Summary of the major aflatoxins produced by the
\\n\\n
These books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\\n\\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\\n\\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
\\n\\n\\n\\n\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
IntechOpen and Knowledge Unlatched formed a partnership to support researchers working in engineering sciences by enabling an easier approach to publishing Open Access content. Using the Knowledge Unlatched crowdfunding model to raise the publishing costs through libraries around the world, Open Access Publishing Fee (OAPF) was not required from the authors.
\n\nInitially, the partnership supported engineering research, but it soon grew to include physical and life sciences, attracting more researchers to the advantages of Open Access publishing.
\n\n\n\nThese books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\n\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\n\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
\n\n\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:"6237",leadTitle:null,fullTitle:"GABA And Glutamate - New Developments In Neurotransmission Research",title:"GABA And Glutamate",subtitle:"New Developments In Neurotransmission Research",reviewType:"peer-reviewed",abstract:"This book collates the contributions of a selected number of neuroscientists that are interested in the molecular, preclinical, and clinical aspects of neurotransmission research. The seven chapters in this book address the latest research/review data related to GABA/glutamate system's organization and function, the structure of receptors, subtypes and their ligands, as well as the translational approach and clinical implications. The book offers readers a rich collection of data regarding current and future applications of GABA and glutamate neurotransmission, including promising research strategies and potential clinical benefits.",isbn:"978-953-51-3822-8",printIsbn:"978-953-51-3821-1",pdfIsbn:"978-953-51-4069-6",doi:"10.5772/intechopen.68762",price:119,priceEur:129,priceUsd:155,slug:"gaba-and-glutamate-new-developments-in-neurotransmission-research",numberOfPages:138,isOpenForSubmission:!1,isInWos:1,isInBkci:!1,hash:"9883dc7bb642e8ae919261b2519547ba",bookSignature:"Janko Samardzic",publishedDate:"March 21st 2018",coverURL:"https://cdn.intechopen.com/books/images_new/6237.jpg",numberOfDownloads:12308,numberOfWosCitations:19,numberOfCrossrefCitations:13,numberOfCrossrefCitationsByBook:0,numberOfDimensionsCitations:37,numberOfDimensionsCitationsByBook:1,hasAltmetrics:1,numberOfTotalCitations:69,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 26th 2017",dateEndSecondStepPublish:"May 17th 2017",dateEndThirdStepPublish:"October 29th 2017",dateEndFourthStepPublish:"November 29th 2017",dateEndFifthStepPublish:"January 29th 2018",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"188756",title:"Dr.",name:"Janko",middleName:null,surname:"Samardzic",slug:"janko-samardzic",fullName:"Janko Samardzic",profilePictureURL:"https://mts.intechopen.com/storage/users/188756/images/4710_n.jpg",biography:"Dr. Janko Samardzic is an Assistant Professor and researcher at the Medical Faculty, University of Belgrade. He holds PhD in Medical Pharmacology and has extensive experience and expertise in Basic and Applied Neuroscience. Dr. Samardzic completed his postdoctoral studies at the University KU Leuven in Belgium and postgraduate specialty courses at the Erasmus University Medical Center Rotterdam. Currently, he also holds the position of Visiting Fellow at the University Children\\'s Hospital Basel, Switzerland. Dr. Samardzic is a member of European Colleague of Neuropsychopharmacology, Austrian Pharmacological Society, Swiss Society for Clinical Pharmacology and Toxicology and Serbian Pharmacological Society. He is the author of a large number of peer reviewed papers and the regular speaker at the international scientific conferences. Janko is looking forward to continue juggling between the Serbia and Switzerland.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of Belgrade",institutionURL:null,country:{name:"Serbia"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"212",title:"Molecular Neuroscience",slug:"molecular-neuroscience"}],chapters:[{id:"59071",title:"Introductory Chapter: GABA/Glutamate Balance: A Key for Normal Brain Functioning",doi:"10.5772/intechopen.74023",slug:"introductory-chapter-gaba-glutamate-balance-a-key-for-normal-brain-functioning",totalDownloads:1614,totalCrossrefCites:5,totalDimensionsCites:12,hasAltmetrics:0,abstract:null,signatures:"Janko Samardzic, Dragana Jadzic, Boris Hencic, Jasna Jancic and\nDubravka Svob Strac",downloadPdfUrl:"/chapter/pdf-download/59071",previewPdfUrl:"/chapter/pdf-preview/59071",authors:[{id:"188756",title:"Dr.",name:"Janko",surname:"Samardzic",slug:"janko-samardzic",fullName:"Janko Samardzic"},{id:"398264",title:"Dr.",name:"Dragana",surname:"Jadzic",slug:"dragana-jadzic",fullName:"Dragana Jadzic"},{id:"398265",title:"Dr.",name:"Boris",surname:"Hencic",slug:"boris-hencic",fullName:"Boris Hencic"},{id:"398266",title:"Dr.",name:"Jasna",surname:"Jancic",slug:"jasna-jancic",fullName:"Jasna Jancic"},{id:"398267",title:"Dr.",name:"Dubravka Svob",surname:"Strac",slug:"dubravka-svob-strac",fullName:"Dubravka Svob Strac"}],corrections:null},{id:"58028",title:"Early Life Experience, Maternal Separation, and Involvement of GABA and Glutamate Transporters",doi:"10.5772/intechopen.70868",slug:"early-life-experience-maternal-separation-and-involvement-of-gaba-and-glutamate-transporters",totalDownloads:1143,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"The physiological response initiates with activation of the hypothalamic-pituitary-adrenal axis, the autonomic nervous, and the immune systems. All actions promoted cellular adaptive changes in cells and tissues that protect the body and promote their survival. Diverse protocols of maternal separation (MS) in rodents presented alterations in central nervous system (CNS) such as learning disabilities, voluntary alcohol intake, and neurochemical changes. It is believed that the properties of these early life procedures are mediated by the high plasticity of the developing CNS. During critical development stage, brain regions, mainly those related to aggressive conditions, can have advancement abnormalities occasionally irreversible and thus adjust emotional processing when they grow to be adults. Early postnatal period and relationship between mother and infant are essential of normal stress response and emotional behavior. Probably, it involves the activation of intracellular signaling pathways, genome adaptations, adjusts in gene expression, and neural action. The objective of this article is to provide an overview of the current state of knowledge in the field focused on the maternal separation model, early life experience of postnatal stress, and the involvement of γ-aminobutyric acid (GABA) and glutamate transporters.",signatures:"Gabriela Beatriz Acosta",downloadPdfUrl:"/chapter/pdf-download/58028",previewPdfUrl:"/chapter/pdf-preview/58028",authors:[{id:"111733",title:"Dr.",name:"Gabriela",surname:"Acosta",slug:"gabriela-acosta",fullName:"Gabriela Acosta"}],corrections:null},{id:"58809",title:"Notch Signaling in the Astroglial Phenotype: Relevance to Glutamatergic Transmission",doi:"10.5772/intechopen.73318",slug:"notch-signaling-in-the-astroglial-phenotype-relevance-to-glutamatergic-transmission",totalDownloads:1376,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Glutamate (Glu), the major excitatory neurotransmitter, elicits its action through the activation of membrane receptors and transporters expressed in neurons and glial cells. Glial glutamate transporters, EAAT1 and EAAT2, remove this transmitter from the synaptic cleft preventing an excitotoxic insult. The Notch pathway is a signaling system involved in neuro- and gliogenesis. Radial glia (RG) generates neurons, oligodendrocytes, and astrocytes in a spatial and temporal pattern, in which Notch represses neurogenesis, maintaining the self-renewal potential of RG. Astrogenesis depends on several stimuli, Notch being a master regulator of the differentiation process. The cAMP-PKA-CREB signaling cascade cross talks with the Notch pathway, acting synergistically by reducing progenitor markers and inducing astrocytic differentiation. Notch1 mRNA is upregulated in a PKA/γ-secretase/NICD/CSL-dependent manner, suggesting a feedback loop to keep Notch active until astrocytic differentiation is complete. Glial differentiation is also modulated by PKC, which acts over NICD. In RG cells and astrocytes enwrapping glutamatergic synapses, EAAT1 transcriptional regulation is mediated by PKC, increasing Notch expression and its receptor intracellular traffic. It is clear that Notch represents an activity-dependent molecular key in RG cells that enable them to shape glutamatergic transmission through the expression of genes involved in glial/neuronal interactions.",signatures:"López-Bayghen Esther, Angulo-Rojo Carla, López-Bayghen Bruno,\nHernández-Melchor Dinorah, Ramírez Leticia and Ortega Arturo",downloadPdfUrl:"/chapter/pdf-download/58809",previewPdfUrl:"/chapter/pdf-preview/58809",authors:[{id:"40836",title:"Prof.",name:"Esther",surname:"Lopez-Bayghen",slug:"esther-lopez-bayghen",fullName:"Esther Lopez-Bayghen"},{id:"208829",title:"Prof.",name:"Arturo",surname:"Ortega",slug:"arturo-ortega",fullName:"Arturo Ortega"},{id:"237405",title:"Prof.",name:"Carla",surname:"Angulo-Rojo",slug:"carla-angulo-rojo",fullName:"Carla Angulo-Rojo"},{id:"237406",title:"BSc.",name:"Dinorah",surname:"Hernandez-Melchor",slug:"dinorah-hernandez-melchor",fullName:"Dinorah Hernandez-Melchor"},{id:"237407",title:"BSc.",name:"Bruno",surname:"Lopez-Bayghen",slug:"bruno-lopez-bayghen",fullName:"Bruno Lopez-Bayghen"},{id:"237411",title:"Dr.",name:"Leticia",surname:"Ramirez",slug:"leticia-ramirez",fullName:"Leticia Ramirez"}],corrections:null},{id:"57935",title:"Pharmacological Studies with Specific Agonist and Antagonist of Animal iGluR on Root Growth in Arabidopsis thaliana",doi:"10.5772/intechopen.72121",slug:"pharmacological-studies-with-specific-agonist-and-antagonist-of-animal-iglur-on-root-growth-in-arabi",totalDownloads:1154,totalCrossrefCites:4,totalDimensionsCites:7,hasAltmetrics:0,abstract:"Ionotropic glutamate receptors (iGluRs) are a group of proteins with a high degree of sequence homology. At least 20 type of putative ionotropic glutamate receptor (iGluR)-like channels have been identified in Arabidopsis thaliana. To uncover the role of iGluR-like channels in plant root growth, we used a comprehensive set of compounds known to alter iGluR channels in the neurons. We found that Arabidopsis root system is highly sensitive to these compounds. iGluR competitive antagonists 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitroquinoxaline-2,3-dione acted (DNQX) acts as a negative regulator of primary root and lateral root density. Continuous growth on antagonist also leads to impairment of root meristem size, which suggests that iGluR-like channels may play a role in meristem maintenance. However, application of iGluR agonists L-glutamate recovered Arabidopsis root growth. Taken together, these results suggest a correlation between the putative iGluR-like channel function and the alteration of root growth and development in the Arabidopsis roots.",signatures:"Shashi Kant Singh and Ing-Feng Chang",downloadPdfUrl:"/chapter/pdf-download/57935",previewPdfUrl:"/chapter/pdf-preview/57935",authors:[{id:"56567",title:"Prof.",name:"Ing-Feng",surname:"Chang",slug:"ing-feng-chang",fullName:"Ing-Feng Chang"},{id:"230147",title:"Dr.",name:"Shashi",surname:"Singh",slug:"shashi-singh",fullName:"Shashi Singh"}],corrections:null},{id:"57103",title:"GABA and Glutamate: Their Transmitter Role in the CNS and Pancreatic Islets",doi:"10.5772/intechopen.70958",slug:"gaba-and-glutamate-their-transmitter-role-in-the-cns-and-pancreatic-islets",totalDownloads:3477,totalCrossrefCites:3,totalDimensionsCites:9,hasAltmetrics:1,abstract:"Glutamate and gamma-aminobutyric acid (GABA) are the major neurotransmitters in the mammalian brain. Inhibitory GABA and excitatory glutamate work together to control many processes, including the brain’s overall level of excitation. The contributions of GABA and glutamate in extra-neuronal signaling are by far less widely recognized. In this chapter, we first discuss the role of both neurotransmitters during development, emphasizing the importance of the shift from excitatory to inhibitory GABAergic neurotransmission. The second part summarizes the biosynthesis and role of GABA and glutamate in neurotransmission in the mature brain, and major neurological disorders associated with glutamate and GABA receptors and GABA release mechanisms. The final part focuses on extra-neuronal glutamatergic and GABAergic signaling in pancreatic islets of Langerhans, and possible associations with type 1 diabetes mellitus.",signatures:"Christiane S. Hampe, Hiroshi Mitoma and Mario Manto",downloadPdfUrl:"/chapter/pdf-download/57103",previewPdfUrl:"/chapter/pdf-preview/57103",authors:[{id:"210220",title:"Prof.",name:"Christiane",surname:"Hampe",slug:"christiane-hampe",fullName:"Christiane Hampe"},{id:"210485",title:"Prof.",name:"Mario",surname:"Manto",slug:"mario-manto",fullName:"Mario Manto"},{id:"210486",title:"Prof.",name:"Hiroshi",surname:"Mitoma",slug:"hiroshi-mitoma",fullName:"Hiroshi Mitoma"}],corrections:null},{id:"58832",title:"Antagonists of Ionotropic Receptors for the Inhibitory Neurotransmitter GABA: Therapeutic Indications",doi:"10.5772/intechopen.72678",slug:"antagonists-of-ionotropic-receptors-for-the-inhibitory-neurotransmitter-gaba-therapeutic-indications",totalDownloads:1517,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,abstract:"Agents that antagonize the action of GABA on ionotropic receptors are widely used to probe the function of this neurotransmitter. Three such agents are in common use: bicuculline, gabazine, and picrotoxinin. These three agents produce convulsions on systemic administration but act in significantly different ways. Bicuculline is a competitive antagonist of GABAA receptors. Gabazine is also a competitive antagonist of GABAA receptors, interacting with different residues on the receptors. Picrotoxinin is a noncompetitive antagonist acting on the chloride channel of GABAA and several other ionotropic CYS-loop receptors including glycine, GABAC, and 5-HT3 receptors. Many other structurally diverse agents are now known to act as GABA receptor antagonists, providing opportunities for the discovery of agents with selectivity for the myriad of ionotropic GABA receptors. TPMPA is a selective antagonist for GABAC receptors, which are insensitive to bicuculline. Like TPMPA, many antagonists of ionotropic GABA receptors are not convulsants, indicating that there is still much to be learnt about GABA function in the brain from the study of such agents and their possible therapeutic uses. The most recently discovered GABAA receptor nonconvulsive antagonist is S44819, which is subtype selective for α5-containing receptors, and is arousing much interest in relation to cognition.",signatures:"Tina Hinton and Graham A. R. Johnston",downloadPdfUrl:"/chapter/pdf-download/58832",previewPdfUrl:"/chapter/pdf-preview/58832",authors:[{id:"199156",title:"Emeritus Prof.",name:"Graham",surname:"Johnston",slug:"graham-johnston",fullName:"Graham Johnston"},{id:"199160",title:"Dr.",name:"Tina",surname:"Hinton",slug:"tina-hinton",fullName:"Tina Hinton"}],corrections:null},{id:"58817",title:"Clinical Application of MR Spectroscopy in Identifying Biochemical Composition of the Intracranial Pathologies",doi:"10.5772/intechopen.71728",slug:"clinical-application-of-mr-spectroscopy-in-identifying-biochemical-composition-of-the-intracranial-p",totalDownloads:2028,totalCrossrefCites:0,totalDimensionsCites:5,hasAltmetrics:0,abstract:"Magnetic resonance spectroscopy (MRS) provides useful information regarding metabolic composition in the tissues, and advanced spectroscopic methods are used to quantify markers of tumor membrane turnover and proliferation (e.g., choline (Cho)), energy homoeostasis (e.g., creatine (Cr)), intact glioneuronal structures (e.g., N-acetylaspartate (NAA)), and necrosis (e.g., lactate (Lac) or lipids). Results are usually expressed as metabolite ratios rather than absolute metabolite concentrations. Because glial tumors have some specific metabolic characteristics that differ according to the grade of tumor, there is a potential for MR spectroscopy to increase the sensitivity of routinely used diagnostic imaging. MRS also has many diagnostic applications in neurosciences to support the diagnosis in conditions like demyelination, infections, and dementia and in postradiotherapy cases. Biochemical changes in the metabolism of tumor cells related to malignant transformation are reflected in changes of particular metabolite concentration in the tumor tissue. Our prospective study aimed to analyze the usefulness of proton MR spectroscopy in grading of glioma and to correlate various metabolite ratios like choline/creatine, choline/N-acetylaspartate, N-acetylaspartate/creatine, and lactate/creatine with the histopathological grades of glioma.",signatures:"B C Hamsini, Bhavana Nagabhushana Reddy, Sankar Neelakantan\nand Sunitha Palasamudram Kumaran",downloadPdfUrl:"/chapter/pdf-download/58817",previewPdfUrl:"/chapter/pdf-preview/58817",authors:[{id:"211054",title:"Dr.",name:"Sunitha",surname:"P Kumaran",slug:"sunitha-p-kumaran",fullName:"Sunitha P Kumaran"},{id:"221485",title:"Dr.",name:"Sankar",surname:"Neelakantan",slug:"sankar-neelakantan",fullName:"Sankar Neelakantan"},{id:"398223",title:"Dr.",name:"B C",surname:"Hamsini",slug:"b-c-hamsini",fullName:"B C Hamsini"},{id:"398224",title:"Dr.",name:"Bhavana",surname:"Nagabhushana Reddy",slug:"bhavana-nagabhushana-reddy",fullName:"Bhavana Nagabhushana Reddy"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"6998",title:"Synucleins",subtitle:"Biochemistry and Role in Diseases",isOpenForSubmission:!1,hash:"2b4b802fec508928ce8ab9deebd1375f",slug:"synucleins-biochemistry-and-role-in-diseases",bookSignature:"Andrei Surguchov",coverURL:"https://cdn.intechopen.com/books/images_new/6998.jpg",editedByType:"Edited by",editors:[{id:"266540",title:"Dr.",name:"Andrei",surname:"Surguchov",slug:"andrei-surguchov",fullName:"Andrei Surguchov"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6989",title:"Biogenic Amines in Neurotransmission and Human Disease",subtitle:null,isOpenForSubmission:!1,hash:"4c7e866a847bc30d77f37feccdf72dbf",slug:"biogenic-amines-in-neurotransmission-and-human-disease",bookSignature:"Ahmet Uçar",coverURL:"https://cdn.intechopen.com/books/images_new/6989.jpg",editedByType:"Edited by",editors:[{id:"205106",title:"Associate Prof.",name:"Ahmet",surname:"Uçar",slug:"ahmet-ucar",fullName:"Ahmet Uçar"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophile",surname:"Theophanides",slug:"theophile-theophanides",fullName:"Theophile Theophanides"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. 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\r\n\r\n\tThe chapters in this book will be organized into various topics with the intent of taking the readers on a journey of understanding of schizophrenia and its symptoms & diagnosis, epidemiology, mechanisms of actions, brain imaging, psychopharmacology, psycho-behavioral intervention, social inclusion, community care, social action, diversity & inclusion, novel therapeutics, and future direction. People with schizophrenia often face stigma in society, and this book intends to inform on improvement in diagnostics, management of clinical trajectories, and therapeutic intervention to provide the much need relief of help that is on the way.
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Aflatoxins are poisonous by-products from soil-borne fungus
\n\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
Difurocoumarocyclopentenone series | \n\t\t\t\t\t\tAflatoxin B1 (AFB1) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin B2 (AFB2) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin B2a (AFB2a) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin M1 (AFM1) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin M2 (AFM2) | \n\t\t\t\t\t\tMetabolite of aflatoxin B2 in milk of cattle fed on contaminated foods | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin M2A (AFM2A) | \n\t\t\t\t\t\tMetabolite of AFM2\n\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxicol (AFL) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxicol M1\n\t\t\t\t\t\t | \n\t\t\t\t\t\tMetabolite of AFM1\n\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t\t | \n\t\t\t\t\t\tAflatoxin G1 (AFG1) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin G2 (AFG2) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin G2A (AFG2A) | \n\t\t\t\t\t\tMetabolite of AFG2\n\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin GM1 (AFG1) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin GM2 (AFGM2) | \n\t\t\t\t\t\tMetabolite of AFG2\n\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | AFGM2A\n\t\t\t\t\t\t | \n\t\t\t\t\t\tMetabolite of AFGM2\n\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin B3 (AFB3) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Parasiticol (P) | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatrem | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aspertoxin | \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t | \n\t\t\t\t\t
\n\t\t\t\t\t\t | Aflatoxin Q1 (AFQ1) | \n\t\t\t\t\t\tMajor metabolite of AFB1 in in vitro liver preparations of other higher vertebrates | \n\t\t\t\t\t
Summary of the major aflatoxins produced by the
Aflatoxins are a group of approximately 20 related fungal metabolites produced primarily by the fungi
Structures of the major aflatoxins B1, B2, G1, G2, M1, M2, B2A and G2A (Adopted from Reddy, 2012)[
The four major naturally known aflatoxins produced by the
Aflatoxins are highly liposoluble compounds and are readily absorbed from the site of exposure usually through the gastrointestinal tract and respiratory tract into blood stream [22, 23]. Human and animals get exposed to aflatoxins by two major routes (a) direct ingestion of aflatoxin-contaminated foods or ingestion of aflatoxins carried over from feed into milk and milk products like cheese and powdered milk as well as other animal tissues mainly as AFM1 [22](b) by inhalation of dust particles of aflatoxins especially AFB1 in contaminated foods in industries and factories [24]. After entering the body, the aflatoxins are absorbed across the cell membranes where they reach the blood circulation. They are distributed in blood to different tissues and to the liver, the main organ of metabolism of xenobiotics. Aflatoxins are mainly metabolized by the liver to a reactive epoxide intermediate or hydroxylated to become the less harmful aflatoxin M1 [25, 26]. In humans and susceptible animal species, aflatoxins especially AFB1 are metabolized by cytochrome P450 (CYP450) microsomal enzymes to aflatoxin-8,9-epoxide, a reactive form that binds to DNA and to albumin in the blood serum, forming adducts and hence causing DNA damage [25, 26]. Various CYP450 enzymes isoforms occur in the liver and they metabolize aflatoxin into a reactive oxygen species (aflatoxin-8,9-epoxide), which may then bind to proteins and cause acute toxicity (aflatoxicosis) or to DNA and induce liver cancer [25, 26]. The predominant human CYP450 isoforms involved in human metabolism of AFB1 are CYP3A4 and CYP1A2. Both enzymes catalyze the biotransformation of AFB1 to the highly reactive
The epoxidation of AFB1 to the exo-8, 9-epoxide is a critical step in the genotoxic pathway of this carcinogen. The binding of AFB1 to DNA and DNA adduction by AFB1 exo-8,9 epoxide has been reported to cause a functional changes of DNA conformation [31].The epoxide is highly unstable and binds with high affinity to guanine bases in DNA to form afltoxin-N7-guanine [32]. The aflatoxin-N7-guanine has been shown to be capable of forming guanine (purine) to thymine (pyrimidine) transversion mutations in DNA and hence affecting the p53 suppressor gene in the cell cycle [33, 34]. The p53 gene is important in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. The mutations have been reported to affect some base pair locations more than others especially in the third base of codon 249 of the p53 gene in the region corresponding to the DNA binding domain of the corresponding protein [13, 34]and this appears to be more susceptible to aflatoxin-mediated mutations than nearby bases [35]. AFB1 induces the transversion of base G to base T in the third position of codon 249 and similar mutations have been observed in hepatocellular carcinoma (HCC) in high AFB1 contaminated food in regions in East Asia and Africa [34, 36, 37].
\n\t\t\tEpoxide hydrolase and glutathione-S-transferase (GST) are both involved in hepatic detoxification of activated AFB1, but the GST-catalyzed conjugation of glutathione to AFB1-8,9-epoxides is thought to play the most important role in preventing epoxide binding to target macromolecules like DNA and various cell proteins [38]. Glutathione pathway is reported to play a vital role in the detoxification of AFB1 [39, 40]. The AFB1 8,9
Aflatoxin disease pathways in humans (Adopted from Wu, 2010; Wu, 2011)[
Various check points that can be damaged by binding of aflatoxins and AF-8,9-epoxide causing the deregulation of the cell cycle; P –prophase, M-Metaphase, A- Anaphase, T- Telophase, S- Synthetic DNA phase, G1 and G2 – Gaps (growth phase) [
The reactive aflatoxin-8,9-epoxide preferentially binds to mitochondrial DNA (mitDNA) during hepatocarcinogenesis as compared to nuclear DNA that hinder ATP production and FAD/NAD-linked enzymatic functions and this causes the disruption of mitochondrial functions in the various parts of the body that require production of energy in the form of ATP [45]. Aflatoxin damage to mitochondria can lead to mitochondrial diseases and may be responsible for aging mechanisms [45]. It is reported that certain mitochondrial diseases result from the ability of the nucleus to detect energetic deficits in its area. The nucleus attempts to compensate for the ATP shortages by triggering the replication of any nearby mitochondria but unfortunately, the response promotes replication of the very mitochondria that are causing the local energy deficit hence aggravating the problem [46]. The AFB1 also binds to DNA and cause structural DNA alterations that lead to gene mutations as well as changes in the length of the telomeres and the check points in the cell cycle [47-49]. The binding of AFB1 to DNA at the guanine base in liver cells corrupt the genetic code that regulates cell growth, thereby leading to formation of tumors ([45-49]. The damage to mitDNA is caused by adduction and mutations of mitochondrial membranes leading to increased cell death (apoptosis) as well as disruption of energy production (production of ATP) [46, 49, 50]. The reactive aflatoxin-8, 9-epoxide can affect the mitotic (M) phase, growth process (G1 and G2 phase) and DNA synthesis (S phase) in the cell cycle by disrupting the various check points that regulate the cell cycle development and proliferation leading to deregulation of the cell and hence cancer development [47-49], (Figure 3).
\n\t\t\t\tHowever in resistant rodents, their mitDNA is protected from aflatoxins from DNA adducts that effect mitochondrial transcription and translation [46-49]. The mycotoxin alters energy-linked functions of ADP phosphorylation and FAD- and NAD-linked oxidizing substrates and α-ketoglutarate-succinate cytochrome reductases [46-49].
\n\t\t\tAFB causes ultrastuctural changes in mitochondria [46-49]and also induces mitochondrial directed apoptosis thus reducing their function [20, 29, 48-51]. Also the aflatoxins may affect the telomere length and the various check point in the cell cycle causing further damage to the regulatory processes of the cell cycle [51]. Also the extent of aflatoxin binding to DNA and its damage, the level of different proteins changes from cell cycle and apoptotic pathways such as c-Myc, p53, pRb, Ras, protein kinase A (PKA), protein kinase C (PKC), Bcl-2, NF-kB, CDK, cyclins and CKI contribute to the life or death decision making process that may contribute to the deregulation of the cell proliferation leading to cancer development [34, 48, 49](Figure 3).
\n\t\t\tHowever like in hepatic detoxification of aflatoxins and other chemicals, GSH act as antioxidant and has many functions in membrane maintenance and stability as well as in reducing oxidative stress factors and the high reactive oxygen species (ROS) produced from the process of lipid peroxidation [38-41, 46, 52-56]. The increased depletion of GSH leads to abnormally high levels of ROS found in cells affected by aflatoxin due to uncoupling of metabolic processes resulting from the lack of GSH for GSH-peroxidase catalysis of O2 to H2O2 leading to lipid peroxidation and compromised cell membranes. Its reduction further enhances the damage to critical cellular components (DNA, lipids, proteins) by the 8,9 epoxides. However the most serious adverse effects of the AFB1-8,9-epoxide metabolite is that it reacts with amino acids in DNA and forms an adduct [38-41, 46, 52-55]. The adduct are fairly resistant to DNA repair processes and this causes gene mutation that leads to liver cancers especially the hepatocellular carcinomas [38-41, 46, 52-55].
\n\t\t\tAlso in the hepatocytes, AFB1 are converted to other different classes of metabolites by cytoplasmic reductase such as aflatoxicol and by microsomal mixed-function oxidase system to form AFM1, AGFQ1, AFP1 and AFB1 -epoxide (the most toxic and carcinogenic derivative) and these metabolites may be deposited in various body tissues as well as in edible animal products [38-41, 46, 52-55]. These metabolites other than the AFB1 are less toxic and are conjugated with other molecules that enhance their rapid elimination from the body [22]. The metabolite AFQ1 has very little cancer-causing potential and they are usually excreted in urine with little effect on the body.
\n\t\t\tThe aflatoxin binds and interferes with enzymes and substrates that are needed in the initiation, transcription and translation processes involved in protein synthesis. They interacts of with purines and purine nucleosides and impair the process of protein synthesis by forming adducts with DNA, RNA and proteins [57]. Aflatoxin also inhibits RNA synthesis by interacting with the DNA-dependent RNA polymerase activity and thus causes degranulation of endoplasmic reticulum. Also the reduction in protein content in body tissues like in skeletal muscle, heart, liver and kidney could be due to increased liver and kidney necrosis [58]. AFB1 is a potent mutagenic, carcinogenic, teratogenic, and immunosuppressive and all these may interfere with normal process of protein synthesis as well as inhibition of several metabolic systems thus causing damages to various organs especially the liver, kidney and heart [59, 60].
\n\t\t\tAflatoxins especially AFB1, AFG1 and AFM1 are the most toxic, naturally occurring carcinogens known with AFB1 the most hepatocarcinogenic compound, causing various cancers of the liver and other body organs in humans and animals [4, 14, 45, 61]. Aflatoxin’s cancer-causing potential is due to its ability to produce altered forms of DNA adducts. The primary disease associated with aflatoxin intake is hepatocellular carcinoma (HCC, or liver cancer). This disease is the third-leading cause of cancer death globally [4, 45, 61], with about 550,000–600,000 new cases each year. The incidence of liver cancer has been consistently higher in men than in women with a sex ratio ranging from 2 to 3 in most countries [9]. Eighty-three percent of these cancer deaths occur in East Asia and sub-Saharan Africa [62-64]. Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide with extremely poor prognosis. The majority of cases occur in south-east Asia and sub-Saharan Africa where the major risk factors of chronic infection with hepatitis B and C viruses (HBV and HCV) as well as dietary exposure to aflatoxins are a problem [9, 25, 61, 65]. Aflatoxin B1, the most commonly occurring and potent of the aflatoxins is associated with a specific AGG to AGT amino acid transversion mutation at codon 249 of the p53 gene in human HCC, providing mechanistic support to a causal link between exposure and disease [25, 26, 66, 67]. Liver cancer has an increasing incidence that parallels the rise in chronic hepatitis B (HBV) and hepatitis C (HCV) infection [25, 67, 68]. Chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV) can progress to advanced liver disease, including cirrhosis and hepatocellular carcinoma (HCC), a form of primary liver cancer [25, 61, 67, 68]. HCC is the third leading cause of cancer-related mortality worldwide [69]. The data show that individuals positive for the hepatitis B virus and exposed to aflatoxin in the diet are about 60 times of risk for developing hepato-biliary carcinoma or liver cancer [26, 66, 67] especially in poor developing countries worldwide [67]. Reports have shown that a number of interactions exist between HBV and aflatoxins in development of hepatocellular carcinoma in humans. They may include the fixation of AFB1-induced mutations in the presence of liver regeneration and hyperplasia induced by chronic HBV infection, the predisposition of HBV-infected hepatocytes to aflatoxin induced DNA damage, an increase in susceptibility to chronic HBV infection in aflatoxin exposed individuals and oxidative stress exacerbated by co-exposure to aflatoxins and chronic hepatitis infection [61](Figure 4).
\n\t\t\t\tIn humans, epidemiological studies in Africa, Southeast Asia, USA and other countries of the west where there is a high incidence of hepatocellular carcinoma, have revealed an association between cancer incidence and the aflatoxin content of the diet [5, 6, 70]. Aflatoxin B1 (AFB1) is a major risk factor in the pathogenesis of liver cancer in Asia and sub-Saharan Africa [71]. Aflatoxin B1 is a potent liver carcinogen in a variety of experimental animals. It causes liver tumours in mice, rats, fish, marmosets, tree shrews and monkeys following administration by various routes. Types of cancers described in research animals include hepatocellular carcinoma (rats) colon and kidney (rats), cholangiocellular cancer (hamsters), lung adenomas (mice), and osteogenic sarcoma, adenocarcinoma of the gall bladder and carcinoma of the pancreas (monkeys) [5, 6, 12, 70].
\n\t\t\tAflatoxicosis is a condition caused by aflatoxins in both humans and animals. It occurs in two general forms (1) the acute primary aflatoxicosisis produced when moderate to high levels of aflatoxins are consumed. Specific acute episodes of disease may include hemorrhage, acute liver damage, edema, alteration in digestion, absorption and/or metabolism of nutrients, and possibly death [5, 6, 12, 69, 70]. Acute dietary exposure to AFB1 has been implicated in epidemics of acute hepatic injury [13, 72]. Evidence of acute aflatoxicosis in humans has been reported worldwide especially in the third world countries like Taiwan, Uganda, India, Kenya and many others [7]. (2) The chronic primary aflatoxicosis results from ingestion of low to moderate levels of aflatoxins (USAID, 2012). The effects are usually subclinical and difficult to recognize. Some of the common symptoms are impaired food conversion and slower rates of growth with or without the production of an overt aflatoxin syndrome [9]. The chronic forms of aflatoxicosis include (1) teratogenic effects associated with congenital malformations (2) mutagenic effects where aflatoxins cause changes (mutations) in the genetic code, altering DNA and these changes can be chromosomal breaks, rearrangement of chromosome pieces, gain or loss of entire chromosomes, or changes within a gene (3) the carcinogenic effect in which the carcinogenic mechanisms have been identified such as the genotoxic effect where the electrophilic carcinogens alter genes through interaction with DNA and thus becoming a potential for DNA damage and the genotoxic carcinogens that are sometimes effective after a single exposure, can act in a cumulative manner, or act with other genotoxic carcinogens which affect the same organs [50, 60]. Chronic effects of aflatoxin has been reported to impair the normal body immune function by either by reducing phagocytic activity or reduce T cell number and function as observed immunological suppression in animal model. Aflatoxins have also been reported to interfere with nutrition in a dose response relationship between exposure to aflatoxin and rate of growth in infants and children [4, 9, 20, 50, 60]. Aflatoxins also causes nutrient modification like vitamin A or D in animal models and thus making them unavailable for the normal body physiology and hence leads to nutritional deficiencies [7, 20].
\n\t\t\tThe contamination of foods and feeds with aflatoxin can cause serious consequences in human and animal health. It is estimated that more than 5 billion people in developing countries worldwide are at risk of chronic aflatoxin exposure due to consumption of aflatoxin-contaminated foods and of these more than 4 billion people develop aflatoxin related liver cancer especially the hepatocellular carcinoma [64, 69, 73, 74]. Aflatoxin exposure is mainly a problem in poor and developing countries with poor regulatory authorities in food processing and storage as well as with high levels of malnutrition. Aflatoxins have also been linked with kwashiorkor and marasmus in most of the sub-Saharan countries in children [20]. Many people in these countries experience chronic aflatoxicosis associated with long-term exposure to low to moderate levels of aflatoxin in the food supply chain. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney [75]. Aflatoxin B1 exposure results in both steatosis and accumulation of fat and necrosis or cell death of liver cells. The amount of aflatoxins consumed contributes to the mutagenic, carcinogenic, teratogenic, and immunosuppressive health effects in the body. The adverse effect of aflatoxins in humans ranges from acute hepatic toxicity to chronic disease such as liver cancer, haemorrhages, oedema, and even immediate death. Prolonged consumption of aflatoxins has also been reported to cause impaired immune function and malnutrition and stunted growth in children and a number of disabilities and death [7, 76, 77]. Human studies have reported that aflatoxins cause an increase in circulating alpha tumor necrosing factor, suggesting that these mycotoxins are also immunotoxic in humans. Due to the aflatoxin body immunosuppressant, it has been associated with HIV and tuberculosis [66, 67](Figure 2). Aflatoxins also pose a threat to developing fetuses and they are transferred from mother to infant in breast milk. Aflatoxins have been reported to be associated with a Reye-like Syndrome in Thailand, New Zealand, Czechoslovakia, the United States, Malaysia, Venezuela, and Europe [4, 50, 78].
\n\t\t\tAll species of animals are susceptible to aflatoxicosis and the susceptibility of individual animals to aflatoxicosis varies considerably depending on dose, duration of exposure, species, age, sex and nutrition. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney of growing swine when protein and protein-free portions of the diet were separately fed [75]. Chronic exposure of aflatoxins to animals causes immunosuppression and also interferes with protein metabolism and multiple micronutrients that are critical to health due to adduct formation. These adduct are responsible for mutations, cancer, immunosuppression, lung injury and birth defects [46]. In animals, the aflatoxins cause liver damage, decreased milk production, reduced reproductively and suppressed immunity in animals consuming low dietary concentrations. The aflatoxicosis syndrome in animals may also be characterized by vomiting, abdominal pain, pulmonary oedema, convulsions, coma, and death with cerebral edema and fatty involvement of the liver, kidneys, and heart. In dairy and beef cattle, the signs of acute toxicosis include anorexia, depression, dramatic drop in milk production, weight loss, lethargy, gastrointestinal dysfunctions such as ascitis, icterus, tenesmus, abdominal pain, bloody diarrhoea, decreased feed intake and efficiency; weight loss, jaundice, abortion, hepatoencephalopathy, blindness, walking in circles, ear twitching, frothy mouth, photosensitization, bleeding and death [4, 6, 22, 79]. In poultry, beside inappetance, weight loss, decreased egg production, leg and bone problems, poor pigmentation, fatty liver, kidney dysfunction, bruising and death, suppression to natural immunity and susceptibility to parasitic, bacterial and viral infections can occur [6, 22], (Figure 4).
\n\t\t\tAflatoxin disease pathways in humans (Adopted from Wu, 2010; USAID, 2012; WHO, 2011; Wu and Tritscher, 2011) [
Aflatoxins have been reported to affect the various body organs like the liver, kidneys, lungs, brain, testes and many endocrine and exocrine organs, the heart, skeletal muscles and the different body systems.
\n\t\t\tAflatoxins have been reported to cause liver cirrhosis as well as liver cancers [4, 6, 7, 26, 80]. Hepatic injury can be acute or chronic form caused by a variety of toxic agents like aflatoxins, chemicals and drugs, trauma and infectious agents [2, 4, 6, 7, 26, 61, 76, 80, 81]. The reduced level of total protein is indicative of the toxic effect of AFB1 to the liver due to the failure in synthesis of the proteins and kidney in which aflatoxins are known to impair protein biosynthesis by forming adducts with DNA, RNA and proteins, inhibits RNA synthesis, DNA-dependent RNA polymerase activity and causes degranulation of endoplasmic reticulum [58-60]. Acute hepatic injury due to aflatoxin causes a rise in serum enzymes including aspartate aminotransferase, lactate dehydrogenase, glutamate dehyrogenase, gamma-glutamyltransferase and alkaline phosphatase and bilirubin that reflect liver damage as well as other biochemical changes such as proteinura, ketonuria, glycosuria and hematuria [4, 5, 40]. The other frequently used liver enzymes are the alkaline phosphatase (ALP) and Gamma-glutamyltransferase and gamma-glutamyltranspeptidase (GGT and GGTP) that indicate obstruction to the biliary system, either within the liver or in the larger bile channels outside the liver [9, 45, 61]. The presence of jaundice and neurological disorders due to brain damage leading to hepatic encephalopathy are associated with liver failure. Chronic liver failure leads to accumulation of metabolites in circulation such as ammonia and fatty acids that eventually lead to brain damage and hence hepatic encephalopathy [40, 82]. The liver failure makes it unable to detoxify ammonia, the product of protein and amino acid metabolism leading to hyperammonemia that may cross the blood brain barrier leading to increased synthesis of glutamate neurotransmitters henceleading to cytotoxicity of the brain cells and hence the hepatic encephalopathy [82-84]. AFB1 has been reported to cause pallor discoloration of liver and enlargement of liver and kidneys, congestion of liver parenchyma, cytoplasmic vaculation or fatty change of hepatocytes, necrosis of hepatocytes and newly formed bile ducts, mononuclear and heterophilic cell infiltration are reported in aflatoxin fed broiler chicks [85]. It is also reported that there is a decrease in protein content in skeletal muscle, heart, liver and kidney in aflatoxin-fed animals due to the AFB1’s potent mutagenic, carcinogenic, teratogenic, immunosuppressive and its ability to inhibits several metabolic systems such as protein synthesis thus leading to liver, kidney and heart damage [58-60]. In chicken, the activity of serum or plasma enzymes like the sorbitol dehydrogenase, glutamic dehydrogenase, lactate dehydrogenase, alkaline phosphatase, acid phosphatase, aspartate aminotransferase and alanine aminotransferase were reported to be increased in aflatoxicated chickens [22].
\n\t\t\tIn the brain or central nervous system, the neurons have a high metabolic rate but little capacity for anaerobic metabolism and subsequently, inadequate oxygen flow to the brain kills the neuronal brain cells within minutes. Some compounds damage neurons or neurotoxic and thus inhibit their function. Mycotoxins especially aflatoxins and its metabolites and other products such as the reactive oxygen species (ROS) like the AFB-8,9-epoxides may interfere with the normal functioning of the nerve cells by forming DNA adducts, protein adducts, oxidative stress factors, mitochondrial directed apoptosis of the nerve cells as well as inhibiting their synthesis of protein, RNA and DNA [40, 44, 47, 50, 52, 54]. Aflatoxins also cause abnormalities in mitochondrial DNA, structure and function, including defective oxidative phosphorylation in the brain cells [29, 49, 50, 54]. The oxidative stress may result in damage to critical cellular macromolecules such as DNA, lipids and proteins. Cellular fatty acids are readily oxidized by ROS to produce lipid peroxyl radicals which can subsequently propagate into MDA that may interact with cellular DNA to cause DNA-MDA adduct that may affect energy production in the brain [29, 49, 50, 54]. The role of ROS has been postulated in the development of aging and chronic degenerative diseases, inflammatory diseases and brain cancers [52]. Aflatoxins may also deplete the myelin sheath of the nerves, an important substance that covers the nerves and hence become exposed to insults. Mycotoxins especially aflatoxins have been reported to be toxic to various aspects of brain chemistry and their function [4, 50, 82]. AFB1 also alters the levels of various biogenic amines (neurotransmitters) and their precursors in rat and mouse brains. Acute AFB1 treatment in experimental animals has been reported to cause a decrease in regional brain acetylcholinesterase enzymes that may affect the cognitive functions as well as memory and learning of the individual while chronic exposure increases adenohypophyseal acetylcholinesterase [24]. Aflatoxin causes a decrease in dopamine, serotonin and alterations in the levels of the precursor’s tyrosine and tryptophan [86-88]. Deficiencies in these neurotransmitter lead to neurological symptoms such as neurocognitive decline and alteration of sleep cycle and symptoms of brain damage like dullness, restlessness, muscle tremor, convulsions, loss of memory, epilepsy, idiocy, loss of muscle coordination, and abnormal sensations [89, 90]. AFB1 has also been reported to increase the central and peripheral nervous system Na+/K+-ATPase, β-glucuronidase and β-galactosidase while inhibiting the Mg2+-ATPse in experimental animals and this also is important in the normal functioning of the glutamate neurotransmitter and their NMDA receptors [24, 53, 91-93]. The liver failure makes it unable to detoxify ammonia, the product of protein and amino acid metabolism leading to hyperammonemia that may cross the blood brain barrier leading to increased synthesis of glutamate neurotransmitters hence leading to cytotoxicity of the brain cells and hence the hepatic encephalopathy [82-84]. Toxic encephalopathy was originally described in children with Reye’s syndrome associated with consumption of Aflatoxin B1 and/or salicylates [78] and subsequently in cases of aflatoxicosis in canines and Chinese children were reported [94]. Aflatoxins also have been linked to Reye\'s syndrome that is characterized by symptoms of encephalopathy and fatty degeneration of the viscera. It is a pediatric disease characterized by cerebral edema and neuronal degeneration. Toxic encephalopathy due to aflatoxins involves multiple symptoms like loss of balance, recent memory decline, headaches, lightheadedness, spaciness/disorientation, insomnia, loss of coordination [4, 18, 50, 82]. Aflatoxins have been reported to be associated with a Reye-like Syndrome in Thailand, New Zealand, Czechoslovakia, the United States, Malaysia, Venezuela and Europe [4, 9, 24, 50, 78]. Aflatoxins especially AFB1 have been reported to cause tumors in both the central and peripheral nervous system and several nonepithelial neurogenic tumors like the schwannomas, gliomas, meningiomas and granular cell tumors have been reported [24].
\n\t\t\tThe gastrointestinal tract (GIT) is the main route of entry of aflatoxins as a result of consumption of aflatoxin-contaminated foods especially AFB1. It is also the main route of excretion aflatoxin metabolites from the bile. The aflatoxins, metabolites and AF-8,9-epoxides have been reported to cause intestinal tumors especially the human colon cancers like colon carcinomas and similar results have been reported in experimental animals [24]. Aflatoxins have also been reported to cause serious acute effects on the GIT [95]. Aflatoxins have been implicated as potential factors in the increased incidence of human gastrointestinal and hepatic neoplasms in Africa, Philippines and China [22]. Aflatoxins have been reported to cause digestive system effects such as diarrhea, vomiting, intestinal hemorrhage, and liver necrosis and fibrosis [89]. Aflatoxins have been reported also to damage the integrity of the pancreas. In domestic animals, aflatoxins cause changes in the GIT physiology especially decreased rumen motility and function in cows [24]. In birds, aflatoxins interfere with intestinal morphology, sialic acid production and apparent digestible energy [96].
\n\t\t\tAflatoxins have reported to have serious acute effects on the respiratory systems [95].The respiratory tract is the only organ system with vital functional elements in constant and direct contact with the environment [97]. Many people working in food industries as their occupational setting get exposed to aflatoxins especially AFB1 when they inhale aflatoxin-contaminated dusts like during grain shelling and processing and have been reported to have a higher incidences of upper respiratory tract and lung cancers [24, 95]. In experimental animals, AFB1 was reported to induce 100% pulmonary adenomas. In the respiratory tract, aflatoxins may also be converted to active metabolites like in the nasal mucosa [23]. It is also reported that the intranasal administration of AFB1 lead to formation of tissue-bound metabolites in subtentacular cells, bowman\'s glands and in neuronal cells in the olfactory mucosa but there is no evidence that AFB1 may induce tumours in olfactory bulbs [98]. Epoxide hydrolase and glutathione-S-transferase (GST) are both involved in hepatic detoxification of activated AFB1 but the GST-catalyzed conjugation of glutathione to AFB1-8,9-epoxides is thought to play more important role in preventing epoxide binding to target macromolecules [23, 89, 99]. However, the low capacity for GST-catalyzed detoxification of bio-activated AFB1 in lung may be an important factor in the susceptibility of the lung to AFB1 toxicity ([41]. Nose-only inhalation exposure of rats to AFB1 aerosols suppressed alveolar macrophage (AM). Intratracheal administration of AFB1 also suppressed the release of tumor necrosis factor-alpha from AMs and impaired systemic innate and acquired immune defenses as well as suppression of peritoneal macrophage phagocytosis and the primary splenic antibody response thus leading to suppression of respiratory tract defenses system [99].
\n\t\t\tAflatoxins have reported to have serious acute effects on the cardiovascular systems including vascular fragility and hemorrhaging in tissues [58, 89, 95] as well as heart damage and teratogenic effects [59, 60]. It is reported that there is a decrease in protein content of the muscles of these tissues and organs as well as inhibition of their metabolic processes attributable by the aflatoxin consumption of contaminated foods [59, 60].
\n\t\t\tThe aflatoxins and its metabolites as well as the generated reactive oxygen species(ROS) has been reported to have a deleterious effects on the bone and blood cells as well as induction of cancers on the hemopoietic system in bone marrow and lymphoid organs where blood, blood cells and blood components are produced [52]. The blood system can be damaged by agents that affect blood cell production (bone marrow), the components of blood (platelets, red blood cells, and white blood cells), or the oxygen-carrying capacity of red blood cells or impair blood clotting and their poor growth rates. Oxidative damage by the AFB1 on human lymphocytes has been reported [100] and significant declines in both the proportion of peripheral blood lymphocytes and in the percentages of ANAE-positive peripheral blood lymphocytes (T-lymphocytes) in a dose dependent manner has been observed [101]. Aflatoxins have been linked to anemia in pregnancy [7, 102] and alterations in erythrocytes during induced chronic aflatoxicosis in rabbit also have been reported [103, 104]. Aflatoxin causes hematopietic suppression and anemia, decrease in total erythrocytes, packed-cell volume and hemoglobin [16] as well as toxicity to red blood cells [103]. Aflatoxin is known to produce hemolytic anemia by decreasing the circulating mature erythrocytes [104]and consequently the spleen appear congested because of an unusually high concentration of inorganic iron and debris from the circulation [103, 104]. In birds, AFB1 is reported to causes hematological changes [105]. Aflatoxicosis has been reported to cause lymphocytopenia and monocytopenia and increased percentage of neutrophil counts [106]. In cattle, aflatoxins are reported to cause blood coagulation defects that may involve impairment of prothrombin, factors VII and X and possibly factor IX and similar effects are reported in dogs [5]. Generally aflatoxins have been reported to depress growth and alter many aspects of humoral and cellular immunity and thus affecting the hematological parameters [101, 107].
\n\t\t\tThe kidney is susceptible to many toxic agents due to the high amount of blood it receives and about 20-25% of blood that flows in at rest coupled with the large amounts of circulating toxicants that reach the kidneys [89]. The kidneys also have high oxygen and nutrient requirements because of their workload and therefore filters one-third of the blood reaching them and reabsorb 98-99% of the salt and water. Different parts of the nephrone are exposed to aflatoxins especially the AFB1 and its metabolites leading to nephrotoxicity before it is excreted in the urine [24, 58]. The aflatoxin induced reduction in protein content has been reported to be due to increased necrosis of the kidney [58-60, 90]. AFB1 has been reported to cause kidney tumors in experimental animals and a mixture of AFB and AFG was observed to cause renal and hepatic tumors in 80% of hamsters [24]. There were also renal lesions with features of megalocytosis in the proximal renal tubules. In Africa, birds exposed to AFB1 were reported to develop fatty and hemorrhagic kidney syndrome, thickening of the glomerular basement membrane, abnormal development of glomerular epithelial cells and degenerative changes in renal tubular cells, congestion and parenchyma hemorrhage [24, 85]. In other animals, there was a reduction in the glomerular filtration rate, glucose reabsorption and tubular transport of electrolytes and organic anions, reduced activities of renal glutamate-oxaloacetate and pyruvate transaminases and alkaline phosphatase in rats attributed to by the aflatoxins and their metabolites as well as the generated ROS. There was induced aggregation and loss of chromatin, mitochondrial degeneration and loss of microvilli induced by AFB1 in cultured kidney cell lines [24, 85].
\n\t\t\tAflatoxin especially AFB has been reported to interfere with the functioning of the various endocrine gland by disrupting the enzymes and their substrates that are responsible for the synthesis of the various hormones. Aflatoxins and their metabolites as well as the generated ROS have been reported to cause various cancers in different endocrine glands like pituitary gland, granulosa cell tumors of the ovary and adenomas and adenocarcinomas of the adrenal gland, kidneys, thyroid gland, ovaries, testes, thyroid gland, parathyroid glands and endocrine pancreas [4, 90, 108]. The plasma testosterone and luteinizing hormone (LH) concentrations have been reported to reduce in aflatoxin-fed birds [90]. In laboratory animals, aflatoxin causes delayed maturation of both males and females [4, 22, 90, 109]. Aflatoxicosis in white leghorn males chicken decreased feed consumption, body weight, testes weight and semen volume (Sharlin et al., 1980) and decreased plasma testosterone values [22].
\n\t\t\tIn humans exposed to chronic aflatoxin-contaminated foods, it has been reported that higher concentrations of aflatoxins occur in the semen of infertile men [3]. It is also associated with low birth weight, a risk factor for jaundice in infants as well as presence of AFM in maternal breast milk where it can cause deleterious effect in the newborns [102]. In Nigeria, about 37% of the infertile men had aflatoxin in their blood and semen hence contributing to the incidence of infertility in Nigerians [110]. Experimental results indicate that certain agents like aflatoxins can interfere with the reproductive capabilities of sexes, causing sterility, infertility, and abnormal sperm, low sperm count, and/or affect hormone activity in animals. Aflatoxins have been reported to disrupt the reproductive system in both male and female animals after ingestion of aflatoxin-contaminated foods. Aflatoxins also cause pathological alterations in the form of coagulative necrosis especially in the growing and mature follicles and decrease in number and size of graffian and growing follicles with increased number of atretic follicles and small areas of degenerative changes in experimental animals [111]. AFB1 has been reported to have a deleterious effect on the reproductive capacity of laboratory and domestic female animals where they cause reductions in ovarian and uterine sizes, increases fetal resorption, implantation loss and intra-uterine death in the aflatoxin exposed female rats [111]. They also cause a reduction in the primary spermatocytes and spermatids [112] and affect the morphology of the sperm cells produced [113]. Stillbirths were reported in the 15th to the 18th days of pregnancy in rats [108]. The levels of plasma testosterone, plasma 5a-DHT and absolute and relative testes weights were reported in experimental animals of aflatoxin-treated males remained low in all age groups and a delay in the onset of sexual maturation during aflatoxicosis [114]. In cows, aflatoxins affected the reproductive system by causing abortion, the birth of weak, deformed calves, reduced fertility due to reduced vitamin A levels [109]. The teratogenic effects of AFB1 were described as enlarged eye sockets and enlarged liver of embryos [60]. In poultry, AFB1 cause a reduction in semen volume, testes weight, spermatocrit and plasma testosterone as well as a reduction in egg output [24].
\n\t\t\tChronic consumption of aflatoxin-contaminated foods has been reported to cause immunosuppression in both humans and animals worldwide [7, 89]. In human, aflatoxins affect both the cellular and humoral immune responses where they alter immunological parameters in participants with high AFB1 levels resulting in impairments in cellular immunity hence decreasing the host resistance to infections [115-117]. Aflatoxin exposure has been shown to cause immune suppression, particularly in cell-mediated responses [115-117]. Chronic exposures of the individual to aflatoxins depress the phagocytic efficiency of the phagocytes and the delayed hypersensitivity reactions in birds [24]. Aflatoxins also deplete the cell populations of the thymus; reduce the bone marrow and the red and white blood cells count, macrophage numbers and the phagocytic activity of the cells [24]. It also depresses the T-cell-dependent functions of splenic lymphocytes in mice. The natural killer cell function of the peripheral blood lymphocytes are also affected by aflatoxins especially AFB1 [24]. A reduction in the leukocyte immunophenotypes in peripheral blood, CD4+ T cell proliferative response, CD4+ T and CD8+ T cell cytokine profiles and monocyte phagocytic activity were reported. Children in developing countries appear to be naturally exposed to aflatoxin through their diet at levels that compromise the immune system. In general, the proportion of childhood growth stunting is directly correlated with the proportion of the population living below the national poverty line and is inversely correlated with gross domestic product per capita [7, 45]. As is the case with liver cancer, childhood stunting is prominent in regions such as Southeast Asia and Sub-Saharan Africa, where aflatoxin exposure through consuming contaminated food is common [7, 45]. It has been reported that the immunosuppression and nutritional effects of chronic aflatoxin exposure may be linked to the high prevalence of HIV in Southern Africa [7, 74, 118, 119]. The CD4 proteins that have been weakened by aflatoxin exposure have been reported to correlate positively with HIV infection [116]. Also high aflatoxin levels have been reported to increase risk of developing tuberculosis in HIV positive individuals. Persons who are exposed to aflatoxin and are HIV positive have decreased plasma vitamin A and vitamin E in the blood, although there was no interaction detected between aflatoxin and HIV infection [120]. HIV infection is likely to increase aflatoxin exposure by two possible routes: (1) HIV infection decreases the levels of antioxidant nutrients that promote the detoxification of aflatoxin, or (2) the high degree of co-infection of HIV-infected people with hepatitis B also increases the biological exposure to aflatoxin [7, 118, 119]. Aflatoxin induce immunosuppression and increases susceptibility of toxicated birds and animals to bacterial, viral and parasitic infections [58]. It also affects the lymphoid follicles of caecum thus depleting the lymphocytes that may contribute to the observed immunosuppression [117]. Aflatoxin decreases the concentrations of immunoglobulins IgM, IgG and IgA in birds as well as decrease complement activity in chickens [22, 121]. The low dose of AFB1 slightly decrease both mRNA and protein levels of lymphocytic IL-2, IFNγ and it preferentially affects macrophage functions as well as IL-1α, IL-6 and TNF production by these cells [121, 122]. Aflatoxin suppression of the immune system therefore subjects the individual to high risk of susceptible to infectious diseases like parasitic, bacterial and viral infections [123].
\n\t\tChronic consumption of aflatoxin-contaminated foods is a common problem in both humans and animals worldwide especially in poor developing nations of south East Asia and sub-Saharan Africa where there is poor food harvesting, processing and storage of food and food products thus allowing the growth of mold on them. Aflatoxins, their metabolites, the aflatoxin-8,9-epoxide and the generated ROS causes deleterious effects on the various body organs and body systems including the development of cancers especially the liver cancer mainly due to AFB1 exposure. Aflatoxins are also responsible for the suppression of both the humoral and cell-mediated immunity and thus making individuals susceptible to infectious diseases. Aflatoxins also responsible for the malabsorption of various nutrients thus leading to nutritional deficiencies, impaired immune function, malnutrition and stunted growth and hence the development of kwashiorkor and marasmus in infants. Aflatoxins also can affect almost all the different body systems and hence the health of the affected individuals especially in poor developing nations of south East Asia and sub-saharan Africa where there is poor food harvesting, processing and storage thus allowing the growth of mold on them.
\n\t\tThis paper discusses the implications of climate change in Indonesia and discusses the challenges to and opportunities for climate change mitigation and adaptation within Indonesia.
It is widely known that one of the reasons for climate change is global warming which is marked by an increase in air temperature. Climate change is associated with increased atmospheric temperature caused by the “Green House Effect” which occurs due to the increase in green house gases (GHG) in the atmosphere. Carbon dioxide (CO2) is one of the gases that causes global warming. According to the IPCC [1], the average temperature of the earth’s surface over the past century has increased by 1.30 F. The presence of CO2 is related to the condition of forests in an area. The trees that make up forests of various types and growth rates, known as forest structure and composition, have a role in storing CO2. Forests are dominated by vegetation that has chlorophyll which functions in the photosynthesis process by requiring light energy, water and CO2 to form carbohydrates. Thus the forest will absorb carbon from the air and accumulate in the plant body in the form of stems, branches, twigs, leaves, flowers, fruit and roots and soil. In general, this process is known as Carbon Sequestration [2, 3]. Thus the forest can function as a carbon sink. Therefore, well-well-maintained forests can increase carbon sequestration or reduce the amount of carbon in the atmosphere. In addition, by expanding the forest area, of course, its ability to absorb carbon will be higher. The development of various ecosystems over millions of years has resulted in certain patterns of carbon flow in global ecosystems. However, human (anthropogenic) activities in the use of fossil fuels, conversion of forest land and others have resulted in changes in the exchange of carbon in the atmosphere, land and marine ecosystems. As a result of these activities, there was an increase in the concentration of CO2 into the atmosphere by 28% from the CO2 concentration that occurred more than 150 years ago.
Indonesia’s swamplands, which are around 33 million ha, 20.6 million ha of which are peatlands. Most of the peatlands are spread across three major islands, namely Sumatra (35%), Kalimantan (32%), Papua (30%), Sulawesi (3%), and the rest (3%) is spread over a narrow area [4]. The role of peatland is important because it has a high carbon sequestration and is a natural resource that has a hydrorological function. The existing peatlands need to be protected from fire. Because if a fire occurs in the peat forest, it will cause large CO2 emissions and the resulting smoke will disrupt airlines and cause shortness of breath, etc. Peatlands play a major role in the development of agriculture, oil palm plantations or industrial plantations. For this reason, peatlands are managed with the principle of sustainable peatland management so that they can minimize environmental damage. Apart from peatlands, there are also mangrove forests that are found on the coast of the Indonesian archipelago which have a high carbon content known as blue carbon.
Peatlands planted with oil palm and acacia function as a carbon sequester through the photosynthetic process and carbon is stored as plant biomass. The carbon tethering process through the photosynthesis process is able to offset the loss of carbon stocks in the soil which are oxidized to CO2 gas emissions. However, if the expansion of oil palm plantations is excessive to the point where many natural forests are converted, it will have a negative impact on the biodiversity of the peatlands. The existing mangrove forests have also suffered a lot of damage because the area is used for the construction of ponds, excessive mangrove wood extraction and the large number of mangrove forests that have turned into settlements in coastal areas. The area of mangrove forests in Indonesia reaches 3.49 million ha but 52% or 1.82 million ha is in a damaged condition [5].
Carbon emissions from forest land including peat and mangrove forests generally fluctuate depending on many factors including climate, soil and hydrology. Environmental factors that greatly influence the amount of carbon emissions, especially from peatlands, are temperature, soil moisture and electrical conductivity (EC) [6]. These three factors fluctuate greatly from day to day depending on climatic and hydrological factors, resulting in high fluctuations in carbon emissions [7, 8]. High carbon content in natural and plantation forests is usually found in forests where the potential for wood or wood volume unit (m3/ha) is also very high. Therefore, if an area is only used for seasonal plant development, of course the carbon content is low. The lowest carbon content is when forest land has been converted into urban areas with the development of housing, markets, offices, development of road networks and infrastructure. Even with the construction of urban areas with various tall buildings, it has triggered the emergence of a heat island. One of the safety valves so that forest areas can maintain carbon content is the application of the agroforestry system. This system is a cultivation in an area with a mixture of perennials and seasonal plants.
In an effort to increase the prosperity of a country, a lot of forest is transferred to other uses such as the development of oil palm plantations, agricultural land, livestock grazing and urban expansion etc. In fact, many agricultural lands have changed their function into settlements. If this happens, the forest area will continue to decrease again because after the agricultural land has turned into residential land, the forest land is converted again for agricultural expansion, this happens continuously. In other words, deforestation and forest degradation have triggered climate change.
If viewed from the CO2 flux, there will also be changes in the basic CO2 flux from forest land, plantation land, agriculture and urban areas. It is certain and inevitable that the forest area will decrease and be used for non-forestry development. One of the reasons is the increase in population which is difficult to control every year. Thus, changing a forest area to non-forest will have an impact on the lack of carbon sequestration as shown in Figure 1.
The lower carbon sequestration of forest to non-forest areas. (a) Forests: very high carbon sequestration, (b) Agroforestry: high carbon sequestration, (c) Agricultural crops: low carbon sequestration, (d) Cities with infrastructure: very low carbon sequestration.
The conversion of forest land to non-forest land actually occurs as a result of economic motivation. For example, more forest land will be converted into oil palm plantations if the results of oil palm management turn out to be more profitable from an economic perspective. Therefore, forest management must endeavor to be able to generate more tangible benefits from non-forest uses.
Indonesian oil palm plantations have grown rapidly in large parts of Indonesia. Sumatra and Kalimantan are two large islands which are the main centers of oil palm plantations in Indonesia. About 90% of oil palm plantations in Indonesia are located on these two oil palm islands, and the two islands produce 95% of Indonesia’s crude palm oil (CPO) production. In the period 1990–2015, there was a revolution in the exploitation of oil palm plantations in Indonesia, which was marked by the rapid growth and development of smallholder plantations, namely 24% per year during 1990–2015. During this period, the forest land changed into oil palm plantations. This marks the end of the logging era and the drastic reduction of the plywood industry. The Ministry of Forestry has revoked many HPH licenses and an increasing number of plywood industries have closed due to a shortage of log raw materials. So in addition to the development of oil palm plantations, it is also planting industrial tree plantations which encourage the construction of pulp and paper mills. The area of Indonesian oil palm plantations in 2015 reached 11.3 million ha [9]. In 2017 it has reached 16 million ha. The largest proportion of oil palm plantations is smallholder plantations 53%, large private plantations 42%, and state plantations 5%. The rapid development of the palm oil industry has attracted the attention of the world community, particularly the world’s major vegetable oil producers. In 2019 the area of oil palm plantations has reached 14.6 million ha [10]. Indonesia has become the world’s largest palm oil producing country since 2006. Indonesia managed to surpass Malaysia in 2016 where Indonesia’s CPO production share has reached 53.4% of the world’s total CPO. Meanwhile, Malaysia only has a share of 32%. Likewise in the global vegetable oil market, palm oil has also managed to outperform soybean oil since 2004. In 2004, total CPO production reached 33.6 million tons, while soybean oil was 32.4 million tons. In 2016, the share of world CPO production reached 40% of the world’s main vegetable products, while soybean oil had a 33.18% share [11].
Indonesia with its enormous reserves of oil palm plantations needs to ensure that these resources contribute to its national energy plan. Therefore the central government has compiled a Biodiesel Mandate which is among the most ambitious in the world. By 2016, liquid fuels must contain at least 20 percent of biofuels (and by 2025, 30 percent). A subsidy program has also been established to account for the substantial difference in production costs between biofuels and conventional diesel. One can feel considerable optimism because this funding is based on taxes on Crude Palm Oil (CPO) exports rather than on national budget expenditures which are negotiated annually [12]. With the mandate of biodiesel, in an effort to achieve national energy independence, expansion of oil palm plantations is something that cannot be avoided.
The rapidly increasing share of palm oil in the world vegetable oil market has influenced the dynamics of competition between vegetable oils and has even led to a negative / black campaign against palm oil. In addition, the sustainability aspect of oil palm plantations is under the spotlight. The development of oil palm plantations in Indonesia is perceived as unsustainable and is accused of being the main cause of deforestation and loss of wildlife habitat. The rapid clearing of forest land into oil palm plantations has led to the perception that Indonesia has carried out deforestation on a large scale. Actually this action was taken by the Government of Indonesia in carrying out national development in order to improve the welfare of its people. So there are stages for a country to deforest for the welfare of its people. When viewed from the development history of a number of major countries in the world, both the United States and Europe have deforested their countries. Therefore, it is unfair if the issue of deforestation is used to suppress the growth of Indonesian oil palm plantations.
So far there have been many accusations stating that 67% of oil palm plantations are obtained from forest conversion [13]. Gunarso et al. [14] tried to examine the truth of forest conversion in Indonesia for oil palm plantations. This is done by using data from disturbed and undisturbed forest land cover classes according to the carbon stock sequence published by the Forestry Planning Agency in 2011. Carbon stock of natural/production forests, either undisturbed forest or disturbed forest, contains carbon stocks higher than carbon. Oil palm plantation stock. Thus, if there is conversion of production forest to oil palm plantations, there will be a decrease in land carbon stock or deforestation. Meanwhile, timber plantation, agricultural land (mixed tree crops, dry cultivation land) and shrubs/ abandoned land (schrub) contain lower carbon stocks than oil palm plantations. Thus, the conversion of scrub agricultural land/abandoned land, including industrial plantation forest land, into oil palm plantations is categorized as an increase in land carbon stock or reforestation. This study turns out to provide conclusions that are different from the allegations by Koh and Wilcove [13]. The Indonesian oil palm plantations planted until 2010, namely 8.1 million ha, turned out to be 5.5 million ha of which came from the conversion of agricultural land and abandoned land (reforestation). While the rest, namely 2.5 million ha, comes from conversion of production forests (deforestation). Because the area of deforestation for oil palm plantations is much less than the area of reforestation for oil palm plantations, in net terms, the expansion of Indonesian oil palm plantations to reach 10.4 million ha in 2013 is a form of reforestation and not deforestation. This means that the expansion of Indonesian oil palm plantations to 10.4 million ha in 2013 on a net basis is to increase land carbon stock or reforestation [15]. However, the conversion of forest land which was converted into oil palm plantations in 2019 has reached 14.6 million ha, so that deforestation cannot be avoided. This is what causes a huge source of CO2 emissions that actually triggers climate change.
The remaining forest area in Indonesia in 2019 is 94.1 million ha or 50.1% of the total land area [16] These forests play an important role in climate change mitigation and adaptation, so various strategies are needed and identification of opportunities to strengthen the results for both. a logical step. Therefore, the existence of the REDD+ Program will be very useful to support various steps that will help reduce the vulnerability of forest communities to the impacts of climate change. Reducing Emissions from Deforestation and Forest Degaradation (REDD+) is an effort to reduce emissions from deforestation and forest degradation, the role of conservation, sustainable forest management and increasing forest carbon stocks using a national approach and sub-national implementation. In its implementation, mitigation-adaptation synergy is needed which aims to find ways to take advantage of the synergy between REDD+ and climate change adaptation. Thus there is certainty that REDD+ will have impacts that go beyond mitigation and are sustainable in a climate that changes over time [17].
Indonesia still dominantly uses fossil energy sources that are not environmentally friendly and contribute to the increase in GHG which has been scientifically proven to change climate patterns with the emergence of global warming. Climate change will affect the duration of the dry and rainy seasons. This will certainly affect the yields in the agricultural-plantation sector and also the results of fishing in the sea. Therefore, people whose income depends on these two livelihoods will definitely be affected directly. To overcome this, it is necessary to implement climate change mitigation and adaptation programs. Here there are funding opportunities to carry out climate change mitigation and adaptation sourced from (1) public funds through the State Budget (APBN), (2) funds from abroad in the form of grants or loans (3) Funds from the private sector through Corporate Social Responsibility (CSR) and Green Bond [18].
The selection of the types of adaptation that can be carried out in various regions is basically a follow-up to the National Action Plan - Climate Change Adaptation (RAN-API). Understanding the impacts of climate change varies depending on location or region. In this condition, an assessment of the impacts and vulnerability of climate change specific to the economic sector in a location or region is required as a first step in selecting climate change adaptation options. Furthermore, an evaluation of adaptation options is carried out considering that the implementation of climate change adaptation requires additional costs [19]. One of the important elements needed in conducting a climate change impact and vulnerability assessment is climate information. This climate information plays a vital role in identifying the impact of global climate change on climate conditions in a region. The trend of climatic elements such as rainfall and air temperature observations is the earliest stage to see the effects of climate change in an area. Climate information is needed to (1) undergo impact models, for example: crop simulation models to assess the impact of climate variability in a region on the agricultural sector, (2) validate climate model outputs for projecting future climate conditions, compiling climate change scenarios. The uncertainty of future climate change is often approached by using more than one climate model or emission scenario. To understand the capabilities of climate models, validation of climate model outputs for the current period (control) is carried out using observational climate information. Compiling climate change scenarios also requires observational climate information, for example by changing (adjusting) observational climate information with differences between future climate projections and control periods [20].
Indonesia is the fourth largest country with GHG emissions in the world but does not make climate change a national priority agenda. At the international level, Indonesia has ratified the PARIS Agreement and has committed to reduce GHG emissions without conditions by 29% under a business as usual scenario in 2030 and up to 41% with international assistance. The government has established a policy framework such as RAN GRK SINCE 2011 and RAN API in 2014. These policies must be broken down to sub-national levels in the form of RAD GRK and RAD API. However, in practice, the policy framework and implementation often do not go hand in hand because local governments do not fully implement the policies set by the central government [21]. Addressing this challenge requires a strong synergy between the central government and local governments.
For indigenous community activists, fighting for community rights to support the implementation of REDD+ is very important. This is because the role of indigenous peoples is very real in protecting the forest and its environment. Those with local wisdom have the knowledge to protect and protect their territory with customary laws, customary institutions and tenure systems that are different from the Western system. In general, they apply communal ownership and do not understand property rights [22]. Tenure issues cannot be eliminated in forestry management in Indonesia. This is due to overlapping control of forest areas because there are claims of state blasphemy over customary forests which are controlled by customary law communities. State forest claims provide room for the State’s unilateral control over the forest through the various companies it owns or granting permits on it with the authority of the regional government. This has resulted in legislation and policies that are not clearly formulated, uncoordinated granting of permits and denial of recognition of indigenous peoples and other local forest users [23]. Indigenous peoples have a special role in REDD+, especially from the policy context, namely their participatory role. They have long lived in the forest and are able to care for and protect the forest for their survival from generation to generation. In addition, their cultural and spiritual relationship with the land and forest where they live is very deep [24]. Actually, the existence of this tenurial conflict has been eliminated somewhat by the implementation of the Social Forestry Program. In general, indigenous peoples have been given access to be able to carry out activities and manage in State forests. Tenure conflicts do not only occur on land already owned by companies that have forest concession permits but also in forest areas that have implemented the REDD+ program. So this is a challenge that must be resolved in the future.
Before REDD+ is fully implemented, a Demonstration Activity (DA) is carried out in the early stages. The implementation of DA is based on international guidelines from COP’s decision in the form of International Guidance for DA. The aim is to find out progress, evaluate the implementation of activities and lessons learned related to DA REDD+. In the implementation of DA REDD+, various activities carried out refer to the methodology issued by the IPCC but the mechanisms mostly follow the schemes issued by the Voluntary Standard such as VCS, CCBS and Plan Vivo. The implementation of REDD+ provides benefits and provides opportunities because it is in accordance with the principles of forest sustainability and provides benefits to the community and biodiversity preservation. The current conditions for DA REDD+ are various, many lessons learned have ended and are also results-based with varying progress which still needs further guidance [25]. A crucial implementation stage is the implementation of the Measuring, Reporting and Verifying (MRV) System. Developing country governments at the COP 16 meeting in Cancun 2010 were encouraged to carry out various mitigation activities, including: reducing emissions from deforestation and forest degradation, conserving forest carbon stocks, sustainable forest management, and increasing carbon stocks (FCCC/CP/2010/7/Add.1/C/Par. 70). In connection with these activities, a suitable and transparent measurement and reporting system needs to be established (FCCC/CP/2010/7/Add.1/C/Par.71). Specifically for activities funded by international or domestic sources, verification must be carried out based on the conventions / guidelines that will be developed (FCCC/CP/2010/7/Add.1/C/Par.71; FCCC/CP/2010/7/Add 1/B/Par. 61 and 62). During its development, the Monitoring, Reporting and Verification system was changed to Measurement, Reporting and Verification (MRV) at the Subsidiary Body for Scientific and Technological Advice (SBSTA) 36 in Bonn, 2012. MRV system is the basic and main requirement of implementing the REDD+ program using the principles incentives that are assessed based on performance or pay for performance [26].
MRV activities include measuring and reporting the effectiveness of GHG reduction or absorption quantitatively using methods and procedures that are reliable, transparent and accountable. MRV is part of a monitoring system where measurement methods and results are conveyed using standard and consistent scientific principles. These activities will serve as the basis for payment for the performance of reducing emissions. Each MRV activity must be in line with the reporting principles of the IPCC (Intergovernmental Panel on Climate Change), which must be transparent, accurate, consistent, complete, comparable and have minimal uncertainty. The MRV system implementer is an independent body but still coordinates with the REDD+ Agency as a governing council. The UN-REDD Program has recommended a set of key considerations for the development of a national MRV system. As a system, MRV can be applied to several scales, namely national, sub-national (province, district) and projects. The MRV system can also be reported to certain agencies and verified or validated by certain agencies or associations related to carbon. The use of MRV at the local and national levels is highly recommended. At the international level, reporting to the UNFCCC is a must or a requirement. Because the MRV system reporting must be based on scientific principles, this is a challenge for scientists and foresters in implementing the MRV system [27]. This is very important because the MRV principle is applied to collect data on each type of forest, forest cover and the amount of carbon content contained therein. Forest conditions in Indonesia are very diverse and categorized as mega-biodiversity. Of course, there will be many difficulties in implementing MRV. The challenge that is often faced is the calculation of the biomass present in each forest type. Ideally, biomass calculations are carried out by developing an allometric equation for each tree species which is very expensive. If this is done per tree type in each forest type, it certainly requires a large biomass measurement fund. The REDD+ program is known for leakage, additionality and uncertainity. In REDD+ activities, forest land which is designated as the location for REDD+ implementation according to the stipulated time period must be able to prevent leakage from occurring[28]. Here it is necessary to take intensive care for the location of the implementation of REDDD + so that there is no leakage originating from the work area and the surrounding area. Thus, year after year additionality must be guaranteed. Given the prevalence of forest conversion to non-forest, unresolved tenurial conflicts and illegal logging, etc., it will definitely be difficult to avoid uncertainty.
Global warming has caused climate change around the world. The impact of climate change is very large which affects the joints of life from an economic, ecological, and social perspective. The main cause is deforestation and forest degradation which releases CO2 emissions into the atmosphere. Thus, if deforestation and forest degradation cannot be controlled, the earth’s temperature will get warmer. The warming of the earth’s temperature is also triggered by the use of fossil energy which is not environmentally friendly. Nowadays there is awareness from each country to start replacing fossil energy with biofuels that are more environmentally friendly. Indonesia has planned the production of biofuels to be independent of national energy that is environmentally friendly. One of them is by converting forest land for expansion of oil palm plantations and of course it will cause deforestation. So on the one hand developing environmentally friendly energy but on the other hand, sacrificing the area of the forest so that it becomes a contributor to CO2 emissions that trigger climate change. Therefore, it requires a strong determination from the Government to be able to find the best way that can benefit both of them in controlling climate change. In every program that is executed, there are always opportunities and challenges that must be faced. One of them is the implementation of climate change mitigation and adaptation programs, such as opportunities for implementing the REDD+ program, financing climate change management, and the availability of climate information. There are also challenges faced, such as the lack of synergy in the policy framework and implementation of climate change control, recognition of indigenous peoples’ rights, and uncertainty in the implementation of the REDD+ program.
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\\n\\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\\n\\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\\n\\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\\n\\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
\\n\\n\\n"}]'},components:[{type:"htmlEditorComponent",content:'
The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\n\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\n\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\n\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\n\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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Flawed sample preparations can undermine the quality of results and lead to false conclusions. Thus, the aim of this chapter is to equip researchers, post graduate students and technicians with essential knowledge required to prepare samples for scanning electron microscopy (SEM) investigations in the life sciences.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Mogana Das Murtey and Patchamuthu Ramasamy",authors:[{id:"176330",title:"Dr.",name:"Mogana",middleName:"Das",surname:"Murtey",slug:"mogana-murtey",fullName:"Mogana Murtey"},{id:"181159",title:"Mr.",name:"Patchamuthu",middleName:null,surname:"Ramasamy",slug:"patchamuthu-ramasamy",fullName:"Patchamuthu Ramasamy"}]},{id:"49537",doi:"10.5772/61781",title:"Electron Diffraction",slug:"electron-diffraction",totalDownloads:10067,totalCrossrefCites:9,totalDimensionsCites:30,abstract:"Electron microscopes are usually supplied with equipment for obtaining diffraction patterns and micrographs from the same area of a specimen and the best results are attained if the complete use is to be made of these combined facilities. Electron diffraction patterns are used to obtain quantitative data including phase identification, orientation relationship and crystal defects in materials, etc. At first, a general introduction including a geometrical and quantitative approach to electron diffraction from a crystalline specimen, the reciprocal lattice and electron diffraction in the electron microscope are presented. The scattering process by an individual atom as well as a crystal, the Bragg law, Laue conditions and structure factor are also discussed. Types of diffraction patterns such as ring pattern, spot pattern and Kikuchi pattern, and general and unique indexing diffraction patterns are explained. The procedure for indexing simple, complicated and imperfect patterns as well as Kikuchi lines and a combination of Kikuchi lines and spots is outlined. The known and unknown materials are identified by indexing patterns. 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Finally, electron diffraction patterns of new materials are investigated.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Mohsen Asadi Asadabad and Mohammad Jafari Eskandari",authors:[{id:"176352",title:"Dr.",name:"Mohsen",middleName:null,surname:"Asadi Asadabad",slug:"mohsen-asadi-asadabad",fullName:"Mohsen Asadi Asadabad"},{id:"177600",title:"Dr.",name:"Mohammad",middleName:null,surname:"Jafari Eskandari",slug:"mohammad-jafari-eskandari",fullName:"Mohammad Jafari Eskandari"}]},{id:"49526",doi:"10.5772/61634",title:"Focused Ion Beams (FIB) — Novel Methodologies and Recent Applications for Multidisciplinary Sciences",slug:"focused-ion-beams-fib-novel-methodologies-and-recent-applications-for-multidisciplinary-sciences",totalDownloads:4268,totalCrossrefCites:4,totalDimensionsCites:9,abstract:"Considered as the newest field of electron microscopy, focused ion beam (FIB) technologies are used in many fields of science for site-specific analysis, imaging, milling, deposition, micromachining, and manipulation. Dual-beam platforms, combining a high-resolution scanning electron microscope (HR-SEM) and an FIB column, additionally equipped with precursor-based gas injection systems (GIS), micromanipulators, and chemical analysis tools (such as energy-dispersive spectra (EDS) or wavelength-dispersive spectra (WDS)), serve as multifunctional tools for direct lithography in terms of nano-machining and nano-prototyping, while advanced specimen preparation for transmission electron microscopy (TEM) can practically be carried out with ultrahigh precision. Especially, when hard materials and material systems with hard substrates are concerned, FIB is the only technique for site-specific micro- and nanostructuring. 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In addition, recent studies concerning the active use of dual-beam platforms are mentioned",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Meltem Sezen",authors:[{id:"176338",title:"Associate Prof.",name:"Meltem",middleName:null,surname:"Sezen",slug:"meltem-sezen",fullName:"Meltem Sezen"}]},{id:"49520",doi:"10.5772/61719",title:"Immunogold Techniques in Electron Microscopy",slug:"immunogold-techniques-in-electron-microscopy",totalDownloads:4383,totalCrossrefCites:1,totalDimensionsCites:7,abstract:"Ever since electron microscopy became an important tool in the scientific research, the focus had been mainly on ultrastructural analysis with little success in the development and application of suitable techniques for the localization of macromolecules in cells. The emergence of immunogold techniques in the 1960s managed to fill this gap in serving this function. The aim of this chapter is to equip researchers, postgraduate students, and technicians with essential knowledge to utilize immunogold techniques for ultrastructural investigations in the life sciences. The principles and factors involved have been highlighted to give researchers a quick review of the techniques before embarking on their ultrastructural localization procedures. The advantages and limitations of the four types of immunogold labeling techniques have been discussed.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Mogana Das Murtey",authors:[{id:"176330",title:"Dr.",name:"Mogana",middleName:"Das",surname:"Murtey",slug:"mogana-murtey",fullName:"Mogana Murtey"}]},{id:"49496",doi:"10.5772/61811",title:"Evaluation of the Glomerular Filtration Barrier by Electron Microscopy",slug:"evaluation-of-the-glomerular-filtration-barrier-by-electron-microscopy",totalDownloads:2723,totalCrossrefCites:3,totalDimensionsCites:6,abstract:"The plasma filtration and formation of the urine is a very complex process necessary for the elimination of metabolites, toxins, and excessive water and electrolytes from the body. The initial process of urine formations is done by the glomerular filtration barrier inside the glomeruli. This specialized barrier consists of three layers, fenestrated endothelium, basement membrane, and podocytes, which ensure that water and small molecules pass through while cells and large molecules are retained. The glomerular filtration barrier is found with abnormal morphology in several diseases and is associated with renal malfunction; thus, it is interesting to study these structures in different experimental and clinical conditions. The normal glomerular barrier and its alterations in some conditions (hypertension, diabetes, and fetal programming) are discussed in this chapter. Furthermore, some methods for studying the glomerular filtration barrier by electron microscopy, both by qualitative and quantitative methods, are present.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Diogo Benchimol de Souza, Bianca Martins Gregório, Marlene\nBenchimol and Fernanda Amorim de Morais Nascimento",authors:[{id:"176343",title:"Dr.",name:"Diogo Benchimol",middleName:null,surname:"De Souza",slug:"diogo-benchimol-de-souza",fullName:"Diogo Benchimol De Souza"},{id:"176436",title:"Prof.",name:"Bianca Martins",middleName:null,surname:"Gregório",slug:"bianca-martins-gregorio",fullName:"Bianca Martins Gregório"},{id:"176437",title:"Prof.",name:"Fernanda Amorim De Morais",middleName:null,surname:"Nascimento",slug:"fernanda-amorim-de-morais-nascimento",fullName:"Fernanda Amorim De Morais Nascimento"},{id:"177637",title:"Prof.",name:"Marlene",middleName:null,surname:"Benchimol",slug:"marlene-benchimol",fullName:"Marlene Benchimol"}]}],mostDownloadedChaptersLast30Days:[{id:"49526",title:"Focused Ion Beams (FIB) — Novel Methodologies and Recent Applications for Multidisciplinary Sciences",slug:"focused-ion-beams-fib-novel-methodologies-and-recent-applications-for-multidisciplinary-sciences",totalDownloads:4265,totalCrossrefCites:4,totalDimensionsCites:9,abstract:"Considered as the newest field of electron microscopy, focused ion beam (FIB) technologies are used in many fields of science for site-specific analysis, imaging, milling, deposition, micromachining, and manipulation. Dual-beam platforms, combining a high-resolution scanning electron microscope (HR-SEM) and an FIB column, additionally equipped with precursor-based gas injection systems (GIS), micromanipulators, and chemical analysis tools (such as energy-dispersive spectra (EDS) or wavelength-dispersive spectra (WDS)), serve as multifunctional tools for direct lithography in terms of nano-machining and nano-prototyping, while advanced specimen preparation for transmission electron microscopy (TEM) can practically be carried out with ultrahigh precision. Especially, when hard materials and material systems with hard substrates are concerned, FIB is the only technique for site-specific micro- and nanostructuring. Moreover, FIB sectioning and sampling techniques are frequently used for revealing the structural and morphological distribution of material systems with three-dimensional (3D) network at micro-/nanoscale.This book chapter includes many examples on conventional and novel processes of FIB technologies, ranging from analysis of semiconductors to electron tomography-based imaging of hard materials such as nanoporous ceramics and composites. In addition, recent studies concerning the active use of dual-beam platforms are mentioned",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Meltem Sezen",authors:[{id:"176338",title:"Associate Prof.",name:"Meltem",middleName:null,surname:"Sezen",slug:"meltem-sezen",fullName:"Meltem Sezen"}]},{id:"49537",title:"Electron Diffraction",slug:"electron-diffraction",totalDownloads:10058,totalCrossrefCites:9,totalDimensionsCites:30,abstract:"Electron microscopes are usually supplied with equipment for obtaining diffraction patterns and micrographs from the same area of a specimen and the best results are attained if the complete use is to be made of these combined facilities. Electron diffraction patterns are used to obtain quantitative data including phase identification, orientation relationship and crystal defects in materials, etc. At first, a general introduction including a geometrical and quantitative approach to electron diffraction from a crystalline specimen, the reciprocal lattice and electron diffraction in the electron microscope are presented. The scattering process by an individual atom as well as a crystal, the Bragg law, Laue conditions and structure factor are also discussed. Types of diffraction patterns such as ring pattern, spot pattern and Kikuchi pattern, and general and unique indexing diffraction patterns are explained. The procedure for indexing simple, complicated and imperfect patterns as well as Kikuchi lines and a combination of Kikuchi lines and spots is outlined. The known and unknown materials are identified by indexing patterns. Practical comparisons between various methods of analysing diffraction patterns are also described. The basic diffraction patterns and the fine structure in the patterns including specimen tilting experiments, orientation relationship determination, phase identification, twinning, second phases, crystallographic information, dislocation, preferred orientation and texture, extra spots and streaks are described in detail. Finally, electron diffraction patterns of new materials are investigated.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Mohsen Asadi Asadabad and Mohammad Jafari Eskandari",authors:[{id:"176352",title:"Dr.",name:"Mohsen",middleName:null,surname:"Asadi Asadabad",slug:"mohsen-asadi-asadabad",fullName:"Mohsen Asadi Asadabad"},{id:"177600",title:"Dr.",name:"Mohammad",middleName:null,surname:"Jafari Eskandari",slug:"mohammad-jafari-eskandari",fullName:"Mohammad Jafari Eskandari"}]},{id:"49846",title:"Scanning Electron Microscopy with a Retarded Primary Beam",slug:"scanning-electron-microscopy-with-a-retarded-primary-beam",totalDownloads:1999,totalCrossrefCites:1,totalDimensionsCites:2,abstract:"The general trend for reducing the energies of primary electrons in electron microscopy has been faced with a gradual deterioration of the image resolution. Biasing the sample to a high negative voltage and making the electrons arbitrarily slow solely on and inside the sample has shown itself to be far more feasible than originally expected. The fundamental aberration coefficients (spherical and chromatic) of a combination of an objective lens and an immersion electrostatic lens formed by the biased sample decrease with the decreasing landing energy of the electrons. As a result, the spot size in scanning systems may become nearly independent of the landing energy of the electrons. The requirements placed on samples are strict but feasible, and detection of signal electrons is greatly facilitated by the acceleration of both reflected and transmitted electrons in the field of the biased sample and their collimation toward the optical axis. The interaction of slow electrons is not only more intensive than that at standard energies but even scattering phenomena appear which are not otherwise observed. Several application examples are presented. The benefits of very low energy EM are still being uncovered after its having been in routine use for several years.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Luděk Frank",authors:[{id:"16460",title:"Dr.",name:"Ludek",middleName:null,surname:"Frank",slug:"ludek-frank",fullName:"Ludek Frank"}]},{id:"49627",title:"Observation of Fungi, Bacteria, and Parasites in Clinical Skin Samples Using Scanning Electron Microscopy",slug:"observation-of-fungi-bacteria-and-parasites-in-clinical-skin-samples-using-scanning-electron-microsc",totalDownloads:3596,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"This chapter highlights the description of the clinical manifestation and its pathogen and the host tissue damage observed under the Scanning Electron Microscope, which helps the clinician to understand the pathogen’s superstructure, the change of host subcell structure, and the laboratory workers to understand the clinical characteristics of pathogen-induced human skin lesions, to establish a two-way learning exchange database with vivid images",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Ran Yuping, Zhuang Kaiwen, Hu Wenying, Huang Jinghong, Feng\nXiaowei, Chen Shuang, Tang Jiaoqing, Xu Xiaoxi, Kang Daoxian, Lu\nYao, Zhang Ruifeng, Ran Xin, Wan Huiying, Lama Jebina, Dai Yalin\nand Zhang Chaoliang",authors:[{id:"174134",title:"Dr.",name:"Yuping",middleName:null,surname:"Ran",slug:"yuping-ran",fullName:"Yuping Ran"}]},{id:"49519",title:"Microstructure Evolution in Ultrafine-grained Magnesium Alloy AZ31 Processed by Severe Plastic Deformation",slug:"microstructure-evolution-in-ultrafine-grained-magnesium-alloy-az31-processed-by-severe-plastic-defor",totalDownloads:1912,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Commercial MgAlZn alloy AZ31 was processed by two techniques of severe plastic deformation (SPD): equal channel angular pressing and high pressure torsion. Several microscopic techniques, namely light, scanning and transmission electron microscopy, electron backscatter diffraction, and automated crystallographic orientation mapping were employed to characterize the details of microstructure evolution and grain fragmentation of the alloy as a function of strain imposed to the material using these SPD techniques. The advantages and drawbacks of these techniques, as well as the limits of their resolution, are discussed in detail. The results of microstructure observations indicate the effectiveness of grain refinement by severe plastic deformation in this alloy. The thermal stability of ultrafine-grained structure that is important for practical applications is also discussed.",book:{id:"5075",slug:"modern-electron-microscopy-in-physical-and-life-sciences",title:"Modern Electron Microscopy in Physical and Life Sciences",fullTitle:"Modern Electron Microscopy in Physical and Life Sciences"},signatures:"Jitka Stráská, Josef Stráský, Peter Minárik, Miloš Janeček and Robert\nKrál",authors:[{id:"15744",title:"Dr.",name:"Milos",middleName:null,surname:"Janecek",slug:"milos-janecek",fullName:"Milos Janecek"},{id:"177102",title:"Dr.",name:"Jitka",middleName:null,surname:"Stráská",slug:"jitka-straska",fullName:"Jitka Stráská"},{id:"177103",title:"Dr.",name:"Josef",middleName:null,surname:"Strasky",slug:"josef-strasky",fullName:"Josef Strasky"},{id:"177104",title:"Dr.",name:"Petr",middleName:null,surname:"Minarik",slug:"petr-minarik",fullName:"Petr Minarik"},{id:"177105",title:"Dr.",name:"Robert",middleName:null,surname:"Kral",slug:"robert-kral",fullName:"Robert Kral"}]}],onlineFirstChaptersFilter:{topicId:"1224",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[],lsSeriesList:[],hsSeriesList:[],sshSeriesList:[],testimonialsList:[]},series:{item:{id:"22",title:"Business, Management and Economics",doi:"10.5772/intechopen.100359",issn:"2753-894X",scope:"
\r\n\tThis series will provide a comprehensive overview of recent research trends in business and management, economics, and marketing. Topics will include asset liability management, financial consequences of the financial crisis and covid-19, financial accounting, mergers and acquisitions, management accounting, SMEs, financial markets, corporate finance and governance, managerial technology and innovation, resource management and sustainable development, social entrepreneurship, corporate responsibility, ethics and accountability, microeconomics, labour economics, macroeconomics, public economics, financial economics, econometrics, direct marketing, creative marketing, internet marketing, market planning and forecasting, brand management, market segmentation and targeting and other topics under business and management. This book series will focus on various aspects of business and management whose in-depth understanding is critical for business and company management to function effectively during this uncertain time of financial crisis, Covid-19 pandemic, and military activity in Europe.
",coverUrl:"https://cdn.intechopen.com/series/covers/22.jpg",latestPublicationDate:"May 18th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:1,editor:{id:"356540",title:"Prof.",name:"Taufiq",middleName:null,surname:"Choudhry",slug:"taufiq-choudhry",fullName:"Taufiq Choudhry",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000036X2hvQAC/Profile_Picture_2022-03-14T08:58:03.jpg",biography:"Prof. Choudhry holds a BSc degree in Economics from the University of Iowa, as well as a Masters and Ph.D. in Applied Economics from Clemson University, USA. In January 2006, he became a Professor of Finance at the University of Southampton Business School. He was previously a Professor of Finance at the University of Bradford Management School. He has over 80 articles published in international finance and economics journals. His research interests and specialties include financial econometrics, financial economics, international economics and finance, housing markets, financial markets, among others.",institutionString:null,institution:{name:"University of Southampton",institutionURL:null,country:{name:"United Kingdom"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:5,paginationItems:[{id:"91",title:"Sustainable Economy and Fair Society",coverUrl:"https://cdn.intechopen.com/series_topics/covers/91.jpg",isOpenForSubmission:!0,editor:{id:"181603",title:"Dr.",name:"Antonella",middleName:null,surname:"Petrillo",slug:"antonella-petrillo",fullName:"Antonella Petrillo",profilePictureURL:"https://mts.intechopen.com/storage/users/181603/images/system/181603.jpg",biography:"Antonella Petrillo is a Professor at the Department of Engineering of the University of Naples “Parthenope”, Italy. She received her Ph.D. in Mechanical Engineering from the University of Cassino. Her research interests include multi-criteria decision analysis, industrial plant, logistics, manufacturing and safety. She serves as an Associate Editor for the International Journal of the Analytic Hierarchy Process. She is a member of AHP Academy and a member of several editorial boards. She has over 160 Scientific Publications in International Journals and Conferences and she is the author of 5 books on Innovation and Decision Making in Industrial Applications and Engineering.",institutionString:null,institution:{name:"Parthenope University of Naples",institutionURL:null,country:{name:"Italy"}}},editorTwo:null,editorThree:null},{id:"92",title:"Health and Wellbeing",coverUrl:"https://cdn.intechopen.com/series_topics/covers/92.jpg",isOpenForSubmission:!0,editor:{id:"348225",title:"Prof.",name:"Ann",middleName:null,surname:"Hemingway",slug:"ann-hemingway",fullName:"Ann Hemingway",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000035LZFoQAO/Profile_Picture_2022-04-11T14:55:40.jpg",biography:"Professor Hemingway is a public health researcher, Bournemouth University, undertaking international and UK research focused on reducing inequalities in health outcomes for marginalised and excluded populations and more recently focused on equine assisted interventions.",institutionString:null,institution:{name:"Bournemouth University",institutionURL:null,country:{name:"United Kingdom"}}},editorTwo:null,editorThree:null},{id:"93",title:"Inclusivity and Social Equity",coverUrl:"https://cdn.intechopen.com/series_topics/covers/93.jpg",isOpenForSubmission:!0,editor:{id:"210060",title:"Prof. Dr.",name:"Ebba",middleName:null,surname:"Ossiannilsson",slug:"ebba-ossiannilsson",fullName:"Ebba Ossiannilsson",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002g6LkBQAU/Profile_Picture_2022-02-28T13:31:48.png",biography:'Professor Dr. Ebba Ossiannilsson is an independent researcher, expert, consultant, quality auditor and influencer in the fields of open, flexible online and distance learning (OFDL) and the "new normal". Her focus is on quality, innovation, leadership, and personalised learning. She works primarily at the strategic and policy levels, both nationally and internationally, and with key international organisations. She is committed to promoting and improving OFDL in the context of SDG4 and the future of education. Ossiannilsson has more than 20 years of experience in her current field, but more than 40 years in the education sector. She works as a reviewer and expert for the European Commission and collaborates with the Joint Research Centre for Quality in Open Education. Ossiannilsson also collaborates with ITCILO and ICoBC (International Council on Badges and Credentials). She is a member of the ICDE Board of Directors and has previously served on the boards of EDEN and EUCEN. Ossiannilsson is a quality expert and reviewer for ICDE, EDEN and the EADTU. She chairs the ICDE OER Advocacy Committee and is a member of the ICDE Quality Network. She is regularly invited as a keynote speaker at conferences. She is a guest editor for several special issues and a member of the editorial board of several scientific journals. She has published more than 200 articles and is currently working on book projects in the field of OFDL. Ossiannilsson is a visiting professor at several international universities and was recently appointed Professor and Research Fellow at Victoria University of Wellington, NZ. Ossiannilsson has been awarded the following fellowships: EDEN Fellows, EDEN Council of Fellows, and Open Education Europe. She is a ICDE OER Ambassador, Open Education Europe Ambassador, GIZ Ambassador for Quality in Digital Learning, and part of the Globe-Community of Digital Learning and Champion of SPARC Europe. On a national level, she is a quality developer at the Swedish Institute for Standards (SIS) and for ISO. She is a member of the Digital Skills and Jobs Coalition Sweden and Vice President of the Swedish Association for Distance Education. She is currently working on a government initiative on quality in distance education at the National Council for Higher Education. She holds a Ph.D. from the University of Oulu, Finland.',institutionString:"Swedish Association for Distance Education, Sweden",institution:null},editorTwo:null,editorThree:null},{id:"94",title:"Climate Change and Environmental Sustainability",coverUrl:"https://cdn.intechopen.com/series_topics/covers/94.jpg",isOpenForSubmission:!1,editor:null,editorTwo:null,editorThree:null},{id:"95",title:"Urban Planning and Environmental Management",coverUrl:"https://cdn.intechopen.com/series_topics/covers/95.jpg",isOpenForSubmission:!0,editor:{id:"181079",title:"Dr.",name:"Christoph",middleName:null,surname:"Lüthi",slug:"christoph-luthi",fullName:"Christoph Lüthi",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRHSqQAO/Profile_Picture_2022-04-12T15:51:33.png",biography:"Dr. Christoph Lüthi is an urban infrastructure planner with over 25 years of experience in planning and design of urban infrastructure in middle and low-income countries. He holds a Master’s Degree in Urban Development Planning from the University College of London (UCL), and a Ph.D. in Urban Planning & Engineering from TU Berlin. He has conducted applied research on urban planning and infrastructure issues in over 20 countries in Africa and Asia. In 2005 he joined Eawag-Sandec as Leader of the Strategic Environmental Sanitation Planning Group. Since 2015 he heads the research department Sanitation, Water and Solid Waste for Development (Sandec) at the Swiss Federal Institute of Aquatic Research and Technology (Eawag).",institutionString:"Swiss Federal Institute of Aquatic Science and Technology, Switzerland",institution:null},editorTwo:{id:"290571",title:"Dr.",name:"Rui Alexandre",middleName:null,surname:"Castanho",slug:"rui-alexandre-castanho",fullName:"Rui Alexandre Castanho",profilePictureURL:"https://mts.intechopen.com/storage/users/290571/images/system/290571.jpg",biography:"Rui Alexandre Castanho has a master\\'s degree in Planning, Audit, and Control in Urban Green Spaces and an international Ph.D. in Sustainable Planning in Borderlands. Currently, he is a professor at WSB University, Poland, and a visiting professor at the University of Johannesburg, South Africa. Dr. Castanho is a post-doc researcher on the GREAT Project, University of Azores, Ponta Delgada, Portugal. He collaborates with the Environmental Resources Analysis Research Group (ARAM), University of Extremadura (UEx), Spain; VALORIZA - Research Center for the Enhancement of Endogenous Resources, Polytechnic Institute of Portalegre (IPP), Portugal; Centre for Tourism Research, Development and Innovation (CITUR), Madeira, Portugal; and AQUAGEO Research Group, University of Campinas (UNICAMP), Brazil.",institutionString:"University of Johannesburg, South Africa and WSB University, Poland",institution:{name:"University of Johannesburg",institutionURL:null,country:{name:"South Africa"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:11,paginationItems:[{id:"81920",title:"Rethinking an Approach for Sustainable Globalization",doi:"10.5772/intechopen.105141",signatures:"Parakram Pyakurel",slug:"rethinking-an-approach-for-sustainable-globalization",totalDownloads:0,totalCrossrefCites:null,totalDimensionsCites:null,authors:null,book:{title:"Globalization and Sustainability - Recent Advances, New Perspectives and Emerging Issues",coverURL:"https://cdn.intechopen.com/books/images_new/11476.jpg",subseries:{id:"91",title:"Sustainable Economy and Fair Society"}}},{id:"81297",title:"Legumes Cropping and Nitrogen Fixation under Mediterranean Climate",doi:"10.5772/intechopen.104473",signatures:"Fernando Teixeira",slug:"legumes-cropping-and-nitrogen-fixation-under-mediterranean-climate",totalDownloads:3,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Food Systems Resilience",coverURL:"https://cdn.intechopen.com/books/images_new/10897.jpg",subseries:{id:"91",title:"Sustainable Economy and Fair Society"}}},{id:"81493",title:"Rust Disease Classification Using Deep Learning Based Algorithm: The Case of Wheat",doi:"10.5772/intechopen.104426",signatures:"Shivani Sood, Harjeet Singh and Suruchi Jindal",slug:"rust-disease-classification-using-deep-learning-based-algorithm-the-case-of-wheat",totalDownloads:40,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Food Systems Resilience",coverURL:"https://cdn.intechopen.com/books/images_new/10897.jpg",subseries:{id:"91",title:"Sustainable Economy and Fair Society"}}},{id:"81428",title:"Observatory of Sustainable Development in Postgraduate Study Programs in Baja California",doi:"10.5772/intechopen.104641",signatures:"Rodolfo Martinez-Gutierrez, Maria Marcela Solis-Quinteros, Maria Esther Ibarra-Estrada and Angel Ernesto Jimenez-Bernardino",slug:"observatory-of-sustainable-development-in-postgraduate-study-programs-in-baja-california",totalDownloads:9,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Globalization and Sustainability - Recent Advances, New Perspectives and Emerging Issues",coverURL:"https://cdn.intechopen.com/books/images_new/11476.jpg",subseries:{id:"91",title:"Sustainable Economy and Fair Society"}}}]},overviewPagePublishedBooks:{paginationCount:0,paginationItems:[]},openForSubmissionBooks:{},onlineFirstChapters:{paginationCount:17,paginationItems:[{id:"81751",title:"NanoBioSensors: From Electrochemical Sensors Improvement to Theranostic Applications",doi:"10.5772/intechopen.102552",signatures:"Anielle C.A. 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