Names and abbreviations of ionic liquids.
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:{caption:"IntechOpen Maintains",originalUrl:"/media/original/113"}},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\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:"6060",leadTitle:null,fullTitle:"Mitochondrial Diseases",title:"Mitochondrial Diseases",subtitle:null,reviewType:"peer-reviewed",abstract:"Mitochondria are crucial organelles for any cell type. Mitochondria take responsibility for not only energy production but also regulation of cell death, also called apoptosis; calcium storage; and heat production. Therefore, mitochondrial disease is implicated in the mode of action of many harmful factors for cells such as drugs and environmental contaminants, dysfunction of the oxygen transport system, malnutrition, intense exercise, and genetic variations. This book presents up-to-date knowledge about mitochondrial disease and its complex relation to some diseases such as cardiac failure, cancer, and Alzheimer's and Parkinson's diseases. This book will, therefore, be essential for readers who are interested in life sciences, especially in medicine.",isbn:"978-1-78923-675-0",printIsbn:"978-1-78923-674-3",pdfIsbn:"978-1-83881-272-0",doi:"10.5772/67963",price:139,priceEur:155,priceUsd:179,slug:"mitochondrial-diseases",numberOfPages:496,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"66c079bd70478fcc63072a8a42da4c33",bookSignature:"Eylem Taskin, Celal Guven and Yusuf Sevgiler",publishedDate:"August 29th 2018",coverURL:"https://cdn.intechopen.com/books/images_new/6060.jpg",numberOfDownloads:20913,numberOfWosCitations:24,numberOfCrossrefCitations:23,numberOfCrossrefCitationsByBook:0,numberOfDimensionsCitations:48,numberOfDimensionsCitationsByBook:0,hasAltmetrics:1,numberOfTotalCitations:95,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 22nd 2017",dateEndSecondStepPublish:"March 15th 2017",dateEndThirdStepPublish:"July 15th 2017",dateEndFourthStepPublish:"October 14th 2017",dateEndFifthStepPublish:"December 20th 2017",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"192567",title:"Prof.",name:"Eylem",middleName:null,surname:"Taskin",slug:"eylem-taskin",fullName:"Eylem Taskin",profilePictureURL:"https://mts.intechopen.com/storage/users/192567/images/system/192567.png",biography:"Eylem Taskin is a physiologist. She worked as a postdoctoral researcher at New York University for two years. She has published more than twenty articles and four international book chapters. She has also edited a book. She has worked on the editorial board for several scientific journals.",institutionString:"Nigde Omer Halisdemir University",position:"Associate Professor",outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"3",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"205580",title:"Dr.",name:"Celal",middleName:null,surname:"Guven",slug:"celal-guven",fullName:"Celal Guven",profilePictureURL:"https://mts.intechopen.com/storage/users/205580/images/7792_n.jpg",biography:"Celal Guven graduated from the Department of Biophysics, Istanbul University. He has been working on protein-chemical interactions. He has published almost ten articles and four international book chapters. He has also edited a book. Dr. Guven has worked on an editorial board for a national journal.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorTwo:{id:"205581",title:"Dr.",name:"Yusuf",middleName:null,surname:"Sevgiler",slug:"yusuf-sevgiler",fullName:"Yusuf Sevgiler",profilePictureURL:"https://mts.intechopen.com/storage/users/205581/images/system/205581.jpeg",biography:"Yusuf Sevgiler graduated from the Department of Biology, Çukurova University. He has published twenty articles about oxidative and neurotoxic potentials of xenobiotics and reviewed many. Dr Sevgiler has also published two international book chapters and has edited a book as well.",institutionString:"Adiyaman University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Adıyaman University",institutionURL:null,country:{name:"Turkey"}}},coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1049",title:"Mitochondrial Genetics",slug:"mitochondrial-genetics"}],chapters:[{id:"56803",title:"Mitochondria and Metabolism in Right Heart Failure",doi:"10.5772/intechopen.70450",slug:"mitochondria-and-metabolism-in-right-heart-failure",totalDownloads:1062,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Heart failure (HF) is a clinically complex and heterogenous disease characterized by an inability of the heart to pump sufficient blood to the periphery. As such, it has historically been thought of and studied as a disease of the left ventricle (LV). While LV failure is the most common form of HF, it is the ability of the right heart to function that predicts survival in many clinical settings. Extrapolation of mechanisms of left HF to the right ventricle (RV) has yet to prove fruitful in identification of therapeutic approaches, in large part due to a lack of basic mechanistic understanding of the RV which is embryologically, anatomically, and physiologically distinct from the LV. The failing LV is characterized by mitochondrial dysfunction and a metabolic switch, both of which contribute to an energetically starved heart with poor contractile ability. These mechanisms, however, are far less described in the failing RV. The purpose of this chapter is to present the current literature examining the role of mitochondria and metabolism in the healthy right heart, treatments to target deficits in the failing RV, and to identify knowledge gaps for future research in this clinically important area.",signatures:"Danielle R. Bruns and Lori A. Walker",downloadPdfUrl:"/chapter/pdf-download/56803",previewPdfUrl:"/chapter/pdf-preview/56803",authors:[{id:"95273",title:"Dr.",name:"Lori A.",surname:"Walker",slug:"lori-a.-walker",fullName:"Lori A. Walker"},{id:"206035",title:"Dr.",name:"Danielle R.",surname:"Bruns",slug:"danielle-r.-bruns",fullName:"Danielle R. Bruns"}],corrections:null},{id:"58177",title:"Mitochondria and Heart Disease",doi:"10.5772/intechopen.72611",slug:"mitochondria-and-heart-disease",totalDownloads:1283,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:1,abstract:"Mitochondria play a key role in the normal functioning of the heart and in the pathogenesis and development of various types of heart disease. In addition, specific mitochondrial cardiomyopathies due to mutations in mitochondrial DNA have been identified. Increasing studies demonstrate that mitochondrial function has emerged as a therapeutic target in heart disease. This chapter addresses the recent studies of the role and the mechanism of mitochondria in the development of heart disease, and the progress in clinical diagnosis and treatments on a mitochondrial basis. Consequently, the aim of this chapter is to outline current knowledge about mitochondria in the heart disease.",signatures:"Shaunrick Stoll, Christiana Leimena and Hongyu Qiu",downloadPdfUrl:"/chapter/pdf-download/58177",previewPdfUrl:"/chapter/pdf-preview/58177",authors:[{id:"207057",title:"Dr.",name:"Hongyu",surname:"Qiu",slug:"hongyu-qiu",fullName:"Hongyu Qiu"},{id:"217395",title:"Mr.",name:"Shaunrick",surname:"Stoll",slug:"shaunrick-stoll",fullName:"Shaunrick Stoll"},{id:"217396",title:"Dr.",name:"Christiana",surname:"Leimena",slug:"christiana-leimena",fullName:"Christiana Leimena"}],corrections:null},{id:"57765",title:"Interplay Between Mitochondrial Proteins and Age-Associated Risk of Cardiovascular Diseases",doi:"10.5772/intechopen.71789",slug:"interplay-between-mitochondrial-proteins-and-age-associated-risk-of-cardiovascular-diseases",totalDownloads:912,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Normal functioning of mitochondria is crucial for cardiac performance. Mitochondria undergo mitophagy (mitochondrial autophagy) and biogenesis, and mitochondrial proteins are subject to extensive post-translational modifications (PTMs). The state of mitochondrial homeostasis reflects overall cellular fitness and longevity. Perturbed mitochondria produce less adenosine triphosphate (ATP), release greater amounts of reactive molecules, and are more prone to apoptosis. Therefore mitochondrial turnover is an integral aspect of quality control in which dysfunctional mitochondria are selectively eliminated through mitophagy. Currently, the progressive deterioration of physiological functions is seen as accumulation of modified/damaged proteins with limiting regenerative ability throughout aging in myocardial cells. Mitochondrial stress response to reactive species was evaluated as electron transport chain (ETC) complexes, redox-active molecules, and their possible communication. Protein-protein interactions revealed a strong linkage between age and ETC protein subunits. Redox state was strongly affected in senescent mitochondria with shift in favor of more pro-oxidizing condition within cardiomyocytes. Assume all together, dysfunctional proteostasis can play a causative role in aging and restoration of protein homeostasis machinery is protective against aging and possibly age-related disorders.",signatures:"Zuzana Tatarkova, Martin Kolisek, Ivana Pilchova, Peter Racay and\nPeter Kaplan",downloadPdfUrl:"/chapter/pdf-download/57765",previewPdfUrl:"/chapter/pdf-preview/57765",authors:[{id:"188509",title:"Prof.",name:"Peter",surname:"Kaplan",slug:"peter-kaplan",fullName:"Peter Kaplan"},{id:"213111",title:"Associate Prof.",name:"Zuzana",surname:"Tatarkova",slug:"zuzana-tatarkova",fullName:"Zuzana Tatarkova"},{id:"213298",title:"Dr.",name:"Martin",surname:"Kolisek",slug:"martin-kolisek",fullName:"Martin Kolisek"},{id:"213299",title:"Dr.",name:"Ivana",surname:"Pilchova",slug:"ivana-pilchova",fullName:"Ivana Pilchova"},{id:"213300",title:"Prof.",name:"Peter",surname:"Racay",slug:"peter-racay",fullName:"Peter Racay"}],corrections:null},{id:"58893",title:"Differential Effect of Atpenin A5 on ROS Production from Wild- Type Mitochondrial Complex II in Human Cancer Cells and Normal Cells",doi:"10.5772/intechopen.71638",slug:"differential-effect-of-atpenin-a5-on-ros-production-from-wild-type-mitochondrial-complex-ii-in-human",totalDownloads:970,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Human mitochondrial complex II is an intriguing enzyme, which has been the focus of medical research during the past few decades since it contributes to pathogenesis of mitochondrial diseases as well as a target for chemotherapy. Reactive oxygen species (ROS) produced by this enzyme has been implicated in both these conditions. While ROS produced from mutated mitochondrial complex II has been implicated in pathogenesis of mitochondrial diseases, ROS produced from pharmacologically inhibited mitochondrial complex II has been implicated in cancer cell death. In this chapter, we show that inhibition of mitochondrial complex II in human cancer cells with atpenin A5 produces detectable levels of ROS while normal cells do not. Thus, this enzyme may be used as a potential target for developing new anticancer drugs to trigger ROS-mediated selective death of cancer cells.",signatures:"Madhavi P. Paranagama and Kiyoshi Kita",downloadPdfUrl:"/chapter/pdf-download/58893",previewPdfUrl:"/chapter/pdf-preview/58893",authors:[{id:"173425",title:"Prof.",name:"Kiyoshi",surname:"Kita",slug:"kiyoshi-kita",fullName:"Kiyoshi Kita"},{id:"212640",title:"Dr.",name:"Madhavi Priyanka",surname:"Paranagama",slug:"madhavi-priyanka-paranagama",fullName:"Madhavi Priyanka Paranagama"}],corrections:null},{id:"57487",title:"A New Insight into the Development of Novel Anti-Cancer Drugs that Improve the Expression of Mitochondrial Function-Associated Genes",doi:"10.5772/intechopen.71095",slug:"a-new-insight-into-the-development-of-novel-anti-cancer-drugs-that-improve-the-expression-of-mitocho",totalDownloads:1016,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Recent analyses of the whole genome sequencing data enable us to predict cancer incidence for healthy people at present. In addition, metabolome analyses rediscovered that “cancer is a metabolic disease”. Importantly, it has been suggested that mitochondrial dysfunction might precede the metabolic change. In this chapter, we would discuss if “cancer is a transcriptional disease”. Analyzing 5′-upstream non-protein-encoding regions of the human mitochondrial function-associated genes, we speculate that mitochondrial functions could be recovered or improved at a transcriptional level. In the near future, novel chemo-/gene-therapies might be applied to treat cancer patient converting cancerous cells into normal differentiated cells.",signatures:"Fumiaki Uchiumi, Jun Arakawa, Yutaka Takihara, Motohiro Akui,\nHiroshi Hamada and Sei-ichi Tanuma",downloadPdfUrl:"/chapter/pdf-download/57487",previewPdfUrl:"/chapter/pdf-preview/57487",authors:[{id:"47235",title:"Dr.",name:"Fumiaki",surname:"Uchiumi",slug:"fumiaki-uchiumi",fullName:"Fumiaki Uchiumi"},{id:"56771",title:"Dr.",name:"Sei-Ichi",surname:"Tanuma",slug:"sei-ichi-tanuma",fullName:"Sei-Ichi Tanuma"},{id:"217239",title:"BSc.",name:"Jun",surname:"Arakawa",slug:"jun-arakawa",fullName:"Jun Arakawa"},{id:"217242",title:"BSc.",name:"Yutaka",surname:"Takihara",slug:"yutaka-takihara",fullName:"Yutaka Takihara"},{id:"217245",title:"BSc.",name:"Motohiro",surname:"Akui",slug:"motohiro-akui",fullName:"Motohiro Akui"},{id:"217246",title:"BSc.",name:"Hiroshi",surname:"Hamada",slug:"hiroshi-hamada",fullName:"Hiroshi Hamada"}],corrections:null},{id:"58888",title:"Mitochondria at the Base of Neuronal Innate Immunity in Alzheimer’s and Parkinson’s Diseases",doi:"10.5772/intechopen.72612",slug:"mitochondria-at-the-base-of-neuronal-innate-immunity-in-alzheimer-s-and-parkinson-s-diseases",totalDownloads:1098,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Mitochondria are exceptionally primed to play a key role in neuronal cell survival since they are involved in energy production and function as the metabolic center of cells. Several findings provide evidence for the role of mitochondria in neurodegeneration associated with Alzheimer’s and Parkinson’s diseases (AD and PD). Recent data highlight the role of mitochondrial proteins and mitochondrial reactive oxygen species in the intracellular signaling that regulates innate immunity and inflammation. In this chapter, we will discuss the relevance of the interplay between mitochondria and innate immunity, focusing on mitochondrial damage-associated molecular patterns (DAMPs) and how they can activate innate immunity and elicit AD and PD neurodegenerative process.",signatures:"A. Raquel Esteves, Diana F. Silva, Daniel Santos, Emanuel Candeias,\nFilipa Filipe and Sandra M. Cardoso",downloadPdfUrl:"/chapter/pdf-download/58888",previewPdfUrl:"/chapter/pdf-preview/58888",authors:[{id:"164998",title:"Ph.D.",name:"Ana",surname:"Esteves",slug:"ana-esteves",fullName:"Ana Esteves"},{id:"164999",title:"Prof.",name:"Sandra",surname:"Cardoso",slug:"sandra-cardoso",fullName:"Sandra Cardoso"},{id:"213149",title:"Dr.",name:"Diana F",surname:"Silva",slug:"diana-f-silva",fullName:"Diana F Silva"},{id:"213153",title:"Dr.",name:"Daniel",surname:"Santos",slug:"daniel-santos",fullName:"Daniel Santos"},{id:"213154",title:"Dr.",name:"Emanuel",surname:"Candeias",slug:"emanuel-candeias",fullName:"Emanuel Candeias"},{id:"213155",title:"Dr.",name:"Filipa",surname:"Filipe",slug:"filipa-filipe",fullName:"Filipa Filipe"}],corrections:null},{id:"57582",title:"Protein Kinases and Regulation of Mitochondrial Function in Ischemia/Reperfusion Injury",doi:"10.5772/intechopen.71094",slug:"protein-kinases-and-regulation-of-mitochondrial-function-in-ischemia-reperfusion-injury",totalDownloads:965,totalCrossrefCites:1,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Ischemic heart disease and stroke are the leading causes of death worldwide. Nonetheless, our understanding of the molecular mechanisms regulating cardiac and cerebral ischemic injury is very modest and our ability to develop therapies arresting and/or reversing detrimental events that spread from the ischemic core to the surrounding tissue is limited. Ischemia occurs when oxygen is unavailable to tissues due to occlusion of an artery (myocardial infarction, stroke, and pulmonary embolism), hemorrhage, organ transplantation, or hypotension in septic shock. The mitochondrion is a key target of ischemia. Alterations in mitochondrial morphology, dynamics, and functions result in energy deficits and contribute to the pathogenesis of ischemic injury. Phosphorylations of mitochondrial proteins and protein kinases that mediate them are important regulators of mitochondrial functions and tissue ATP levels. Thus, mitochondrial protein kinases could serve as targets for therapeutic interventions to mitigate the effects of ischemic injury. This will review the mitochondrial proteins regulated by phosphorylation, protein kinases mediating these reactions, and their implications in mitochondrial functions in ischemia/reperfusion (I/R)-induced injury.",signatures:"Grażyna Nowak",downloadPdfUrl:"/chapter/pdf-download/57582",previewPdfUrl:"/chapter/pdf-preview/57582",authors:[{id:"206134",title:"Prof.",name:"Grazyna",surname:"Nowak",slug:"grazyna-nowak",fullName:"Grazyna Nowak"}],corrections:null},{id:"60594",title:"Mitochondrial Trafficking by Prohibitin-Kinesin-Myosin- Cadherin Complex in the Eye",doi:"10.5772/intechopen.75994",slug:"mitochondrial-trafficking-by-prohibitin-kinesin-myosin-cadherin-complex-in-the-eye",totalDownloads:1184,totalCrossrefCites:1,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Disruption of the mitochondrial-nuclear network leads to accelerated aging and age-related diseases, including age-related macular degeneration. The current study tested the hypothesis that mitochondrial morphology could be demonstrated quantitatively using a mathematic model and mitochondrial trafficking complex under stress conditions. To test our hypothesis, normal and aberrant mitochondria were examined quantitatively based on mitochondrial size, shape, position, composition, and dynamics. Adaptation of the mitochondrial network to changes in the intracellular oxidation and reduction milieu is critical for the survival of retinal pigment epithelial cells. Our mitochondrial interactome mapping demonstrated that a positive correlation may exist between oxidative stress-mediated phosphorylation and age-related disease progression. The current interactome may provide a potential therapeutic approach to treat mitochondria-induced neurodegeneration, including age-related macular degeneration.",signatures:"Srinivas R. Sripathi, Weilue He, Johnpaul Offor, Diana R. Gutsaeva\nand Wan Jin Jahng",downloadPdfUrl:"/chapter/pdf-download/60594",previewPdfUrl:"/chapter/pdf-preview/60594",authors:[{id:"205781",title:"Associate Prof.",name:"Wan Jin",surname:"Jahng",slug:"wan-jin-jahng",fullName:"Wan Jin Jahng"},{id:"244413",title:"Dr.",name:"Srinivasa R.",surname:"Sripathi",slug:"srinivasa-r.-sripathi",fullName:"Srinivasa R. Sripathi"},{id:"244414",title:"Dr.",name:"Weilue",surname:"He",slug:"weilue-he",fullName:"Weilue He"},{id:"244415",title:"Dr.",name:"Johnpaul",surname:"Offor",slug:"johnpaul-offor",fullName:"Johnpaul Offor"},{id:"244416",title:"Dr.",name:"Diana R.",surname:"Gutsaeva",slug:"diana-r.-gutsaeva",fullName:"Diana R. Gutsaeva"}],corrections:null},{id:"59622",title:"18 kDa Translocator Protein in Mitochondria-Related Pathology: The Case of Traumatic Brain Injury",doi:"10.5772/intechopen.74057",slug:"18-kda-translocator-protein-in-mitochondria-related-pathology-the-case-of-traumatic-brain-injury",totalDownloads:955,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Translocator protein (TSPO) takes part in mitochondrial adenine triphosphate (ATP) production and transport. Mitochondrial TSPO is a part of the apoptotic and cell necrotic mechanism. Ligands to TSPO, endogenous and synthetic, have different effects on metabolism and protein expression in human well-differentiated metabolically active cells. In general, most of the TSPO ligands affect the cellular function or metabolism in the same general direction, but different specific TSPO ligands have their own unique effects in human cells. Regulation of gene expression via the actions of TSPO ligands on the mitochondrial TSPO may form an essential mechanism for the regulation of cellular functions, especially during acute organ injury, such as acute brain damage. The exact mode of action of the specific TSPO ligands is not clear enough and should be further investigated. TSPO is a potential target for therapeutic efforts to mitigate secondary tissue injury caused by programmed cell death.",signatures:"Nahum Rosenberg, Nasra Yasin, Leo Veenman, Orit Rosenberg,\nAbraham Weizman and Moshe Gavish",downloadPdfUrl:"/chapter/pdf-download/59622",previewPdfUrl:"/chapter/pdf-preview/59622",authors:[{id:"68911",title:"Dr.",name:"Nahum",surname:"Rosenberg",slug:"nahum-rosenberg",fullName:"Nahum Rosenberg"},{id:"217534",title:"MSc.",name:"Nasra",surname:"Yassin",slug:"nasra-yassin",fullName:"Nasra Yassin"},{id:"217535",title:"Dr.",name:"Leo",surname:"Veenman",slug:"leo-veenman",fullName:"Leo Veenman"},{id:"217536",title:"Dr.",name:"Orit",surname:"Rosenberg",slug:"orit-rosenberg",fullName:"Orit Rosenberg"},{id:"217538",title:"Prof.",name:"Abraham",surname:"Weizman",slug:"abraham-weizman",fullName:"Abraham Weizman"},{id:"217540",title:"Prof.",name:"Moshe",surname:"Gavish",slug:"moshe-gavish",fullName:"Moshe Gavish"}],corrections:null},{id:"61883",title:"Hereditary Disorders and Human Mutations of Iron-Sulfur Assembly Genes",doi:"10.5772/intechopen.78006",slug:"hereditary-disorders-and-human-mutations-of-iron-sulfur-assembly-genes",totalDownloads:1049,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Multiple mitochondrial dysfunctions syndrome (MMDS) is a group of autosomal recessive mitochondrial disorders that is associated with deficiencies related to nuclear genes: ISCA2, ISCA1, NFU1, IBA57, and BOLA3. The syndromes are relatively new and recently discovered. Individuals with MMDS have reduced function of energy production stages in mitochondria. The dysfunctions are mostly related to iron-sulfur (Fe-S) clustering system (ISC) and its biogenesis. The signs and symptoms of the patients may begin early in life, and can be quite severe leading to death more or less during infancy. Affected individuals have various symptoms including brain dysfunction (encephalopathy), hypotonia, seizures, delayed developmental milestones, and cognition and psychomotor impairments. These individuals often have difficulty growing and gaining weight at the expected rate. Diagnosis of the disease can be challenging as in the case with most of the mitochondrial disorders. However, since the genetic causes of the MMDS are known, a laboratory test focusing on the causative genes will be helpful to determine the pathogenic mutations. This in turn would facilitate reducing the number of the diseases through carrier testing and genetic counseling and utilization of preimplantation genetic diagnosis in populations, especially those that display high rate of consanguinity, which are prone to have such autosomal recessive disorders.",signatures:"Namik Kaya, Zuhair Al-Hassnan, Maha Abdulrahim, Mazhor\nAldosary and Dilek Colak",downloadPdfUrl:"/chapter/pdf-download/61883",previewPdfUrl:"/chapter/pdf-preview/61883",authors:[{id:"99664",title:"Dr.",name:"Namik",surname:"Kaya",slug:"namik-kaya",fullName:"Namik Kaya"},{id:"209159",title:"Prof.",name:"Zuhair",surname:"Al-Hassnan",slug:"zuhair-al-hassnan",fullName:"Zuhair Al-Hassnan"},{id:"209160",title:"Dr.",name:"Dilek",surname:"Colak",slug:"dilek-colak",fullName:"Dilek Colak"},{id:"209161",title:"Dr.",name:"Mazhor",surname:"Aldosary",slug:"mazhor-aldosary",fullName:"Mazhor Aldosary"},{id:"209162",title:"M.Sc.",name:"Maha",surname:"Abdurrahim",slug:"maha-abdurrahim",fullName:"Maha Abdurrahim"}],corrections:null},{id:"58879",title:"Nuclear Encoded Mitochondrial Proteins in Metabolite Transport and Oxidation Pathway Connecting Metabolism of Nutrients",doi:"10.5772/intechopen.72937",slug:"nuclear-encoded-mitochondrial-proteins-in-metabolite-transport-and-oxidation-pathway-connecting-meta",totalDownloads:1086,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:"In the mitochondria, there are ongoing processes essential to the survival of cells associated with the production of energy ending in the oxidative phosphorylation and the formation of ATP, constituting a form of energy for majority of metabolic processes. Except for nutrient oxidation in the citric acid cycle interfacing with the process of oxidative phosphorylation, mitochondria are linked to a number of metabolic pathways ongoing directly in mitochondria or indirectly in cell compartments by serving substrates. Mitochondrial activities maintenance requires continual draw of intermediates from cytosol through the double mitochondrial membrane as well as transport in the reverse direction. Interconnection and regulation of all the processes are mediated by transporters and carriers, activities of which are affected by cell and body requirements. In the chapter, the main transport systems localized in membranes of mitochondria, their regulation, affection, and disorders in the background of mitochondria aberrant functions are described. Voltage-dependent anion channels, translocase of mitochondrial outer membrane, deoxynucleotide carrier, ADP/ATP nucleotide translocase, and phosphate carrier in mitochondrial inner membrane are among them. In more detail, the pyruvate carrier and its abnormal activity, but also others as di- and tri-carboxylate, glutamate, and ornithine carriers, are characterized. The uncoupling protein, as solute carrier family members, involvement is also mentioned.",signatures:"Janka Vašková, Jozef Firment and Ladislav Vaško",downloadPdfUrl:"/chapter/pdf-download/58879",previewPdfUrl:"/chapter/pdf-preview/58879",authors:[{id:"140747",title:"Associate Prof.",name:"Janka",surname:"Vašková",slug:"janka-vaskova",fullName:"Janka Vašková"},{id:"207199",title:"Prof.",name:"Ladislav",surname:"Vaško",slug:"ladislav-vasko",fullName:"Ladislav Vaško"},{id:"216720",title:"Prof.",name:"Jozef",surname:"Firment",slug:"jozef-firment",fullName:"Jozef Firment"}],corrections:null},{id:"62948",title:"Pyrethroid Insecticides as the Mitochondrial Dysfunction Inducers",doi:"10.5772/intechopen.80283",slug:"pyrethroid-insecticides-as-the-mitochondrial-dysfunction-inducers",totalDownloads:1459,totalCrossrefCites:4,totalDimensionsCites:8,hasAltmetrics:0,abstract:"Pyrethroids are used to decrease vector-based health concerns and to increase field yield against agricultural pests. Their metabolism is a concern to disrupt a cell’s homeostatic machinery via reactive oxygen species (ROS) production. They interact with lipid membranes to damage the fine balance between membrane lipids and membrane proteins, especially mitochondrial substrate transporters and electron carriers. Pyrethroids cause a shift in the metabolic energy production strategy, resulting in ROS production and intracellular lipid deposition. The change of open/closed conformation of some mitochondrial membrane proteins increases the vulnerability of mitochondria to Ca2+ ions. Membrane lipid fluidity change is also a concern because of permeability to the substrates and ions to produce energy and other substrates necessary for the cell. Pyrethroids can change the Ca2+ signaling and its interaction with ROS signals via disruption of the fine balance between endoplasmic reticulum and mitochondria. They can disrupt the mitochondrial DNA (mtDNA) via their hydrophobic nature or their ROS production capacity. In conclusion, mitochondria are the center of pyrethroid toxicity, and dysfunction of this organelle via pyrethroid toxicity plays an important role in the fate of cell. Their lipophilic and pro-oxidative nature together with Ca2+ homeostasis plays a synergistic role in this mitochondrial effect.",signatures:"Celal Guven, Yusuf Sevgiler and Eylem Taskin",downloadPdfUrl:"/chapter/pdf-download/62948",previewPdfUrl:"/chapter/pdf-preview/62948",authors:[{id:"192567",title:"Prof.",name:"Eylem",surname:"Taskin",slug:"eylem-taskin",fullName:"Eylem Taskin"}],corrections:null},{id:"63034",title:"Mitochondrial Dysfunction Associated with Doxorubicin",doi:"10.5772/intechopen.80284",slug:"mitochondrial-dysfunction-associated-with-doxorubicin",totalDownloads:1690,totalCrossrefCites:6,totalDimensionsCites:13,hasAltmetrics:0,abstract:"Cancer prevalence is scaling up each year. Anthracycline groups are still the best chemotherapeutic agent. The most popular anticancer drug in the group is doxorubicin (DOX). Unfortunately, DOX has potent toxicity on noncancerous tissues, e.g., heart, kidneys, etc. However, it is well documented that the severest toxicity of the drug affects heart tissue. Of course, some reasons have been suggested why and/or how the heart is so vulnerable to toxicity. The primary mechanism responsible for DOX’s cardiospecific toxicity remains unidentified so far; however, mitochondrial dysfunction induced by DOX is now considered one of the leading reasons for DOX’s toxicities and undesired side effects. Mitochondrial reactive oxygen production in the heart is a significant contributor to developing mitochondrial dysfunction-exposed DOX based on a variety of evidence. The objective of this review chapter is to critically evaluate and highlight the role of mitochondria in the development of DOX-induced cardiotoxicity.",signatures:"Celal Guven, Yusuf Sevgiler and Eylem Taskin",downloadPdfUrl:"/chapter/pdf-download/63034",previewPdfUrl:"/chapter/pdf-preview/63034",authors:[{id:"192567",title:"Prof.",name:"Eylem",surname:"Taskin",slug:"eylem-taskin",fullName:"Eylem Taskin"},{id:"195229",title:"Dr.",name:"Celal",surname:"Guven",slug:"celal-guven",fullName:"Celal Guven"},{id:"206996",title:"Prof.",name:"Yusuf",surname:"Sevgiler",slug:"yusuf-sevgiler",fullName:"Yusuf Sevgiler"}],corrections:null},{id:"58876",title:"Ethanol Consumption Affects Neuronal Function: Role of the Mitochondria",doi:"10.5772/intechopen.71611",slug:"ethanol-consumption-affects-neuronal-function-role-of-the-mitochondria",totalDownloads:1098,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:1,abstract:"Ethanol is a licit drug consumed by a large part of the population, from adolescence to adulthood. High ethanol consumption is a public health problem due to its addictiveness and the risk it produces of developing other diseases, including cardiovascular, hepatic, and mental pathologies. Different patterns of ethanol consumption and its toxic effects in the brain have been reported. Current studies suggest to mitochondria, one of the principal mediators for ethanol neurotoxicity. In this chapter, we will review the effects of ethanol on neurons in different scenarios of ethanol consumption and its relation with mitochondrial function. Finally, we will propose a mechanism of ethanol toxicity in which the mitochondria are the main mediator and in which the mitochondrial alterations correlate with the severity of ethanol consumption. Thus, improving mitochondrial health of brain cells could be considered as a potential therapeutic target to treat ethanol-associated disorders.",signatures:"Cheril Tapia-Rojas, María José Pérez, Claudia Jara, Erick H. Vergara\nand Rodrigo A. Quintanilla",downloadPdfUrl:"/chapter/pdf-download/58876",previewPdfUrl:"/chapter/pdf-preview/58876",authors:[{id:"182849",title:"Dr.",name:"Rodrigo",surname:"Quintanilla",slug:"rodrigo-quintanilla",fullName:"Rodrigo Quintanilla"},{id:"183872",title:"MSc.",name:"María José",surname:"Pérez",slug:"maria-jose-perez",fullName:"María José Pérez"},{id:"183873",title:"Dr.",name:"Claudia",surname:"Jara",slug:"claudia-jara",fullName:"Claudia Jara"},{id:"217065",title:"Dr.",name:"Cheril",surname:"Tapia-Rojas",slug:"cheril-tapia-rojas",fullName:"Cheril Tapia-Rojas"},{id:"217066",title:"BSc.",name:"Erick H",surname:"Vergara",slug:"erick-h-vergara",fullName:"Erick H Vergara"}],corrections:null},{id:"58965",title:"Mitochondrial Oxidative Stress and Calcium-Dependent Permeability Transition are Key Players in the Mechanisms of Statins-Associated Side Effects",doi:"10.5772/intechopen.71610",slug:"mitochondrial-oxidative-stress-and-calcium-dependent-permeability-transition-are-key-players-in-the-",totalDownloads:1184,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"Statins are cholesterol-lowering medicines utilized worldwide and are associated with reduced risk of cardiovascular mortality and events. However, 0.5–10% of patients suffer from adverse effects especially on skeletal muscle. Recently, new onset of diabetes has been reported in subjects on statin therapy. Pro- and anti-oxidant effects of statins have been reported, thus fostering a debate. Previously reported data provide evidence that statins induce alterations in intracellular calcium homeostasis and mitochondrial dysfunctions that can be counteracted by antioxidants (e.g., CoQ10, creatine, and L-carnitine). Therefore, we have proposed that statin-induced inhibition of mitochondrial respiration leads to oxidative stress that opens a calcium-dependent permeability transition pore, an event that may lead to cell death. In addition, mitochondrial oxidative stress caused by statin treatment may be a signal for cellular antioxidant system responses such as catalase upregulation, possibly explaining the alleged statins’ antioxidant properties. Muscle mitochondrial dysfunction induced by statin treatment may be associated with the peripheral insulin resistance and may explain statins-induced new onset of diabetes. Together, the data presented in this review suggest that the statins’ detrimental effects can be prevented by co-administration of antioxidants.",signatures:"Estela N.B. Busanello, Ana C. Marques, Estela Lorza-Gil, Helena C.F.\nde Oliveira and Anibal E. Vercesi",downloadPdfUrl:"/chapter/pdf-download/58965",previewPdfUrl:"/chapter/pdf-preview/58965",authors:[{id:"206665",title:"Dr.",name:"Anibal",surname:"Vercesi",slug:"anibal-vercesi",fullName:"Anibal Vercesi"},{id:"206915",title:"Dr.",name:"Estela",surname:"Busanello",slug:"estela-busanello",fullName:"Estela Busanello"},{id:"206916",title:"BSc.",name:"Ana Carolina",surname:"Marques",slug:"ana-carolina-marques",fullName:"Ana Carolina Marques"},{id:"206917",title:"Dr.",name:"Estela",surname:"Lorza-Gil",slug:"estela-lorza-gil",fullName:"Estela Lorza-Gil"},{id:"206919",title:"Dr.",name:"Helena",surname:"Oliveira",slug:"helena-oliveira",fullName:"Helena Oliveira"}],corrections:null},{id:"58701",title:"Ketamine Induces Neuroapoptosis in Stem Cell–Derived Developing Human Neurons Possibly through Intracellular Calcium/Mitochondria/microRNA Signaling Pathway",doi:"10.5772/intechopen.72939",slug:"ketamine-induces-neuroapoptosis-in-stem-cell-derived-developing-human-neurons-possibly-through-intra",totalDownloads:893,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"Ketamine, one of the commonly used agents in pediatric anesthesia, has been linked to neurodegeneration and cognitive dysfunction in developing animal models. Previous studies on developing neurons derived from human embryonic stem cells (hESCs) indicate that ketamine induces neuroapoptosis and the mechanisms remain largely unknown. This study aims to investigate the effect of ketamine on intracellular calcium, mitochondrial signaling, and microRNA profiles in hESCs-derived 2-week-old neurons. The neurons were exposed to ketamine for 6 or 24 hours. Neuroapoptosis was assessed by TUNEL staining. Intracellular calcium level was analyzed using Fluo-4 AM staining. The mitochondria-related neuroapoptosis pathway including mitochondrial membrane potential, cytochrome c release from mitochondria to cytosol, and mitochondrial fission was also investigated. miScript miRNA arrays were used in microRNA target identification studies. The results showed that ketamine exposure induced neuroapoptosis and alterations in intracellular calcium levels. In addition, ketamine decreased mitochondrial membrane potential, resulted in cytochrome c release from mitochondria into cytosol, and increased mitochondrial fission. Among 88 microRNAs investigated, let-7a/e, miR-21, miR-23b, miR-28-5p, and miR-423-5p were found downregulated, while miR-96 was upregulated in the neurons treated with ketamine. Collectively, our findings indicate that ketamine induces neuroapoptosis possibly through the dysregulated intracellular calcium, mitochondria, and microRNA pathway.",signatures:"Danielle Twaroski, Yasheng Yan, Congshan Jiang, Sarah Logan,\nZeljko J. Bosnjak and Xiaowen Bai",downloadPdfUrl:"/chapter/pdf-download/58701",previewPdfUrl:"/chapter/pdf-preview/58701",authors:[{id:"208378",title:"Dr.",name:"Xiaowen",surname:"Bai",slug:"xiaowen-bai",fullName:"Xiaowen Bai"},{id:"212867",title:"Dr.",name:"Danielle",surname:"Twaroski",slug:"danielle-twaroski",fullName:"Danielle Twaroski"},{id:"212868",title:"Mr.",name:"Yasheng",surname:"Yan",slug:"yasheng-yan",fullName:"Yasheng Yan"},{id:"212869",title:"Dr.",name:"Congshan",surname:"Jiang",slug:"congshan-jiang",fullName:"Congshan Jiang"},{id:"212871",title:"Ms.",name:"Sarah",surname:"Logan",slug:"sarah-logan",fullName:"Sarah Logan"},{id:"212872",title:"Dr.",name:"Zeljko J",surname:"Bosnjak",slug:"zeljko-j-bosnjak",fullName:"Zeljko J Bosnjak"}],corrections:null},{id:"58886",title:"Modulation of Mitochondria During Viral Infections",doi:"10.5772/intechopen.73036",slug:"modulation-of-mitochondria-during-viral-infections",totalDownloads:1786,totalCrossrefCites:5,totalDimensionsCites:7,hasAltmetrics:1,abstract:"Mitochondria are organelles critical for cell survival because they produce ATP and modulate programmed cell death (PCD) pathways. PCD pathways are important in many clinical disorders, such as ischemia/reperfusion injuries, trauma, and toxic/metabolic syndromes, as well as in chronic neurodegenerative conditions, such as amyotrophic lateral sclerosis, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Moreover, many viruses and other pathogens target the mitochondria. Viruses induce the production of various proteins in their hosts that have proapoptotic and anti-apoptotic activities, depending on the cellular environment. More specifically, many viruses that target mitochondria regulate the balance between the anti- and proapoptotic Bcl-2 family proteins and thereby increase their own survival within the host cell. Recent studies indicated that mitochondria centralize several critical innate immune responses based on the presence of several important signaling proteins within the mitochondria: mitochondrial antiviral signaling (MAVS), stimulation of interferon genes (STING), and NLR family member X1. Therefore, mitochondria are not only vital because they regulate cell survival and death but also they have broad roles in the control of cell functions following pathogen invasion. This chapter highlights the tight interplay between viral infection and mitochondria.",signatures:"Latif Reshi, Hao-Ven Wang and Jiann-Ruey Hong",downloadPdfUrl:"/chapter/pdf-download/58886",previewPdfUrl:"/chapter/pdf-preview/58886",authors:[{id:"66487",title:"Prof.",name:"Jiann",surname:"Hong",slug:"jiann-hong",fullName:"Jiann Hong"},{id:"206951",title:"Dr.",name:"Lateef",surname:"Reshi",slug:"lateef-reshi",fullName:"Lateef Reshi"},{id:"213164",title:"Dr.",name:"Hao -Ven",surname:"Wang",slug:"hao-ven-wang",fullName:"Hao -Ven Wang"}],corrections:null},{id:"58585",title:"Estrogen and Mitochondrial Function in Disease",doi:"10.5772/intechopen.73015",slug:"estrogen-and-mitochondrial-function-in-disease",totalDownloads:1223,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,abstract:"Anecdotal and scientific evidence suggest that the sex hormone estrogen provides significant health benefits in women. Women have higher estrogen levels than men. Circulating estrogen reaches its highest level during the reproductive period and steadily declines with the onset of menopause. The role of estrogen and estrogen receptors in both cellular physiology and pathophysiology has been controversial. Estrogen has anti-inflammatory and anti-oxidant effects, which preserve cell viability during cardiovascular incidents, but it enhances disease progression in the context of breast cancer. Estrogen mediates these responses via activation of estrogen receptor subtypes located in the cell membrane, nucleus, and mitochondrion. Further, transcription of nuclear and mitochondrial genes by estrogen yields products that play an important role in regulating mitochondrial function. Mitochondria are part of a highly dynamic network and undergo fission and fusion, produce cellular energy, adenosine 5′ triphosphate (ATP), and regulate cell death. Herein, we review the cell and receptor specific effects of estrogen on mitochondrial structure, function, and cell death under normal physiological conditions and in the context of cardiovascular disease, inflammation, neurodegeneration, and cancer. Further research is needed to elucidate the specific role of estrogenic control of mitochondria in health and disease.",signatures:"Ved P. Mooga, C. Roger White and Samantha Giordano-Mooga",downloadPdfUrl:"/chapter/pdf-download/58585",previewPdfUrl:"/chapter/pdf-preview/58585",authors:[{id:"193624",title:"Prof.",name:"C. Roger",surname:"White",slug:"c.-roger-white",fullName:"C. Roger White"},{id:"213186",title:"Dr.",name:"Samantha",surname:"Giordano-Mooga",slug:"samantha-giordano-mooga",fullName:"Samantha Giordano-Mooga"},{id:"213187",title:"Dr.",name:"Ved",surname:"Mooga",slug:"ved-mooga",fullName:"Ved Mooga"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"6684",title:"Mitochondrial DNA",subtitle:"New Insights",isOpenForSubmission:!1,hash:"326a9354db0c23d8a26659e8a0c26872",slug:"mitochondrial-dna-new-insights",bookSignature:"Hervé Seligmann",coverURL:"https://cdn.intechopen.com/books/images_new/6684.jpg",editedByType:"Edited by",editors:[{id:"118814",title:"Dr.",name:"Herve",surname:"Seligmann",slug:"herve-seligmann",fullName:"Herve Seligmann"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5232",title:"Restricted Growth",subtitle:"Clinical, Genetic and Molecular Aspects",isOpenForSubmission:!1,hash:"c604493aaeaf8258adc42b2d7dc9b22d",slug:"restricted-growth-clinical-genetic-and-molecular-aspects",bookSignature:"Maria del Carmen Cardenas- Aguayo",coverURL:"https://cdn.intechopen.com/books/images_new/5232.jpg",editedByType:"Edited by",editors:[{id:"169616",title:"Dr.",name:"Maria del Carmen",surname:"Cardenas-Aguayo",slug:"maria-del-carmen-cardenas-aguayo",fullName:"Maria del Carmen Cardenas-Aguayo"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"7850",title:"Mitochondria and Brain Disorders",subtitle:null,isOpenForSubmission:!1,hash:"e4cb9b34e45c6177ede9cf78fbda4b82",slug:"mitochondria-and-brain-disorders",bookSignature:"Stavros Baloyannis",coverURL:"https://cdn.intechopen.com/books/images_new/7850.jpg",editedByType:"Edited by",editors:[{id:"156098",title:"Emeritus Prof.",name:"Stavros J.",surname:"Baloyannis",slug:"stavros-j.-baloyannis",fullName:"Stavros J. Baloyannis"}],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. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],ofsBooks:[]},correction:{item:{id:"80207",slug:"corrigendum-to-aspects-regarding-thermal-mechanical-fatigue-of-shape-memory-alloys",title:"Corrigendum To: Aspects Regarding Thermal-Mechanical Fatigue of Shape Memory Alloys",doi:null,correctionPDFUrl:"https://cdn.intechopen.com/pdfs/80207.pdf",downloadPdfUrl:"/chapter/pdf-download/80207",previewPdfUrl:"/chapter/pdf-preview/80207",totalDownloads:null,totalCrossrefCites:null,bibtexUrl:"/chapter/bibtex/80207",risUrl:"/chapter/ris/80207",chapter:{id:"62954",slug:"aspects-regarding-thermal-mechanical-fatigue-of-shape-memory-alloys",signatures:"Petrică Vizureanu and Dragoș-Cristian Achiței",dateSubmitted:"April 12th 2018",dateReviewed:"April 25th 2018",datePrePublished:null,datePublished:"September 26th 2018",book:{id:"7213",title:"Shape-Memory Materials",subtitle:null,fullTitle:"Shape-Memory Materials",slug:"shape-memory-materials",publishedDate:"September 26th 2018",bookSignature:"Alicia Esther Ares",coverURL:"https://cdn.intechopen.com/books/images_new/7213.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"91095",title:"Dr.",name:"Alicia Esther",middleName:null,surname:"Ares",slug:"alicia-esther-ares",fullName:"Alicia Esther Ares"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"12354",title:"Prof.",name:"Petrică",middleName:null,surname:"Vizureanu",fullName:"Petrică Vizureanu",slug:"petrica-vizureanu",email:"peviz2002@yahoo.com",position:null,institution:{name:"Gheorghe Asachi Technical University of Iași",institutionURL:null,country:{name:"Romania"}}},{id:"209329",title:"Dr.",name:"Mirabela Georgiana",middleName:null,surname:"Minciuna",fullName:"Mirabela Georgiana Minciuna",slug:"mirabela-georgiana-minciuna",email:"mirabela.minciuna@yahoo.ro",position:null,institution:{name:"Gheorghe Asachi Technical University of Iași",institutionURL:null,country:{name:"Romania"}}},{id:"245668",title:"Dr.",name:"Dragos Cristian",middleName:null,surname:"Achitei",fullName:"Dragos Cristian Achitei",slug:"dragos-cristian-achitei",email:"dragos_adc@tuiasi.ro",position:null,institution:null},{id:"245669",title:"Dr.",name:"Manuela Cristina",middleName:null,surname:"Perju",fullName:"Manuela Cristina Perju",slug:"manuela-cristina-perju",email:"cryss_ela@yahoo.com",position:null,institution:null}]}},chapter:{id:"62954",slug:"aspects-regarding-thermal-mechanical-fatigue-of-shape-memory-alloys",signatures:"Petrică Vizureanu and Dragoș-Cristian Achiței",dateSubmitted:"April 12th 2018",dateReviewed:"April 25th 2018",datePrePublished:null,datePublished:"September 26th 2018",book:{id:"7213",title:"Shape-Memory Materials",subtitle:null,fullTitle:"Shape-Memory Materials",slug:"shape-memory-materials",publishedDate:"September 26th 2018",bookSignature:"Alicia Esther Ares",coverURL:"https://cdn.intechopen.com/books/images_new/7213.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"91095",title:"Dr.",name:"Alicia Esther",middleName:null,surname:"Ares",slug:"alicia-esther-ares",fullName:"Alicia Esther Ares"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"12354",title:"Prof.",name:"Petrică",middleName:null,surname:"Vizureanu",fullName:"Petrică Vizureanu",slug:"petrica-vizureanu",email:"peviz2002@yahoo.com",position:null,institution:{name:"Gheorghe Asachi Technical University of Iași",institutionURL:null,country:{name:"Romania"}}},{id:"209329",title:"Dr.",name:"Mirabela Georgiana",middleName:null,surname:"Minciuna",fullName:"Mirabela Georgiana Minciuna",slug:"mirabela-georgiana-minciuna",email:"mirabela.minciuna@yahoo.ro",position:null,institution:{name:"Gheorghe Asachi Technical University of Iași",institutionURL:null,country:{name:"Romania"}}},{id:"245668",title:"Dr.",name:"Dragos Cristian",middleName:null,surname:"Achitei",fullName:"Dragos Cristian Achitei",slug:"dragos-cristian-achitei",email:"dragos_adc@tuiasi.ro",position:null,institution:null},{id:"245669",title:"Dr.",name:"Manuela Cristina",middleName:null,surname:"Perju",fullName:"Manuela Cristina Perju",slug:"manuela-cristina-perju",email:"cryss_ela@yahoo.com",position:null,institution:null}]},book:{id:"7213",title:"Shape-Memory Materials",subtitle:null,fullTitle:"Shape-Memory Materials",slug:"shape-memory-materials",publishedDate:"September 26th 2018",bookSignature:"Alicia Esther Ares",coverURL:"https://cdn.intechopen.com/books/images_new/7213.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"91095",title:"Dr.",name:"Alicia Esther",middleName:null,surname:"Ares",slug:"alicia-esther-ares",fullName:"Alicia Esther Ares"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},ofsBook:{item:{type:"book",id:"11536",leadTitle:null,title:"Recent Advances in Gasification Technologies",subtitle:null,reviewType:"peer-reviewed",abstract:"
\r\n\tThe recent strong interest in clean gas and hydrogen as energy sources has revived the gasification technology development that aims to meet a carbon-neutral, clean, and renewable energy. Instead of using fossil fuels, like coal, that are considered responsible for global warming, biomass and wastes are becoming inevitable feedstock for gasification. Conventional complex and big-scale gasification technologies used for fossil fuels should be replaced with compact, medium-size, more-economical blocks of gasification technologies. In particular, the possibility of hydrogen production as a distributed facility at the exact required site envisions a bright future of developing gasification and related technologies. To meet the current climate-change consciousness, gasification technologies should be equipped with more agile cleaning, conversion, purifying parts that remove CO2 and generate high-grade hydrogen for fuel cells and hydrogen vehicles.
\r\n\r\n\t
\r\n\tThis book aims to cover recent developments and novel components in gasification technologies that suit the requirements related to CO2 reduction, syngas conversion, hydrogen production, renewable usage, and reliability as an economic process. The conventional gasification process is inherently expensive due to the toxicity and explosiveness of syngas in addition to the difficulty of the impurities removal process. Many novel ideas and processes have tried to overcome these inherent limitations. This book hopes to provide more insights on the future of the utility of gasification technologies at this climate-conscious time.
Medication-overuse headache (MOH) is defined by the International Classification of Headache Disorders (ICHD) as a headache in patients with primary headache disorders occurring on ≥15 days per month for >3 months, that is induced by overuse of medications taken as symptomatic treatment for acute headaches.
In ICHD-3, chronic headache syndromes are described by professional consensus as headache disorders that share traits with pre-existing headache syndromes, happen for a specific duration of time (at least three months in Chronic tension-type headache (CTTH), Chronic migraine (CM); or at least 12 months in Chronic trigeminal autonomic cephalalgia (TAC)) and have an extra time-rule (e.g.headache days per month in CTTH and CM, or the absence of remissions for greater than three months in TAC’s).
MOH occurs if the number of days of acute medicine taken for headache per month exceeds a threshold level [1] i.e., 15 or more days for simple painkillers and 10 or more days for triptans, opioids and combination analgesics. The diagnosis of MOH as per ICHD-3 is given as follows:
A
Headache on ≥15 days/month
Pre-existing headache disorder
B
Overuse of acute and/or symptomatic headache medications for >3 months*C
Not better represented by any other ICHD-3 diagnosis
*Regular consumption of tablets on ≥10 days/month for ergotamines, triptans, opioids and mixture analgesics and on ≥15 days/month for paracetamol (also recognised as acetaminophen), acetylsalicylic acid and NSAIDs.
As ICHD defines MOH as a secondary headache, one must identify the primary headache disorder associated with it for example episodic or chronic migraine. The classification identifies further sub-groups based on the substance misused (e.g., 2.2.1.2 triptan-overuse headache). Many sufferers take more than one drug [2] or are overusing combination analgesics and/or multiple drugs at different times which are identified in the classification as headache attributed to numerous drug classes (2.2.5). The comprehensive classification of MOH from ICHD-3 is given here:
Headache happening on ≥15 days/month in a affected person with a pre-existing headache disorder
Regular overuse for > three months of one or more drugs that can be taken for acute and/or symptomatic treatment of headache
Not better represented by means of any other ICHD-3 diagnosis.
Headache satisfying standards for 2.2.1 Medication- overuse headache
Regular consumption of ergotamine on ≥10 days/month for >three months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular consumption of one or greater triptans, 1 in any formulation, on ≥10 days/month for >3 months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular consumption of paracetamol on ≥15 days/month for > three months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular consumption of one or extra non-steroidal anti- inflammatory drugs (NSAIDs) (other than acetylsalicylic acid) on ≥15 days/month for >3 months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular intake of acetylsalicylic acid on ≥15 days/month for >three months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular intake of a non-opioid analgesic other than paracetamol or non-steroidal anti-inflammatory tablets (including acetylsalicylic acid) on ≥15 days/month for> three months.
Headache satisfying criteria for 2.2.1 Medication- overuse headache
Regular consumption of one or more opioids on ≥10 days/month for >3 months.
Headache fulfilling standards for 2.2.1 Medication- overuse headache
Regular consumption of one or more combination-analgesic medicines on ≥10 days/month for >three months.
Headache satisfying standards for 2.2.1 Medication- overuse headache
Regular intake of any aggregate of ergotamine, triptans, non-opioid analgesics and/or opioids on a total of ≥10 days/month for >3 months besides overuse of any single drug or drug type alone.
Headache satisfying standards for 2.2.1 Medication- overuse headache
Both of the following: 1. regular consumption of any mixture of ergotamine, triptans, non-opioid analgesics and/or opioids on ≥10 days/month for >3 months
Headache fulfilling standards for 2.2.1 Medication- overuse headache
Regular overuse, on ≥10 days/month for >3 months, of one or greater medicines other than these described above, 1 taken for acute or symptomatic cure of headache
MOH was first identified in 1951 in relation to overuse of ergotamine [3]. It was in 1984 that relationship between analgesic consumption and exacerbation of headaches were recognised with improvement in headaches on stopping them [4]. It was given the name as ‘drug-induced headache’ in the first classification of the headache disorders (ICHD-1) [5]. The ICHD-2 described this as ‘medication-overuse headache’ in 2004. The condition was said to be probable as the definitive diagnosis was only given following reduction of headache days 2 months after withdrawal of the overused medication [6]. The 2006 modification broadened the definition [7] by abolishing the required improvement after discontinuation and this has persisted in both ICHD-3 beta and ICHD-3 criteria [8].
The headache of medication overuse is that of the primary headache disorder [9]. Patients with migraines who overuse triptan will observe increase in the frequency of pre-existing headaches to almost daily in frequency that exacerbates intermittently and more so if a dose of triptan is missed. The patient gets in a vicious circle with increasing headaches proportional to the triptans consumed. In the same way patients with tension-type headache will report exacerbation of their featureless headaches [9]. A few people are able to differentiate between their primary headaches and a constant dull and diffuse headache that they attribute as MOH. It has been observed that MOH develops more quickly with triptan and resolves more quickly on withdrawal compared to combination and simple analgesics. This perception was confirmed by a French study [10].
The diagnostic criteria for MOH do not fully demonstrate the complexity of making the diagnosis of MOH. It is important to realise that medication overuse and MOH are two different entities that can have different implications and outcomes. Medication-overuse only signifies the number of days a person consumes painkiller and not necessarily a cause for on-going headache. In certain chronic painful conditions e.g., back pain; arthritis etc. there is medication overuse but no accompanying headache. Another observation has been that not every individual will develop headache with acute medication overuse [11]. It is not entirely clear why overuse worsens headache in some and not the others. Considered a secondary headache disorder, MOH should be identified by the type of medication being overused. The primary headache disorder must also be identified.
Majority of research have reported the general prevalence of MOH in the normal population to be 0.5–2.6% [12]. Higher rates have been seen in Russia (7.6%) [13] and Iran (4.6%), where medication overuse is a lot more frequent than in other nations [14]. However, no speculative reason or hypothesis has been provided for this.
The prevalence for MOH is 0.5–2.6% although it varies based on the availability of painkillers over the counter (OTC) and hence reported much higher in Russia (7.6%) and Iran (4.6%). The availability of OTC varies with codeine-based analgesics available in the UK, while barbiturates containing painkillers in the USA. Figures from the third world countries such as India and Pakistan are difficult to obtain considering all forms of painkillers are available over the counter with no definitive prescription system existing in the country. The prevalence is less common in adolescents (0.3%–0.5%) than adults observed in two epidemiological studies in Norway and Taiwan [15, 16]. Overall females are affected more than males (5:4) and those with chronic migraine have a very high incidence of medication overuse (11–70%) much more than observed in the general population [17].
On the basis of current scientific knowledge, all pain medications have the capacity to cause MOH. Dependency-like behaviour is most commonly seen in patients who overuse opioids, although it is also seen in patients overusing triptans [18, 19, 20]. Medication overuse was found to be an important risk factor for chronification of primary headaches [21]. A study in the USA found majority of patients with medication overuse were taking combined painkillers containing caffeine or opioids than simple painkillers [22]. They concluded that the risk of MOH is less with simple painkillers although this does not prove a link between overuse and a specific medication.
In a large prospective population-based study, Hagen et al. studied 25.596 patients who did not suffer from chronic daily headache at baseline but had MOH 11 years later (n = 201,0.8%) and the risk factors that were found to be associated with development of MOH: regular use of tranquillisers, combination of chronic musculoskeletal complaints, gastrointestinal complaints and hospital anxiety depression scale (HADS) score > =11, physical inactivity and smoking [23]. Migraine headaches was more strongly linked with MOH than non-migraine headaches and the risk was higher with those having a high frequency i.e., 7–14 days per month, although it remains unclear as to whether this is because of a higher analgesic intake or frequent migraine attacks. Some of the non-modifiable risk factors for MOH include young age, female gender, family history of analgesic or substance overuse and low education level. Smoking and physical inactivity were other risk factors for MOH that were not associated with chronic daily headache without medication overuse suggesting that the two conditions are phenotypically different [23]. In 80% of patients with MOH, migraine is the underlying primary headache disorder [24] and majority of remaining patients have tension-type headache or more rarely post traumatic headache [25, 26, 27].
AGE(<50 years) 1.8(1.3–2.4) |
Female sex 1.9(1.4–2.6) |
Low degree of education 1.9(1.2–3.0) |
Chronic Musculoskeletal problems 1.9(1.4–2.7) |
Gastrointestinal problems 1.6(1.1–2.2) |
Depression or Anxiety (HADS score ≥ 11) 4.7(2.4–9.0) |
Tranquillisers 5.2(3.0–9.0) |
Aspirin 0.5(0.3–0.9) |
Ibuprofen 0.7(0.5–1.0) |
Opioids 2.3(1.3–3.9) |
Smoking 1.8(1.2–2.5) |
Physical Inactivity 2.7(1.2–6.3) |
Metabolic Syndrome 5.3(1.6–24.6) |
High daily Caffeine intake 1.4(0.8–2.5) (>540 mg versus ≤240 mg) |
Figure shown are derived from population-based studies [23] in Norway [15, 16], the USA [22] and China.CI, confidence interval; HADS, Hospital Anxiety and Depression; MOH, medication-overuse headache; OR, odds ratio.
The pathophysiology of MOH remains unclear. The fact that patients with migraine or tension type headache are more likely to develop MOH may mean that the underlying mechanism for MOH could be related to a brain with these primary headache disorders [28]. Patients with cluster headache (another primary headache disorder) do not develop MOH in spite of regular painkillers unless they also suffer from or have a family history for migraine [29]. It is possible that a genetic risk factor in a migrainous brain could make the person more susceptible to MOH (Figure 1).
Current perception of the pathophysiology of medication-overuse headache (MOH) [
The renin-angiotensin system is well known for blood pressure control. Angiotensin II can cause increase in blood pressure and require Angiotensin-converting enzyme (ACE) for its formation from Angiotensin I. It also has a role in regulating neural plasticity [31] and its interaction with monoaminergic synaptic transmission contributes towards dependence behaviour [32]. Polymorphism (insertion/deletion) in the gene that encodes ACE may well play a role in the condition particularly the D/D genotype [33].
Brain-derived neurotrophic factor (BDNF) has been linked to substance overuse [34, 35]. Certain BDNF genotypes (non G/G) [36, 37] are associated with increased consumption behaviour for the painkillers than others.
Many affective disorders such as depression, anxiety and substance abuse are associated with variants of SLC6A4 that encodes for SERT (Serotonin transporter) [38, 39]. Patients with SLC6A4 variants that have MOH are extremely difficult to respond to withdrawal therapy and have a high relapse rate following withdrawal [40].
COMT is an enzyme that metabolises catecholamines such as dopamine, adrenaline and nor-adrenaline and influences pain modulation [41]. Certain genotypes of COMTSNP (rs4680 and rs6269) have a low rate of relapse following withdrawal of analgesics than others indicating its role [40].
All forms of painkillers are associated with MOH although certain classes of analgesics can cause the condition much quicker than others. For example patients with triptan overuse develop MOH much quicker than opioids, ergotamine and combination analgesics [42]. In the same way triptans withdrawal responds much quicker and has a much lower relapse rate. This indicates that the underlying pathophysiological mechanism may be medication specific. Platelets of those with migraine and medication overuse have higher 5-HT2 receptors than those without medication overuse [43]. The research has also shown a reduction of serotonin levels and a reduction of the primary endogenous cannabinoids, anandamide and 2-acylglycerol in those with Migraine and medication overuse compared to those without it [44]. Research has also shown that those with MOH have a high consumption of other medicines such as nasal decongestants, eye drops, laxatives, tranquillisers and sleeping drugs.
One of the pathways for head pain in migraine is activation of the trigeminal primary afferent neurons innervating the intracranial and dural blood vessels. Stimulation of these vessels have shown to induce pain similar to migrainous headache [45, 46], although the exact underlying mechanism that activates the trigeminovascular system remains unclear. Among possible explanations include the spreading depression with subsequent neuronal depolarisation and activation of the trigeminovascular system and release of chemicals that produce neurogenic inflammation around the intracranial and dural blood vessels. Chronic use of paracetamol has shown to be associated with an increased activation of the nociceptive pathway involved in headache. Hence it is proposed that prolonged exposure to analgesics may lead to MOH via up-regulation of neural regulators of vasodilation and neurogenic inflammation. It has been known for some time that sustained systemic delivery of morphine exposure increases CGRP content in dorsal root ganglion neurons [47, 48]. Plentiful studies documenting continuous, persistent exposure of rats to triptans for a period of days was shown to result in a marked increase in the numbers of trigeminal ganglion cell bodies expressing CGRP and a modest increase in expression of substance P.
Imaging studies have demonstrated functional [49, 50, 51], structural [52, 53] and metabolic [54] adjustments of the central pain network in patients with MOH. In a voxel-based morphometric study [55] of individuals with MOH, grey matter volume was increased in the thalamus, midbrain, and striatum, and reduced in the frontal regions [52] that resolved in sufferers who show clinical improvement of MOH [53]. Another study indicated that grey matter volume of the orbitofrontal cortex estimated response to medication-overuse treatment [56].
Functional MRI studies have shown MOH associated hypoactivitiy in certain cortical region including the right supramarginal gyrus, right inferior and superior parietal area that constitute the lateral pain system [49, 50]. This was further demonstrated in PET study where hypometabolism was also demonstrated in thalami and cerebellar vermis [54]. These changes resolved at the end of the overuse except in the orbito-frontal cortex [54]. It is to be emphasised that such changes are not unique to MOH and can be seen to some extent in other headache disorders (migraine) and pain conditions [55].
Co- morbidity is defined as the presence of one and more additional conditions co-occurring with a primary condition. Psychiatric co-morbidities in MOH are noticeably frequent and have been studied extensively since the earliest literature of patients with MOH [57]. MOH and mood disorders such as anxiety and depression are thought to be co morbid disorders by more than chance [57, 58, 59, 60].
In the Norwegian BIMOH study, (double-blind pragmatic cluster randomised controlled trial carried out among 50 general practitioners in Norway) sixty MOH patients and 40 population controls were included. The MOH patients had significantly higher headache disability and anxiety scores than the population controls. Hospital Anxiety and Depression Scale (HADS) scores were collected in patients with MOH (before and after a brief intervention) and controls. MOH patients were found to show significantly higher HADS scores for anxiety [61].
In the European and Latina “COMOESTAS” trial, (694 patients with MOH from six centres had been included, of whom 492 completed the study) in a seven-month cohort study. The study used Hospital Anxiety and Depression (HAD) scoring and found more than half (56%) of MOH patients had anxiety while 40% suffered from depression [62]. Similar findings were seen in the ‘Eurolight’ trial conducted in ten European countries. The association was considerably stronger in contrast to a group of patients with migraine without overuse [63]. A study on Sodium Valproate in Medication Overuse Headache (SAMOHA) found substantially higher number of patients with moderate to severe anxiety compared to those with episodic migraine or healthy controls [64]. Moreover, MOH are more likely to have one or more psychiatric co-morbidities and some authors found a third of patient with clinically relevant obsessive–compulsive disorders (OCD) [65].
Subclinical OCD may be an additional risk factor for chronic headaches [64, 65]. MOH can also be associated to substance-related disorder spectrum, moreover since MOH and dependence share common neurobiological pathways; noticeably MOH patients do not share common personality characteristics seen with drug addicts [66, 67].
In a Chinese cohort, an association was found between MOH and metabolic disturbances namely obesity and hypertension was shown in female patients [68]. A Danish cross-sectional analysis confirmed an association between MOH and those metabolic derangements (smoking, physical inactivity and obesity, although causality could not be proven [69]. Lastly, patients with chronic headache and MOH present with a high prevalence of sleep symptomatology [70].
There is adequate evidence that withdrawal therapy is the best treatment for MOH. The aim is not only to break the cycle of regular analgesic consumption but to improve responsiveness to both acute and prophylactic medications [71]. The following questions remain under discussion among headache experts:
Should preventive treatments be commenced at the time or following withdrawal of the analgesics?
Should the withdrawal be abrupt or gradual?
Should this be done as out-patient or done through in-patient admission.
There is argument on both sides and researchers are divided with respect to whether prophylactic medications are given at the time of withdrawal or after withdrawal. Study conducted in Germany found all patients should be offered a non-drug treatment and in the majority, additional preventive drug therapy. Taking evidence from randomised controlled trials into consideration, topiramate or OnabotulinumtoxinA should be offered as a treatment for this condition. About 50% of patients with chronic migraine and medication overuse will respond and show a significant reduction in headache days [72]. Similar results were seen with OnabotulinumtoxinA treatment in a large prospective study from Hull, UK. OnabotulinumtoxinA significantly reduced the headache and migraine days whilst increasing headache-free days and the benefit is equally seen in those with or without co-existing medication overuse. We acknowledge the value of analgesic withdrawal although we recommend that this can be achieved alongside preventive treatment [73].
No study has ever compared abrupt withdrawal with tapered withdrawal in prospective randomised trials; therefore, no formal evidence-based recommendation or guideline can be deduced. However, the majority of headache specialists consider drug withdrawal to be more effective if done abruptly than gradual [74, 75, 76].
Abrupt withdrawal is recommended for overuse of triptans, ergots, paracetamol, aspirin and NSAIDs and could be done in outpatients. Most patients have a less protracted suffering and resolution of withdrawal symptoms is much quicker. Those on opioids, barbiturates, benzodiazepines and combination analgesics a tapered withdrawal is more appropriate as withdrawal symptoms are more severe. Patients are warned that their headaches may get worse before getting better and symptoms of nausea, vomiting, sleep disturbances, palpitations, restlessness and anxiety are troublesome for a week to 10 days and in some cases may persist for up to 4 weeks before showing improvement. The duration of worsening is shorter with triptans (4.1 days) than ergotamine (6.7 days) and NSAID (9.5 days) [77].
A study in Italy of 137 patients aiming to study the effectiveness of an educational strategy (advice to withdraw the overused medication/s) with that of two structured pharmacological detoxification programmes in patients with complicated medication overuse headache (MOH) plus migraine concluded that inpatient withdrawal is significantly more effective than advice alone or an outpatient strategy in complicated MOH patients [78]. Another multicentre study (N = 376) on MOH subjects in four European and two Latin American centres comparing in-patient or out-patient detoxification programme with optional prophylaxis and a follow up for 6 months concluded equal effectiveness of both strategies with or without prophylaxis [79]. Carlsen et al. (N = 72) in a prospective, outpatient study randomised patients to two groups with one taking no analgesic or acute migraine-medication and the other restricted to no more than two days of painkillers per week. Patients were followed up for 12 months. The primary outcome was percentage reduction in headache days per month after 6 months. The outcome was better in complete withdrawal and more patients reverted to episodic migraine in this group [80].
The decision has to be taken on individual circumstances that include the type of overused medication, length of the overuse, patients’ motivation and history of previous detoxification failures and presence of co-morbidities. Out-patient withdrawal is more suited to simple analgesic, brief overuse period and highly motivated patients [81]. Evidence in favour of inpatient withdrawal comes from an observational study from Austria showing statistically significant improvement of quality of life, depression and anxiety at 6-month follow-up [82]. Alternatively a study conducted in Milan has shown that direct comparison between inpatient withdrawal and outpatient withdrawal treatment showed that both methods were effective and revealed a significant reduction in headache days per month after 12 months and a decrease in the scores of migraine disability without superiority of one method [83].
There is no standardised accepted protocol for both in-patient withdrawal. Every clinic use their own method that does include intravenous dehydration, complete stoppage of oral painkillers and treatment with anti-emetics and intramuscular painkillers as and when required with or without steroids [84, 85, 86, 87, 88].
With respect to corticosteroids, there is low evidence for change in various headache outcome measures (i.e. use of rescue medication, days with severe or moderate headache, days without headache, headache days, and frequency of headache) [89, 90]. There is plentiful literature evidence to suggest that majority of patients will get worse before they get better [91].
Early and effective prophylaxis remains the key to avoid chronification of episodic migraine. As nearly two-thirds of patients with chronic migraine have co-existing medication overuse, the question remains largely unanswered whether prophylaxis should commence before or after analgesic withdrawal. There are arguments on both sides and the jury remains out as to which approach is better. Some argue that patients with previous failure would show a good prophylactic response following withdrawal [92]; others recommend prophylaxis at the same time as withdrawal [93].
There are open-label studies showing improved outcome for using valproic acid and topiramate in patients with chronic daily headache with medication overuse. A double-blind study on topiramate in patients with chronic migraine and medication overuse showed reduction of migraine days per month significantly higher in the topiramate group (−3.5 vs. 0.2 in placebo p < 0.05), although side effects were considerably higher in the topiramate group (75% versus 37% in placebo) [94]. This supported using topiramate use before analgesic withdrawal although the reduction on headache days were not large enough to change it to episodic form. A similar observation was observed in another topiramate study where the reduction in migraine days per month was significantly higher for topiramate than placebo (6.4 versus 4.7) [95].
In a Danish study consisting of 335 patients with MOH where abrupt detoxification was initiated, the headache frequency was reduced by 67% in migraine patients and by 37% in those with combined migraine and tension-type headache after a 2-month observation period without prophylactic medication [92]. There are randomised controlled trials to show that with patients affected by chronic migraine and MOH suggest the use of onabotulinumtoxinA and topiramate without early discontinuation. However, the quality of the data is limited due to the fact that it is based on post hoc analysis [96]. Two further studies in the states have shown improvement in headache days in patients with chronic migraine and medication overuse treated with onabotulinumtoxinA and concluded that withdrawal prior to prophylaxis may not be required in all patients with MOH [97].
Steroids and NSAID have so far been studied but their effectiveness remains inconclusive. Few studies have used a short course of steroids as bridging treatment with different outcomes. The first study from Brazil used a short course of oral prednisolone in an out-patient setting. They studied 400 patients with daily headaches for longer than 6 months. Symptomatic medications were stopped suddenly and prednisone was initiated in tapering doses during 6 days, followed by the introduction of preventive treatment. The study found eighty-five per cent of the patients experienced a reduction in headache frequency and no patients presented severe attacks during the first 6 days. 10 day follow up, 46% of the patients experienced at least 2 days without headache and 58% less intense attacks [98]. Another German randomised, placebo-controlled, double-blind study showed efficacy of prednisone for the treatment of withdrawal symptoms in patients with MOH (N = 20). The total number of hours with severe or moderate headache within the first 72 and 120 h was significantly lower in the prednisone group. The results show that prednisone might be effective in the treatment of medication withdrawal headache [99]. Another randomised, double-blind, and placebo controlled Norwegian study negated the use of steroids as prophylaxis in MOH. Patients (N = 100) were randomly assigned to prednisolone or placebo pills for six days. Study concluded prednisolone has no effect on withdrawal headache in unselected patients with chronic daily headache and medication overuse [100]. A brief period of prophylaxis with naproxen 500 mg bd for 10–20 days has been recommended based on experience [101], there are other doses used for different durations [102, 103].
As a rule of thumb, overuse of acute treatment can lead to a poor prognosis of chronic headache and lower quality of life by itself [104]. The outcome for MOH patients withdrawing from their acute treatments has been reported in multiple literature citations. An accepted endpoint as mentioned in many studies for good response to therapy is a ≥ 50% reduction from baseline headache frequency and/or headache index. Successful withdrawal was found in around 50–70% of MOH patients after 1 year [105, 106, 107, 108, 109, 110, 111, 112, 113]. Managing to retain full withdrawal after 1 year was found to be a good predictor for long-term success [114, 115].A successful withdrawal leads to a better response for prophylactic treatment, even in patients with little improvement in headache frequency [116].Tension-type headache have documented to have a higher relapse risk [105, 106, 107, 117, 118]. Patients who kept overusing medication in the long-term had a poor response to withdrawal therapy and had a higher frequency of chronic headache [114]. Risk factors for short term relapse (1 year) were: high number of acute treatments, smoking, alcohol consumption and return to overused drugs [119]. Patients withdrawn from triptans have a lower relapse risk, while combined drug therapy had a higher relapse rate [106, 118, 120]. Drugs with codeine, low self-reported sleep quality and high self-reported bodily pain are probable predictors for poor outcome after 1 yr. [113]. A prospective study from Germany followed 96 patients with MOH of which 75 completed 4 years. 26 patients (31%) relapsed within first six months and a total of 32 (41%) in the first year. The following three years only two more relapsed totalling 34 (45%). The authors concluded that most of the patients who relapse do that in the first year (94%) and the long-term success is dependent on the type of primary headache and the type of overused painkiller [121].
Most recent evidence on the most effective treatment strategy comes from an Open-label, randomised clinical trial to compare 3 treatment strategies for MOH [122] which was conducted at the Danish headache Centre, Glostrup form October 2016 to June 2019. Random assignments (1:1:1 allocation) to 1 of the 3 outpatient treatments consisted of [1] Withdrawal Plus Preventive treatment [2] Preventive treatment without Withdrawal, or [3] Withdrawal with optional Preventive treatment 2 months after Withdrawal. The Primary outcome was change in the headache days per month after 6 months. Of 120 patients, 102 completed the 6 month follow-up and the headache days per month were reduced by 12.3 (95% CI, 9.3–15.3) in the withdrawal plus preventive group, by 9.9 (95% CI,7.2–12.6) in the preventive group, and by 8.5 (95% CI 5.6–11.5) in the withdrawal group (P = 0.20). In the withdrawal plus preventive group, 23 of 31 patients (74.2%) reverted to episodic migraine, compared with 21 of 35 (60%) in the preventive group and 15 of 36 (41.7%) in the withdrawal group (P = 0.03). Moreover, 30 of 31 patients (96.8%) were cured of MOH in the withdrawal plus preventive group, compared with 26 of 35 (74.3%) in the preventive group and 32 of 36 (88.9%) in the withdrawal group (P = 0.03). These findings correspond to a 30% (RR, 1.3; 95% CI 1.1–.16) increased chance of MOH cure in the withdrawal plus preventive group compared with the preventive group (P = 0.03), therefore based on these findings, withdrawal therapy combined with preventive medication from the start of the withdrawal is recommended as the preferred management for MOH.
MOH is a common and worldwide problem with a prevalence of 1% in the general population but accounts for nearly 11 to 70% in those with chronic daily headaches, often under-recognised and un treated correlates with a significant negative impact on the patient’s quality of life. Opiates and combination analgesics carry an increased risk for MOH needs to be recognised and accepted as per literature. Among the multiple risk factors for the development of MOH, some are noted to be modifiable and require MDT approach for attention and action. Anxiety and depression are the most common co morbidities, and up to approximately 50% of patients show dependence-type behaviours like tolerance or inability to control pain medication usage.
Treatment trials are still required to determine for clinicians the best evidence-based approach for helping these patients break their obnoxious headache cycle (?), but intervention will require patient counselling, detoxification, and prevention therapy. The future needs to be tailored to include a focus on increased awareness of MOH for the general population and primary prevention strategies for patients and providers. To achieve success in treatment, it is essential that the primary care provider, nurse practitioner, pharmacist, and hospital doctors openly communicate with the neurologist when MOH is suspected.
Gas chromatography is a widely used technique for the characterization of complex systems in chemical industries but also for the determination of physicochemical properties of solute in the stationary phase. This approach is also known as inverse gas chromatography (IGC) is used to quantify the solute-stationary interactions or the polarity of the last one. At the end of the twentieth century, numerous solvation models were proposed to represent retention data from chromatography. The most well-known models are called Linear Free Energy Relationship (LFER) or Linear Solvation Energy Relationship (LSER). The most recent representation of the LSER model proposed by Abraham [1, 2, 3, 4] is given by Eq. (1).
Where SP is a solvation parameter related with the free energy change such as gas–liquid partition coefficient, specific retention volume, or adjusted retention time at a given temperature. The capital letters represent the solutes properties and the lowercase letters the complementary properties of the ionic liquids. The solute descriptors are the excess molar refraction
A large databank of experimental LSER parameters for organic compounds can be found in the literature. Platts et al. proposed to determine these parameters using group contribution methods [5, 6].
In order to improve the predictive applicability of the Abraham model for ionic liquids, Sprunger et al. [8, 9, 10, 11] have proposed a method for predicting log
Other approaches reported in the literature to calculate log KL are based on group contribution methods (GC). This method is useful because we need only to know the structure of the material (IL). Revelli et al. [12] proposed to splits the cation with its alkyl chains into 21 different contributions to estimate log
In this chapter, we propose to extend the model temperature-dependent GC-LSER (TDGC-LSER) based on the group contribution method to correlate and analysis of log KL values for different solutes in ILs as a function of the temperature from 293.15 to 396.35 K. A new decomposition but also new groups are proposed in this approach. The database includes the alkyl-based ILs as well as functionalized ILs (task-specific ILs) such as alcohols and ethers. The largest number of ILs used in this database was composed of imidazolium cation-based ILs (73 ILs). Three new cations were included, choline, quinolinium, and octanium, each cation occurs only once in the database as well as Sulphonium-Based ILs.
Partition coefficients
The objective of this study is to extend the potential applicability of the TDGC-LSER model for the prediction of log
No. | Abbreviation | Ionic liquid Name | Reference |
---|---|---|---|
1 | [MMIM]+ [MeSO4]− | 1-metyl-3-methylimidazolium methylsulfate | [14] |
2 | [BMIM]+ [MeSO4]− | 1-butyl-3-methylimidazolium methylsulfate | [15] |
3 | [EMIM]+ [F3AC]− | 1-ethyl-3-methylimidazolium trifluoroacetate | [16] |
4 | [HMIM]+ [F3AC]− | 1-hexyl-3-methylimidazolium trifluoroacetate | [17] |
5 | [EMIM]+ [Tf2N]− | 1-Ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imidate | [18] |
6 | [EMIM]+ [Tf2N]− | 1-Ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)Amide | [18] |
7 | [EMIM]+ [Tf2N]− | 1-Ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [19] |
8 | [EMIM]+ [Tf2N]− | 1-Ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imidate | [18] |
9 | [EMIM]+ [Tf2N]− | 1-Ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl)Amide | [18] |
10 | [MMIM]+ [Tf2N]− | 1-methyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [19] |
11 | [BMIM]+ [Tf2N]− | 1-butyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [20] |
12 | [BMIM]+ [Tf2N]− | 1-butyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [19] |
13 | [BMIM]+ [Tf2N]− | 1-butyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [21] |
14 | [BMIM]+ [Tf2N]− | 1-butyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [22] |
15 | [MEIM]+ [Tf2N]− | 1-methyl-3-ethylimidazolium bis(trifluoromethylsulfonyl) amide | [23] |
16 | [M2EIM]+ [Tf2N]− | 1,2-dimethyl-3-ethylimidazolium bis(trifluoromethylsulfonyl) amide | [23] |
17 | [HMIM]+ [Tf2N]− | 1-hexyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [20] |
18 | [HMIM]+ [Tf2N]− | 1-hexyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [24] |
19 | [HMIM]+ [Tf2N]− | 1-hexyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [25] |
20 | [OMIM]+ [Tf2N]− | 1-octyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [25] |
21 | [OMIM]+ [Tf2N]− | 1-octyl-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [22] |
22 | [(CH2)4SO3HMIM]+ [Tf2N]− | 1-(4-sulfobutyl)-3-methylimidazolium bis(trifluoromethanesulfonyl)imide | [26] |
23 | [EtOHMIM]+ [Tf2N]− | 1-ethanol-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [27] |
24 | [MeoeMIM]+ [Tf2N]− | 1-(methylethylether)-3-methylimidazolium bis(trifluoromethylsulfonyl)imide | [27] |
25 | [(MeO)2IM]+ [Tf2N]− | 1,3-dimethoxyimidazolium bis(trifluoromethylsulfonyl)imide | [27] |
26 | [(CH2)4SO3HMIm]+ [TFO]− | 1-(4-sulfobutyl)-3-methylimidazolium trifluoromethanesulfonate | [26] |
27 | [(CH2)4SO3HMIm]+ [HSO4]− | 1-(4-sulfobutyl)-3-methylimidazolium hydrogen sulfate | [26] |
28 | [BMIM]+ [TDI]− | 1-butyl-3-methylimidazolium 4,5-dicyano-2 (trifluoromethyl)imidazolide | [28] |
29 | [C2OHMIM]+ [FAP]− | 1-(2-hydroxyethyl)-3-methylimidazolium tris(pentafluoroethyl)trifluorophosphate | [29] |
30 | [C2OHMIM]+ [FAP]− | 1-(2-hydroxyethyl)-3-methylimidazolium tris(pentafluoroethyl)trifluorophosphate | [30] |
31 | [EMIM]+ [FAP]− | 1-ethyl-3-methylimidazolium tris(pentafluoroethyl)trifluorophosphate | [31] |
32 | [BMIM]+ [N(CN)3]− | 1-butyl-3-methylimidazolium tricyanomethanide | [32] |
33 | [EMIM]+ [BF4]− | 1-ethyl-3-methylimidazolium tetrafluoroborate | [33] |
34 | [EMIM]+ [BF4]− | 1-ethyl-3-methylimidazolium tetrafluoroborate | [34] |
35 | [BMIM]+ [BF4]− | 1-butyl-3-methylimidazolium tetrafluoroborate | [20] |
36 | [BMIM]+ [BF4]− | 1-butyl-3-methylimidazolium tetrafluoroborate | [33] |
37 | [BMIM]+ [BF4]− | 1-butyl-3-methylimidazolium tetrafluoroborate | [35] |
38 | [BMIM]+ [BF4]− | 1-butyl-3-methylimidazolium tetrafluoroborate | [21] |
39 | [HMIM]+ [BF4]− | 1-hexyl-3-methylimidazolium tetrafluoroborate | [33] |
40 | [HMIM]+ [BF4]− | 1-hexyl-3-methylimidazolium tetrafluoroborate | [36] |
41 | [OMIM][BF4]− | 1-octyl-3-methylimidazolium tetrafluoroborate | [33] |
42 | [OMIM][BF4]− | 1-octyl-3-methylimidazolium tetrafluoroborate | [21] |
43 | [C2OHMIM]+ [BF4]− | 1-(2-hydroxyethyl)-3-methylimidazolium tetrafluoroborate | [37] |
44 | [PM2IM]+ [BF4]− | 1-propyl-2,3-dimethylimidazolium tetrafluoroborate | [38] |
45 | [PM2IM]+ [BF4]− | 1-propyl-2,3-dimethylimidazolium tetrafluoroborate | [39] |
46 | [EMIM]+ [(MeO)(H)PO2]− | 1-ethyl-3-methylimidazolium methylphosphonate | [40] |
47 | [M2MIM]+ [(MeO)(H)PO2]− | 1.3-dimethylimidazolium methylphosphonate | [40] |
48 | [EMIM]+ [EtSO4]− | 1-ethyl-3-methylimidazolium ethylsulfate | [41] |
49 | [EMIM]+ [EtSO4]− | 1-ethyl-3-methylimidazolium ethylsulfate | [19] |
50 | [BMIM]+ [OcSO4]− | 1-butyl-3-methylimidazolium octylsulfate | [20] |
51 | [BMIM]+ [OcSO4]− | 1-butyl-3-methylimidazolium octylsulfate | [42] |
52 | [EMIM]+ [SCN]− | 1-ethyl-3-methyl-imidazolium thiocyanate | [43] |
53 | [EMIM]+ [SCN]− | 1-ethyl-3-methyl-imidazolium thiocyanate | [22] |
54 | [BMIM]+ [SCN]− | 1-butyl-3-methylimidazolium thiocyanate | [44] |
55 | [BMIM]+ [SCN]− | 1-butyl-3-methylimidazolium thiocyanate | [22] |
56 | [HMIM]+ [SCN]− | 1-hexyl-3-methylimidazolium thiocyanate | [45] |
57 | [MMIM]+ [CH3OC2H4SO4]− | 1-methyl-3-methylimidazolium methoxyethylsulfate | [14] |
58 | [MMIM]+ [(CH3)2PO4]− | 1-methyl-3-methylimidazolium dimethylphosphate | [14] |
59 | [BMIM]+ [PF6]− | 1-butyl-3-methylimidazolium hexafluorophosphate | [46] |
60 | [HMIM]+ [PF6]− | 1-hexyl-3-methylimidazolium hexafluorophosphate | [47] |
61 | [HMIM]+ [PF6]− | 1-hexyl-3-methylimidazolium hexafluorophosphate | [47] |
62 | [MOIM]+ [PF6]− | 1-methyl-3-octylimidazolium hexafluorophosphate | [48] |
63 | [EMIM]+ [CF3SO3]− | 1-ethyl-3-methylimidazolium trifluoromethanesulfonate | [49] |
64 | [BMIM]+ [CF3SO3]− | 1-butyl-3-methylimidazolium trifluoromethanesulfonate | [22] |
65 | [HMIM]+ [CF3SO3]− | 1-hexyl-3-methylimidazolium trifluoromethanesulfonate | [50] |
66 | [HMIM]+ [CF3SO3]− | 1-hexyl-3-methylimidazolium trifluoromethanesulfonate | [22] |
67 | [BMIM]+ [NO3]− | 1-Butyl-3-methylimidazolium nitrate | [51] |
68 | [OMIM]+ [NO3]− | 1-octyl-3-methylimidazolium nitrate | [52] |
69 | [B4MPY]+ [N(CN)2]− | 1-butyl-4-methylpyridinium dicyanamide | [53] |
70 | [BMPY]+ [TDI]− | 1-Butyl-3-methylpyridinium 4,5-dicyano-2-(trifluoromethyl)imidazolide | [28] |
71 | [BMPY]+ [N(CN)3]− | 1-butyl-4-methylpyridinium tricyanomethanide | [32] |
72 | [NEPY]+ [Tf2N]− | N-ethylpyridinium bis(trifluoromethylsulfonyl)imide | [14] |
73 | [4MBPY]+ [BF4]− | 4-methyl-N-butylpyridinium tetrafluoroborate | [54] |
74 | [4MBPY]+ [BF4]− | 4-methyl-N-butylpyridinium tetrafluoroborate | [55] |
75 | [4MBPY]+ [BF4]− | 4-methyl-N-butylpyridinium tetrafluoroborate | [46] |
76 | [BMPY]+ [Tf2N]− | 1-butyl-3-methylpyridinium bis(trifluoromethylsulfonyl)imide | [56] |
77 | [1,3BMPY]+ [CF3SO3]− | 1-butyl-3-methylpyridinium trifluoromethanesulfonate | [57] |
78 | [C2PY]+ [Tf2N]− | 2-alkylpyridinium bis(trifluoromethylsulfonyl)imide | [22] |
79 | [C4PY]+ [Tf2N]− | 4-alkylpyridinium bis(trifluoromethylsulfonyl)imide | [22] |
80 | [C5PY]+ [Tf2N]− | 5-alkylpyridinium bis(trifluoromethylsulfonyl)imide | [22] |
81 | [BMPYR]+ [N(CN)3]− | 1-butyl-1-methylpyrrolidinium tricyanomethanide | [58] |
82 | [MeoeMPYR]+ [FAP]− | 1-(2-methoxyethyl)-1-methylpyrrolidinium tris(pentafluoroethyl)trifluorophosphate | [59] |
83 | [MeoeMPYR]+ [FAP]− | 1-(2-methoxyethyl)-1-methylpyrrolidinium tris(pentafluoroethyl)trifluorophosphate | [29] |
84 | [PrMPYR]+ [Tf2N]− | 1-propyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide | [60] |
85 | [BMPYR]+ [Tf2N]− | 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide | [25] |
86 | [BMPYR]+ [Tf2N]− | 1-butyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide | [60] |
87 | [PeMPYR]+ [Tf2N]− | 1-pentyl-1-methylpyrrolidinium Bis(trifluoromethylsulfonyl)imide | [60] |
88 | [HMPYR]+ [Tf2N]− | 1-hexyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide | [61] |
89 | [OMPYR]+ [Tf2N]− | 1-octyl-1-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide | [61] |
90 | [BMPYR]+ [CF3SO3]− | 1-butyl-1-methylpyrrolidinium trifluoromethanesulfonate | [62] |
91 | [C5C1PIP]+ [Tf2N]− | 1-5-alkyl-1-methylpiperidinium bis(trifluoromethylsulfonyl)imide | [63] |
92 | [C6C1PIP]+ [Tf2N]− | 1-6-alkyl-1-methylpiperidinium bis(trifluoromethylsulfonyl)imide | [63] |
93 | [MeoeMPIP]+ [FAP]− | 1-(2-methoxyethyl)-1-methylpiperidinium trifluorotris(perfluoroethyl)phosphate | [64] |
94 | [PMPIP]+ [Tf2N]− | 1-propyl-1-methylpiperidiniumbis(trifluoromethylsulfonyl)imide | [65] |
95 | [H3TdP]+ [L-Lact]− | trihexyl(tetradecyl)phosphonium L-lactate | [66] |
96 | [H3TdP]+ [+CS]− | trihexyl(tetradecyl)phosphonium (1S)-(+)-10-camphorsulfonate | [66] |
97 | [H3TdP]+ [Tf2N]− | Trihexyl(tetradecyl)phosphonium bis(trifluoromethylsulfonyl)imide | [67] |
98 | [H3TdP]+ [Tf2N]− | Trihexyl(tetradecyl)phosphonium bis(trifluoromethylsulfonyl)imide | [25] |
99 | [BMMOR]+ [N(CN)3]− | 1-butyl-1-methylmorpholinium tricyanomethanide | [68] |
100 | [N-C3OHMMOR]+ [Tf2N]− | 4-(3-hydroxypropyl)-4-methylmorpholinium bis(trifluoromethylsulfonyl)amide | [69] |
101 | [Et3S]+ [Tf2N]− | triethylsulphonium bis(trifluoromethylsulfonyl)imide | [70] |
102 | [O3MAM]+ [Tf2N]− | trioctylmethylammonium bis(trifluoromethylsulfonyl)imide | [71] |
103 | [O3MAM]+ [Tf2N]− | trioctylmethylammonium bis(trifluoromethylsulfonyl)imide | [71] |
104 | [M3BAM] + [NTf2]− | trimethyl-butylammonium bis(trifluoromethylsulfonyl)imide | [72] |
105 | [Cho]+ [Tf2N]− | choline bis(trifluoromethylsulfonyl)imide | [73] |
106 | [HiQuin]+ [SCN]− | N-hexylisoquinolinium thiocyanate | [74] |
107 | [HDABCO]+ [Tf2N]− | 1-hexyl-1,4-diaza[2.2.2]bicyclooctanium bis(trifluoromethylsulfonyl)imide | [75] |
Names and abbreviations of ionic liquids.
Number of cation-based ILs used for the prediction of log
The collection of organic solutes includes alkanes, cycloalkanes, alkenes, alkynes, aromatics, alcohols, ethers, aldehydes, ketones, chloroalkanes cyanoalkanes, thiophene, pyridine, water, and other solutes. The values of the five solute descriptors for different organic compounds considered in this work can be found in the literature [1, 2, 3, 4, 5, 6]. The solute descriptors used in the calculations were taken from earlier studies on ILs and cover the range from:
Definition | Group | Definition | Group |
---|---|---|---|
CH3 from alkyl chain | CH3 | Trifluorotris(perfluoroethyl)phosphate | [FAP]─ |
CH2 from alkyl chain | CH2 | Bis(trifluoromethylsulfonyl)imide | [Tf2N]─ |
-O- in alkyl chain | O | Hexafluorophosphate | [PF6]─ |
Hydroxyl in alkyl | OH | Tetrafluoroborate | [BF4]─ |
Sulfonyl hydroxide | SO3H | Methylsulfate | [MeSO4]─ |
N ammonium’s cation | [N]+ | Ethylsulfate | [EtSO4]─ |
S sulfonium’s cation | [S]+ | Octylsulfate | [OcSO4]─ |
1,4-diaza [2] bicyclooctanium | [DABCO]+ | Thiocyanate | [SCN]─ |
Imidazolium cation | [IM]+ | Trifluoromethylsulfonate | [CF3SO3]─ |
Pyridinium cation | [PY]+ | Trifluoroacetate | [F3AC]─ |
Pyrrolidinium cation | [PYR]+ | Methoxyethylsulfate | [CH3OC2H4SO4]─ |
Piperidinium cation | [PIP]+ | 4,5-Dicyano-2-(trifluoromethyl)imidazolium | [TDI]─ |
Phosphonium cation | [P]+ | Methylphosphonate | [(MeO)(H)PO2]─ |
Morpholium cation | [MOR]+ | Hydrogen sulfate | [HSO4]─ |
Quinolinium cation | [Quin]+ | Dimethylphosphate | [(CH3)2PO4]─ |
Choline cation | [Cho]+ | L-lactate | [L-Lact]─ |
Dicyanamide | [N(CN)2]─ | (1S)-(+)-10-Camphorsulfonate | [+CS]─ |
Tricyanomethanide | [N(CN)3]─ | Nitrate | [NO3]─ |
Description of the 36 groups used for the estimation of log
In the present study, the database contains 14,762 experimental data for about 107 ILs at the temperature range of 293.15–396.35 K, the main objective of this study is to extend the predictive applicability of the TDGC-LSER model to a new cation and anion based ILs, that have not been reported previously, as the ILs having cyano-based anions (thiocyanate [SCN]─; dicyanamide, [N(CN)2]─; tricyanomethanide, [C(CN)3]─ and perfluorinated anions (e.g. trifluorotris(perfluoroethyl)phosphate, [FAP]). The model adopted in this work is capable of representing log
The TDGC-LSER model may represent the partition coefficient of solutes in ILs using the Eq. 6:
Where ni is the number of group i present in the ionic liquid. Values of ci, ei, si, ai, bi, and li and their standard errors in parentheses are given in Table 3.
Group | ||||||
---|---|---|---|---|---|---|
CH3 | −82.195 (8.697) | 67.71 (13.14) | 1.38 (15.33) | 133.26 (16.50) | 5.69 (14.63) | 4.18 (2.594) |
CH2 | 11.093 (1.523) | −25.428 (2.319) | −15.933 (2.836) | −14.017 (2.827) | −3.663 (3.065) | 8.57 (0.4577) |
O | −18.818 (6.703) | −9.581 (8.681) | 21.984 (8.577) | −30.93 (11.21) | 21.494 (9.081) | −13.017 (1.732) |
OH | −193 (12.76) | 98.11 (17.90) | 39.42 (20.01) | 168.51 (22.02) | 293.86 (19.65) | −17.394 (3.687) |
[N]+ | 2316.75 (64.96) | 353.55 (90.42) | −297.80 (112.6) | −387.6 (120.5) | 98.1 (123.9) | −263.57 (17.99) |
[S]+ | 1892.89 (47.02) | −69.03 (61.36) | 71.74 (73.65) | −358.17 (80.73) | 190.98 (67.59) | −59.51 (11.93) |
SO3H | −401.01 (27.18) | 211.14 (25.90) | 29.56 (29.25) | 963.61 (46.37) | 646.47 (35.68) | −0.109 (5.620) |
DABCO | 1804.97 (41.71) | 116.87 (41.93) | −89.01 (46.46) | −141.72 (70.03) | 232.09 (53.11) | −60.643 (9.825) |
[IM]+ | 1929.34 (39.51) | −29.8 (39.59) | −8.73 (44.00) | −267.56 (65.70) | 180.46 (47.66) | −63.12 (9.213) |
[PY]+ | 1899.81 (39.00) | 8.09 (39.56) | −20.39 (44.43) | −254.68 (65.27) | 189.68 (47.58) | −59.425 (9.001) |
[PYR]+ | 1891.63 (40.38) | −5.33 (40.98) | 16.51 (45.52) | −222.69 (67.02) | 117.9 (49.23) | −50.992 (9.509) |
[PIP]+ | 1896.55 (40.90) | 6.56 (42.01) | 30.75 (46.89) | −231.35 (67.60) | 65.98 (50.61) | −46.801 (9.668) |
[P]+ | 1942.67 (72.12) | 410.56 (98.99) | 48.1 (116.4) | −402.1 (128.0) | 191.7 (122.5) | −243.72 (20.34) |
[MOR]+ | 1834.41 (41.57) | 44.92 (42.28) | 107.86 (46.83) | −119.24 (68.33) | 88.14 (50.55) | −72.741 (9.943) |
[Quin]+ | 1849.71 (40.76) | 25.7 (42.69) | 33.16 (48.08) | −145.85 (66.40) | 33.22 (49.85) | −46.729 (9.584) |
[Cho]+ | −183.29 (35.99) | −522.76 (58.38) | 333.14 (78.77) | −30.32 (75.04) | −49.82 (93.81) | 185.55 (10.51) |
[N(CN)2]─ | −970.82 (36.63) | 150.74 (33.05) | 810.89 (35.05) | 1249.76 (61.39) | −81.18 (40.34) | 197.042 (8.294) |
[N(CN)3] ─ | −896.18 (34.95) | 82.95 (28.43) | 725.96 (29.59) | 894.88 (56.33) | 13.96 (36.19) | 199.506 (7.598) |
[FAP] ─ | −830.7 (34.70) | −74.84 (29.00) | 736.99 (30.24) | 372.32 (56.58) | 52.4 (36.71) | 214.343 (7.509) |
[Tf2N] ─ | −899.66 (33.67) | −29.2 (27.04) | 734.55 (28.17) | 640.99 (55.10) | −10.5 (34.81) | 207.618 (7.095) |
[PF6]─ | −977.77 (36.33) | 85.23 (38.82) | 758.26 (47.71) | 528.15 (64.97) | 125.04 (49.75) | 208.42 (8.180) |
[BF4]─ | −958.9 (34.01) | 144.71 (27.81) | 733.41 (29.17) | 979.13 (56.03) | −40.58 (35.85) | 187.379 (7.214) |
[MeSO4]─ | −912.02 (38.32) | 179.36 (34.98) | 439.56 (38.88) | 1866.13 (72.09) | 112.7 (49.26) | 147.143 (9.112) |
[EtSO4]─ | −959.72 (36.50) | −12.58 (35.09) | 792.73 (39.00) | 1467.31 (65.24) | −194.98 (48.93) | 198.684 (7.880) |
[OcSO4] ─ | −883.39 (45.40) | −65.96 (41.05) | 575.78 (42.09) | 1395.39 (73.88) | −231.21 (50.54) | 249.11 (11.64) |
[SCN]─ | −1120.06 (34.61) | 239.28 (32.03) | 720.87 (36.59) | 1388.16 (56.41) | 64.13 (38.49) | 210.298 (7.459) |
[CF3SO3] ─ | −971.54 (34.72) | 84.5 (30.51) | 708.98 (34.13) | 1048.13 (57.45) | 35.85 (39.56) | 205.302 (7.504) |
[F3AC]─ | −948.31 (36.54) | 192.18 (32.62) | 516.67 (34.42) | 1654.6 (60.42) | −41.21 (40.15) | 201.913 (8.340) |
[CH3OC2H4SO4]─ | −864.62 (60.40) | −117.89 (90.33) | 1150.9 (142.0) | −190.7 (776.4) | −563.9 (186.0) | 128.97 (19.99) |
[TDI]─ | −900.02 (34.69) | 8.82 (28.82) | 719.91 (29.78) | 868.4 (56.35) | −50.29 (36.22) | 228.757 (7.537) |
[(MeO)(H)PO2]─ | −837.19 (39.44) | −110.29 (34.18) | 772.28 (36.82) | 1843.42 (68.33) | −103.52 (42.76) | 175.47 (8.406) |
[HSO4]─ | −718.34 (91.93) | −438.37 (52.51) | 991.64 (66.58) | −457.3 (283.4) | −1113.4 (101.0) | 171.09 (16.10) |
[(CH3)2PO4]─ | −1189.85 (64.54) | 327.11 (52.20) | 379.11 (68.71) | 1887.4 (79.33) | 445.78 (81.67) | 242.14 (17.61) |
[L-Lact] ─ | −935.34 (46.66) | −35.01 (45.39) | 869.85 (46.65) | 2176.62 (89.53) | −254.38 (59.97) | 227.99 (11.50) |
[+CS]─ | −1008.33 (44.06) | −29.46 (43.56) | 822.58 (43.45) | 1674.07 (74.84) | −160.92 (51.68) | 228.68 (10.48) |
[NO3]─ | −937.17 (33.75) | 215.29 (26.72) | 565.62 (29.28) | 1483.74 (45.69) | 125.91 (29.89) | 188.276 (7.003) |
TDGC-LSER coefficients for the calculation of log
The experimental log KL data for all ILs were reproduced using Eq. (6) with average absolute deviation (AARD) at the level of 6.39%. The model developed is statistically good, and describes the experimental log
The average absolute deviation AARD
The AARD values on the prediction of log
Ionic liquids | Log KL (%) | Ionic liquids | Log KL (%) | ||
---|---|---|---|---|---|
[MMIM]+ [MeSO4]− | 22.82 | 56.93 | [EMIM]+ [EtSO4]− | 6.71 | 21.63 |
[BMIM]+ [MeSO4]− | 13.17 | 27.03 | 10.20 | 19.59 | |
[EMIM]+ [F3AC]− | 5.91 | 15.16 | [BMIM]+ [OcSO4]− | 6.70 | 33.60 |
[HMIM]+ [F3AC]− | 4.54 | 32.12 | 2.78 | 14.49 | |
[MMIM]+ [Tf2N]− | 6.56 | 26.59 | [MMIM]+ [CH3OC2H4SO4]− | 13.82 | 11.28 |
[EMIM]+ [Tf2N]− | 13.55 | 98.45 | [MMIM]+ [(CH3)2PO4]− | 10.73 | 29.15 |
9.36 | 54.05 | [EMIM]+ [CF3SO3]− | 3.24 | 11.55 | |
5.38 | 29.87 | [BMIM]+ [CF3SO3]− | 3.38 | 11.03 | |
13.69 | 101.29 | [HMIM]+ [CF3SO3]− | 10.11 | 23.18 | |
10.64 | 64.23 | 6.93 | 21.79 | ||
[MEIM]+ [Tf2N]− | 6.10 | 17.00 | [BMIM]+ [NO3]− | 6.31 | 29.82 |
[M2EIM]+ [Tf2N]− | 6.73 | 24.15 | [OMIM]+ [NO3]− | 6.12 | 32.88 |
[BMIM]+ [Tf2N]− | 3.90 | 22.78 | |||
5.11 | 24.57 | [B4MPY]+ [N(CN)2]− | 4.54 | 12.64 | |
6.99 | 39.58 | [BMPY]+ [TDI]− | 3.35 | 14.75 | |
3.54 | 27.55 | [BMPY]+ [C(CN)3]− | 3.77 | 19.51 | |
[HMIM]+ [Tf2N]− | 3.15 | 21.65 | [BMPY]+ [Tf2N]− | 5.18 | 16.77 |
3.17 | 16.04 | [4MBPY]+ [BF4]− | 3.88 | 21.36 | |
2.90 | 15.23 | 4.82 | 15.22 | ||
2.86 | 20.70 | 2.67 | 16.47 | ||
0.87 | 5.15 | [1,3BMPY]+ [CF3SO3]− | 9.98 | 42.38 | |
[OMIM]+ [Tf2N]− | 3.12 | 11.35 | [NEPY]+ [Tf2N]− | 9.54 | 29.23 |
2.62 | 11.09 | [C2PY]+ [Tf2N]− | 5.37 | 21.46 | |
[(CH2)4SO3HMIm]+ [Tf2N]− | 7.40 | 34.57 | [C4PY]+ [Tf2N]− | 9.63 | 32.88 |
[EtOHmim]+ [Tf2N]− | 7.12 | 26.81 | [C5PY]+ [Tf2N]− | 9.63 | 32.88 |
[(MeO)2IM]+ [Tf2N]− | 8.05 | 21.27 | |||
[MeoeMIM]+ [Tf2N]− | 4.70 | 20.21 | [BMPYR]+ [C(CN)3]− | 3.09 | 11.06 |
[EMIM]+ [BF4]− | 9.64 | 60.61 | [MeoeMPyrr]+ [FAP]− | 4.70 | 18.65 |
11.71 | 38.35 | 5.61 | 29.68 | ||
[PM2IM]+ [BF4]− | 6.18 | 23.63 | [PrMPYR]+ [Tf2N]− | 4.23 | 16.02 |
35.41 | 35.51 | [BMPYR]+ [Tf2N]− | 4,10 | 15.54 | |
[BMIM]+ [BF4]− | 5.15 | 11.76 | [PeMPYR]+ [Tf2N]− | 3.79 | 14.22 |
12.10 | 22.42 | [HMPYR]+ [Tf2N]− | 1.95 | 7.89 | |
4.25 | 21.49 | [OMPYR]+ [Tf2N]− | 3.27 | 12.20 | |
5.32 | 29.16 | [BMPYR]+ [CF3SO3]− | 7.97 | 14.51 | |
5.55 | 28.39 | [BMPYR]+ [Tf2N]− | 4.60 | 22.93 | |
[HMIM]+ [BF4]− | 6,02 | 19.93 | |||
9.63 | 51.73 | [PMPIP]+ [Tf2N]− | 3,19 | 13.44 | |
[OMIM]+ [BF4]− | 3.57 | 14.14 | [C5C1PiP]+ [Tf2N]− | 2.42 | 10.89 |
3.71 | 22.32 | [C6C1PIP]+ [Tf2N]− | 2.47 | 10.12 | |
5.69 | 29.40 | [MeoeMPIP]+ [FAP]− | 3.74 | 15.66 | |
11.37 | 90.97 | ||||
[C2OHMIM]+ [BF4]− | 10.65 | 38,39 | [H3TdP]+ [L-Lact]− | 3.06 | 16.80 |
[BMIM]+ [PF6]− | 2.70 | 18.20 | [H3TdP]+ [+CS]− | 5.90 | 33.28 |
[HMIM]+ [PF6]− | 3.36 | 14.79 | [H3TdP]+ [Tf2N]− | 3.58 | 16.19 |
3.32 | 14.51 | 4.55 | 23.55 | ||
[MOIM]+ [PF6]− | 2.91 | 12.12 | |||
[(CH2)4SO3HMIm]+ [TFO]− | 12.52 | 31.50 | [BMMOR]+ [C(CN)3]− | 5.94 | 13.17 |
[(CH2)4SO3HMIm]+ [HSO4]− | 8.56 | 36.71 | [N-C3OHMMOR]+ [Tf2N]− | 12.42 | 15.87 |
[BMIM]+ [TDI]− | 3.42 | 13.01 | |||
[EMIM]+ [FAP]− | 8.41 | 23.43 | [Et3S]+ [Tf2N]− | 3.63 | 8.95 |
[C2OHMIM]+ [FAP]− | 8.25 | 54.98 | |||
4.71 | 21.68 | [M3BA]+ [Tf2N]− | 11.08 | 91.05 | |
[EMIM]+ [SCN]− | 14.50 | 14.31 | [O3MA]+ [Tf2N]− | 8.61 | 52.55 |
9.17 | 19.02 | [O3MA]+ [Tf2N]− | 8.72 | 50.13 | |
[BMIM]+ [SCN]− | 10.20 | 18.10 | |||
14.21 | 29.36 | [Cho]+ [Tf2N]− | 4.82 | 13.95 | |
[HMIM]+ [SCN]− | 5.44 | 18.68 | |||
[BMIM]+ [C(CN)3]− | 3.14 | 10.86 | [HiQuin]+ [SCN]− | 7.93 | 16.65 |
[EMIM]+ [(MeO)(H)PO2]− | 15.89 | 50.54 | |||
[DIMIM]+ [(MeO)(H)PO2]− | 9.70 | 47.47 | [HDABCO]+ [Tf2N]− | 4.28 | 18.48 |
Average absolute deviation for the ionic liquids that are used in this study.
The values obtained for each ILs vary from 0.87 to 35.41%. Figure 2 shows a plot of calculated log
Comparison of calculated log KL values based on Eq.
The ILs with the highest AARD are [MMIM]+ [MeSO4]−, [PM2IM]+ [BF4]−, [BMIM]+ [NO3]−, [OMIM]+ [NO3]−, This may be related to the quality of the experimental data or the number of experimental data.
The predictive power of TDGC-LSER was evaluated calculating log KL of organic compounds in four ILs not included in the database: 1-butyl-3-methylimidazolium chloride [BMIM]+ [Cl]─ [76], 1-butyl-3-methylimidazolium dimethyl phosphate [BMIM]+ [(CH3)2PO4]─ [76], 1-butyl-3-methylimidazolium dicyanamide [BMIM]+ [N(CN)2]─ [77], 1-Dodecyl-3-methylimidzolium Bis(trifluoromethylsulfonyl)-imide [DoMIM]+ [Tf2N]─ [78]. In the case of [BMIM]+ [Cl]─, 224 experimental log
The TDGC-LSER model was used for the prediction of log
The list of groups used for the estimation of calculated log
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",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"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)
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\\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.
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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
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\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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His studies in robotics lead him not only to a PhD degree but also inspired him to co-found and build the International Journal of Advanced Robotic Systems - world's first Open Access journal in the field of robotics.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"441",title:"Ph.D.",name:"Jaekyu",middleName:null,surname:"Park",slug:"jaekyu-park",fullName:"Jaekyu Park",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/441/images/1881_n.jpg",biography:null,institutionString:null,institution:{name:"LG Corporation (South Korea)",country:{name:"Korea, South"}}},{id:"465",title:"Dr",name:"Christian",middleName:null,surname:"Martens",slug:"christian-martens",fullName:"Christian Martens",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"479",title:"Dr.",name:"Valentina",middleName:null,surname:"Colla",slug:"valentina-colla",fullName:"Valentina Colla",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/479/images/358_n.jpg",biography:null,institutionString:null,institution:{name:"Sant'Anna School of Advanced Studies",country:{name:"Italy"}}},{id:"494",title:"PhD",name:"Loris",middleName:null,surname:"Nanni",slug:"loris-nanni",fullName:"Loris Nanni",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/494/images/system/494.jpg",biography:"Loris Nanni received his Master Degree cum laude on June-2002 from the University of Bologna, and the April 26th 2006 he received his Ph.D. in Computer Engineering at DEIS, University of Bologna. On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. His research interests include pattern recognition, bioinformatics, and biometric systems (fingerprint classification and recognition, signature verification, face recognition).",institutionString:null,institution:null},{id:"496",title:"Dr.",name:"Carlos",middleName:null,surname:"Leon",slug:"carlos-leon",fullName:"Carlos Leon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Seville",country:{name:"Spain"}}},{id:"512",title:"Dr.",name:"Dayang",middleName:null,surname:"Jawawi",slug:"dayang-jawawi",fullName:"Dayang Jawawi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Technology Malaysia",country:{name:"Malaysia"}}},{id:"528",title:"Dr.",name:"Kresimir",middleName:null,surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/528/images/system/528.jpg",biography:"K. Delac received his B.Sc.E.E. degree in 2003 and is currentlypursuing a Ph.D. degree at the University of Zagreb, Faculty of Electrical Engineering andComputing. His current research interests are digital image analysis, pattern recognition andbiometrics.",institutionString:null,institution:{name:"University of Zagreb",country:{name:"Croatia"}}},{id:"557",title:"Dr.",name:"Andon",middleName:"Venelinov",surname:"Topalov",slug:"andon-topalov",fullName:"Andon Topalov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/557/images/1927_n.jpg",biography:"Dr. Andon V. Topalov received the MSc degree in Control Engineering from the Faculty of Information Systems, Technologies, and Automation at Moscow State University of Civil Engineering (MGGU) in 1979. He then received his PhD degree in Control Engineering from the Department of Automation and Remote Control at Moscow State Mining University (MGSU), Moscow, in 1984. From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. His current research interests are in the fields of intelligent control and robotics.",institutionString:null,institution:{name:"Technical University of Sofia",country:{name:"Bulgaria"}}},{id:"585",title:"Prof.",name:"Munir",middleName:null,surname:"Merdan",slug:"munir-merdan",fullName:"Munir Merdan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/585/images/system/585.jpg",biography:"Munir Merdan received the M.Sc. degree in mechanical engineering from the Technical University of Sarajevo, Bosnia and Herzegovina, in 2001, and the Ph.D. degree in electrical engineering from the Vienna University of Technology, Vienna, Austria, in 2009.Since 2005, he has been at the Automation and Control Institute, Vienna University of Technology, where he is currently a Senior Researcher. His research interests include the application of agent technology for achieving agile control in the manufacturing environment.",institutionString:null,institution:null},{id:"605",title:"Prof",name:"Dil",middleName:null,surname:"Hussain",slug:"dil-hussain",fullName:"Dil Hussain",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/605/images/system/605.jpg",biography:"Dr. Dil Muhammad Akbar Hussain is a professor of Electronics Engineering & Computer Science at the Department of Energy Technology, Aalborg University Denmark. Professor Akbar has a Master degree in Digital Electronics from Govt. College University, Lahore Pakistan and a P-hD degree in Control Engineering from the School of Engineering and Applied Sciences, University of Sussex United Kingdom. Aalborg University has Two Satellite Campuses, one in Copenhagen (Aalborg University Copenhagen) and the other in Esbjerg (Aalborg University Esbjerg).\n· He is a member of prestigious IEEE (Institute of Electrical and Electronics Engineers), and IAENG (International Association of Engineers) organizations. \n· He is the chief Editor of the Journal of Software Engineering.\n· He is the member of the Editorial Board of International Journal of Computer Science and Software Technology (IJCSST) and International Journal of Computer Engineering and Information Technology. \n· He is also the Editor of Communication in Computer and Information Science CCIS-20 by Springer.\n· Reviewer For Many Conferences\nHe is the lead person in making collaboration agreements between Aalborg University and many universities of Pakistan, for which the MOU’s (Memorandum of Understanding) have been signed.\nProfessor Akbar is working in Academia since 1990, he started his career as a Lab demonstrator/TA at the University of Sussex. After finishing his P. hD degree in 1992, he served in the Industry as a Scientific Officer and continued his academic career as a visiting scholar for a number of educational institutions. In 1996 he joined National University of Science & Technology Pakistan (NUST) as an Associate Professor; NUST is one of the top few universities in Pakistan. In 1999 he joined an International Company Lineo Inc, Canada as Manager Compiler Group, where he headed the group for developing Compiler Tool Chain and Porting of Operating Systems for the BLACKfin processor. The processor development was a joint venture by Intel and Analog Devices. In 2002 Lineo Inc., was taken over by another company, so he joined Aalborg University Denmark as an Assistant Professor.\nProfessor Akbar has truly a multi-disciplined career and he continued his legacy and making progress in many areas of his interests both in teaching and research. He has contributed in stochastic estimation of control area especially, in the Multiple Target Tracking and Interactive Multiple Model (IMM) research, Ball & Beam Control Problem, Robotics, Levitation Control. He has contributed in developing Algorithms for Fingerprint Matching, Computer Vision and Face Recognition. He has been supervising Pattern Recognition, Formal Languages and Distributed Processing projects for several years. He has reviewed many books on Management, Computer Science. Currently, he is an active and permanent reviewer for many international conferences and symposia and the program committee member for many international conferences.\nIn teaching he has taught the core computer science subjects like, Digital Design, Real Time Embedded System Programming, Operating Systems, Software Engineering, Data Structures, Databases, Compiler Construction. 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Its uses have recorded good success rate in controlling major plant diseases. Knowledge on the mechanisms employed by Trichoderma spp. could be further studied to improve its ability as an efficient biocontrol agent. The Trichoderma ability to curb plant diseases were mainly based on the activation of single or multiple control mechanisms. It is known that the Trichoderma-based biocontrol mechanisms mainly rely on mycoparasitism, production of antibiotic and/or hydrolytic enzymes, competition for nutrients, as well as induced plant resistance; numerous secondary metabolites produced by Trichoderma species could directly inhibit the growth of several plant pathogens. These mechanisms may act directly or indirectly against the targeted plant pathogen. This chapter reviews the recent updates on published research findings on mechanisms used by Trichoderma as biological control of plant diseases particularly on basal stem rot disease of oil palm caused by Ganoderma spp.",book:{id:"8081",slug:"trichoderma-the-most-widely-used-fungicide",title:"Trichoderma",fullTitle:"Trichoderma - The Most Widely Used Fungicide"},signatures:"Syed Ali Nusaibah and Habu Musa",authors:null}],onlineFirstChaptersFilter:{topicId:"366",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:32,numberOfPublishedChapters:318,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:106,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:15,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. 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Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. 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Other positions she has held at the university include Vice-Dean of Master Programs, Vice-Dean of the Degree in Biology and Vice-Dean for Mobility and Enterprise and Engagement at the Faculty of Science (University of Alicante). She received her Bachelor in Biology in 1998 (University of Alicante) and her PhD in 2003 (Biochemistry, University of Alicante). She undertook post-doctoral research at the University of East Anglia (Norwich, U.K. 2004-2005; 2007-2008).\nHer multidisciplinary research focuses on investigating archaea and their potential applications in biotechnology. She has an H-index of 21. She has authored one patent and has published more than 70 indexed papers and around 60 book chapters.\nShe has contributed to more than 150 national and international meetings during the last 15 years. Her research interests include archaea metabolism, enzymes purification and characterization, gene regulation, carotenoids and bioplastics production, antioxidant\ncompounds, waste water treatments, and brines bioremediation.\nRosa María’s other roles include editorial board member for several journals related\nto biochemistry, reviewer for more than 60 journals (biochemistry, molecular biology, biotechnology, chemistry and microbiology) and president of several organizing committees in international meetings related to the N-cycle or respiratory processes.",institutionString:null,institution:{name:"University of Alicante",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"15",title:"Chemical Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/15.jpg",isOpenForSubmission:!0,editor:{id:"441442",title:"Dr.",name:"Şükrü",middleName:null,surname:"Beydemir",slug:"sukru-beydemir",fullName:"Şükrü Beydemir",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003GsUoIQAV/Profile_Picture_1634557147521",biography:"Dr. Şükrü Beydemir obtained a BSc in Chemistry in 1995 from Yüzüncü Yıl University, MSc in Biochemistry in 1998, and PhD in Biochemistry in 2002 from Atatürk University, Turkey. He performed post-doctoral studies at Max-Planck Institute, Germany, and University of Florence, Italy in addition to making several scientific visits abroad. He currently works as a Full Professor of Biochemistry in the Faculty of Pharmacy, Anadolu University, Turkey. Dr. Beydemir has published over a hundred scientific papers spanning protein biochemistry, enzymology and medicinal chemistry, reviews, book chapters and presented several conferences to scientists worldwide. He has received numerous publication awards from various international scientific councils. He serves in the Editorial Board of several international journals. 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He is a member of the Turkish Biochemical Society, American Chemical Society, and German Genetics society. Dr. Ekinci published around ninety scientific papers, reviews and book chapters, and presented several conferences to scientists. He has received numerous publication awards from several scientific councils. 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He worked on the structure-function relationships of glycoconjugates and his main project was the investigations on the biological roles of the de-N-glycosylation enzymes (Endo-N-acetyl-β-D-glucosaminidase and peptide-N4-(N-acetyl-β-glucosaminyl) asparagine amidase). From 2002 he contributes to the understanding of the Blood-brain barrier functioning using proteomics approaches. He has published more than 70 papers. 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Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. 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She gained considerable experience in developing and validating new methodologies whose applications allowed her to determine both the amount of biomarkers (Desmosine and Isodesmosine) in the urine of patients affected by COPD, and the activity of proteolytic enzymes (HNE, Cathepsin G, Pseudomonas aeruginosa elastase) in the sputa of these patients. Simona Viglio was also involved in research dealing with the supplementation of amino acids in patients with brain injury and chronic heart failure. She is presently engaged in the development of 2-DE and LC-MS techniques for the study of proteomics in biological fluids. The aim of this research is the identification of potential biomarkers of lung diseases. She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:36,paginationItems:[{id:"82195",title:"Endoplasmic Reticulum: A Hub in Lipid Homeostasis",doi:"10.5772/intechopen.105450",signatures:"Raúl Ventura and María Isabel Hernández-Alvarez",slug:"endoplasmic-reticulum-a-hub-in-lipid-homeostasis",totalDownloads:4,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Updates on Endoplasmic Reticulum",coverURL:"https://cdn.intechopen.com/books/images_new/11674.jpg",subseries:{id:"14",title:"Cell and Molecular Biology"}}},{id:"82409",title:"Purinergic Signaling in Covid-19 Disease",doi:"10.5772/intechopen.105008",signatures:"Hailian Shen",slug:"purinergic-signaling-in-covid-19-disease",totalDownloads:5,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82374",title:"The Potential of the Purinergic System as a Therapeutic Target of Natural Compounds in Cutaneous Melanoma",doi:"10.5772/intechopen.105457",signatures:"Gilnei Bruno da Silva, Daiane Manica, Marcelo Moreno and Margarete Dulce Bagatini",slug:"the-potential-of-the-purinergic-system-as-a-therapeutic-target-of-natural-compounds-in-cutaneous-mel",totalDownloads:10,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82103",title:"The Role of Endoplasmic Reticulum Stress and Its Regulation in the Progression of Neurological and Infectious Diseases",doi:"10.5772/intechopen.105543",signatures:"Mary Dover, Michael Kishek, Miranda Eddins, Naneeta Desar, Ketema Paul and Milan Fiala",slug:"the-role-of-endoplasmic-reticulum-stress-and-its-regulation-in-the-progression-of-neurological-and-i",totalDownloads:6,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Updates on Endoplasmic Reticulum",coverURL:"https://cdn.intechopen.com/books/images_new/11674.jpg",subseries:{id:"14",title:"Cell and Molecular Biology"}}}]},overviewPagePublishedBooks:{paginationCount:32,paginationItems:[{type:"book",id:"7006",title:"Biochemistry and Health Benefits of Fatty Acids",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7006.jpg",slug:"biochemistry-and-health-benefits-of-fatty-acids",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Viduranga Waisundara",hash:"c93a00abd68b5eba67e5e719f67fd20b",volumeInSeries:1,fullTitle:"Biochemistry and Health Benefits of Fatty Acids",editors:[{id:"194281",title:"Dr.",name:"Viduranga Y.",middleName:null,surname:"Waisundara",slug:"viduranga-y.-waisundara",fullName:"Viduranga Y. Waisundara",profilePictureURL:"https://mts.intechopen.com/storage/users/194281/images/system/194281.jpg",biography:"Dr. Viduranga Waisundara obtained her Ph.D. in Food Science\nand Technology from the Department of Chemistry, National\nUniversity of Singapore, in 2010. She was a lecturer at Temasek Polytechnic, Singapore from July 2009 to March 2013.\nShe relocated to her motherland of Sri Lanka and spearheaded the Functional Food Product Development Project at the\nNational Institute of Fundamental Studies from April 2013 to\nOctober 2016. She was a senior lecturer on a temporary basis at the Department of\nFood Technology, Faculty of Technology, Rajarata University of Sri Lanka. She is\ncurrently Deputy Principal of the Australian College of Business and Technology –\nKandy Campus, Sri Lanka. She is also the Global Harmonization Initiative (GHI)",institutionString:"Australian College of Business & Technology",institution:null}]},{type:"book",id:"6820",title:"Keratin",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/6820.jpg",slug:"keratin",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Miroslav Blumenberg",hash:"6def75cd4b6b5324a02b6dc0359896d0",volumeInSeries:2,fullTitle:"Keratin",editors:[{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}}]},{type:"book",id:"7978",title:"Vitamin A",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7978.jpg",slug:"vitamin-a",publishedDate:"May 15th 2019",editedByType:"Edited by",bookSignature:"Leila Queiroz Zepka, Veridiana Vera de Rosso and Eduardo Jacob-Lopes",hash:"dad04a658ab9e3d851d23705980a688b",volumeInSeries:3,fullTitle:"Vitamin A",editors:[{id:"261969",title:"Dr.",name:"Leila",middleName:null,surname:"Queiroz Zepka",slug:"leila-queiroz-zepka",fullName:"Leila Queiroz Zepka",profilePictureURL:"https://mts.intechopen.com/storage/users/261969/images/system/261969.png",biography:"Prof. Dr. Leila Queiroz Zepka is currently an associate professor in the Department of Food Technology and Science, Federal University of Santa Maria, Brazil. She has more than fifteen years of teaching and research experience. She has published more than 550 scientific publications/communications, including 15 books, 50 book chapters, 100 original research papers, 380 research communications in national and international conferences, and 12 patents. She is a member of the editorial board of five journals and acts as a reviewer for several national and international journals. 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The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:null},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. She is a professor in the Stomatology Faculty, St. Petersburg State University. She has expertise in the development and evaluation of a wide range of live mucosal vaccines against influenza and bacterial complications. Her research interests include immunity against influenza and COVID-19 and the development of immunization schemes for high-risk individuals.",institutionString:'Federal State Budgetary Scientific Institution "Institute of Experimental Medicine"',institution:null},{id:"238958",title:"Mr.",name:"Atamjit",middleName:null,surname:"Singh",slug:"atamjit-singh",fullName:"Atamjit Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/238958/images/6575_n.jpg",biography:null,institutionString:null,institution:null},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:null},{id:"252058",title:"M.Sc.",name:"Juan",middleName:null,surname:"Sulca",slug:"juan-sulca",fullName:"Juan Sulca",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/252058/images/12834_n.jpg",biography:null,institutionString:null,institution:null},{id:"191392",title:"Dr.",name:"Marimuthu",middleName:null,surname:"Govindarajan",slug:"marimuthu-govindarajan",fullName:"Marimuthu Govindarajan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191392/images/5828_n.jpg",biography:"Dr. M. Govindarajan completed his BSc degree in Zoology at Government Arts College (Autonomous), Kumbakonam, and MSc, MPhil, and PhD degrees at Annamalai University, Annamalai Nagar, Tamil Nadu, India. He is serving as an assistant professor at the Department of Zoology, Annamalai University. His research interests include isolation, identification, and characterization of biologically active molecules from plants and microbes. He has identified more than 20 pure compounds with high mosquitocidal activity and also conducted high-quality research on photochemistry and nanosynthesis. He has published more than 150 studies in journals with impact factor and 2 books in Lambert Academic Publishing, Germany. He serves as an editorial board member in various national and international scientific journals.",institutionString:null,institution:null},{id:"274660",title:"Dr.",name:"Damodar",middleName:null,surname:"Paudel",slug:"damodar-paudel",fullName:"Damodar Paudel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/274660/images/8176_n.jpg",biography:"I am DrDamodar Paudel,currently working as consultant Physician in Nepal police Hospital.",institutionString:null,institution:null},{id:"241562",title:"Dr.",name:"Melvin",middleName:null,surname:"Sanicas",slug:"melvin-sanicas",fullName:"Melvin Sanicas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241562/images/6699_n.jpg",biography:null,institutionString:null,institution:null},{id:"337446",title:"Dr.",name:"Maria",middleName:null,surname:"Zavala-Colon",slug:"maria-zavala-colon",fullName:"Maria Zavala-Colon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Puerto Rico, Medical Sciences Campus",country:{name:"United States of America"}}},{id:"338856",title:"Mrs.",name:"Nur Alvira",middleName:null,surname:"Pascawati",slug:"nur-alvira-pascawati",fullName:"Nur Alvira Pascawati",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universitas Respati Yogyakarta",country:{name:"Indonesia"}}},{id:"441116",title:"Dr.",name:"Jovanka M.",middleName:null,surname:"Voyich",slug:"jovanka-m.-voyich",fullName:"Jovanka M. Voyich",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Montana State University",country:{name:"United States of America"}}},{id:"330412",title:"Dr.",name:"Muhammad",middleName:null,surname:"Farhab",slug:"muhammad-farhab",fullName:"Muhammad Farhab",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"349495",title:"Dr.",name:"Muhammad",middleName:null,surname:"Ijaz",slug:"muhammad-ijaz",fullName:"Muhammad Ijaz",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Veterinary and Animal Sciences",country:{name:"Pakistan"}}}]}},subseries:{item:{id:"12",type:"subseries",title:"Human Physiology",keywords:"Anatomy, Cells, Organs, Systems, Homeostasis, Functions",scope:"Human physiology is the scientific exploration of the various functions (physical, biochemical, and mechanical properties) of humans, their organs, and their constituent cells. The endocrine and nervous systems play important roles in maintaining homeostasis in the human body. Integration, which is the biological basis of physiology, is achieved through communication between the many overlapping functions of the human body's systems, which takes place through electrical and chemical means. Much of the basis of our knowledge of human physiology has been provided by animal experiments. Because of the close relationship between structure and function, studies in human physiology and anatomy seek to understand the mechanisms that help the human body function. The series on human physiology deals with the various mechanisms of interaction between the various organs, nerves, and cells in the human body.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/12.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11408,editor:{id:"195829",title:"Prof.",name:"Kunihiro",middleName:null,surname:"Sakuma",slug:"kunihiro-sakuma",fullName:"Kunihiro Sakuma",profilePictureURL:"https://mts.intechopen.com/storage/users/195829/images/system/195829.jpg",biography:"Professor Kunihiro Sakuma, Ph.D., currently works in the Institute for Liberal Arts at the Tokyo Institute of Technology. He is a physiologist working in the field of skeletal muscle. He was awarded his sports science diploma in 1995 by the University of Tsukuba and began his scientific work at the Department of Physiology, Aichi Human Service Center, focusing on the molecular mechanism of congenital muscular dystrophy and normal muscle regeneration. His interest later turned to the molecular mechanism and attenuating strategy of sarcopenia (age-related muscle atrophy). His opinion is to attenuate sarcopenia by improving autophagic defects using nutrient- and pharmaceutical-based treatments.",institutionString:null,institution:{name:"Tokyo Institute of Technology",institutionURL:null,country:{name:"Japan"}}},editorTwo:{id:"331519",title:"Dr.",name:"Kotomi",middleName:null,surname:"Sakai",slug:"kotomi-sakai",fullName:"Kotomi Sakai",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000031QtFXQA0/Profile_Picture_1637053227318",biography:"Senior researcher Kotomi Sakai, Ph.D., MPH, works at the Research Organization of Science and Technology in Ritsumeikan University. She is a researcher in the geriatric rehabilitation and public health field. She received Ph.D. from Nihon University and MPH from St.Luke’s International University. Her main research interest is sarcopenia in older adults, especially its association with nutritional status. Additionally, to understand how to maintain and improve physical function in older adults, to conduct studies about the mechanism of sarcopenia and determine when possible interventions are needed.",institutionString:null,institution:{name:"Ritsumeikan University",institutionURL:null,country:{name:"Japan"}}},editorThree:null,series:{id:"10",title:"Physiology",doi:"10.5772/intechopen.72796",issn:"2631-8261"},editorialBoard:[{id:"213786",title:"Dr.",name:"Henrique P.",middleName:null,surname:"Neiva",slug:"henrique-p.-neiva",fullName:"Henrique P. 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