\\n\\n
IntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\\n\\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\\n\\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\\n\\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\\n\\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\\n\\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\\n\\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\\n\\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\\n\\nFeel free to share this news on social media and help us mark this memorable moment!
\\n\\n\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/237"}},components:[{type:"htmlEditorComponent",content:'
After years of being acknowledged as the world's leading publisher of Open Access books, today, we are proud to announce we’ve successfully launched a portfolio of Open Science journals covering rapidly expanding areas of interdisciplinary research.
\n\n\n\nIntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\n\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\n\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\n\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\n\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\n\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\n\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\n\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\n\nFeel free to share this news on social media and help us mark this memorable moment!
\n\n\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"10542",leadTitle:null,fullTitle:"Molecular Epidemiology Study of Mycobacterium Tuberculosis Complex",title:"Molecular Epidemiology Study of Mycobacterium Tuberculosis Complex",subtitle:null,reviewType:"peer-reviewed",abstract:"Tuberculosis (TB), which is caused by the infectious agent Mycobacterium tuberculosis (MTB), is a major global public health problem that infects one third of the world’s population. This book provides an overview of the molecular epidemiology pattern, transmission dynamics, host response, evolution, and pathogenesis mechanisms of TB. Chapters explore such topics as mechanisms associated with increasing trends of drug-resistant TB, the development of anti-mycobacterial drugs, genotyping tools, diagnosis and treatment of latent tuberculosis infection, and more.",isbn:"978-1-83968-100-4",printIsbn:"978-1-83968-099-1",pdfIsbn:"978-1-83968-101-1",doi:"10.5772/intechopen.92916",price:119,priceEur:129,priceUsd:155,slug:"molecular-epidemiology-study-of-mycobacterium-tuberculosis-complex",numberOfPages:120,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"29279e34f971687dc28de62534335ac4",bookSignature:"Yogendra Shah",publishedDate:"September 15th 2021",coverURL:"https://cdn.intechopen.com/books/images_new/10542.jpg",numberOfDownloads:1335,numberOfWosCitations:0,numberOfCrossrefCitations:1,numberOfCrossrefCitationsByBook:0,numberOfDimensionsCitations:1,numberOfDimensionsCitationsByBook:0,hasAltmetrics:1,numberOfTotalCitations:2,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 8th 2020",dateEndSecondStepPublish:"November 23rd 2020",dateEndThirdStepPublish:"January 22nd 2021",dateEndFourthStepPublish:"April 12th 2021",dateEndFifthStepPublish:"June 11th 2021",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"278914",title:"Ph.D.",name:"Yogendra",middleName:null,surname:"Shah",slug:"yogendra-shah",fullName:"Yogendra Shah",profilePictureURL:"https://mts.intechopen.com/storage/users/278914/images/system/278914.jpg",biography:"Dr. Yogendra Shah is a consultant microbiologist/virologist, senior research microbiologist, and lecturer at Seti Provincial Hospital, COVID-19 PCR laboratory, National Zoonoses and Food Hygiene Research Center, and Kathmandu College of Science and Technology, Nepal. He obtained a Ph.D. in Veterinary Medicine (Bacteriology) from the Graduate School of Veterinary Medicine, Hokkaido University, Japan, in 2017. His research focuses on better understanding the molecular epidemiological features/transmission dynamics of infectious diseases and zoonotic infectious diseases in Nepal by employing molecular techniques like ELISA, polymerase chain reaction (PCR), loop-mediated isothermal amplification (LAMP), and DNA sequencing. He was awarded the Young Science and Technology Award from the Nepal Academy of Science and Technology (NAST) in 2019. His research interests include infectious diseases, zoonotic infectious diseases, and vector-borne diseases. He has published more than thirty-five research articles in peer-reviewed journals and twelve books.",institutionString:"National Zoonoses and Food Hygiene Research Centre",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"2",institution:{name:"National Zoonoses and Food Hygiene Research Centre",institutionURL:null,country:{name:"Nepal"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1047",title:"Pulmonology",slug:"pulmonology"}],chapters:[{id:"77861",title:"Introductory Chapter: Plan to Prevent and Combat against the Drug-Resistant Tuberculosis/Zoonotic Tuberculosis",doi:"10.5772/intechopen.99548",slug:"introductory-chapter-plan-to-prevent-and-combat-against-the-drug-resistant-tuberculosis-zoonotic-tub",totalDownloads:97,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:1,abstract:null,signatures:"Yogendra Shah",downloadPdfUrl:"/chapter/pdf-download/77861",previewPdfUrl:"/chapter/pdf-preview/77861",authors:[{id:"278914",title:"Ph.D.",name:"Yogendra",surname:"Shah",slug:"yogendra-shah",fullName:"Yogendra Shah"}],corrections:null},{id:"76741",title:"Challenges in Drug Discovery against Tuberculosis",doi:"10.5772/intechopen.97857",slug:"challenges-in-drug-discovery-against-tuberculosis",totalDownloads:272,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Tuberculosis (TB) is one of the deadly diseases in the present era caused by Mycobacterium tuberculosis. Principally, this bacterium attacks the lungs, however, MTB Has been observed affecting any part of the human body including the kidney, spine, and brain. Drug-resistant progression and other associated properties of MTB become a major hurdle in drug discovery to fight against tuberculosis. Moreover, some of the challenging situations such as the low range of chemical agents, the time-consuming process of drug development, the shortage of predictive animal models, and inadequate information of the physicochemical evidence required for effective bacterial penetration, are additional hindrances for the pharmaceutical scientist. In the current chapter, we focus on challenges encountered during drug discovery and need to be overcome as M. tuberculosis has a substantial barrier in its lipid-containing cell wall to inhibit the influx of drugs which is the initial requirement of the drug to show its therapeutic effect. There is also an immediate need for efficient vaccine development which may show its effect on adolescents and adults along with infants. Investigation on key bacterial targets has been troublesome, in light of the vulnerability around the microenvironments found in vivo and subsequently, the importance of exceptional metabolic pathways. The manuscript is prepared after the extensive literature survey to explore the vigorous approaches in novel drug designing and in proposing potent drug targets. The re-engineering and repositioning of prominent antitubercular drugs are required to attain viable control.",signatures:"Manish Dwivedi and Priya Giri",downloadPdfUrl:"/chapter/pdf-download/76741",previewPdfUrl:"/chapter/pdf-preview/76741",authors:[{id:"337061",title:"Assistant Prof.",name:"Manish",surname:"Dwivedi",slug:"manish-dwivedi",fullName:"Manish Dwivedi"},{id:"337625",title:"Ms.",name:"Priya",surname:"Giri",slug:"priya-giri",fullName:"Priya Giri"}],corrections:null},{id:"74782",title:"Study of Various Chemically and Structurally Diverse Currently Clinically Used and Recently Developed Antimycobacterial Drugs",doi:"10.5772/intechopen.95538",slug:"study-of-various-chemically-and-structurally-diverse-currently-clinically-used-and-recently-develope",totalDownloads:249,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Infectious diseases originate from pathogens and increased severely in current years. Despite numerous important advances in antimicrobial therapy, the extensive use and misuse of these antimicrobial drugs have caused the emergence of microbial resistance, which is a serious risk to public health. In particular, the emergence of multidrug-resistant pathogens has become a serious difficulty in the therapy of pathogenic diseases. Therefore, the progress of novel drugs to deal with resistant pathogens has become one of the most essential areas of antimicrobial research today. In addition to the development of novel and efficient antimicrobial agents against multidrug-resistant pathogens, recent attention has focused on the treatment of tuberculosis. Therefore, recent developments have been directed towards examining currently used and newly developed antimycobacterial drugs and their toxicities and mechanism of action.",signatures:"Saad Alghamdi and Mohammad Asif",downloadPdfUrl:"/chapter/pdf-download/74782",previewPdfUrl:"/chapter/pdf-preview/74782",authors:[{id:"334959",title:"Prof.",name:"Mohammad",surname:"Asif",slug:"mohammad-asif",fullName:"Mohammad Asif"},{id:"336639",title:"Dr.",name:"Saad",surname:"Alghamdi",slug:"saad-alghamdi",fullName:"Saad Alghamdi"}],corrections:null},{id:"76023",title:"Genealogy of Resistant Tuberculosis in Latin America and the Caribbean until 2020",doi:"10.5772/intechopen.96280",slug:"genealogy-of-resistant-tuberculosis-in-latin-america-and-the-caribbean-until-2020",totalDownloads:196,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:1,abstract:"History hallmarks different out brakes events during the last century. Being caught in the in the middle of the catastrophic COVID-19 pandemic, that initiated in 2019 makes possible to forget other causalities. Tuberculosis makes the case. The pathogen has been present more than hundredth years. Relevance rest in worldwide prevalence, pathogen spread, treatment resistance and the need for eradication. Drug treatment resistance is considered as one of the criteria to prioritize a country in the World Health Organization’s intention to eradicate tuberculosis infection in the world. For decades in Latin America, including the Caribbean, there have been a persistent high rate of drug resistance with an overall prevalence to one or more drug rounds 13.0%. Approximately 30% of previously treated cases have a multidrug resistance. In this chapter, we intend to review the epidemiology of resistant tuberculosis, and the causes of resistance associated to the community of people in the Latin American and the Caribbean. We intend to describe the genetic response of Mycobacterium tuberculosis from its migratory journey throughout decades from areas of Europa and Asia to Latin America, its genetic transformation secondary to inadequate drug exposure and the characteristics of the infected host, and how a change in the healthcare system and tuberculosis control strategies access are needed to change the surge of multidrug resistance tuberculosis.",signatures:"Onix J. Cantres-Fonseca and Francisco Del Olmo-Arroyo",downloadPdfUrl:"/chapter/pdf-download/76023",previewPdfUrl:"/chapter/pdf-preview/76023",authors:[{id:"229701",title:"M.D.",name:"Onix",surname:"Cantres-Fonseca",slug:"onix-cantres-fonseca",fullName:"Onix Cantres-Fonseca"},{id:"346572",title:"Dr.",name:"Francisco",surname:"Del Olmo",slug:"francisco-del-olmo",fullName:"Francisco Del Olmo"}],corrections:null},{id:"76718",title:"Latent Tuberculous Infection: Influence on Patient’s Quality of Life",doi:"10.5772/intechopen.96901",slug:"latent-tuberculous-infection-influence-on-patient-s-quality-of-life",totalDownloads:108,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Latent tuberculosis infection is an asymptomatic condition in which patients carry the bacteria, but do not show any sign of illness, however they are at risk of disease activation at any time in the future. Understanding of influence of latent tuberculosis infection on the physical and mental well-being of these patients is important as successful strategies to reduce the tuberculosis burden globally. Our purpose is to explore patients during diagnosis and treatment of latent tuberculosis infection, measure their quality of life. Materials and methods: during 2017–2019 was examined 100 children 4–7 years age. Children were divided in 3 groups. First group (n = 40) - a children with LTI. Group of the comparison (n = 40) has comprised preschool age children with tuberculosis. Group of the checking (n = 20) have constituted the preschool age healthy children. Estimation of children health was conducted by analysis health factors: social, genetic, biological. In addition were studied criteria of health. It was used study anamnestic data, questioning, estimation quality of life, anthropometry, data of objective examination, laboratory data and parameters of functioning, electrocardiography, vegetative nervous system spectrography (VNS-spectrography), manual ergometry. Physical development valued with the help of specialized tables. Leukocyte intoxication index is calculated on formula Shemitova V.F. Variety heart rhythm (VHR) was studied by method VNS-spectrography on vegetotester “VNS-Micro” with computer program “Polispectr” of company “Neyrosoft”. Interpretation source vegetative tone and vegetative reactivity was realized according to recommendation N.A. Belokon. Vegetative provision of activity was valued on tolerance to steady-state load by method manual ergometry (MEM) in help of manual dynamometer. Quality of life was defined with the help of questionnaire PedsQL version 4.0 (the Russian version). Results and their discussion: in children with active tuberculosis, specific process has a most negative influence upon quality of life, comparatively temporary negative influence has LTI. Revealed changes in general have brought to reduction of QL indicators both in first and second group. With provision of latency currents of infecting with mycobacteria of tuberculosis, indicators of quality of life should be considered as one of defining, reflecting psychological component adaptation of child, and can be recommended to enter in program of examination and dispensary observation of children with LTI. Conclusions: our study has shown that preschool age children with LTI have rather significant deflections of health condition, revealing by symptoms of intoxication, expressed breaches adaptation and regulation mechanisms. Results of study have logistical confirmed need of improvement of the preventive maintenance and dispensary observation at children with LTI and active participation in its base of the interdepartmental approach. All of this allows newly taking a look at problem of the latent tuberculous infection at preschool age children and role general practitioner in preventive maintenance of the development such dangerous diseases as tuberculosis.",signatures:"Dinara Namazovna Adjablaeva",downloadPdfUrl:"/chapter/pdf-download/76718",previewPdfUrl:"/chapter/pdf-preview/76718",authors:[{id:"260358",title:"Ms.",name:"Dinara Namazovna",surname:"Adjablaeva",slug:"dinara-namazovna-adjablaeva",fullName:"Dinara Namazovna Adjablaeva"}],corrections:null},{id:"75569",title:"Molecular Characterization of Mycobacterium spp. Isolated from Cattle and Wildlife in Poland",doi:"10.5772/intechopen.96695",slug:"molecular-characterization-of-em-mycobacterium-em-spp-isolated-from-cattle-and-wildlife-in-poland",totalDownloads:218,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:1,abstract:"Although Poland is officially tuberculosis (TB) free, meaning that less than 0.1% of her cattle herd is TB-positive, the problem of bovine TB in Poland may be re-emerging: its presence has recently been confirmed in domestic and companion animals, wildlife such as the European bison, and even humans. The aim of this chapter was to review all reports of bovine TB in Poland described to date, with particular emphasis on molecular studies, and determine further research directions. These studies include a range of molecular methods for diagnosis, including genotyping, spoligotyping and MIRU- VNTR; such methods successfully identifies a tuberculosis-positive European bison as the source of wild boar infection in the Bieszczady Mountains based on its spoligotype. This chapter argues that identified trains should be better archived, as such records would allow detailed epidemiological investigations and shed greater light on the activity of Mycobacterium spp. The current epidemiological situation in Poland highlights the need for further studies to determine epidemiological links and confirm possible routes of transmission based on whole genome sequencing; this need is accentuated by the zoonotic potential of such infections and the endangered species at risk.",signatures:"Anna Didkowska, Monika Krajewska-Wędzina, Blanka Orłowska, Monika Kozińska, Ewa Augustynowicz-Kopeć and Krzysztof Anusz",downloadPdfUrl:"/chapter/pdf-download/75569",previewPdfUrl:"/chapter/pdf-preview/75569",authors:[{id:"336132",title:"Prof.",name:"Krzysztof",surname:"Anusz",slug:"krzysztof-anusz",fullName:"Krzysztof Anusz"},{id:"345337",title:"Dr.",name:"Anna",surname:"Didkowska",slug:"anna-didkowska",fullName:"Anna Didkowska"},{id:"345339",title:"Dr.",name:"Monika",surname:"Krajewska-Wędzina",slug:"monika-krajewska-wedzina",fullName:"Monika Krajewska-Wędzina"},{id:"345340",title:"Dr.",name:"Blanka",surname:"Orłowska",slug:"blanka-orlowska",fullName:"Blanka Orłowska"},{id:"345341",title:"Dr.",name:"Monika",surname:"Kozińska",slug:"monika-kozinska",fullName:"Monika Kozińska"},{id:"345342",title:"Prof.",name:"Ewa",surname:"Augustynowicz-Kopeć",slug:"ewa-augustynowicz-kopec",fullName:"Ewa Augustynowicz-Kopeć"}],corrections:null},{id:"75835",title:"Humeral Artery Aneurysm Revealing a Rare Association between Tuberculosis and Behçet’s Disease",doi:"10.5772/intechopen.95465",slug:"humeral-artery-aneurysm-revealing-a-rare-association-between-tuberculosis-and-beh-et-s-disease",totalDownloads:197,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"The association of pulmonary tuberculosis and Behçet’s disease revealed by an aneurysm of the humeral artery is exceptional with a complicated management. We report a case in which the two conditions occurred concomitantly with the vascular complication, apart from any use of immunosuppressive therapy, something that has never been reported in the literature. We report an extremely rare case of a spontaneous rupture of an aneurysm of the humeral artery of a 29-year-old woman, with no history. The patient underwent axillo-humeral bypass. Investigations concluded the diagnosis of Behçet’s disease associated with pulmonary and lymph node tuberculosis. Anti-tuberculous chemotherapy followed by corticosteroids, immunosuppressants and colchicine have been administrated. Based on this observation, we insist on the necessity of searching the symptoms of Behçet’s disease in the presence of arterial involvement when having a young patient. Therapeutic management must include medical treatment to control inflammation and limit the risk of recurrence. Endovascular or surgical treatment is necessary if the arterial involvement is threatening. The association with tuberculosis complicates management and requires close monitoring.",signatures:"Rabie Ayari, Ramy Triki, Youssef Mallat, Achraf Abdennadher, Khalil Amri, Raja Amri and Mohamed Ali Sbai",downloadPdfUrl:"/chapter/pdf-download/75835",previewPdfUrl:"/chapter/pdf-preview/75835",authors:[{id:"336309",title:"Dr.",name:"Rabie",surname:"Ayari",slug:"rabie-ayari",fullName:"Rabie Ayari"},{id:"351589",title:"Dr.",name:"Ramy",surname:"Triki",slug:"ramy-triki",fullName:"Ramy Triki"},{id:"351590",title:"Dr.",name:"Youssef",surname:"Mallat",slug:"youssef-mallat",fullName:"Youssef Mallat"},{id:"351591",title:"Dr.",name:"Achraf",surname:"Abdennadher",slug:"achraf-abdennadher",fullName:"Achraf Abdennadher"},{id:"351592",title:"Dr.",name:"Khalil",surname:"Amri",slug:"khalil-amri",fullName:"Khalil Amri"},{id:"351593",title:"Dr.",name:"Raja",surname:"Amri",slug:"raja-amri",fullName:"Raja Amri"},{id:"351594",title:"Dr.",name:"Mohamed",surname:"Ali Sbai",slug:"mohamed-ali-sbai",fullName:"Mohamed Ali Sbai"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"9018",title:"Some RNA Viruses",subtitle:null,isOpenForSubmission:!1,hash:"a5cae846dbe3692495fc4add2f60fd84",slug:"some-rna-viruses",bookSignature:"Yogendra Shah and Eltayb Abuelzein",coverURL:"https://cdn.intechopen.com/books/images_new/9018.jpg",editedByType:"Edited by",editors:[{id:"278914",title:"Ph.D.",name:"Yogendra",surname:"Shah",slug:"yogendra-shah",fullName:"Yogendra Shah"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"956",title:"Cystic Fibrosis",subtitle:"Renewed Hopes Through Research",isOpenForSubmission:!1,hash:"703f0969078948d82535b7b0c08ab613",slug:"cystic-fibrosis-renewed-hopes-through-research",bookSignature:"Dinesh Sriramulu",coverURL:"https://cdn.intechopen.com/books/images_new/956.jpg",editedByType:"Edited by",editors:[{id:"91317",title:"Dr.",name:"Dinesh",surname:"Sriramulu",slug:"dinesh-sriramulu",fullName:"Dinesh Sriramulu"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"969",title:"Lung Diseases",subtitle:"Selected State of the Art Reviews",isOpenForSubmission:!1,hash:"b4344208b8b993d83e0131d23db46343",slug:"lung-diseases-selected-state-of-the-art-reviews",bookSignature:"Elvis Malcolm Irusen",coverURL:"https://cdn.intechopen.com/books/images_new/969.jpg",editedByType:"Edited by",editors:[{id:"87213",title:"Prof.",name:"Elvis",surname:"Irusen",slug:"elvis-irusen",fullName:"Elvis Irusen"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"648",title:"Chronic Obstructive Pulmonary Disease",subtitle:"Current Concepts and Practice",isOpenForSubmission:!1,hash:"d52ddc19c473a70b91e5a64f41760a04",slug:"chronic-obstructive-pulmonary-disease-current-concepts-and-practice",bookSignature:"Kian-Chung Ong",coverURL:"https://cdn.intechopen.com/books/images_new/648.jpg",editedByType:"Edited by",editors:[{id:"103585",title:"Dr.",name:"Kian Chung",surname:"Ong",slug:"kian-chung-ong",fullName:"Kian Chung Ong"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3843",title:"Lung Inflammation",subtitle:null,isOpenForSubmission:!1,hash:"92938e8752fa3444849d88b776cd7892",slug:"lung-inflammation",bookSignature:"Kian Chung Ong",coverURL:"https://cdn.intechopen.com/books/images_new/3843.jpg",editedByType:"Edited by",editors:[{id:"103585",title:"Dr.",name:"Kian Chung",surname:"Ong",slug:"kian-chung-ong",fullName:"Kian Chung Ong"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5444",title:"Hypoxia and Human Diseases",subtitle:null,isOpenForSubmission:!1,hash:"331b1aa8d399bc404988a8bc5e431582",slug:"hypoxia-and-human-diseases",bookSignature:"Jing Zheng and Chi Zhou",coverURL:"https://cdn.intechopen.com/books/images_new/5444.jpg",editedByType:"Edited by",editors:[{id:"89898",title:"Dr.",name:"Jing",surname:"Zheng",slug:"jing-zheng",fullName:"Jing Zheng"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3309",title:"Respiratory Disease and Infection",subtitle:"A New Insight",isOpenForSubmission:!1,hash:"2e85d47bf0576f1c2ccf642156ccbda2",slug:"respiratory-disease-and-infection-a-new-insight",bookSignature:"Bassam H. 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Later in 1854, Rudolph Virchow observed similar deposits in human nervous tissue that reacted in an analogous manner as the deposits in plants after the addition of Schleiden’s iodine-sulfuric acid stain [1]. With the advance in technological power and the advent of microscopy, researchers found that the starch-like deposits found in the diseased tissues of humans were made of proteinaceous structures that were organized as fibrils (termed “amyloid fibrils”) and coated with carbohydrates, hence the reaction to iodine-sulfuric acid stains [1]. More than 40 pathologies are part of the family of diseases characterized as “Amyloid Diseases” [2]. The criteria that allow such characterization rely on the fact that these pathologies contain a very specific hallmark: the accumulation of amyloid fibrils in cells, tissues and/or organs. Fibrils are formed after native proteins partly unfold and aggregate into oligomers or amorphous aggregates that later organize themselves into mature, β-sheet-rich fibrillar structures [2]. On a molecular level, amyloid fibrils extracted from different patients can be indistinguishable from each other [2]. These structures can be formed outside the cell or inside the cell [2], and when they accumulate, they cause cellular damage or mechanical damage (if accumulating in between or on top of tissues).
For decades, scientists believed that amyloid fibrils were stable and inert, and the end result of a nontoxic natural pathway that serves to scavenge and store highly reactive and toxic oligomeric intermediates formed during the process of protein folding [3, 4, 5]. The reactive hydrophobic residues found exposed in oligomeric intermediates are hidden in mature amyloid fibrils, thus unable to react with important cellular components [6]. Although the latter is true about amyloid fibrils, research in the last two decades shows that these structures are neither inert nor nontoxic [5, 7]. When extracellular, amyloid fibrils are readily identified by the host immune system, mainly by macrophages or neutrophils [8, 9, 10]. These immune cells have receptors that recognize and bind to the amyloid fibrils and intermediates, activating a signaling cascade that results in the production of proinflammatory molecules [8, 9, 10]. In this chapter, we will review the inflammatory component of some clinically important amyloid diseases, such as Alzheimer’s disease (AD) and familial amyloid pathologies, such as hereditary TTR amyloidosis (hATTR or familial amyloid polyneuropathy—FAP). We will also discuss how inflammatory cells contribute to disease progression by causing bystander damage to tissues or by enhancing protein aggregation, in the case of AA amyloidosis. Finally, we will provide the recent therapeutic approaches based on immune regulatory strategies for these diseases.
Inflammation is the term given to a form of immune defense that is widespread and requires a complex network of immune effector mechanisms to address tissue dysfunction or injury. The notion that inflammation is involved in amyloid pathogenesis was first suggested in the 1970s in two reports on serum amyloid A (SAA) [11, 12]. Nowadays, it is known that this particular amyloidogenic protein expression is regulated by IL-6, an inflammatory cytokine, which results in increased levels of SAA [13]. Hyperexpression of SAA for long periods of time results in amyloid formation and deposition in tissue, characterizing amyloid A (AA) amyloidosis [13]. This particular type of amyloidosis occurs in chronic inflammation conditions, such as autoimmune diseases or cancer [13]. With the exception of inflammation-induced amyloidosis, such as AA amyloidosis, the role of inflammation in most amyloid diseases is a more recent concept that emerged in the late 1980s with the observation of microglia, a brain immune cell, found near amyloid plaques in postmortem brain tissue from Alzheimer’s disease (AD) patients [14, 15, 16]. After these first observations, more evidence on the involvement of inflammatory mechanism in amyloid pathogenesis has emerged.
Alzheimer’s disease (AD) is known as the most common neurodegenerative disease worldwide. It afflicts over 40 million people in the world, and because aging is the major risk factor for developing AD, its incidence will likely increase in the future as medical advances lead to increasing life span [17]. Although there is no definite known causative agent, most scientists agree that amyloid-β peptide (Aβ) is an important factor leading to AD [18]. Aβ is highly amyloidogenic, meaning that it has great potential to aggregate in solution [18]. Aβ is a small peptide ranging from 25 to 42 amino acids [18]. Extracellular aggregates of Aβ are the main protein present in amyloid plaques, a hallmark of AD [18]. Moreover, a small fraction of AD patients is diagnosed with familial AD, which is known to be the result of an infrequently inherited autosomal dominant mutation in one of the three genes involved with the production of Aβ: the amyloid precursor protein (APP) gene, presenilin 1 (PSEN1), and presenilin 2 (PSEN2) [19]. The first findings pointing to a possible involvement of inflammatory mechanisms emerged around 1980 when scientists reported reactive microglia and astrocytes surrounding amyloid plaques of AD patients [14, 15, 16]. Nowadays, after years of research, inflammation is known to be implicated in AD by having a role in neuronal damage [20], Aβ generation [21], increased hyperphosphorylation of tau protein [22] (another hallmark of AD), and cognitive impairment [23]. In this part of the chapter, we will be focusing on summarizing the role of microglia in the progression of AD.
Microglia are the immune cells of the brain. They derive from myeloid precursors which migrate into the brain during early embryonic development and play a major role in maintaining a healthy environment in the brain [24, 25]. Microglia use their surface receptors to constantly scan the central nervous system (CNS) for microbes or other damaging molecules [26]. When activated by a stimulus, microglia mediate innate and adaptive immune responses or perform various functions in response to CNS disease or injury [26]. Microglia are of great importance for brain homeostasis, but uncontrolled or overactivated microglia can also contribute to brain diseases, such as AD.
Years of research is allowing deeper understanding of how microglia contribute to AD. Microglia produce inflammatory mediators, such as TNF-α [26], that can have a detrimental role when overproduced for long periods of time. Microglia are able to produce large quantities of TNF-α upon exposure to fibrillar and oligomeric Aβ [23, 27]. TNF-α is increased in the serum and CSF of AD patients and has additionally been detected in amyloid plaques [28, 29, 30, 31, 32]. Inhibiting TNF-α production with the use of unspecific anti-inflammatory compounds, such as minocycline, or a specific neutralizing TNF-α antibody, (infliximab) results in downregulated inflammatory pathways (e.g., MAPK, AKT, and NF-κB) and abrogates cognitive deficits in mice [23, 33]. It has been shown that fibrillar and oligomeric Aβ can induce production of not only TNF-α but also other important inflammatory cytokines in microglia by binding and activating several receptors [23, 34]. This suggests the existence of a universal epitope found in aggregated material and a nonspecific response to amyloids. Also supporting this idea is the fact that two generic, widely used, conformation-specific antibodies have been generated (A11 and OC antibodies) that recognize mutually exclusive structural epitopes in a range of amyloid-forming proteins, including Aβ, independently of any primary amino acid sequence similarities. A11 antibodies recognize anti-parallel β-sheet structures found in intermediate states, and OC antibodies detect parallel β-sheets found in mature amyloid fibrils [35]. Inflammation is a downstream consequence of aggregated Aβ binding to receptors such as TLR-4 (toll-like receptor 4), RAGE (receptor for advanced glycation end products), CD36 [23, 36, 37], etc. It is important to note that some of these receptors are also able to recognize other aggregated non-Aβ materials [38]. Interestingly, these receptors are not only present in microglia, but some are also present in endothelial cells and neurons [39]. This suggests that the role of Aβ in AD is very complex.
Some receptors that primarily bind monomeric Aβ are not involved in pathological, inflammatory processes. Receptors such as LRP1 (low-density lipoprotein receptor-related protein 1), PrPc (cellular prion protein), and PICALM (phosphatidylinositol-binding clathrin assembly protein) are able to bind monomeric Aβ and are thought to be involved in Aβ clearance, decreasing the Aβ burden and plaque formation in the brain [40]. Moreover, mutations in PICALM, which is a gene that encodes a clathrin assembly protein and thus is involved in endocytosis, have been shown to be a risk factor for developing late-onset AD [41]. More convincing evidence of the significant role of neuroinflammation in AD is found in recent genome-wide association studies (GWAS). These studies have identified more than 20 gene variants as risk factors for developing late-onset AD. These disease-modifying genes include genes involved in both innate and adaptive immune system responses:
An emerging concept based on recent work is that peripheral inflammation, in addition to local, brain inflammation, also affects AD pathogenesis. Studies suggest that myeloid cells, such as neutrophils, can enter the brain and may also involve in Aβ clearance [10, 43]. Neutrophils can recognize fibrillar Aβ and produce
Acute systemic inflammation, caused by bacterial infection, exacerbates AD pathology [45], and chronic systemic inflammation, occurring in diseases such as rheumatoid arthritis (RA), depression, and obesity, has also been reported to modify the amyloid phenotype of AD mice and is considered common co-morbid states of AD patients. In autoimmune disease, chronic inflammation can increase the risk of developing AD. Patients with the autoimmune disease Sjögren’s syndrome (SS) are twice as likely to develop AD [46]. In RA, it has been shown that anti-TNF-α therapy has a protective effect on dementia [47]. In the case of depression, Aβ accumulation in AD mouse models induces depressive-like behavior, which is dependent on inflammation [23]. Inflammatory cytokine production reduces serotonin levels and contributes to behavioral changes in mice with AD [23]. Again, this can be prevented by anti-TNF-α therapy [23]. Obesity is a known comorbidity of AD and a low-grade chronic inflammatory disease. In humans and AD mouse models, cafeteria diet consumption and a higher BMI are known to accelerate AD pathology [48, 49]. For example, in humans, for every 1.0 increase in BMI at age 70 years, AD risk increased by 36% in female patients [49].
In an attempt to cure AD, active immunization against Aβ was performed in mice and humans [50, 51]. Studies reported that immunization had a therapeutic effect on mouse models of AD [50, 51, 52]. Unfortunately, clinical Aβ vaccination trials have been interrupted due to the development of meningoencephalitis in 6% of the patients, likely involving the appearance of pro-inflammatory macrophages, CD4+ and CD8+ T cells [50]. As well as myeloid cells, T cells can enter the brain. There are myriads of T-cell subtypes surveilling the CSF and the meningeal membranes [53], and they can enter the brain parenchyma upon cell injury [53]. It is not only brain-local T cells that react to Aβ but also blood T cells have been shown to have hyperreactivity to the Aβ peptide [54], specifically to epitopes within the residues 15–42 [54]. This evidence together suggests that the immune system and inflammation play significant roles in AD: not only helping with homeostatic Aβ clearance and preventing AD plaque formation but also by contributing to cell injury. Unfortunately, to date, tackling the immune system to prevent AD has yet to prove clinically effective.
Transthyretin (TTR) is a 55-kDa tetrameric protein expressed and secreted mainly not only by the liver, but also by the choroid plexus in the brain [55]. This protein received this specific name due to its function: once in the plasma or in the cerebrospinal fluid, TTR acts as a retinol-binding protein and thyroxine transporter across the body [55]. More than 100 point mutations in the TTR gene have been described worldwide and most of them culminate in the production of abnormal protein with a high thermodynamic instability compared to its wild-type counterpart [55]. Only a handful of mutations are not pathogenic, such as the T119M mutation [56]. The pathogenic V30M variant is the most common mutation affecting a large population of people worldwide and results in the accumulation of TTR in various tissues, such as cardiac and nervous tissue [57]. Most TTR mutations have a high propensity to aggregate under denaturing and even physiological conditions [58], forming amyloid fibrils that deposit in various tissues and organs [58]. For decades, most physicians and pathologists still regard hATTR amyloidosis as a disease without an inflammatory component, since most biopsies and
The diagnosis of FAP is challenging, often relying on genetic screening to identify TTR mutations as well as on the identification of Congo red-positive amyloid deposits in biopsies. These biopsies are generally invasive, and tissue is usually taken from the sural nerve, abdominal fat, or salivary glands [59]. The main
Since the first study in 2001, the new concept that inflammation may play a role in the pathogenesis of FAP has emerged. Sousa and colleagues showed the presence of proinflammatory markers such as TNF-α and IL-1β in biopsies of FAP patients [63, 64]. Interestingly, the levels of proinflammatory and oxidative markers in
These studies altogether suggest that inflammation in FAP consists of two different phases. One phase in which inflammation possibly begins at the moment of TTR production in the liver. The synthesis and abnormal folding process of the mutated and unstable TTR in the liver requires a high energetic state and thus, may cause endoplasmic reticulum (ER) stress and the activation of the liver unfolding protein response (UPR). ER stress and the activation of UPR in liver were shown to cause pro-inflammatory cytokines production, such as IL-6 [71, 72]. IL-6 is known to increase the production of other proinflammatory intermediates and could enhance inflammation levels locally in the liver by activating liver-associated macrophages as seen in other nonamyloid diseases [73, 74]. It is ultimately important to understand whether the liver plays an important role in the inflammation observed in FAP patients due to the fact that most of these patients undergo domino liver transplant. In this procedure, a liver failure patient receives a liver from a FAP patient. However, a five-year study described that 35% of patients that underwent domino liver transplantation presented FAP symptoms earlier than donor FAP patients [75]. These data indicate that FAP patients may have altered liver capacity and a low-grade chronic inflammation, decreasing the success of liver transplants. The second phase occurs after unstable TTR reaches the bloodstream and aggregation starts. TTR oligomers have been found in blood from FAP patients [76] and could elicit the production of various inflammatory cascades in circulating leukocytes and T cells. Amyloid oligomers are formed before fibril deposition and have been shown to be toxic to cells [77] and elicit inflammation when presented to immune cells [23]. Small, toxic oligomers can also be produced in situ after the cleavage of mature fibrils through the action of local proteases, such as elastase and metalloproteinase-9 [10, 66].
So far, in FAP patients and hATTR mouse models as well as in vitro, TTR fibrils are able to elicit inflammation and activate a myriad of cell types. In a broader clinical context, the underlying inflammation that begins in asymptomatic patients and continues chronically might be important for the development of FAP-associated symptoms. Patients with FAP present symptoms other than neuropathy, such as gastrointestinal symptoms, cachexia, malnutrition, diarrhea, and others [59]. Inflammatory molecules are known to change neuroendocrine pathways leading to anorexia and thus cachexia in FAP patients. These new data point to an explanation for a lot of unknowns concerning the pathogenesis of FAP. Additionally, understanding the role of inflammation in hATTR will help improve the quality of life and disease management in affected patients. There are currently no studies showing if inflammation can increase the risk of developing hATTR. However, it is possible that an inflammatory environment could decrease liver function and predispose an individual for the production of misfolded proteins, such as TTR.
Although recent papers have confirmed that amyloid fibrils present polymorphisms in topology, amyloids still possess an unchangeable structural fingerprint that is shared across species [78]. A lot of different proteins are able to form amyloid fibrils and not all amyloids are pathogenic. Various hormones are present in amyloid form in the pituitary gland [79], and melanocytes possess amyloids, which contribute to melanin formation [80], etc. What makes an amyloid pathogenic or not is still unclear. However, amyloids also possess another universal characteristic: they are able to activate the immune system and induce inflammation. This suggests that inflammation may be an important component of many other amyloid diseases. Indeed, inflammation has been described in many other amyloid diseases. In Parkinson’s disease (PD), the involvement of inflammation in the disease process is supported by data showing the infiltration of activated microglia and T cells in post-mortem PD brains [81, 82] Additionally, there is accumulation of proinflammatory cytokines such as TNF-α, IFN-γ, and IL-6 IL-1β in the brain and cerebrospinal fluid of PD patients [83, 84]. The PD culprit protein, α-synuclein, is able to bind to several immune receptors and elicits
Prion disease is another widely studied amyloid disease and is also known as Creutzfeldt-Jakob disease, fatal insomnia, spongiform encephalopathy, and Kuru. Prion diseases are rare, progressive neurodegenerative disorders that affect both humans and animals [87]. They are caused by the aggregation of PrPc (cellular prion protein) into transmissible, pathogenic prions [87]. These diseases are accompanied by long incubation periods and brain changes associated with neuronal loss [87]. Identifying a role of inflammation in these diseases is rather recent and begun with studies showing that the pathological hallmarks of the prion diseases are associated with the presence of activated astrocytes and microglia [88]. CD8+ T cells are also present in prion-affected brains and usually are found near activated microglia and prion amyloid plaques [89]. As inflammation progresses, inflammatory cytokines are also detected in prion-containing brains [88], and these are thought to play an important role in behavioral changes and neuronal loss observed in affected mice. And this is yet another example of inflammation being widely present and contributing to pathogenesis in an amyloid disease which was first thought to not have an inflammatory component.
Most amyloid diseases are still incurable. However, most of them can be managed using palliative care and drugs to decrease symptoms and extend the patients’ lives. In AD, efforts are concentrated in decreasing symptoms such as cognitive deficits [90]. Currently, there are five FDA-approved drugs to treat cognitive symptoms associated with AD. These drugs are basically acting on two different neurotransmitter systems in the brain: the cholinergic system and the glutamatergic system [90]. They act by blocking glutamate receptors and inhibiting cholinesterase activity, thus these drugs, when combined, can decrease excitotoxicity induced by an overload of glutamate in the synapse and making acetylcholine more available for a healthy synaptic transmission [90]. While in theory, and as seen in mouse models of AD, these drugs seem effective, in humans they work to certain extent decreasing the symptoms. Although these drugs can temporarily decrease symptoms, they are not able to stop the progression of AD, as they do not address amyloid accumulation [90]. Although great results were seen in mouse models, in AD patients, clinical trial using nonsteroidal anti-inflammatory drugs (NSAID) were unsuccessful to prevent or treat the disease, but these drugs only account for a small part of inflammatory pathways dependent on cyclooxygenases (COX) and have diverse side effects. For PD, treatment using drugs is aimed at enhancing cholinergic and dopaminergic transmissions and hence decreasing motor and gut-related symptoms, such as tremors and constipation [91]. Deep-brain stimulation is a surgical treatment available for PD and can also decrease motor symptoms [91]. Most treatments, as the ones described above, are aimed at treating the consequence of amyloid accumulation rather than treating the amyloid accumulation itself or the inflammatory components of these many amyloid diseases.
For the hATTR diseases, two FDA-approved drugs have been developed to prevent amyloid accumulation in patients: tafamidis, a drug that stabilizes TTR and decreases TTR aggregation and antisense oligonucleotides against TTR, a drug that aims in reducing TTR production in the liver [61, 62]. In structure, tafamidis resembles most NSAID, and hence, it does not have any NSAID activity [92]. Notably, many other NSAID drugs also bind to TTR, stabilizing it [93]. However, many have not been to clinical trials at all or have not been successful in clinical trials because chronic use of NSAIDs is not indicated for patients with liver, renal, and heart problems [94], which are part of the symptoms affecting FAP patients. NSAIDs have also been used for treating other amyloid diseases, such as AD and PD, but again without success [95, 96]. Indeed, many AD and PD patients are older individuals that also possess additional conditions that exclude them from the chronic use of NSAIDs. The use of immunotherapies, especially for AD, has been thought to be an effective approach to treating the disease, but clinical trials have shown that autoimmune meningoencephalitis develops in a significant number of patients undergoing immunotherapy [50]. Usually these treatments aim to use antibodies to neutralize the culprit of the disease, in the case of AD, the Aβ peptide [50]. Unfortunately, the autoimmune response, consisting of hyperreactive T cells, of patients has prevented the clinical trials from continuing further. Researchers are still investigating immunotherapies as a way to treat AD and managing the T cell response.
The use of antisense nucleotides (ASOs) for successfully decreasing the amount of native protein in the body remains the most effective therapy and maybe the path to cure amyloid diseases. ASOs have already been shown to be effective in hATTR disease [62], without eliciting any further autoimmune inflammatory response in patients receiving the therapy. There is growing interest in using ASOs in AD and PD, since many proteins that cause amyloid diseases have unknown or redundant physiological function [2]. This suggests that decreasing the levels of native, healthy protein in individuals may not cause problems for most bodily functions. By reducing the levels of native protein, ASOs ultimately decrease amyloid formation and accumulation and finally, all the immune responses that might come with unstable protein synthesis, aggregation, and amyloid deposition in tissue.
Amyloid diseases have been described in humans and animals since the 1800s. This family of diseases has one defining characteristic: the presence of extracellular proteinaceous aggregates (amyloid fibrils or plaques) in tissues and organs. These amyloid fibrils arise from the unfolding of native protein, which vary according to the disease (for example, Aβ peptide in AD). Another common characteristic of amyloid diseases is the installment of inflammation during and after amyloid formation. Amyloid fibrils and tissue damage elicit local and nonlocal immune cell infiltration into tissue and proinflammatory cytokine production. Together, these fuel a vicious cycle that can increase amyloid production, as seen in AA amyloidosis, and create an environment of chronic inflammation. A chronically inflamed tissue, as seen in autoimmune diseases, rapidly loose function and deteriorates. This is especially true for the nervous system, a delicate tissue in which self-repair is almost impossible. As most amyloid diseases affect the CNS, and inflammation is a fundamental component of amyloid disease, studying inflammation in the CNS is imperative to our understanding of how to treat amyloid disease. Many current treatments focus on the consequences of amyloid accumulation and fail to address the basic underlying causes. The use of ASOs brings promise of improvements in amyloid disease therapeutics and fortunately is growing as an important tool used in disease therapy. Recognizing that inflammation plays a significant role in amyloid disease is essential to understand the pathogenesis of amyloidosis and important for developing new targeted treatments in an era of growing demand.
I would like to thank Dr. Kristina Hedbacker for careful proof reading of this chapter.
We report no conflict of interest.
Death is often considered in terms of medical, legal, ethical, philosophical, societal, cultural, and religious rationales. The biomedical definition of death is primarily a scientific issue supported by the best available evidence. A medical practitioner has certain ethical and legal responsibilities regarding death, such as the effort for prevention of death, determination of death, determination of time/moment of death, declaration of death, issuing the certificate, and if needed, autopsy or organ removal for transplantation. That aspect has a lot of ethical, legal, emotional, and scientific issues. Dying is considered as a process, which affects different functions and cells of the body at different rates of decay. Doctors must decide at what moment along this process there is permanence and death can be appropriately declared. Diagnosis of death and a record of the time of the death, in most countries, are the legal responsibility of a medical practitioner. Determining the moment of death is vital to avoid the use of unnecessary medical interventions on patients who have already died and to make sure that the method of organ donation is obvious and transparent. Also, the time of death is important because of survivorship clauses in wills.
For the millennia, human has struggled with the concept and criteria of death, and thus, the line between life and death continues to be debated. The profound changes caused by the life support in organ failure, organ substitution technology, and transplantation still continue to challenge our notions of life and death [1]. Despite scientific progress in the last few decades, there remain big variations in the diagnosis criteria applied in each country with legal regulations resulting in misunderstandings among the public and health care professionals. Since the ample decades, the academic literature and the media have raised the voice in alarming language in issues of death determination and dead donation practices [2]. Difficulty arises to distinguish valid scientific critique from those criticisms supported by the fear of death itself, mistaken diagnosis or a premature declaration of death, or the fear of retrieving organs from the living.
The challenges in discussions about death are complex due to philosophical, religious, and cultural differences in the concept and definitions of death; debate about ethics, law, and religion; problems in performing research and the resultant shortfall in information and evidence on various aspects of the dying process; dispute in the validity of death determination practices; lack of understanding and/or awareness by general public and health professionals; last but not the least the emotionally charged nature of the subject matter. There are plentiful ways of dying but just one way to be dead. Hence, the baseline determination of death criteria should be rigorous, global, and acceptable for medical practice worldwide, while remaining respectful of diversities. International consensus on the clinical criteria for the death determination is of central importance to preserve public trust and promote ethical practices that respect the fundamental rights of people and promote quality health services [3].
In medical practice and law, the separation between being alive and dead should not be ambiguous. It designates the moments that follow events such as no medical or legal need to maintain resuscitation or life support, loss of personhood and individual rights, decedent’s legal will execution, disposal of the estate, life insurance settlement, burial or cremation of the body for final disposition, and religious or social ceremonies to mark the end of a life [4]. Dying is not an event rather a process, which affects various functions of the body at different rates of decay. The physician must confirm the moment along this process that there is permanence and death can be accurately declared [5]. Biological criteria of death are associated with biological features and irreversible loss of certain cognitive capabilities [6]. A patient could be declared dead legally as lack of brain function and may still have a heartbeat when on a mechanical ventilator. Though there is no justification in supporting the ventilation of a dead person, withdrawing the ventilator before the legal criteria of death may involve the doctor in both civil and criminal proceedings. The legitimate moment of death could be a wide range of time after the death has actually occurred. Many accident victims actually died at the scene of the accident but were declared dead officially on arrival at a hospital.
The scientific, biological, and medical aspects of the determination of death are still controversial. Certain ancillary and/or complementary laboratory tests could also be useful in situations where clinical testing cannot be executed or if confounding or special conditions are present. It had been recognized that there are limitations to the utilization of a number of these tests and further work will confirm the reliability of these tests. Death is a biological phenomenon, with profound social, religious, and psychological traditions, but very little background experience and available scientific information. The understanding of the biological aspect has gradually developed and strengthened as a direct result of technology, cell biology, organ donation, and transplantation, but was inadequately adjust in law, health policy, and bioethical discourse. Organ donation has forced the understanding of moment of death and acceptance or persisting controversy of where that line is.
It is urgent time demanding notion to adopt a minimum determination of death criteria to be acceptable for medical practice worldwide to achieve international consensus on clinical criteria to maintain public trust and promote ethical practices.
The concepts and practices of death undoubtedly are influenced by values and social practice. The definition of death affects not only that consider to count as death, but also questions of grieving, medical treatment, asset disposal, organ donation, and a myriad of other legal and ethical issues [7].
The philosophical investigation of human death has focused on some overarching questions—What is human death? The conceptualization (definition) of death is the answer to this ontological question that defines death as the irreversible cessation of organismic functioning along with the irreversible loss of personhood. Next question, how can be determine that death has occurred? The answer is epistemological one, which furnishes both the
Finally, how do the deaths relate, conceptually, to the essence and identity as human persons? The metaphysics of the body and soul does so in terms of the logical dualism between the material body and consciousness or the immaterial mind. In the philosophy of mind, mental phenomena are nonphysical and thus distinct and separable from the body. The dualism of body and soul/mind suggests that while being a person is, undoubtedly, a matter of having a biologically human body. The existence of a person entails the presence of a thinking being, which has reason and reflection, and can consider itself as itself, in different times and places. The individual identity of psychological persons is dependent on the brains’ neurophysiology [9]. The brain death need not be considered as biological death rather a proxy for the loss of individual identity, that is, personhood [10]. When a person has died, it does not merely mean that some biological entity no longer functions. It means some unique mind or person, realized as a cognitive or psychological entity, has ceased to exist. The personhood admits of application of the terms life and death. It has been exceedingly rare for the demise of a biological human organism to take place sometime after the death of a person. Artificial life support can maintain the biological life of an individual in the absence of their continued psychological existence. Such brain dead individuals have been considered living cadavers and twice dead [11]. Human life is operationally defined by the onset and cessation of organismal function [12]. There are two different meanings to human death being alive and having a life, the notion of personhood allows us to focus on the autobiographical meaning of death—the loss of a person [13].
Other philosophical questions—When does a human being die? Is the organismic and denouement conception of death have any practical use? Schofield et al. present a definition of death focused on the final denouement of human beings as biological organisms. According to their view, the moment of death is the last process in bodily functions that maintain homeostasis and finally ceases [14]. Reducing death to the biological denies an important characteristic of being human, intellectual, or psychological nature. The conception of death acknowledges the cognitive aspect of human existence, at the same time, accommodating embodiment, that we both have and are biological bodies [15].
Generally, people believe that death terminates the whole existence of a person. According to Christians’ belief, death puts an end to human existence on earth but does not end existence, instead opens an entrance into another sphere where existence continues either in heaven or hell after the final judgment that everybody will face it. Death is considered
Life is fundamentally grounded on the continuation of individual and collective cell function, dependent on the supply of nutrients and oxygen. Cell biology has exhibited that a layer of human cells, separated from the human organism, could also be grown in laboratory culture pending till bathed in a steady supply of nutrients and oxygen. The human being, a complex package of trillions of cells organized into organ systems, requires a cardiopulmonary delivery system for oxygen and nutrients to reach the cells. The development and evolution of modern cardiopulmonary resuscitation evolving into cardiopulmonary support technologies have been important advances informing our concepts of life and death.
The introduction of advanced medical technology poses new problems for the old standards that constitute death. The values automatically shape thinking of the death of a person, not merely a descriptive, scientific concept, but unequivocally contain evaluative content. The changing frontiers of the death drive to confront basic questions of persons and values that will adapt to address future questions. It is vital to examine the evaluative content of concepts and practices relating to death, and reflects on what it is that we value or should value in persons. The philosophical definitions of death in the absence of indisputable objective signs of death should be considered, loss of integrative functioning of the whole organism, failure to engage the environment spontaneously by respiration, loss of consciousness and sentiency, and the separation of some vital principles from the body.
The neurological criteria for death represent an interesting advance in the ways of responding to changes in death and dying. The development of medical technology and life support techniques insist increasingly on precise notions to identify the most important aspect of neurological lives. However, the whole brain standard of death suffices in the vast majority of cases, but does not fully line up the value in persons. Time has come to decide the position of the current brain death standard as it mismatch with the values and negative consequences in determining death and in organ donation. Advances in technologies seem as if they will inevitably make this question inescapable. The prominence of
Ideally, the definition of death would link the concept of life or death with its clinical manifestations as closely as possible that fall in both two categories, the
Death is the transition from being a living mortal organism to being something that, though dead, retains a physical continuity with the once-living organism. Death is a process involving the cessation of physiological functions and the determination of death is the final event in that process. Death is a gradual process at the cellular level with tissues varying in their ability to withstand deprivation of oxygen. A distinction is now being made between death at the cellular and tissue levels and death of the person. Sydney declaration states, clinically, death lies not in the preservation of isolated cells but in the fate of a person. Korein’s view of the life of the multicellular organism as a whole could no longer be explained in terms of a cellular task alone. The life of a typical unicellular organism encompasses fundamental tasks of the metabolic and reproductive attributes of a particular organism, empowering it to amplify in a direction of decreased entropy production (bacteria, amoeba, or zygote). In a multicellular organism, a large mass of cells could be alive but this does not indicate that the organism as a whole was alive. Machado refused the hypothesis that an explanation of death should include the function that contributes to the key human attributes and the highest level of control in the hierarchy of integrating functions within the human organism [18, 19, 20, 21, 22, 23, 24].
The full version of death includes three unique ingredients such as the definition of death, yardstick of brain death, and the tests to prove that the standard has been satisfied. The definition of death is typically a philosophical task, while the criteria and tests are medical tasks. Particular standards and tests must match with a given definition. The definition must represent attributes that are so important and significant to a living entity that its absence is designate death [25, 26]. The nonfunctioning entire brain provokes the permanent cessation of the functioning of the organism as a whole.
Biologically death is defined as the extinction of biological properties of life. Human death can be defined as the irreversible cessation of three interdependent and interlink vital functions of the body—the tripod of life (heart, lung, and brain). Another way death can be defined as a person is said to be dead, if he cannot take up spontaneous respiration or maintain circulation. There is growing medical consensus in a unifying concept of human death, which involves the irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe.
Uniform determination of death (UDDA) act defines death as, an individual who has sustained either irreversible cessation of circulatory and respiratory functions, or irreversible cessation of all the functions of the entire brain, including the brain stem, is dead. Montreal forum defines death as the irreversible loss of the capability for consciousness and loss of all brainstem functions. That could result as a consequence of permanent stoppage of circulation and/or after catastrophic brain injury. In the determination of death, “permanent” refers to the cessation of function that cannot resume automatically even not be restored through intervention. The determination of death must be made in accordance with accepted medical standards.
The presence of the two vital functions, circulation and respiration in a body, is a sure sign of life. The patient who was diagnosed with entire brain failure and has been pronounced dead the vital functions are dependent on external support from the ventilator. The supporter of neurological standard designates these apparent signs of life are artifacts of the mechanical support that conceal the very fact that death has already occurred. To judge that logic, the essential facts of mechanical assistance for these vital functions be achieved if the interrelationship of three-body systems involved in breathing and circulation is understood. The three systems are the heart and circulatory system, the lungs and respiratory system, and the central nervous system. The pathophysiological processes that eventually end in mortal condition,
The prime functions of respiration are ventilation and diffusion. The ventilation involves both inhalation and exhalation; the diffusion involves the exchange of oxygen and carbon dioxide between atmospheric air and blood. The respiratory system brings atmospheric air by inhaling process to the alveoli where oxygen from the atmospheric air is able to move into the blood by the process of diffusion. The exhaling process of breathing facilitates to rid the body of the waste products—carbon dioxide. The walls of the alveoli are extremely thin, formed to facilitate the diffusion of gases between the sacs and the blood vessels. Oxygen is essential to the continued metabolic work of the trillions of cells in the body. The absence of an endless delivery of oxygen, brought into the body through inhalations and transported to the tissues by the
The CNS plays a crucial role in maintaining an organism’s vital functions. The reticular activating system of the brainstem is also critical to the organism’s conscious life, essential for maintaining a state of wakefulness, which is a prerequisite for any of the activities associated with consciousness. The contraction of the muscles of respiration is brought about by a signal sent from the respiratory center located at the brainstem. A relatively high level of CO2 in the blood stimulates the respiratory center to send a signal to the muscles of respiration, which excites them to contract. For life to continue, the CO2 must be expelled and new oxygen brought in. Other parts of the CNS also be involved in signaling the muscles of respiration to contract, like
To prevent the death of the organism, some external device (mechanical ventilator) for the breathing process is essential. The mechanical ventilator works by altering the pressure in the lung cavities in order that oxygen-rich atmospheric air will travel down and CO2-rich air will travel back up the respiratory tree. Gas exchange in the lungs will be of no benefit to the patient unless the blood is kept moving as well. Incoming oxygen must be delivered to tissues that required it, and accumulating carbon dioxide must be a shift to the lungs for expulsion from the body. Hence, a ventilator will help the patient as long as another vital system is functional, constituting the heart (working as a pump) and network of arteries, veins, and capillaries. The movement of blood occurs only within the body, whereas the movement of air is an exchange between the body and the surrounding atmosphere. Another relevant rationale of external support of vital systems is the indisputable fact that there is no part of the CNS that is absolutely essential for heart contractions within the way as the respiratory center in the brainstem is unconditionally essential in breathing. The heart is the most essential active part of the circulatory system and the vessels of circulation, being rigid plumbing lines that passively convey blood, pumped by the heart, are living tissues that undergo changes (some driven by CNS) to sustain a proper blood pressure. Patients of ventilator support must also be given drugs to maintain the blood pressure in a healthy range. Ventilator support designates the external supports of vital functions of breathing and circulation, in lieu of breathing effort of organism, stimulated by the respiratory centers of CNS, an external device moves the lungs and facilitates the inflow and outflow of needed air. It offers the heart muscle still to function, as the myocardium, like other cells in the body, needs oxygen to stay alive. The argument for the neurological standard of determination of death begins with facts that the respiratory motion supported in this way is not in itself a symbol of life, rather an artifact of technological intervention. Neither a beating heart, in this instance, a symbol of life, or merely the continuation of a spontaneous process would quickly cease if the ventilator is withdrawn [27].
Humans have long used criteria and technology to assist in the diagnosis of death. The link between breath and life is equally as ancient and found in both Genesis (2:7) and the Qur’an (32:9). Somatic criteria, such as the presence of decomposition and rigor mortis, are the oldest in human history. Over 800 years ago, when Maimonides codified the diagnosis of death as the absence of the heartbeat and respiration with cooling of the body [28], he was likely documenting a standard used from down of civilization.
In the eighteenth century, the physician was confirmed about death if the heart and lungs break off, but lacked adequate tests to certify it. In the twentieth century, the moment of death became less clear, and thus, the tests physicians had finally perfected proved insufficient. Historically, until the early twentieth century, physicians’ inexperience in human anatomy and physiology left them poorly equipped to accurately test for death. From the eighteenth through the mid-twentieth centuries, a person was declared dead when the heart stopped beating and lungs ceased to function. In the early part of the twentieth century, while the standard to check death was well established, the understanding of when the death occurred became the subject of great debate. The fear of premature burial was replaced by the fear of apparent death sustained by life support systems. These issues reach a climax in the latter part of the twentieth century when the cardiorespiratory definition of death was reevaluated and a novice addition of brain death was introduced. Intensifying new questions as to the moment of death, the brain death criterion demands further revision of the empirical tests. The nature of death, however, does not lend itself to one discipline rather considers metaphysics, sociology, theology, and medicine. Historically, the irreversible stoppage of heart and lung functions constituted death as the absence of heart and lung activity immediately leading to failure of the entire organism. It has become apparent that cardiac and respiratory activities were significant for separating the living from the dead. The moment of death was firmly estimated but the task of confirming criteria to check for irreversible quiescence of functions proved more challenging and often had catastrophic consequences. A consensus emerged that once the heart and lungs ceased to function the person was dead, although the empirical criteria to test for death were suspect. Because of this critical divide between theory and practice, instances of premature burial occurred. To safeguard premature burial date back to antiquity with the Thracians, Romans, and Greeks, each waited 3 days for putrefaction to start before burying their dead. The Romans took a more extreme approach by amputation of a finger to ascertain if the stump bled, in addition to calling out the person’s name three times while on the funeral pyre. Hence, the premature burial was a great worry, though it did not attain climax until the eighteenth century, accelerated by the intellectual climate. The knowledge and scientific revolution instituted a radical change in the insight of life and death [29].
Belief in the afterlife was not as important as life here due to the works of Bacon, Descartes, and Galileo, which emphasized the notion that life might be improved if not perfected by scientific manipulation. There is little practical obligation to worry oneself with an afterlife if this life could be manipulated by the art of medicine. Revulsion (drawing of disease) by the dissection of cadaver found in the sixteenth and seventeenth centuries as the study of human anatomy revealed the secrets of the
During this era, fear for early burial was so prominent that led to the establishment of waiting mortuaries and security coffins with alarm mechanisms and permanent air supply. The “Academy of sciences prize” was awarded in 1846 to Dr. Eugene Bouchut for his best work on the “signs of death and the means of avoiding premature burials.” He suggested the utilization of the stethoscope, invented in 1819 by Laennec, as a technological aid to diagnose death. Other popular practices for death determination were inserting leeches near the anus, applying specially designed pincers to the nipples, or piercing the heart with a long needle with a flag at the end, which wave if the heart is still beating. Bouchut suggested that a person could be declared dead if a heartbeat was absent for 2 min. He extended the period to 5 min, in the face of opposition [36, 37, 38, 39]. Case reports from physicians (Harvey Cushing) writing around the beginning of the twentieth century had evident that patients of cerebral pathology would die from respiratory arrest and subsequent circulatory collapse. Loss of electrical activity in the brain and cerebral circulatory arrest might signify human death that was evident in subsequent decades. The advent of mechanical ventilation, halting the inevitable circulatory collapse that follows the cessation of spontaneous respiration with the advent of mechanical ventilation, and the relevance to diagnosing death using neurological standard were understood.
In 1959, two historical landmarks were published, Mollaret and Goulon proposed the term
A group of anesthesiologists observed problems of sustaining the body alive in the absence of total brain function. This problem was presented to Pope Pius XII and resulted in the publication of a papal allocution describing that
The papal allocution culminate research, by three categories of French neurologists and neurophysiologists during 1959, separately studied comatose and apneic patients separately, narrated terms death of the “systema nervosum and coma de´passe´” translated as beyond coma or ultra-coma and subsequently by others as irreversible coma. These patients were respirator dependent, in an unresponsive coma, and areflexive. EEG and deep intracranial electrical activity were entirely absent. The investigators’ conclusion was that the brains of these patients were irreversibly dysfunctional. The WMA ethical committee and its council undertake dialogue and conference on death, 2 years earlier the first heart transplant by Christian Barnard in 1967. Wijdicks wrote that the first idea for the formation of the Harvard committee was recorded in a letter from Henry Beecher to Robert H. Ebert in September 1967. The Sydney and Harvard committees worked in parallel for several months, without either being aware of the other’s work [41, 42, 43, 44, 45].
The year 1968 was a crucial time for defining human death on the neurological ground and a milestone event in the history of medical science. On August 5, 1968, the Ad Hoc committee of the Harvard medical school to examine the definition of brain death published a report, as
Since 1968, the concept of brain death has been extensively analyzed, debated, and reworked. Still, there remain much misunderstanding and confusion, especially for the general public [50]. The Declaration of Sydney touched on key philosophical issues on human death. It proclaimed that in most situations physicians could diagnose death by the classical cardiorespiratory criteria. In spite of this, two modern practices in medicine force them to revise the time of death: first the ability to maintain circulation by artificial means and second the use of cadaver organs for transplantation. The essential public addresses death as a progressive process at the cellular level with tissues varying in their capability to cope with deprivation of oxygen, but clinically death “lies not in the preservation of isolated cells but in the fate of a person.” Also, it is described that the death determination must be grounded on clinical judgment, supplemented if necessary by a number of diagnostic aids, emphasizing the EEG. Nonetheless, it asserted that the overall judgment of the physician could not be replaced by any ancillary test. The declaration went further, proposing a more philosophical and conceptual explanation about the relationship between death and the fate of a person. The Harvard committee did not provide a clear concept of death but emphasized a clinical explanation of brain death, describing in detail the anatomical substratum and tests. The Sydney declaration did not use the term brain death but declared the clinical judgment for death determination and the Harvard committee, although mentioned the term brain death, finally select irreversible coma along with a detailed set of clinical criteria for death declaration. Both the Sydney and the Harvard committees suggest the use of EEG. For the purpose of the death diagnosis and transplantation, the Sydney declaration advocates two or more physicians not involved in transplantation should make the diagnosis, while the Harvard committee voiced that the death declaration should be made first, and then, physicians not involved in the transplantation procedure should be the one to turn off the respirator. Both committees justify a legal regulation of this issue [49]. Sydney declaration was amended at 35th WMA, by the addition of a key point declaring that “It is essential to determine the irreversible cessation of all functions of the whole brain, including the brain stem” for diagnosis of brain death but the EEG was not mentioned and no other issues were modified [49, 50].
In July 1981, the President commission for the study of ethical problems in medicine and behavioral research published a report,
A scientific basis was suggested to justify brain death with the theory of the brain as the central integrator of the body. According to this theory, the organism becomes a rapidly disintegrating collection of organs following the brain death (BD). Consequently, the concept of BD is not only an ethical and/or social concept or a matter of values, rather a matter of scientific facts such as irreversible stoppage of functioning of the organism as a whole is death. The guiding principles of irreversible cessations of functioning of the entire brain are absolutely correlated with the permanent cessation of functioning of the organism as a whole as the brain is necessary for the functioning of the organism. The brain integrates, generates, interrelates, and controls complex bodily activities. A patient on a ventilator with entirely destroyed brain is merely a group of artificially sustained subsystems since the organism as a whole has ceased to function. President’s Commission report also supports that rationale, convincing the gravity of the brain and recognized the profound instability of the brain-dead organism. In adults who have an irreversible stoppage of the whole brain’s function, the mechanically generated functioning could exist only for a limited time as the heart usually stops beating within 2–10 days [51].
The enabling legislation for the President’s Commission directs it to study the ethical and legal implications of the matter of defining death, including the probability of developing a uniform definition of death [51]. The central conclusions were that the recent developments in medical treatment necessitate a restatement of the standards traditionally recognized for determining that death has occurred and such a restatement ought preferably to be a matter of statutory law, which should be uniform among all the states. The definition embodied in the statute ought to address general physiological standards instead of medical criteria and tests, which will change with advances in biomedical knowledge and refinements in technique. The death is a unique episode that could accurately be confirmed either on the traditional grounds of permanent cessation of heart and lung functions or on the basis of permanent loss of functions of the entire brain. Any statutory definition must be separate and distinct from provisions governing the donation of cadaver organs and any legal rules on decisions to terminate life-sustaining treatment. American Bar Association, American Medical Association, and the National conference of commissioners on uniform state laws together have declared the statute, the Uniform Determination of Death Act (UDDA) affirmed: “an individual is dead who has
The UDDA is a statute, to address the societal problem created in the mid-twentieth century, due to the development of mechanical ventilation and other organ-sustaining technologies, to support permanently brain-injured individuals. The justification of the UDDA was to establish a uniform definition of death, determined by
In the executive summary update of task force recommendations, declare requisite for the diagnosis of brain death in children of two neurologic examinations is performed by two independent physicians and two apnea tests, both of which may be organized by the physician managing ventilator care [56, 57]. Examinations should follow an observation period of 24 hours for neonates less than 30 days old and 12 hours for older infants and children up to age 18. It is significant to note that there may be institutional variance in the way these criteria are interpreted, and pediatricians may adapt their brain death testing methods to take into account the age-related anatomical and physiological differences between neonates, infants, and children. Parents and other family members of children undergoing brain death testing may require close attention and additional support [58, 59]. The pediatric guidelines were updated in 2011 by the American Academy of Pediatrics. A recent study reveals widespread disparities in adherence to the guidelines nationwide. It is essential to follow a standardized process to ensure accuracy in the diagnosis and inconsistencies in diagnosis could lead to false-positive brain death determinations, which could erode the public trust in the ability of physicians to declare death [58, 59, 60].
In December 2008, the President’s council on bioethics published a white paper (controversies in the determination of death) in which the neurological standard was carefully reexamined [27]. The council built the insight in biological reality by appropriately describing the clinical and pathophysiological understanding of brain death, which offers substantial reassurance to the ultimate validity of the neurological standard. It effectively gives a new foundation to the justification for the neurological standard of death. The council strongly agreed that “
The council works was a historical decision that answers lot of
Whether a patient in the condition of total brain failure is actually dead and can it be said with sufficient certainty to ground a course of action as the mortal remains of a human being. To ascertain those, up to this time, two facts about the diagnosis of total brain failure have been taken to provide basic support for a declaration of death: first, that the body of a patient with
Another view of the neurological standard was also pointed within the council for certainty about the vital status of patients with total brain failure, the only rational and defensible conclusion of such patients are severely injured, but not yet dead. Hence, only the traditional signs of permanent cessation of heart and lung function should be used to declare a patient dead. Accordingly, medical interventions for patients with total brain failure should be withdrawn only after they have been judged to be
The understanding of medical futility [61, 62] has been developed in several papers by Edmund D. Pellegrino. Futility is the condition of a patient’s disease, which is beyond medical rescue, such as beyond the powers of medical technology to help. Clinical futility is present when any medical intervention is considered as ineffective, non-beneficial, and disproportionately burdensome for the patient. The clinical judgments of the futility of a given therapeutic intervention involve a rational balancing of three factors: efficacy of the given intervention, the purpose of which doctor alone can make; second, the advantage of that intervention, the patients and/or their surrogates can make; and third, the burdens of the intervention (cost, discomfort, pain, or inconvenience), jointly assessed by both physicians and patients and/or their surrogates. Adjusting the relationship among those three criteria is at the heart of prudent, precautionary, and proportionate action [27].
Lastly, the council members on bioethics had opined that the current neurological standard for declaring death, grounded in a careful diagnosis of total brain failure, is biologically and philosophically defensible. The council also concluded that,
The DDR has been secured for the ethical and social acceptability of organ transplantation protocols from their primitive days. This rule demands assurance of the death of the donor as the first step in any ethically legitimate transplantation protocol (other than those involving healthy, living donors). Additionally, the death of the patient must not be accelerated, nor end-of-life care made vulnerable in any way, to accommodate the transplantation protocols [27]. No protocol can demand ethical approval without trustiness to the present rule, in any ethically legitimate transplantation protocol (other than those involving healthy, living donors).
Relaxation of the DDR is a morally and ethically inappropriate and rationally specious way to deal with the uncertainties of the standard for the death of the donor. It leaves the options of the criteria for death to individual preference, amounting to the eventual abolition of any stable criteria for death. Numerous additional dangers are the use of assisted suicide to facilitate organ donation, legitimizing the utilization of patients in permanent vegetative states or of less-than-perfect infants as donors [27]. It exposes “undeclared” patients to “presumed” consent to donation [27, 62, 63].
Montreal forum was formed to address the global challenge in response to the request from various countries to “WHO and Transplantation Society” to provide guidance for leading practices and health policy in death determination by neurological and/or circulatory criteria. The guidelines would promote safe practices assuring the absence of diagnostic errors in death determination, safeguarding patients and health care professionals, upgrading public and professional confidence in the dead donation process along with strengthening the availability of organs obtained by ethically legitimate donation and procurement practices. The principles adopted by the forum for discussion were the safeguarding the interests of dying patients overrides facilitating deceased donation for transplantation; task restricted to a scientific, medical, and biological basis for death determination; the principle of the “dead donor rule” applied to deceased donation practices; use of available best scientific and medical evidence for decisions; guidelines and recommendations must have utility, applicability, and be workable in a wide range of global health care practice settings. The key issues of the forum considered death as a biological event with a focus on the physiological aspect of the dying process and death determination and respectfully recognized the impact of attending religious, ethical, legal, spiritual, philosophical, and cultural aspects of death [1].
Forum outcome of the review developed some
The forum came to a consensus on an operational (practical and concrete) definition of human death based on measurable and observable biomedical standards that “Death occurs when there is permanent loss of capacity for consciousness and irreversible loss of all brainstem functions.” This might result from permanent stoppage of circulation and/or after catastrophic brain injury. The “permanent” refers to loss of function that cannot resume automatically and will not be returned through intervention. Death is a single phenomenon founded on stoppage of brain function (loss of capacity for consciousness and brainstem reflexes) with two mechanisms to reach that point: permanent absence of circulation or subsequent to a catastrophic brain injury—two entrances, one exit. It is understood that the overwhelming majority of death determination in the world occurs after the stoppage of circulation and usually occurs external to health care settings. In some regions, the dead donation practices include re-establishing circulation (CPR, extracorporeal organ support) following death for the preservation of organs. Future research will enrich this issue for the clarity that constitutes re-establishing circulation, physiologically meaningful circulation, circulation versus oxygenation, and distinctions between organ targeted, regional, and whole-body circulation [1, 64].
During the 50 years since the publication of reports on the determination of death by neurologic criteria by Harvard University and the WMA (Sydney declaration) in 1968, brain death/death on neurological criteria (BD/DNC) protocols have been developed in many countries around the world. However, some countries still do not have medical standards for BD/DNC, and there is also international and intranational variability between the protocols that do exist [65, 66, 67, 68].
Discrepancies were noted in the studies by Wijdicks, Wahlster et al., and Chua et al. between protocols in this region in the criteria used for diagnosis of BD/DNC. Nonetheless, these studies were all limited reviews, though they addressed a number of examiners, observation time, the time between examinations, concordance/discordance with AAN—brain death/death by neurological criteria practice parameters, target value and methods of apnea testing, and requirement for ancillary testing. They did not explore the more distinct aspects of BD/DNC protocols, such as the technique used to rule out the effect of drugs on the evaluation, minimum temperature and blood pressure for an evaluation to be performed, a technique used to assess each component of the examination and findings of BD/DNC, preparation for rationale to discard apnea testing, accepted ancillary tests, need for communication with a person’s family, time of death, and stopping of organ support [68]. The existence of a protocol in a given country is dependent on acceptance of BD/DNC as death, access to resources (neurosciences/critical care experts), the presence of a transplant network, and local laws. Religious beliefs markedly influence the acceptance of BD/DNC as death. Although religious views in these countries are distinct from those in the rest of the world, the diversity of political, economic, legal, social, and religious climates throughout the region mirrors that globally [65, 66, 67, 68].
A review by Lewisa et al. in 2020 was published in a clinical neurology journal to find out the similarities and differences in the official protocols for the determination of death in Asia Pacific countries (57 of 197 UN) and concluded that protocols for conducting a BD/DNC determination vary markedly. In their report, only 24 of the 37 countries had brain death protocols (69%), but vary in definition such as whole-brain death and brain stem death; a number of examinations vary from single to double, separated by 6–48 hours; and the prerequisites, clinical examination, apnea testing procedure, and indications for/selection of ancillary tests varied. But agreed on that the damage to be irreversible or be permanent, all function/all activities are to be absent before declaring BD/DNC. Also, it is emphasized to harmonize protocols both within this region and worldwide [65, 66, 67, 68].
Traditionally, death occurs with the confirmation of irreversible cessation of cardiorespiratory function [3, 53, 54, 55, 56, 57, 58]. The use of artificial maintenance of life support and organ transplant leads to introduce a new criterion of death determination of permanently nonfunctioning brain, called irreversible coma equated to brain death. In recent years, however, controversy has arisen about the clinical and ethical validity of the neurological standard.
Source: Ref. [
AAN clinical criteria on the determination of brain death [53, 54, 55, 56] can be considered to consist of four steps: Prerequisites, Neurological assessment (coma, absence of brain stain reflex, apnea), Ancillary test, and Documentation.
Prerequisites for clinical criteria of brain death determination.
Establish permanent and predicted explanation of coma:
The explanation of coma is often establish by history, clinical examination, neuroimaging, and laboratory tests.
Rule out the existence of any CNS-depressant drug effect by history, drug screen, calculation of clearance; or, if available, drug plasma levels below the therapeutic range. Prior use of hypothermia (following CPR) may delay drug metabolism. The legitimate alcohol limit for driving (blood alcohol content 0.08%) is a practical threshold below which an examination to determine brain death could adequately proceed.
Should be no current administration or existence of neuromuscular blocking agents (train of four twitches with maximal ulnar nerve stimulation).
Should be no critical electrolyte, acid–base, or endocrine disorder (severe acidosis or laboratory values markedly deviated from the norm).
Ensure normal core temperature.
Raise the body temperature and to sustain a normal or near-normal temperature (36°C) use a warming blanket. To prevent delaying an increase in PaCO2, normal or near-normal core temperature is preferred during the apnea test.
Ensure normal systolic blood pressure. Hypotension or hypovolemia should be corrected by vasopressors or vasopressin. Neurologic examination is commonly reliable with a systolic blood pressure ≥ 100 mm Hg.
Perform neurologic examination (one neurological examination is enough to declare brain death in the USA). A certain period of time has to be passed since the onset of the brain insult to rule out the possibility of recovery (usually several hours). However, some US state statutes require two examinations.
Legally, all physicians are authorized to determine brain death in the USA. Neurologists, neurosurgeons, and intensive care specialists may have specialized expertise. It appears rational that all physicians making a determination of brain death be absolutely familiar with brain death criteria and have demonstrated competence in this complex examination.
Neurological assessment for clinical criteria for brain death determination.
Coma:
Profound loss of consciousness with no response to any stimuli. No evidence of responsiveness. No motor response on noxious stimuli other than spinally mediated reflexes.
Absence of brainstem reflexes:
Lack of pupillary response to bright light is produced in both eyes. Usually, pupils are fixed in a midsize or dilated position (4–9 mm). Constricted pupils signify the possibility of drug intoxication. A magnifying glass can be used in doubtful cases.
Oculocephalic testing and oculovestibular reflex testing: Absence of ocular movements. Once the integrity of the cervical spine is ensured, the head is briskly rotated horizontally and vertically. No movement of the eyes relative to head movement. The oculovestibular reflex is tested by irrigating each ear with ice water after the patency of the external auditory canal is confirmed. The head is elevated to 30°. Each external auditory canal is irrigated (one ear at a time) with approximately 50 ml of ice water. Eye movement was absent during 1 minute of observation. Both sides are tested, with an interval of several minutes.
Absence of corneal reflex: Touching the cornea with a piece of tissue paper, a cotton swab, or squirts of water, no eyelid movement will be demonstrated.
Absence of facial muscle movement to a noxious stimulus: Deep pressure on the supraorbital ridge and the condyles at temporomandibular joints produce no grimacing or facial muscle movement.
Lack of pharyngeal and tracheal reflexes. This reflex is tested after stimulation of the posterior pharynx with a tongue blade or suction device. The tracheal reflex is most reliably tested by examining the cough response to tracheal suctioning.
Apnea test:
Absence of a breathing drive is tested with a CO2 challenge. Usually, a rise in PaCO2 above normal levels is the typical practice but requires preparation before the test.
Prerequisites for apnea test: (1) Normotension, (2) Normothermia, (3) Euvolemia, (4) Eucapnia (PaCO2 35–45 mm Hg), (5) Lack of hypoxia, and (6) No prior evidence of CO2 retention (COPD, excessive obesity).
Procedure:
Ensure a systolic blood pressure ≥ 100 mm Hg, if needed by vasopressors.
It is mandatory to pre-oxygenate with 100% oxygen for at least 10 minutes to a PaO2 > 200 mm Hg.
Diminish frequency of ventilation to 10 breaths per minute to eucapnia.
Diminish positive end-expiratory pressure (PEEP) to 5 cm H2O (oxygen desaturation with decreasing PEEP suggest problems with apnea testing).
If pulse oximetry oxygen saturation persists >95%, obtain a baseline blood gas.
Detach the patient from the ventilator.
Maintain oxygenation (deliver 100% O2 at 6 L/min by endotracheal tube).
Observe closely for 8–10 minutes for respiratory movements. Respiration may be abdominal or may include a brief gasp.
Exclude if systolic blood pressure decreases to <90 mm Hg.
Exclude if oxygen saturation measured by pulse oximetry is <85% for 30 seconds.
If the respiratory drive is absent, repeat blood gas (PaO2, PaCO2, pH, bicarbonate, base excess) after approx. 8 minutes.
The apnea test is positive if respiratory movements are absent and arterial PCO2 is ≥60 mm Hg (supports the clinical diagnosis of brain death).
If the test is inconclusive but the patient is hemodynamically stable during the procedure, the test could be repeated for a longer period of time (10–15 minutes) after the patient is again adequately pre-oxygenated.
Supportive tests to diagnose brain death.
The ancillary tests such as EEG, cerebral angiography, nuclear scan, TCD, CTA, and MRI/MRA are at present used for adults in clinical practice. Three tests may be preferred such as EEG, nuclear scan, or cerebral angiogram, as the most hospital has the logistic to perform and interpret. The supportive tests can be done when there is no scope for apnea test or uncertainty exists. The ancillary tests are usually practiced to shorten the duration of the observation period. The interpretation of each of these tests requires expertise. In adults, ancillary tests are not needed for the clinical diagnosis of brain death and cannot replace a neurologic examination.
Documentation of the time of death.
The moment of brain death must be documented in medical records and is the time the arterial PCO2 reached the target value. But in patients where the apnea test is discarded, the time of death is when the ancillary test has been officially interpreted. A checklist is filled out, signed, and dated.
For the millennia, the human has fought with the concept and criteria of and the line between life and death continues to be debated. The profound changes caused by life-sustaining technology and transplantation continue to challenge our notions of life and death. The cardiopulmonary approach is an age-old practice for the determination of death that ensures social acceptance without any debate. The public is also used to rely on the somatic standard for criteria of death such as cooling of the body, absence of breath, loss of consciousness, rigor mortis, putrefaction, and so on.
Despite scientific progress in the last few decades, there remain big variations in the diagnosis criteria applied in each country with legal regulations resulting in misunderstandings among the public and health care professionals. However, the Harvard committee in 1968 develops a set of criteria of the permanently nonfunctioning brain, called irreversible coma equated to brain death. On the same date, the WMA declared a guideline for the determination of death known as the
The global philosophical, ethical, legal, and biomedical controversies of determining death due to life support, organ supports, and organ transplantation issues console us in the historic report published (1981) by President commission for the study of ethical problems in medicine and behavioral research,
WHO in 2014 published clinical criteria on the determination of death, mentioning various ways to determine death but there is only one way of being dead, so the two classic algorithms of brain death and circulatory death merge into a single endpoint identified as death and should not imply that brain death and circulatory death are two distinct phenomena [3]. They prepare a workable flowchart of cardiocirculatory algorithm and neurological algorithm to declare death. That guideline provides a minimum determination of death criteria to be acceptable for medical practice worldwide to achieve international consensus on clinical criteria to maintain public trust and promote ethical practices that respect fundamental rights of people and minimize philosophical, ethical, and biomedical debate in the human death. The WHO clinical criteria of 2014 did not mention the detail of clinical examination. Harvard report describes the clinical criteria and AAN guidelines on clinical criteria already accepted globally.
American Association of Neurology (AAN) in 2019 validated that brain death is the irreversible loss of all functions of the entire brain and is also equivalent to circulatory death. The testing methods of brain death take into account the age-related anatomical and physiological differences between neonates, infants, and children. Parents and other family members of children undergoing brain death testing may require close attention and additional support [58, 59].
International Guidelines for the Determination of Death—Phase I. Montreal Forum Report; 2012. Available from: http://www.who.int/patientsafety/montreal-forum-report.pdf
Clinical Criteria for the Determination of Death. Geneva: World Health Organization; 2017. Licence: CC BY-NC-SA 3.0 IGO
Controversies in the Determination of death: A white paper by the President Council on Bioethics (2008). Available from: http://hdl.handle.net/10822/559343
Evidence-based guideline update: Determining brain death in adults (Report of the Quality Standards Subcommittee of the American Academy of Neurology). Neurology 2010;74(23):1911–1918. DOI:10.1212/WNL.0b013e3181e242a8
All praise to Almighty to bless me with good health to complete this chapter. Acknowledge to all staff of the Forensic Medicine department of IMC and my family member for their sincere cooperation. Special thanks to Prof. Sharfuddin Ahmed, VC of BSMMU for encouraging me to complete. Also thanks to Dr. Ferdausi Rahman for her review of some portion of scripts.
The authors declare no conflict of interest.
Prof. Md Shah Alam developed the conception and design of the article and drafted the manuscript, providing important intellectual content.
Not applicable.
AAN | American Association of Neurology |
BD | brain death |
CNS | central nervous system |
CTA | computed tomography angiography |
CDD | controlled death donor |
COPD | chronic obstructive pulmonary disease |
DDR | death donor rule |
MRA | magnetic resonance angiogram |
PVS | persistent vegetative state |
TCD | transcranial Doppler |
CCA | cerebral circulatory arrest |
BSMMU | Bangabandhu Sheikh Mujib Medical University, Bangladesh |
DNC | death on neurological criteria |
UDDA | unifying determination of death act |
WHO | World Health Organization |
WMA | World Medical Association/World Medical Assembly |
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The direct problem of reflection and transmission of acoustic waves by a slab of porous material is studied. The inverse problem is solved using experimental reflected and transmitted signals. Both high- and low-frequency domains are studied. Different acoustic methods are proposed for measuring physical parameters describing the acoustic propagation as porosity, tortuosity, viscous and thermal characteristic length, and flow resistivity. Some advantages and perspectives of this method are discussed.",book:{id:"5708",slug:"computational-and-experimental-studies-of-acoustic-waves",title:"Computational and Experimental Studies of Acoustic Waves",fullTitle:"Computational and Experimental Studies of Acoustic Waves"},signatures:"Zine El Abiddine Fellah, Mohamed Fellah, Claude Depollier, Erick\nOgam and Farid G. Mitri",authors:[{id:"143693",title:"Dr.",name:"Zine El Abiddine",middleName:null,surname:"Fellah",slug:"zine-el-abiddine-fellah",fullName:"Zine El Abiddine Fellah"},{id:"144519",title:"Prof.",name:"Claude",middleName:null,surname:"Depollier",slug:"claude-depollier",fullName:"Claude Depollier"},{id:"178778",title:"Prof.",name:"Mohamed",middleName:null,surname:"Fellah",slug:"mohamed-fellah",fullName:"Mohamed Fellah"},{id:"209074",title:"Dr.",name:"Erick",middleName:null,surname:"Ogam",slug:"erick-ogam",fullName:"Erick Ogam"},{id:"227468",title:"Dr.",name:"Farid G",middleName:null,surname:"Mitri",slug:"farid-g-mitri",fullName:"Farid G Mitri"}]},{id:"56872",doi:"10.5772/intechopen.70590",title:"Acoustic Wave Monitoring of Fluid Dynamics in the Rock Massif with Anomaly Density, Stressed and Plastic Hierarchic Inclusions",slug:"acoustic-wave-monitoring-of-fluid-dynamics-in-the-rock-massif-with-anomaly-density-stressed-and-plas",totalDownloads:1110,totalCrossrefCites:1,totalDimensionsCites:5,abstract:"The geological environment is an open system, on which external and internal factors act. They lead it to an unstable state, which, as a rule, manifests itself locally in the form of zones, called dynamically active elements, which are indicators of potential catastrophic sources. These objects differ from the host geological environment by structural forms, which are often forming of a hierarchical type. The process of their activation can be observed using monitoring with wave fields, for mathematical support of which new modeling algorithms have been developed using the method of integral and integral-differential equations. A new approach to the interpretation of wave fields has been developed, to determine contours or surfaces of locally stressed hierarchical objects. An iterative process of solving the theoretical inverse problem for the case of determining configurations of 2D hierarchical inclusions of the k-th rank is developed. When interpreting monitoring results, it is necessary to use data from such monitoring systems that are tuned to study the hierarchical structure of the environment.",book:{id:"5708",slug:"computational-and-experimental-studies-of-acoustic-waves",title:"Computational and Experimental Studies of Acoustic Waves",fullTitle:"Computational and Experimental Studies of Acoustic Waves"},signatures:"Olga Hachay and Andrey Khachay",authors:[{id:"150801",title:"Prof.",name:"Olga",middleName:"Alexandrovna",surname:"Hachay",slug:"olga-hachay",fullName:"Olga Hachay"},{id:"219182",title:"MSc.",name:"Andrey",middleName:null,surname:"Khachay",slug:"andrey-khachay",fullName:"Andrey Khachay"}]},{id:"57258",doi:"10.5772/intechopen.71203",title:"Sound Waves in Complex (Dusty) Plasmas",slug:"sound-waves-in-complex-dusty-plasmas",totalDownloads:1398,totalCrossrefCites:5,totalDimensionsCites:5,abstract:"Wave properties of strongly coupled complex dusty (SCCD) plasmas evaluated using the equilibrium molecular dynamics (EMD) simulation technique. In this work, the plasma normalized longitudinal current correlation function CL(k,t) and transverse current CT(k,t) are calculated for a large range of plasma parameters of Coulomb coupling parameter (Γ) and screening strength (κ) with varying wave’s number (k). In EMD simulations, we have analysed different modes of wave propagation in SCCD plasmas with increasing and decreasing sequences of different combinations of plasmas parameters (κ, Γ) at varying simulation time step (Δt). Our simulation results show that the fluctuation of waves increases with an increase of Γ and decreases with increasing κ. Additional test shows that the presented results for waves are slightly dependent on number of particles (N). The amplitude and time period of CL(k,t) and CT(k,t) also depend on different influenced parameters of κ, Γ, k and N. The new results obtained through the presented EMD method for complex dusty plasma discussed and compared with earlier simulation results based on different numerical methods. It is demonstrated that the presented model is the best tool for estimating the behaviour of waves in strongly coupled complex system (dusty plasmas) over a suitable range of parameters.",book:{id:"5708",slug:"computational-and-experimental-studies-of-acoustic-waves",title:"Computational and Experimental Studies of Acoustic Waves",fullTitle:"Computational and Experimental Studies of Acoustic Waves"},signatures:"Aamir Shahzad, Muhammad Asif Shakoori, Maogang He and Sajid\nBashir",authors:[{id:"288354",title:"Dr.",name:"Aamir",middleName:null,surname:"Shahzad",slug:"aamir-shahzad",fullName:"Aamir Shahzad"}]},{id:"57674",doi:"10.5772/intechopen.71647",title:"Optimized Finite Difference Methods for Seismic Acoustic Wave Modeling",slug:"optimized-finite-difference-methods-for-seismic-acoustic-wave-modeling",totalDownloads:1526,totalCrossrefCites:1,totalDimensionsCites:3,abstract:"The finite difference (FD) methods are widely used for approximating the partial derivatives in the acoustic/elastic wave equation. Grid dispersion is one of the key numerical problems and will directly influence the accuracy of the result because of the discretization of the partial derivatives in the wave equation. Therefore, it is of great importance to suppress the grid dispersion by optimizing the FD coefficient. Various optimized methods are introduced in this chapter to determine the FD coefficient. Usually, the identical staggered grid finite difference operator is used for all of the first-order spatial derivatives in the first-order wave equation. In this chapter, we introduce a new staggered grid FD scheme which can improve the efficiency while still preserving high accuracy for the first-order acoustic/elastic wave equation modeling. It uses different staggered grid FD operators for different spatial derivatives in the first-order wave equation. The staggered grid FD coefficients of the new FD scheme can be obtained with a linear method. At last, numerical experiments were done to demonstrate the effectiveness of the introduced method.",book:{id:"5708",slug:"computational-and-experimental-studies-of-acoustic-waves",title:"Computational and Experimental Studies of Acoustic Waves",fullTitle:"Computational and Experimental Studies of Acoustic Waves"},signatures:"Yanfei Wang and Wenquan Liang",authors:[{id:"218676",title:"Prof.",name:"Yanfei",middleName:null,surname:"Wang",slug:"yanfei-wang",fullName:"Yanfei Wang"}]},{id:"66196",doi:"10.5772/intechopen.85275",title:"Analysis of Energy Relations between Noise and Vibration Produced by a Low-Field MRI Device",slug:"analysis-of-energy-relations-between-noise-and-vibration-produced-by-a-low-field-mri-device",totalDownloads:883,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Magnetic resonance imaging (MRI) tomography is often used for noninvasive scanning of various parts of a human body without undesirable effects present in X-ray computed tomography. In MRI devices, slices of a tested subject are selected in 3D coordinates by a system of gradient coils. The current flowing through these coils changes rapidly, which results in mechanical vibration. This vibration is significant also in the equipment working with a low magnetic field, and it causes image blurring of thin layer samples and acoustic noise significantly degrading a speech signal recorded simultaneously during MR scanning of the vocal tract. There are always negative physiological and psychological effects on a person exposed to vibration and acoustic noise. In order to minimize these negative impacts depending on intensity and time duration of exposition, we mapped relationship between energy of vibration and noise signals measured in the MRI scanning area and its vicinity.",book:{id:"7778",slug:"noise-and-vibration-control-from-theory-to-practice",title:"Noise and Vibration Control",fullTitle:"Noise and Vibration Control - From Theory to Practice"},signatures:"Jiří Přibil, Anna Přibilová and Ivan Frollo",authors:[{id:"34650",title:"Dr.",name:"Anna",middleName:null,surname:"Pribilova",slug:"anna-pribilova",fullName:"Anna Pribilova"},{id:"180699",title:"Dr.",name:"Jiri",middleName:null,surname:"Pribil",slug:"jiri-pribil",fullName:"Jiri Pribil"},{id:"180785",title:"Prof.",name:"Ivan",middleName:null,surname:"Frollo",slug:"ivan-frollo",fullName:"Ivan Frollo"}]}],mostDownloadedChaptersLast30Days:[{id:"65699",title:"How Do Acoustic Materials Work?",slug:"how-do-acoustic-materials-work-",totalDownloads:1668,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Acoustic quality of closed spaces is an increasing concern all around the world, since noise pollution is one of the main nowadays pollutants, but also one of the less considered when building designing and construction. In 2011, the World Health Organization stated that noise pollution should be treated as a public health concern: about 1 million years of human healthy life are lost yearly because of the environmental noise pollution, emphasizing on traffic noise in the cities. There are some physics phenomena that are the rule of thumb for room acoustic projects. This chapter introduces the main concepts about them: sound absorption, insulation, and diffusion. Their principles, main implementation, and computing are presented for each one.",book:{id:"7364",slug:"acoustics-of-materials",title:"Acoustics of Materials",fullTitle:"Acoustics of Materials"},signatures:"Alice Elizabeth González",authors:[{id:"64836",title:"Prof.",name:"Alice Elizabeth",middleName:null,surname:"Gonzalez",slug:"alice-elizabeth-gonzalez",fullName:"Alice Elizabeth Gonzalez"}]},{id:"65785",title:"Acoustics from Interior Designer Perspective",slug:"acoustics-from-interior-designer-perspective",totalDownloads:1749,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Should we consider the acoustics as engineering science or as architectural elements or as interior design applications? The main purpose of this chapter will focus on the differences between the three aspects of the acoustics with a special focus on the interior acoustical design. The arguments that favor the acoustic in each field are many. This chapter will clarify, strengthen, and explore the importance that has the acoustic study for the interior designing layout. From the historical eras where only material schemes were used, the acoustical treatment reached a great achievement. Nowadays, electrical, acoustical devices took place in different situations where only the materials could solve the acoustic needs. The considerations of using the electrical-acoustical devices remain under request, while their usage, only in specific conditions, a topic to highlight in this chapter.",book:{id:"7364",slug:"acoustics-of-materials",title:"Acoustics of Materials",fullTitle:"Acoustics of Materials"},signatures:"Naglaa Sami AbdelAziz Mahmoud",authors:[{id:"199698",title:"Dr.",name:"Naglaa",middleName:null,surname:"Sami AbdelAziz",slug:"naglaa-sami-abdelaziz",fullName:"Naglaa Sami AbdelAziz"}]},{id:"66196",title:"Analysis of Energy Relations between Noise and Vibration Produced by a Low-Field MRI Device",slug:"analysis-of-energy-relations-between-noise-and-vibration-produced-by-a-low-field-mri-device",totalDownloads:883,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Magnetic resonance imaging (MRI) tomography is often used for noninvasive scanning of various parts of a human body without undesirable effects present in X-ray computed tomography. In MRI devices, slices of a tested subject are selected in 3D coordinates by a system of gradient coils. The current flowing through these coils changes rapidly, which results in mechanical vibration. This vibration is significant also in the equipment working with a low magnetic field, and it causes image blurring of thin layer samples and acoustic noise significantly degrading a speech signal recorded simultaneously during MR scanning of the vocal tract. There are always negative physiological and psychological effects on a person exposed to vibration and acoustic noise. In order to minimize these negative impacts depending on intensity and time duration of exposition, we mapped relationship between energy of vibration and noise signals measured in the MRI scanning area and its vicinity.",book:{id:"7778",slug:"noise-and-vibration-control-from-theory-to-practice",title:"Noise and Vibration Control",fullTitle:"Noise and Vibration Control - From Theory to Practice"},signatures:"Jiří Přibil, Anna Přibilová and Ivan Frollo",authors:[{id:"34650",title:"Dr.",name:"Anna",middleName:null,surname:"Pribilova",slug:"anna-pribilova",fullName:"Anna Pribilova"},{id:"180699",title:"Dr.",name:"Jiri",middleName:null,surname:"Pribil",slug:"jiri-pribil",fullName:"Jiri Pribil"},{id:"180785",title:"Prof.",name:"Ivan",middleName:null,surname:"Frollo",slug:"ivan-frollo",fullName:"Ivan Frollo"}]},{id:"67498",title:"Ultrasonic Vibration-Assisted Hot Glass Embossing Process",slug:"ultrasonic-vibration-assisted-hot-glass-embossing-process",totalDownloads:1002,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"This chapter is intended to provide the reader with background information about the assistance of ultrasonic vibration in hot glass embossing process. For this purpose, the description of the conventional hot glass embossing process and the ultrasonic vibration-assisted hot glass embossing process will be defined first. Based on the comparison between these two processes, components of the ultrasonic vibration device which produces ultrasonic vibration will be discussed in principle. Among these components, ultrasonic horn will be especially analyzed. After that, each interesting effect of ultrasonic vibration on hot glass embossing process will be explained in detail. With the development and application of simulation tools on forming process, this chapter will finally describe some results of finite element analysis (FEA) of ultrasonic vibration-assisted hot glass embossing process.",book:{id:"7778",slug:"noise-and-vibration-control-from-theory-to-practice",title:"Noise and Vibration Control",fullTitle:"Noise and Vibration Control - From Theory to Practice"},signatures:"Lanphuong Nguyen",authors:[{id:"290694",title:"Dr.",name:"Lanphuong",middleName:null,surname:"Nguyen",slug:"lanphuong-nguyen",fullName:"Lanphuong Nguyen"}]},{id:"58101",title:"Wave Propagation in Porous Materials",slug:"wave-propagation-in-porous-materials",totalDownloads:1554,totalCrossrefCites:1,totalDimensionsCites:5,abstract:"This chapter provides different models for the acoustic wave propagation in porous materials having a rigid and an elastic frames. The direct problem of reflection and transmission of acoustic waves by a slab of porous material is studied. 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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:null},{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. 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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. 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