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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
\n\n\n\n\n'}],latestNews:[{slug:"intechopen-supports-asapbio-s-new-initiative-publish-your-reviews-20220729",title:"IntechOpen Supports ASAPbio’s New Initiative Publish Your Reviews"},{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"}]},book:{item:{type:"book",id:"1373",leadTitle:null,fullTitle:"Ionic Liquids: Applications and Perspectives",title:"Ionic Liquids",subtitle:"Applications and Perspectives",reviewType:"peer-reviewed",abstract:"This book is the second in the series of publications in this field by this publisher, and contains a number of latest research developments on ionic liquids (ILs). This promising new area has received a lot of attention during the last 20 years. Readers will find 30 chapters collected in 6 sections on recent applications of ILs in polymer sciences, material chemistry, catalysis, nanotechnology, biotechnology and electrochemical applications. The authors of each chapter are scientists and technologists from different countries with strong expertise in their respective fields. You will be able to perceive a trend analysis and examine recent developments in different areas of ILs chemistry and technologies. The book should help in systematization of knowledges in ILs science, creation of new approaches in this field and further promotion of ILs technologies for the future.",isbn:null,printIsbn:"978-953-307-248-7",pdfIsbn:"978-953-51-4519-6",doi:"10.5772/1782",price:159,priceEur:175,priceUsd:205,slug:"ionic-liquids-applications-and-perspectives",numberOfPages:688,isOpenForSubmission:!1,isInWos:1,isInBkci:!0,hash:"5e9ae5ae9167cde4b344e499a792c41c",bookSignature:"Alexander Kokorin",publishedDate:"February 21st 2011",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",numberOfDownloads:166753,numberOfWosCitations:422,numberOfCrossrefCitations:84,numberOfCrossrefCitationsByBook:73,numberOfDimensionsCitations:264,numberOfDimensionsCitationsByBook:115,hasAltmetrics:0,numberOfTotalCitations:770,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"May 12th 2010",dateEndSecondStepPublish:"June 9th 2010",dateEndThirdStepPublish:"September 14th 2010",dateEndFourthStepPublish:"November 13th 2010",dateEndFifthStepPublish:"January 27th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7,8",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"3",institution:{name:"Semenov Institute of Chemical Physics",institutionURL:null,country:{name:"Russia"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"935",title:"Fluid Dynamics",slug:"materials-science-fluid-mechanics-fluid-dynamics"}],chapters:[{id:"13719",title:"Advanced Applications of Ionic Liquids in Polymer Science",doi:"10.5772/15224",slug:"advanced-applications-of-ionic-liquids-in-polymer-science",totalDownloads:10409,totalCrossrefCites:3,totalDimensionsCites:13,hasAltmetrics:0,abstract:null,signatures:"Elaheh Kowsari",downloadPdfUrl:"/chapter/pdf-download/13719",previewPdfUrl:"/chapter/pdf-preview/13719",authors:[{id:"16210",title:"Dr.",name:"Elaheh",surname:"Kowsari",slug:"elaheh-kowsari",fullName:"Elaheh Kowsari"}],corrections:null},{id:"13720",title:"Ionic Liquids in Biphasic Ethylene Polymerisation",doi:"10.5772/14448",slug:"ionic-liquids-in-biphasic-ethylene-polymerisation",totalDownloads:2911,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:null,signatures:"Wioletta Ochędzan-Siodłak",downloadPdfUrl:"/chapter/pdf-download/13720",previewPdfUrl:"/chapter/pdf-preview/13720",authors:[{id:"17827",title:"Dr.",name:"Wioletta",surname:"Ochędzan-Siodłak",slug:"wioletta-ochedzan-siodlak",fullName:"Wioletta Ochędzan-Siodłak"}],corrections:null},{id:"13721",title:"Synthesis of Ionic Liquids, Solubility for Wood and Its Application for Graft Copolymer with Acrylamide",doi:"10.5772/14082",slug:"synthesis-of-ionic-liquids-solubility-for-wood-and-its-application-for-graft-copolymer-with-acrylami",totalDownloads:3037,totalCrossrefCites:0,totalDimensionsCites:1,hasAltmetrics:0,abstract:null,signatures:"Guo Liying",downloadPdfUrl:"/chapter/pdf-download/13721",previewPdfUrl:"/chapter/pdf-preview/13721",authors:[{id:"16622",title:"Dr.",name:"Liying",surname:"Guo",slug:"liying-guo",fullName:"Liying Guo"}],corrections:null},{id:"13722",title:"Selective Breakdown of (Ligno)cellulose in Ionic Liquids",doi:"10.5772/14681",slug:"selective-breakdown-of-ligno-cellulose-in-ionic-liquids",totalDownloads:3971,totalCrossrefCites:3,totalDimensionsCites:6,hasAltmetrics:0,abstract:null,signatures:"Haibo Xie and Zongbao K. 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Marco Aurélio dos Santos Bernardes serves as a postdoc researcher at the Centre de Recherche Public Henri Tudor in Luxembourg. His expertise is in the area of energy analysis, life cycle assessment, renewable energy and biofuels. Dr.-Ing. Bernardes has had 10 papers published in journals such as Solar Energy, International Journal of Life Cycle Assessment, ASME Heat Transfer, a book and book chapters as well. Dr.-Ing. Bernardes' areas of interest include CFD, heat transfer modelling, Solar Chimney Power Plants, thermal processes, thermodynamics. He received his Ph.D. in Mechanical Engineering at Stuttgart University in Germany and conducted a postdoctoral research at the Stellenbosch University in South Africa. He was awarded with the UNEP/SETAC Life Cycle Assessment Award for LCA Projects in Development Countries. Dr.-Ing. Bernardes served as a full professor in the Department of Mechanical Engineering at CEFET-MG in Belo Horizonte for more than 13 years.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"5",institution:{name:"Luxembourg Institute of Science and Technology",institutionURL:null,country:{name:"Luxembourg"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"857",title:"Bioenergy",slug:"environmental-sciences-environmental-management-bioenergy"}],chapters:[{id:"17875",title:"Implications for the Feed Industry",slug:"implications-for-the-feed-industry",totalDownloads:3363,totalCrossrefCites:0,authors:[{id:"25080",title:"Prof.",name:"Paul",surname:"Iji",slug:"paul-iji",fullName:"Paul Iji"},{id:"87616",title:"MSc",name:"Mohammad Reza",surname:"Barekatain",slug:"mohammad-reza-barekatain",fullName:"Mohammad Reza Barekatain"}]},{id:"18035",title:"The Future Crops for Biofuels",slug:"the-future-crops-for-biofuels",totalDownloads:2602,totalCrossrefCites:0,authors:[{id:"25156",title:"Dr.",name:"Chuanxin",surname:"Sun",slug:"chuanxin-sun",fullName:"Chuanxin Sun"},{id:"100933",title:"Dr.",name:"Chunlin",surname:"Liu",slug:"chunlin-liu",fullName:"Chunlin Liu"}]},{id:"17877",title:"A Comparison Between Raw Material and Technologies for a Sustainable Biodiesel Production Industry",slug:"a-comparison-between-raw-material-and-technologies-for-a-sustainable-biodiesel-production-industry",totalDownloads:3929,totalCrossrefCites:1,authors:[{id:"27114",title:"Dr.",name:"Jorge",surname:"Marchetti",slug:"jorge-marchetti",fullName:"Jorge Marchetti"}]},{id:"17878",title:"How to Balance Biofuel and Food Production for Optimal Global Health and Nutrition - The Food Crop-Feed Crop-Fuel Crop Trilemma",slug:"how-to-balance-biofuel-and-food-production-for-optimal-global-health-and-nutrition-the-food-crop-fee",totalDownloads:2919,totalCrossrefCites:1,authors:[null]},{id:"17879",title:"The Post 2008 Food Before Fuel Crisis: Theory, Literature, and Policies",slug:"the-post-2008-food-before-fuel-crisis-theory-literature-and-policies",totalDownloads:2196,totalCrossrefCites:0,authors:[{id:"34199",title:"Prof.",name:"Michael",surname:"Wetzstein",slug:"michael-wetzstein",fullName:"Michael Wetzstein"},{id:"34204",title:"Ms.",name:"Cheng",surname:"Qiu",slug:"cheng-qiu",fullName:"Cheng Qiu"},{id:"34205",title:"Dr.",name:"Gregory",surname:"Colson",slug:"gregory-colson",fullName:"Gregory Colson"}]},{id:"17880",title:"Can Biofuels be an Engine for Growth in Small Developing Economies – The Case of Paraguay",slug:"can-biofuels-be-an-engine-for-growth-in-small-developing-economies-the-case-of-paraguay",totalDownloads:2637,totalCrossrefCites:1,authors:[{id:"25155",title:"Dr.",name:"Anil",surname:"Hira",slug:"anil-hira",fullName:"Anil Hira"}]},{id:"18291",title:"Biofuels and World Agricultural Markets: Outlook for 2020 and 2050",slug:"biofuels-and-world-agricultural-markets-outlook-for-2020-and-2050",totalDownloads:3723,totalCrossrefCites:4,authors:[{id:"39590",title:"Dr.",name:"Yves",surname:"Dronne",slug:"yves-dronne",fullName:"Yves Dronne"},{id:"48595",title:"Mr.",name:"Hervé",surname:"Guyomard",slug:"herve-guyomard",fullName:"Hervé Guyomard"},{id:"48596",title:"Mrs.",name:"Agneta",surname:"Forslund",slug:"agneta-forslund",fullName:"Agneta Forslund"}]},{id:"17882",title:"The Potential for Production of Biomass for Biofuel by the Cultivation of Hybrid Poplar and Hybrid Aspen in the South of Sweden",slug:"the-potential-for-production-of-biomass-for-biofuel-by-the-cultivation-of-hybrid-poplar-and-hybrid-a",totalDownloads:2457,totalCrossrefCites:0,authors:[{id:"27549",title:"Prof.",name:"Lars",surname:"Christersson",slug:"lars-christersson",fullName:"Lars Christersson"}]},{id:"17883",title:"Theoretical and Practical Evaluation of Jatropha as Energy Source Biofuel in Tanzania",slug:"theoretical-and-practical-evaluation-of-jatropha-as-energy-source-biofuel-in-tanzania",totalDownloads:4777,totalCrossrefCites:1,authors:[{id:"25235",title:"Dr.",name:"Stelyus L.",surname:"Mkoma",slug:"stelyus-l.-mkoma",fullName:"Stelyus L. 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Anxiety, fear and worry are all completely natural human feelings. If these feelings occur and endure for an extended period, it affects both physical and mental health. This leads to clinical anxiety disorders. There are many types of treatment available to treat anxiety disorders. This article outlines more common herbal remedies to treat anxiety disorders.
\n\t\t\tAnxiety is an aversive emotional state, in which the feeling of fear is disproportionate to the threat (Weinberger, 2001). Anxiety is implicated in a number of psychiatric disorders, such as depression, panic attacks, phobias, generalized anxiety disorder, obsessive-compulsive disorder and post-traumatic stress disorder (Gross and Hen, 2004). Anxiety disorders are the most common class of neuropsychiatric disorders in USA (Kessler et al., 2005) and many other countries (Alonso and Lepine, 2007). The life time prevalence of panic attacks (a form of anxiety disorder) is around 7-9% in most countries and 1% alone in India with the prevalence of generalized anxiety disorder is very high i.e. 8.5% in the general population (WHO, 2001). Anxiety disorders affect 16.6% of population worldwide (Somers et al., 2006) and numerous efforts have been made to understand the pathophysiology of the disease and treatments.
\n\t\t\tAccording to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), anxiety is characterized by a feeling of persistent worry that hinders an individual’s ability to relax [Diagnostic and Statistical Manual of Mental Disorders Washington D.C.: American Psychiatric Association, 4 2000]. Anxiety disorders are described and classified in DSM and several anxiety disorders share common clinical symptoms such as widespread anxiety, physiological anxiety symptoms, and behavioral disturbances.
\n\t\tGeneralized anxiety disorder is a syndrome of ongoing anxiety and worry about many events or feelings that the patient generally recognizes as extreme and inappropriate (DSM-IV-TR). Individuals manifest both physical and psychological symptoms leading to significant distress or impairment.
\n\t\t\tPeople suffering from OCD tend to have bothersome and intrusive thoughts that generate anxiety (obsession) and perform repetitive actions (compulsion). Obsessions include unwanted thoughts, impulses, or images that cause great anxiety. Compulsions include repetitive behaviors or mental acts that those affected feel driven to perform.
\n\t\t\tPeople suffering from panic disorders often have panic attacks, defined as discrete periods of sudden symptom onset usually peaking in 10 minutes and can occur with most anxiety disorders.
\n\t\t\tIndividuals with PTSD avoid stimuli associated with the trauma and feel an extreme amount of fear and anxiety after presenting stimuli. Stress is a condition which affects physiological and psychological homeostasis. Evidence indicates that chronic repeated stress precipitates neuropsychiatric disorders like anxiety and depression (Holsboer, 1988; Mc Ewen and Stellar, 1993; Mc Ewen, 2000; Vyas et al., 2002; Veena et al., 2009b; \n\t\t\t\t\t\t\n\t\t\t\t\t\t\t2011\n\t\t\t\t\t\t\n\t\t\t\t\t). Previous work in an animal model of stress revealed that chronic stress impairs learning in the T-maze (Sunanda et al., 2000a) and radial arm maze (Srikumar et al., 2006; 2007; Veena et al., 2009a) tasks in addition to inducing anxiety-like behavior (Adamec et al., 1999; Vyas et al., 2002; Govindarajan et al., 2006). Stress-induced behavioral impairments are associated with structural (Ramkumar et al., 2008; Shankaranarayana Rao et al., 2001; Shankaranarayana Rao & Raju, 2004; 2005; 2007), biochemical (Sunanda et al., 2000b), molecular (Bennur et al., 2007; Pawlak et al., 2005; \n\t\t\t\t\t\t\n\t\t\t\t\t\t\tVeena et al., 2011\n\t\t\t\t\t\t\n\t\t\t\t\t) and electrophysiological (Hegde et al., 2008) alterations in the hippocampus and amygdala regions. Recent studies have clearly demonstrated the abnormal synaptic plasticity is responsible for cognitive deficits including enhanced anxiety in fragile X mental retardation and autism (Dolen et al., 2007; Hayashi et al., 2007). Induction of progressive plasticity is known to be responsible for amelioration of stress-induced cognitive deficits and depression-like behavior by enriched environment and brain stimulation rewarding experience (Asha Devi et al., 2011; Ramkumar et al., 2008; Shankaranarayana Rao, 2009; 2010; Veena et al., 2009a).
\n\t\t\t\tAnxiety and other psychiatric conditions are one of the most frequent conditions seen by clinicians and often require long-term treatment with medications. Selective serotonin reuptake inhibitor (SSRI) and benzodiazepines are important class of drugs used to treat generalized anxiety disorders (Davidson, 2001; Davidson, 2009) and depression (Bhagya et al., 2008; Bhagya et al., 2011). With the increasing cost of anti-anxiety medications and their increased side effects like suicidal ideation, decreased alertness, sexual dysfunction and dependency (Hu et al., 2004; Gunnell et al., 2005; O\'brien, 2005; Lader et al., 2009), drugs of natural origin are promising alternatives to treat neuropsychiatric disorders (Kienzle-Horn, 2002; Carlini, 2003).
\n\t\t\tAyurveda, the Indian traditional system of medicine uses herbs and their preparations to treat various neuropsychiatric disorders. Numerous herbs have been used for centuries in folk and other traditional medicine to calm the mind and positively enhance mood. Herbal medicine which plays an important role in developing countries, are once again becoming popular throughout developing and developed countries. Study by Sparreboom et al. (2004) revealed that use of herbal medicine is increasing enormously in the Western world. In spite of the large number of animal studies evaluating the potential anxiolytic effects of plant extracts, very few controlled studies have been conducted in a clinical setup. The efficacy and safety of utilizing these natural drugs to treat anxiety, has only just begun to be exactly tested in clinical trials within the last 10 to 15 years (Saeed et al., 2007; Garcia-Garcia et al., 2008; Kinrys et al., 2009). For instance, both Kava-kava (
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There is substantial evidence that kava has a positive effect on the symptoms of anxiety disorders. Animal studies have demonstrated anti-anxiety activity of kava (Garrett et al., 2003; Bruner and Anderson, 2009). Several randomized double-blind clinical studies in GAD patients showed beneficial effect of kava-kava in reducing anxiety (Watkins et al., 2001; Connor and Davidson, 2002; Boerner et al., 2003; Sarris et al., 2009). Kava-kava was used in numerous controlled clinical studies to treat anxiety disorders, but the subjects included in these studies were heterogeneous i.e., they were diagnosed with agoraphobia, specific phobia, social phobia, adjustment disorder with anxiety (Volz and Kieser, 1997; Malsch and Kieser, 2001; Gastpar and Klimm, 2003; Lehrl, 2004). In the study by Connor & Davidson, kava extract was compared with placebo in GAD patients (2002). In another 8-week randomized, double-blind multi-center clinical trial, the efficacy of
St. John’s wort is a popular supplement for treating depression but is much less popular for treating anxiety disorders. Studies conducted by Flausino et al. and Singewald et al. have shown that chronic administration of
Studies specifically testing the effects of St. John’s wort on patients with anxiety are extremely limited. The evidence of positive effects of St. John’s wort on anxiety disorders is weak. No placebo-controlled, randomized, double-blind trials have shown St. John’s wort to be effective in treating generalized anxiety disorder, post-traumatic stress disorder, obsessive-compulsive disorder (OCD), or phobias. Volz et al. (2002) showed that Hypericum extract to 149 out patients diagnosed with somatization disorder, undifferentiated somatoform disorder, or somatoform autonomic dysfunctions, significantly reduced anxiety scores in HAMA scale. Another open-label uncontrolled observation with 500 subjects showed beneficial effect of St. John’s wort extract in reducing anxiety disorder symptoms in patients diagnosed with depression comorbid with anxiety (Muller et al., 2003). However, stronger evidence is needed before St. John’s wort should be considered as a treatment option for patients with diagnosable anxiety disorders.
\n\t\t\tValerian is one of the most popularly used herbal medicines for insomnia (Donath et al., 2000) and is also used to treat anxiety. Hydroalcoholic and aqueous extracts of valerian roots have shown affinity for the GABA-A receptor in the brains of rats (Benke et al., 2009). In humans, valerian has been successful in the treatment of insomnia and tension (Schmidt-Voigt, 1986; Vorbach, 1996; Leathwood, 1985; Donath et al., 2000; Stevinson and Ernst, 2000; Ziegler, 2002). Andreatini et al. (2002) compared the extract of
Extract of
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Chamomile is one of the most popular single ingredient of herbal teas, or tisanes. Chamomile tea, brewed from dried flower heads is used traditionally for several medicinal purposes like gastrointestinal tract ailments. Other uses include allergic rhinitis, attention deficit-hyperactivity disorder (ADHD), restlessness, insomnia, dysmenorrhea, mastitis and varicose ulcers. Chamomile contains flavonoids, which exert benzodiazepine-like activity (Avallone et al., 2000) and also has a phosphodiesterase inhibitory action, which leads to increased cAMP levels (Kuppusamy and Das, 1992). A recent study evaluated the efficacy of a standardized extract of
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In Indian traditional medicine, several herbs have been used as nerve tonics. The most popular of these herbs is
Previous clinical study demonstrated that administration of
This has been an important herb in use within Ayurvedic and indigenous medical systems for over 3000 years. Both preclinical and clinical studies demonstrate the use of
In Ayurveda, compound formulations are generally used in the therapy as the combination of many drugs provides a synergistic therapeutic effect and also includes ingredients which help to minimize the adverse effects of few other major drugs. A recent study demonstrated adaptogenic potential of a compound natural health product which had
Mentat (BR-16A) is an herbal medication contains 20 different ingredients. The main herbs present in the mentat are
\n\t\t\t\tAgrawal et al. (1990a,b) reported that BR-16A improves memory parameters and decreases anxiety parameters in normal volunteers. Also, mentat (BR-16) brought about marked improvement in memory in all age groups and caused decrease in anxiety level and neuroticism index (Agrawal et al., 1991). Mentat in the form of syrup was given to patients of anxiety neurosis and depression in a placebo controlled study. Both anxiety and depressive patients showed memory impairment and also increased fatiguability. 3 month treatment with Mentat improved memory and decreased fatiguability in these patients (Sharma et al., 1990). Psychological problems like stress, anxiety and depression play an important role in the prognosis, quality of life as well as the survival rate of cancer patients. Treatment with mentat in cancer patients reduced stress, anxiety and depressive symptoms (Durgesh Kumar, 2000).
\n\t\t\tAnother polyherbal formulation Geriforte showed significant anxiolytic effect in clinical studies. Geriforte contains Chyavanprash concentrate and the extracts of
Another common polyherbal formulation Euphytose, which is a combination of six extracts: Crataegus, Ballota, Passiflora and Valeriana, which have mild sedative effects, and Cola and Paullinia, which mainly act as mild stimulants. Euphytose reduced HAMA scores in outpatients with adjustment disorder with anxious mood in multicenter, double-blind, placebo-controlled study (Bourin et al., 1997).
\n\t\t\tRecent preclinical studies have shown anxiolytic activity of several herbal drugs.
Our own studies have demonstrated the role of different herbs and herbal formulations namely
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Despite a large number of animal studies evaluating the potential anxiolytic effects of herbal drugs, very few controlled clinical studies have been conducted. These studies have methodological problems like small number of subjects, lack of placebo and control groups, and inclusion of heterogeneous subjects and short treatment duration, which hinders consistent conclusion about these herbal preparations. Some herbs like kava-kava, gingko showed promising results with substantial clinical significance when compared with benzodiazepines, buspirone and antidepressants. Although evidence of effectiveness of herbs and their preparations in treating neuropsychiatric disorders is increasing, translating these results to treat patients effectively is slowed down by the limited knowledge regarding chemical composition of the products, lack of standardization of these preparations and the paucity of well controlled studies. Preliminary evidence suggests that herbal medicines may have a role in the treatment of anxiety disorders and warrants further research. However, we would like to clearly warn that most of the remedies are not approved for clinical use and herbal remedies are not solely alternatives of clinical treatment regimens. Also some of the herbal remedies may interact with other medicines leading to drug-drug interactions, which may cause severe side effects and in some cases it may be fatal. Accordingly, it is advised to use herbal drugs under strict supervision of qualified ayurvedic physicians with periodic follow-ups.
\n\t\tWe acknowledge the financial support from the Council of Scientific and Industrial Research (CSIR), New Delhi, India through a Senior Research Associate fellowship to BV, Research grants from Department of Biotechnology (DBT) and Department of Science and Technology (DST), Government of India to BSS, Fondation pour la recherche médicale (FRM) fellowship to BNS.
\n\t\tMetabolic dysregulation of carbohydrate and lipid metabolism is frequent in cancer cells, facilitating growth and survival through adaptive mechanisms. Otto Warburg was the first to recognize that cancer cells favor glycolysis as compared to oxidative phosphorylation for the generation of energy (ATP) [1]. While the former is less efficient in terms of energy production per molecule of glucose, it also generates precursor molecules (amino acids, fatty acids, etc.) for replication and facilitates survival under oxidative stress [2]. This is in contrast to normal cells, which typically use oxidative metabolism to derive more energy (ATP) per molecule of glucose [3, 4]. Nearly a century later, we now recognize that cancer cells may utilize either aerobic or anaerobic respiration. The majority of cancer cells also have alterations of mitochondrial respiration, further providing a selective advantage to facilitate cancer growth and survival [5]. More specifically, it may increase intracellular reactive oxygen species by disruption of the mitochondrial electron transport chain to reduce the mitochondrial membrane potential in BC or act directly to inhibit the mitochondrial respiratory-chain complex 1 (MRCC1) [6, 7, 8].
Chronic energy excess and physical inactivity lead to systemic alterations of carbohydrate and fatty acid metabolism characterized by systemic hyperglycemia, hyperinsulinemia with insulin resistance followed by hypoinsulinemia, an increase in inflammatory cytokines and adipokines, alterations of steroid and growth hormones, and downregulation of immune surveillance and tissue oxygenation [3, 9, 10]. These changes are frequent but variable in patients with obesity and type 2 diabetes and can be modified by drugs, exercise, body weight, socioeconomic factors, access to healthcare, genetic risk, and other factors. Patients with these disorders are at an increased risk of cardiovascular disease, cancer, and other diseases associated with significant morbidity and mortality. In the U.S., there are ~13.8 million type 2 diabetics, 5 million undiagnosed diabetics, and 41 million persons with prediabetes/metabolic syndrome [11, 12, 13]. Obesity is a frequent comorbidity, often proceeding diabetes by years or decades.
Energy-sensing systems are integral to maintaining homeostasis in normal and transformed cells. Energy deprivation is frequent in cancer cells due to an inadequate vascular supply to meet the needs of increased cell replication. In energy-stressed cells, AMPK is allosterically modified by binding to AMP and ADP, rendering them targetable by AMPK kinases. AMPK activation induces signaling, upregulates energy production, and inhibits energy programming for cell growth and motility. In cancerous cells, this shift often fails to occur even with stress. As a result, cancer cells typically prioritize replication and motility to favor cancer growth and metastasis. Drugs that activate AMPK, most notably metformin, reengage the AMPK failsafe to inhibit proliferation and motility. Thus, metformin provides a unique and generally less-toxic approach to combat the emergence or growth of cancers through inhibition of cell replication. This is particularly important for patients with obesity and type 2 diabetes, who lack homeostasis and experience wide swings in systemic glucose, insulin, and other energy precursors and growth factors that contribute to systemic energy stress.
Abundant epidemiologic and clinical data have shown that obesity and type 2 diabetes increase the risk and severity of cardiovascular disease and human cancer. Each of these chronic metabolic disorders as a single variable significantly increases the risk of breast cancer (BC) [10, 14]. In combination, the risk is increased by 20–50%, depending on the severity of disease and other variables. It is highest in women with abdominal (central) obesity in the postmenopausal setting, in women of all ethnic backgrounds [15, 16, 17]. Obesity also promotes BC in premenopausal women of color, especially African Americans and Latinos [18, 19, 20, 21, 22, 23]. In patients with obesity and diabetes, BC also presents at a higher disease stage and is more resistant to treatment, resulting in a shorter disease-free interval and a significantly higher mortality rate [24, 25].
Steroid receptor-positive BC (luminal A) and basal (triple negative) BC cells are the most responsive to extracellular glucose at or above 7 mM of glucose to promote cell replication, tumor growth, and motility. In contrast, steroid receptor-positive BC cells that also express high HER2 (luminal B) and steroid receptor-negative, HER2 positive (the HER2 subtype) are less responsive to hyperglycemia, even at levels associated with untreated type 2 diabetes (10 mM glucose or higher) [26]. Glucose directly promotes signaling in epithelial cells or can act indirectly by interacting with molecular signaling proteins, such as the insulin-like growth factor (IGF-1), sex hormones, and adipokines [3, 27, 28]. Insulin and insulin-like growth factors are frequently increased in newly diagnosed BC patients [28, 29, 30, 31]. These potent growth factors promote BC growth and are associated with a worse prognosis, both in overweight and ‘normal’ weight women [24, 29, 32, 33, 34]. Epidemiological and clinical data show that obesity and type 2 diabetes are particularly associated with luminal A (estrogen and progesterone responsive) as well as triple negative BCs [19, 21, 27, 35, 36].
Metformin (N′, N′-dimethylbiguanide) is the most frequently used drug to treat patients with metabolic syndrome (prediabetes) and type 2 diabetes worldwide. It has been used successfully for over six decades and has a very favorable benefit-risk profile [37]. Metformin is stable at room temperature with a long shelf life, is inexpensive and orally administered, and has low rates of significant toxicity or drug-drug interaction. Metformin is best known for its effects on liver and skeletal muscle cells, where it downregulates insulin resistance, lowers serum insulin, stimulates insulin receptor tyrosine kinase activity, inhibits hepatic glucose output (thus lowering A1C), increases glucose uptake by skeletal muscle cells, and can alter fatty acid metabolism.
Epidemiologic data show a significant lowering of cancer risk in patients with metabolic dysregulation (obesity, diabetes, or metabolic syndrome) who take metformin [29, 34, 38, 39]. Metformin use by BC patients has also been associated with improved treatment response and survival. In one meta-analytic study of BC patients with diabetes, metformin use was associated with a 65% improvement in BC-specific survival as compared to nonusers [40]. The anticancer properties of metformin are in contrast to other antidiabetic agents, including sulfonylureas and insulin, which promote cancer growth [9].
It is also taken for its ‘antiaging’ properties in individuals without obesity or metabolic dysregulation, particularly outside of the US [10, 41, 42].
Numerous clinical trials are currently underway in BC patients to evaluate the benefit of metformin combined with or following the administration of other therapeutic agents [29, 32, 33, 43, 44, 45, 46]. Studies designed to test the benefit of metformin in patients in only specific molecular subtypes of BC have not been performed, although some have looked at molecular cohort interactions as a secondary goal [30, 47, 48, 49, 50, 51]. There are limited data on the use of metformin in metabolically ‘normal’ BC patients. However, our preclinical data suggest that metformin is most active in all molecular subtypes with physiological levels of extracellular glucose [26]. This evidence provides a rationale for testing metformin in otherwise healthy BC patients.
Cellular uptake of metformin requires expression and functionality of the organic cation transporter 1 (OCT1) protein, which in some individuals or BCs may be altered (more or less effective in transporting metformin into the cell) by polymorphism or genetic error [52]. Polymorphisms have also been associated with a decrease in metformin efficacy in diabetic patients [53, 54, 55]. In BC cells, we have demonstrated that OCT1 expression is associated with the anticancer activity
Metformin AMPK-dependent mechanism of action on breast cancer. Metformin activates AMPK directly through insulin-like growth factor (IGF-I) or insulin receptor, which in turn can activate PI3K/Akt/mTOR or RAS/Raf/MEK/ERK to increase cell growth, survival, angiogenesis, migration, and invasion. Metformin indirectly activates AMPK, which activates mTORC2, CREB, and gluconeogenesis. Lastly, glucose can enter BC cell through GLUT-1, and metformin can directly downregulate GLUT-1 receptor.
Activation of mTOR-dependent protein synthesis and cell growth (downstream of the PI3K/Akt signaling axis), along with AMPK, provides a robust signaling platform for BC cell growth, proliferation, and chemotherapy resistance. In addition to activating AMPK, metformin inhibits mTOR and downstream signaling components of this critical pathway. Mutation of the PI3K catalytic subunit (PIK3CA) occurs in 20-35% of BCs [62, 63]. Mutation or loss of the tumor suppressor gene PTEN has also been demonstrated in 40% of BC [64, 65]. Metformin can also inhibit gluconeogenesis and mTOR signaling independent of AMPK and the tuberous sclerosis 2 (TSC2) gene in some experimental systems (in hepatic cells that lack AMPK or its kinase, LKB1). In this model system, metformin induces downregulation of hepatic gluconeogenesis through non-AMPK–associated mechanisms [66, 67].
Signaling systems and thus metformin sensitivity by dose or mechanism vary by the molecular subtype of BC as well as unique genomic changes in each patient’s BC. For example, we have shown that metformin-induced partial S phase arrest increased P-AMPK and reduced P-EGFR, P-MAPK, P-Src, cyclin D1, and cyclin E, with the induction of PARP cleavage and apoptosis only in triple negative BCs [44]. In this tumor subtype, metformin specifically targets Stat3 and is not dependent on mTOR signaling [44]. In non-triple negative BCs (luminal and HER2), metformin induces partial cell cycle arrest at the G1 checkpoint, reduces cyclin D1 and E2F1 expression, and inhibits AMPK, MAPK, Akt, and mTOR activity [44, 57, 68]. Metformin-associated AMPK activation may also inactivate the insulin receptor substrate 1 (IRS1), which in turn regulates IGF-IR and PI3K/Akt signaling pathways to block the progrowth effects of hyperinsulinemia and insulin-like growth factors typically associated with type 2 diabetes [66, 67, 69].
Metformin is unique in the breadth and complexity of AMPK-dependent direct and indirect targets that inhibit cancer. Several new mechanisms fall into the rapidly expanding field of immuno-oncology. Metformin-induced activation of AMPK activates the programmed death ligand-1 (PDL-1) at S195, reducing stability and membrane localization and thus increasing PDL-1 degradation [70]. Metformin also promotes cytotoxic T cell lymphocyte activity in tumor tissue and enhances tumor-associated immune surveillance [6, 70, 71]. Additionally, metformin upregulates pro-inflammatory cytokines (tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6), IL-1β, the nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB), the hypoxia-inducible factor 1-alpha (HIF-1α), and the vascular endothelial growth factor (VEGF), reviewed in [72, 73]).
AMPK-dependent mechanisms of action have been validated using clinical trial–derived BC samples as well as preclinical model systems, reviewed in detail elsewhere [43]. Some of these were especially important to spur the expansion of metformin use in BC patients. The timing, dose, and duration of metformin treatment in BC patients with or without other chemotherapy are actively under investigation. Neoadjuvant metformin, in particular, has shown benefit with a higher rate of complete pathological response, as compared to similar BC patients [74].
AMPK plays an integral role in the regulation of cell cycle and cell division. The ability of metformin to activate AMPK thus has a significant inhibitory effect on cell-cycle associated proteins. This mechanism is represented in Figure 2. Expression profiling of BC derived from metformin-treated patients as compared to controls has shown consistent downregulation of many gene encoding proteins involved in mitosis, including kinesins, tubulins, histones, Aurora, as well as Polo-like kinases and ribosomal proteins (critical for protein and macromolecular biosynthesis, respectively) [75]. Given the targeted effects of metformin, it is not surprising that its actions are synergistic with drugs like paclitaxel that induce defects in mitotic spindle assembly, chromosome segregation, and cell division. In combination, metformin and paclitaxel dramatically increase the number of cells arrested in G2-M and apoptosis, as compared to either agent alone [76]. Metformin may also induce GO/G1 arrest due to activation of AMPK, downregulation of cyclin D1, and enhanced binding of CDK2 by p27Kip1 and p21cip1 [60, 61], especially in non-triple negative cells. Some have shown that metformin sensitivity to GO/G1 arrest is linked to overexpression of p27Kip1 p21cip1 [60, 61]. We have demonstrated that metformin induces cycle arrest at the G1 checkpoint in luminal A, B and HER2 BC [75] associated with a reduction of cyclin D1 and E2F1 expression, with no changes in p27Kip1 or p21waf1. While these authors describe how metformin can increase CDK chemical inhibitors to control BC growth [57, 61], others have utilized cell cycle-dependent kinases (CDK) inhibitors with metformin and report that this combination should be used with caution [77].
AMPK-dependent action on cell cycle and alternate mechanisms. Metformin activates AMPK directly through insulin-like growth factor (IGF-I) or insulin receptor, which in turn can activate PI3K/Akt/mTOR or RAS/Raf/MEK/ERK signaling pathway. Metformin can also inhibit downstream signaling intermediates to attenuate autophagy, mRNA translation, cell growth, ribosome biogenesis, protein synthesis, and cell cycle growth. Metformin can also activate AMPK, which blocks P53 and induces cell cycle arrest. Lastly, metformin can block complex I of mitochondrial biogenesis to increase intracellular O2, which can block HIF-1 and VEGF production.
In addition to downregulating cell replication under stress, metformin upregulates the cellular DNA-damage response, resulting in a decline in the mutational burden for those cancer cells that survive. Mechanisms underlying this effect include selective activation of the ataxia telangiectasia mutated (ATM) gene as well as ATM targets, such as protein kinase CHK2 gene and attenuation of reactive oxygen species ROS that result in DNA damage [78]. Algire et al. have postulated that downregulation of ROS production and thus somatic mutation are likely contributing mechanisms for the reduction in cancer risk associated with metformin use [8].
In summary, AMPK plays a central regulatory role in human cells, including BC where it regulates energy metabolism, cell growth and motility, response to insulin and growth factors, and estrogen production. Metformin induces AMPK activation in a robust manner, to affect numerous target pathways and intermediate molecules. The activity of AMPK and thus metformin can be modified by interacting factors including hormones, growth factors, and energy sensors. Selective targeting of AMPK-dependent pathways has shown less efficacy than metformin alone against BC [79], consistent with the findings that not all mechanisms of metformin action are AMPK dependent.
Upregulation of bioavailable glucose, insulin, and other growth factors increase the risk and promote BC aggression [16, 23, 27, 80, 81]. In addition to shifts in host metabolism, glycolytic reprogramming occurs in breast epithelial cells during malignant transformation. This process is accentuated by systemic dysregulation of carbohydrate and lipid metabolism, as bioavailable sugars and fat typically increase in these patients. Glycolytic reprogramming includes dependence on aerobic respiration, providing less-efficient energy (ATP) production per molecule of glucose from and incomplete oxidative phosphorylation. Cancer cell reprogramming includes activation of numerous signaling intermediaries, including phosphatidyl-inositide 3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), phosphatase and tensin homolog (PTEN), and AMPK [82, 83, 84]. Changes in other factors including c-MYC, hypoxia-inducible factor 1-alpha (HIF1α), epidermal growth factor receptor (EGFR), tumor protein 53 (P53), and the Met receptor may also facilitate cancer cell dependence on aerobic glycolysis [16, 85, 86, 87].
We have focused on the effects of extracellular glucose and other carbohydrates, combined with or without metformin using BC cell lines and animal models of obesity, metabolic syndrome, and mammary tumorigenesis, summarized in Figure 3 and detailed elsewhere [26, 47, 49, 52, 57, 68, 88, 89, 90, 91, 92, 93]. Importantly, most
Metformin action on glucose and metabolism breast cancer. Metformin enters the BC cell through OCT 1 transporter to attenuate inner membrane fluidity/permeability, the Krebs cycle (TCA), and complex I of the mitochondria. Metformin can also block downstream signaling intermediates involved in the PI3K/Akt/mTOR or RAS/Raf/MEK/ERK signaling pathways, which can control BC cell growth. Lastly, metformin blocks GLUT1 transporter and key enzymes that are involved in carbohydrate synthesis.
Luminal A and some subsets of triple negative BC cell lines show the greatest increase in proliferation when cultured in media with supraphysiologic glucose or insulin. In contrast, luminal B and HER2 BC cells were significantly less responsive to glucose or insulin, even at the highest concentrations examined. This responsivity pattern was similar to the cellular response to metformin by molecular BC subtype, with triple negative being the most responsive. From a molecular standpoint, triple negative BC cell responsivity to high glucose and metformin by dose was unique (efficacy at lower EC50s). Triple negative BC cells are especially dependent on glucose/glucosamine (metabolized through glycolysis) and lipids for energy and building block production, cell division, phenotypic aggression, and motility [94]. When grown with media containing supraphysiologic glucose, they upregulate specific genes, including EGFR, P-EGFR, IGF1R, P-IGF1R, IRS2, cyclin D1, and cyclin E expression, and inhibit AMPK/P-AMPK and p38 in a dose-dependent manner [26]. With the addition of metformin, there is a downregulation of these genes and the upregulation of genes associated with cell killing and growth control [49, 94]. Our report showed that glucose promotes phenotypic aggression and reduces metformin efficacy by targeting key enzymes that are required for glucose metabolism in TNBC. Such enzymes include G6PD, Fructose-2-6-BP, PGK, PGM, ENO, PKM2, and LDH-A (shown in Figure 3 and reviewed in [49]). Further, we reported that metformin attenuated the expression of over 20 critical genes involved in glucose metabolism, glucose transporters, gluconeogenesis, and tricarboxylic acid cycle [49]. Metformin-associated gene expression changes also reduced phenotypic aggressiveness and stem-like progenitor cell pool [26, 49, 90, 92]. Metformin treatment also restricted cell proliferation with S phase arrest, motility (through downregulation of intermediate filament proteins), and increased apoptosis (through activation of both the intrinsic and extrinsic pathways) [26, 47, 57, 88, 89, 92]. Metformin significantly inhibits carbohydrate induced pro-oncogenic metabolic and biologic characteristics of triple negative BC cells [26]. Altogether, metformin’s ability to target key glucose transporters, such a GLUT1, along with key genes involved in glucose and carbohydrate metabolism, highlights the role that this agent may play to control highly aggressive malignant BC cells via downregulation of the cellular metabolic machinery.
We have also shown that inhibition of lipid biosynthesis was requisite to the anticancer effects of metformin in triple negative BC cells. It downregulates both fatty acid synthase (FASN) and the cholesterol biosynthesis pathway, as detailed below. Other studies have focused on interactions between obesity, weight gain, hormonal status, and BC, and more specifically if metformin could be used to disrupt this process. Using a rat model of mammary tumor development after exposure to a carcinogen, animals were overfed and then segregated into lean and obese. Both subsets were subjected to ovary removal, half were given metformin, and they were followed for the development and progression of mammary tumors [52, 93, 95]. Obese rats experienced marked changes in metabolism, akin to metabolic syndrome. Mammary tumors from these obese rats showed enhanced tumor growth and tumor-associated glucose uptake, 50% higher than nonobese rats in association with upregulation of the progesterone receptor. In contrast, the lean rats preferentially deposited excess nutrients in mammary (nontumor) and peripheral tissues. Metformin abrogated systemic metabolic dysregulation, reduced tumorigenesis, tumor progression, and tumor-associated PR expression in obese rats. Similar changes in body weight and obesity are frequent after female menopause has been observed in BC of postmenopausal females with obesity, providing additional clues for the use and timing of metformin associated with BC risk and treatment for future study.
The mevalonate pathway, also known as the β-hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase pathway, is critical for cancer cell survival. Inhibition of the pathway by statins or other agents has been shown to have anticancer effects [96, 97]. In contrast, elevated cholesterol has been strongly associated with BC risk, a worse BC-associated outcome and chemotherapeutic resistance. This reflects the pivotal role of lipids including cholesterol in cancer survival and growth, including upregulation of signaling through membrane-bound receptors, facilitation of intracellular signaling pathways, and serving as an anchor for intracytoplasmic filaments to promote motility and invasion and as a precursor for cellular metabolism to generate energy and facilitate replication [98, 99]. We have shown that triple negative BC cells are especially dependent on the upregulation of lipid and cholesterol biosynthesis [100].
Statins are widely prescribed for patients with high cholesterol or lipid abnormalities, most often to reduce the risk of cardiovascular disease. Statins also benefit women to reduce the risk and disease progression of BC. Two population-based studies from Northern Europe are particularly compelling. A Finnish study involving over 30,000 women showed that statin use, pre- or post-BC diagnosis, reduced BC-specific mortality by about 50% [101]. A large Danish study showed a benefit for BC patients as well, with significantly lower recurrence rates in statin users as compared to nonusers. They also reported that lipophilic statins (rather than hydrophilic satins) had the most anti-BC activity [102]. A recent study from MD Anderson Cancer Center suggests that statin use is particularly beneficial for BC patients with triple negative tumors, especially in patients with higher stage disease [95]. Their data are consistent with our preclinical data, showing significant upregulation of lipid metabolism-associated gene triple negative BC as compared to other molecular subtypes. See for further discussion elsewhere [103]. A major issue with statin use is toxicity, which reportedly occurs in up to half of patients. Some statin drugs are also expensive and thus may be unaffordable by many patients.
Metformin, in contrast, is relatively nontoxic and inexpensive. We have demonstrated that metformin has potent effects in lipid and cholesterol biosynthesis in BC cells. More specifically, it inhibits transcriptional activation of HMGCo-A (the enzyme targeted by statins), as well as over 20 other genes in the cholesterol biosynthesis pathway. We have also shown that it induces translational activation of downstream signaling, including the genes ACAA2, HMGCS1, HMGCR, MVK, MVD, LSS, and DHCR24 (Figure 4). Through broad inhibition of cholesterol biosynthesis in triple negative BC, metformin induces a significant reduction of membrane-associated and intracellular cholesterol and reduces GM1 lipid rafts through decreased synthesis and destabilization (disassociation). GM1 lipid raft stability has a profound effect on some receptors that rely on GM1 lipid rafts (like EGFR) for stability, ligand binding, and thus activation, resulting in downstream signaling. We have shown that metformin inhibits cholesterol biosynthesis and raft production, reducing membranous EGFR and its activation associated with downstream signaling in TNBC [91]. We have also shown that in combination, metformin and the statin-mimetic MβCD were synergistic in attenuating cholesterol biosynthesis and cell proliferation [91]. Others have validated our observation that metformin downregulates genes involved in cholesterol biosynthesis, reporting downregulation of HMGCR, LDLR, and SREBP1 [104]. A particularly exciting corollary of these findings is the potential of metformin to synergize with receptor tyrosine kinase inhibitors (RTKIs) against BC. This is an underexplored area of breast oncology research with tremendous translational potential, given the growing use of RTKIs against BC.
Metformin action on cholesterol synthesis and lipid rafts. Metformin blocks epidermal growth factor receptor (EGFR), human epidermal growth factor receptors 2/3 (HER2/HER3), which in turn can block key enzymes involved in cholesterol synthesis pathway. Metformin and statins both can inhibit rate limiting step HMG-CoA Reductase, HMGCR. Metformin can also decrease cellular membrane rigidity, increase fluidity, and decrease cholesterol content to allow for the internalization of EGFR, HER2, or HER3 receptors. Internalization of these receptors is through GM1 lipid rafts, which are degraded and allow for BC cell death.
MiRNAs are endogenous, short (21-25) nucleotide sequences that control gene expression during post-transcriptional translation. It has previously been reported that more than half of human genes are regulated by miRNAs [105]. A growing body of evidence has highlighted the role of miRNAs as master regulators of metabolic processes, such as lipid and cholesterol synthesis [92, 105, 106]. Perturbations of these processes are important for tumor development. Modulation of these regulators using synthetic antagomirs to block the activity of specific miRNAs is an important new area of breast research. Metformin exerts some of its anticancer activity through modulation of miRNAs that target genes in metabolic and other pathways (Figure 5) [92, 107, 108]. miRNAs have been reported to be potential biomarkers for BC (i.e.,
Metformin action on lipid synthesis and miRNAs metformin blocks EGFR, HER2, and HER3, which in turn can block key enzymes involved in cholesterol synthesis pathway as described in
We have shown that metformin increases several members of the miR-193 family. It upregulates miR-193b, which in turn targets and downregulates the FASN 3’UTR. FASN is an important component of
The PI3K/Akt/mTOR pathway plays a central role in regulating protein synthesis, cell proliferation, tumorigenesis, angiogenesis, tumor growth, and metastasis [63]. While AMPK-dependent phosphorylation is frequently described in metformin-mediated inhibition of the PI3K/Akt/mTOR signaling pathway, AMPK activation is not mandatory for these effects; see schematic in Figure 6 [57]. We have shown that metformin inhibits Akt and mTOR and inhibits cellular proliferation and colony formation and causes a partial G1 cell cycle arrest in all ER-positive, HER2 normal or abnormal BC cell lines examined [57]. Metformin-mediated inhibition of the PI3K/Akt/mTOR signaling pathway has also been shown to induce inhibition of cell replication, S phase arrest, and apoptosis, with a reduction in E2F1 and cyclin D1 expression in triple negative BC cell lines [57].
Metformin action in breast cancer. Metformin can block receptor tyrosine kinase (RTK), such as EGFR, HER2, and HER3. Metformin further blocks downstream signaling intermediates involved in PI3K/Akt/mTOR or RAS/Raf/MEK/ERK signaling pathway, such as AKT, mTOR, MEK, or ERK, which can decrease cell growth, angiogenesis, and migration/invasion. Further, metformin can further block cytokine and growth factor receptors such as the TGF-RII. Metformin can block IL-6/STAT3 pathway and TGF-signaling pathway, which in turn can decrease cell growth, angiogenesis, migration/invasion, inflammation, and EMT.
TNBC shows high activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway, which in turn promotes cell growth, invasion, migration, metastasis, angiogenesis, immune evasion, and drug resistance and inhibits apoptosis [88]. We have shown that metformin specifically targets STAT3 signaling to reduce P-STAT3 at both Ser727 and Tyr705 phosphorylation sites but not STAT3 expression in TNBC, schematically represented in Figure 6. In combination with a Stat3 inhibitor, metformin significantly downregulated STAT3 expression and was synergistic in reducing cell growth and the induction of apoptosis in TNBC [88]. Given that TNBC also shows an upregulation/activation of the PI3K/Akt/mTOR signaling pathways, we then combined metformin with an mTOR inhibitor rapamycin, to determine if it would reduce metformin efficacy. Significant interactions with metformin were not observed; thus, mechanisms underlying its effects are not dependent on mTOR.
The JAK/STAT pathway is upregulated by obesity-associated mechanisms that promote BC growth. Others have demonstrated that metformin attenuates Janus kinase (JAK)/STAT3 signaling at Ser515 and Ser518 within the Src homology 2 domain of JAK1 [110]. Metformin has also been shown to preferentially inhibit nuclear translocation of NK-𝜅B and phosphorylation of STAT3 in cancer stem cells (CSCs) as compared to non-CSCs [111]. Given the procarcinogenic and prometastatic role that JAK/STAT pathways play in TNBC, the development of therapeutic strategies to attenuate these pathways using metformin may provide benefit with limited toxicity.
A subset of TNBC subclassified as mesenchymal-stem like/claudin-low (MSL/CL) characteristically shows high expression and activation of TGF-β signaling, phenotypic aggression, and a worse outcome. In addition to TGF-β receptor 2 expression, BC in this group shows upregulation of Smad2, Smad3, ID1, and ID3 [90]. They are especially responsive to TGF-β ligand 1 (TGF-β1), resulting in cell proliferation, migration, and invasion. MSL/CL cell lines also demonstrate downregulation of several growth factor receptors in response to metformin, including fibroblast growth factor receptors (FGFR2 and FGFR3), hormone receptors (AR, ESR1, and PGR), and claudin integral membrane proteins of tight junctions (CLDN3, CLDN4, and CLDN7) in the MSL/CL BC subtypes [90]. Metformin directly attenuated TGF-β signaling pathway by downregulating activation of Smad2/Smad3, ID1, and ID3 (Figure 6). In combination with TGF-β inhibitors (TβRI-KIs; LY2197s299 or SB431542), metformin synergistically enhanced cell death in MSL/CL BC cells [90]. Overall, these data suggest that targeting TGF-β signaling using metformin with or without a TGF-β inhibitor may provide benefit for patients with MSL/CL BCs.
The process of epithelial-mesenchymal transition (EMT) is also common in TNBC and has been associated with biologic aggression and stem-like properties. Metformin reportedly inhibits EMT in a metastatic canine model of mammary cancer [112]. Others have shown that metformin reduces EMT through blockade of transcription factors like ZEB1, TWIST1, and SNAIL (Slug) [113, 114, 115]. Given that TGF-β pathway activation and EMT promote breast cancer stem cells (BCSC), therapeutic resistance, dormancy, and a poor outcome [113], and that metformin has been shown to block these in TNBC, inhibitors against TGF-β-induced EMT combined with metformin may provide benefit in some TNBC patients.
Clinical studies have demonstrated that diabetic patients treated with metformin are less likely to develop cardiovascular disease, independent of glycemic control. It is unclear whether this outcome reflects downregulation of hyperglycemia and systemic inflammatory triggers or vascular damage, or whether metformin has a direct effect on endothelial cells, vascular resistance, elasticity, and damage [12, 80, 116]. In the context of breast cancer, it has long been demonstrated that high-stage and grade cancers with a worse prognosis have the capacity to upregulate peri- and intratumoral neo-angiogenesis [117]. The induction of new vessels provides metabolic and oxygen delivery advantages to the cancer cells, facilitating survival and growth. Neo-angiogenesis is also associated with an increased capacity of the BC to metastasize, particularly to distant sites including the visceral organs and brain. We have demonstrated a reduction in vascular density and growth, in association with metformin treatment in preclinical models. Others have shown that metformin is associated with reduced tumor angiogenesis in many different cancer cell types. Metformin and alternate biguanides, such as phenformin, downregulate VEGF-dependent activation of ERK1, inhibiting neo-angiogenesis and reducing microvessel density (MVD) [118]. Wang et al. have shown that metformin also downregulates the expression of two other genes, platelet-derived growth factor B (PDGF-B) and fibroblast growth factor (FGF-2), to reduce angiogenesis [119]. Downregulation of PDGF-B also restricts BC cell proliferation, survival, and migration, [117]. Metformin’s effect on the microenvironment and angiogenesis has also been shown to enhance chemo-sensitivity, via a reduction in MVD leakage and cancer cell hypoxia
Cancer stem cells (CSCs), also known as tumor-initiating cells (TICs), are the progenitor cells that give rise to BC as well as heterogeneity within transformed populations. CSCs are maintained as a subpopulation within the neoplasm that perpetuates clonal expansion and may facilitate dormancy, metastasis, chemo-resistance, and relapse. Among the molecular BC subtypes, TNBC shows the highest enrichment of CSCs, identified by expression patterns with flow cytometry as CD44+, CD24−/low CSC [120]. BC CSCs are particularly sensitive to metformin, which induces rapid cell death facilitated through a number of pathways involved in cell differentiation, renewal, metastasis, and metabolism (Figure 7). It directly targets key CSC gene signatures such as Notch 1, NF
Metformin action on breast cancer stem cells. Metformin can block a myriad of signaling pathways involved in BCSCs, including WNT, transforming growth factor (TGF), NOTCH, hypoxia inducible factor (HIF), and STAT3 signaling pathways. These pathways are thought to enrich for BCSC through the enrichment of CD44 positive receptor and aldehyde dehydrogenase (ALDH+) and decrease in CD24 expression. Metformin can be given as a monotherapy or combinatorial therapy with alternate chemotherapeutic agents, which in turn can induce BCSC death with an increase in apoptosis, cell cycle arrest, and DNA damage. Overall, reduction in BCSCs can result in reduction of tumor growth and prevention in therapy-mediated relapse.
The capacity of metformin to induce CSC cell death has significant clinical relevance, given their role in therapeutic resistance, dormancy, and disease progression. Metformin reduces cancer recurrence through the preferential killing of differentiated rather than undifferentiated CSCs [122]. In combination with chemotherapy, metformin is especially active against BC CSCs [111]. In studies of trastuzumab-resistant BC cells as well as xenograft models, the combination of trastuzumab and metformin significantly reduced CD44+, CD24−/low CSC subpopulations and reduced tumor volume [111, 123, 124]. In combination with doxorubicin, paclitaxel, or carboplatin, metformin can also eradicate CSCs and reduce the effective dosage required of the highly toxic chemotherapeutic agents, minimizing patient risk [111, 123].
The pleiotropic oncostatic effects of metformin have been explored as an adjuvant therapeutic option for the management of BC [43, 125, 126]. Epidemiological studies have demonstrated associations between metformin use in patients with type 2 diabetes and decreased cancer incidence and cancer-related mortality [10]. Several observational and randomized trials have evaluated a number of biomarker changes after metformin administration, increasing the footage of metformin as an off-label agent for BC. Over 11 ongoing and 13 completed clinical trials have tested the efficacy of metformin as a monotherapy or in combination with chemotherapy and/or radiotherapy for the management of BC (reviewed in [43, 127]). Goodwin et al. have shown that after six months of metformin treatment, a reduction in insulin by 22% had improved metabolic indices, such as insulin sensitivity, body weight, and cholesterol levels in nondiabetic patients with early-stage BC [29]. This information suggests that metformin is effective in the nondiabetic population. These data and other clinical trials further provide support in using metformin as an adjuvant agent as it is the only agent that does not promote BC but actually retards tumor growth. In addition, these clinical trials further support the need to screen for metabolic dysfunction and evaluate whether or not metformin should be integrated into the treatment for BC therapy. Further, BC patients receiving 1500 mg/day of metformin showed a significant reduction in insulin levels and insulin resistance [44, 128]. The effect of metformin in response to neoadjuvant chemotherapy has been examined in diabetic BC patients. This study included 2529 women with BC and confirmed that metformin could achieve higher pathological complete response with neoadjuvant therapy relative to non-metformin users [129]. Dowling et al. have further examined neoadjuvant metformin in a prospective window of opportunity study [32]. Clinical and biological effects of metformin on nondiabetic BC patients were evaluated. These patients were treated with 500 mg of metformin three times daily for 2 weeks. Significant attenuated expression of the insulin receptor was observed in treated breast tumors and had high expression of OCT1 (organic cation transporter 1) [32]. The effect of metformin in nondiabetic BC patients was previously reviewed [43]. Systemic reviews and meta-analyses, highlighting a summary of studies involving metformin therapy in nondiabetic patients and diabetic patients, were reviewed in [43].
Pharmacokinetic profiling of mouse tumors provided preclinical analysis of appropriate human doses to provide efficient inhibition of tumor growth [130]. Based on this evidence, metformin-mediated activation of AMPK and antitumor function was dependent on cellular uptake of the drug, which is primarily controlled by membrane transporters OCT1, OCT2, and OCT3 [131]. Based on the high expression of OCT transporters, 850 mg/day of metformin is required to inhibit tumor growth efficiently. If a tumor expresses low levels of OCT transporter, then 2250 mg/day is recommended [132]. Additionally, a dose of metformin of 500–850 mg/day is typically recommended with standard chemotherapy (including anthracyclines, platinum, taxanes, and capecitabine) for first- or second-line therapy (please see https://www.drugbank.ca/drugs/DB00331). The combination of metformin with a chemotherapeutic agent is recommended for a number of cycles until progression is unacceptable or toxicity develops.
Metformin is not approved for clinical use by the FDA and is still considered investigational for the treatment for BC. While metformin is well established as an inexpensive, well-tolerated, and effective for the treatment of diabetes, adjuvant use of metformin for BC remains to be defined. Current clinical trials have not outlined indications and contraindications for metformin use as adjuvant therapy for BC. Generally, metformin hydrochloride tablets are contraindicated in patients with (1) severe renal impairment (eGFR below 30 mL/min/1.73 m2), (2) hypersensitivity to metformin, and (3) acute or chronic metabolic acidosis including diabetic ketoacidosis. Additionally, current clinical trials with metformin have been listed (https://clinicaltrials.gov/ct2/show/NCT01310231 and https://clinicaltrials.gov/ct2/show/NCT01101438). The NCIC CTG MA.32 Phase III randomized clinical trial has completed enrollment of 3649 nondiabetic women receiving standard surgical, chemotherapeutic, hormonal, biologic, and radiation treatment for T1-3, N0-3, M0 breast cancer. This trial has provided preliminary findings [33] and has not defined clear indications and/or contraindications for metformin use as adjuvant therapy for breast cancer.
A preponderance of clinical, epidemiological, and scientific evidence indicates that metabolic dysregulation of carbohydrate and lipid metabolism promote BC pathogenesis and a worse outcome, for women who have the disease [9, 10, 30, 40, 45, 129, 133]. One of the therapeutic agents commonly used in patients with metabolic syndrome or type 2 diabetes, metformin, has demonstrated significant anti-BC activity. Metformin inhibits gluconeogenesis, reduces circulating levels of glucose, increases insulin sensitivity, and reduces hyperinsulinemia associated with insulin [134]. These factors have been associated with BC prognosis. Several mechanisms of metformin action involve AMPK-dependent and AMPK-independent signaling pathways, and these effects are remarkably broad and potent. Its ability to target metabolic dysregulation of carbohydrate and lipid metabolism as well as cancer stem cells appear to be equally important in its anticancer activity against BC [129, 133, 134, 135, 136, 137]. Furthermore, the effects of metformin are unique among molecular subsets of BC. A better understanding of these mechanisms will facilitate targeted applications in patients with specific subtypes, fostering the goal of more personalized cancer care.
A number of clinical trials are underway to evaluate metformin in BC patients [30, 44, 45, 46, 50, 136]. Most have been designed to evaluate its efficacy, in combination with various chemo- or radiotherapy agents; see (https://clinicaltrials.gov/ct2/results?term=+cancer+AND+metformin). Most ongoing or completed clinical trials have evaluated metformin’s effect on cellular proliferation or death, pathological response rate, progression-free or overall survival. Some have also sought to compare its efficacy in patients with or without metabolic dysregulation, as a secondary aim. None have specifically been designed to evaluate interactions with CSCs, or in selected molecular subtypes, although correlative studies have provided some data in this regard. The ALTTO trial has shown that metformin improves outcomes for patients with diabetes and either HER2+ or hormone receptor positive BC [30]. The NCIC Clinical Trials Group (NCIC CTG) MA.32 has shown benefit from metformin, as compared to placebo on outcomes in early stage BC [33]. It demonstrated efficacy with improvements in body weight, insulin, glucose, and leptin levels in BC patients examined, regardless of baseline BMI or fasting insulin levels [33].
In conclusion, metformin is a unique drug with a long track record of human use, which has demonstrated robust efficacy against type 2 diabetes and metabolic dysregulation. Epidemiologic data show independent and significant benefit in preventing cardiovascular disease and cancer in these patients. Metformin is an inexpensive oral agent that is currently available worldwide. It is generally well tolerated and has a low risk:benefit ratio. Epidemiological and clinical data have shown that metformin reduces BC incidence and mortality in women with metabolic dysregulation, obesity, and type 2 diabetes. This subpopulation of woman is at significantly higher risk for BC, particularly in the postmenopausal setting. Preclinical and clinical evidence shows that metformin inhibits BC cell replication and tumor growth, decreases tumor aggression, reduces the stem cell pool, and slows motility/metastasis and can promote cell death through apoptosis, autophagy, or upregulation of immunity. Metformin has unique effects on molecular subsets of BC, with the aggressive triple negative BC showing the most sensitivity and lowest EC50 data. TNBC is particularly sensitive to metformin’s downregulation of fatty acid and cholesterol biosynthesis, glucose transport, and carbohydrate metabolism. This cancer subtype is typically the most aggressive and is less responsive to traditional chemotherapy; thus, metformin’s potency may provide significant benefit especially in these patients.
Grant support provided in part by Susan G Komen for the Cure K100575 to RSW, SME, and ADT; ACS-IRG 16-184-56 RSW from the American Cancer Society; CCL-C92110 RSW and ADT from the Colorado Cancer League.
The authors have declared that no conflict of interest exists.
ACAA2 | Acetyl-coenzyme A acetyltransferase 2 |
ADP | Adenosine di-phosphate |
AKT | Protein kinase B |
ALTTO | Adjuvant lapatinib and/or trastuzumab treatment optimization |
AMP | Adenosine monophosphate |
AMPK | AMP-activated protein kinase |
AMPKK | AMP-activated protein kinase kinase |
ATP | Adenosine triphosphate |
AR | Androgen receptor |
BC | Breast cancer |
BCSCs | Breast cancer stem cells |
CDK | Cyclin-dependent kinase |
CL | Claudin-low |
CLDN | Claudin integral membrane proteins of tight junctions |
CSC | Cancer stem cells |
DHCR24 | 24-dehydrocholesterol reductase |
ESR1 | Estrogen receptor |
HIF-1α | Hypoxia-inducible factor 1-alpha |
EC | Effective concentration/Inhibitory concentration |
EGFR | Epidermal growth factor receptor |
EMT | Epithelial mesenchymal transition |
FASN | Fatty acid synthase |
FDA | Food and Drug Administration |
FGFR2 | Fibroblast growth factor receptor 2 |
FGFR3 | Fibroblast growth factor receptor 3 |
GLUT1 | Glucose transporter 1 |
GM1 | GM1 gangliosidosis marker |
HER2 | Human epidermal growth factor receptor 2 |
HER3: | Human epidermal growth factor receptor 3 |
HMGCo-A | β-Hydroxy β-methylglutaryl-CoA |
HMGCS1 | Hydroxymethylglutaryl-CoA synthase |
HMGCR | 3-Hydroxy-3-Methylglutaryl-CoA Reductase |
ID1 | Inhibitor of differentiation-1 |
IGFIR | Insulin-like growth factor receptor |
IGF1 | Insulin-like growth factor-1 |
IRS1 | Insulin receptor substrate 1 |
IL-1𝛽 | Interleukin 1 beta |
IL-6 | Interleukin-like 6 |
JAK | Janus kinase |
LDLR | Low-density lipoprotein receptor |
LKB1 | Liver kinase B1 |
LSS | Lanosterol synthase |
MAPK | Mitogen-activated protein kinases |
MβCD | Methyl-β-cyclodextrin |
MTOR | Mammalian target of rapamycin |
MRCC1 | Mitochondrial respiratory-chain complex 1 |
MSL | Mesenchymal stem-like |
MVD | Mevalonate diphosphate decarboxylase |
MVK | Mevalonate kinase |
NCIC CTG | NCIC Clinical Trials Group |
NF-𝜅B | Nuclear factor kappa-light-chain-enhancer of activated B-cells |
OCT1 | Organic cation transporter 1 |
OCT2 | Organic cation transporter 2 |
OCT3 | Organic cation transporter 2 |
P- | Phosphorylated |
P53 | Tumor protein 53 |
PARP | Poly (ADP-ribose) polymerase |
PGR | Progesterone receptor |
PI3K | Phosphatidyl-inositide 3-kinase |
PTEN | Phosphatase and tensin homolog |
RNA | Ribonucleic acid |
ROS | Reactive oxygen species |
SRC | Proto-oncogene c-Src |
SREBP1 | Sterol regulatory element-binding transcription factor 1 |
STAT3 | Signal transducer and activator of transcription 3 |
TGF-β | Transforming growth factor beta |
TNBC | Triple negative breast cancer |
TNF-α | Tumor necrosis factor alpha |
TSC2 | Tuberous sclerosis complex 2 |
US | United States |
VEGF | Vascular endothelial growth factor |
This is a brief overview of the main steps involved in publishing with IntechOpen Compacts, Monographs and Edited Books. Once you submit your proposal you will be appointed a Author Service Manager who will be your single point of contact and lead you through all the described steps below.
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\\n\\n5. LANGUAGE COPYEDITING, TECHNICAL EDITING AND TYPESET PROOF
\\n\\nYour manuscript will be sent to Straive, a leader in content solution services, for language copyediting. You will then receive a typeset proof formatted in XML and available online in HTML and PDF to proofread and check for completeness. The first typeset proof of your manuscript is usually available 10 days after its original submission.
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\\n\\nIntechOpen will help you complete your payment safely and securely, keeping your personal, professional and financial information safe.
\\n\\n7. ONLINE PUBLICATION, PRINT AND DELIVERY OF THE BOOK
\\n\\nIntechOpen authors can choose whether to publish their book online only or opt for online and print editions. IntechOpen Compacts, Monographs and Edited Books will be published on www.intechopen.com. If ordered, print copies are delivered by DHL within 12 to 15 working days.
\\n\\nIf you feel that IntechOpen Compacts, Monographs or Edited Books are the right publishing format for your work, please fill out the publishing proposal form. For any specific queries related to the publishing process, or IntechOpen Compacts, Monographs & Edited Books in general, please contact us at book.department@intechopen.com
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\n\nPlease complete the publishing proposal form. The completed form should serve as an overview of your future Compacts, Monograph or Edited Book. Once submitted, your publishing proposal will be sent for evaluation, and a notice of acceptance or rejection will be sent within 10 to 30 working days from the date of submission.
\n\n2. SUBMIT YOUR MANUSCRIPT
\n\nAfter approval, you will proceed in submitting your full-length manuscript. 50-130 pages for compacts, 130-500 for Monographs & Edited Books.Your full-length manuscript must follow IntechOpen's Author Guidelines and comply with our publishing rules. Once the manuscript is submitted, but before it is forwarded for peer review, it will be screened for plagiarism.
\n\n3. PEER REVIEW RESULTS
\n\nExternal reviewers will evaluate your manuscript and provide you with their feedback. You may be asked to revise your draft, or parts of your draft, provide additional information and make any other necessary changes according to their comments and suggestions.
\n\n4. ACCEPTANCE AND PRICE QUOTE
\n\nIf the manuscript is formally accepted after peer review you will receive a formal Notice of Acceptance, and a price quote.
\n\nThe Open Access Publishing Fee of your IntechOpen Compacts, Monograph or Edited Book depends on the volume of the publication and includes: project management, editorial and peer review services, technical editing, language copyediting, cover design and book layout, book promotion and ISBN assignment.
\n\nWe will send you your price quote and after it has been accepted (by both the author and the publisher), both parties will sign a Statement of Work binding them to adhere to the agreed upon terms.
\n\nAt this step you will also be asked to accept the Copyright Agreement.
\n\n5. LANGUAGE COPYEDITING, TECHNICAL EDITING AND TYPESET PROOF
\n\nYour manuscript will be sent to Straive, a leader in content solution services, for language copyediting. You will then receive a typeset proof formatted in XML and available online in HTML and PDF to proofread and check for completeness. The first typeset proof of your manuscript is usually available 10 days after its original submission.
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\n\nThe invoice is generally paid by the author, the author’s institution or funder. The payment can be made by credit card from your Author Panel (one will be assigned to you at the beginning of the project), or via bank transfer as indicated on the invoice. We currently accept the following payment options:
\n\nIntechOpen will help you complete your payment safely and securely, keeping your personal, professional and financial information safe.
\n\n7. ONLINE PUBLICATION, PRINT AND DELIVERY OF THE BOOK
\n\nIntechOpen authors can choose whether to publish their book online only or opt for online and print editions. IntechOpen Compacts, Monographs and Edited Books will be published on www.intechopen.com. If ordered, print copies are delivered by DHL within 12 to 15 working days.
\n\nIf you feel that IntechOpen Compacts, Monographs or Edited Books are the right publishing format for your work, please fill out the publishing proposal form. For any specific queries related to the publishing process, or IntechOpen Compacts, Monographs & Edited Books in general, please contact us at book.department@intechopen.com
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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. 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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. 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The literature source was Web of Science and SSCI, SCI-EXPANDED, A&HCI, CPCI-S, CPCI-SSH, and ESCI indexes. Fifty-two articles were reviewed; however, 14 of them were not been included in the study. As a result, 38 articles were examined. Level of education, field of education, and material types of AR used in education and reported educational advantages of AR have been investigated. All articles are categorized according to target groups, which are early childhood education, primary education, secondary education, high school education, graduate education, and others. AR technology has been mostly carried out in primary and graduate education. “Science education” is the most explored field of education. Mobile applications and marker-based materials on paper have been mostly preferred. 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The more active a lesson, the more students tend to engage intellectually and emotionally in the learning activities. Cooperative learning is the foundation on which many of the active learning procedures are based. Cooperative learning is the instructional use of small groups so that students work together to maximize their own and each other’s learning. Most of the active learning procedures, such as problem-based learning, team-learning, collaborative learning, and PALS, require that students work cooperatively in small groups to achieve joint learning goals. Cooperative learning is based on two theories: Structure-Process-Outcome theory and Social Interdependence theory. Four types of cooperative learning have been derived: formal cooperative learning, informal cooperative learning, cooperative base groups, and constructive controversy. There is considerable research confirming the effectiveness of cooperative learning. 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Currently, you can hear a lot of criticism that the classroom has not changed significantly compared to the last century or even like two centuries ago. Do the teachers succeed in modern changes? The purpose of the chapter is to summarize the current changes in didactics for the use of innovative teaching methods and study the understanding of changes by teachers. In this chapter, we consider four areas: the expansion of the subject of pedagogy, environmental approach to teaching, the digital generation and the changes taking place, and innovation in teaching. The theory of education, figuratively speaking, has two levels. At the macro-level, in the “education-society” relationship, decentralization and diversification, internationalization of education, and the introduction of digital technologies occur. At the micro-level in the “teacher-learner” relationship, there is an active mix of traditional and innovative methods, combination of an activity approach with an energy-informational environment approach, cognition with constructivism and connectivism.",book:{id:"5980",slug:"new-pedagogical-challenges-in-the-21st-century-contributions-of-research-in-education",title:"New Pedagogical Challenges in the 21st Century",fullTitle:"New Pedagogical Challenges in the 21st Century - Contributions of Research in Education"},signatures:"Aigerim Mynbayeva, Zukhra Sadvakassova and Bakhytkul\nAkshalova",authors:[{id:"201997",title:"Dr.",name:"Aigerim",middleName:null,surname:"Mynbayeva",slug:"aigerim-mynbayeva",fullName:"Aigerim Mynbayeva"},{id:"209208",title:"Dr.",name:"Zukhra",middleName:null,surname:"Sadvakassova",slug:"zukhra-sadvakassova",fullName:"Zukhra Sadvakassova"},{id:"209210",title:"Dr.",name:"Bakhytkul",middleName:null,surname:"Akshalova",slug:"bakhytkul-akshalova",fullName:"Bakhytkul Akshalova"}]},{id:"59468",doi:"10.5772/intechopen.74344",title:"Virtual and Augmented Reality: New Frontiers for Clinical Psychology",slug:"virtual-and-augmented-reality-new-frontiers-for-clinical-psychology",totalDownloads:2364,totalCrossrefCites:13,totalDimensionsCites:21,abstract:"In the last decades, the applied approach for the use of virtual reality (VR) and augmented reality (AR) on clinical and health psychology has grown exponentially. These technologies have been used to treat several mental disorders, for example, phobias, stress-related disorders, depression, eating disorders, and chronic pain. The importance of VR/AR for the mental health field comes from three main concepts: (1) VR/AR as an imaginal technology, people can feel “as if they are” in a reality that does not exist in external world; (2) VR/AR as an embodied technology, the experience to feel user’s body inside the virtual environment; and (3) VR/AR as connectivity technology, the “end of geography’. In this chapter, we explore the opportunities provided by VR/AR as technologies to improve people’s quality of life and to discuss new frontiers for their application in mental health and psychological well-being promotion.",book:{id:"6543",slug:"state-of-the-art-virtual-reality-and-augmented-reality-knowhow",title:"State of the Art Virtual Reality and Augmented Reality Knowhow",fullTitle:"State of the Art Virtual Reality and Augmented Reality Knowhow"},signatures:"Sara Ventura, Rosa M. Baños and Cristina Botella",authors:[{id:"106036",title:"Dr.",name:"Rosa Maria",middleName:null,surname:"Baños",slug:"rosa-maria-banos",fullName:"Rosa Maria Baños"},{id:"227763",title:"Ph.D.",name:"Sara",middleName:null,surname:"Ventura",slug:"sara-ventura",fullName:"Sara Ventura"},{id:"229056",title:"Dr.",name:"Cristina",middleName:null,surname:"Botella",slug:"cristina-botella",fullName:"Cristina Botella"}]},{id:"64583",doi:"10.5772/intechopen.81714",title:"Evaluating a Course for Teaching Advanced Programming Concepts with Scratch to Preservice Kindergarten Teachers: A Case Study in Greece",slug:"evaluating-a-course-for-teaching-advanced-programming-concepts-with-scratch-to-preservice-kindergart",totalDownloads:1422,totalCrossrefCites:13,totalDimensionsCites:18,abstract:"Coding is a new literacy for the twenty-first century, and as a literacy, coding enables new ways of thinking and new ways of communicating and expressing ideas, as well as new ways of civic participation. A growing number of countries, in Europe and beyond, have established clear policies and frameworks for introducing computational thinking (CT) and computer programming to young children. In this chapter, we discuss a game-based approach to coding education for preservice kindergarten teachers using Scratch. The aim of using Scratch was to excite students’ interest and familiarize them with the basics of programming in an open-ended, project-based, and personally meaningful environment for a semester course in the Department of Preschool Education in the University of Crete. For 13 weeks, students were introduced to the main Scratch concepts and, afterward, were asked to prepare their projects. For the projects, they were required to design their own interactive stories to teach certain concepts about mathematics or physical science to preschool-age students. The results we obtained were more satisfactory than expected and, in some regards, encouraging if one considers the fact that the research participants had no prior experiences with computational thinking.",book:{id:"6936",slug:"early-childhood-education",title:"Early Childhood Education",fullTitle:"Early Childhood Education"},signatures:"Stamatios Papadakis and Michail Kalogiannakis",authors:null}],mostDownloadedChaptersLast30Days:[{id:"58060",title:"Pedagogy of the Twenty-First Century: Innovative Teaching Methods",slug:"pedagogy-of-the-twenty-first-century-innovative-teaching-methods",totalDownloads:8832,totalCrossrefCites:17,totalDimensionsCites:23,abstract:"In the twenty-first century, significant changes are occurring related to new scientific discoveries, informatization, globalization, the development of astronautics, robotics, and artificial intelligence. This century is called the age of digital technologies and knowledge. How is the school changing in the new century? How does learning theory change? Currently, you can hear a lot of criticism that the classroom has not changed significantly compared to the last century or even like two centuries ago. Do the teachers succeed in modern changes? The purpose of the chapter is to summarize the current changes in didactics for the use of innovative teaching methods and study the understanding of changes by teachers. In this chapter, we consider four areas: the expansion of the subject of pedagogy, environmental approach to teaching, the digital generation and the changes taking place, and innovation in teaching. The theory of education, figuratively speaking, has two levels. At the macro-level, in the “education-society” relationship, decentralization and diversification, internationalization of education, and the introduction of digital technologies occur. At the micro-level in the “teacher-learner” relationship, there is an active mix of traditional and innovative methods, combination of an activity approach with an energy-informational environment approach, cognition with constructivism and connectivism.",book:{id:"5980",slug:"new-pedagogical-challenges-in-the-21st-century-contributions-of-research-in-education",title:"New Pedagogical Challenges in the 21st Century",fullTitle:"New Pedagogical Challenges in the 21st Century - Contributions of Research in Education"},signatures:"Aigerim Mynbayeva, Zukhra Sadvakassova and Bakhytkul\nAkshalova",authors:[{id:"201997",title:"Dr.",name:"Aigerim",middleName:null,surname:"Mynbayeva",slug:"aigerim-mynbayeva",fullName:"Aigerim Mynbayeva"},{id:"209208",title:"Dr.",name:"Zukhra",middleName:null,surname:"Sadvakassova",slug:"zukhra-sadvakassova",fullName:"Zukhra Sadvakassova"},{id:"209210",title:"Dr.",name:"Bakhytkul",middleName:null,surname:"Akshalova",slug:"bakhytkul-akshalova",fullName:"Bakhytkul Akshalova"}]},{id:"61746",title:"Facilitation of Teachers’ Professional Development through Principals’ Instructional Supervision and Teachers’ Knowledge- Management Behaviors",slug:"facilitation-of-teachers-professional-development-through-principals-instructional-supervision-and-t",totalDownloads:3384,totalCrossrefCites:2,totalDimensionsCites:2,abstract:"With the rise of global competition and the focus on teacher quality, teacher professional development is becoming increasingly crucial, and the stress and challenges for principals are more severe than ever. Teachers can improve their professional abilities through principals’ instructional supervision and their own knowledge-management (KM) behaviors to benefit students. Thus, this chapter analyzes the relationship among principals’ instructional supervision, teachers’ KM, and teachers’ professional development. The author believes that principals’ instructional supervision and effective KM can facilitate the professional development of teachers. The author also believes the readers can know the relationships among them, and teachers’ professional development can be improved through principal’s instructional supervision and teachers’ KM behaviors.",book:{id:"6674",slug:"contemporary-pedagogies-in-teacher-education-and-development",title:"Contemporary Pedagogies in Teacher Education and Development",fullTitle:"Contemporary Pedagogies in Teacher Education and Development"},signatures:"Chien-Chin Chen",authors:[{id:"232569",title:"Ph.D.",name:"Chien Chih",middleName:null,surname:"Chen",slug:"chien-chih-chen",fullName:"Chien Chih Chen"}]},{id:"75908",title:"From the Classroom into Virtual Learning Environments: Essential Knowledge, Competences, Skills and Pedagogical Strategies for the 21st Century Teacher Education in Kenya",slug:"from-the-classroom-into-virtual-learning-environments-essential-knowledge-competences-skills-and-ped",totalDownloads:519,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"As teachers in Kenya begin to migrate from the classroom to virtual learning spaces following COVID 19 pandemic, there is pressing need to realign Teacher Education to requisite Knowledge, competences, skills, and attitudes that will support online teaching. This chapter explores these needs using a combination of lived experiences and literature review that captured a meta-analysis of research trends on e-learning. While trends in Teacher Education indicate progression towards adoption of technology, there are disparities between the theory and practice. Evidence from recent research and reports; and the recollected experiences confirmed knowledge, competence, skills and pedagogical gaps in the implementation of online learning, that have been exacerbated by COVID-19. The researcher recommends that teacher education should sensitize and train teacher trainees on how to access, analyze and use new knowledge emerging with technology; they also should be coached on how learners learn with technology and on fundamentals of the communication process. Particularly the course on educational technology, should focus on how to create and manage online courses. The 5-stage E-Moderator Model and Universal Design for Learning (UDL) are recommended as effective pedagogical scaffold for online teaching.",book:{id:"10229",slug:"teacher-education-in-the-21st-century-emerging-skills-for-a-changing-world",title:"Teacher Education in the 21st Century",fullTitle:"Teacher Education in the 21st Century - Emerging Skills for a Changing World"},signatures:"Catherine Adhiambo Amimo",authors:[{id:"333482",title:"Dr.",name:"Catherine Adhiambo",middleName:null,surname:"Amimo",slug:"catherine-adhiambo-amimo",fullName:"Catherine Adhiambo Amimo"}]},{id:"75224",title:"Decoding the Digital Gap in Teacher Education: Three Perspectives across the Globe",slug:"decoding-the-digital-gap-in-teacher-education-three-perspectives-across-the-globe",totalDownloads:589,totalCrossrefCites:0,totalDimensionsCites:4,abstract:"Educational use of technology is regularly assessed, and results often show a gap between educational policies and what is actually practiced. This chapter will help clarify how teacher educators experience the changing educational contexts due to the digital revolution, how their meaning-making shifts, and how outside forces influence those processes. The results are based on comparative international studies. Central for this study is practitioners’ professional digital competence, their attitudes towards digital technology and the use of digital technology in education. We found that the influence and contribution of digital practice is carried out quite differently across the globe. Our research questions were: How do practitioners experience teaching in a rapidly changing context? How do attitudes change due to top-down governing of education? and What motivates teacher educators to implement digital technology?",book:{id:"10229",slug:"teacher-education-in-the-21st-century-emerging-skills-for-a-changing-world",title:"Teacher Education in the 21st Century",fullTitle:"Teacher Education in the 21st Century - Emerging Skills for a Changing World"},signatures:"Steinar Thorvaldsen and Siri Sollied Madsen",authors:[{id:"332624",title:"Associate Prof.",name:"Siri Sollied",middleName:null,surname:"Madsen",slug:"siri-sollied-madsen",fullName:"Siri Sollied Madsen"},{id:"332626",title:"Prof.",name:"Steinar",middleName:null,surname:"Thorvaldsen",slug:"steinar-thorvaldsen",fullName:"Steinar Thorvaldsen"}]},{id:"75416",title:"Self-Study Research: Challenges and Opportunities in Teacher Education",slug:"self-study-research-challenges-and-opportunities-in-teacher-education",totalDownloads:777,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"This article aims to describe what self-study research is, why self-study can be a good approach to teacher educators’ professional development and improvements in practice and highlight some challenges and opportunities in this research approach. In addition, the article will shed light on some methodological aspects related to self-study. Self-study refers to teacher educators who in an intentionally and systematically way examine their practice to improve it, based on a deeper understanding of practice, as well as the context practice takes place. In the article, I argue that engaging in self-study is a learning and development process and an approach to developing personal professionalism, collective professionalism and improvements in practice.",book:{id:"10229",slug:"teacher-education-in-the-21st-century-emerging-skills-for-a-changing-world",title:"Teacher Education in the 21st Century",fullTitle:"Teacher Education in the 21st Century - Emerging Skills for a Changing World"},signatures:"Kåre Hauge",authors:[{id:"332053",title:"Associate Prof.",name:"Kåre",middleName:null,surname:"Hauge",slug:"kare-hauge",fullName:"Kåre Hauge"}]}],onlineFirstChaptersFilter:{topicId:"265",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:90,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:108,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:33,numberOfPublishedChapters:330,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:14,numberOfPublishedChapters:145,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:9,numberOfPublishedChapters:141,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:124,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:112,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:22,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:11,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:"2753-6580",doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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",coverUrl:"https://cdn.intechopen.com/series/covers/23.jpg",latestPublicationDate:"August 12th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:0,editor:{id:"280770",title:"Dr.",name:"Katherine K.M.",middleName:null,surname:"Stavropoulos",slug:"katherine-k.m.-stavropoulos",fullName:"Katherine K.M. Stavropoulos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRdFuQAK/Profile_Picture_2022-05-24T09:03:48.jpg",biography:"Katherine Stavropoulos received her BA in Psychology from Trinity College, in Connecticut, USA and her Ph.D. in Experimental Psychology from the University of California, San Diego. She completed her postdoctoral work at the Yale Child Study Center with Dr. James McPartland. Dr. Stavropoulos’ doctoral dissertation explored neural correlates of reward anticipation to social versus nonsocial stimuli in children with and without autism spectrum disorders (ASD). She has been a faculty member at the University of California, Riverside in the School of Education since 2016. Her research focuses on translational studies to explore the reward system in ASD, as well as how anxiety contributes to social challenges in ASD. She also investigates how behavioral interventions affect neural activity, behavior, and school performance in children with ASD. She is also involved in the diagnosis of children with ASD and is a licensed clinical psychologist in California. She is the Assistant Director of the SEARCH Center at UCR and is a faculty member in the Graduate Program in Neuroscience.",institutionString:null,institution:{name:"University of California, Riverside",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:2,paginationItems:[{id:"89",title:"Education",coverUrl:"https://cdn.intechopen.com/series_topics/covers/89.jpg",isOpenForSubmission:!1,annualVolume:null,editor:{id:"260066",title:"Associate Prof.",name:"Michail",middleName:null,surname:"Kalogiannakis",slug:"michail-kalogiannakis",fullName:"Michail Kalogiannakis",profilePictureURL:"https://mts.intechopen.com/storage/users/260066/images/system/260066.jpg",biography:"Michail Kalogiannakis is an Associate Professor of the Department of Preschool Education, University of Crete, and an Associate Tutor at School of Humanities at the Hellenic Open University. He graduated from the Physics Department of the University of Crete and continued his post-graduate studies at the University Paris 7-Denis Diderot (D.E.A. in Didactic of Physics), University Paris 5-René Descartes-Sorbonne (D.E.A. in Science Education) and received his Ph.D. degree at the University Paris 5-René Descartes-Sorbonne (PhD in Science Education). His research interests include science education in early childhood, science teaching and learning, e-learning, the use of ICT in science education, games simulations, and mobile learning. He has published over 120 articles in international conferences and journals and has served on the program committees of numerous international conferences.",institutionString:"University of Crete",institution:{name:"University of Crete",institutionURL:null,country:{name:"Greece"}}},editorTwo:{id:"422488",title:"Dr.",name:"Maria",middleName:null,surname:"Ampartzaki",slug:"maria-ampartzaki",fullName:"Maria Ampartzaki",profilePictureURL:"https://mts.intechopen.com/storage/users/422488/images/system/422488.jpg",biography:"Dr Maria Ampartzaki is an Assistant Professor in Early Childhood Education in the Department of Preschool Education at the University of Crete. Her research interests include ICT in education, science education in the early years, inquiry-based and art-based learning, teachers’ professional development, action research, and the Pedagogy of Multiliteracies, among others. She has run and participated in several funded and non-funded projects on the teaching of Science, Social Sciences, and ICT in education. She also has the experience of participating in five Erasmus+ projects.",institutionString:"University of Crete",institution:{name:"University of Crete",institutionURL:null,country:{name:"Greece"}}},editorThree:null},{id:"90",title:"Human Development",coverUrl:"https://cdn.intechopen.com/series_topics/covers/90.jpg",isOpenForSubmission:!0,annualVolume:11974,editor:{id:"191040",title:"Dr.",name:"Tal",middleName:null,surname:"Dotan Ben-Soussan",slug:"tal-dotan-ben-soussan",fullName:"Tal Dotan Ben-Soussan",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSBf1QAG/Profile_Picture_2022-03-18T07:56:11.jpg",biography:"Tal Dotan Ben-Soussan, Ph.D., is the director of the Research Institute for Neuroscience, Education and Didactics (RINED) – Paoletti Foundation. Ben-Soussan leads international studies on training and neuroplasticity from neurophysiological and psychobiological perspectives. As a neuroscientist and bio-psychologist, she has published numerous articles on neuroplasticity, movement and meditation. She acts as an editor and reviewer in several renowned journals and coordinates international conferences integrating theoretical, methodological and practical approaches on various topics, such as silence, logics and neuro-education. She lives in Assisi, Italy.",institutionString:"Research Institute for Neuroscience, Education and Didactics, Patrizio Paoletti Foundation",institution:null},editorTwo:null,editorThree:null}]},overviewPageOFChapters:{paginationCount:42,paginationItems:[{id:"82914",title:"Glance on the Critical Role of IL-23 Receptor Gene Variations in Inflammation-Induced Carcinogenesis",doi:"10.5772/intechopen.105049",signatures:"Mohammed El-Gedamy",slug:"glance-on-the-critical-role-of-il-23-receptor-gene-variations-in-inflammation-induced-carcinogenesis",totalDownloads:15,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Chemokines Updates",coverURL:"https://cdn.intechopen.com/books/images_new/11672.jpg",subseries:{id:"18",title:"Proteomics"}}},{id:"82875",title:"Lipidomics as a Tool in the Diagnosis and Clinical Therapy",doi:"10.5772/intechopen.105857",signatures:"María Elizbeth Alvarez Sánchez, Erick Nolasco Ontiveros, Rodrigo Arreola, Adriana Montserrat Espinosa González, Ana María García Bores, Roberto Eduardo López Urrutia, Ignacio Peñalosa Castro, María del Socorro Sánchez Correa and Edgar Antonio Estrella Parra",slug:"lipidomics-as-a-tool-in-the-diagnosis-and-clinical-therapy",totalDownloads:9,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82440",title:"Lipid Metabolism and Associated Molecular Signaling Events in Autoimmune Disease",doi:"10.5772/intechopen.105746",signatures:"Mohan Vanditha, Sonu Das and Mathew John",slug:"lipid-metabolism-and-associated-molecular-signaling-events-in-autoimmune-disease",totalDownloads:17,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82483",title:"Oxidative Stress in Cardiovascular Diseases",doi:"10.5772/intechopen.105891",signatures:"Laura Mourino-Alvarez, Tamara Sastre-Oliva, Nerea Corbacho-Alonso and Maria G. Barderas",slug:"oxidative-stress-in-cardiovascular-diseases",totalDownloads:10,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Importance of Oxidative Stress and Antioxidant System in Health and Disease",coverURL:"https://cdn.intechopen.com/books/images_new/11671.jpg",subseries:{id:"15",title:"Chemical Biology"}}}]},overviewPagePublishedBooks:{paginationCount:33,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. 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She is also the Global Harmonization Initiative (GHI)",institutionString:"Australian College of Business & Technology",institution:{name:"Kobe College",institutionURL:null,country:{name:"Japan"}}}]},{type:"book",id:"6820",title:"Keratin",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/6820.jpg",slug:"keratin",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Miroslav Blumenberg",hash:"6def75cd4b6b5324a02b6dc0359896d0",volumeInSeries:2,fullTitle:"Keratin",editors:[{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. 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