Classification of the flow regimes.
\\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:"1388",leadTitle:null,fullTitle:"Autoimmune Disorders - Current Concepts and Advances from Bedside to Mechanistic Insights",title:"Autoimmune Disorders",subtitle:"Current Concepts and Advances from Bedside to Mechanistic Insights",reviewType:"peer-reviewed",abstract:'Autoimmune disorders are caused due to break down of the immune system, which consequently fails in its ability to differentiate "self" from "non-self" in the context of immunology. The diseases are intriguing, both clinically and immunologically, for their diversified clinical phenotypes and complex underlying immunological mechanisms. This book offers cutting-edge information on some of the specific autoimmune disease phenotypes, respective diagnostic and prognostic measures, classical and new therapeutic options currently available, pathogenesis and underlying mechanisms potentially involved, and beyond. In the form of Open Access, such information is made freely available to clinicians, basic scientists and many others who will be interested regarding current advances in the areas. Its potential readers will find many of the chapters containing in-depth analysis, interesting discussions and various thought-provoking novel ideas.',isbn:null,printIsbn:"978-953-307-653-9",pdfIsbn:"978-953-51-6563-7",doi:"10.5772/1851",price:159,priceEur:175,priceUsd:205,slug:"autoimmune-disorders-current-concepts-and-advances-from-bedside-to-mechanistic-insights",numberOfPages:630,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"f3365e915e5d7c7299da6c076aa5cf24",bookSignature:"Fang-Ping Huang",publishedDate:"November 14th 2011",coverURL:"https://cdn.intechopen.com/books/images_new/1388.jpg",numberOfDownloads:103598,numberOfWosCitations:28,numberOfCrossrefCitations:2,numberOfCrossrefCitationsByBook:1,numberOfDimensionsCitations:27,numberOfDimensionsCitationsByBook:2,hasAltmetrics:0,numberOfTotalCitations:57,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 2nd 2010",dateEndSecondStepPublish:"November 30th 2010",dateEndThirdStepPublish:"April 6th 2011",dateEndFourthStepPublish:"May 6th 2011",dateEndFifthStepPublish:"July 5th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"42618",title:"Dr.",name:"Fang-Ping",middleName:null,surname:"Huang",slug:"fang-ping-huang",fullName:"Fang-Ping Huang",profilePictureURL:"https://mts.intechopen.com/storage/users/42618/images/1665_n.jpg",biography:"Dr. Huang received his initial medical education in China (Shantou, 1977-82). He was later awarded the Li Ka Shing Academic Foundation Scholarship to undertake postgraduate training in the UK (1987-90), and subsequently became engaged in active immunology research and teaching at the Universities of Glasgow (1990-7), Oxford (1997-2000) and Hong Kong (2000-7). He is currently a Senior Lecturer affiliated to the Imperial College London (since 2007). Immunology has been his major field of research, with a focus on immune regulation in autoimmune diseases. His current research focuses on the roles of dendritic cells (DC), regulatory T (Treg) and B (Breg) cells in systemic autoimmunity (lupus). Based on their findings, he and his research group members are trying to understand how the immune system is normally regulated, why dysregulation of which may cause diseases, and whether the so-called 'self-reactivity” (autoimmunity) can be alternatively switched on, and then effectively redirected for cancer treatment (anti-tumour immunity).",institutionString:null,position:null,outsideEditionCount:null,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Imperial College London",institutionURL:null,country:{name:"United Kingdom"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1035",title:"Clinical Immunology",slug:"immunology-allergology-and-rheumatology-clinical-immunology"}],chapters:[{id:"20659",title:"Autoimmune Disorders Associated to Type 1 Diabetes Mellitus in Children and Adolescents",doi:"10.5772/20612",slug:"autoimmune-disorders-associated-to-type-1-diabetes-mellitus-in-children-and-adolescents",totalDownloads:5691,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:null,signatures:"Giuseppe d’Annunzio and Chiara Russo, Ramona Tallone and Renata Lorini",downloadPdfUrl:"/chapter/pdf-download/20659",previewPdfUrl:"/chapter/pdf-preview/20659",authors:[{id:"39758",title:"Dr.",name:"Giuseppe",surname:"D'Annunzio",slug:"giuseppe-d'annunzio",fullName:"Giuseppe D'Annunzio"},{id:"52571",title:"Dr.",name:"Chiara",surname:"Russo",slug:"chiara-russo",fullName:"Chiara Russo"},{id:"52572",title:"Prof.",name:"Renata",surname:"Lorini",slug:"renata-lorini",fullName:"Renata Lorini"},{id:"53744",title:"Dr.",name:"Ramona",surname:"Tallone",slug:"ramona-tallone",fullName:"Ramona Tallone"}],corrections:null},{id:"20660",title:"Hashimoto's Thyroiditis in Children and Adolescents",doi:"10.5772/24755",slug:"hashimoto-s-thyroiditis-in-children-and-adolescents",totalDownloads:16528,totalCrossrefCites:0,totalDimensionsCites:5,hasAltmetrics:0,abstract:null,signatures:"Erkan Sarı, Abdulbaki Karaoglu and Ediz Yeşilkaya",downloadPdfUrl:"/chapter/pdf-download/20660",previewPdfUrl:"/chapter/pdf-preview/20660",authors:[{id:"59265",title:"Dr.",name:"Ediz",surname:"Yesilkaya",slug:"ediz-yesilkaya",fullName:"Ediz Yesilkaya"},{id:"59267",title:"Dr.",name:"Erkan",surname:"Sari",slug:"erkan-sari",fullName:"Erkan Sari"},{id:"91048",title:"Dr.",name:"Abdulbaki",surname:"Karaoglu",slug:"abdulbaki-karaoglu",fullName:"Abdulbaki Karaoglu"}],corrections:null},{id:"20661",title:"Primary Sjögren’s Syndrome: Current Pathophysiological, Diagnostic and Therapeutic Advances",doi:"10.5772/20848",slug:"primary-sjo-gren-s-syndrome-current-pathophysiological-diagnostic-and-therapeutic-advances",totalDownloads:2784,totalCrossrefCites:0,totalDimensionsCites:3,hasAltmetrics:0,abstract:null,signatures:"Christine Delporte, Jason Perret and Muhammad S. 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\r\n\tElectrodeposition has been an active research field of vast technological significance for many decades and continues to be an area of active discovery and development. Under electrochemical control, it is possible to create coatings of alloys, metals, colloids, magnetic materials, pigments, and nanoparticles or nanostructures of precise composition, thickness, and ordering. Electrodeposited coatings and thin films have served many both protective and decorative functions in commercial products. Electrodeposited films and coating are also essential for microelectronics, biomedical devices, corrosion and wear protection, batteries, photovoltaics, other energy devices, and the development of chemical and biochemical sensors. The long investigated and commercially applied fields of electroplating, electrophoretic deposition, and electroless plating will also be the focus of this book. The more recent area of electrodeposition of nanoparticles has resulted in the formation of surfaces covered by nanoparticles of controlled composition, size, and morphology that have enhanced electrochemical and optical, and plasmonic properties for use in catalysis and sensing. Electrodeposition under precisely controlled conditions has also been used to produce other structures on substrates having unique electrochemical and optical properties. The field of patterned surfaces generated by combining electrodeposition and lithographic methods is also a leading area of basic research and technological development.
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Stine",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/11764.jpg",keywords:"Nanoparticle, Nanostructure, Electrode, Plasmon, Monolayer, Electrodeposition, Metal, Alloy, Coating, Electroless, Electroforming, Plating Bath",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 3rd 2022",dateEndSecondStepPublish:"July 7th 2022",dateEndThirdStepPublish:"September 5th 2022",dateEndFourthStepPublish:"November 24th 2022",dateEndFifthStepPublish:"January 23rd 2023",dateConfirmationOfParticipation:null,remainingDaysToSecondStep:"9 days",secondStepPassed:!1,areRegistrationsClosed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:"Dr. Keith J. Stine (h-index 25) is a productive researcher in the fields of nanostructures formed and studied using electrochemical methods, and a member of the Center for Nanoscience at the University of Missouri - Saint Louis. Professor Stine received his BS from Fairleigh Dickinson University and his Ph.D. from MIT. He was a postdoctoral fellow at UCLA and joined the UMSL faculty in 1990. He served as Chair of the Faculty Senate and University Assembly for two years and was appointed department chair.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"192643",title:"Prof.",name:"Keith J.",middleName:null,surname:"Stine",slug:"keith-j.-stine",fullName:"Keith J. Stine",profilePictureURL:"https://mts.intechopen.com/storage/users/192643/images/system/192643.jpg",biography:"Keith J. Stine was born in Jersey City, New Jersey in 1962 and grew up in New Jersey. He received his BS from Fairleigh Dickinson University in 1984 and his Ph.D. in 1988 from MIT under the direction of Carl W. Garland. He was a postdoctoral fellow at UCLA in the lab of Charles M. Knobler. He joined the UMSL faculty in 1990. He served as Chair of the Faculty Senate and University Assembly for two years and was appointed department chair in August 2019. Dr. Stine's research effort involves studies of modified surfaces and nanostructures. The surface modification of nanostructures is pursued with a focus on their prospective applications in bioanalytical chemistry such as in immunoassays, sensors, or in separations. Other projects concern the study of lipid monolayers and bilayers as models of processes occurring at the surface of cell membranes, and the use of these monolayers in molecular recognition studies. Collaborative efforts related to the automated synthesis of carbohydrates are also a focus.",institutionString:"University of Missouri–St. Louis",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"3",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Missouri–St. Louis",institutionURL:null,country:{name:"United States of America"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"14",title:"Materials Science",slug:"materials-science"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"453622",firstName:"Tea",lastName:"Jurcic",middleName:null,title:"Ms.",imageUrl:"//cdnintech.com/web/frontend/www/assets/author.svg",email:"tea@intechopen.com",biography:null}},relatedBooks:[{type:"book",id:"6320",title:"Advances in Glass Science and Technology",subtitle:null,isOpenForSubmission:!1,hash:"6d0a32a0cf9806bccd04101a8b6e1b95",slug:"advances-in-glass-science-and-technology",bookSignature:"Vincenzo M. 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Kawsar Alam",coverURL:"https://cdn.intechopen.com/books/images_new/6805.jpg",editedByType:"Edited by",editors:[{id:"199691",title:"Dr.",name:"Md. Kawsar",surname:"Alam",slug:"md.-kawsar-alam",fullName:"Md. 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However, the quality of water in most streams and rivers is being threatened worldwide due to pollution connected with human activities [1]. The situation is worsened with increasing industrial pollution and use of fertilizers and other agro-chemicals in agriculture, rapid urbanization, and continuing use of improper sanitation systems especially in developing countries [2]. Consequently, aquatic ecosystems that depend on water flows and seasonal changes within these water bodies are often threatened by poor water quality [3]. Water quality problems represent a major global challenge. For example, pollution of water bodies, especially nutrient loading, has worsened water quality in almost all rivers in Africa, Asia, and Latin America. Therefore, future global water demands cannot be met unless concerted efforts are made to address water quality and wastewater management challenges.
\nTherefore, sustainable management of freshwater resources needs to aim at protecting or reducing pollution load of freshwater sources especially streams and rivers to avoid negative impacts on water quality and ecosystems. In this regard, constructed wetlands are recognized as potential technology for meeting water quality and other requirements of these important freshwater sources. The use of constructed wetlands for water quality improvement is increasing with new applications and technological possibilities [4, 5]. In recent times, the use of river diversion wetlands is gaining more relevance for improving quality of water in riverine systems [6, 7, 8]. The incorporation of constructed wetlands into management strategies for rivers and streams may help to reduce pollution load and enhance their absorbing capacity against impacts [9].
\nDespite the recognition of constructed wetlands as an effective and economical way of improving water quality, many of those in operation are underperforming. The shortcomings are partly attributed to limitation and inconsistencies of equations used in designing them [10, 11, 12]. Besides, most of the available design methods are either related to municipal wastewater treatment or stormwater quality improvement with the primary aim of peak flow retention to attenuate flood water which may lead to overestimation. For river diversion wetlands, specific design criteria have not been fully established, and further research is needed to optimize existing approach in order to enhance performance capabilities of these types of wetlands [7]. However, the design of constructed wetlands is generally based on empirical equations using zero- or first-order plug flow kinetics as basis for predicting pollutants’ removal and improving water quality [13].
\nThis chapter aimed to provide guidance on the design of a typical river diversion constructed wetland intended to improve quality of river water. The chapter provides an overview of factors to be considered for the wetland design, water quality characterization, wetland inflow estimation, computation of the wetland hydrodynamic parameters, wetland sizing, and configuration and guide on designing of conveying and inlet and outlet structures. The approach presented may be useful to wetland experts as some of the procedures adopted are not popular in wetland studies.
\nBasically, two main types of constructed wetlands exist. These are free water surface (FWS) flow and subsurface flow (SSF) systems. FWS flow wetlands operate with water surface open to the atmosphere, while for SSF, water flow is below the ground through a sand or gravel bed without direct contact with the atmosphere [14, 15]. Both are characterized by shallow basins usually less than 1 m deep. FWS wetlands require more land than SSF wetlands for the same pollution reduction but are easier and cheaper to design and build [16].
\nFWS flow wetlands are further sub-classified based on the dominant type of vegetation planted in them such as emergent, submerged, or floating aquatic plants. SSF wetlands which are often planted with emergent aquatic plants are best sub-classified according to their flow direction as horizontal subsurface flow (HSSF), vertical subsurface flow (VSSF), and hybrid system [17]. Another sub-division of constructed wetland types which have emerged recently is river diversion wetlands. These are mostly FWS wetlands located near or within a stream or river system. They are distinguished according to their location as off-stream and in-stream wetlands. Off-stream wetlands are constructed nearby a river or stream where only a portion of the river flow enters the wetland. On the other hand, in-stream wetlands are constructed within the river bed, and all flows of the river enter into the wetland [18]. Figure 1 shows a typical arrangement of both types.
\nArrangement of off-stream and in-stream river diversion wetlands. (a) Off-stream river diversion wetland and (b) in-stream river diversion wetland.
Potential benefits of river diversion wetlands include merits relating to river water quality improvement, flood attenuation, increasing connectivity between rivers and floodplains, and creation of mixed habitat of flora and fauna communities [8, 19]. The systems are also cost-effective due to their simple designs and construction when compared to conventional treatment systems. Major drawbacks of these types of wetland systems relate to emissions of greenhouse gases and losses of biodiversity which may result from continued pollution loading [20]. Unlike the in-stream wetlands, a major advantage of the off-stream river diversion wetlands is that they can be used to mitigate non-point source pollution from agricultural lands before reaching the river channel. However, off-stream wetlands may require storage and flow control structures to regulate flow and a large space for layout of the wetlands which may result in high initial costs for land easements. Additionally, only part of the river flow volume can be treated at a time. On the other hand, space availability may not be a big issue for in-stream wetlands as they are constructed within the river bed, and as such the whole river flow volume can be subjected to treatment. However, it may be difficult to regulate flow especially during river peak flows and consequently retention time which is an important aspect of wetland for effective pollutant removal.
\nThe design of a constructed river diversion wetland is an iterative process involving site-specific data. Prior to design and construction, site conditions must be evaluated to assess the appropriateness of the site for the proposed constructed wetland system [4]. Thus, the following are recommended as part of the design process:
Investigation of site characteristics
Water quality characterization
Wetland design inflow estimation
Site condition is a very important factor in the design of a constructed river diversion wetland. This is particularly necessary when a suitable site or land is not readily available as the situation often limits possible options the designer may utilize. Thus, site investigation enables the designer to have an idea of the site characteristics including size of area or land available for the design. However, where there is sufficient suitable site or land, it gives the designer the latitude and flexibility of several design options. Therefore, identifying the required area available for optimal layout of the wetland is vital for effective reduction of pollutants.
\nSite characteristics to be evaluated when designing and possibly constructing a river diversion wetland include:
Proximity of the site to the river system (the site should be situated close to the source of water to be treated for easy diversion or within the river channel depending on the type (in-stream or off-stream))
Climate (climate can affect type and size of the space required for the wetland; climatic factors that are important include rainfall, evaporation, evapotranspiration, insolation, and wind velocity)
Topography of the land (topographic conditions such as natural depressions and slopes are important consideration; the gradient of the land should preferably have a gentle slope so that water can easily flow by gravity)
Groundwater condition (assess groundwater levels within the site in different seasons to guide against possible contamination)
Soil and environmental condition of the site (the site should contain soils that can be sufficiently compacted to minimize seepage to groundwater, or necessary measures should be put in place to minimize groundwater contamination)
Distance of the site from residential buildings to avoid creating an environment that is not conducive for inhabitants
After due consideration of the above conditions, a suitable location can be selected for siting the wetland system, and the designer can then take cognizance of the space available for the system design.
\nCharacterization of pollutant concentration of the river water to be treated is essential for sizing of a constructed river diversion wetland and in creating a clear understanding of whether the wetland can effectively treat the water or not. Thus, the constituents of the river water and their respective concentrations need to be known before beginning the design process of the constructed river diversion wetland. However, water quality is highly variable especially in rivers due to fluctuations and variability of discharge and contaminant concentration from pollution sources [21]. Thus, a clear definition of water quality is essential, and it may be necessary to take into account previous distribution of the contaminants’ concentrations in the water over time [4]. According to [22], characterization of the river water quality can be done based on available data which provides information on temporal and spatial distribution of parameters of interest and their level of concentrations in the water to be treated. Water quality parameters that are characterized in most situations include biochemical oxygen demand (BOD), nitrogen, phosphorus, suspended solids, and coliform bacteria [23]. These are pollutants that originate mostly from organic sources and are considered of most interest in treatment wetland design [24]. Others include metals, phenols, pesticides, and surfactants which may also be treated. However, these parameters require specific applications as opposed to organic pollutants [18].
\nBOD reflects the degree of organic matter pollution, and it is a measure of the amount oxygen removed by aerobic microorganisms for their metabolic requirement during decomposition of organic materials. Nitrogen and phosphorus are considered as primary drivers of nutrient pollution, and they occur in organic and inorganic forms. Nitrogen in water is usually measured as total nitrogen, ammonium ion, nitrate, nitrite, and total Kjeldahl nitrogen (sum of organic nitrogen and ammonium ion) or as a combination of these parameters to estimate organic or inorganic nitrogen concentrations [25]. Phosphorus in water is usually measured as total phosphorus which is the sum of organic and inorganic forms of phosphorus and includes orthophosphate (PO4\n3−), polyphosphates, and organic phosphates [1]. For microbial contamination, indicator organisms are used to detect the presence of pathogens (disease causing organisms). Microorganisms mostly considered are those of fecal origin, and coliform bacteria are most often used to indicate the presence of fecal pollution [26]. Suspended solids are constituents that remain in solid state in water and often occur as part of sediments carried in the water. Measurement of suspended solids is essential as sediments are responsible for contaminant transport in water. Metals can exist as dissolved, colloidal, or suspended forms in water, and their toxicity depends on the degree of oxidation of the metal ion together with the forms in which it occurs [1]. Metals mostly considered with high priority in water pollution are arsenic (As), cadmium (Cd), copper (Cu), chromium (Cr), lead (Pb), mercury (Hg), nickel (Ni), and zinc (Zn) [23]. Nevertheless, selection of any pollutant or combination of pollutants for water quality improvement will depend on the objectives for which the wetland is designed. Based on the river water quality characterization, appropriate equations can be used to determine the required area and organic loading rates of the wetland system.
\nThe amount of water flow per unit time that passes through a wetland system is one of the important parameters required in the design of a constructed river diversion wetland. Flow rate of water is an important hydrological parameter required to facilitate sizing of a constructed wetland [4]. Even though flow into a wetland can be continuous or intermittent, it however passes through the system at low velocities. There are different approaches employed to determine the quantity of inflow (volumetric inflow rate) into a wetland, depending on the wetland type, treatment objectives, and incoming water to be treated.
\nFor wastewater treatment wetlands, inflow is mostly based on wastewater concentration and generation rates [27]. Mass loading charts with reference to the required level of pollutant removal are mostly used in the United States, while in Europe estimation is based on wastewater generation volume and pollutant concentration [27, 28]. For stormwater constructed wetlands, a range of hydrologic methods are applied to estimate design flows. Typical approaches include the use of routing in response to a storm event like the average recurrence interval (ARI) flow criterion, level-pool routing, and estimation of peak runoff flow rate using curve number (CN) model and rational method [29, 30, 31]. The ARI is applied in Australia and level-pool in Malaysia, and the CN is mostly used in the United States. While all these methods are mainly applied to stormwater treatment wetlands, they are however used with reference to specific available data and scenarios in these countries [29]. Moreover, not all wetlands are designed for treatment of maximum expected peak flows; otherwise the vegetation are likely to be damaged due to high flows, and the wetland system would need to be extremely large or the outflow water quality requirement considerably relaxed. Furthermore, the CN model has been examined to be inaccurate due to inherent limitation associated with inconsistency of the fixed ratio (λ) between initial abstraction (\n
For river diversion wetlands, a specific method for estimating design inflow has not been fully established [7]. However, more recently, [8] evaluated the performance of a river diversion wetland for improving quality of river water using relations that can be used to estimate design inflow for a similar wetland system. These relations are presented below.
\nwhere
Application of the above equations requires estimation of average flow volume of a river. However, flow rates vary over time because of normal variability in precipitation patterns, and a key factor governing hydrological regime of rivers is their discharge variability [35]. Therefore, to determine river flow or discharge regimes, historical flow data are required, including possible seasonality trend of the flows, pattern of past flows (low, moderate, and high flows), and stream gauge information close to the wetland site location [4, 36]. Flow data are important to facilitate understanding of fluctuations in the amount of flowing water in the river and to support development of a rating curve for the river where it is not available. The rating curve has been an important tool widely used for routing purposes in hydrology to estimate discharge in natural rivers [37]. It is a graphical representation that gives relationship between flow regimes and stage heights or water levels of a river at a given site and over a period of time [35, 38]. However, very few rivers have absolutely stable flow characteristics, and thus the rating curve may require revision over time and under unsteady conditions. A comprehensive review of the various equations developed by several authors for correcting unsteady to steady flow condition was presented by [38].
\nAnother crucial aspect of wetland design is the estimation of average river flow regimes. The river flow regimes are required to:
Guide in determining the amount of water per unit time that can be diverted into the wetland system without compromising the flow needed for survival of the river ecosystem.
Aid the design and estimation of inflow regime(s) for which the wetland system will be operated since the goal of the wetland is to improve quality of river water.
Therefore, obtaining or developing appropriate rating curve may be necessary to facilitate characterization of flow regimes of the river. Based on the rating curve, the river flows can be classified into low, moderate, and high flows. Figure 2 shows a typical river rating curve with flows classified into three regimes as indicated. For example, based on the rating curve (Figure 2), three flow regimes (0.29 m3/s, 1.97 m3/s, and 3.96 m3/s) (marked with dotted red lines) were selected corresponding to low, moderate, and high flows of the river, respectively. The classification of the flow regimes into low, moderate, and high flows was based on their computed flow velocities as presented in Table 1.
\nTypical river rating curve with flows classified into three regimes.
Flow regimes (m3/s) | \nMean cross-sectional area of river gauging section (m2) | \nVelocity (m/s) | \nVelocity\n*\n groups (m/s) | \nClassification | \n
---|---|---|---|---|
0.29 | \n3.34 | \n0.09 | \n<0.10 | \nLow flow | \n
1.97 | \n3.34 | \n0.59 | \n0.10–0.60 | \nModerate flow | \n
3.96 | \n3.34 | \n1.19 | \n≥0.70 | \nHigh flow | \n
For flood or peak flow control wetlands, high flows are often considered for the design, while for water quality improvement, moderate to low flows are mostly the target. Where high flow is to be used for design of river diversion wetland intended for water quality improvement, it may be necessary to include a retention basin in the design to slow down flow energy and allow for gradual release into the system.
\nSince the river diversion wetland under discussion is intended to be designed for water quality improvement, only a portion of the river flow regimes is required to be diverted into the wetland system per unit time. Thus, to determine the quantity of the design inflow rate of the wetland, Eq. (3) derived from Eqs. (1) and (2) can be used together with the average river flow regime(s).
\nwhere all parameters remain the same as previously defined in Eqs. (1) and (2).
\nThe wetland can be designed to operate with the three river flow regimes (low, moderate, and high) to take into account seasonal flow variability or a single flow regime depending on the objective and availability of space within the site.
\nThe design of constructed wetlands is generally based on empirical equations using zero- or first-order plug flow kinetics as basis for predicting pollutant removal and improving water quality [13]. With zero-order kinetics, the reaction rate does not change with concentration but varies with temperature [4], while first-order kinetics simply implies that the rate of removal of a particular pollutant is directly proportional to the remaining concentration of the pollutant at any point within the wetland [40]. Plug flow means that every portion of flow entering into the wetland takes almost the same amount of time to pass through it which is rarely the case [41]. The kinetic equations also considered FWS wetlands as attached growth biological reactors similar to those found in conventional wastewater treatment systems [23]. Generally, two types of equations are popular that use two different approaches in the design of FWS wetlands based on “rule-of-thumb” (no account for the many complex reactions that occur in a constructed wetland). There is the volume-based or zero-order kinetic equation which uses hydraulic retention time to optimize pollutant removal [42, 43]. The second is the area-based or first-order kinetic equation where the entire wetland area is used to provide the desired pollutant treatment [44]. The key difference between the two equations is in the use of kinetic rate constants. Volume-based equation assumes horizontal or linear kinetics and uses volumetric and temperature-dependent rate constant, with calculations being based on available volume of the wetland and average water temperature. The area-based equation assumes vertical or areal kinetics and uses rate constants which are independent of temperature but related to the wetland surface area. The volume-based equation was developed by [43], and the equations are presented below:
\nwhere \n
The area-based model equation was developed by [44], and the equations are presented below:
\nwhere \n
The volume-based model was developed based on those parameters that are removed primarily by biological processes such as biochemical oxygen demand (BOD), ammonia (NH4), and nitrate (NO3). The areal equation considered more parameters and in addition includes total suspended solids (TSS), total phosphorus (TP), total nitrogen (TN), and fecal coliform (FC). According to [45], while the [43] method provides a relatively conservative area estimate, [44] approach may require considerable land space, depending on the pollutant concentration limit. Furthermore, the [45] model appears to be less sensitive to different climatic conditions as temperature changes are only considered significant for nitrogen removal [46]. However, temperature plays an important role in constructed wetland systems as it enhances higher biological activity and productivity which may lead to better performance of the systems [47, 48]. For this reason, the use of these models may lead to wide variations in performance due to effect of changes in climatic conditions. Additionally, many authors have developed more complex models like the Monod-type and mechanistic compartmental models [49, 50]. However, the [43, 44] models appear to be more straightforward and can be applied with ease by wetland designers [13]. Data limitation on operational performance of constructed wetlands prevented the development of equations which can clearly describe the kinetics of known wetland processes [23]. Thus, optimal design of constructed wetland systems has not yet been determined. However, in order to take advantage of [43, 44] models and ease complexity of computation, [24] presented a simplified approach for the design and sizing of FWS constructed wetlands using the two equations. The approach was based on performance criteria for the removal of four water quality parameters that included BOD, nitrogen, phosphorus, and coliform bacteria. According to [24], rates of BOD and nitrogen removal are principally temperature dependent and therefore utilized equations proposed by [43] model for removal of these parameters. On the other hand, the reduction of phosphorus and coliform bacteria was assumed to be governed by physical processes which are less temperature-dependent, and thus [44] equations were used. In addition, [24, 51] proposed the following relationships for nominal hydraulic retention time and removal of total nitrogen (TN), respectively.
\nwhere \n
The authors recommended that the above equations can be used together with those presented by [43, 44] to determine the hydrodynamic and size parameters of a new FWS flow constructed wetland, depending on the target pollutant or combination of pollutants (BOD, nitrogen, phosphorus, and coliform bacteria) required to be removed from the wastewater. As indicated by [52], the approach presented by [24] is useful in the design of a new FWS constructed wetland and for performance evaluation of existing ones.
\nThe use of a combination of wetland design equations proposed by [24, 51] was found to be useful for determination of river diversion wetlands’ hydrodynamic parameters. These parameters include nominal hydraulic retention time and hydraulic loading rate.
\nDetermination of nominal hydraulic retention time is important for design guide and estimating possible pollutant removal ability of the wetland system. Thus, the nominal HRT for a river diversion wetland can be estimated based on the kinetic equations governing the removal of basic water quality parameters (BOD, nitrogen, phosphorus, and coliform bacteria), often used for sizing of constructed wetlands. Table 2 shows the parameters and kinetic equation used for determining the nominal HRT.
\nParameter | \nEmpirical equations | \nEquation no. | \nSource | \n
---|---|---|---|
BOD (mg/l) | \n\n\n | \n(1) | \n[41] | \n
\n | \n\n | \n(11) | \n[12] | \n
TN (mg/l) | \n\n\n | \n(9) | \n[12] | \n
\n | \n\n | \n(12) | \n\n |
\n | \n\n | \n(13) | \n\n |
TP (mg/l) | \n\n\n | \n(10) | \n[22] | \n
\n | \n\n | \n(14) | \n[13] | \n
FC (CFU/100 ml) | \n\n\n | \n(10) | \n[22] | \n
\n | \n\n | \n(14) | \n[13] | \n
Parameters and equations for computing design HRT.
Note: \n
The HLR of the wetlands system can be computed using Eq. (7) by [44]. The determination of the HLR is essential to guide in the design and can assist to avoid overloading the system. Thus, the design may confirm the organic loading rate is within the wetland limit; an equation developed by [51] can be used to compare the \n
where all parameters remain the same as defined in Eqs. (1), (2), and (4).
\nSizing is an important component of wetland design and vital for pollutant removal processes to take place. Most of the design recommendations provided certain approaches to wetland sizing to maximize removal of pollutants. For wastewater treatment wetlands, population equivalent (PE) is mostly employed for the determination of design wetland area. The required surface area is usually expressed as unit area per population equivalent (m2/PE). For example, 5–10 m2/PE was recommended for FWS, while for SSF it ranges between 2 and 5 m2/PE depending on the type (HSSF, VSF, and hybrids) [27]. For stormwater wetlands, the typical approach is to consider relative percentage of the contributing catchment area or connected impervious area, and 1–5% of the contributing watershed was recommended as actual sizing criterion [4]. For full-scale river diversion wetlands, a minimum of 2–7% of the total catchment area was recommended as wetland area [20]. However, such sizing criteria pose challenges of overestimation and do not account for any performance consideration [53]. Therefore, such prescribed wetland sizing criteria may be unrealistic due to space limitation and cost. Nevertheless, an approach derived based on empirical determination of actual area required for pollutant removal with reference to hydraulic loading rate as presented by [24] appears to be more realistic for estimating actual area of river diversion wetlands intended for water quality improvement. Thus, the actual area required for such a wetland system can be determined using Eq. (16) which was derived from Eq. (8) by [24].
\nwhere \n
For ease of operational control (flow control and water level adjustment) and increased removal efficiency, multiple wetland units often referred to as cells may be used where possible than a single unit wetland. This is particularly more applicable to design of off-stream river diversion wetland. Multiple cells have the advantages of providing greater flexibility in design and operation and enhancing the performance of the system by decreasing the potential for short-circuiting. Wetland cell size depends primarily on water quality treatment needs and cost considerations.
\nThe actual area of the wetland is then computed using Eq. (16). Based on the computed values, the actual area of the wetland is thus selected as the maximum of areas obtained for each of the target pollutants (BOD, nitrogen, phosphorus, and coliform bacteria).
\nWetland system configuration is an important element in the design of river diversion constructed wetland technology. After determining an appropriate wetland size, it is necessary to define the system configuration or layout by choosing an appropriate aspect ratio. Aspect ratio represents length (L) to width (W) ratio (L/W) of the wetland. It was suggested that choosing a good aspect ratio can assist to minimize short-circuiting and maximize flow distribution within the wetland system for biological activities [54]. Aspect ratio of as low as 1:1 was recommended for SSF [55], while length to width ratio of between 3:1 and 5:1 was recommended for FWS from an optimal point of view by [23]. However, based on findings by [56], 10:1 was recommended for FWS for good hydraulic efficiency. For water quality improvement, a river diversion wetland should be designed to operate with the most efficient aspect ratio.
\nWetland bed slopes are also critical to maintain a uniform water depth throughout the wetland system and facilitate drainage. In order to minimize short-circuiting, a uniform bed slope from inlet to outlet is recommended. Thus, the bed slope for SSF should be 2% or less, while that for FWS should be 0.5% or less [14]. A river diversion wetland can also be designed to operate with similar bed slope as recommended for FWS since they are related in mode of operation.
\nThis aspect of the wetland design focused on selecting or designing a water conveying system, inlet and outlet control structures that can facilitate flow and distribute inflow and drain outflow water from the wetland effectively. Depending on the type of river diversion wetland, flow diversion structure may be designed to consist of either a pipe or channel system and should function to provide a controlled flow of water to the wetland. However, it is necessary to be explicit about flow capacity at the time of design so that appropriate sizing of flow diversion structure can be made. Generally, the design flow conveyance structure is based on hydraulic; therefore the reader is referred to hydraulic books for detailed information.
\nIn order to ensure that the inflow water is uniformly distributed across the entire wetland area, multiple entry openings or gates should be considered rather than single to deliver the range of design flow regimes required. Flow control structures should be used to control inflow rate and maintain water levels. Control valves or weirs or a combination can be used depending on the type of inlet structured selected. Since the wetland system is for water quality improvement, high incoming water velocities should be discouraged. Therefore, energy dissipation system may be required for the incoming water to provide protection for the wetland inlet. The inlet openings should be designed large enough to avoid obstruction. Inlet zones should provide access for sampling and flow monitoring.
\nWetland outlet design is essential in avoiding possible dead zones and controlling water level and for monitoring flow and water quality. Depending on the size of the wetland, a combination of outlets (primary and secondary) or multiple outlets consisting of hydraulic control structures can be considered to collect and discharge treated water for the range of design flow regimes and maintain required water storage level. The purpose of the primary outlets is for water quality control, while the secondary is to act as a spillway and control flows in excess of the maximum design flow regime. Different types of control structures are available that can be used to control water level within the wetland. These may include number of individual pipes that fit together in a combination to obtain the desired water level, drop structures, or weirs. The design requirements of drop control structures and weirs can be found in hydraulic books. The outlet or water level control structure should be able to completely dewater the wetland when needed and allow for changes to be made easily.
\nThe management and restoration of water bodies like rivers should go beyond protection through the use of regulations. It should also make the most of opportunities that arise from using ecosystem properties to enhance self-purification capacity of rivers for water quality improvement. A key consideration is the use of constructed river diversion wetlands.
\nThis chapter provided guidance on the design of a river diversion constructed wetland aimed at improving quality of river water. The use of a combination of empirical equations was presented to guide in the estimation of the actual wetland area rather than relying on an assumed rate. The design approach using these equations may present a promising method for the design of river diversion wetlands. Furthermore, this novel approach may be useful to wetland experts as some of the procedures adopted are not popular in wetland studies. This may provide opportunity for wetland designers to document approaches that have been found promising and come up with suitable design criteria for constructed river diversion wetlands.
\nThe authors wish to express appreciation for the funding support provided by the Regional Water and Environmental Sanitation Centre, Kumasi (RWESCK), at the Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, which is funded by the Government of Ghana and the World Bank under the Africa Centres of Excellence Project. Also, the authors wish to thank the National Water Resources Institute (NWRI), Nigeria, for providing opportunity and support for the study that led to the generation of knowledge and information presented in this chapter. We declare that the views expressed in this chapter are those of the authors and do not necessarily reflect those of the World Bank, Ghana Government, KNUST, and NWRI.
\nNone declared.
In a prior review (2012), literature describing the etiology of fetal brain injury, and its presentation, evolution and management in the neonate was summarized [2]. However, recent advances have considerably increased our knowledge of the nature and prognosis of brain injury, and what can be done to treat and prevent it.
The importance of maternal and fetal health throughout the nine months of intrauterine life remains. But the vulnerability of the fetus to adverse events related to labor and delivery is better understood, and more readily anticipated. Substantial progress has also been made in the care of neonates, our understanding of the pathogenesis of injury, and protective strategies which can help to prevent or mitigate permanent injury. It is now clear that acute brain injury is a continuum; hypoxia and ischemia in particular generate a sequence of physiologic consequences where the acute phase of injury is followed by a period of latency, and then brain cells undergo secondary energy failure where a cascade of disruptive events occurs which leads ultimately to programmed cell death. This understanding is particularly valuable, as it now guides investigation linked to both the diagnosis and prognosis of injury, and provides critical opportunities for novel care strategies.
The birth and care of infants born prematurely remains challenging. The inherent immaturity of their organ systems and complex therapies they require makes them vulnerable physiologically to a spectrum of potentially adverse events; the result is a significant incidence of long-term cognitive and motor deficits. In spite of advances in obstetric and neonatal care lowering the overall prevalence of complications, the incidence of cerebral palsy has not reduced significantly. But it is clear now that a strong relationship exists between gestational age at delivery and the probability of both survival and discharge without major handicap, with every additional week in utero tending to improve the chances of a good outcome [3].
Fetal and neonatal brain injury, and the long-term neurodevelopmental handicap caused, is an extremely important problem, and especially so in premature infants, because of the large absolute number born. Research documents that infants born very prematurely (<32 weeks gestation), and those with an extremely low birth weight (<1000 g), are at increased risk for neurobehavioral impairments (cerebral palsy, blindness, deafness), lower general intelligence, specific cognitive defects, learning disabilities, and behavioral and emotional problems [2, 3]. Modern neonatal care does now enable an increasing number of these infants to survive and escape significant handicaps. Survival of extremely preterm infants (<25 weeks gestation) remains rare, but in Europe and the USA 75-90% of infants who weigh <1500 g at birth now survive, however 5-10% of them develop cerebral palsy subsequently, and many have cognitive, behavioral, attention-related or socialization deficits.
Normal fetal growth is a continuum that must be appreciated in order to fully understand the causes, evolution, and consequences of abnormalities in brain development. Key factors have been reviewed previously [2]. Genetic anomalies are the principal cause of fetal loss, and structural abnormalities are commonly evident at a macroscopic and microscopic level. Advances in genetic screening and analysis have led to genetic studies becoming an integral part of the workup of an increasing number of infants. Genetic counseling is central to prevention in situations where there is a family history of a genetic brain abnormality, birth of a prior infant with an anomaly, or predisposition to a genetic problem due to racial or age-related factors. An autopsy and placental pathology are important after fetal loss.
Embryonic development progresses rapidly after conception, so that a large proportion of the brain’s structure is already formed by the time many women become aware that they are pregnant. By the end of the first trimester (3 months of gestation), all the main structures of the central nervous system are formed and so brain growth alone follows between this time and fetal maturity (40 weeks). Hence the relevance of more people understanding the concepts currently articulated in the developmental origins of health and disease (DOHaD) [4] and the importance of:
health at the time of conception (both paternal and maternal);
the detrimental effects on the fetal brain of drugs, alcohol and nicotine;
the beneficial effects of a maternal diet that provides essential nutrients
maternal nutrition and weight gain that avoids fetal stunting or overweight
Impaired fetal growth secondary to poor maternal nutrition or placental insufficiency can be associated with reduced brain development; growth retarded infants are at increased risk of hypoxic stress and hypoxic ischemic (HI) brain injury due to altered placental blood flow and sub-optimal fetal oxygenation, particularly at the time of delivery. Suboptimal nutrition also poses the risk of hypoglycemic brain injury immediately after birth; the impact of this form of brain injury can now be defined through neuroimaging [5]. At the opposite end of the spectrum, being large for gestational age, post mature, or the product of a multiple pregnancy poses unique challenges, and increases the risk of HI injury [2]. In addition, surviving infants born small or large for gestational age are at increased risk of developing adult-onset chronic diseases (e.g. hypertension, cardiovascular disease, stroke, type 2 diabetes, obesity); the current epidemic of non-communicable diseases has been shown to be linked to early stunting of growth and excessive infant weight gain [4].
Importantly many of the causes of brain damage are now avoidable or amenable to treatment. Neuroimaging protocols help to define both the timing and geographic location of injury, and document the evolution of neuronal changes through defined phases over time [6, 7]. In the acute phase, damage follows decreased cerebral blood flow and reduced oxygen and glucose delivery and resulting ischemia and acidosis. A period of latency follows with transient recovery of energy metabolism. Then an ‘excito-oxidative’ cascade leads to cerebral energy failure and progression to cell death [8, 9, 10]. In this phase, reduced adenosine triphosphate (ATP) production affects membrane integrity; intracellular accumulation of sodium and water follows, and brain cell injury is caused by neuronal depolarization, glutamate release, an influx of calcium, and release of toxic nitric oxide free radicals. The ‘therapeutic window’ offered by the ‘latent phase’ now allows interventions to ameliorate the effects of HI injury, and hypothermia initiated within 6 hours of age shows particular promise.
Clinical effects of hypoxia include a disturbance of acid base status. An unrelieved hypoxic event in the fetus causes progressive acidosis which leads to systemic organ dysfunction, including cardiac depression, where compromised contractility and filling reduce cardiac output leading to a reduction in CBF and high risk of brain insult when cerebral hypoxia and ischemia occur. Importantly, cardiac functional impairment can precede depression of fetal heart rate. Hypoxic insults depress brain function, so following intrapartum insults infants are neurologically abnormal at birth, often require resuscitation to initiate breathing, and cardiovascular support can be needed to stimulate heart function and provide adequate blood pressure and circulation. Tone and behavior usually remain abnormal on admission to the nursery; encephalopathy developing in the hours or days after birth is confirmation that a significant HI insult resulting in brain injury has occurred.
Hypoxic ischemic brain injury is estimated to occur in about 3 out of every 1000 births [8]. Diagnostic features include problems with level of consciousness, tone, respiratory drive, and coordination of sucking and swallowing, and seizure activity which is commonly refractory. In the longer term, the consequences of injury vary between death (15-20%) and complete recovery, with the spectrum of permanent brain injury ranging from mild motor and cognitive defects, to cerebral palsy and severe cognitive disabilities. The pattern and consequences of injury depend on the severity and duration of the insult. The neurovascular and anatomical maturity of the brain relative to the gestational age of the fetus is also a primary factor; co-related elements include the adequacy of metabolic reserves available to the fetus to compensate for oxidative stress, the presence or absence of infection, and pre-existing abnormalities in brain growth and development. Different regions of the fetal brain and individual cell lines have gestation specific vulnerability to damage.
Periventricular leukomalacia (PVL) is predominately a condition affecting the preterm infant. The primary causal mechanism is HI injury, with ischemia being the major component. PVL acquired intrapartum is usually associated with abnormal neurological findings at birth, but may manifest as lower limb weakness evident in the first weeks of life. PVL can be aggravated by, or generated as a result of postnatal events. Neurobiologic research has shown that maturational dependent oligodendroglial precursor cells are a major target in PVL, and these are exquisitely vulnerable to damage by free radicals generated during ischemia and reperfusion. PVL is associated with intraventricular hemorrhage (IVH) in approximately 25% of cases. The pathogenesis of IVH is usually multifactorial, and related to: fluctuating CBF; increased cerebral venous pressure; decreased CBF followed by reperfusion; and disorders of coagulation, platelet function and capillary integrity [11].
The commonest clinical situation where pathogenic factors combine to generate sufficient ischemia to cause PVL is when a sick preterm infant requires mechanical ventilation, and problems occur during ‘uncontrolled’ intubation, with ‘fighting the ventilator,’ or when a pneumothorax (air leak) compresses the lung, which raises intrathoracic pressure and disrupts normal blood return to the heart; in turn, this reduces cardiac output and brain blood flow. Vascular factors are also relevant; blood transfusion or rapid IV volume replacement pose potential risk due to the pressure passive nature of the immature cerebral circulation; systemic variations in blood pressure, sequelae of sepsis, and the cerebral effects of hypocarbia can render an infant symptomatic. Many infants with PVL have a normal neurologic outcome. Those with permanent sequelae exhibit a range of problems with varying degrees of severity; including intellectual and visual deficits, usually superimposed on spastic paresis involving the extremities, where the lower limbs are predominantly affected.
In late prematurity (34 weeks to 36 weeks plus 6 days gestation), the vulnerability of the brain to injury, and the pattern of damage commonly seen are different, due to increased structural and functional maturation; at 34 weeks of gestation the brain has 65% of its term volume compared to 13% at 28 weeks, and a fivefold increase in white matter volume occurs between 35 and 41 weeks of gestation.
Gestation in weeks | 23 | 24 | 25 | 26 | 27-31 | 32-34 |
Percentage of survivors | 0% | 11.6% | 30% | 47.5% | 81.3% | 96.8% |
Gestation-related survival without grade 3/4 intraventricular hemorrhage, cystic periventricular leukomalacia, retinopathy of prematurity stage 3 or higher, severe bronchopulmonary dysplasia, or necrotizing enterocolitis stage 2-3 [3].
Ischemia is the principal mechanism underlying brain damage; lesions include white matter infarction, intra-ventricular hemorrhage, hydranencephaly, and porencephaly. In up to 58% of TTTS affected pregnancies combined US evidence is reported of antenatally acquired brain abnormalities and IVH, and periventricular echogenicity assumed to be perinatally acquired [20]. Fetal MRI can identify CNS injury; findings range from ischemic or hemorrhagic lesions in the brain to marked dilation of the cerebral venous sinuses secondary to central venous hypertension.
US can also evaluate flow in the umbilical vein (UV) and ductus venosus (DV). Normally, the UV blood flow velocity waveform has an even non-pulsating pattern, since the pulse waves caused by atrial contractions are not propagated backwards through the narrow ductus venosus. However, if the DV widens, the pulse waves propagate into the UV and result in a pulsating pattern. UV pulsations were first described in fetuses in imminent danger of asphyxia, then in those hydropic due to heart failure. In fetuses exposed to chronic hypoxia, UV pulsations predict poor outcome [21]. The presence of absent or reversed flow in the DV during atrial systole (defined as absent/reversed a-wave) is associated with poor perinatal outcomes because of compromise to mechanisms that normally preferentially supply the fetal brain with well oxygenated blood. The function of the DV is to shunt a portion of the oxygenated blood arriving from the placenta directly to the inferior vena cava, allowing oxygenated blood to bypass the liver. Consequently, DV flow plays a critical role in preferentially supplying oxygen to the fetal brain, in parallel with the other fetal shunts (foramen ovale and ductus arteriosus). And so, US evidence of an absent or reversed a-wave in the DV identifies those fetuses who are at the highest risk of hypoxic brain injury in utero [13, 22, 23].
The expectation of maternal treatment, even for severe TTTS, is for improvement, with probable resolution in utero [24], including regression of fetal cardiovascular pathology and improved myocardial performance. Recovery may take longer in more severely affected pregnancies, but this is not the case in all series. Survival, particularly for the recipient twin, is likely to be compromised if treatment is delayed [25] hence the relevance of US surveillance and early diagnosis [17].
Many cytokines are vasoactive, so in the immature brain, focal variations in brain perfusion could result in local ischemia followed by reperfusion; such perturbations may cause cumulative injury to brain white matter due to the primitive neuro-vascular architecture, immature autoregulatory control mechanisms, and sensitivity of maturational dependent cells to free radical damage. The germinal matrix is also particularly vulnerable to variations in brain blood flow and blood pressure [11]; consequently, it has been hypothesized that periventricular hemorrhage would be more likely to occur in the preterm fetus exposed to FIRS.
The initial literature supported a role for inflammatory mediators in premature labor and delivery; linked maternal infection and pro-inflammatory mediators in the neonatal systemic circulation with increased risk of periventricular leukomalacia and/or spastic diplegia; emphasized the synergistic role of inflammation and hypoxia and ischemia when they occur together; and reported a higher incidence of HI brain damage where fetal exposure to maternal inflammation/infection occurred [2]. This literature also states: “For the premature fetus, once clinical chorioamnionitis occurs, rates of sepsis, pneumonia, respiratory distress syndrome and death are all increased by 2-4-fold and long-term neurologic injury is substantially more likely to occur” [29]. Strategies can be used to down-regulate the inflammatory response and treat mothers with signs and symptoms of infection; some antibiotic therapies reduce cytokine production; because of the independent association of elevated maternal temperature with worse fetal outcome, appropriate management to control fever is also cited as a treatment of potential benefit [30, 31].
Recent literature reappraises prior FIRS-related research. Isolated cytokine-mediated injury is not reported in term infants [11], and in the premature newborn, newer studies have found the relationship between chorioamnionitis and brain injury to be attenuated; this difference may result from heterogeneity of the studies, or possibly improved neonatal intensive care [32]. Current literature does conflict on whether or not histopathological chorioamnionitis is linked to an increased risk of white matter injury and intraventricular hemorrhage, or with abnormalities of brain development identifiable via MRI (e.g. variations in cortical thickness). But research continues to emphasize that postnatal complications from infections, particularly when associated with hypotension in the premature newborn, are associated with an increased risk of white matter injury [33, 34].
Population data indicate that blood glucose levels as low as 2.0 mmol/L (or even 1.8 mmol/L at 1 hour of age) are not uncommon in healthy newborns. However, various syndromes and metabolic conditions cause or contribute to hypoglycemia. Importantly, HI injury can disrupt normal metabolic adaptation, as anaerobic glycolysis depletes hepatic glycogen and hyperinsulinism can also occur; there is a correlation between lower serum glucose levels and higher Sarnat stages in hypoxic ischemic encephalopathy (HIE).
For at-risk infants, outcome data support raising the intervention threshold from conventional levels. Current screening and management guidelines are that neonates with hypoglycemia persisting beyond the first 72 should be investigated further when levels remain ≤2.8 mmol/L, and ≥ 3.3 mmol/L should be the therapeutic glucose target level in symptomatic/at risk infants. Also, before discharge, those experiencing persistent hypoglycemia should have a 5-6 hour fast, while maintaining blood glucose levels ≥3.3 mmol/L, to ensure safety at home [39].
Differing patterns of damage now help to distinguish hypoglycemic from HI brain injury [5, 40, 41]; the combination on MRI of selective edema in the posterior white matter and pulvinar appears specific even in absence of hypoglycemic laboratory values. In neonates with concurrent hypoglycemia and HIE, injury is synergistic, and the imaging features of both HI injury and hypoglycemia may be detected [5].
As the physiologist Haldane said: “Hypoxia not only stops the machine it wrecks the machinery” [2]. A healthy fetus can respond to, and tolerate, the early effects of hypoxia, and the degree of acidosis that occurs initially in response to the associated retention of carbon dioxide. Acute hypoxia promotes adenosine release, which reduces fetal cerebral oxygen consumption via action on neuronal A1 receptors on the cerebral arteries, and initiates vasodilatation through activation of A2 receptors; release of nitric oxide and opioids and direct effects of hypoxia on the vascular endothelium also contribute [53]. As a result, while fetal vascular resistance can decrease up to 50%, the net effect is to maintain CBF with only minimal reduction in oxygen delivery; but normal or elevated mean arterial blood pressure is critical in parallel, and once hypotension ensues the brain suffers from the resulting ischemia.
With moderate HI stress and evolving acidosis, the fetus also has the physiologic ability to preferentially perfuse the deep structures of the brain that have higher metabolic rates (brainstem, cerebellum, basal ganglia). However, this compensatory redistribution of blood from the anterior to the posterior circulation results in the brain’s cortical areas being less well perfused, and hence, if ongoing hypoxia remains unrecognized and unrelieved over the course of an hour or more, the end result is damage to cortical white matter, and the watershed areas of the cerebral hemispheres. In contrast to this partial prolonged pattern of injury, situations occur where the HI event is near total in nature and the effect profound. With such insults, acidosis develops relatively abruptly, and little or no compensatory redistribution of blood to the deep brain structures occurs, because there is no time for effective redistribution of CBF to maintain their perfusion. Hence it is the basal ganglia and thalami that are predominantly injured, and damage happens over a much shorter time frame [9, 54, 55, 56]. In the premature, mild to moderate HI injury results in periventricular leukomalacia and germinal matrix bleeds, and in full term neonates parasagittal watershed infarcts are seen [55, 57]; severe injury in both term and preterm infants involves deep gray matter.
Distinction between partial/prolonged and near total/profound/patterns of injury is important from a diagnostic and prognostic standpoint, for understanding potential mechanisms for prevention, and over issues of causation in a medico-legal context. Modern neuroimaging is the definitive way to distinguish between them based on the selective geographic patterns of brain damage caused. Importantly however, mixed patterns of injury are also seen that involve both the cortex and deep structures [55, 57]. The mechanisms involved can be either superimposed insults involving periods of both partial/prolonged and near total/profound injury, or, situations where partial and prolonged injury is severe enough to extend to involve the deep brain nuclei, or vice versa, when a near total, profound event is extensive enough to also involve cortical damage [11, 58].
The time line of near-total HI events can be extrapolated from data obtained in animal studies, where fetal monkeys were exposed to complete (i.e. total) hypoxia and ischemia, generated by ligating the umbilical cord and preventing breathing. These animals could tolerate 10 minutes of HI insult without permanent effects if delivered and resuscitated immediately, but, where the HI event was continued beyond this 10-minute period for an additional 10 minutes, a progressive and cumulative increase in the level of neurological damage was then evident. Where the whole insult extended beyond 20 minutes, the fetal monkeys died, in spite of delivery and immediate resuscitation.
In applying these data to the human fetus, it is recognized that what occurs most often is a near total (profound) interruption of brain blood flow and oxygen delivery, rather than an event where hypoxia and ischemia are absolutely total in nature. Hence the time-line for tolerance of such events, and the period over which brain damage evolves, are accepted as being longer than in the landmark animal studies conducted by Myers [59, 60, 61, 62]. For this reason, it is generally agreed that approximately 15 minutes, and possibly up to 20 minutes, of sudden profound asphyxia can be tolerated by the human fetus prior to brain damage beginning (in contrast to the 10 minutes seen in the animal model). Then, after this ‘grace’ period, damage to the brain begins to occur, and over a further period of 15 to 20 minutes the extent and severity of injury become progressively more profound over time. And beyond this time frame, a human fetus is usually born dead. It is important to recognize that the principal mechanism that causes fetal asphyxial brain injury is cerebral ischemia caused by the severe reduction in CBF that occurs as a result of hypoxic myocardial depression significantly reducing cardiac output (CO). The fetal heart has a fixed stroke volume, which means that CO, and the amount of blood supplied to the brain are a direct function of the rate of contraction; so, for example, with bradycardia where fetal heart rate slows to half normal, this equates to a 50% fall in CO, and a comparable reduction in CBF will result. CO also decreases where tachycardia accompanies hypoxic stress; at high heart rates poor contractility secondary to acidosis is then compounded by incomplete atrial filling in diastole.
The relationships between the geographic pattern of asphyxial brain injury and type of resulting disability have been defined [63], and the predictors of long-term morbidity delineated [64]. Near-total insults of moderate duration and degree which have the basal ganglia and thalamic pattern of damage, predominantly lead to athetoid or dystonic cerebral palsy, with intact or mildly impaired cognitive development. When severe, near-total insults damage the cerebral cortex in addition to the deep brain structures; and severe spastic quadriplegia results, with microcephaly, significant cognitive deficits and cortical visual impairment. The extent of injury is strongly associated with the intensity of resuscitation, the degree of encephalopathy, and severity of seizures [55, 65]. Prolonged partial insults of moderate degree with injury confined to watershed regions cause variable degrees of cognitive deficit and epilepsy, and can be associated with spastic quadriplegia. But, when more severe or prolonged, injury causes extensive cortical brain involvement, or global brain injury; the end result is spastic quadriplegia, severe cognitive impairment, cortical visual impairment, and microcephaly. In addition, symptomatic brainstem involvement can be associated with severe patterns of injury, and lead to non-survival [66].
Hallmarks of neonatal encephalopathy are neurological depression, with altered level of consciousness and often respiratory depression, abnormal muscle tone and power, disturbances of cranial nerve function, and seizures. HI injury is strongly suggested in a neurologically depressed infant by associated acidosis, and further confirmed by concomitant multi-organ injury [58, 65, 68].
Acidosis has two components: respiratory - from retained carbon dioxide, and metabolic - from accumulation of fixed acids (lactic acid and β-hydroxybutyrate). While acidosis present at birth usually resolves in the first hours of life, HIE progresses with further depression of consciousness, abnormalities in tone and movement, and onset of seizures. Infants exhibit a range of behaviors and alterations of conscious level from lethargy and obtundation to irritability and a hyper-alert state. Similarly, disorders of tone range from a marked decrease to hyper-tonicity. Abnormal movements include tremors, jitteriness, mouthing and blinking, and ‘bicycling’ of the legs, through to frank seizures. Other manifestations include apnea, with bradycardia and impaired oxygen saturation, shrill cry, feeding difficulty (due to poor coordination of suck or altered peristalsis, and occasionally brain stem damage), absence of the Moro and/or gag reflexes, and exaggeration of deep tendon reflexes. Decerebrate or decorticate posturing may be seen. Sarnat et al. defined three levels of severity (mild, moderate and severe); these are linked to the probability that HIE will result in permanent neurological consequences [69].
The pathophysiology of HIE is now better understood and treatment with hypothermia has become the foundation of therapy [67]. All affected infants require supportive management that anticipates and limits the adverse effects on the brain of fluctuations in cerebral perfusion, metabolic instability, sepsis, sub-optimal respiration, and any situation that increases oxygen and energy demands. This involves correction of hypotension, attention to glucose, fluid and electrolyte homeostasis, maintenance of PaCO2 in the normal range, and treatment of seizures [58, 67]. Neuroimaging (US, CT, MRI) is best done at defined periods after injury [41, 57]; MRI in particular can then define the diagnosis, pattern, severity, timing and prognosis, and help rationalize hypothermia and other interventions, including the withdrawal of support. Several neuroprotective agents that can be combined with hypothermia have entered clinical trials; new biomarkers for HIE are being sought [70]. Affected survivors need follow up to manage their handicaps.
The effects of hypoxia extend beyond the brain [9, 11, 67, 68], associated injury to other organs principally occurs due to compensatory redistribution of blood during partial and prolonged insults, but can follow profound, near total episodes; 60-80% of affected neonates exhibit single or multiple organ injury [68].
The fetus often passes meconium (fetal bowel contents) in utero due to hypoxia; a combination of gut ischemia and reduced sphincter tone secondary to neurological depression is the likely mechanism, hence, the presence of meconium is a marker for probable HI. Following a recent event, meconium seen is usually thick and green; after a remote event, because mixing with amniotic fluid disperses and thins the meconium, the liquor is evenly discolored, and the fetal skin may be stained green.
In the neonate, multiple organs can show varying effects from hypoxia.
Normally, oxygenated blood from the placenta flows through the UV and preferentially supplies the fetal brain and heart via shunts that bypass the liver; repeated uterine contractions during labor exert a significant, but manageable metabolic stress on the fetus. But when labor is precipitous, or contractions are abnormally frequent or prolonged, uterine artery blood flow becomes restricted, and inter-contraction restoration of placental perfusion is delayed as it is dependent on uterine relaxation; in this and similar scenarios maternal to fetal oxygen transfer via the UV can suffer sufficiently for HI injury to occur. Where blood return through the UA is also affected, normal removal of carbon dioxide from the fetus is reduced.
Acidosis occurs as a consequence of cellular hypoxia (inadequate oxygenation), tissue ischemia (inadequate blood flow) and retention of carbon dioxide; the unit of measurement, pH, is on a logarithmic scale, so small differences represent a major change in the degree of acidosis. Bicarbonate naturally buffers acid production; as reserves are depleted, base deficit increases. With resolution of acidosis, PCO2 values are restored first, followed by bicarbonate and pH; base deficit remains abnormal longest. Normal cell metabolism only occurs when pH is held within a narrow range, beyond these limits, cells progressively lose their ability to sustain normal function and maintain their metabolic integrity, and organs begin to fail.
Blood gas data are compared to the reference range of the testing laboratory. Significant, recent HI stress usually manifests with low oxygen, elevated PCO2, low pH, low bicarbonate and high base deficit, with UA values most affected. However, it is most relevant clinically to define pathological acidosis as the threshold at which the incidence of adverse events starts to correlate strongly [83]. Criteria to define an acute intrapartum event as sufficient to cause cerebral palsy include UA pH <7.00 and base deficit of >12; infants with a pH <7.0 who are not vigorous are at high risk of adverse outcome [84], and the threshold for moderate or severe newborn complications is defined as a UA base deficit of >12 [85]. With worsening acidosis progression of adverse sequelae rises sharply; in one reported series, HIE occurred in 12% of infants with cord pH <7.0, in 33% with pH <6.9, and in 80% with pH <6.7; a pH <6.8 equated with the probability of neonatal death [86]. Persisting lactic acidosis is associated with severe encephalopathy [82]. Identifying those at risk is especially important now, since neuroprotection strategies are available.
Hemoglobin concentration and hematocrit are used to identify anemia and polycythemia where too few or too many red cells are circulating respectively. Both circumstances compromise oxygen delivery; anemia by limiting the amount of oxygen that can be transported, and polycythemia by reducing the ease with which blood flows, which also increases the risk of blood vessel occlusion (thrombosis), and is one of the mechanisms underlying stroke. Also, by following serial measurements from birth, situations can be identified where bleeding occurred while the fetus was in utero. After significant blood loss, the volume of the blood in the circulation is reduced, but the hemoglobin concentration remains the same initially, then, as physiological compensation for the blood lost occurs, fluid is drawn into the circulation to restore blood volume and, as a consequence, hemoglobin concentration and the number of red cells per unit of volume (hematocrit) fall.
Like US and CT, MRI scans are best done at defined intervals after birth (3-5 and 10-14 days of life) for accurate diagnosis, timing and evolution of injury [55, 57]. Pathology identified includes structural developmental abnormalities, edema, hemorrhage, early ischemic damage, localization of the predominant injury to either cortical tissue or deep brain structures, the evolution and end stages of scarring, and, onset and progression of hydrocephalus or microcephaly. Importantly, intrapartum and late antepartum HI damage can be distinguished from congenital structural effects or lesions due to acquired causes that occurred well prior to birth, so MRI scans can identify damage caused to an otherwise normal and pristine brain.
MRI, magnetic resonance spectroscopy, and diffusion-weighted MRI have identified the patterns of brain injury that evolve after HI insults. Studies also define the severity of the insult and can indicate the age at which it probably occurred. Injury evolves over days, if not weeks before the final stage with scarring is evident. The anatomical regions of the brain affected define the mechanism of injury. Distinction can be made between an insult that involved a relatively short period of total or near total hypoxia/ischemia (profound hypotension), or one occurring over a more prolonged period where HI was partial in degree (moderate hypotension).
In near total insults, the most metabolically active brain structures are damaged; the lentiform nuclei, especially the posterior putamina, the ventrolateral thalami, the Rolandic cortex and the hippocampi are predominantly injured, while there is little or no involvement of the remainder of the cerebral cortex.
In contrast, in partial and prolonged hypoxia, cortical white matter integrity is compromised, and there is relative preservation of the basal ganglia and thalami. In severe cases the whole cortex may be involved, while with milder injury, the principal areas damaged are the interfaces between the perfusion zones of the anterior, middle and posterior cerebral arteries. An excellent schematic derived from a medicolegal database of MR images of term neonates with partial-prolonged HI injury illustrates the geography of the inter-arterial watershed zone [89].
While these are the two distinctive and predominant patterns of HI brain injury seen, in reality, the type, pattern, duration and variability in severity of HI are a continuum, so there is a spectrum of MRI findings, and mixed patterns of damage are seen, with changes of varying degree in both the basal ganglia thalami and cortical regions [55, 57]. Very severe injury from moderate or profound hypotension can also cause global brain involvement, and extend to include the brainstem [66].
MRI detectable changes take time to evolve; the first abnormality seen is diffusion restriction which peaks at about 72 hours [57]; brain edema, identified as T2 hyperintensity, reflects the progression of energy failure that follows brain cell damage, and precedes cell death due to the apoptosis necrosis continuum. Where there is significant involvement of the cortex, abnormal T1 hyperintensity is evident from about 1 week following the HI event; this can persist for several weeks. T1 hyperintensity due to basal ganglia damage is visualized over a similar time frame. The end result of injury is permanent scaring (gliosis), and compensatory enlargement of the ventricles (ventriculomegaly) [7, 55, 57].
Destructive lesions characterized by periventricular hyperintensity, focal defects in the germinal matrix, and areas of abnormal signal intensity occur in developing white matter. In encephalopathic term newborns, non-cystic white matter injury is a distinct and common pattern. A helpful sign in those >37 weeks gestation is loss of normal signal intensity in the posterior limb of the internal capsule. Hemorrhage is associated with hypointense areas; signal intensity depends on degree of evolution.
Periventricular leukomalacia can develop during fetal life and in the newborn period. Imaging predominantly identifies PVL in preterm infants, but importantly, lesions also occur in term and late preterm infants (those born between 34 weeks and 0 days and 36 weeks plus 6 days gestation) [90].
Fetal MR imaging is a technique that complements prenatal sonography as it has higher contrast resolution and allows direct visualization of the fetal brain, and hence more readily identifies both cerebral malformations and destructive lesions, including agenesis of the corpus callosum, cerebellar dysplasia, germinal matrix hemorrhage, IVH, multicystic encephalomalacia, periventricular leukomalacia, periventricular nodular heterotopias, porencephaly, and sulcation anomalies. For post-natal studies, diffusion-weighted MR imaging and proton MR spectroscopy are the most sensitive modalities for diagnosis in the early hours following injury.
Future advances in MRI hardware and software will likely enable neuroimaging technologies to contribute more by further delineating the site(s), progression and extent of injury; this will aid evaluation of causation and timing, and advance care strategies able to reverse or mitigate the long-term effects of perinatal brain injury.
Prevention of brain damage requires knowledge of the etiologies underlying injury, awareness of the availability of preventive measures, and timely employment of them to address the underlying cause. In addition, situations that may aggravate existing or evolving brain injury need to be anticipated, recognized, and appropriate evidence-based care provided that is capable of improving outcome.
In future, earlier initiation of cooling after resuscitation may prove beneficial; ongoing research aims to identify other neuroprotective approaches that can be used in parallel, and evaluate potentially beneficial therapeutic agents; ways that may help reduce the incidence of IVH during rewarming are also being explored.
Many causes of fetal and neonatal brain injury are now preventable. The consequences of cerebral hypoxia and ischemia remain considerable. Evidence-based care strategies during pregnancy and for premature and sick newborns infants are improving outcome.
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Castro",authors:[{id:"107041",title:"Dr.",name:"Maite A",middleName:null,surname:"Castro",slug:"maite-a-castro",fullName:"Maite A Castro"},{id:"109692",title:"Mr.",name:"Felipe A",middleName:null,surname:"Beltran",slug:"felipe-a-beltran",fullName:"Felipe A Beltran"},{id:"109695",title:"Mr.",name:"Aníbal",middleName:"I.",surname:"Acuña",slug:"anibal-acuna",fullName:"Aníbal Acuña"},{id:"109696",title:"Ms.",name:"Maria Paz",middleName:null,surname:"Miro",slug:"maria-paz-miro",fullName:"Maria Paz Miro"}]},{id:"54565",doi:"10.5772/67828",title:"The Role of the Amygdala in Regulating the Hypothalamic-Pituitary-Adrenal Axis",slug:"the-role-of-the-amygdala-in-regulating-the-hypothalamic-pituitary-adrenal-axis",totalDownloads:3554,totalCrossrefCites:6,totalDimensionsCites:9,abstract:"We investigated the regulatory role of the amygdala upon the function of the hypothalamic-pituitary-adrenal (HPA) axis as measured by median eminence corticotrophin releasing hormone (CRH) content and serum levels of adrenocorticotrophic hormone (ACTH) and corticosterone. Our findings showed that (1) lesions of the central amygdala inhibited the HPA axis responses to a variety of stressful stimuli. (2) Depletion of norepinephrine or serotonin in the amygdala and hypothalamus and local injections of norepinephrine and serotonin receptor antagonists into the central amygdala inhibited the HPA axis responses to neural stress. Norepinephrine and serotonin agonists injected into the amygdala caused an increase in HPA axis activity. The activation of the amygdala facilitated the in vivo release of serotonin from the paraventricular nucleus following electrical stimulation of the brainstem raphe nuclei. (3) Electrical stimulation of the amygdala impaired the glucocorticoid negative feedback action following neural stressful stimuli probably via a decrease in hippocampal corticosteroid receptors.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Joseph Weidenfeld and Haim Ovadia",authors:[{id:"190851",title:"Ph.D.",name:"Haim",middleName:null,surname:"Ovadia",slug:"haim-ovadia",fullName:"Haim Ovadia"},{id:"192823",title:"Prof.",name:"Joseph",middleName:null,surname:"Weidenfeld",slug:"joseph-weidenfeld",fullName:"Joseph Weidenfeld"}]},{id:"32393",doi:"10.5772/34852",title:"The Neurochemical Anatomy of Trigeminal Primary Afferent Neurons",slug:"the-neurochemical-anatomy-of-trigeminal-primary-afferent-neurons",totalDownloads:4712,totalCrossrefCites:0,totalDimensionsCites:9,abstract:null,book:{id:"1592",slug:"neuroscience-dealing-with-frontiers",title:"Neuroscience",fullTitle:"Neuroscience - Dealing With Frontiers"},signatures:"Nikolai E. Lazarov",authors:[{id:"101891",title:"Prof.",name:"Nikolai",middleName:null,surname:"Lazarov",slug:"nikolai-lazarov",fullName:"Nikolai Lazarov"}]},{id:"54301",doi:"10.5772/67585",title:"Revisiting the Role of the Amygdala in Posttraumatic Stress Disorder",slug:"revisiting-the-role-of-the-amygdala-in-posttraumatic-stress-disorder",totalDownloads:2172,totalCrossrefCites:2,totalDimensionsCites:8,abstract:"Over the past 20 years, the reactivity of amygdala to emotive stimuli has been explored by emerging neuroimaging techniques in an effort to understand the role of amygdala in the pathophysiology of posttraumatic stress disorder (PTSD). A fear neurocircuitry model, whereby the amygdala is hyperactive due to poor top-down control from the anterior cingulate and ventromedial prefrontal cortices, has been supported by numerous experimental studies and meta-analyses. However, this model has not always been upheld by experimental data and clinical observations. In particular, many neuroimaging studies find that the amygdala fails to activate in response to negative stimuli in individuals with PTSD. Several technical and design issues may explain disparate results regarding amygdala reactivity in PTSD. However, biological and symptom-based factors emerge as possible mediators of amygdala function in PTSD, leading to the conclusion that symptoms of emotional disengagement and dissociation are associated with amygdala hyporeactivity, and symptoms of hypervigilance/hyperarousal and problems with fear conditioning and extinction are reflected by amygdala hyperactivity. Therefore, treatment of PTSD should take into account the nature of amygdala dysfunction in the individual to optimize treatment outcomes.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Gina L. Forster, Raluca M. Simons and Lee A. Baugh",authors:[{id:"145620",title:"Dr.",name:"Gina",middleName:null,surname:"Forster",slug:"gina-forster",fullName:"Gina Forster"},{id:"195109",title:"Dr.",name:"Raluca",middleName:null,surname:"Simons",slug:"raluca-simons",fullName:"Raluca Simons"},{id:"195110",title:"Dr.",name:"Lee",middleName:null,surname:"Baugh",slug:"lee-baugh",fullName:"Lee Baugh"}]},{id:"55211",doi:"10.5772/intechopen.68618",title:"The Amygdala and Anxiety",slug:"the-amygdala-and-anxiety",totalDownloads:2984,totalCrossrefCites:4,totalDimensionsCites:8,abstract:"The amygdala has a central role in anxiety responses to stressful and arousing situations. Pharmacological and lesion studies of the basolateral, central, and medial subdivisions of the amygdala have shown that their activation induces anxiogenic effects, while their inactivation produces anxiolytic effects. Many neurotransmitters and stress mediators acting at these amygdalar nuclei can modulate the behavioral expression of anxiety. These mediators may be released from different brain regions in response to different types of stressors. The amygdala is in close relationship with several brain regions within the brain circuitry that orchestrates the expression of anxiety. Recent developments in optogenetics have begun to unveil details on how these areas interact.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Sergio Linsambarth, Rodrigo Moraga-Amaro, Daisy Quintana-\nDonoso, Sebastian Rojas and Jimmy Stehberg",authors:[{id:"144923",title:"Dr.",name:"Jimmy",middleName:null,surname:"Stehberg",slug:"jimmy-stehberg",fullName:"Jimmy Stehberg"},{id:"194182",title:"Ph.D. Student",name:"Rodrigo",middleName:null,surname:"Moraga-Amaro",slug:"rodrigo-moraga-amaro",fullName:"Rodrigo Moraga-Amaro"},{id:"194183",title:"M.Sc.",name:"Sergio",middleName:null,surname:"Linsambarth",slug:"sergio-linsambarth",fullName:"Sergio Linsambarth"}]}],mostDownloadedChaptersLast30Days:[{id:"54675",title:"The Key Role of the Amygdala in Stress",slug:"the-key-role-of-the-amygdala-in-stress",totalDownloads:2939,totalCrossrefCites:3,totalDimensionsCites:4,abstract:"Several data highlighted that stress exposure is strongly associated with several psychiatric disorders. The amygdala, an area of the brain that contributes to emotional processing, has a pivotal role in psychiatric disorders and it has been demonstrated to be highly responsive to stressful events. Here we will review evidences indicating how the amygdala changes its functionality following exposure to stress and how this contributes to the onset of anxiety disorders.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Diego Andolina and Antonella Borreca",authors:[{id:"190318",title:"Dr.",name:"Diego",middleName:null,surname:"Andolina",slug:"diego-andolina",fullName:"Diego Andolina"},{id:"192832",title:"Dr.",name:"Antonella",middleName:null,surname:"Borreca",slug:"antonella-borreca",fullName:"Antonella Borreca"}]},{id:"55211",title:"The Amygdala and Anxiety",slug:"the-amygdala-and-anxiety",totalDownloads:2984,totalCrossrefCites:4,totalDimensionsCites:8,abstract:"The amygdala has a central role in anxiety responses to stressful and arousing situations. Pharmacological and lesion studies of the basolateral, central, and medial subdivisions of the amygdala have shown that their activation induces anxiogenic effects, while their inactivation produces anxiolytic effects. Many neurotransmitters and stress mediators acting at these amygdalar nuclei can modulate the behavioral expression of anxiety. These mediators may be released from different brain regions in response to different types of stressors. The amygdala is in close relationship with several brain regions within the brain circuitry that orchestrates the expression of anxiety. Recent developments in optogenetics have begun to unveil details on how these areas interact.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Sergio Linsambarth, Rodrigo Moraga-Amaro, Daisy Quintana-\nDonoso, Sebastian Rojas and Jimmy Stehberg",authors:[{id:"144923",title:"Dr.",name:"Jimmy",middleName:null,surname:"Stehberg",slug:"jimmy-stehberg",fullName:"Jimmy Stehberg"},{id:"194182",title:"Ph.D. Student",name:"Rodrigo",middleName:null,surname:"Moraga-Amaro",slug:"rodrigo-moraga-amaro",fullName:"Rodrigo Moraga-Amaro"},{id:"194183",title:"M.Sc.",name:"Sergio",middleName:null,surname:"Linsambarth",slug:"sergio-linsambarth",fullName:"Sergio Linsambarth"}]},{id:"32387",title:"The Mystery of P2X7 Ionotropic Receptor: From a Small Conductance Channel to a Large Conductance Channel",slug:"the-mystery-of-p2x7-receptor-from-a-small-channel-to-a-big-pore",totalDownloads:2418,totalCrossrefCites:0,totalDimensionsCites:0,abstract:null,book:{id:"1592",slug:"neuroscience-dealing-with-frontiers",title:"Neuroscience",fullTitle:"Neuroscience - Dealing With Frontiers"},signatures:"R.X. Faria, L.G.B. Ferreira and L.A. Alves",authors:[{id:"76663",title:"Prof.",name:"Luiz A.",middleName:null,surname:"Alves",slug:"luiz-a.-alves",fullName:"Luiz A. Alves"},{id:"76674",title:"Mr.",name:"Leonardo",middleName:null,surname:"Braga",slug:"leonardo-braga",fullName:"Leonardo Braga"},{id:"79615",title:"Dr.",name:"Robson",middleName:null,surname:"Faria",slug:"robson-faria",fullName:"Robson Faria"}]},{id:"32399",title:"Brain Energy Metabolism in Health and Disease",slug:"brain-energy-metabolism-in-health-and-disease",totalDownloads:9132,totalCrossrefCites:1,totalDimensionsCites:10,abstract:null,book:{id:"1592",slug:"neuroscience-dealing-with-frontiers",title:"Neuroscience",fullTitle:"Neuroscience - Dealing With Frontiers"},signatures:"Felipe A. Beltrán, Aníbal I. Acuña, María Paz Miró and Maite A. Castro",authors:[{id:"107041",title:"Dr.",name:"Maite A",middleName:null,surname:"Castro",slug:"maite-a-castro",fullName:"Maite A Castro"},{id:"109692",title:"Mr.",name:"Felipe A",middleName:null,surname:"Beltran",slug:"felipe-a-beltran",fullName:"Felipe A Beltran"},{id:"109695",title:"Mr.",name:"Aníbal",middleName:"I.",surname:"Acuña",slug:"anibal-acuna",fullName:"Aníbal Acuña"},{id:"109696",title:"Ms.",name:"Maria Paz",middleName:null,surname:"Miro",slug:"maria-paz-miro",fullName:"Maria Paz Miro"}]},{id:"54509",title:"The Contribution of the Amygdala to Reward-Related Learning and Extinction",slug:"the-contribution-of-the-amygdala-to-reward-related-learning-and-extinction",totalDownloads:1742,totalCrossrefCites:3,totalDimensionsCites:3,abstract:"There has been substantial research into the role of the amygdala in fear conditioning and extinction of conditioned fear. The role of the amygdala in appetitive conditioning is relatively less explored. Here, we will review research into the role of the amygdala in reward‐related learning. Research to date suggests that the basolateral and central amygdala are responsible for learning about distinct aspects of a reinforcing event. For example, the basolateral amygdala is essential for distinguishing and choosing between specific rewards based on the specific‐sensory properties of those rewards as well as updating the relative value of specific rewarding events. In contrast, the central amygdala is involved in encoding reinforcement more generally and for regulating motivational influences on responding. We will also review what is known about the role of the amygdala in extinction of reward‐related behaviours and highlight areas for future research.",book:{id:"5485",slug:"the-amygdala-where-emotions-shape-perception-learning-and-memories",title:"The Amygdala",fullTitle:"The Amygdala - Where Emotions Shape Perception, Learning and Memories"},signatures:"Rose Chesworth and Laura Corbit",authors:[{id:"193670",title:"Dr.",name:"Laura",middleName:null,surname:"Corbit",slug:"laura-corbit",fullName:"Laura Corbit"},{id:"194020",title:"Dr.",name:"Rose",middleName:null,surname:"Chesworth",slug:"rose-chesworth",fullName:"Rose Chesworth"}]}],onlineFirstChaptersFilter:{topicId:"1176",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:31,numberOfPublishedChapters:314,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:11,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:105,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:14,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}}]},series:{item:{id:"11",title:"Biochemistry",doi:"10.5772/intechopen.72877",issn:"2632-0983",scope:"Biochemistry, the study of chemical transformations occurring within living organisms, impacts all areas of life sciences, from molecular crystallography and genetics to ecology, medicine, and population biology. Biochemistry examines macromolecules - proteins, nucleic acids, carbohydrates, and lipids – and their building blocks, structures, functions, and interactions. Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. This Biochemistry Series will address the current research on biomolecules and the emerging trends with great promise.",coverUrl:"https://cdn.intechopen.com/series/covers/11.jpg",latestPublicationDate:"June 24th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:31,editor:{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:4,paginationItems:[{id:"14",title:"Cell and Molecular Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/14.jpg",isOpenForSubmission:!0,annualVolume:11410,editor:{id:"165627",title:"Dr.",name:"Rosa María",middleName:null,surname:"Martínez-Espinosa",slug:"rosa-maria-martinez-espinosa",fullName:"Rosa María Martínez-Espinosa",profilePictureURL:"https://mts.intechopen.com/storage/users/165627/images/system/165627.jpeg",biography:"Dr. Rosa María Martínez-Espinosa has been a Spanish Full Professor since 2020 (Biochemistry and Molecular Biology) and is currently Vice-President of International Relations and Cooperation development and leader of the research group 'Applied Biochemistry” (University of Alicante, Spain). Other positions she has held at the university include Vice-Dean of Master Programs, Vice-Dean of the Degree in Biology and Vice-Dean for Mobility and Enterprise and Engagement at the Faculty of Science (University of Alicante). She received her Bachelor in Biology in 1998 (University of Alicante) and her PhD in 2003 (Biochemistry, University of Alicante). She undertook post-doctoral research at the University of East Anglia (Norwich, U.K. 2004-2005; 2007-2008).\nHer multidisciplinary research focuses on investigating archaea and their potential applications in biotechnology. She has an H-index of 21. She has authored one patent and has published more than 70 indexed papers and around 60 book chapters.\nShe has contributed to more than 150 national and international meetings during the last 15 years. Her research interests include archaea metabolism, enzymes purification and characterization, gene regulation, carotenoids and bioplastics production, antioxidant\ncompounds, waste water treatments, and brines bioremediation.\nRosa María’s other roles include editorial board member for several journals related\nto biochemistry, reviewer for more than 60 journals (biochemistry, molecular biology, biotechnology, chemistry and microbiology) and president of several organizing committees in international meetings related to the N-cycle or respiratory processes.",institutionString:null,institution:{name:"University of Alicante",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"15",title:"Chemical Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/15.jpg",isOpenForSubmission:!0,annualVolume:11411,editor:{id:"441442",title:"Dr.",name:"Şükrü",middleName:null,surname:"Beydemir",slug:"sukru-beydemir",fullName:"Şükrü Beydemir",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003GsUoIQAV/Profile_Picture_1634557147521",biography:"Dr. Şükrü Beydemir obtained a BSc in Chemistry in 1995 from Yüzüncü Yıl University, MSc in Biochemistry in 1998, and PhD in Biochemistry in 2002 from Atatürk University, Turkey. He performed post-doctoral studies at Max-Planck Institute, Germany, and University of Florence, Italy in addition to making several scientific visits abroad. He currently works as a Full Professor of Biochemistry in the Faculty of Pharmacy, Anadolu University, Turkey. Dr. Beydemir has published over a hundred scientific papers spanning protein biochemistry, enzymology and medicinal chemistry, reviews, book chapters and presented several conferences to scientists worldwide. He has received numerous publication awards from various international scientific councils. He serves in the Editorial Board of several international journals. Dr. Beydemir is also Rector of Bilecik Şeyh Edebali University, Turkey.",institutionString:null,institution:{name:"Anadolu University",institutionURL:null,country:{name:"Turkey"}}},editorTwo:{id:"13652",title:"Prof.",name:"Deniz",middleName:null,surname:"Ekinci",slug:"deniz-ekinci",fullName:"Deniz Ekinci",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYLT1QAO/Profile_Picture_1634557223079",biography:"Dr. Deniz Ekinci obtained a BSc in Chemistry in 2004, MSc in Biochemistry in 2006, and PhD in Biochemistry in 2009 from Atatürk University, Turkey. He studied at Stetson University, USA, in 2007-2008 and at the Max Planck Institute of Molecular Cell Biology and Genetics, Germany, in 2009-2010. Dr. Ekinci currently works as a Full Professor of Biochemistry in the Faculty of Agriculture and is the Head of the Enzyme and Microbial Biotechnology Division, Ondokuz Mayıs University, Turkey. He is a member of the Turkish Biochemical Society, American Chemical Society, and German Genetics society. Dr. Ekinci published around ninety scientific papers, reviews and book chapters, and presented several conferences to scientists. He has received numerous publication awards from several scientific councils. 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He was associate professor at the University of Limoges (1987) before becoming full professor of biochemistry at the Université d’Artois (1996). He worked on the structure-function relationships of glycoconjugates and his main project was the investigations on the biological roles of the de-N-glycosylation enzymes (Endo-N-acetyl-β-D-glucosaminidase and peptide-N4-(N-acetyl-β-glucosaminyl) asparagine amidase). From 2002 he contributes to the understanding of the Blood-brain barrier functioning using proteomics approaches. He has published more than 70 papers. His teaching areas are energy metabolism and regulation, integration and organ specialization and metabolic adaptation.",institutionString:null,institution:{name:"Artois University",institutionURL:null,country:{name:"France"}}},editorTwo:null,editorThree:null},{id:"18",title:"Proteomics",coverUrl:"https://cdn.intechopen.com/series_topics/covers/18.jpg",isOpenForSubmission:!0,annualVolume:11414,editor:{id:"200689",title:"Prof.",name:"Paolo",middleName:null,surname:"Iadarola",slug:"paolo-iadarola",fullName:"Paolo Iadarola",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSCl8QAG/Profile_Picture_1623568118342",biography:"Paolo Iadarola graduated with a degree in Chemistry from the University of Pavia (Italy) in July 1972. He then worked as an Assistant Professor at the Faculty of Science of the same University until 1984. In 1985, Prof. Iadarola became Associate Professor at the Department of Biology and Biotechnologies of the University of Pavia and retired in October 2017. Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. In this context, he has developed and validated new methodologies (e.g., Capillary Electrophoresis coupled to Laser-Induced Fluorescence, CE-LIF) whose application enabled him to determine both the amounts of biochemical markers (Desmosines) in urine/serum of patients affected by Chronic Obstructive Pulmonary Disease (COPD) and the activity of proteolytic enzymes (Human Neutrophil Elastase, Cathepsin G, Pseudomonas aeruginosa elastase) in sputa of these patients. More recently, Prof. Iadarola was involved in developing techniques such as two-dimensional electrophoresis coupled to liquid chromatography/mass spectrometry (2DE-LC/MS) for the proteomic analysis of biological fluids aimed at the identification of potential biomarkers of different lung diseases. He is the author of about 150 publications (According to Scopus: H-Index: 23; Total citations: 1568- According to WOS: H-Index: 20; Total Citations: 1296) of peer-reviewed international journals. He is a Consultant Reviewer for several journals, including the Journal of Chromatography A, Journal of Chromatography B, Plos ONE, Proteomes, International Journal of Molecular Science, Biotech, Electrophoresis, and others. He is also Associate Editor of Biotech.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorTwo:{id:"201414",title:"Dr.",name:"Simona",middleName:null,surname:"Viglio",slug:"simona-viglio",fullName:"Simona Viglio",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRKDHQA4/Profile_Picture_1630402531487",biography:"Simona Viglio is an Associate Professor of Biochemistry at the Department of Molecular Medicine at the University of Pavia. She has been working since 1995 on the determination of proteolytic enzymes involved in the degradation process of connective tissue matrix and on the identification of biological markers of lung diseases. She gained considerable experience in developing and validating new methodologies whose applications allowed her to determine both the amount of biomarkers (Desmosine and Isodesmosine) in the urine of patients affected by COPD, and the activity of proteolytic enzymes (HNE, Cathepsin G, Pseudomonas aeruginosa elastase) in the sputa of these patients. Simona Viglio was also involved in research dealing with the supplementation of amino acids in patients with brain injury and chronic heart failure. She is presently engaged in the development of 2-DE and LC-MS techniques for the study of proteomics in biological fluids. The aim of this research is the identification of potential biomarkers of lung diseases. 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He received his Ph.D. in Environmental Analytical Chemistry from Assiut University, Egypt, in 1989. His research interest is in analytical and environmental chemistry with special emphasis on: (1) monitoring and assessing biological trace elements and toxic metals in human blood, urine, water, crops, vegetables, and medicinal plants; (2) relationships between environmental heavy metals and human diseases; (3) uses of biological indicators for monitoring water pollution; (4) environmental chemistry of lakes, rivers, and well water; (5) water and wastewater treatment by adsorption and photocatalysis techniques; (6) soil and water pollution monitoring, control, and treatment; and (7) advanced oxidation treatment. Prof. Rashed has supervised several MSc and Ph.D. theses in the field of analytical and environmental chemistry. He served as an examiner for several Ph.D. theses in analytical chemistry in India, Kazakhstan, and Botswana. 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She is now a lecturer at the University of Witwatersrand, South Africa, and a principal researcher at the Health Economics and Epidemiology Research Office (HE2RO), South Africa. Dr. Moolla holds a Ph.D. in Psychology with her research being focused on mental health and resilience. In her professional work capacity, her research has further expanded into the fields of early childhood development, mental health, the HIV and TB care cascades, as well as COVID. She is also a UNESCO-trained International Bioethics Facilitator.",institutionString:"University of the Witwatersrand",institution:{name:"University of the Witwatersrand",country:{name:"South Africa"}}},{id:"342152",title:"Dr.",name:"Santo",middleName:null,surname:"Grace Umesh",slug:"santo-grace-umesh",fullName:"Santo Grace Umesh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/342152/images/16311_n.jpg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"333647",title:"Dr.",name:"Shreya",middleName:null,surname:"Kishore",slug:"shreya-kishore",fullName:"Shreya Kishore",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333647/images/14701_n.jpg",biography:"Dr. Shreya Kishore completed her Bachelor in Dental Surgery in Chettinad Dental College and Research Institute, Chennai, and her Master of Dental Surgery (Orthodontics) in Saveetha Dental College, Chennai. She is also Invisalign certified. She’s working as a Senior Lecturer in the Department of Orthodontics, SRM Dental College since November 2019. She is actively involved in teaching orthodontics to the undergraduates and the postgraduates. Her clinical research topics include new orthodontic brackets, fixed appliances and TADs. She’s published 4 articles in well renowned indexed journals and has a published patency of her own. Her private practice is currently limited to orthodontics and works as a consultant in various clinics.",institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"323731",title:"Prof.",name:"Deepak M.",middleName:"Macchindra",surname:"Vikhe",slug:"deepak-m.-vikhe",fullName:"Deepak M. Vikhe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/323731/images/13613_n.jpg",biography:"Dr Deepak M.Vikhe .\n\n\t\n\tDr Deepak M.Vikhe , completed his Masters & PhD in Prosthodontics from Rural Dental College, Loni securing third rank in the Pravara Institute of Medical Sciences Deemed University. He was awarded Dr.G.C.DAS Memorial Award for Research on Implants at 39th IPS conference Dubai (U A E).He has two patents under his name. He has received Dr.Saraswati medal award for best research for implant study in 2017.He has received Fully funded scholarship to Spain ,university of Santiago de Compostela. He has completed fellowship in Implantlogy from Noble Biocare. \nHe has attended various conferences and CDE programmes and has national publications to his credit. His field of interest is in Implant supported prosthesis. Presently he is working as a associate professor in the Dept of Prosthodontics, Rural Dental College, Loni and maintains a successful private practice specialising in Implantology at Rahata.\n\nEmail: drdeepak_mvikhe@yahoo.com..................",institutionString:null,institution:{name:"Pravara Institute of Medical Sciences",country:{name:"India"}}},{id:"204110",title:"Dr.",name:"Ahmed A.",middleName:null,surname:"Madfa",slug:"ahmed-a.-madfa",fullName:"Ahmed A. Madfa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204110/images/system/204110.jpg",biography:"Dr. Madfa is currently Associate Professor of Endodontics at Thamar University and a visiting lecturer at Sana'a University and University of Sciences and Technology. He has more than 6 years of experience in teaching. His research interests include root canal morphology, functionally graded concept, dental biomaterials, epidemiology and dental education, biomimetic restoration, finite element analysis and endodontic regeneration. Dr. Madfa has numerous international publications, full articles, two patents, a book and a book chapter. Furthermore, he won 14 international scientific awards. Furthermore, he is involved in many academic activities ranging from editorial board member, reviewer for many international journals and postgraduate students' supervisor. Besides, I deliver many courses and training workshops at various scientific events. Dr. Madfa also regularly attends international conferences and holds administrative positions (Deputy Dean of the Faculty for Students’ & Academic Affairs and Deputy Head of Research Unit).",institutionString:"Thamar University",institution:null},{id:"210472",title:"Dr.",name:"Nermin",middleName:"Mohammed Ahmed",surname:"Yussif",slug:"nermin-yussif",fullName:"Nermin Yussif",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/210472/images/system/210472.jpg",biography:"Dr. Nermin Mohammed Ahmed Yussif is working at the Faculty of dentistry, University for October university for modern sciences and arts (MSA). Her areas of expertise include: periodontology, dental laserology, oral implantology, periodontal plastic surgeries, oral mesotherapy, nutrition, dental pharmacology. She is an editor and reviewer in numerous international journals.",institutionString:"MSA University",institution:null},{id:"204606",title:"Dr.",name:"Serdar",middleName:null,surname:"Gözler",slug:"serdar-gozler",fullName:"Serdar Gözler",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/204606/images/system/204606.jpeg",biography:"Dr. Serdar Gözler has completed his undergraduate studies at the Marmara University Faculty of Dentistry in 1978, followed by an assistantship in the Prosthesis Department of Dicle University Faculty of Dentistry. Starting his PhD work on non-resilient overdentures with Assoc. Prof. Hüsnü Yavuzyılmaz, he continued his studies with Prof. Dr. Gürbüz Öztürk of Istanbul University Faculty of Dentistry Department of Prosthodontics, this time on Gnatology. He attended training programs on occlusion, neurology, neurophysiology, EMG, radiology and biostatistics. In 1982, he presented his PhD thesis \\Gerber and Lauritzen Occlusion Analysis Techniques: Diagnosis Values,\\ at Istanbul University School of Dentistry, Department of Prosthodontics. As he was also working with Prof. Senih Çalıkkocaoğlu on The Physiology of Chewing at the same time, Gözler has written a chapter in Çalıkkocaoğlu\\'s book \\Complete Prostheses\\ entitled \\The Place of Neuromuscular Mechanism in Prosthetic Dentistry.\\ The book was published five times since by the Istanbul University Publications. Having presented in various conferences about occlusion analysis until 1998, Dr. Gözler has also decided to use the T-Scan II occlusion analysis method. Having been personally trained by Dr. Robert Kerstein on this method, Dr. Gözler has been lecturing on the T-Scan Occlusion Analysis Method in conferences both in Turkey and abroad. Dr. Gözler has various articles and presentations on Digital Occlusion Analysis methods. He is now Head of the TMD Clinic at Prosthodontic Department of Faculty of Dentistry , Istanbul Aydın University , Turkey.",institutionString:"Istanbul Aydin University",institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"240870",title:"Ph.D.",name:"Alaa Eddin Omar",middleName:null,surname:"Al Ostwani",slug:"alaa-eddin-omar-al-ostwani",fullName:"Alaa Eddin Omar Al Ostwani",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/240870/images/system/240870.jpeg",biography:"Dr. Al Ostwani Alaa Eddin Omar received his Master in dentistry from Damascus University in 2010, and his Ph.D. in Pediatric Dentistry from Damascus University in 2014. Dr. Al Ostwani is an assistant professor and faculty member at IUST University since 2014. \nDuring his academic experience, he has received several awards including the scientific research award from the Union of Arab Universities, the Syrian gold medal and the international gold medal for invention and creativity. Dr. Al Ostwani is a Member of the International Association of Dental Traumatology and the Syrian Society for Research and Preventive Dentistry since 2017. He is also a Member of the Reviewer Board of International Journal of Dental Medicine (IJDM), and the Indian Journal of Conservative and Endodontics since 2016.",institutionString:"International University for Science and Technology.",institution:{name:"Islamic University of Science and Technology",country:{name:"India"}}},{id:"42847",title:"Dr.",name:"Belma",middleName:null,surname:"Işik Aslan",slug:"belma-isik-aslan",fullName:"Belma Işik Aslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/42847/images/system/42847.jpg",biography:"Dr. Belma IşIk Aslan was born in 1976 in Ankara-TURKEY. After graduating from TED Ankara College in 1994, she attended to Gazi University, Faculty of Dentistry in Ankara. She completed her PhD in orthodontic education at Gazi University between 1999-2005. Dr. Işık Aslan stayed at the Providence Hospital Craniofacial Institude and Reconstructive Surgery in Michigan, USA for three months as an observer. She worked as a specialist doctor at Gazi University, Dentistry Faculty, Department of Orthodontics between 2005-2014. She was appointed as associate professor in January, 2014 and as professor in 2021. Dr. Işık Aslan still works as an instructor at the same faculty. She has published a total of 35 articles, 10 book chapters, 39 conference proceedings both internationally and nationally. Also she was the academic editor of the international book 'Current Advances in Orthodontics'. She is a member of the Turkish Orthodontic Society and Turkish Cleft Lip and Palate Society. She is married and has 2 children. Her knowledge of English is at an advanced level.",institutionString:"Gazi University Dentistry Faculty Department of Orthodontics",institution:null},{id:"178412",title:"Associate Prof.",name:"Guhan",middleName:null,surname:"Dergin",slug:"guhan-dergin",fullName:"Guhan Dergin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178412/images/6954_n.jpg",biography:"Assoc. Prof. Dr. Gühan Dergin was born in 1973 in Izmit. He graduated from Marmara University Faculty of Dentistry in 1999. He completed his specialty of OMFS surgery in Marmara University Faculty of Dentistry and obtained his PhD degree in 2006. In 2005, he was invited as a visiting doctor in the Oral and Maxillofacial Surgery Department of the University of North Carolina, USA, where he went on a scholarship. Dr. Dergin still continues his academic career as an associate professor in Marmara University Faculty of Dentistry. He has many articles in international and national scientific journals and chapters in books.",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"178414",title:"Prof.",name:"Yusuf",middleName:null,surname:"Emes",slug:"yusuf-emes",fullName:"Yusuf Emes",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178414/images/6953_n.jpg",biography:"Born in Istanbul in 1974, Dr. Emes graduated from Istanbul University Faculty of Dentistry in 1997 and completed his PhD degree in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery in 2005. He has papers published in international and national scientific journals, including research articles on implantology, oroantral fistulas, odontogenic cysts, and temporomandibular disorders. Dr. Emes is currently working as a full-time academic staff in Istanbul University faculty of Dentistry Department of Oral and Maxillofacial Surgery.",institutionString:null,institution:{name:"Istanbul University",country:{name:"Turkey"}}},{id:"192229",title:"Ph.D.",name:"Ana Luiza",middleName:null,surname:"De Carvalho Felippini",slug:"ana-luiza-de-carvalho-felippini",fullName:"Ana Luiza De Carvalho Felippini",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/192229/images/system/192229.jpg",biography:null,institutionString:"University of São Paulo",institution:{name:"University of Sao Paulo",country:{name:"Brazil"}}},{id:"256851",title:"Prof.",name:"Ayşe",middleName:null,surname:"Gülşen",slug:"ayse-gulsen",fullName:"Ayşe Gülşen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256851/images/9696_n.jpg",biography:"Dr. Ayşe Gülşen graduated in 1990 from Faculty of Dentistry, University of Ankara and did a postgraduate program at University of Gazi. \nShe worked as an observer and research assistant in Craniofacial Surgery Departments in New York, Providence Hospital in Michigan and Chang Gung Memorial Hospital in Taiwan. \nShe works as Craniofacial Orthodontist in Department of Aesthetic, Plastic and Reconstructive Surgery, Faculty of Medicine, University of Gazi, Ankara Turkey since 2004.",institutionString:"Univeristy of Gazi",institution:null},{id:"255366",title:"Prof.",name:"Tosun",middleName:null,surname:"Tosun",slug:"tosun-tosun",fullName:"Tosun Tosun",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/255366/images/7347_n.jpg",biography:"Graduated at the Faculty of Dentistry, University of Istanbul, Turkey in 1989;\nVisitor Assistant at the University of Padua, Italy and Branemark Osseointegration Center of Treviso, Italy between 1993-94;\nPhD thesis on oral implantology in University of Istanbul and was awarded the academic title “Dr.med.dent.”, 1997;\nHe was awarded the academic title “Doç.Dr.” (Associated Professor) in 2003;\nProficiency in Botulinum Toxin Applications, Reading-UK in 2009;\nMastership, RWTH Certificate in Laser Therapy in Dentistry, AALZ-Aachen University, Germany 2009-11;\nMaster of Science (MSc) in Laser Dentistry, University of Genoa, Italy 2013-14.\n\nDr.Tosun worked as Research Assistant in the Department of Oral Implantology, Faculty of Dentistry, University of Istanbul between 1990-2002. \nHe worked part-time as Consultant surgeon in Harvard Medical International Hospitals and John Hopkins Medicine, Istanbul between years 2007-09.\u2028He was contract Professor in the Department of Surgical and Diagnostic Sciences (DI.S.C.), Medical School, University of Genova, Italy between years 2011-16. \nSince 2015 he is visiting Professor at Medical School, University of Plovdiv, Bulgaria. \nCurrently he is Associated Prof.Dr. at the Dental School, Oral Surgery Dept., Istanbul Aydin University and since 2003 he works in his own private clinic in Istanbul, Turkey.\u2028\nDr.Tosun is reviewer in journal ‘Laser in Medical Sciences’, reviewer in journal ‘Folia Medica\\', a Fellow of the International Team for Implantology, Clinical Lecturer of DGZI German Association of Oral Implantology, Expert Lecturer of Laser&Health Academy, Country Representative of World Federation for Laser Dentistry, member of European Federation of Periodontology, member of Academy of Laser Dentistry. Dr.Tosun presents papers in international and national congresses and has scientific publications in international and national journals. He speaks english, spanish, italian and french.",institutionString:null,institution:{name:"Istanbul Aydın University",country:{name:"Turkey"}}},{id:"171887",title:"Prof.",name:"Zühre",middleName:null,surname:"Akarslan",slug:"zuhre-akarslan",fullName:"Zühre Akarslan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/171887/images/system/171887.jpg",biography:"Zühre Akarslan was born in 1977 in Cyprus. She graduated from Gazi University Faculty of Dentistry, Ankara, Turkey in 2000. \r\nLater she received her Ph.D. degree from the Oral Diagnosis and Radiology Department; which was recently renamed as Oral and Dentomaxillofacial Radiology, from the same university. \r\nShe is working as a full-time Associate Professor and is a lecturer and an academic researcher. \r\nHer expertise areas are dental caries, cancer, dental fear and anxiety, gag reflex in dentistry, oral medicine, and dentomaxillofacial radiology.",institutionString:"Gazi University",institution:{name:"Gazi University",country:{name:"Turkey"}}},{id:"256417",title:"Associate Prof.",name:"Sanaz",middleName:null,surname:"Sadry",slug:"sanaz-sadry",fullName:"Sanaz Sadry",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/256417/images/8106_n.jpg",biography:null,institutionString:null,institution:null},{id:"272237",title:"Dr.",name:"Pinar",middleName:"Kiymet",surname:"Karataban",slug:"pinar-karataban",fullName:"Pinar Karataban",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/272237/images/8911_n.png",biography:"Assist.Prof.Dr.Pınar Kıymet Karataban, DDS PhD \n\nDr.Pınar Kıymet Karataban was born in Istanbul in 1975. After her graduation from Marmara University Faculty of Dentistry in 1998 she started her PhD in Paediatric Dentistry focused on children with special needs; mainly children with Cerebral Palsy. She finished her pHD thesis entitled \\'Investigation of occlusion via cast analysis and evaluation of dental caries prevalance, periodontal status and muscle dysfunctions in children with cerebral palsy” in 2008. She got her Assist. Proffessor degree in Istanbul Aydın University Paediatric Dentistry Department in 2015-2018. ın 2019 she started her new career in Bahcesehir University, Istanbul as Head of Department of Pediatric Dentistry. In 2020 she was accepted to BAU International University, Batumi as Professor of Pediatric Dentistry. She’s a lecturer in the same university meanwhile working part-time in private practice in Ege Dental Studio (https://www.egedisklinigi.com/) a multidisciplinary dental clinic in Istanbul. Her main interests are paleodontology, ancient and contemporary dentistry, oral microbiology, cerebral palsy and special care dentistry. She has national and international publications, scientific reports and is a member of IAPO (International Association for Paleodontology), IADH (International Association of Disability and Oral Health) and EAPD (European Association of Pediatric Dentistry).",institutionString:null,institution:null},{id:"202198",title:"Dr.",name:"Buket",middleName:null,surname:"Aybar",slug:"buket-aybar",fullName:"Buket Aybar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/202198/images/6955_n.jpg",biography:"Buket Aybar, DDS, PhD, was born in 1971. She graduated from Istanbul University, Faculty of Dentistry, in 1992 and completed her PhD degree on Oral and Maxillofacial Surgery in Istanbul University in 1997.\nDr. Aybar is currently a full-time professor in Istanbul University, Faculty of Dentistry Department of Oral and Maxillofacial Surgery. She has teaching responsibilities in graduate and postgraduate programs. Her clinical practice includes mainly dentoalveolar surgery.\nHer topics of interest are biomaterials science and cell culture studies. She has many articles in international and national scientific journals and chapters in books; she also has participated in several scientific projects supported by Istanbul University Research fund.",institutionString:null,institution:null},{id:"260116",title:"Dr.",name:"Mehmet",middleName:null,surname:"Yaltirik",slug:"mehmet-yaltirik",fullName:"Mehmet Yaltirik",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/260116/images/7413_n.jpg",biography:"Birth Date 25.09.1965\r\nBirth Place Adana- Turkey\r\nSex Male\r\nMarrial Status Bachelor\r\nDriving License Acquired\r\nMother Tongue Turkish\r\n\r\nAddress:\r\nWork:University of Istanbul,Faculty of Dentistry, Department of Oral Surgery and Oral Medicine 34093 Capa,Istanbul- TURKIYE",institutionString:null,institution:null},{id:"172009",title:"Dr.",name:"Fatma Deniz",middleName:null,surname:"Uzuner",slug:"fatma-deniz-uzuner",fullName:"Fatma Deniz Uzuner",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/172009/images/7122_n.jpg",biography:"Dr. Deniz Uzuner was born in 1969 in Kocaeli-TURKEY. After graduating from TED Ankara College in 1986, she attended the Hacettepe University, Faculty of Dentistry in Ankara. \nIn 1993 she attended the Gazi University, Faculty of Dentistry, Department of Orthodontics for her PhD education. After finishing the PhD education, she worked as orthodontist in Ankara Dental Hospital under the Turkish Government, Ministry of Health and in a special Orthodontic Clinic till 2011. Between 2011 and 2016, Dr. Deniz Uzuner worked as a specialist in the Department of Orthodontics, Faculty of Dentistry, Gazi University in Ankara/Turkey. In 2016, she was appointed associate professor. Dr. Deniz Uzuner has authored 23 Journal Papers, 3 Book Chapters and has had 39 oral/poster presentations. She is a member of the Turkish Orthodontic Society. Her knowledge of English is at an advanced level.",institutionString:null,institution:null},{id:"332914",title:"Dr.",name:"Muhammad Saad",middleName:null,surname:"Shaikh",slug:"muhammad-saad-shaikh",fullName:"Muhammad Saad Shaikh",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Jinnah Sindh Medical University",country:{name:"Pakistan"}}},{id:"315775",title:"Dr.",name:"Feng",middleName:null,surname:"Luo",slug:"feng-luo",fullName:"Feng Luo",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Sichuan University",country:{name:"China"}}},{id:"423519",title:"Dr.",name:"Sizakele",middleName:null,surname:"Ngwenya",slug:"sizakele-ngwenya",fullName:"Sizakele Ngwenya",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of the Witwatersrand",country:{name:"South Africa"}}},{id:"419270",title:"Dr.",name:"Ann",middleName:null,surname:"Chianchitlert",slug:"ann-chianchitlert",fullName:"Ann Chianchitlert",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"419271",title:"Dr.",name:"Diane",middleName:null,surname:"Selvido",slug:"diane-selvido",fullName:"Diane Selvido",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"419272",title:"Dr.",name:"Irin",middleName:null,surname:"Sirisoontorn",slug:"irin-sirisoontorn",fullName:"Irin Sirisoontorn",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Walailak University",country:{name:"Thailand"}}},{id:"355660",title:"Dr.",name:"Anitha",middleName:null,surname:"Mani",slug:"anitha-mani",fullName:"Anitha Mani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"355612",title:"Dr.",name:"Janani",middleName:null,surname:"Karthikeyan",slug:"janani-karthikeyan",fullName:"Janani Karthikeyan",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"334400",title:"Dr.",name:"Suvetha",middleName:null,surname:"Siva",slug:"suvetha-siva",fullName:"Suvetha Siva",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"SRM Dental College",country:{name:"India"}}},{id:"334239",title:"Prof.",name:"Leung",middleName:null,surname:"Wai Keung",slug:"leung-wai-keung",fullName:"Leung Wai Keung",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Hong Kong",country:{name:"China"}}}]}},subseries:{item:{id:"6",type:"subseries",title:"Viral Infectious Diseases",keywords:"Novel Viruses, Virus Transmission, Virus Evolution, Molecular Virology, Control and Prevention, Virus-host Interaction",scope:"The Viral Infectious Diseases Book Series aims to provide a comprehensive overview of recent research trends and discoveries in various viral infectious diseases emerging around the globe. The emergence of any viral disease is hard to anticipate, which often contributes to death. A viral disease can be defined as an infectious disease that has recently appeared within a population or exists in nature with the rapid expansion of incident or geographic range. This series will focus on various crucial factors related to emerging viral infectious diseases, including epidemiology, pathogenesis, host immune response, clinical manifestations, diagnosis, treatment, and clinical recommendations for managing viral infectious diseases, highlighting the recent issues with future directions for effective therapeutic strategies.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/6.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11402,editor:{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. 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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. 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