System measured vs. theoretical supply air temperature.
\\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:"intechopen-supports-asapbio-s-new-initiative-publish-your-reviews-20220729",title:"IntechOpen Supports ASAPbio’s New Initiative Publish Your Reviews"},{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"}]},book:{item:{type:"book",id:"137",leadTitle:null,fullTitle:"Sustainable Wireless Sensor Networks",title:"Sustainable Wireless Sensor Networks",subtitle:null,reviewType:"peer-reviewed",abstract:"Wireless Sensor Networks came into prominence around the start of this millennium motivated by the omnipresent scenario of small-sized sensors with limited power deployed in large numbers over an area to monitor different phenomenon. The sole motivation of a large portion of research efforts has been to maximize the lifetime of the network, where network lifetime is typically measured from the instant of deployment to the point when one of the nodes has expended its limited power source and becomes in-operational - commonly referred as first node failure. Over the years, research has increasingly adopted ideas from wireless communications as well as embedded systems development in order to move this technology closer to realistic deployment scenarios. In such a rich research area as wireless sensor networks, it is difficult if not impossible to provide a comprehensive coverage of all relevant aspects. In this book, we hope to give the reader with a snapshot of some aspects of wireless sensor networks research that provides both a high level overview as well as detailed discussion on specific areas.",isbn:null,printIsbn:"978-953-307-297-5",pdfIsbn:"978-953-51-5530-0",doi:"10.5772/663",price:159,priceEur:175,priceUsd:205,slug:"sustainable-wireless-sensor-networks",numberOfPages:586,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:null,bookSignature:"Winston Seah and Yen Kheng Tan",publishedDate:"December 14th 2010",coverURL:"https://cdn.intechopen.com/books/images_new/137.jpg",numberOfDownloads:65530,numberOfWosCitations:118,numberOfCrossrefCitations:60,numberOfCrossrefCitationsByBook:34,numberOfDimensionsCitations:145,numberOfDimensionsCitationsByBook:35,hasAltmetrics:1,numberOfTotalCitations:323,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 13th 2010",dateEndSecondStepPublish:"May 11th 2010",dateEndThirdStepPublish:"September 15th 2010",dateEndFourthStepPublish:"October 15th 2010",dateEndFifthStepPublish:"December 14th 2010",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"78857",title:"Dr.",name:"Tan Yen",middleName:null,surname:"Kheng",slug:"tan-yen-kheng",fullName:"Tan Yen Kheng",profilePictureURL:"https://mts.intechopen.com/storage/users/78857/images/system/78857.jpg",biography:"Dr. Tan Yen Kheng is the CEO and co-founder of Printed Power, a high-tech company headquartered in Singapore that develops edge computers for smarter buildings and manufacturing globally (China and the Association of Southeast Asian Nations [ASEAN]). The company empowers customers with sensor-end to application-end platform solutions to discover opportunities and capture value from actionable insights as well as co-create with domain experts using advanced artificial intelligence (AI)/machine learning (ML) tools. Dr. Tan is concurrently the associate editor of the IEEE Sensors Journal and the industrial chair of IEEE Singapore section. He was also chair/professor at the School of Electrical Engineering/Hanergy School of Renewable Energy at Beijing Jiaotong University (BJTU) where he built international partnership programs, delivered seminars and short courses, and performed research exchanges with research staff and students.",institutionString:"Printed Power LTD",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"3",totalChapterViews:"0",totalEditedBooks:"6",institution:{name:"Nanyang Technological University",institutionURL:null,country:{name:"Singapore"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"45110",title:"Prof.",name:"Winston",middleName:null,surname:"Seah",slug:"winston-seah",fullName:"Winston Seah",profilePictureURL:"https://mts.intechopen.com/storage/users/45110/images/1643_n.jpg",biography:"Winston K.G. Seah received the Dr.Eng. degree from Kyoto University, Kyoto, Japan, in 1997. He is currently Professor of Network Engineering in the School of Engineering and Computer Science, Victoria University of Wellington, New Zealand. Prior to this, he has worked for more than 16 years in mission-oriented research, taking ideas from theory to prototypes, most recently, as a Senior Scientist (Networking Protocols) in the Institute for Infocomm Research (I2R), Singapore. He is actively involved in research in the areas of mobile ad hoc and sensor networks, and co-developed one of the first Quality of Service models for mobile ad hoc networks. He is a Senior Member of the IEEE and Professional Member of the ACM.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"540",title:"Wireless Communication Network",slug:"communications-and-security-wireless-communication-network"}],chapters:[{id:"12417",title:"A Survey on Routing Protocols for Wireless Sensor Networks",doi:"10.5772/13942",slug:"a-survey-on-routing-protocols-for-wireless-sensor-networks",totalDownloads:4363,totalCrossrefCites:8,totalDimensionsCites:10,hasAltmetrics:0,abstract:null,signatures:"Abbas Mohammed and Zhe Yang",downloadPdfUrl:"/chapter/pdf-download/12417",previewPdfUrl:"/chapter/pdf-preview/12417",authors:[{id:"2559",title:"Dr.",name:"Zhe",surname:"Yang",slug:"zhe-yang",fullName:"Zhe Yang"},{id:"8423",title:"Prof.",name:"Abbas",surname:"Mohammed",slug:"abbas-mohammed",fullName:"Abbas Mohammed"}],corrections:null},{id:"12418",title:"Review of Energy Harvesting Technologies for Sustainable WSN",doi:"10.5772/13062",slug:"review-of-energy-harvesting-technologies-for-sustainable-wsn",totalDownloads:4525,totalCrossrefCites:4,totalDimensionsCites:55,hasAltmetrics:0,abstract:null,signatures:"Yen Kheng Tan and Sanjib Kumar Panda",downloadPdfUrl:"/chapter/pdf-download/12418",previewPdfUrl:"/chapter/pdf-preview/12418",authors:[{id:"78857",title:"Dr.",name:"Tan Yen",surname:"Kheng",slug:"tan-yen-kheng",fullName:"Tan Yen Kheng"},{id:"15547",title:"Dr.",name:"Sanjib Kumar",surname:"Panda",slug:"sanjib-kumar-panda",fullName:"Sanjib Kumar Panda"}],corrections:null},{id:"12419",title:"Monitoring of Wireless Sensor Networks",doi:"10.5772/13239",slug:"monitoring-of-wireless-sensor-networks",totalDownloads:3472,totalCrossrefCites:2,totalDimensionsCites:2,hasAltmetrics:0,abstract:null,signatures:"Khelifa Benahmed, Haffaf Hafid and Madjid Merabti",downloadPdfUrl:"/chapter/pdf-download/12419",previewPdfUrl:"/chapter/pdf-preview/12419",authors:[{id:"14166",title:"Dr.",name:"Haffaf",surname:"Hafid",slug:"haffaf-hafid",fullName:"Haffaf Hafid"},{id:"14175",title:"Prof.",name:"Khelifa",surname:"Benahmed",slug:"khelifa-benahmed",fullName:"Khelifa Benahmed"},{id:"23870",title:"Prof.",name:"Madjid",surname:"Merabti",slug:"madjid-merabti",fullName:"Madjid Merabti"}],corrections:null},{id:"12420",title:"Diversity Techniques for Robustness and Power Awareness in Wireless Sensor Systems for Railroad Transport Applications",doi:"10.5772/13165",slug:"-diversity-techniques-for-robustness-and-power-awareness-in-wireless-sensor-systems-for-railroad-tra",totalDownloads:1795,totalCrossrefCites:1,totalDimensionsCites:4,hasAltmetrics:0,abstract:null,signatures:"Mathias Grudén, Magnus Jobs and Anders Rydberg",downloadPdfUrl:"/chapter/pdf-download/12420",previewPdfUrl:"/chapter/pdf-preview/12420",authors:[{id:"13993",title:"Dr.",name:"Mathias",surname:"Grudén",slug:"mathias-gruden",fullName:"Mathias Grudén"},{id:"15732",title:"MSc.",name:"Magnus",surname:"Jobs",slug:"magnus-jobs",fullName:"Magnus Jobs"},{id:"23322",title:"Prof.",name:"Anders",surname:"Rydberg",slug:"anders-rydberg",fullName:"Anders Rydberg"}],corrections:null},{id:"12421",title:"Energy Efficient Transmission Techniques in Continuous-Monitoring and Event-Detection Wireless Sensor Networks",doi:"10.5772/13333",slug:"energy-efficient-transmission-techniques-in-continuous-monitoring-and-event-detection-wireless-senso",totalDownloads:2367,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Nizar Bouabdallah, Mario E. Rivero-angeles, Sofiane Moad and Bruno Sericola",downloadPdfUrl:"/chapter/pdf-download/12421",previewPdfUrl:"/chapter/pdf-preview/12421",authors:[{id:"14446",title:"Prof.",name:"Bruno",surname:"Sericola",slug:"bruno-sericola",fullName:"Bruno Sericola"},{id:"15722",title:"Dr.",name:"Nizar",surname:"Bouabdallah",slug:"nizar-bouabdallah",fullName:"Nizar Bouabdallah"},{id:"15723",title:"Dr.",name:"Mario E.",surname:"Rivero-Angeles",slug:"mario-e.-rivero-angeles",fullName:"Mario E. Rivero-Angeles"},{id:"15724",title:"MSc.",name:"Sofiane",surname:"Moad",slug:"sofiane-moad",fullName:"Sofiane Moad"}],corrections:null},{id:"12422",title:"On Clustering in Sensor Networks",doi:"10.5772/13685",slug:"on-clustering-in-sensor-networks-",totalDownloads:2195,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Marot Michel",downloadPdfUrl:"/chapter/pdf-download/12422",previewPdfUrl:"/chapter/pdf-preview/12422",authors:[{id:"15612",title:"Dr.",name:"Marot",surname:"Michel",slug:"marot-michel",fullName:"Marot Michel"}],corrections:null},{id:"12423",title:"Cluster-based Routing Protocols for Energy-Efficiency in Wireless Sensor Networks",doi:"10.5772/13274",slug:"cluster-based-routing-protocols-for-energy-ef-ciency-in-wireless-sensor-networks-",totalDownloads:4567,totalCrossrefCites:17,totalDimensionsCites:24,hasAltmetrics:0,abstract:null,signatures:"Moufida Maimour, Houda Zeghilet and Francis Lepage",downloadPdfUrl:"/chapter/pdf-download/12423",previewPdfUrl:"/chapter/pdf-preview/12423",authors:[{id:"13808",title:"Dr.",name:"Moufida",surname:"Maimour",slug:"moufida-maimour",fullName:"Moufida Maimour"},{id:"23887",title:"Prof.",name:"Houda",surname:"Zeghilet",slug:"houda-zeghilet",fullName:"Houda Zeghilet"},{id:"23888",title:"Prof.",name:"Francis",surname:"Lepage",slug:"francis-lepage",fullName:"Francis Lepage"}],corrections:null},{id:"12424",title:"An Energy-aware Clustering Technique for Wireless Sensor Networks",doi:"10.5772/13714",slug:"-energy-aware-clustering-techniques-for-wireless-sensor-networks-",totalDownloads:2336,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,abstract:null,signatures:"Wibhada Naruephiphat and Chalermpol Charnsripinyo",downloadPdfUrl:"/chapter/pdf-download/12424",previewPdfUrl:"/chapter/pdf-preview/12424",authors:[{id:"13284",title:"Dr.",name:"Chalermpol",surname:"Charnsripinyo",slug:"chalermpol-charnsripinyo",fullName:"Chalermpol Charnsripinyo"},{id:"15762",title:"Mr.",name:"Wibhada",surname:"Naruephiphat",slug:"wibhada-naruephiphat",fullName:"Wibhada Naruephiphat"}],corrections:null},{id:"12425",title:"EECED: An Energy Efficient Clustering Algorithm for Event-Driven Wireless Sensor Networks",doi:"10.5772/13722",slug:"eeced-an-energy-efficient-clustering-algorithm-for-event-driven-wireless-sensor-networks",totalDownloads:2265,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Otgonchimeg Buyanjargal and Youngmi Kwon",downloadPdfUrl:"/chapter/pdf-download/12425",previewPdfUrl:"/chapter/pdf-preview/12425",authors:[{id:"15716",title:"Dr.",name:"Youngmi",surname:"Kwon",slug:"youngmi-kwon",fullName:"Youngmi Kwon"},{id:"15718",title:"Dr.",name:"Otgonchimeg",surname:"Buyanjargal",slug:"otgonchimeg-buyanjargal",fullName:"Otgonchimeg Buyanjargal"}],corrections:null},{id:"12426",title:"Topology Control in Large Scale WSNs : Routing and Base Station Placement",doi:"10.5772/13763",slug:"topology-control-in-large-scale-wsns-routing-and-base-station-placement",totalDownloads:1839,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Ines Slama",downloadPdfUrl:"/chapter/pdf-download/12426",previewPdfUrl:"/chapter/pdf-preview/12426",authors:[{id:"15769",title:"Dr.",name:"ines",surname:"slama",slug:"ines-slama",fullName:"ines slama"}],corrections:null},{id:"12427",title:"Dynamic Routing Framework for Wireless Sensor Networks",doi:"10.5772/13495",slug:"dynamic-routing-framework-for-wireless-sensor-networks",totalDownloads:1607,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Numerous routing protocols have been proposed for wireless sensor networks. Each such protocol carries with it a set of assumptions about the trafï¬c type that it caters to, and hence has limited interoperability. Also, most protocols are validated over workloads which only form a fraction of an actual deployment’s requirement. Most real world and commercial deployments, however, would generate multiple trafï¬c types simultaneously throughout the lifetime of the network. For example, most deployments would want all of the following to happen concurrently from the network: periodic reliable sense and disseminate, real time streams, patched updates, network reprogramming, query-response dialogs, mission critical alerts and so on. Naturally, no one routing protocol can completely cater to all of a deployments requirements. This chapter presents a routing framework that captures the communication intent of an application by using just three bits. The traditional routing layer is replaced with a collection of routing components that can cater to various communication patterns. The framework dynamically switches routing component for every packet in question. Data structure requirements of component protocols are regularized, and core protocol features are distilled to build a highly composable collection of routing modules. This creates a framework for developing, testing, integrating, and validating protocols that are highly portable from one deployment to another. Communication patterns can be easily described to lower layer protocols using this framework. One such real world application scenario is also investigated: that of predictive maintenance (PdM). The requirements of a large scale PdM are used to generate a fairly complete and realistic trafï¬c workload to drive an evaluation of such a framework.",signatures:"Mukundan Venkataraman, Mainak Chatterjee and Kevin Kwiat",downloadPdfUrl:"/chapter/pdf-download/12427",previewPdfUrl:"/chapter/pdf-preview/12427",authors:[{id:"14904",title:"Dr.",name:"Mainak",surname:"Chatterjee",slug:"mainak-chatterjee",fullName:"Mainak Chatterjee"},{id:"14911",title:"Prof.",name:"Mukundan",surname:"Venkataraman",slug:"mukundan-venkataraman",fullName:"Mukundan Venkataraman"},{id:"14912",title:"Dr.",name:"Kevin",surname:"Kwiat",slug:"kevin-kwiat",fullName:"Kevin Kwiat"}],corrections:null},{id:"12428",title:"Routing Security Issues in Wireless Sensor Networks: Attacks and Defenses",doi:"10.5772/12952",slug:"routing-security-issues-in-wireless-sensor-networks-attacks-and-defenses",totalDownloads:3119,totalCrossrefCites:5,totalDimensionsCites:11,hasAltmetrics:0,abstract:null,signatures:"Jaydip Sen",downloadPdfUrl:"/chapter/pdf-download/12428",previewPdfUrl:"/chapter/pdf-preview/12428",authors:[{id:"4519",title:"Prof.",name:"Jaydip",surname:"Sen",slug:"jaydip-sen",fullName:"Jaydip Sen"}],corrections:null},{id:"12429",title:"Optimization Approaches in Wireless Sensor Networks",doi:"10.5772/13093",slug:"optimization-approaches-in-wireless-sensor-networks",totalDownloads:3487,totalCrossrefCites:8,totalDimensionsCites:15,hasAltmetrics:0,abstract:null,signatures:"Arslan Munir and Ann Gordon-ross",downloadPdfUrl:"/chapter/pdf-download/12429",previewPdfUrl:"/chapter/pdf-preview/12429",authors:[{id:"13813",title:"Prof.",name:"Arslan",surname:"Munir",slug:"arslan-munir",fullName:"Arslan Munir"},{id:"14191",title:"Prof.",name:"Ann",surname:"Gordon-Ross",slug:"ann-gordon-ross",fullName:"Ann Gordon-Ross"}],corrections:null},{id:"12430",title:"A k-covered Mobile Target Tracking in Voronoi-based Wireless Sensor Networks",doi:"10.5772/13682",slug:"a-k-covered-mobile-target-tracking-in-voronoi-based-wireless-sensor-networks",totalDownloads:2361,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Jiehui Chen, Mariam B. Salim and Mitsuji Matsumoto",downloadPdfUrl:"/chapter/pdf-download/12430",previewPdfUrl:"/chapter/pdf-preview/12430",authors:[{id:"13597",title:"Dr.",name:"Jiehui",surname:"Chen",slug:"jiehui-chen",fullName:"Jiehui Chen"},{id:"15576",title:"Prof.",name:"Mitsuji",surname:"Matsumoto",slug:"mitsuji-matsumoto",fullName:"Mitsuji Matsumoto"},{id:"15606",title:"Dr.",name:"Mariam B.",surname:"Salim",slug:"mariam-b.-salim",fullName:"Mariam B. Salim"}],corrections:null},{id:"12431",title:"Power Efficient Target Coverage in Wireless Sensor Networks",doi:"10.5772/13377",slug:"power-efficient-target-coverage-in-wireless-sensor-networks",totalDownloads:3328,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:null,signatures:"Dimitrios Zorbas and Christos Douligeris",downloadPdfUrl:"/chapter/pdf-download/12431",previewPdfUrl:"/chapter/pdf-preview/12431",authors:[{id:"14561",title:"Dr.",name:"Dimitrios",surname:"Zorbas",slug:"dimitrios-zorbas",fullName:"Dimitrios Zorbas"},{id:"15646",title:"Prof.",name:"Christos",surname:"Douligeris",slug:"christos-douligeris",fullName:"Christos Douligeris"}],corrections:null},{id:"12432",title:"Node Deployment and Mobile Sinks for Wireless Sensor Networks Lifetime 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Mitochondria are abundantly present in mammalian cells. Their fraction varies from tissue to tissue, ranging from <1% (volume) in white blood cells to 35% in heart muscle cells. However, mitochondria should not be thought of as single entities, but rather a dynamic network that continuously undergoes fission and fusion processes. In skeletal muscle, mitochondria exist as a reticular membrane network. The subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria are located in distinct subcellular regions, and they possess subtle differences in biochemical and functional properties that are characterized by their anatomical locations. SS mitochondria lie directly beneath the sarcolemmal membrane and the IMF mitochondria are located in close contact with the myofibril. Their different properties are likely to influence their capacity for adaptation. SS mitochondria account for 10-15% of the mitochondrial volume and this population has been shown to be more susceptible to adaptation than the IMF mitochondria. However, the IMF mitochondria were found to have higher rates of protein synthesises, enzyme activities and respiration (1).
The mitochondria are equipped with double membranes, crating the intermembrane space between the outer and inner membranes as well as the inner matrix compartment, where most of the metabolic processes take place. The inner membrane is highly folded, forming so-called cristate, to accommodate its large surface area. Embedded in the inner mitochondria membrane are the five complexes that make up the respiratory chain where oxidative phosphorylation takes place. In this process, a proton gradient across the inner membrane is coupled to ATP synthesis at complex V (2). In addition to producing ATP essential for cell survival, the mitochondria are a source for free radical or reactive oxygen species (ROS), production. ROS are small, highly reactive molecules that can be generated by mitochondrial respiration and in active skeletal muscle.
Mitochondria are unique organelles in that they contain their own DNA, which consists of a circular DNA molecule of about 16.6 kb in humans and 16.3 in mice. It encodes 13 of the around 90 proteins that make up the respiratory chain. In addition, mtDNA also encodes 2 ribosomal RNAs (rRNA) and 22 transfer RNAs (tRNA) (3). The presence of mtDNA is explained by the evolutionary origin of mitochondrion as a free-living prokaryotic organism. During the course of time, genes have been transferred to the nuclear genome, and mitochondrial function is highly depended on close coordination between the nuclear and mitochondrial genomes. In mammals, mtDNA is maternally inherited, the paternal mtDNA being destroyed during the first embryonic cell divisions. The individual stands of mtDNA are termed heavy (H) and light (L) stand. Introns are lacking, but there is a long non-coding region, the D loop, which contains control elements for transcription and replication of mtDNA.
The mitochondria are often referred to as the powerhouses of the cell. In turn, It is well stabilised that mitochondria are the site of oxidative energy production in eukaryotic cells and provide the majority of the total ATP required to maintain normal cellular function and homeostasis. Within skeletal muscle, ATP is primarily required for the energy-dependent cross-bridge cycling between actin and myosin, as well as for Ca2+ cycling. Within the mitochondrial matrix, enzymes oxidize fatty acids and carbohydrates producing the reducing equivalents, NADH and FADH2. These reducing equivalents are then used to produce a proton gradient across the inner mitochondrial membrane. Dissipation of this gradient through the F0F1-ATPase results in the resynthesis of the ATP that drives every energy-dependent process in the cell. Studies showed Changes in metabolic demand can directly alter the concentration of mitochondria within the cell. Proliferation of mitochondria occurs in muscle in response to endurance exercise training, chronic electrical stimulation and thyroid hormone, while loss of mitochondria is associated with inactivity and aging.
Skeletal muscle is a highly malleable tissue, capable of considerable metabolic and morphological adaptations in response to repeated bouts of contractile activity (i.e. exercise). It is well established that chronic contractile activity, in the form of repeated bouts of endurance exercise, usually interspersed with recovery periods, results in the altered expression of a wide variety of gene products, leading to an altered muscle phenotype with improved fatigue resistance. This improved endurance is highly correlated with the increase in muscle mitochondrial density and enzyme activity, referred to as ‘mitochondrial biogenesis’. Mitochondrial biogenesis within muscle consists of two possible mutually inclusive alterations: [1] an increase in mitochondrial content per gram of tissue and/or [2] a change in mitochondrial composition, with an alteration in mitochondrial protein-to-lipid ratio (4). Although this phenomenon resulting from exercise has long been established, many of the detailed molecular mechanisms remain to be identified. This has particular relevance for our understanding of the pathophysiology of mitochondrially based diseases, and may improve our understanding of mitochondrial pathways involved in programmed cell death. Additionally, it has been suggested that an age-related accumulation of dysfunctional mitochondria may result in progressive reactive oxygen species-induced damage, producing a further impairment of oxidative capacity in aged muscle. Moreover, dysfunctional mitochondria have also been implicated in the age-related loss of muscle mass known as sarcopenia. Thus, mitochondrial biogenesis induced by chronic exercise is now recognized to have implications for a broader range of health issues than just the enhancement of endurance performance.
Therefore, the present chapter will highlight important molecular mechanisms that involved in mitochondrial biogenesis and then we will investigate the exercise effects on theses mechanisms. In the second Section of theses chapter, we examine the effects of aging on mitochondrial content and function and potential role of exercise in attenuation of age-related mitochondrial dysfunction.
One of the most fascinating aspects of mitochondrial synthesis is that it requires the cooperation of the nuclear and mitochondrial genomes (Figure-1). Mitochondria are unique in the fact that they house multiple copies of a small circular DNA molecule (mtDNA) comprising 16,659 nucleotides. As noted above, this mtDNA is minuscule compared with the 3 billion nucleotides found in the nuclear genome, it nonetheless contributes 13 mRNA, 22 tRNA, and 2 rRNA molecules that are essential for mitochondrial function. The thirteen mRNA molecules all encode protein components of the respiratory chain, responsible for electron transport and ATP synthesis.
Where does the cooperation between the genomes come in? First, these thirteen components comprise only a small fraction of the total respiratory chain proteins. Some act as single protein subunits, but many are combined nuclear-encoded proteins to form multisubunit holoenzymes, like COX or NADH dehydrogenase (Figure-1). The function of these holoenzymes is clearly impaired if contributions from either genome is absent (5). Second, it is known that mtDNA transcription and replication require the import of nuclear gene products, which act as polymerases or transcription factors. Given the diverse promoter regions of nuclear genes encoding mitochondrial proteins, as well as the sequences of the mtDNA promoters, it is not surprising that this coordination can be disrupted. Evidence for this has been presented in cases of thyroid hormone treatment, suggesting that a coordination of gene expression responses leading to strict stoichiometric relationships is not absolutely necessary for the formation of a functional organelle (6).
A longstanding question has been related to how the two genomes are regulated, or coordinated, in response to a stimulus leading to mitochondrial biogenesis. Williams et al. (7-8) were the first to show that chronic contractile activity led to increases in mRNA levels encoding both nuclear and mitochondrial gene products. Subsequently, this was demonstrated for subunit mRNAs belonging to the same COX holoenzyme. Because COX contains 10 nuclear encoded and 3 mitochondrial-encoded subunits, this enzyme is a useful model for studying the interactions of the two genomes. The mRNA expression of these subunits is also coordinated across a variety of tissues possessing a wide range of mitochondrial contents. In addition, some evidence for a coordinated regulation of the two genomes was found during the mitochondrial biogenesis induced by cardiac hypertrophy, as well as in human muscle when trained and untrained individuals were compared.
Overall synopsis of mitochondrial biogenesis in a muscle cell. Signals originating at the neuromuscular junction (NMJ) include propagated action potentials and the release of trophic substances, which interact with the postsynaptic membrane. Electrical activity in the sarcolemma is coupled to the release of calcium from the sarcoplasmic reticulum (SR). Calcium acts as a second messenger to activate phosphatases and/or kinases, which are ultimately translocated to the nucleus to affect the activation of transcription factors and which influence the expression of nuclear genes encoding mitochondrial proteins. mRNA produced by transcription is translated into protein in the cytosol, which can either be translocated back to the nucleus (transcription factor) or chaperoned to the protein import machinery and taken up by the organelle. Within mitochondria it may act as a single protein subunit or be combined with other subunits to form a multisubunit holoenzyme (e.g., cytochrome c oxidase). Some subunits of the holoenzyme may be derived from the mitochondrial genome (mtDNA), which also undergoes transcription and translation to synthesize a limited number (13) of proteins that are essential components of the electron transport chain.
The expansion of the mitochondrial reticulum in skeletal muscle is a highly regulated and complex process that appears to require the co-ordinated expression of a large number of genes. Thus, an important aspect of mitochondrial biogenesis is the import machinery regulating the transport of nuclear encoded precursor proteins into the organelle. The vast majority of mitochondrial proteins (>90%) are encoded by nuclear genes and synthesized in the cytosol as preproteins containing a mitochondria import sequence.
Notwithstanding the importance of the mitochondrial genome in contributing proteins to the mitochondrial respiratory chain, it is nevertheless true that most mitochondrial proteins are derived from nuclear DNA. Therefore, a mechanism must exist for targeting these proteins to specific mitochondrial compartments once they have been synthesized in the cytosol. Most proteins are fabricated as “precursor” proteins with a signal sequence, often either located at the NH2 terminus or as an internal sequence (Figure-2).
Although pathways of protein targeting to the outer membrane, inner membrane, matrix, or intermembrane space differ somewhat from each other (9), the most widely studied path is that of proteins destined for the matrix. In this case, the positively charged NH2-terminal signal sequence interacts with a cytosolic molecular chapter that unfolds the precursor and directs it to the outer membrane import receptor complex, termed the translocase of the outer membrane (Tom complex). Cytosolic chaperones include 70-kDa heat shock protein (HSP70) and mitochondrial import stimulating factor (MSF). Precursor proteins can be directed to one of two subcomplexes within the Tom machinery. One of these, consisting of the Tom20 and Tom22 receptors, is the preferential route for HSP70 chaperone precursors.
On the other hand, proteins interacting with MSF are largely directed to the Tom70-Tom37 heterodimer (10). Precursors are then transferred from the Tom receptors to Tom40 and the small Tom proteins 5, 6, and 7, which form an aqueous channel through which the precursor protein passes. Proteins are then sorted to the outer membrane, to the inner membrane, or to the translocase of the inner membrane (Tim), another protein complex that allows movement of precursor proteins to either the matrix or the inner membrane. Those proteins involved in the translocation of the precursor to the matrix are Tim17, Tim23, and Tim44. Tim17 and Tim23 act as integral membrane proteins, spanning the mitochondrial inner membrane and having domains associated with both the matrix and intermembrane space. In a manner similar to the Tom receptor complexes, Tim17 and Tim23 bind the precursor protein, prevent any untimely folding that would inhibit the precursor from translocating into the matrix, and form an aqueous pore through which the precursor can travel. In contrast, Tim44 is a peripheral membrane protein that is secured to the inner face of the inner mitochondrial membrane. Tim44 anchors the matrix chaperone HSP70 (mtHSP70), which acts in a ratchet like manner to pull the precursor into the matrix (Figure-2). Along with these proteins, the inner membrane phospholipid cardiolipin is imperative for protein translocation because it appears to orient the precursor into the correct position for interaction with the Tim44-mtHSP70 complex. The importance of this phospholipid has been shown by studies in which cardiolipin function has been blocked using the drug Adriamycin, resulting in an attenuation of the import of proteins destined for the matrix (11-12).
Left: mitochondrial transcription factor A (Tfam) is a nuclear-encoded transcription factor that is synthesized in the cytosol as a larger, “precursor” protein with a positively charged NH2-terminal presequence (blue). It must interact with the protein import machinery to enter the organelle. Once inside the matrix, mature Tfam will bind within the D-loop region of the circular (not shown) mtDNA on the heavy-strand (HSP) and light-strand promoters (LSP) and stimulate the transcription and replication of mtDNA. Right: enlarged view of the components of the protein import machinery. A typical matrix-destined precursor like Tfam is unfolded and directed to the import machinery by a cytosolic chaperone, either cytosolic 70-kDa heat shock protein (cHSP70) or mitochondrial import stimulating factor (MSF). On interaction with the translocase of the outer membrane (Tom complex), it is correctly oriented by interacting with the inner membrane phospholipid cardiolipin (not shown) before being transferred to the translocase of the inner membrane (Tim complex). The matrix chaperone mtHSP70 pulls in the precursor, and the signal sequence is cleaved by the mitochondrial processing peptidase (MPP). Subsequently, the mature protein is refolded by matrix chaperonins HSP60 and Cpn10. ATP is required at multiple steps during the import process. The number within each import machinery component refers to its size in kDa.
Two other elements are required for correct import of precursor proteins into the matrix. These are 1) the presence of an inner membrane potential (DC, negative inside) across the inner membrane to help pull the positively charged presequence into the matrix and 2) the availability of ATP both in the cytosol and in the matrix. Uncoupling agents that dissipate DC reduce protein import, whereas ATP depletion prevents the unfolding of the precursor in the cytosol and/or the action of mtHSP70 in the matrix. Thus reductions in cellular ATP levels such as that produced by severe contractile activity or defects in ATP production as might be encountered in cells with mtDNA mutations could affect the rate of import into mitochondria.
After its arrival in the matrix, the NH2-terminal signal sequence is cleaved by a mitochondrial processing peptidase (MPP) to form the mature protein. It is then refolded into its active conformation by a mitochondrial chaperonin system consisting in part of 60-kDa heat shock protein (HSP60) and 10-kDa chaperonin (Cpn10). The vast majority of work that defines the components of the protein import machinery, as well as their cellular function, has been done in Saccharomyces cerevisiae and Neurospora crassa. This is now being extended to mammalian cells. For example, the kinetics of matrix precursor protein that import into skeletal muscle SS and IMF mitochondrial fractions, the ATP and cardiolipin dependence of the process, and the relationship to mitochondrial respiration have all been defined (13). IMF mitochondria import precursor proteins more rapidly than SS mitochondria, and there is a direct relationship between the capacity for mitochondrial respiration (and thus ATP production) and the rate of protein import. It has also been shown that a number of protein import machinery components are induced in response to chronic contractile activity. These include the chaperones MSF, cytosolic HSP70 (cHSP70), mtHSP70, HSP60, Cpn10, as well as the import receptor Tom20. Coincident with these increases are contractile activity-induced increases in the rate of import into the matrix but not into the outer membrane. This differential effect on protein targeting to mitochondrial compartments provides an example of how contractile activity can result in an altered mitochondrial protein stoichiometry. The accelerated rate of protein import into the matrix can be reproduced in cardiac mitochondria obtained from animals treated with thyroid hormone. Thus the effect is not a unique response to contractile activity but appears to be common to stimuli that increase mitochondrial biogenesis. To more easily define the role of specific components of the import pathway in determining the kinetics of import, measurement of import in intact cells can be employed. When C2C12 cells were incubated with [35S] methionine and the import of radiolabeled MDH into mitochondria was measured, a greater rate of import was found during the progress of mitochondrial biogenesis occurring coincident with muscle differentiation. As expected, thyroid hormone accelerated the rate of import and induced the expression of Tom20. To evaluate the role of Tom20 alone in mediating the accelerated import rate, forced overexpression of Tom20 in these cells using a mammalian expression construct was used. Parallel increases in the rate of import and the magnitude of overexpression were observed. Conversely, inhibition of Tom20 expression using specific antisense oligonucleotides led to equivalent decreases in MDH import. These data suggest that the import of matrix-destined proteins is controlled, at least in part, by the expression of Tom20. The protein import pathway represents an example of intracellular trafficking that is important for organelle biogenesis, and it may, under some conditions, determine the increase in mitochondrial content as a result of chronic exercise. For this to be the case, it must be shown that it is inducible and that it operates at a rate that limits the overall pathway under some conditions (i.e., chronic exercise). If the import rate was slow enough to limit mitochondrial biogenesis, then a pool of precursor proteins in the cell cytosol would be measurable. In the absence of such a pool, the assumption is that newly synthesized precursor proteins are rapidly taken up by mitochondria, and the kinetics does not limit the synthesis of the organelle as a whole. This has yet to be rigorously tested in a cellular system in which any other fates of the precursor (i.e., cytosolic degradation) are blocked. It is possible that the import of proteins might become limiting under conditions of chronic contractile activity if upstream steps (i.e., transcription, translation) are accelerated such that a saturating abundance of precursor proteins are presented to the import machinery.
In any event, the physiological value of the observed contractile activity-induced increases in mitochondrial protein import is that mitochondria are more sensitive to changes in precursor protein concentration, a situation that would be advantageous for mitochondrial biogenesis at any given upstream production rate of cytosolic precursor proteins. Progress in the area of protein import will advance substantially as additional mammalian homologues of the import machinery are identified. Recently, the first disease that can solely be attributed to a mutation in a protein component of the import machinery has been identified. A mutation in deafness dystonia protein (DPP) results in a neurodegenerative disorder characterized by muscle dystonia, sensorineural deafness, and blindness. DPP has been shown to be a mitochondrial protein that closely resembles Tim8p, a protein of the intermembrane space involved in the import process. In addition, mutations in the import receptor Tom70 have been shown to produce mtDNA rearrangements in the fungus Podospora anserina, presumably because of defective import of a component involved in mtDNA maintenance. The cloning of Tom22, as well as members of the Tim machinery, will be of help in elucidating the functional roles of individual import machinery components in the import process and the relevance of import in mitochondrially based diseases and in organelle biogenesis.
As noted above, exercise has been shown to induce the expression of several protein import machinery components, occurring coincident with an increased rate of translocation into the mitochondria. In turn, activity-induced changes have been observed in Tom20, Hsp60 and mtHSP70 protein and cpn10 mRNA levels, as well as cytosolic concentrations of Hsp70 and MSF (13-15). Coincident with these changes is acceleration in the rate of protein import into the matrix. Thus, the upregulation of protein import machinery components appears to be an important aspect of mitochondrial biogenesis which occurs with contractile activity. This greater capacity for protein import is physiologically relevant because it means that a greater rate of translocation into the organelle will occur at any given concentration of cytosolic protein produced by translation.
Expression of genes promoting mitochondrial biogenesis is predominantly controlled by the global principles of gene regulation, that is, transcription initiation and interaction at the gene promoter. Therefore, transcription factors and transcriptional co-activators represent critical regulators of mitochondrial biogenesis.
Numerous transcription factors have been implicated in mediating the physiological and metabolic adaptations associated with expression of genes involved in mitochondrial biogenesis. While no single transcription factor has been found to be responsible for the co-ordination of mitochondrial gene expression, several candidates appear to be important for mitochondrial biogenesis. These include two nuclear respiratory factors (NRF-1 and NRF-2), two peroxisome proliferator-activated receptors (PPAR-γ and PPAR-α), specificity protein 1 (Sp1), mitochondrial transcription factor A (Tfam), early growth response gene-1 (Egr-1) and the products of the immediate early genes, c-jun and c-fos. This diversity is important given that the characterization of an assortment of upstream promoter regions of genes encoding mitochondrial proteins has revealed considerable variability in their composition.
NRF-1 and NRF-2 are implicated in the transcriptional control of multiple mitochondrial genes including mitochondrial transcription factor A (Tfam) and identified mitochondrial transcription specificity factors TFB1M and TFB2M, while Egr-1 is associated with promoting transcription of the electron transport chain protein cytochrome C oxidase (COX). The peroxisome proliferator receptor gamma co-activator-1 alpha (PGC-1α) has been established as an important regulator of mitochondria content in skeletal muscle due to its apparent co-activation of multiple mitochondrial transcription factors. Indeed, PGC-1α is the founding member of a family of transcriptional co-activators that has been proposed as a potential “master regulator” of mitochondrial biogenesis (16). In support of this contention, Lin and co-workers (2002) over expressed PGC-1α in mice skeletal muscle and observed increased proportions of type I fibers and increased resistance to fatigue (17). In addition, the biogenesis and maintenance of mitochondrial architecture is controlled by altered rates of mitochondrial protein fusion and fission, a role for which mitofusin (Mfn) 1/2 proteins have been strongly implicated (18).
Similarly, PGC-1α also mediates Tfam activation, a key component in mitochondrial DNA replication and transcription. The NRF-1 transcription factor has been shown to activate Tfam which enhances the capacity for assembly of protein complexes within the mitochondria. Therefore, as a co-activator of NRF-1 transcription PGC-1α is involved in regulating Tfam function. Importantly, Tfam activity appears to increase in response to contractile activity and exercise suggesting enhanced mitochondrial protein assembly with endurance training. Most notably, PGC-1α is the co-activator of the peroxisome proliferator activated receptor (PPAR) family (19). The three PPAR sub-types α, γ and δ have distinct functions but all appear to regulate lipid homeostasis via expression of genes involved in mitochondrial fatty acid oxidation. The initial cellular perturbations associated with the onset of muscle activity leading to the activation of these transcription factors are beginning to be defined (Figure-3).
Researchers showed NRF-1, Tfam and PPAR-γ (has emerged as a potential master regulator of mitochondrial biogenesis) mRNA in response to contractile activity in cell cutlers and endurance exercise in vivo is increased. In turn, studies have been shown that PGC-1α mediates a regulatory pathway involving estrogen-related receptor alpha (ERRα) and Mfn1/2, and this pathway has been shown to be up-regulated following a 10-km cycling time trial (20). Also, this suggests that a PGC- 1α activated pathway promotes an increase in mitochondrial content in response to endurance exercise through enhanced mitochondrial protein fusion. This provokes an increase in mtDNA transcription and replication. The result is that PGC-1 overexpression can produce an overall increase in cellular oxygen consumption and subsequently, increases the aerobic capacity in endurance activities. The physiological significance of increased PGC-1α-PPAR activated gene expression with endurance training is an enhanced capacity for fat utilisation during prolonged exercise, and may also be related to fast-to-slow fibre type conversion (21). Indeed, this was highlighted by Wang and colleagues (2004) who generated transgenic mice over expressing PPARδ that resulted in a 2.3-fold increase in mitochondrial DNA content, significant type I fibre transformation and a 90% increase in running performance (22).
Transcription factors and mitochondrial biogenesis
The small numbers of studies investigating PPAR activation following exercise support these findings where both acute (21, 23-24) and chronic (25-27) endurance exercise induces PPAR transcription. The initial cellular perturbations associated with the onset of muscle activity leading to the activation and increment of these transcription factors are beginning to be defined. A considerable amount of evidence implicates alterations of intracellular Ca2+ (28-29) and ATP (30-31) turnover as the initial triggers eliciting the activation of signalling cascades which provoke changes in these gene expressions, as noted above.
Mitochondria are cited regularly as the main site of superoxide generation that contributes to the majority of reactive oxygen species (ROS) to the cell, although other sites of ROS production within the cell are documented. The potential for ROS to induce oxidative damage has significant implications for the cellular integrity of highly metabolic, long-lived and post-mitotic tissues such as brain, heart, and skeletal muscle. In addition, the effect of ROS is exacerbated by its potential to induce mutations in mtDNA, which is located in close proximity to the source of ROS generation. mtDNA has no protective histones and has substantially less repair mechanisms than nuclear DNA. Thus, ROS-induced accumulations in faulty proteins, oxidized fatty acids, and mtDNA mutations would result in a progressive, feed-forward, and irreversible cycle of cellular dysfunction that leads to the onset of phenotypes associated with aging. These observations are the major features of the mitochondrial theory of aging, which was first proposed, and then refined, by Denham Harman (32-33), suggesting that changes to mitochondrial integrity, content, and function could have a determining role on the rate at which we age. The role of mitochondria in promoting sarcopenia was uncovered by studies showing that muscle fibers containing dysfunctional mitochondria were atrophied compared to fibers that did not. As well, these authors and other groups (34-36) have reported that histochemical analyses of skeletal muscle fibers revealed an increase in the number of ragged red fibers, characterized by elevated levels of succinate dehydrogenase and a deficiency in COX activity. An in-depth description on the involvement of ROS in mitochondrial dysfunction associated with aging is provided in a later section.
Along with their role in ROS production, mitochondria play a critical role in maintaining cellular integrity through the regulation of programmed cell death, also termed apoptosis. Within mitochondria reside proteins, which upon release from the organelle, can initiate a cascade of proteolytic events that converge onto the nucleus leading to the fragmentation of DNA. This compromises cell viability and ultimately leads to cell death (37). The release of these apoptotic proteins, such as cytochrome C (cytoC), endonuclease G (EndoG) and apoptosisinducing factor (AIF), through either the mitochondrial permeability transition pore (mtPTP) or the homo-oligomeric BAX pores in the outer membrane, occurs in response to cellular stressors such as reactive oxygen species (ROS), chronic elevations in intracellular Ca2+ concentration, or gamma irradiation. Thus, the intimate connection between mitochondrial function and the viability of skeletal muscle suggests that this organelle plays a significant role in the progression of aging. Indeed, it is evident that in skeletal muscle of aged individuals, the induction of apoptosis is greater when compared with younger subjects. The increase in cytoC and EndoG release from the mitochondria of aged individuals is paralleled by an increase in caspase-3 cleavage, and p53 mediated apoptosis. The result of apoptosis is a loss in myonuclear number, resulting in a reduction in myofiber diameter to maintain a constant myonuclear domain size. Alternatively, a consequence of fiber atrophy may be the initial activation of apoptotic events that lead to a decrease in myonuclear number. Irrespective of the mechanism involved, mitochondria appear to have an involvement in the progression of sarcopenia. A discussion of the importance of apoptotic signalling during the development of age-related phenotypes caused by mtDNA mutations follows below.
Electron microscopic (EM) analyses reveal that the volume of mitochondria within skeletal muscle declines by 66% with age when compared with younger counterparts (38). Similar EM findings are documented in a human study, revealing a 25% decrease in the density of mitochondria within the vastus lateralis muscle of males and females aged greater than 60 years (39). Related to mitochondrial content is the level of cardiolipin found within skeletal muscle. Cardiolipin is a fatty acid that is exclusively found within the inner membrane of mitochondria, and it is linked to the optimal function and structure of the multitude of enzymes and respiratory complexes. The proximity of cardiolipin to the sites of ROS production makes it particularly vulnerable to oxidative damage. Numerous studies have investigated whether aging has an effect on cardiolipin content or oxidation in cardiac muscle. Some results have indicated that cardiolipin content is decreased along with an increased degree of peroxidation (40). This is linked to decreased activities of COX, ANT, and carrier complexes. However, other reports have failed to indicate a decline in cardiolipin content or its peroxidation within either SS or IMF mitochondria with age. One study in skeletal muscle has illustrated that cardiolipin content in 36-monthold rats is not decreased when compared with 6-month-old rats in isolated SS and IMF mitochondria (41). However, whether cardiolipin is oxidatively modified with age in skeletal muscle remains to be determined. The morphology of mitochondria may also be altered with age in skeletal muscle, in that a proportion of the organelles are enlarged, depolarized, and non-functional. When compared with the elongated morphology of mitochondria in skeletal muscles of young animals, mitochondria tend to be more rounded in shape within aged skeletal muscle, suggesting that mitochondrial fusion events may be impaired in skeletal muscle. Indeed, decreased OPA1 protein expression has been documented in experimentally-generated, giant mitochondria which may have physiological relevance to the morphology of mitochondria seen in aged individuals (42). Mitochondria have also been shown to undergo significant swelling with age because of the increased retention of calcium. EM has also identified losses in mitochondrial cristae formation, leading to homogenization of the materials found within the mitochondrial Compartments.
Upstream of the synthesis of ATP, the activities of the metabolic enzymes in Krebs’ cycle and those involved in lipid oxidation are altered with age. Citrate synthase activity is significantly decreased with age and the activities of b-hydroxyacyl-CoA dehydrogenase (b-HAD) and succinate dehydrogenase are also reduced with age (43). Oxidation of lipids is also impaired within skeletal muscle of aged individuals. Aged muscle also exhibits characteristics of decreased mitochondrial respiratory capacity and ETC enzyme activities. Functional analyses reveal decreased activities of complex I and IV. In line with these alterations, the activity of COX has been shown to decrease with age and the activities of complexes I, II, III, and IV decrease by 28–43%. Reduced oxidative capacity of approximately 30% has also been reported per mitochondrion (44). As a result of decreased enzyme and complex activities, ATP synthesis and content within aged skeletal muscle is reduced. Thus, there is an increased probability of affecting cellular processes reliant on a constant supply of ATP, such as muscle contractions, protein turnover, and the maintenance of membrane potential.
Skeletal muscle oxidative capacity is a reflection of the ability of working muscle to regenerate ATP through aerobic metabolism. Studies support that whole body maximal oxygen consumption (VO2max) declines with age and there is reduced aerobic capacity per kilogram of muscle in late-middle aged individuals. Oxidative phosphorylation capacity decreased by 50% in 70-year-old human subjects, evaluated using in vivo measurements (39). ATP production rates were decreased by 50% in the gastrocnemius of aged animals (45). Assessments of mitochondrial respiration that was stimulated with a variety of substrates in the presence of ADP revealed that this parameter decreased in aged skeletal muscle. At rest, muscle ATP synthesis was reduced in 30-month, compared with 7-month-old mice (46). In addition, the ATP content in aged gastrocnemius muscle is 50% lower when compared with that found in young animals (45), and a lower ATP/ADP ratio in 30-month-old mice has been illustrated as well (46).
Despite this evidence, numerous studies have also demonstrated that the oxidative capacity of skeletal muscle does not change with age and discrepancies in results can arise for a number of reasons. One is the lack of consistency of the ages used to make comparisons. Studies may pool together subjects in their late teenage years with middle-aged subjects to represent an ‘‘adult’’ group, whereas the ‘‘old’’ group could encompass subjects ranging from 40 to 90 years of age. Another variable between aging studies is the differences in the species used, which can range from rats, mice, monkeys, yeast, flies, worms, and humans. The selection of muscle studied, and the method of preparation are also not standardized, such that measurements have been made using either whole muscle homogenates or isolated mitochondrial populations. Related to this, many studies have ignored the potential biochemical differences between the SS and IMF mitochondria and report their findings on mixed mitochondrial samples. It is very possible that these skeletal muscle mitochondrial populations are affected differentially by the aging process. Finally, many studies fail to control for physical activity levels in their subjects, and there is evidence that the majority of age-related declines in mitochondrial oxidative capacity disappear after accounting for this variable (47). Thus, it is controversial whether mitochondrial dysfunction is due to aging per se, or whether the lack of regular physical activity is the major reason for the divergent age-related phenotypes of skeletal muscle. Then again, a reduced oxidative capacity was observed in aged subjects even after accounting for physical activity and fat-free mass. Thus, more research is needed to fully clarify these important issues.
The impairment in mitochondrial biogenesis may be due to a plethora of causes that lead to the propagation of mitochondrial dysfunction. As discussed below, a change in the content of mitochondria may be due to a decrease in the expression of genes coding for mitochondrial proteins, and/or alterations in the control of protein turnover that occur with aging. In addition, alterations in mitochondrial function may be due to oxidative modifications resulting from an increase of ROS, an elevation of mtDNA mutations, or increased uncoupling of oxidative phosphorylation with age.
Declines in mitochondrial content and function may be related to the altered expression of nuclear genes encoding mitochondrial proteins (NUGEMPS) in skeletal muscle of the elderly. The huge reliance of mitochondria on the nuclear genome suggests that impaired protein synthesis rates could lead to the decline in mitochondrial biogenesis that is observed with old age, especially if the transcription of NUGEMPS is decreased with age. An interesting study by Zahn et al. revealed that expression of mitochondrial ETC transcripts decreased, whereas cytosolic ribosomal transcripts were increased in skeletal muscle with age (48). This increased expression of ribosomal subunits may represent a compensatory response for decreased translational efficiency, particularly because protein synthesis has been illustrated to decrease with age. Deficits in ETC enzyme activities have been observed in number of studies and may be linked to a reduction in the transcription of genes located within mtDNA, or to a reduction in the content of mtDNA with age. However, in response to the decline in mitochondrial respiratory function, compensatory increases in mtDNA content in tissues such as skeletal muscle, kidney, and cardiac muscle have been observed. Conversely, the preponderance of evidence seems to suggest that mitochondrial mRNA content is reduced with age. Mitochondrial DNA copy number and mtDNA transcript levels of COX I and COX III have been shown to decrease in 27-month aged animals versus 6-month young animals (49). Similarly in humans, mtDNA content was significantly decreased in muscle biopsies obtained from 67-year-old subjects (50), whereas Welle et al. revealed that mRNA transcripts of components of the respiratory complexes also decrease in their abundance in aged skeletal muscle (51). It has been illustrated that in skeletal muscle of aged humans the rate of mitochondrial protein synthesis is decreased and this may have contributed to the decrease in COX and CS activities observed.
Mitochondrial function and morphology depend on the balance between protein synthesis and assembly, and the clearance of damaged or improperly assembled proteins. A reduced ability of degradation pathways to remove whole or damaged compartments of mitochondria could lead to impaired organelle bioenergetics. These effects likely manifest as decreased ATP synthesis, increased ROS generation, accumulated mtDNA mutations and cell death, characteristics which are observed in skeletal muscle of aging individuals. The major pathways that contribute to mitochondrial protein quality control include intramitochondrial proteases and autophagy. Studies have illustrated that with increasing age, the activity and expression of the intramitochondrial Lon protease is reduced, reflected by an accumulation of dysfunctional aconitase (52). Decreased activity of the Lon protease is likely due to oxidative modifications by elevated ROS levels within the mitochondrial matrix. In the cytosolic environment, lipofuscin has been implicated in contributing to the progressive decline in mitochondrial protein turnover and the onset of dysfunction that occurs with age. Lipofuscin, referred to as the aging pigment, is a non-degradable protein that is the product of incomplete autophagic degradation followed by the peroxidation of remaining contents within the lysosome by reactive oxygen species. Lipofuscin localizes within vesicles throughout tissues in aged individuals, which may reduce the availability of vesicles to form autophagosomes to remove damaged and dysfunctional mitochondria (53). Thus, it appears that the activities of these housekeeping pathways related to protein quality control are altered with aging, resulting in the accumulation of damaged mitochondria and cellular dysfunction. More research is required in this area with skeletal muscle as a function of age.
Research unequivocally indicates that ROS production increases in aging skeletal muscle (54). Chabi et al. observed that the generation of ROS is elevated in both the SS and IMF mitochondrial pools of fast-twitch muscles isolated from senescent animals (41). One consequence of increased aberrant ROS production is oxidative damage to complex V leading to a decrease in ATP synthesis and content within skeletal muscle. Additionally, increases in oxidative modifications in DNA occur with age, reflected by higher levels of 8-oxodeoxyguanosine, (8-oxoG) and the corresponding repair enzyme, 8-oxoguanine-DNA glycosylase 1 (OGG1) in skeletal muscle. Increased levels of protein carbonyls have also been associated with aging skeletal muscle. It is well known that slower respiration rates increase the likelihood of the donation of electrons to oxygen at complexes I or III (55), and this may be a feature of mitochondrial respiration in aged individuals. It has also been hypothesized that during aging, there is increased dysfunction of these two complexes, leading to increased ROS generation.
Antioxidant enzymes have evolved to buffer the deleterious, effects of ROS. Enzymes such as manganese superoxide dismutase (MnSOD), catalase (CAT), and glutathione peroxidise (GPX), can ultimately reduce ROS to hydrogen peroxide (H2O2), and then finally into water. The role of ROS in limiting lifespan was elucidated in an elegant study, in which human CAT was targeted to the mitochondria. This resulted in improved aconitase activity, decreased mtDNA mutations, and increased mean lifespan (56). Conversely, transgenic mice lacking copper/zinc SOD (CuZnSOD) showed rapid aging and muscle atrophy similar to sarcopenia in concert with elevated oxidative modifications in proteins, lipids, and DNA, when compared with wild-type animals (57). However, whether the activity or content of these antioxidant enzymes is truly altered with age remains an equivocal issue. A number of studies have illustrated that there is an increase in antioxidant activities with age, as this would be the intuitive hypothesis in response to the elevated ROS generation that occurs during aging (58-59). However, other studies suggest that CuZnSOD, MnSOD, CAT, and GPX activities decrease with age in skeletal muscle, even though the protein and mRNA content of these enzymes were either unchanged or decreased with age (60-61). To add more complexity to this issue, it remains to be determined whether antioxidant enzyme activities are differentially affected by age in the two mitochondrial subfractions. One study suggests that there is no change in the content of MnSOD in SS and IMF mitochondria from tibialis anterior and extensor digitorum longus muscles of aged, compared with young animals. In cardiac muscle, IMF mitochondria exhibit increased levels of GPX, CAT, and MnSOD with age, whereas SS mitochondria exhibit increased levels of GPX and MnSOD and a decrease in CAT activity (62). Because it is clear that oxidative modifications to mitochondrial macromolecules are indeed occurring in skeletal muscle with age, it is likely that the increased ROS production overwhelms the buffering capacity of the antioxidant enzymes that are available. This suggests that other means to reduce ROS, independent of antioxidant enzyme activities, would be beneficial in reducing cellular oxidative damage.
An important component of the free radical theory of aging is that mitochondrial dysfunction is a result of accumulated oxidative damage to mtDNA, leading to mutations in coding regions for ETC proteins. The last point is especially critical because mtDNA contains no introns or spacer regions (63), thus even point mutations could lead to the expression of faulty proteins. It is accepted that ROS generation by skeletal muscle mitochondria increases with age and is accompanied by an increase in mtDNA mutations, impaired energy production, mitochondrial dysfunction, and a greater susceptibility to undergo apoptotic signalling that results in the downfall of skeletal muscle function. The most common mtDNA mutation associated with aging has a frequency rate of 30–35%, is found within the D-loop region, and is a deletion mutation that affects the expression of seven of the 13 proteins encoded by mtDNA (64-65). In addition, mtDNA deletion mutations appear to be highly localized in small regions of muscle fibers in mosaic patterns, rather than distributed ubiquitously throughout aged skeletal muscle.
Interestingly, research has illustrated that mtDNA mutations may be an important contributor to the aging process. Genetically altered mice lacking DNA polymerase gamma (Polg) activity exhibited an elevated accumulation of random mtDNA point mutations, in conjunction with a severe deficiency in ATP synthesis and the early onset of aging-related phenotypes. However, these occurred in the absence of increased ROS production, protein carbonylation or mtDNA damage (66). Although there was no evidence for increased oxidative stress in this study, apoptotic signalling was significantly elevated in the Polg mice, and it is conceivable that areas of the cell with accumulated oxidative modifications may have been cleared away by cell death and subsequent autophagy processes. In future experiments, it would be interesting to determine whether the enhanced expression of Polg activity could result in extended lifespan in normal animals. A definite role for ROS in producing mutations and mitochondrial dysfunction was illustrated in a mouse model with compromised MnSOD activity and content. Age-related alterations observed included 25% decreases in complex I and V activities, a 50% increase in basal ROS generation and a 45% increase in 8-oxoG content (67). However, both the mean and maximum lifespan were not altered. As a result of this, there is considerable debate regarding the validity of the mitochondrial theory of aging. As Conley et al. reviewed, mitochondrial dysfunction can be observed in skeletal muscle before the detection of mtDNA mutations (68). In addition, the theory postulates that mitochondrial dysfunction is irreversible; however, much evidence exists to contradict this point. Clearly, more research is required, with a focus on when and how mtDNA mutations are involved with aging. Despite this, the associations between dysfunctional mitochondria, mtDNA mutations, and apoptosis remain strong themes in the description of mechanisms that may be causative to the aging process.
Coupling of the energy generated from electron transfer through the respiratory complexes to the synthesis of ATP is a major function of the mitochondrial network. However, the flow of protons through complex V can be bypassed and redirected through protein channels which serve to uncouple respiration. The result of uncoupling is a decrease in ATP synthesis, despite increased oxygen consumption and respiratory rates (69). There is evidence which suggests that coupling is reduced with age. When compared with young individuals, coupling was lower by 50% in 30-month-old mice, resulting in decreased ATP production per O2 consumed (46). Another study supplemented this finding with the observation that uncoupling occurs in human skeletal muscle of subjects greater than 65 year of age that was accompanied with reduced ATP content (70). In the same study, it was determined that uncoupling affects muscles with a high type II fibre composition, compared with those that are composed of predominately type I fibers (41). Ghabi et al. also observed 21 and 40% decreases in the coupling of the IMF and SS mitochondria, respectively, in 36-month-old animals when compared with their younger counterparts (41). Potential causes for uncoupling of oxidative phosphorylation occurring with age may involve the increased activity and expression of uncoupling protein 3 (UCP3) that can be stimulated by oxidative stress. An increased activity of UCP3 has been proposed to lend protection to the cell, in response to increased oxidative stress that occurs with age. Indeed, mitochondria from UCP3 null mice demonstrated elevated levels of ROS production and oxidative modifications to cellular components. Whether the expression of uncoupling proteins in skeletal muscle is altered with aging is not well established. Some studies have observed a trend for increased UCP3 content (43), whereas others have suggested there is an age-related decrease or no change in this protein content (46, 71). Thus, if UPC3 content is not increased with age, it is likely that a greater proton leak with age could occur through increased permeability of the inner membrane by ROS-induced oxidative modifications of the lipid bilayer.
Although it has long been established that exercise training increases, and muscle disuse decreases, the activity of mitochondrial oxidative enzymes in skeletal muscle, a lack of consideration of this notion in aging studies has led to discrepancies in our overall understanding of the effect of aging on muscle mitochondrial function. Indeed, some of the age-associated alterations found in mitochondrial activity can be the result of a reduction in the level of voluntary physical activity as individuals age (31). In this regard, it is notable that the adaptation to exercise is not limited to young individuals, because older athletes can increase the activity of mitochondrial oxidative enzymes as a result of training (72). This likely happens through increases in expression of the coactivator PGC-1a and the specific transcription factors NRF-1 and Tfam, the main regulators of organelle biogenesis and protein expression. One can assume that if mitochondrial function deteriorates with age, organelle biogenesis induced by exercise may attenuate this age-related decline, and therefore may have a protective role. However, despite the fact that exercise-induced increases in enzyme activities and mitochondrial content have been reported in aging individuals, less is known about the effects of exercise on the expansion of mtDNA mutations, ROS balance, and apoptosis in aged skeletal muscle. For example, in patients suffering from mitochondrial diseases due to mtDNA mutations, the introduction of an exercise program to improve muscle oxidative capacity and mitochondrial function has been approached with caution. In those patients, exercise induced mitochondrial biogenesis but also increased both wild-type and mutant mtDNA, worsening the heteroplasmy ratio in muscle fibers (73). Thus, one might expect that this phenomenon could also occur in older individuals. However, in view of the evidence that chronic exercise can attenuate proapoptotic protein release from mitochondria in young animals, and reduce ROS production in intermyofibrillar mitochondria, it is worth investigating whether exercise can attenuate he enhanced apoptotic susceptibility evident in muscle from aged individuals.
Several lines of evidence support the fact that exercise may be beneficial in attenuating an aging-induced ROS imbalance. Old animals that were submitted to an 8-week treadmill exercise program, or 1 year of swimming, were found to have reduced oxidative damage compared with untrained old rats, notably due to alterations in antioxidant defences (74). At the mitochondrial level, recent work has revealed a 10% decrease in mitochondrial hydrogen peroxide production in animals as a result of lifelong voluntary wheel running (75). This may occur through the exercise-induced increase in mitochondrial content, a better redistribution of electrons through the electron transport chain, and (or) a better coupling between oxygen consumption and ATP synthesis in the exercised muscle of old animals. The precise mechanism for this effect remains to be determined.
Skeletal muscle is a remarkably adaptive tissue that is capable of changing its morphological, physiological, and biochemical properties in response to various perturbations. One of the most profound changes in skeletal muscle is mitochondrial biogenesis. Mitochondrial biogenesis is a very complex cellular process that requires the coordination of several mechanisms involving nuclear-mitochondrial corporation, mitochondrial protein expression and import, mtDNA gene expression, transcription factors activity, assembly of multisubunit enzyme complexes, regulation of mitochondrial fission and fusion as well as mitochondrial turnover. In turn, it seems with recognition of variant component of mitochondria of skeletal muscle; we can understand precisely the function of theses component in mitochondrial biogenesis process and effects of many interventions (e.g. Aging and diseases) on them. Also, we can comprehend the uncountable positive effects of exercise on these components. But, many vast and precise researches are needed to fully clarify these important issues.
Higher ventilation rates are dictated both by better comfort requirements and by the most recent standards such as ASHRAE (62-2019) and various CIBSE guides. However, post-COVID 19 pandemics, these ventilation rates require re-consideration. People shall also maintain social distancing regulations, which impact occupied spaces both indoor and outdoor. Eventually, higher fresh air rates are required and researchers will continue to work on the additional fresh air amounts. The more outdoor air is used, the larger the cooling or heating loads required, particularly cooling loads in hot and humid regions. In addition, the uncontrol of the ventilation air physical parameters will impact human comfort and health. For instance, the fresh air must be treated and conditioned to the desired comfort level of humidity and temperature before being supplied to the occupied spaces.
Cooling of outdoor air is usually obtained with refrigeration equipment and often in humid climates and some post-heating is required to heat the air before it is supplied to the rooms. Figure 1 demonstrates the ventilation air mixing in a typical HVAC system. Conventional energy resources are more depleted and the energy demands of a growing global population continue to increase.
Main items for building services operation [
According to Fang et al. [2], individuals spend 90% of their time indoors, resulting in a significant rise in energy consumption to maintain indoor thermal comfort. The characteristics of humid tropical climates are that they are hot and humid. These climates cover a huge portion of the globe and are home to more than 33% of the world’s population as stated by Bonell et al. [3]. As a result, achieving thermal comfort outside is also becoming increasingly crucial. For outdoors, however, thermal comfort is difficult to accomplish since humans are directly exposed to the environment, which is influenced by the combination of air temperature, air velocity, relative humidity and radiation fluxes. These are among the environmental parameters. Clothing insulation and metabolic rate are two human personal factors, which are also variables that influence thermal comfort.
Binarti et al. [4] noted that in these hot-humid locations, a pleasant thermal environment is difficult to establish due to the combination of high temperatures and humidity. These variables also vary and are not uniform in large outdoor spaces, which creates difficulty in monitoring and managing them to achieve thermal comfort. Wind speeds will also impair cooling techniques in hot, humid areas.
If outdoor thermal comfort is accomplished, this will increase city liveability whilst simultaneously reducing building heating and air conditioning energy usage by reducing time spent indoors. To correctly analyse the outside thermal environment, it is important to utilise appropriate outdoor thermal comfort models.
Due to the outbreak of COVID-19, it has become increasingly difficult to have many occupants in the same room inside buildings such as restaurants and cafes. Therefore, outdoor spaces must be utilised to accommodate for a larger group of people. However, in hot-humid climates thermal comfort is difficult to achieve outdoors as previously discussed. The presented ventilation system in this chapter achieves outdoor thermal comfort whilst boasting low energy consumption.
There are challenges related to intensifying energy consumption majorly by the installed air conditioners especially related to hot-humid climates (46°C dry bulb, 31°C wet bulb) due to the fact that evaporative cooling systems will certainly fail to meet the comfort criteria due to the high wet bulb temperature. Despite searing temperatures and high humidity, people will find it interesting to go to places such as markets, cultural venues and other tourist destinations if given a cool and suitable ambiance. Evaporative cooling is often used for outdoors but it will not be enough to relieve people’s discomfort with the weather during the hot months. Cooling is usually obtained with refrigeration machinery, and often some post-heating is required to heat the air before it is supplied to the rooms. Conventional air conditioning systems (e.g. vapour compression systems) address these issues by cooling air below its dew point such that water vapour condenses on a cooling coil, thus removing moisture from the air.
Nevertheless, achieving thermal comfort in using fresh air in hot and humid regions is energy intensive. Countries with extreme climatic conditions impose a heavy reliance on cooling, mostly electricity-based, and thus a strong and structural dependency of a high energy resource. In hot-humid climate, the average highest outdoor temperatures during a year is 37.0°C; however, high-temperature values that exceed 46°C could be observed in summer. As illustrated by Figure 2, the temperature exceeds the 40°C for more than 300 hours, which anticipated to be doubled when considering hot-humid climate climate change in 2025. Air conditioning counts for more than 60% of the electricity consumption in the Gulf Region as explained by Elsarrag [5]. Moreover, this lack of responsiveness to the local climatic conditions also leads to problems of indoor air quality, user comfort and user productivity. With energy being cheaply available, the incentive for building users to save on their energy consumption is weak.
Temperature range in hot-humid climate in Doha City [
In hot-humid climates, not only the total annual energy consumption in buildings is very high, but peak demands for electricity also put a heavy burden on the infrastructures needed to respond to such demand pattern. In this context, building energy efficiency strategies can help to realise peak shaving by load reduction and load shifting.
Improving the energy efficiency measures has taken the attention of researchers in hot-humid climate in the Gulf Region. Experimental and theoretical studies were conducted recently to improve building fabric efficiency and promote enhanced indoor air quality in hot-humid climates as conducted by Elsarrag [5]. High-rise building passive design attracted researchers from different parts of the world [6, 7, 8, 9]. In hot-humid climate, it is vital to cool and dehumidify the ventilation air before being supplied to the space. Alternative fresh air cooling and dehumidification methods to conventional refrigeration system were presented by Elsarrag [10, 11].
The use of efficient systems and effective means of control is vital to reduce the energy consumption. Several resilience cooling strategies are identified by Zhang et al. [12]. The study by Siroky et al. [13] showed that the energy saving of a building heating system by adopting controls could be reached the range of 15 to 28%. At times when ventilation and daylight cannot alone meet the needs of occupants, the building services should meet the remaining demands as simply and effectively as practicable, in harmony with the occupants and the building as a whole. An essential part of the integrated design is to ensure that the energy supply and monitoring strategy are as coherent and environmentally sustainable as possible.
Figure 3 shows about 83% of the ambient weather conditions are not in the comfort zone; therefore, the following strategies are used to design a high efficient cost effective system. Several strategies can be used to reduce the need of conventional vapour compression systems. Such strategies include the use of desiccants and evaporative cooling (direct and indirect).
Extreme weather conditions of hot-humid climate Doha City [
In hot climates, it is desirable to reduce the ambient air temperature in order to improve comfort levels; however, in hot and humid climates (as in some Gulf countries), removal of moisture from the air (dehumidification) is almost as important as cooling [15].
Conventional air conditioning systems (e.g. vapour compression systems) address these issues by cooling air below its dew point such that water vapour condenses on a cooling coil, thus removing moisture from the air. The dehumidified air is then reheated to the desired temperature [16]. This process of deep cooling to dew point and reheating consequently leads to higher energy requirement.
This chapter discusses the integration of the innovative and efficient fresh air cooling and filtration system that has been designed, manufactured and tested to reduce the need of vapour compression cycles and provide better liveability for urban environments.
The innovative smart air conditioning system is a fully integrated and controlled—beCOOL Innovation—ventilating and air conditioning system that provides efficient, cost-effective and sustainable fresh air cooling for open spaces or enclosed spaces in moderate, hot or humid climates. The system can be used tool open spaces such as restaurants, coffee shops, open markets, parks, playgrounds. It can also be used to provide fresh air (ventilation air) to enclosed spaces such as offices, schools, retails. The integrated unit consists of a multistage that can dehumidify and cool the air to the required comfort level. The system utilises the condensate water. The ‘all in one’ HVAC system can be fully driven by renewable energy. Figure 4 shows the proposed system that combines air filtration system, and a three-stream water temperature control system, a multistage fresh air cooling heat exchanger and water collection/makeup system. The system is integrated with a variable frequency drives and smart controls. Initially, fresh air is filtered and used to cool three water streams. The scavenging outdoor air is exhausted to the atmosphere again. The innovative heat exchanger is a compact heat exchanger that allows more than one water stream to circulate. The first water stream is so called the high grade as the water temperature is higher than the second water stream (low grade). The supply hot and/or humid air will be initially filtered, precooled by the first stage in the heat exchanger, dehumidified in the second stage and cooling enhanced in the third stage. Dry cold fresh air is then supplied to spaces. The system is installed at different facilities for testing in a coffee shop, residential external sitting area and industrial workshop in Doha, Qatar. The tests were conducted during the months of June and July where temperature exceeds 47°C in the afternoon and humidity exceeds the 75% at night. Several temperature and humidity sensors are used to verify the readings. At the air intake and outlet, two type of sensors were incorporated, the first is directly integrated with the beCOOL-Innovation control system and the second is connected to the cloud for monitoring and verification.
The innovative system schematics.
The system was placed at a coffee shop—an open sitting area as shown inFigure 5. The system was placed 2.5 m away from the sitting area. To maintain effective outdoor cooling, the use of beCOOL-Innovation must be aligned with outdoor energy efficiency strategies to improve resilience to extreme heat in order to maintain comfortable outdoor thermal conditions during heat waves, such as the use of solar shading and wind barriers. Here, the system was placed between buildings that have shading and act as wind barriers for most of the day.
beCOOL-innovation outdoor testing setup.
Temperature and humidity sensors were placed at the air intake of the unit (behind the unit), and the supply temperature and humidity are measured at the diffuser outlet. Air flow is measured using anemometer. The measured data were used to obtain the enthalpy of the entering and exit air, hence calculating the total cooling energy of the unit. A multimetre was used to measure the voltage and current to calculate the electrical energy. The coefficient of performance (COP) of the system is equal to the cooling energy divided by the electrical energy. Typical COP of conventional air conditioning in hot-humid climate varies between 2 and 2.5 for air-cooled direct expansion units. In this study, the COP for conventional system is considered the highest value (COP = 2.5) to ensure that energy savings are compared with the best practices for similar systems.
The temperature metre accuracy is 0.1°C and the humidity metre is 1%. Energy is measured
Figure 6 shows the beCOOL-Innovation actual system. Jet diffusers are used to supply air to far distances.
The actual beCOOL-innovation system.
Figure 7 compares the theoretical monthly cooling coil load of the conventional fresh air handling unit and the beCOOL-Innovation cooling load. beCOOL-Innovation supplies 2500–3400 m3/h of treated fresh air with a considerable reduction in the cooling coil load compared with conventional. The system is designed to provide fresh air supply without assistant of any mechanical refrigeration in dry season and to provide cooling and dehumidification in humid season. The theoretical analysis showed that it will correspond to an annual cooling load reduction (cooling capacity reduction) of around 60% as shown in Figure 8. The overall predicted monthly and annual system electricity consumption is compared with system cooled
Monthly cooling coil load (kWh).
Annual cooling coil load (kWh).
Monthly system electrical energy (kWh).
Annual system electrical energy (kWh).
Table 1 shows the theoretical and measured results for average summer days. It can be clearly noticed that the discrepancy between the theoretical and experimental is below 8%, which provides confidence to the system design. For thermal comfort comparison, the apparent temperature analysis is used. The apparent temperature (AT) is the temperature perceived by the human body from the combined effects of ambient temperature, wind speed, humidity and solar radiation more objectively reflecting the thermal sensations experienced by the human body than temperature alone, especially in highly humid environments [17, 18].
Ambient air temperature °C | Ambient air humidity % | Measured supply air temperature °C | Theoretical supply air temperature °C | Discrepancy |
---|---|---|---|---|
44.8 | 26.8% | 22.4 | 21.4 | 4.7% |
44.1 | 16.2% | 15.8 | 14.7 | 7.5% |
44 | 22.0% | 18.1 | 17.1 | 5.8% |
42.8 | 31.6% | 21.8 | 21.5 | 1.4% |
41.5 | 43.2% | 23.6 | 23.3 | 1.3% |
37.6 | 65.2% | 26.8 | 26.3 | 1.9% |
36.1 | 74.8% | 28 | 27.5 | 1.8% |
System measured vs. theoretical supply air temperature.
The apparent temperature (AT) is a suitable comfort index for climates with high temperatures and humidity. As shown in Figure 11, the apparent temperature at air speed for afternoon shaded is at 1 m/s air speed 50°C. If evaporative cooling is used, AT is reduced to 36.5°C. A two-stage indirect direct evaporative cooling system will reduce AT to 31.6°C. beCOOL-Innovation can reduce AT to 22.7°C at the same speed (1 m/s), which will have good impact on human comfort compared with traditional technologies.
Comparison of different systems on thermal comfort.
The beCOOL-Innovation is a 100% fresh air system; therefore, the water consumption is directly related to the weather conditions. The average hourly water is found to be 10 litres/hour; however, the system produces 17.5 kW of cooling and consumes 3.4 kW electricity.
This chapter presented the drivers, challenges and the beCOOL-Innovation technology to provide efficient treated fresh air for outdoor comfort whilst reducing energy consumption especially for hot or humid climates. Outdoor comfort is vital to improve urban liveability. The system has shown 50–62% reduction in energy consumption compared with conventional refrigeration systems. The efficient cooling system can shrink clients’ carbon footprints using cost-effective means. In addition to enclosed spaces, typical applications include open spaces such as stadiums and walkways, hospitals, health centres, laboratories, and greenhouses that would reduce food imports and strengthen national and regional food security. The testing results have shown less than 8% discrepancy between the theoretical and actual air supply temperatures.
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Over the past few decades, no major new types of antibiotics have been produced and almost all known antibiotics are increasingly losing their activity against pathogenic microorganisms. The levels of multi-drug resistant bacteria have also increased. It is known that worldwide, more than 60% of all antibiotics that are produced find their use in animal production for both therapeutic and non-therapeutic purposes. The use of antimicrobial agents in animal husbandry has been linked to the development and spread of resistant bacteria. Poultry products are among the highest consumed products worldwide but a lot of essential antibiotics are employed during poultry production in several countries; threatening the safety of such products (through antimicrobial residues) and the increased possibility of development and spread of microbial resistance in poultry settings. This chapter documents some of the studies on antibiotic usage in poultry farming; with specific focus on some selected bacterial species, their economic importance to poultry farming and reports of resistances of isolated species from poultry settings (farms and poultry products) to essential antibiotics.",book:{id:"6978",slug:"antimicrobial-resistance-a-global-threat",title:"Antimicrobial Resistance",fullTitle:"Antimicrobial Resistance - A Global Threat"},signatures:"Christian Agyare, Vivian Etsiapa Boamah, Crystal Ngofi Zumbi and\nFrank Boateng Osei",authors:[{id:"182058",title:"Dr.",name:"Christian",middleName:null,surname:"Agyare",slug:"christian-agyare",fullName:"Christian Agyare"},{id:"261271",title:"MSc.",name:"Crystal Ngofi",middleName:null,surname:"Zumbi",slug:"crystal-ngofi-zumbi",fullName:"Crystal Ngofi Zumbi"},{id:"261272",title:"MSc.",name:"Frank Boateng",middleName:null,surname:"Osei",slug:"frank-boateng-osei",fullName:"Frank Boateng Osei"},{id:"261273",title:"Dr.",name:"Vivian Etsiapa",middleName:null,surname:"Boamah",slug:"vivian-etsiapa-boamah",fullName:"Vivian Etsiapa Boamah"}]},{id:"49246",doi:"10.5772/61300",title:"Chitosan as a Biomaterial — Structure, Properties, and Electrospun Nanofibers",slug:"chitosan-as-a-biomaterial-structure-properties-and-electrospun-nanofibers",totalDownloads:4727,totalCrossrefCites:27,totalDimensionsCites:63,abstract:"Chitosan is a polysaccharide derived from chitin; chitin is the second most abundant polysaccharide in the world, after cellulose. Chitosan is biocompatible, biodegradable and non-toxic, so that it can be usedin medicalapplications such as antimicrobial and wound healing biomaterials. It also used as chelating agent due to its ability to bind with cholesterol, fats, proteins and metal ions.",book:{id:"4648",slug:"concepts-compounds-and-the-alternatives-of-antibacterials",title:"Concepts, Compounds and the Alternatives of Antibacterials",fullTitle:"Concepts, Compounds and the Alternatives of Antibacterials"},signatures:"H. M. Ibrahim and E.M.R. El- Zairy",authors:[{id:"90645",title:"Dr.",name:"Hassan",middleName:null,surname:"Ibrahim",slug:"hassan-ibrahim",fullName:"Hassan Ibrahim"},{id:"175694",title:"Dr.",name:"Enas",middleName:null,surname:"El- Zairy",slug:"enas-el-zairy",fullName:"Enas El- Zairy"}]},{id:"70919",doi:"10.5772/intechopen.90891",title:"Antimicrobial Effect of Titanium Dioxide Nanoparticles",slug:"antimicrobial-effect-of-titanium-dioxide-nanoparticles",totalDownloads:1817,totalCrossrefCites:21,totalDimensionsCites:47,abstract:"The widespread use of antibiotics has led to the emergence of multidrug-resistant bacterial strains, and therefore a current concern for food safety and human health. The interest for new antimicrobial substances has been focused toward metal oxide nanoparticles. Specifically, titanium dioxide (TiO2) has been considered as an attractive antimicrobial compound due to its photocatalytic nature and because it is a chemically stable, non-toxic, inexpensive, and Generally Recognized as Safe (GRAS) substance. Several studies have revealed this metal oxide demonstrates excellent antifungal and antibacterial properties against a broad range of both Gram-positive and Gram-negative bacteria. These properties were significantly improved by titanium dioxide nanoparticles (TiO2 NPs) synthesis. In this chapter, latest developments on routes of synthesis of TiO2 NPs and antimicrobial activity of these nanostructures are presented. Furthermore, TiO2 NPs favor the inactivation of microorganisms due to their strong oxidizing power by free radical generation, such as hydroxyl and superoxide anion radicals, showing reductions growth against several microorganisms, such as Escherichia coli and Staphylococcus aureus. Understanding the main mechanisms of antimicrobial action of these nanoparticles was the second main purpose of this chapter.",book:{id:"9521",slug:"antimicrobial-resistance-a-one-health-perspective",title:"Antimicrobial Resistance",fullTitle:"Antimicrobial Resistance - A One Health Perspective"},signatures:"Carol López de Dicastillo, Matias Guerrero Correa, Fernanda B. Martínez, Camilo Streitt and Maria José Galotto",authors:[{id:"244902",title:"Dr.",name:"Carol",middleName:null,surname:"Lopez De Dicastillo",slug:"carol-lopez-de-dicastillo",fullName:"Carol Lopez De Dicastillo"},{id:"315494",title:"Mr.",name:"Matias",middleName:null,surname:"Guerrero Correa",slug:"matias-guerrero-correa",fullName:"Matias Guerrero Correa"},{id:"315495",title:"Ms.",name:"Fernanda",middleName:null,surname:"B. Martínez",slug:"fernanda-b.-martinez",fullName:"Fernanda B. Martínez"},{id:"315496",title:"Mr.",name:"Camilo",middleName:null,surname:"Zuñiga",slug:"camilo-zuniga",fullName:"Camilo Zuñiga"},{id:"315497",title:"Dr.",name:"Maria José",middleName:null,surname:"Galotto",slug:"maria-jose-galotto",fullName:"Maria José Galotto"}]},{id:"65613",doi:"10.5772/intechopen.84411",title:"The Methods for Detection of Biofilm and Screening Antibiofilm Activity of Agents",slug:"the-methods-for-detection-of-biofilm-and-screening-antibiofilm-activity-of-agents",totalDownloads:9283,totalCrossrefCites:15,totalDimensionsCites:26,abstract:"Biofilm producer microorganisms cause nosocomial and recurrent infections. Biofilm that is a sticky exopolysaccharide is the main virulence factor causing biofilm-related infections. Biofilm formation begins with attachment of bacteria to biotic surface such as host cell or abiotic surface such as prosthetic devices. After attachment, aggregation of bacteria is started by cell-cell adhesion. Aggregation continues with the maturation of biofilm. Dispersion is started by certain conditions such as phenol-soluble modulins (PSMs). By this way, sessile bacteria turn back into planktonic form. Bacteria embedded in biofilm (sessile form) are more resistant to antimicrobials than planktonic bacteria. So it is hard to treat biofilm-embedded bacteria than planktonic forms. For this reason, it is important to detect biofilm. There are a few biofilm detection and biofilm production methods on prosthetics, methods for screening antibacterial effect of agents against biofilm-embedded microorganism and antibiofilm effect of agents against biofilm production and mature biofilm. The aim of this chapter is to overview direct and indirect methods such as microscopy, fluorescent in situ hybridization, and Congo red agar, tube method, microtiter plate assay, checkerboard assay, plate counting, polymerase chain reaction, mass spectrometry, MALDI-TOF, and biological assays used by antibiofilm researches.",book:{id:"8427",slug:"antimicrobials-antibiotic-resistance-antibiofilm-strategies-and-activity-methods",title:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods",fullTitle:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods"},signatures:"Sahra Kırmusaoğlu",authors:[{id:"179460",title:"Associate Prof.",name:"Sahra",middleName:null,surname:"Kırmusaoğlu",slug:"sahra-kirmusaoglu",fullName:"Sahra Kırmusaoğlu"}]},{id:"63397",doi:"10.5772/intechopen.80624",title:"Antibiotic Resistance in Lactic Acid Bacteria",slug:"antibiotic-resistance-in-lactic-acid-bacteria",totalDownloads:2486,totalCrossrefCites:12,totalDimensionsCites:21,abstract:"Most starter cultures belong to the lactic acid bacteria group (LAB) and recognized as safe by the US Food and Drug Administration (FDA) and the European Food Safety Authority (EFSA). However, LAB may act as intrinsic or extrinsic reservoirs for antibiotic resistance (AR) genes. This fact may not constitute a safety concern itself, as the resistance gene transfer is vertical. Nevertheless, external genetic elements may induce changes that favor the horizontal transfer transmission of resistance from pathogens as well as from the human intestinal microbiota, which represents a severe safety issue. Some genus of AR LAB includes Enterococcus, Lactobacillus, Lactococcus, Leuconostoc, Pediococcus, and Streptococcus isolated from fermented meat and milk products. Currently, the WHO recommends that LAB used in the food industry should be free of resistance. Therefore, the objective of this chapter is to present an overview of the LAB antibiotic resistance and some methods to determine the same.",book:{id:"6978",slug:"antimicrobial-resistance-a-global-threat",title:"Antimicrobial Resistance",fullTitle:"Antimicrobial Resistance - A Global Threat"},signatures:"Yenizey M. 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After attachment, aggregation of bacteria is started by cell-cell adhesion. Aggregation continues with the maturation of biofilm. Dispersion is started by certain conditions such as phenol-soluble modulins (PSMs). By this way, sessile bacteria turn back into planktonic form. Bacteria embedded in biofilm (sessile form) are more resistant to antimicrobials than planktonic bacteria. So it is hard to treat biofilm-embedded bacteria than planktonic forms. For this reason, it is important to detect biofilm. There are a few biofilm detection and biofilm production methods on prosthetics, methods for screening antibacterial effect of agents against biofilm-embedded microorganism and antibiofilm effect of agents against biofilm production and mature biofilm. The aim of this chapter is to overview direct and indirect methods such as microscopy, fluorescent in situ hybridization, and Congo red agar, tube method, microtiter plate assay, checkerboard assay, plate counting, polymerase chain reaction, mass spectrometry, MALDI-TOF, and biological assays used by antibiofilm researches.",book:{id:"8427",slug:"antimicrobials-antibiotic-resistance-antibiofilm-strategies-and-activity-methods",title:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods",fullTitle:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods"},signatures:"Sahra Kırmusaoğlu",authors:[{id:"179460",title:"Associate Prof.",name:"Sahra",middleName:null,surname:"Kırmusaoğlu",slug:"sahra-kirmusaoglu",fullName:"Sahra Kırmusaoğlu"}]},{id:"62553",title:"Antibiotic Use in Poultry Production and Its Effects on Bacterial Resistance",slug:"antibiotic-use-in-poultry-production-and-its-effects-on-bacterial-resistance",totalDownloads:7327,totalCrossrefCites:43,totalDimensionsCites:92,abstract:"A surge in the development and spread of antibiotic resistance has become a major cause for concern. Over the past few decades, no major new types of antibiotics have been produced and almost all known antibiotics are increasingly losing their activity against pathogenic microorganisms. The levels of multi-drug resistant bacteria have also increased. It is known that worldwide, more than 60% of all antibiotics that are produced find their use in animal production for both therapeutic and non-therapeutic purposes. The use of antimicrobial agents in animal husbandry has been linked to the development and spread of resistant bacteria. Poultry products are among the highest consumed products worldwide but a lot of essential antibiotics are employed during poultry production in several countries; threatening the safety of such products (through antimicrobial residues) and the increased possibility of development and spread of microbial resistance in poultry settings. This chapter documents some of the studies on antibiotic usage in poultry farming; with specific focus on some selected bacterial species, their economic importance to poultry farming and reports of resistances of isolated species from poultry settings (farms and poultry products) to essential antibiotics.",book:{id:"6978",slug:"antimicrobial-resistance-a-global-threat",title:"Antimicrobial Resistance",fullTitle:"Antimicrobial Resistance - A Global Threat"},signatures:"Christian Agyare, Vivian Etsiapa Boamah, Crystal Ngofi Zumbi and\nFrank Boateng Osei",authors:[{id:"182058",title:"Dr.",name:"Christian",middleName:null,surname:"Agyare",slug:"christian-agyare",fullName:"Christian Agyare"},{id:"261271",title:"MSc.",name:"Crystal Ngofi",middleName:null,surname:"Zumbi",slug:"crystal-ngofi-zumbi",fullName:"Crystal Ngofi Zumbi"},{id:"261272",title:"MSc.",name:"Frank Boateng",middleName:null,surname:"Osei",slug:"frank-boateng-osei",fullName:"Frank Boateng Osei"},{id:"261273",title:"Dr.",name:"Vivian Etsiapa",middleName:null,surname:"Boamah",slug:"vivian-etsiapa-boamah",fullName:"Vivian Etsiapa Boamah"}]},{id:"65914",title:"Introductory Chapter: The Action Mechanisms of Antibiotics and Antibiotic Resistance",slug:"introductory-chapter-the-action-mechanisms-of-antibiotics-and-antibiotic-resistance",totalDownloads:4428,totalCrossrefCites:6,totalDimensionsCites:10,abstract:null,book:{id:"8427",slug:"antimicrobials-antibiotic-resistance-antibiofilm-strategies-and-activity-methods",title:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods",fullTitle:"Antimicrobials, Antibiotic Resistance, Antibiofilm Strategies and Activity Methods"},signatures:"Sahra Kırmusaoğlu, Nesrin Gareayaghi and Bekir S. Kocazeybek",authors:[{id:"179460",title:"Associate Prof.",name:"Sahra",middleName:null,surname:"Kırmusaoğlu",slug:"sahra-kirmusaoglu",fullName:"Sahra Kırmusaoğlu"},{id:"248288",title:"Prof.",name:"Bekir",middleName:null,surname:"Kocazeybek",slug:"bekir-kocazeybek",fullName:"Bekir Kocazeybek"},{id:"406463",title:"Dr.",name:"Nesrin",middleName:null,surname:"Gareayaghi",slug:"nesrin-gareayaghi",fullName:"Nesrin Gareayaghi"}]},{id:"63397",title:"Antibiotic Resistance in Lactic Acid Bacteria",slug:"antibiotic-resistance-in-lactic-acid-bacteria",totalDownloads:2486,totalCrossrefCites:12,totalDimensionsCites:21,abstract:"Most starter cultures belong to the lactic acid bacteria group (LAB) and recognized as safe by the US Food and Drug Administration (FDA) and the European Food Safety Authority (EFSA). However, LAB may act as intrinsic or extrinsic reservoirs for antibiotic resistance (AR) genes. This fact may not constitute a safety concern itself, as the resistance gene transfer is vertical. Nevertheless, external genetic elements may induce changes that favor the horizontal transfer transmission of resistance from pathogens as well as from the human intestinal microbiota, which represents a severe safety issue. Some genus of AR LAB includes Enterococcus, Lactobacillus, Lactococcus, Leuconostoc, Pediococcus, and Streptococcus isolated from fermented meat and milk products. Currently, the WHO recommends that LAB used in the food industry should be free of resistance. Therefore, the objective of this chapter is to present an overview of the LAB antibiotic resistance and some methods to determine the same.",book:{id:"6978",slug:"antimicrobial-resistance-a-global-threat",title:"Antimicrobial Resistance",fullTitle:"Antimicrobial Resistance - A Global Threat"},signatures:"Yenizey M. Álvarez-Cisneros and Edith Ponce-Alquicira",authors:[{id:"256345",title:"Dr.",name:"Yenizey Merit",middleName:null,surname:"Alvarez Cisneros",slug:"yenizey-merit-alvarez-cisneros",fullName:"Yenizey Merit Alvarez Cisneros"},{id:"256347",title:"Dr.",name:"Edith",middleName:null,surname:"Ponce-Alquicira",slug:"edith-ponce-alquicira",fullName:"Edith Ponce-Alquicira"}]},{id:"49246",title:"Chitosan as a Biomaterial — Structure, Properties, and Electrospun Nanofibers",slug:"chitosan-as-a-biomaterial-structure-properties-and-electrospun-nanofibers",totalDownloads:4726,totalCrossrefCites:27,totalDimensionsCites:63,abstract:"Chitosan is a polysaccharide derived from chitin; chitin is the second most abundant polysaccharide in the world, after cellulose. Chitosan is biocompatible, biodegradable and non-toxic, so that it can be usedin medicalapplications such as antimicrobial and wound healing biomaterials. It also used as chelating agent due to its ability to bind with cholesterol, fats, proteins and metal ions.",book:{id:"4648",slug:"concepts-compounds-and-the-alternatives-of-antibacterials",title:"Concepts, Compounds and the Alternatives of Antibacterials",fullTitle:"Concepts, Compounds and the Alternatives of Antibacterials"},signatures:"H. M. Ibrahim and E.M.R. El- Zairy",authors:[{id:"90645",title:"Dr.",name:"Hassan",middleName:null,surname:"Ibrahim",slug:"hassan-ibrahim",fullName:"Hassan Ibrahim"},{id:"175694",title:"Dr.",name:"Enas",middleName:null,surname:"El- Zairy",slug:"enas-el-zairy",fullName:"Enas El- Zairy"}]}],onlineFirstChaptersFilter:{topicId:"897",limit:6,offset:0},onlineFirstChaptersCollection:[{id:"81704",title:"Quorum Sensing Inhibition Based Drugs to Conquer Antimicrobial Resistance",slug:"quorum-sensing-inhibition-based-drugs-to-conquer-antimicrobial-resistance",totalDownloads:22,totalDimensionsCites:0,doi:"10.5772/intechopen.104125",abstract:"Quorum sensing is the cell to cell communication mechanism in microorganism through signalling molecules. Regulation of virulence factor, sporulation, proteolytic enzymes production, biofilm formation, auto-inducers, cell population density are key physiological process mediated through quorum-sensing (QS) signalling. Elevation of innate immune system and antibiotic tolerance of pathogens is highly increased with perspective of quorum-sensing (QS) activity. Development of novel drugs is highly attractive scenario against cell-cell communication of microbes. Design of synthetic drugs and natural compounds against QS signal molecules is vital combat system to attenuate microbial pathogenicity. Quorum sensing inhibitors (QSIs), quorum quenchers (QQs), efflux pump inhibitors (EPIs) act against multi-drug resistance strains (MDR) and other pathogenic microbes through regulation of auto-inducers and signal molecule with perceptive to growth arrest both in-vitro and in-vivo. QQs, QSIs and EPIs compounds has been validated with various animal models for high selection pressure on therapeutics arsenal against microbe’s growth inhibition. Promising QSI are phytochemicals and secondary metabolites includes polyacetylenes, alkaloids, polyphenols, terpenoids, quinones.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Kothandapani Sundar, Ramachandira Prabu and Gopal Jayalakshmi"},{id:"82372",title:"Unlocking the Potential of Ghost Probiotics in Combating Antimicrobial Resistance",slug:"unlocking-the-potential-of-ghost-probiotics-in-combating-antimicrobial-resistance",totalDownloads:20,totalDimensionsCites:0,doi:"10.5772/intechopen.104126",abstract:"Antimicrobial resistance is a global concern that requires immediate attention. Major causes of development of antimicrobial resistance in microbial cells are overuse of antimicrobials along the food chain especially in livestock, in preventing infections as well as misuse of antimicrobials by patients. Probiotics could be a viable alternative to antibiotics in the fight against antimicrobial resistance. Probiotic strains can act as a complement to antimicrobial therapy, improving antimicrobial function and enhancing immunity. However, there are safety concerns regarding the extensive use of live microbial cells especially in immunocompromised individuals; these include microbial translocation, inhibition of other beneficial microorganisms and development of antimicrobial resistance, among other concerns. Inevitably, ghost probiotics have become the favored alternative as they eliminate the safety and shelf-life problems associated with use of probiotics. Ghost probiotics are non-viable microbial cells (intact or broken) or metabolic products from microorganisms, which when administered in adequate amounts have biologic activity in the host and confer health benefits. Ghost probiotics exert biological effects similar to probiotics. However, the major drawback of using ghost probiotics is that the mechanism of action of these is currently unknown, hence more research is required and regulatory instruments are needed to assure the safety of consumers.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Abigarl Ndudzo, Sakhile Ndlovu, Nesisa Nyathi and Angela Sibanda Makuvise"},{id:"82178",title:"Managing Antimicrobial Resistance beyond the Hospital Antimicrobial Stewardship: The Role of One Health",slug:"managing-antimicrobial-resistance-beyond-the-hospital-antimicrobial-stewardship-the-role-of-one-heal",totalDownloads:16,totalDimensionsCites:0,doi:"10.5772/intechopen.104170",abstract:"Infections caused by micro-organisms affect the health of people and animals, causing morbidity and mortality, with Asia and Africa as the epicenters. Some of the infectious diseases are emerging and re-emerging in nature. Examples include viral hepatitis, Lassa fever, Ebola, yellow fever, tuberculosis, covid-19, measles, and malaria, among others. Antimicrobials have been playing an important role in the treatment of infections by these microbes. However, there has been a development of resistance to these antimicrobials as a result of many drivers. This write-up used secondary data to explore the management of antimicrobial resistance (AMR) beyond the hospital antimicrobial resistance steward using the one health concept. The findings showed AMR to be a transboundary, multifaceted ecosystem problem affecting both the developed and developing countries. It is also one of the top ten global public health threats facing mankind. Globally, AMR will cost over US$100 trillion in output loss by 2050, about 700,000 deaths a year, and 4,150,000 deaths in Africa by 2050. About 2.4 million people could die in high-income countries between 2015 and 2050 without a sustained effort to contain AMR. The drivers of AMR are beyond the hospital and hospital AMR stewardship. Therefore, the need for one health concept to manage it.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Istifanus Anekoson Joshua, Mathew Bobai and Clement Sokfa Woje"},{id:"81918",title:"Machine Learning for Antimicrobial Resistance Research and Drug Development",slug:"machine-learning-for-antimicrobial-resistance-research-and-drug-development",totalDownloads:52,totalDimensionsCites:0,doi:"10.5772/intechopen.104841",abstract:"Machine learning is a subfield of artificial intelligence which combines sophisticated algorithms and data to develop predictive models with minimal human interference. This chapter focuses on research that trains machine learning models to study antimicrobial resistance and to discover antimicrobial drugs. An emphasis is placed on applying machine learning models to detect drug resistance among bacterial and fungal pathogens. The role of machine learning in antibacterial and antifungal drug discovery and design is explored. Finally, the challenges and prospects of applying machine learning to advance basic research on and treatment of antimicrobial resistance are discussed. Overall, machine learning promises to advance antimicrobial resistance research and to facilitate the development of antibacterial and antifungal drugs.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Shamanth A. Shankarnarayan, Joshua D. Guthrie and Daniel A. Charlebois"},{id:"81891",title:"Alternatives to Antibiotics in Semen Extenders Used in Artificial Insemination",slug:"alternatives-to-antibiotics-in-semen-extenders-used-in-artificial-insemination",totalDownloads:27,totalDimensionsCites:0,doi:"10.5772/intechopen.104226",abstract:"Antimicrobial resistance is a serious global threat requiring a widespread response. Both veterinarians and medical doctors should restrict antibiotic usage to therapeutic use only, after determining the sensitivity of the causal organism. However, the addition of antibiotics to semen extenders for animal artificial insemination represents a hidden, non-therapeutic use of antimicrobial substances. Artificial insemination for livestock breeding is a huge global enterprise with hundreds of million sperm doses prepared annually. However, reporting of antimicrobial resistance in semen is increasing. This review discusses the consequences of bacteria in semen samples, as well as the effect of antimicrobial substances in semen extenders on bacteria in the environment and even on personnel. Alternatives to antibiotics have been reported in the scientific literature and are reviewed here. The most promising of these, removal of the majority of bacteria by colloid centrifugation, is considered in detail, especially results from an artificial insemination study in pigs. In conclusion, colloid centrifugation is a practical method of physically removing bacteria from semen, which does not induce antibiotic resistance. Sperm quality in stored semen samples may be improved at the same time.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Jane M. Morrell, Pongpreecha Malaluang, Aleksandar Cojkic and Ingrid Hansson"},{id:"81699",title:"Efflux Pumps among Urinary E. coli and K. pneumoniae Local Isolates in Hilla City, Iraq",slug:"efflux-pumps-among-urinary-e-coli-and-k-pneumoniae-local-isolates-in-hilla-city-iraq",totalDownloads:10,totalDimensionsCites:0,doi:"10.5772/intechopen.104408",abstract:"Urinary tract infections (UTI) are the most common bacterial infections affecting humans. Escherichia coli and Klebsiella pneumoniae were common enterobacteria engaged with community-acquired UTIs. Efflux pumps were vital resistance mechanisms for antibiotics, especially among enterobacteria. Overexpression of an efflux system, which results in a decrease in antibiotic accumulation, is an effective mechanism for drug resistance. The ATP-binding cassette (ABC) transporters, small multidrug resistance (SMR), and multidrug and toxic compound extrusion (MATE) families, the major facilitator superfamily (MFS), and the resistance-nodulation- cell division (RND) family are the five superfamilies of efflux systems linked to drug resistance. This chapter highlights the results of studying the prevalence of efflux pump genes among local isolates of E. coli and K. pneumoniae in Hilla City, Iraq. class RND AcrAB-TolC, AcrAD-TolC, and AcrFE-TolC genes detected by conventional PCR of E. coli and K. pneumoniae respectively. The result revealed approximately all studied efflux transporter were found in both E. coli and K. pneumoniae in different percentages. Biofilm formation were observed in 50(100%) of K. pneumoniae and 49(98%) of E. coli isolates were biofilm former and follow: 30(60%), 20(40%) were weak, 12(24%), 22(44%) were moderate and 7(14%) and 8(16%) were Strong biofilm former for E. coli and K. pneumoniae, respectively.",book:{id:"11373",title:"The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions",coverURL:"https://cdn.intechopen.com/books/images_new/11373.jpg"},signatures:"Hussein Al-Dahmoshi, Sahar A. Ali and Noor Al-Khafaji"}],onlineFirstChaptersTotal:13},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:90,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:33,numberOfPublishedChapters:330,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:14,numberOfPublishedChapters:145,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:9,numberOfPublishedChapters:139,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:123,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:112,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:21,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:10,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:"2753-6580",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:"6",title:"Infectious Diseases",doi:"10.5772/intechopen.71852",issn:"2631-6188",scope:"This series will provide a comprehensive overview of recent research trends in various Infectious Diseases (as per the most recent Baltimore classification). Topics will include general overviews of infections, immunopathology, diagnosis, treatment, epidemiology, etiology, and current clinical recommendations for managing infectious diseases. Ongoing issues, recent advances, and future diagnostic approaches and therapeutic strategies will also be discussed. This book series will focus on various aspects and properties of infectious diseases whose deep understanding is essential for safeguarding the human race from losing resources and economies due to pathogens.",coverUrl:"https://cdn.intechopen.com/series/covers/6.jpg",latestPublicationDate:"August 12th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:13,editor:{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},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,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,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. Dr. Ekinci serves as the Editor in Chief of four international books and is involved in the Editorial Board of several international journals.",institutionString:null,institution:{name:"Ondokuz Mayıs University",institutionURL:null,country:{name:"Turkey"}}},editorThree:null},{id:"17",title:"Metabolism",coverUrl:"https://cdn.intechopen.com/series_topics/covers/17.jpg",isOpenForSubmission:!0,editor:{id:"138626",title:"Dr.",name:"Yannis",middleName:null,surname:"Karamanos",slug:"yannis-karamanos",fullName:"Yannis Karamanos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002g6Jv2QAE/Profile_Picture_1629356660984",biography:"Yannis Karamanos, born in Greece in 1953, completed his pre-graduate studies at the Université Pierre et Marie Curie, Paris, then his Masters and Doctoral degree at the Université de Lille (1983). 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,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. She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:42,paginationItems:[{id:"82914",title:"Glance on the Critical Role of IL-23 Receptor Gene Variations in Inflammation-Induced Carcinogenesis",doi:"10.5772/intechopen.105049",signatures:"Mohammed El-Gedamy",slug:"glance-on-the-critical-role-of-il-23-receptor-gene-variations-in-inflammation-induced-carcinogenesis",totalDownloads:9,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Chemokines Updates",coverURL:"https://cdn.intechopen.com/books/images_new/11672.jpg",subseries:{id:"18",title:"Proteomics"}}},{id:"82875",title:"Lipidomics as a Tool in the Diagnosis and Clinical Therapy",doi:"10.5772/intechopen.105857",signatures:"María Elizbeth Alvarez Sánchez, Erick Nolasco Ontiveros, Rodrigo Arreola, Adriana Montserrat Espinosa González, Ana María García Bores, Roberto Eduardo López Urrutia, Ignacio Peñalosa Castro, María del Socorro Sánchez Correa and Edgar Antonio Estrella Parra",slug:"lipidomics-as-a-tool-in-the-diagnosis-and-clinical-therapy",totalDownloads:7,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82440",title:"Lipid Metabolism and Associated Molecular Signaling Events in Autoimmune Disease",doi:"10.5772/intechopen.105746",signatures:"Mohan Vanditha, Sonu Das and Mathew John",slug:"lipid-metabolism-and-associated-molecular-signaling-events-in-autoimmune-disease",totalDownloads:17,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82483",title:"Oxidative Stress in Cardiovascular Diseases",doi:"10.5772/intechopen.105891",signatures:"Laura Mourino-Alvarez, Tamara Sastre-Oliva, Nerea Corbacho-Alonso and Maria G. 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She is also the Global Harmonization Initiative (GHI)",institutionString:"Australian College of Business & Technology",institution:{name:"Kobe College",institutionURL:null,country:{name:"Japan"}}}]},{type:"book",id:"6820",title:"Keratin",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/6820.jpg",slug:"keratin",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Miroslav Blumenberg",hash:"6def75cd4b6b5324a02b6dc0359896d0",volumeInSeries:2,fullTitle:"Keratin",editors:[{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. 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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. 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