neurotransmitter of the ascending reticular activating system.
In Latin, circa means pertaining to and dian means day; circadian is a word used to explain the daily physiological rhythms of an organism, mainly the sleep and wakefulness.
Circadian rhythmicity and sleep-wakefulness homeostasis includes; (1) the modulation of hypothalamic hormones, peptides and molecules, (2) the metabolic pathways influenced by peripheral hormones and (3) autonomous nervous system control of endocrine organs. In the regulation of temporal organization of hormone secretion, processes associated with the electrical signal changes during the sleep stages of brain (NREM-REM) are as effective as circadian rhythm and homeostatic processes. These processes effect different hormonal axes (somatotropic, corticotropic and gonadal axes) and metabolic pathways at different levels. For example thyroid stimulating hormone (TSH) levels might change both with sleep and circadian rhythm while cortisol levels only change with circadian rhythm. Growth hormone (GH) and prolactin (PRL) can be at a certain level during daytime- wakefulness but they increase while sleeping. Glucose and insulin have been shown to be effected by both sleep and the circadian rhythm increasing while being awake at night and while being asleep during daytime. Circadian oscillations can be generated in many peripheral organs under autonomous nervous system control including adipocytes and pancreas beta cells that generate endocrine signals. These “local” oscillators seem to be under the control of central electrical batteries found in suprachiasmatic nuclei either directly through neural and endocrine signals or indirectly via sleep-wakefulness cycle and behavioral rhythms like nutrition. Endocrine secretion of these peripheral oscillators during wakefulness and sleep and their possible participation in the temporal organization of metabolic function are still open to research [30, 31, 32].
The activity of the corticotropic axis is related to stress reaction and behavioral activation. Corticotropic axis activity can be measured peripherally by plasma levels of pituitary adrenocorticotropic hormone (ACTH) and adrenal hormone cortisol that is directly controlled by ACTH stimulation. Plasma levels of these hormones are highest during early hours of morning, they decrease throughout the day reaching lowest limit during late night hours and early stages of sleep period. Therefore, sleep is normally initiates when corticotropic activity is slow. Reactivation of ACTH and cortisol secretion happens suddenly a couple of hours ahead of waking up.
PRL levels begin to increase shortly after the start of sleep and make a night peak at the middle of sleep. The possible primary mechanism underlying this peak is decreased dopaminergic inhibition of PRL during sleep. Thyrotropin releasing hormone (TRH), vasoactive intestinal peptide (VIP), oxytocin, estrogen and angiotensin II increase PRL secretion while dopamine, GABA and acute hypoxia inhibits it. The primary effect of PRL during sleep is to stimulate REM sleep. Rapid PRL increase at the beginning of sleep is thought to be related to SWS. In prolactinoma and lactating mothers SWS increases due to increased PRL secretion. Fragmented sleep decreases PRL secretion (Mechanism: Waking up in the morning and wakefulness that fragment sleep are related to a rapid inhibition of PRL secretion) [41, 42].
The relationship between 24-hour-gonadotropin secretion rhythms and gonadal steroid levels changes based on the stage of maturity and is sex-related during young adulthood [42].
With initiation of sleep, noradrenaline and adrenaline levels decrease as the case with cortisol reaching their minimum levels within an hour. Noradrenaline plays a role in respiratory control while adrenaline is a bronchodilator. Nocturnal catecholamine levels are increased in patients with obstructive apnea syndrome.
Sleep plays an important role in energy balance. Hypocretins and orexins are hypothalamic stimulant neuropeptides with strong wakefulness promoting effects, they also stimulate feeding; their definition created the molecular basis for delineating the interactions between nutrition and sleep regulation.
Nuclei located in hypothalamus (posterior and lateral regions contain sympathetic nuclei, anterior regions have parasympathetic ones) control the autonomic nervous system. Together with hypothalamus and limbic structures, sympathetic and parasympathetic portions of the autonomic nervous system regulate vegetative sensory and motivational behaviors. Norepinephrine (noradrenaline) is the main transmitter for the sympathetic system (catecholaminergic system), and Neuropeptide Y acts as a cotransmitter. In vascular beds, adrenergic endings secrete NPY together with noradrenaline. By itself, NPY has a vasoconstrictor effect. Acetylcholine (Ach) is the main transmitter of the parasympathetic system (cholinergic system) and VIP (vasoactive intestinal peptide) functions as the cotransmitter of this system. In the salivary and perspiratory glands, in the genital system and adrenal medulla cholinergic endings secrete VIP together with ACh. VIP exerts partial vasodilator and strong bronchodilator effects [7, 12, 13, 14].
MCH, is a 19 amino acid long cyclic neuropeptide acting as a neurotransmitter. Neurons containing MCH are primarily found in lateral hypothalamus and incerto-hypothalamic regions and they have widespread projections within the brain. In humans, biological functions of this neuropeptide are realized via two metabotropic receptors, namely MCHR1 and MCHR2, whereas rodents only have MCHR1.
The system and molecules that are in charge of regulating sleep-wakefulness modulate general homeostatic mechanisms as well as orchestrating highly cognitive activities like attention, learning and memory. We need to develop a general perspective for pharmacologic substances influencing these activities.
Ethyl alcohol; blocks glutamate NMDA receptors and is an indirect agonist of GABA receptors. Cerebral granular cells increase GABAergic transmission in cerebellar cortex and hippocampus. Alcohol is neurotoxic at high doses; it can specifically hinder cholinergic input that advances to the cortex through basal forebrain neurons. It can lead to a significant deterioration in motor performance and can result in sleep deprivation. There might be behavioral problems stemming from sleep deficiency as well as memory problems in alcoholics because of apparent effects of alcohol on hippocampus. Individuals having undiagnosed schizophrenia, anxiety disorders and depression might try to benefit from sedative and anxiolytic effects of alcohol by overconsumption. In these individuals, blood circulation to the frontal region deteriorates and their decision making capacity is impaired [14, 15].
Main mechanisms of effect for sleep inducing pharmacological agents are still being delineated. The primary site of action of most anesthetics may be the sleep– wake control system. In anesthesia, considering that arousal and alertness represent a continuum of levels from mania to coma, with physiological and behavioral concomitants, the monitoring of EEG, along with behavioral and autonomic signs, should be used routinely to assess level of anesthesia.
Histaminergic projections at tuberomamillary nucleus are active during waking up. The pathology of this region leads to hypersomnia. Histaminergic inputs coming from TMN to RAS suppress SWS, but they do not have an effect on REM. RAS, basal forebrain, lateral hypothalamus and cortex have high levels of histamine receptors. Antihistamine (histamine receptor blockers) effects on these regions cause dizziness, sleepiness and cognitive dysfunction. In children first and second generation antihistamines can cause poisoning and coma; however, newer (third generation) pediatric formulations (e.g. fexofenadine, loratadine, cetirizine) seem to be safer [57].
The popularity of caffeine is due to its stimulant characteristics. It blocks adenosine receptors in RAS, decreases the inhibitor effect of adenosine; thus, free adenosine levels in the brain are increased resulting in a stimulant activity in the CNS. Caffeine appears to block adenosine A1 and A2a receptors, producing a psychomotor stimulant effect. Because of the high levels of A2a receptors in the striatum, the potential use of caffeine for the treatment of Parkinson’s disease has been advanced. Since adenosine A2a receptor blockade appears to protect dopaminergic neurons from toxic agents, a neuroprotective role has been proposed for caffeine in the treatment of Parkinson’s disease. Caffeine intake has also been associated with a decreased risk of Alzheimer’s disease, again presumably acting as a neuroprotective agent [12].
It is an alkaloid found in abundance in tobacco and eggplants. It is metabolized in the liver and its main metabolite is cotinine. With smoking low dosed of nicotine exerts its effects on sympathetic (tachycardia, high blood pressure) and parasympathetic (tonus in the digestive system, increases in peristaltic movements and acid secretion) effects. (Thromboxane A2 increase, lipolysis, psychomotor stimulation, decreases appetite, analgesic effect, increases the secretion of ADH, ACTH, cortisol and insulin, decreases secretion of LH and PRL). Causes psychological and physical addiction. Inhaled nicotine in cigarette smoke is known to permeate the lungs where more than 80% of the available nicotine is absorbed into the bloodstream. After absorption into the blood, nicotine readily crosses the blood– brain barrier and appears to be rapidly partitioned into brain tissue. Concentrations of nicotine in the brain have been reported to be 5–7 times higher than blood concentrations. Smokers assert that, in addition to its positive effects on concentration and attention, the primary positive effect of smoking is that it calms and relaxes. Recent findings suggest that one of the sites of action of nicotine may be in the RAS, specifically, on PPN neurons. Nicotine, at least initially, has an inhibitory effect on cholinergic RAS neurons, which could produce the calming effect reported upon inhalation of cigarette smoke. The majority of cigarettes are consumed by the mentally ill, especially those with disorders involving hypervigilance or hyperarousal, such as schizophrenia, anxiety disorders, and depression. That is, smoking may be a form of self-medication, presumably because of its calming effects. This effect (inhibition of cholinergic RAS neurons) appears to differ from the role of smoking in reducing the incidence of Parkinson’s disease, which appears to be manifested as a neuroprotective action on dopaminergic neurons by nicotine. Cerebral vasodilation is seen immediately after smoking, but chronic smokers show global reductions in cerebral blood flow. Considering that hypofrontality is present in schizophrenia, anxiety disorders, and depression, the initial beneficial, calming effects of nicotine may be followed by deleterious consequences on cortical blood flow. Such an effect may drive craving for the next cigarette, creating a vicious cycle of continuous self-administration [12, 58, 59].
The most commonly used stimulant, amphetamine, induces release of monoamines, especially dopamine, but also blocks their reuptake and may have neurotoxic effects on nigral neurons and, more recently, is suspected of inducing the degenerations of certain striatal neurons. Unfortunately, this agent is abused for recreational purposes and continues to be prescribed for the treatment of attention deficit disorder (ADD). Fortunately, methylphenidate does not appear to have such neurotoxic effects, although its use has decreased.
Hypofrontality, hypervigilance and sleep irregularities are common symptoms for these disorders. Regions in relation with RAS (cholinergic PPN, noradrenergic LC and serotonergic RN) that we tried to tackle so far, their neurotransmitters and pharmacological agents that are effective on their receptors are used for the treatment of these symptoms. The serotonergic RN is known to inhibit the PPN and LC, with the cholinergic PPN exciting the LC and the noradrenergic LC inhibiting, via alpha-2 adrenergic receptors, the PPN. The PPN sends excitatory cholinergic projections to the substantia nigra (SN), which, in turn, sends dopaminergic projections to the striatum. The treatment of depression previously included tricyclic antidepressants such as amitryptiline, imipramine, and clomipramine, agents that mainly blocked reuptake of noradrenaline and serotonin, and blocked histamine and acetylcholine release, thus accounting for increased sleepiness. The selective serotonin reuptake inhibitors (SSRIs) more selectively affect the RAS by increasing the inhibition. It is not clear if the etiology of depression is related to disinhibition of the PPN and LC by a decrement in serotonergic tone, although this would seem a likely origin for the sleep–wake symptomatology of depression. The treatment of anxiety disorder is involved the use of benzodiazepine amplification of GABAergic inhibition. In addition, the use of the alpha-2 noradrenergic receptor agonist clonidine produces anxiolytic effects, probably by inhibiting autoreceptors in the LC and postsynaptic receptors in the PPN, thus downregulating vigilance. Because of the peripheral cardiovascular effects of clonidine, alpha-2 adrenergic receptor agonists without such actions would be more desirable. One study provided strong evidence for the use of the alpha-2 adrenergic receptor agonist dexmedetomidine as an anxiolytic for the treatment of anxiety disorders like posttraumatic stress disorder, panic attacks, and general anxiety disorder [32]. The etiology of anxiety disorder has been proposed to include downregulation or degeneration of LC outputs (possibly induced by stress hormones), which would act to release, or disinhibit, PPN neurons at site.
The etiology of schizophrenia has been suggested to include increased PPN output, accounting for marked hypervigilance and hallucinations. Excessive PPN output would overactivate the SN and, in turn, increase striatal release of dopamine that is, complying with the dopamine theory of schziophrenia. SWS are reduced in schizophrenics. Consistent with this assumption, lower SWA has been more often reported in institutionalized patients with profound cognitive impairment as well as in schizophrenia patients with prominent negative symptoms. The treatment of schizophrenia previously involved the use of the dopaminergic receptor blocker haloperidol, which induced tardive dyskinesia, among other serious side effects. Newer antipsychotics such as risperidone and quetiapine appear to block dopaminergic, noradrenergic, and serotonergic receptors. More striking antipsychotic effects were provided by the use of clozapine, which was designed as a muscarinic cholinergic blocker for the treatment of Parkinson’s disease [14, 63, 64, 65].
ALS is an incurable neurodegenerative disorder of upper and lower motor neurons, which is characterized by degeneration of the corticospinal tracts, resulting in loss of motor neurons in the brain, brainstem and anterior horn cells of the spinal cord. Loss of motor neurons in the brainstem and spinal cord causes weakness of the pharyngeal, laryngeal, intercostal and diaphragmatic muscles. During non-REM sleep, muscle tone is decreased and during REM sleep muscle tone is almost completely lost. Automatic ventilation during sleep is almost completely dependent on the diaphragm (particularly in REM sleep) therefore diaphragmatic dysfunction (such as that seen in ALS) can predispose to hypoventilation and nocturnal hypoxemia. Parkinson Disease [PD] is the second most common neurodegenerative disorder after Alzheimer’s disease. PD occurs as a result of chronic, progressive decrease in dopamine levels of the substantia nigra, secondary to loss of dopaminergic neurons in the pars compacta and the occurrence of Lewy bodies in the cytoplasm of remaining neurons. It is primarily diagnosed clinically and patients may present with the characteristic motor deficits, which include the resting tremor, bradykinesia, rigidity and postural instability. However, most will have both motor and nonmotor symptoms. The nonmotor symptoms cause disturbances, which affect sleep, mood, cognition, sensation and autonomic function. Among the nonmotor symptoms in PD, sleep disorders are second in frequency only to neuropsychiatric disorder [16, 65, 66, 67, 68].
Particular attention to hormonal conditions is warranted. After all, the first sign of puberty is pulsatile hormone (LH) release during sleep. For example, narcolepsy is tightly linked with certain human leukocyte antigen (HLA) haplotypes, suggesting that it is an autoimmune disorder. Kleine– Levin syndrome, discussed earlier, is linked to similar haplotypes, which suggests an autoimmune etiology. Interestingly, in most cases of narcolepsy, Kleine– Levin syndrome, as well as schizophrenia, panic attacks, obsessive– compulsive disorder, and other disorders, the age of onset is soon after puberty. Along other lines, in about 20% of schizophrenic patients, the mother had an influenza attack during the second trimester, while narcoleptics are born predominantly during the late winter– early spring, that is, after influenza season. It has been suggested that developmental dysregulation, either pre- or perinatally (initial insult), becomes pathologically manifest after exposure to puberty and its hormonal onslaught. These considerations point to complex interactions between development, environment, and hormonal status, all of which seem to affect sleep– wake regulation in as yet unknown ways. These findings suggest that the effects of hormones, either prescribed or taken as dietary supplements, or abused, need to be more closely studied and considered in the design of therapeutic interventions [69, 70].
Brain energy requirements are extraordinarily high; any modification in glucose utilization by the brain may profoundly affect glucose tolerance. Cerebral glucose utilization is lower during SWS than during either REM sleep or wake. Using PET scans, a strong correlation was evidenced between slow-wave activity, an index of the intensity of SWS, and regional blood flow in the prefrontal brain. Furthermore, experimental studies, involving continuous enteral nutrition or intravenous glucose infusion while allowing for normal nocturnal sleep, have shown that glucose tolerance is minimal during the first half of the sleep period, i.e. when SWS is the dominant sleep stage. These findings confirm the existence of a robust link between SWS and glucose tolerance. Both reduction in total sleep duration with slow-wave sleep (SWS) largely preserved and alterations of sleep quality (especially marked reduction of SWS) with preservation of total sleep duration areassociated with insulin resistance without compensatory increase in insulin secretion, resulting in impaired glucose tolerance and increased risk of type 2 diabetes. When performed under rigorously controlled conditions of energy intake and physical activity, sleep restriction is also associated with a decrease in circulating levels of leptin (an anorexigenic hormone) and an increase in circulating levels of ghrelin (an orexigenic hormone), hunger and appetite. Furthermore, sleep restriction is also associated with a stimulation of brain regions sensitive to food stimuli, indicating that sleep loss may lead to obesity through the selection of high-calorie food. There is also evidence that sleep restriction could provide a permissive environment for the activation of genes that promote obesity. Indeed, the heritability of body mass index is increased in short sleepers. Thus, chronic sleep curtailment, which is on the rise in modern society, including in children, is likely to contribute to the current epidemics of type 2 diabetes and obesity [71, 72, 73].
Chronic sleep loss is increasingly common in industrialized societies, affecting about 45% of adults. Sleep deprivation induces behavioral, hormonal, and neurochemical alterations. The stress inherent in sleep deprivation causes changes in the concentration of hormones such as cortisol as well as in prolactin and estradiol, which are known to influence dopaminergic transmission.
Studies have suggested that dopamine (DA) is responsible for the behavioral changes observed after sleep deprivation. Specifically, REM sleep deprivation has been shown to be related to changes in D2 post-synaptic receptor sensitivity in the rat striatum. DA transporter (DAT) knockout mice exhibit increased wakefulness and less SWS. REM sleep would induce increases in dopaminergic activity after sleep deprivation and selective REM sleep deprivation for a prolonged period would result in down-regulation of DAT, enhancing dopaminergic neurotransmission. Amphetamine derivatives inhibit DAT-mediated DA reuptake [74, 75].
Short-term sleep deprivation has shown therapeutic properties for with mood disorders, long-term/ chronic sleep deprivation and disruption have instead been related to the development of mood disorders via monoamine (5-HT, NE, DA) activity dysregulation. The main symptoms of depression are due to a functional deficiency of the brain monoaminergic transmitters: norepinephrine, serotonin and/or dopamine, whereas mania is caused by a functional excess of monoamines at critical synapses in the brain. Although recently some observations have challenged the legitimacy of this theory, a dysregulation in monoamine production and transmission is still considered an important factor in the regulation of mood, emotions, cognition, motivational behaviors and stress responses. Deuschle et al. [81] conducted a study in a group of individuals suffering from chronic insomnia, and found that the short allele of the 5-HT transporter was significantly more frequent in patients suffering from insomnia than in good sleepers. Roman et al. [82] suggested that chronic sleep restriction may increase an individual’s vulnerability to develop mood disorders by impairing serotoninergic transmission throughout the activation of the stress system The genetic makeup of the dopamine system involved in vulnerability to mood disorders has also been shown to be involved in the response to sleep loss and in alterations in responses to reward in humans. A polymorphism in the dopamine 2 receptor, more commonly in the dopamine transporter system, has been related to a vulnerability to psychiatric disorders in the presence of sleep deprivation in humans. It has been widely shown that individuals suffering from insomnia display hyperactivation of the hypothalamic–pituitary– adrenal-axis at both brain and peripheral levels. Increases in norepinephrine, epinephrine and other markers of sympathetic outflow have been related to cognitive and emotional arousal and somatic hyperarousal in individuals suffering from insomnia: it is the key pathophysiological mechanism of insomnia. Changes observed in brain structures in individuals suffering from insomnia include a reduction in the volume of the prefrontal cortex, caudate head and hippocampus, as well as an increase in the amygdala volume, modifications resembling those described in individuals suffering mood disorders. Given these similarities, it has been hypothesized that insomnia may influence the development and maintenance of a mood disorder throughout the activation of the stress system and of its negative consequences on the brain, including hippocampal neurogenesis, synaptic plasticity and connectivity [76, 77, 78, 79, 80, 81, 82, 83, 84, 85].
Finally, we can talk about the relationship between sleep and antidepressants, which are effective on monoamine (5-HT, NE, DA) activity systems in the brain: (1) Tricyclic antidepressants (TCA) (antagonist of 5HT-1, NE, M1, H1 receptors); (a) tertiary TCAs shorten sleep latency and reduce awakenings during sleep. Therefore, it is perceived as a sedative; doxepin and amitriptyline decrease REM rate in sleep EEG, cause prolongation of REM sleep latency, (b) Secondary TCAs such as desipramine are less sedative and relatively stimulating, (c) potent serotoninergic TCAs such as clomipramine increase eye movements in NREM. It increases the periodic leg movements during sleep, (2) nonspecific reuptake inhibitors (5HT, NE DA); trazadone is sedative and nefazodone is less sedative, they increase SWS sleep, (3) monoamine oxidase inhibitors (MAOI) (eg, tranylcypromine, moclobemide), (4) selective serotonin reuptake inhibitors SSRI (eg, fluoxetine, escitalopram, paroxetine, sertraline), (5) serotonin and norepinephrine reuptake inhibitors (SNRI) (eg, venlafaxine, duloxetine, reboxetine) (6) Bupropion (inhibition of norepinephrine and dopamine reuptake) these agents increase SWS, prolong REM latency, shorten REM time, (7) Agomelatine (agonism at melatonin M1 and M2 receptors, antagonism at serotonergic 5-HT2C receptors) have been found to increase SWS [86, 87, 88, 89].
The more we learn about the neurophysiology of sleep and the effects of related molecules, the better we understand the pathological processes in wakefulness. Understanding the functioning of the sleep brain, along with neurotransmitters, hormones, and new molecules, will explain unknown physiological processes and inspire innovative processes in pharmacology.
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On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. 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Delac received his B.Sc.E.E. degree in 2003 and is currentlypursuing a Ph.D. degree at the University of Zagreb, Faculty of Electrical Engineering andComputing. His current research interests are digital image analysis, pattern recognition andbiometrics.",institutionString:null,institution:{name:"University of Zagreb",country:{name:"Croatia"}}},{id:"557",title:"Dr.",name:"Andon",middleName:"Venelinov",surname:"Topalov",slug:"andon-topalov",fullName:"Andon Topalov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/557/images/1927_n.jpg",biography:"Dr. Andon V. Topalov received the MSc degree in Control Engineering from the Faculty of Information Systems, Technologies, and Automation at Moscow State University of Civil Engineering (MGGU) in 1979. He then received his PhD degree in Control Engineering from the Department of Automation and Remote Control at Moscow State Mining University (MGSU), Moscow, in 1984. From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. His current research interests are in the fields of intelligent control and robotics.",institutionString:null,institution:{name:"Technical University of Sofia",country:{name:"Bulgaria"}}},{id:"585",title:"Prof.",name:"Munir",middleName:null,surname:"Merdan",slug:"munir-merdan",fullName:"Munir Merdan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/585/images/system/585.jpg",biography:"Munir Merdan received the M.Sc. degree in mechanical engineering from the Technical University of Sarajevo, Bosnia and Herzegovina, in 2001, and the Ph.D. degree in electrical engineering from the Vienna University of Technology, Vienna, Austria, in 2009.Since 2005, he has been at the Automation and Control Institute, Vienna University of Technology, where he is currently a Senior Researcher. 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Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. She is a professor in the Stomatology Faculty, St. Petersburg State University. She has expertise in the development and evaluation of a wide range of live mucosal vaccines against influenza and bacterial complications. Her research interests include immunity against influenza and COVID-19 and the development of immunization schemes for high-risk individuals.",institutionString:'Federal State Budgetary Scientific Institution "Institute of Experimental Medicine"',institution:null},{id:"238958",title:"Mr.",name:"Atamjit",middleName:null,surname:"Singh",slug:"atamjit-singh",fullName:"Atamjit Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/238958/images/6575_n.jpg",biography:null,institutionString:null,institution:null},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:null},{id:"252058",title:"M.Sc.",name:"Juan",middleName:null,surname:"Sulca",slug:"juan-sulca",fullName:"Juan Sulca",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/252058/images/12834_n.jpg",biography:null,institutionString:null,institution:null},{id:"191392",title:"Dr.",name:"Marimuthu",middleName:null,surname:"Govindarajan",slug:"marimuthu-govindarajan",fullName:"Marimuthu Govindarajan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191392/images/5828_n.jpg",biography:"Dr. M. Govindarajan completed his BSc degree in Zoology at Government Arts College (Autonomous), Kumbakonam, and MSc, MPhil, and PhD degrees at Annamalai University, Annamalai Nagar, Tamil Nadu, India. He is serving as an assistant professor at the Department of Zoology, Annamalai University. His research interests include isolation, identification, and characterization of biologically active molecules from plants and microbes. He has identified more than 20 pure compounds with high mosquitocidal activity and also conducted high-quality research on photochemistry and nanosynthesis. He has published more than 150 studies in journals with impact factor and 2 books in Lambert Academic Publishing, Germany. He serves as an editorial board member in various national and international scientific journals.",institutionString:null,institution:null},{id:"274660",title:"Dr.",name:"Damodar",middleName:null,surname:"Paudel",slug:"damodar-paudel",fullName:"Damodar Paudel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/274660/images/8176_n.jpg",biography:"I am DrDamodar Paudel,currently working as consultant Physician in Nepal police Hospital.",institutionString:null,institution:null},{id:"241562",title:"Dr.",name:"Melvin",middleName:null,surname:"Sanicas",slug:"melvin-sanicas",fullName:"Melvin Sanicas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241562/images/6699_n.jpg",biography:null,institutionString:null,institution:null},{id:"337446",title:"Dr.",name:"Maria",middleName:null,surname:"Zavala-Colon",slug:"maria-zavala-colon",fullName:"Maria Zavala-Colon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Puerto Rico, Medical Sciences Campus",country:{name:"United States of America"}}},{id:"338856",title:"Mrs.",name:"Nur Alvira",middleName:null,surname:"Pascawati",slug:"nur-alvira-pascawati",fullName:"Nur Alvira Pascawati",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universitas Respati Yogyakarta",country:{name:"Indonesia"}}},{id:"441116",title:"Dr.",name:"Jovanka M.",middleName:null,surname:"Voyich",slug:"jovanka-m.-voyich",fullName:"Jovanka M. Voyich",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Montana State University",country:{name:"United States of America"}}},{id:"330412",title:"Dr.",name:"Muhammad",middleName:null,surname:"Farhab",slug:"muhammad-farhab",fullName:"Muhammad Farhab",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"349495",title:"Dr.",name:"Muhammad",middleName:null,surname:"Ijaz",slug:"muhammad-ijaz",fullName:"Muhammad Ijaz",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Veterinary and Animal Sciences",country:{name:"Pakistan"}}}]}},subseries:{item:{id:"26",type:"subseries",title:"Machine Learning and Data Mining",keywords:"Intelligent Systems, Machine Learning, Data Science, Data Mining, Artificial Intelligence",scope:"The scope of machine learning and data mining is immense and is growing every day. 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