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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"9881",leadTitle:null,fullTitle:"Perovskite and Piezoelectric Materials",title:"Perovskite and Piezoelectric Materials",subtitle:null,reviewType:"peer-reviewed",abstract:"Investigating in the area of perovskite materials and the fabrication of devices for properties in optoelectronics, we have presented a brief outline of perovskite materials. The authors present a fairly comprehensive arrangement of this very active area of research, with its past changes and present position and outlooks. Discussions are presented regarding photocatalysis, fabrication of solar cell devices and their stability, lead-free materials, as well as thermoelectric and piezoelectric applications. In view of the present status of perovskite materials, I am assured that each chapter of the book will be of boundless encouragement for researchers, scientists, and academicians working in this field.",isbn:"978-1-78985-666-8",printIsbn:"978-1-78985-665-1",pdfIsbn:"978-1-78985-678-1",doi:"10.5772/intechopen.87690",price:119,priceEur:129,priceUsd:155,slug:"perovskite-and-piezoelectric-materials",numberOfPages:228,isOpenForSubmission:!1,isInWos:null,hash:"8fa0e0f48567bbc50fbb3bfdde6f9a0b",bookSignature:"Someshwar Pola, Neeraj Panwar and Indrani Coondoo",publishedDate:"January 27th 2021",coverURL:"https://cdn.intechopen.com/books/images_new/9881.jpg",numberOfDownloads:1728,numberOfWosCitations:0,numberOfCrossrefCitations:1,numberOfDimensionsCitations:2,hasAltmetrics:0,numberOfTotalCitations:3,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 11th 2019",dateEndSecondStepPublish:"March 9th 2020",dateEndThirdStepPublish:"May 8th 2020",dateEndFourthStepPublish:"July 27th 2020",dateEndFifthStepPublish:"September 25th 2020",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7",editedByType:"Edited by",kuFlag:!1,editors:[{id:"177037",title:"Dr.",name:"Someshwar",middleName:null,surname:"Pola",slug:"someshwar-pola",fullName:"Someshwar Pola",profilePictureURL:"https://mts.intechopen.com/storage/users/177037/images/system/177037.jpg",biography:"Dr. Someshwar Pola has been working as an Assistant Professor\nin the Department of Chemistry, University College of Science,\nOsmania University since 2018. He worked as an Assistant Professor in the Department of Chemistry, Nizam College, Osmania University from 2013 to 2017. He received his B.Sc. from\nKakatiya University, M.Sc from P.G Center, Mirzapur, Osmania\nUniversity, and Ph.D. in chemistry from Kakatiya University,\nWarangal, Telangana State, India. Dr. Pola worked as a visiting faculty member\nat the Institute of Chemistry, Academic Sinica, Taipei, Taiwan for two months in\n2017. He also worked as a Postdoctoral Fellow (PDF) at the Institute of Chemistry,\nAcademic Sinica, Taipei, Taiwan from August 2008 to April 2012. During this period, he focused on the synthesis and characterization of organic functional materials\ntowards single-crystal field-effect transistors. During the period of his doctoral research work (2002 to 2006), he developed various methodologies in inorganic and\nanalytical chemistry. He also has industrial experience in medicinal research and\ndevelopment (AR&D), GVK Biosciences Pvt. Ltd., Hyderabad, India. Dr. Pola has\npublished over 48 research papers in reputed international and national journals\nand has one book chapter to his credit. He has also presented research papers at 35\nnational and 25 international conferences. He has delivered guest/invited lectures\nin various colleges/conferences. He is a Life Member of the Society of Materials\nChemistry (SMC), Materials Research Society of India (MRSI), Indian Science\nCongress Association (ISCA), India, and a member in the American Chemical\nSociety (ACS). He is a reviewer for Elsevier, ACS, and RSC journals. He has 8 years\nof teaching and 20 years of research experience. His research focuses on supramolecular chemistry, solar cell device fabrication studies, organic field-effect transistors, photocatalysis of organic pollutants in the presence of titanates, perovskites\nand related semiconductor and metal-organic frameworks. Under his supervision,\n6 postgraduate students have completed their dissertation work, 3 Ph.D. students\nhave been awarded and 8 scholars are currently working for their Ph.D. degree.\nHis research activities are supported by various funding agencies like NSC-Taiwan,\nUGC, DST and CSIR, New Delhi, India.",institutionString:"Osmania University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Osmania University",institutionURL:null,country:{name:"India"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"289829",title:"Dr.",name:"Neeraj",middleName:null,surname:"Panwar",slug:"neeraj-panwar",fullName:"Neeraj Panwar",profilePictureURL:"https://mts.intechopen.com/storage/users/289829/images/system/289829.jpeg",biography:"Neeraj Panwar, Ph.D., is presently a Senior Assistant Professor in\nthe Department of Physics, Central University of Rajasthan India. He has postdoctoral research experience from the University\nof Puerto Rico, U.S.A. and the University of Aveiro, Portugal. He\nhas had several research collaborations at the international and\nnational levels. He has guided two Ph.D. theses and several master’s and undergraduate students for their dissertation work. He\nhas published more than seventy international research papers. His areas of interest\ninclude magnetism and lead-free piezoelectric and electroceramic materials. He is\nalso interested in practicing yoga.",institutionString:"Central University of Rajasthan",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Central University of Rajasthan",institutionURL:null,country:{name:"India"}}},coeditorTwo:{id:"289832",title:"Dr.",name:"Indrani",middleName:null,surname:"Coondoo",slug:"indrani-coondoo",fullName:"Indrani Coondoo",profilePictureURL:"https://mts.intechopen.com/storage/users/289832/images/system/289832.jpeg",biography:"Dr. Indrani Coondoo has been working as a research scientist at\nthe University of Aveiro, Portugal since 2019. She has worked\nas an FCT postdoctoral researcher at the same university (2010-\n2017). She was a visiting researcher at the University of Puerto\nRico, U.S.A. (2010). She obtained her Doctorate degree from\nthe Faculty of Applied Sciences, University of Delhi (2008). She\nserved as a CSIR Research Associate and Project Fellow at the\nNational Physical Laboratory, India (2008-2009). Her research interest lies in the\nstudy of lead-free piezoelectrics, layered ferroelectrics, and multiferroics. She has\npublished more than fifty research papers in journals of international repute. She\nhas one U.S.A. patent to her credit. She has edited a book entitled “Ferroelectrics”\nand written many book chapters, as well as review articles.",institutionString:"University of Aveiro",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of Aveiro",institutionURL:null,country:{name:"Portugal"}}},coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1169",title:"Condensed Matter Physics",slug:"nanotechnology-and-nanomaterials-material-science-condensed-matter-physics"}],chapters:[{id:"71650",title:"Significant Role of Perovskite Materials for Degradation of Organic Pollutants",doi:"10.5772/intechopen.91680",slug:"significant-role-of-perovskite-materials-for-degradation-of-organic-pollutants",totalDownloads:341,totalCrossrefCites:0,totalDimensionsCites:1,signatures:"Someshwar Pola and Ramesh Gade",downloadPdfUrl:"/chapter/pdf-download/71650",previewPdfUrl:"/chapter/pdf-preview/71650",authors:[{id:"177037",title:"Dr.",name:"Someshwar",surname:"Pola",slug:"someshwar-pola",fullName:"Someshwar Pola"}],corrections:null},{id:"72709",title:"Lead-Free Perovskite Nanocomposites: An Aspect for Environmental Application",doi:"10.5772/intechopen.93052",slug:"lead-free-perovskite-nanocomposites-an-aspect-for-environmental-application",totalDownloads:227,totalCrossrefCites:0,totalDimensionsCites:0,signatures:"Manojit De",downloadPdfUrl:"/chapter/pdf-download/72709",previewPdfUrl:"/chapter/pdf-preview/72709",authors:[{id:"320712",title:"Dr.",name:"Manojit",surname:"De",slug:"manojit-de",fullName:"Manojit De"}],corrections:null},{id:"74453",title:"Perovskite Nanoparticles",doi:"10.5772/intechopen.94588",slug:"perovskite-nanoparticles",totalDownloads:143,totalCrossrefCites:0,totalDimensionsCites:0,signatures:"Burak Gultekin, Ali Kemal Havare, Shirin Siyahjani, Halil Ibrahim Ciftci and Mustafa Can",downloadPdfUrl:"/chapter/pdf-download/74453",previewPdfUrl:"/chapter/pdf-preview/74453",authors:[{id:"176024",title:"Dr.",name:"Mustafa",surname:"Can",slug:"mustafa-can",fullName:"Mustafa Can"},{id:"205447",title:"Dr.",name:"Ali Kemal",surname:"Havare",slug:"ali-kemal-havare",fullName:"Ali Kemal Havare"},{id:"323709",title:"Dr.",name:"Burak",surname:"Gültekin",slug:"burak-gultekin",fullName:"Burak Gültekin"},{id:"323944",title:"Mrs.",name:"Shirin",surname:"Siyahjani",slug:"shirin-siyahjani",fullName:"Shirin Siyahjani"},{id:"323946",title:"Dr.",name:"Halilibrahim",surname:"Çiftçi",slug:"halilibrahim-ciftci",fullName:"Halilibrahim Çiftçi"}],corrections:null},{id:"73856",title:"Organic Inorganic Perovskites: A Low-Cost-Efficient Photovoltaic Material",doi:"10.5772/intechopen.94104",slug:"organic-inorganic-perovskites-a-low-cost-efficient-photovoltaic-material",totalDownloads:99,totalCrossrefCites:0,totalDimensionsCites:0,signatures:"Madeeha Aslam, Tahira Mahmood and Abdul Naeem",downloadPdfUrl:"/chapter/pdf-download/73856",previewPdfUrl:"/chapter/pdf-preview/73856",authors:[{id:"226388",title:"Prof.",name:"Abdul",surname:"Naeem",slug:"abdul-naeem",fullName:"Abdul Naeem"},{id:"305971",title:"Prof.",name:"Tahira",surname:"Mahmood",slug:"tahira-mahmood",fullName:"Tahira Mahmood"},{id:"305974",title:"Ms.",name:"Madeeha",surname:"Aslam",slug:"madeeha-aslam",fullName:"Madeeha Aslam"}],corrections:null},{id:"71279",title:"Structural Phase Transitions of Hybrid Perovskites CH3NH3PbX3 (X = Br, Cl) from Synchrotron and Neutron Diffraction Data",doi:"10.5772/intechopen.91421",slug:"structural-phase-transitions-of-hybrid-perovskites-ch-sub-3-sub-nh-sub-3-sub-pbx-sub-3-sub-x-br-cl-f",totalDownloads:259,totalCrossrefCites:1,totalDimensionsCites:1,signatures:"Carlos Alberto López, María Consuelo Alvarez-Galván, Carmen Abia, María Teresa Fernández-Díaz and José Antonio Alonso",downloadPdfUrl:"/chapter/pdf-download/71279",previewPdfUrl:"/chapter/pdf-preview/71279",authors:[{id:"189662",title:"Prof.",name:"Jose Antonio",surname:"Alonso",slug:"jose-antonio-alonso",fullName:"Jose Antonio Alonso"},{id:"317029",title:"Dr.",name:"C.A.",surname:"Lopez",slug:"c.a.-lopez",fullName:"C.A. 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Breast carcinoma is one of the most frequently diagnosed cancers among women worldwide with a high frequency reported in the West [1, 2]. This highest incidence of breast cancer in American whites and in most European countries reveal the long‐standing high prevalence of reproductive factors associated with increased risk of breast cancer, including early menarche, late child bearing age, few pregnancies, hormone replacement therapy and increased mammography [3, 4]. In Israel, the increased incidence of breast cancer may reflect the disproportionately high prevalence of BRCA1 and BRCA2 mutations [5, 6].
\nWestern lifestyle is another most important factor for Britain’s high number of breast cancer cases fuelled by the women overeating, too much drinking and too little exercise doing in routine life. In addition, breastfeeding is also an important factor, which reduces the chance of developing breast cancer. Eastern women do not drink alcohol than women in the United Kingdom, and obesity ratio is much lower in Asian women than in western women, whereas breastfeeding rates are much higher in Asians (http://www.dailymail.co.uk/news/article‐1301445/Western‐lifestyle‐blame‐soaring‐breast‐cancer‐rates.html). Affected women with breast cancer are usually young and often present with advanced disease [7]. According to a World Health Organization (WHO) estimate, around 25.2% people are diagnosed with breast cancer annually. The exact reason why a woman develops breast cancer is still unrevealed; though certain risk factors enhance a person’s probability of getting breast cancer.
\nThe factors that play a significant role in the aetiology of breast cancer include genetic [8, 9], hormonal [10, 11], environmental [12], lifestyle [13] and reproductive factors [14]. In addition, ovarian hormones (endogenous estrogen) are the key risk factors for the development of breast cancer and their progression among post‐menopausal women [15, 16]. However, it is unclear that to what degree the effects of other risk factors may be mediated by their links with circulating free estradiol. Intake of vegetables and fruits are related with a substantial decrease of breast cancer risk [17, 18]. Vegetables are rich in antioxidants and certain phytochemicals may contribute to the reduced risk of breast cancer [19–21]. Plant‐based diets are also high in fibres, which can decrease serum estrogen and could, in this way, contribute to reduced risk of breast cancer [22, 23]. In addition, increased consumption of fruit and vegetables are associated with lower rates of obesity, which is a crucial risk factor for post‐menopausal breast cancer [24]. High energy intake, physical sluggishness, high body mass index (BMI) and weight put on are coupled to an increased breast [25] cancer risk. Low levels of HDL‐C in breast cancer patients than in control subjects have also been documented [26]. But still, data from prospective studies are very limited (Moorman, 1998). Furthermore, consanguineous marriages are common in certain racial groups, which will increases the risk of breast cancer [27].
\nAmong these contributing factors, vitamin D and its receptor gene polymorphisms may play a pivotal role in the development of mammary gland tumourigenesis [28].
\nVitamin D and VDR are the two most important participants playing a key role in vitamin D endocrine system in the prevention of breast cancer. Vitamin D is a sunshine vitamin, which is involved in a variety of actions and also reduces the risk of many cancers [29, 30].
\nVDR is a member of nuclear receptor (NR) superfamily and transcription regulating factor also called NR1I1 or nuclear receptor subfamily 1, group I and member 1. VDR is a high‐affnity, low‐capacity receptor having a molecular weight of about 48–55 kD. VDR is expressed in majority of human tissues. But some cells have decrease or no VDR expression including RBCs, mature cardiac and skeletal muscles and cerebellar Purkinje cells [31]. Its actions are preceded by the formation of heterodimer with retinoid X receptor (RXR), which causes the conformational changes in VDR and allow the binding of vitamin D3 at ligand binding domain (LBD). In addition, the heterodimer complex then binds with a specific sequence present in the DNA called vitamin D response element (VDRE). Genomic pathway involves the expression of genes in a tissue‐specific manner [28].
\nVDR contain five functional domains (Figure 1) including:\n
A and B domains both are shortest domains contain 20 amino acids.
C domain (DNA binding domain or DBD) having two Zn fingers [32] motifs. Two alpha helices are found at the carboxy terminus of each Zn finger (namely helix A and B which constitutes DNA recognition and phosphate binding sites respectively).
Flexible hinge D domain is present in between C and E domains having the ability to change structural conformation after VDR ligand binding.
E domain (ligand binding domain or LBD) consists of 12 alpha helices along with 3 short beta strands, organized in a manner that it forms three dimensional hormone binding pockets of which vitamin D3 is attached.
Both N‐ter and C‐ter has activation function (called AF‐2) in translation [33].
\nGenomic actions: Vitamin D3 produces its pleiotropic effects by genomic and non‐genomic actions. It mediates its genomic actions upon binding to intracellular nuclear transcription factor called VDR.
Non‐genomic actions: Vitamin D also plays various non‐genomic actions. Non‐genomic actions are also called rapid actions, which are caused by the interaction of vitamin D with the membrane VDR to perform its biological effects through intracellular signalling pathways [35]. However, the contribution of non‐genomic pathway in the development of anti‐neoplastic effects on breast remains unclear.
The crystal structure of VDR showing its functional domains [34]. (A) Schematic representation of VDR domains. (B) LBD of the VDR which contains 12 alpha helices. (C) The binding mode of Vitamin D in the hormone‐binding pocket. (D) The DBD of the Vitamin D. The two zinc atoms are represented in blue in colour, whereas beta sheets are represented in yellow colour.
It is already known that vitamin D affects the breast cancer cell growth but limited information is available about its delivery, uptake and metabolism in mammary cells. Vitamin D is either derived from the gastrointestinal (GIT) absorption or synthesized within the skin under the exposure of UVB radiations, which then undergoes the 25‐hydroxylation in liver in presence of 25‐hydroxylase resulting in the production of 25(OH)D3. 25(OH)D3 is the precursor molecule for the synthesis of active Vitamin D3 (1,25(OH)2D3). It is a major circulating form of vitamin D, which is stored in adipose tissues. It is also an accurate biomarker of vitamin D, which determines the overall status of vitamin D in the body. However, the precursor does not readily binds to the VDR and must be converted into its active form, 1,25(OH)2D3, which has high binding affinity to VDR. The conversion of precursor vitamin D into its active metabolite occurs in the presence of 1‐α‐hydroxylases. Immunohistochemistry and in situ hybridization studies indicated strong expression of 1α‐hydroxylase protein and mRNA in the distal convoluted tubule, the cortical and medullary part of the collecting ducts and the papillary epithelia. Lower expression was observed along the thick ascending limb of the loop of Henle and Bowman’s capsule. Weaker and more variable expression of 1α‐hydroxylase protein and mRNA was seen in proximal convoluted tubules, and no expression was observed in glomeruli or vascular structures [36]. Whereas lesser expression of 1α–hydroxylase was also observed in non–renal cells including keratinocytes, macrophages, prostatic epithelium, colonocytes [37, 38] and breast epithelium [39] to lesser extent. Kidneys and non‐renal 1‐α‐hydroxylases are encoded by the same gene mapped on the chromosome 12 [40]. However, the presence of this enzyme on non‐renal tissues indicated that the non‐renal tissues have the ability of vitamin D bio‐activation, responsible to convert 25(OH)D3 into 1,25(OH)2D3. 1,25(OH)2D3 is virtually not detected in human serum under anephric conditions, which means that kidneys are the major source of 1,25(OH)2D3 in circulation. These observations emphasize that 1,25(OH)2D3 produced by the non‐renal tissues is not released in the bloodstream. However, they act locally upon binding to VDR on the same tissues from where it is synthesized. Such local actions of vitamin D are likely included in proliferation, differentiation and apoptosis, which are discussed below in later sections.
\nThe above information supports the hypothesis that two distinct pathways may be involved in the bio‐synthesis and bio‐activation of vitamin D in breast such as 1,25(OH)2D3 and 25(OH)D3 (vitamin D precursor) pathways [41, 42].
\nThe endocrine pathway is involved with the circulation of 1,25(OH)2D3, which reaches the mammary tissues and produces anti‐neoplastic effects through genomic pathway.
\nThe other pathway is the autocrine/paracrine pathway involved with the 25(OH)D3, which reaches the mammary gland and converts into 1,25(OH)2D3 [43] in the presence of 1‐α‐hydroxylase to prevent breast cancer [41]. Most of the extra‐renal tissues of the body have its own 1‐α‐hydroxylase enzyme needed for the production of active metabolite of vitamin D [37]. The circulating level of 25(OH)D3 seems to be the key regulator of tissue‐specific synthesis of active vitamin D [37, 44]. The locally produced active vitamin D binds with VDRs of mammary epithelium in order to regulate the expression of more than 200 genes, which are involved in controlling cell proliferation, inhibit cell growth, stimulate cell differentiation, induce apoptosis and inhibit angiogenesis [45] and contribute in the prevention of breast tumourogenesis [46]. Moreover, mammary epithelial cells also contain 24‐hydroxylase enzyme (CYP24), which converts active vitamin D into less active metabolites including 24,25‐dihydrohydroxyvitamin D3 and 1,24,25‐trihydroxyvitamin D3 [43]. For this reason, we can say that breast tissues contain all the elements of vitamin D signalling axis, which involve in the local synthesis as well as metabolism of vitamin D and its signal transduction through VDRs.
\nSeveral extra‐renal epithelial cells of body express VDR, for example, epithelial cells of rat, mouse and human mammary glands. VDR expression is highest in breast tissues during puberty, pregnancy and lactation in women [47]. In mice, the expression is highest in ductal epithelium when compared to terminal end‐buds epithelium of mammary gland. In human, VDR‐positive cells are found in basal and luminal layer of breast epithelium [39]. Cap cells and stromal compartments of breast are also rich in VDR [48–50]. The presence of VDR in different cells of breast highlights the complexity of vitamin D signalling in breast tissues.
\nDespite these consistent data, the exact mechanism of breast cancer prevention by vitamin D has yet to be discerned. Both 25(OH)D3 and 1,25(OH)2D3 exert its profound effects on normal VDR‐positive breast epithelium such as hormone‐stimulated growth inhibition, ductal elongation, ductal branching and induction of biomarkers involved in breast differentiation. The expression of VDR and 1‐α‐hydroxylase in mammary adipocytes also takes part in the prevention of cancer in whole tissue since adipocytes secrete diffusible signals in response to 25(OH)D3, which constrain morphogenesis of the nearby ductal tissues [48].
\nFurthermore, alteration in cellular energy metabolism, immune responses and other processes of vitamin D signalling in the prevention of breast cancer on non‐tumourigenic breast epithelium is described below.
\nVitamin D causes cell‐cycle arrest by direct or indirect involvement of growth factors and does not allow the cell to enter in the S phase from G1 phase [51]. It increases the expression of cyclin‐dependent kinases (CDKs) inhibitors, including p21 and p27, and reduces the expression of CDK2, CDK4, cyclin D1, cyclin A1 and cyclin E1, which results in the arrest of cell‐cycle progression [52, 53]. It is also involved in the downregulation of c‐myc oncoprotein and inhibits the cell proliferation [54]. However, all these consequences describe that vitamin D hampers the cell proliferation by affecting the crucial controllers of cell‐cycle progression. Furthermore, vitamin D also enhances the transcription factor CCAT enhancer‐binding protein alpha (C/EBPα), which mediates the anti‐proliferative effects of vitamin D observed in in vitro study on MCF‐7 cells [55]. Tumour suppressor TCF‐4 also hinder cell‐cycle progression [56]. Beside these, vitamin D also causes the induction of BRCA 1 (breast cancer 1) gene, which is inversely associated with the cell proliferation, promotes tumour suppression and inhibits cell‐cycle progression [57].
\nVitamin D plays an important role in the induction of apoptosis in mammary tissues, since in vitro conditions, such as shrinkage of cell, condensation of chromatin network and fragmentation of DNA, have been observed in MCF‐7 cells upon treatment with vitamin D [58]. The mechanism by which vitamin D induced apoptosis has not been fully understood. However, the most probable mechanism is the downregulation of anti‐apoptotic protein, called Bcl2 (51). Vitamin D increases the tumour necrotic factor alpha (TNFα) with or without caspase 3 activation. In the caspase 3‐independent mechanism, vitamin D‐mediated induction of apoptosis in MCF‐7 cells is thought to be correlated with mitochondrial disruption, which causes the release of cytochrome C and formation of reactive oxygen species (ROS) resulting in the apoptosis [59]. Other mechanism of caspase‐independent apoptosis induced by vitamin D‐dependent Ca+ absorption is most likely associated with the increased activation of lysosomal proteases [60]. Finally, vitamin D also acts a pro‐oxidant for breast cancer cells, which generally increase the redox potential [61] of carcinogenic cell, may be one of the most important underlying pro‐aptototic mechanisms of vitamin D. The pro‐oxidant action of vitamin D in MCF‐7 cells could result from increased intra‐cellular reactive oxygen species production during aerobic metabolism. Vitamin D inhibits the expression of one of the major constituents of the cellular defence system against ROS, like superoxide dismutase (SOD) [62]. This decrease could be one of the mechanisms underlying the pro‐oxidant action of vitamin D. Indeed, it was previously reported that overexpression of SOD protects MCF‐7 cells from being injured [63, 64] . Decrease in SOD levels would cause a shift in the balance between superoxides and hydrogen peroxide (H2O2). Increased levels of superoxides can, in turn, cause increased oxidative damage attributable to interaction with NO to form the highly toxic peroxynitrite [65] and to increased availability of free iron that supports hydroxyl radical formation through the Fenton reaction [66].
\nChanges in the redox state could translate into reversible oxidation of cysteines in major proteins that determine cell fate, such as protein kinases, protein tyrosine phosphatases and transcription factors (e.g. Sp1, activator protein‐1, nuclear factor‐κB and p53) [67–73]. The key components of the apoptotic process, such as mitochondrial permeability transition pores and increase caspases, are also subjected to redox regulation [74]. Oxidation of the cysteine in the active site of GAPDH may be considered a sensitive, easily accessible marker for these processes. It is noteworthy that the increase in the cellular redox potential was shown to abolish the DNA‐binding ability of the transcription factors activator protein‐1 and nuclear factor‐κB [75] can cause apoptosis and prevent breast cancer. Notably, a recent study describes the relationship between p53 and VDR. Mutant P53 (mutp53) converts the Vitamin D pro‐apoptotic activity into anti‐apoptotic activity and attain oncogenic activity which demonstrate gain of function (GOF) [76].
\nVitamin D inhibits angiogenesis, which is another important feature for tumour growth and progression. It also has the ability to impede angiogenesis at very minute concentration [77] mediated through the downregulation of vascular endothelial growth factor (VEGF), tenascin‐C, tumour growth factor α (TGF‐α) and epidermal growth factor (EGF) [78, 79].
\nVitamin D inhibits the invasion of tumour in nearby tissues but its deficiency promotes the growth of breast cancer cells in the bones of nude mice and alters the bone micro‐environment [80]. This ability of vitamin D is supposed to be caused by the decrease expression of metalloproteinases (MMP‐9) and serine proteinases (such as urokinase‐type plasminogen activator and tissue‐type plasminogen activator) along with the increased expression of their inhibitors [81]. In addition, vitamin D also downregulates P‐cadherin [82] and upregulates E‐cadherin [83].
\nVitamin D reduces the expression of cyclooxygenase‐2 (COX‐2), which plays a crucial role in the synthesis of prostaglandin in many breast cancer cell lines in human. It increases the upregulation of 15‐hydroxyprostaglandin dehydrogenase, an enzyme which is involved in catalysing the conversion of active prostaglandins into biologically inactive ketoderivatives [84]. Prostaglandins have been supposed to play a role in the breast cancer development and its progression [85]. Prostaglandins are secreted by the breast cancer cells or surrounding tissues promote tumour progression caused by cell proliferation, resistant to apoptosis, tumour invasion and angiogenesis [85]. An increased expression of COX‐2 in breast cancer has been assumed to correlate with high‐grade, large tumour size and poor prognosis [86].
\nVitamin D inhibits estrogen biosynthesis (steroidogenesis) and its biological actions [84]. Vitamin D suppresses the estrogen pathway by inhibiting the expression of gene which encodes aromatase (the enzyme which converts androgens to estrogen) [84]. Vitamin D also reduces the expression of estrogen receptor alpha (ERα‐) [87]. The combined actions of vitamin D can decrease the estrogen and the receptor, which mediates their signalling in the prevention of breast cancer.
\nThe half‐life of circulating vitamin D is approximately about 2–3 weeks which is a better indicator of blood vitamin D. Active vitamin D3 (1,25(OH)2D3) is locally synthesized from its precursor (25‐(OH)D3) in almost all body cells because of the universal presence of 1α‐hydroxylases in all cell type including breast [88]. So, the deficiency of 1‐α hydroxylase may augment the deficiency of vitamin D and thereby associated with increased breast cancer risk and mortality [89].
\nSerum vitamin D concentrations and vitamin D supplementations are the independent predictors of breast cancer risk. Serum level of vitamin D of more than 50 ng/ml is associated with the 50% lower risk of breast cancer in women than serum values less than 30 ng/ml [90, 91]. In addition, breast cancer risk reduces in the pre‐menopausal women who consume calcium and vitamin D orally [92]. Locally advanced breast cancer patients have more severe vitamin D deficiency than those with early‐stage disease [93].
\nDeficiency of vitamin D is related with secondary hyperparathyroidism, which causes increased bone resorption, release of calcium from bones osteoclasts into the blood and may exacerbate osteoporosis with subsequent harsh effects on bone mineral density (BMD). In breast cancer patients, osteopenia and osteoporosis mostly occur because of early menopause and vitamin D deficiency, which is then augmented by chemotherapy and hormone replacement therapy [94]. Therefore, breast cancer patients are necessary to suffer a baseline metabolic bone evaluation along with circulating vitamin D levels and bone mineral densitometry [94, 95].
\nVitamin D deficiency is also associated with the recurrence, tumour size and death from breast cancer. It means that having enough amount of vitamin D may be able to keep a cancer from getting worse. In fact a recent meta‐analysis concluded that high circulating level of vitamin D is weakly related with breast cancer incident; however, strong association was found with better breast cancer survival [89]. So, the maintenance of an optimal vitamin D status at the time of diagnosis and during 1‐year follow‐up period is necessary for improving survival of breast cancer patient.
\nThere are four types of studies which illustrated whether exposure of ultraviolet B (UVB) radiations and low levels of vitamin D decrease the risk of breast cancer.
\nIn these studies, the geographical variation in the incidence or mortality of breast cancer is compared statistically with solar UVB radiations. The lower breast cancer incidence rate was found in the regions of high solar UVB radiations such as in Australia, China, France, Nordic countries, Spain and the United States [96].
\nObservational studies do comparison of vitamin D levels with the incidence of breast cancer among cases and controls. There are two categories of observational studies:\n
The studies in which vitamin D levels is measured near the time of breast cancer diagnosis are called case‐control studies.
The studies in which vitamin D is measured at the time of women enrolment in studies prior to the breast cancer diagnosis are called nested case‐control studies.
Only the case‐control studies have reported that low levels of vitamin D are associated with breast cancer risk [97]. The reason why nested case‐control studies have not reported the same results may be due to\n
breast cancer develops very rapidly, and
without supplementation, vitamin D levels tend to change little over time.
Observational studies have also documented that those females have higher vitamin D levels at the time of diagnosis live longer as compared to those with low vitamin D levels [46, 96]. In addition, the chances of mortality are higher in black women after diagnosis of breast cancer than in white women.
\nLaboratory studies have focused on the mechanisms of vitamin D in the contribution of reduced risk of breast and other cancer types. According to these studies, vitamin D allows the cells to stay alive if they are the right type and present at the right place, or it helps the cells to commit suicide (apoptosis) if cells are not the right type or not present at the right place. Vitamin D also reduces the formation of blood vessels around tumours and decreases the ability of tumours to invade [98]. According to the randomized controlled trials, vitamin D reduced the risk of cancer, including breast cancer [99, 100].
\nThe human VDR (hVDR) gene is located at long arm of chromosome 12 bands 13‐14 (12q13‐14) [101, 102]. The gene is 75 kb long and contains 11 exons [103]. This gene is divided into three regions: one coding region and two non‐coding regions.
\nThe 5’ promoter region of VDR lacks initiator (TATA and CAAT boxes) and is rich in GC content. It provides the putative site for binding of many transcription factors [103]. The promoter region is present at exon 1(1a, 1b, 1c, 1d, 1e, 1f). The promoter region facilitates the transcription activity of VDR target gene. The 3’ UTR contains poly (A) repeats, which is reported to be associated with the mRNA stability.
\nCoding region comprises of exon 2–9. Exon 2, which have translation start codons, contains DNA‐binding site, whereas exon 7, 8 and 9 have ligand (vitamin D) binding site [104].
\nPolymorphism is defined as the presence of two or more clearly different phenotypic variants of a particular DNA sequence in the same population of a species. The most common form of polymorphism is the single nucleotide polymorphism in which variation occurs at a single base pair usually present in approximately 1% of the population. These types of changes can be present in non‐coding region of genes and in introns, which would not affect the translation of proteins, but these changes can affect the degree of gene expression and levels of proteins. The changes can also be present in coding regions of DNA or exons resulting in the formation of an altered protein sequence. Sometimes variation in exons do not cause the change in the structure of protein called synonymous polymorphisms.
\nThese changes often produce or eliminate restriction sites for endonuclease to digest the DNA. As a result, fragments of DNA with a different length will be obtained which can be identified by gel electrophoresis. This process is called restriction fragment length polymorphisms (RFLPs). The produced fragments will be the undigested fragments, which is homozygous dominant, whereas the digested fragments are heterozygous and homozygous recessive.
\nSometimes polymorphic alleles are linked with each other and within a population in non‐random proportion is known as linkage disequilibrium (LD), [105] and the combination of alleles (blocks) or set of SNPs present on the same chromosome which tends to be inherited together is termed as haplotype. The size of these blocks is different ranging between 10 and 20 kb and could be important in determining the reason of genetic disorder.
\nThe variation in the 5’‐promoter region of VDR gene can change the sequence of mRNA as well as protein levels, whereas alteration in 3’ UTR sequence can disturb the stability of mRNA thereby affecting the efficacy of translated protein. Some SNPs have been existed in the VDR gene, including Cdx2 [106], Fok1 [107], Bsm1, Taq1, EcoRV [108], Apa1 [101] and poly (A) [109] microsatellite repeats.
\nThe VDR Cdx2 (G‐1739A) is the single nucleotide polymorphism, which was recognized by the sequence analysis of promoter region. It is an adenine to guanine (A to G) SNP situated at the promoter region of VDR gene at exon 1e. It was initially reported to be located at the 3731 bp upstream exon 1a of promoter region of VDR gene among Japanese women [106], but later identified to be located at 1739 kbp upstream of 1e exon just 2 kb away from the exon 1a among many ethnic population [110]. It is the binding region of Cdx2 protein, a most important intestine‐specific caudal‐related homeodomain protein, which increases the transcription of VDR. When A allele is present in Cdx2 promoter, the Cdx2 protein is bound more strongly as compared to when a G allele is present. The A allele stimulates the initiation of transcription, whereas G allele inhibits [106].
\nGATA (A‐1012G) is located at exon 1a in the core sequence of DNA called AGATAT [111]. It provides the binding of GATA protein and the binding site is present in A allele and absent in G allele. The mechanism of this polymorphism is not identified yet; however, this polymorphism alters the immune responses to cancer cells. A allele is responsible to reduce cytotoxic response to cancer cells. In addition, it is also an important element that if the transcription is begun in exon 1a or 1d. In presence of G allele, exon 1d comprises an alternate start codon which results in a formation of N‐ter extended protein called VDRB1. G allele is most likely associated with the VDRB1 (long) protein, whereas A allele is related with the VDRA (short) protein.
\nFok1 polymorphism is also called start codon polymorphism (SCP). It is a thymine to cytosine (ATG to ACG) polymorphism located at the 10 bp upstream 5’ end of exon 2 on the DNA‐binding domain, which results in a formation of more active transcription factor that is three amino acids shorter [103, 112]. Those individuals who have ACG sequence in the start codon, the initiation of translation occurs at the second ATG site which results in a formation of three less amino acids at NH2 terminus containing 424 amino acids. If the initiation occurs at first ATG sequence, it produces full‐length VDR protein containing 427 amino acids. In the presence of restriction site, alleles are designated as ‘f’, whereas its absence is designated as ‘F’ (active form) [113]. The restriction recognition site of Fok1 is 5’‐GGATG*‐3’; 3’‐CCTAC*‐5’ and enzyme cleaves 9/13 nucleotide downstream of the recognition site.
\nMost of the functional sequence variants identified near the 3’ region of VDR gene were Bsm1, Apa1 and Taq1 SNP. These SNPs are in linkage disequilibrium with each other and are located in the same haplotype block. Therefore, these SNPs may have the potential to influence the mRNA stability. The Apa1 and Bsm1 are located at intron 8, whereas Taq1 is located at exon 9 [114].
\nThe presence of restriction enzyme site in these SNPs is designated as lower case letter such as b, a and t, whereas absence is designated as upper case letter including B, A, T. The restriction site for Bsm1 is 5’‐GAATGCN*‐3’, Apa1 is 5’‐GGGCC*C‐3’ and Taq1 is 5’‐T*CGA‐3’.
\nPoly (A) tail is a variable number of tandem repeats (VNTR) or short tandem repeats (STR) containing variable numbers of adenine nucleotide present at the 3’ UTR of VDR. Poly (A) is also linked with Bsm1, Apa1 and Taq1 polymorphisms and also involved in the mRNA stability of VDR. It varies in length and can be divided into two types:\n
The long (L) Poly (A) sequence in which 18–24 adenine nucleotide is present, and
The short (S) Poly (A) sequence in which 13–17 adenine nucleotide is present.
Because all four polymorphisms (Bsm1, Apa1, Taq1 and Poly (A)) are present in close proximity on the VDR gene, strong linkage disequilibrium exists among them. The two most common haplotypes are:\n
baTL haplotype in which Bsm1 and Apa1 restriction sites are present, whereas Taq1 site is absent along with the presence of long Poly (A) repeats.
BAtS haplotype Bsm1 and Apa1 restriction sites are absent, whereas Taq1 site is absent along with the presence of short Poly (A) repeats [115].
The baTL haplotype is reported to be associated with the increase incidence of breast cancer [116].
\nVDR gene polymorphism is associated with the breast cancer risk [117–125] but insufficient data are available to find the relationship with breast cancer risk [126]. The studies have pointed out allelic variations in VDR gene, such as Cdx2, Fok1, Bsm1, Taq1, Apa1 and Poly A in different ethnic groups with breast cancer incidence with contradictory results [117, 118, 121, 126].
\nThe contradictory observations were reported on the association of Cdx2 polymorphism and breast cancer susceptibility [125]. Recently, a meta‐analysis has documented that Cdx2 polymorphism is linked with breast cancer susceptibility only in Africans [127]. However, no profound relations was observed between Cdx2 polymorphism and breast cancer risk among Pakistani population [126].
\nFok1 polymorphism contain large consensus sequence has no relationship with breast cancer incidence [116, 117]. But the association between Fok1 polymorphism and breast cancer was reported in several ethnic groups [113, 120], mainly in Caucasians [128, 129]. Nemenqani et al. [121] found that Fok1 polymorphism is associated with the ER and PR status of breast cancer and described that Fok1 polymorphism has a significant interaction with the ER status but not with PR status of breast cancer.
\nBsm1 polymorphism is the most important functional VDR gene polymorphism, which is found to be associated with the risk of developing breast cancer [124]. However, it has also been documented that there is no relation between Bsm1 and breast cancer [119]. Rollison et al. [123] describe that Bsm1 is involved to alter the vitamin D intake and overall breast cancer risk. McCullough et al. [130] found that B allele of Bsm1 decreases breast cancer incidence by 20%.
\nMany case‐control studies suggested that Taq1 polymorphism is not associated with breast cancer risk [119–121]. But it has been reported that Taq1 is one of the functional polymorphisms which is linked with increased breast cancer incidence [131, 132]. A meta‐analysis on large ethnic groups revealed that the Taq1 polymorphism increases the risk of breast cancer development in Caucasians; however, no profound association was observed among Asians [133].
\nThis chapter concluded that women with breast cancer are more likely to have low vitamin D levels. Those women who do not get adequate vitamin D may be more likely to develop breast cancer later in life as compared to those who have higher vitamin D levels, who are less likely to develop breast cancer and less likely to die from breast cancer.
\nBecause of the broad spectrum of vitamin D effects on mammary tissue, it is suggested to be a most important physiological growth regulator of mammary gland and could be a potential therapeutic agent. Additionally, due to the expression of VDR to a higher extent on breast epithelial cells, vitamin D signalling should also be monitored during breast cancer treatment. Since breast cancer is a complex disease which may or may not be associated with the decreased vitamin D levels or VDR polymorphisms. However, the functions and role of vitamin D and VDR cannot be neglected during breast cancer treatment.
\nThe Internet of Things (IoT) connects a multiplicity of devices to make life convenient. Smart grids constitute one implementation of IoT, and many countries have launched smart grids to develop integrated energy supply systems. A smart grid incorporates automation, bidirectional communication, and advanced sensor measurement systems to streamline interactions between the client and power supplier [1, 2, 3, 4]. In contrast to traditional grids, smart grids enable power suppliers to distribute power efficiently and to control the use of power during a given period [5]. Furthermore, the data collected from a smart grid enable automatic billing.
The analysis of energy consumption data has many advantages for both consumers and suppliers: Consumers can track their energy usage, particularly as it varies with the seasons. Power suppliers can monitor how power is utilized across the distribution grid, which can help them formulate power management and energy-saving measures [6, 7, 8]. The establishment of advanced metering infrastructure (AMI) constitutes the first step to constructing such an intelligent power gird.
AMI is central to a smart grid system and enables the system to automatically monitor usage. Figure 1 illustrates the architecture of a typical AMI, indicating that it comprises several concentrators and smart meters that are connected to a meter data management system (MDMS) [9]. The smart meters send data to the concentrators, and the concentrators send the data to the MDMS. The AMI architecture requires high-quality and high-speed networks for providing stable service and efficient monitoring, and it comprises two such networks, namely a local area network (LAN) and wide area network (WAN). The LAN connects the concentrators and smart meters and leverages cutting-edge communication technologies such as power-line communication and the Zigbee specification. The WAN connects the concentrators and MDMS and constitutes the most important part of the AMI system; this network supports a host of high-speed technologies such as broadband-over-power-line technology, 3G, and long-term evolution [10].
AMI structure.
Nonetheless, smart meters have a very large data frequency—with a small packet being generated every 15–60 min—that will exceed the capacity of existing communication technologies [11, 12]; this makes data difficult to transmit. Furthermore, smart grids face challenges in storing these large volumes of data. To solve these two problems, data size in both communication and storage should be reduced. This chapter introduces some novel approaches to doing so.
Smart grids have expanded considerably, and many organizations have noticed the advantages engendered by smart meters. Thus, research on smart grids has similarly expanded. Specifically, smart grids enable the automatic distribution of power on the part of suppliers and provide usage data, which can be used to develop various applications.
Smart meters constantly upload data to the MDMS. Such data pertain to, for example, interval data readings, meter remote disconnections, meter remote reconnections, and meter firmware patches. The volume of such data is considerably large, potentially causing network collapse. The reduction of packet size in a smart grid addresses this problem, and such a reduction has become a major topic of research. Thus, this section introduces some basic strategies that are currently adopted to solve this problem.
Among existing methods, the conventional approach is combining the messages sent by multiple meters to reduce either protocol overhead or the frequency of transmission. In this approach of message concatenation, energy consumption data, control signal messages, and firmware update packages are combined. This scheme entails a lower transmission volume because the packet header is reduced, where multiple messages can be sent in a header. However, one issue in this scheme is where messages ought to be concatenated.
Message concatenation at the meter side results in a greater reduction in data size than does that at the concentrator side. Data size reduction is greater at the meter side primarily because a meter generates data within a certain period; thus, a longer interval between instances of meter-to-concentrator data transmission yields disproportionately large savings in data size. However, most meters contain low-performance hardware, hampering this method. Consequently, meters are either overloaded or unable to compress the data.
Messages can also be concatenated at the concentrator side prior to transmission. This is the appropriate site for message concatenation [13, 14] because concentrators have more powerful hardware and process data more efficiently than meters do. In concentrator-side concatenation, meters send packages to the concentrator, the concentrator subsequently aggregates the data into one package, and the compressed message is finally sent to the MDMS. Concentrator-side concatenation not only reduces the volume of messages but also stabilizes the system.
However, despite the advantages of concentrator-side concatenation, existing devices on the market are incapable of supporting such concatenation. Currently, concentrators on the market are capable of executing only simple integrations, and these products all follow the PRIME standard of WAN communication [15].
A message generated by a smart meter contains a 40–60-B header within the packet. Concentrators can collect messages sent from the meter side according to a Poisson process [16] before combining these messages to minimize possible traffic. The aforementioned procedure comprises two steps, namely combination and compaction, which are detailed as follows [17].
Combination entails combining messages into a larger packet to solve the problem of protocol overhead during communication. Figure 2 illustrates how such combination reduces traffic. Combining meter messages on smart grids is efficient because each piece of data generated by a meter have a size of only a few bytes. Concentrators combine messages that have been sent by meters in a specified period, after which they compact the messages.
Concept underlying the combination procedure.
Figure 3 illustrates the operating procedures of a typical combination algorithm. Specifically, the concentrators receive meter messages, place the messages into a combination queue, combine the messages in the queue once some predetermined quantity of messages have been accumulated, and finally compact the messages into a package [17]. This method enables solving the protocol overhead problem. The data compaction scheme is detailed as follows.
Combination procedure.
Compaction reduces the size of headers in large-scale AMI architecture, which is very helpful for reducing data volume. Messages can be compacted through either full compaction (FC) or loose compaction (LC) [17].
Figure 4 illustrates the operating procedures of an FC algorithm. Specifically, any piece of data received from the meter is stored in
FC procedure.
To illustrate the FC procedure, Table 1 lists some energy usage values in an area. First, all values are input into
Meter Number | Previous Usage | Current Usage | Difference |
---|---|---|---|
1 | 2153.232 | 2366.112 | 212.880 |
2 | 5698.564 | 6022.333 | 323.769 |
3 | 23154.003 | 23542.115 | 388.112 |
4 | 1542.121 | 1588.236 | 46.115 |
5 | 56213.225 | 56823.987 | 610.762 |
Example meter data from an area.
An Example of meter data.
LC differs from FC in that LC is recoverable, whereas FC is not. Figure 5 illustrates operating procedures of an LC algorithm. First, the concentrators obtain meter data by dequeuing
LC flow.
To illustrate the LC procedure, consider the values in Table 1. First, the LC algorithm takes the difference between past and present usages and inputs these differences into
After compacting the data, the concentrators send the data to the MDMS. When the MDMS receives the data, it executes the LC recovery (LCR) algorithm to extract the raw data. Figure 6 illustrates the LCR algorithm, which is the reverse of the LC algorithm. First, the LCR algorithm inputs the received data into
LC recovery procedure.
Consider the values for the example presented in Table 1. First, the LCR algorithm recovers the compacted data; specifically, the MDMS inputs [46.112, 166.768, 110.889, 64.343, 222.650] into
First of all, all of messages sent from meters were encoded in ASCII. FC and LC compaction performance are provided in this section. The Figure 7 shows the compression ratio of the FC and LC method. The vertical scale label present the total bytes used before compaction and the horizontal scale label is the number of meter messages compacted when compaction. As the Figure 7 shows, FC has better performance than LC. However, FC does not support recovery, so it can achieve the highly compaction ratio. On the contrary, LC is the trade-off algorithm when recovery function is required and have demand of compression. If the system only need the sum of the energy usage, then FC would be the proper way for compressing the data.
FC and LC analysis.
The choice of compression algorithm has become a critical issue because most IoT devices have hardware limitations, particularly in their low-power-consumption microprocessors. The best compression algorithm provides the best compression ratio given the hardware specifications of an IoT device [18, 19]. This section discusses two well-known approaches to data compression [20].
The Lempel–Ziv–Markov chain algorithm (LZMA) is a member of the LZ-family, and it is based on the LZ77 algorithm, which uses a dictionary-based scheme. The LZMA yields excellent compression ratios without being demanding on hardware, making it suited to IoT environments by virtue of its exclusive dictionary structure [19].
Prediction by partial matching (PPM) can predict a subsequent pattern using present or previous symbols. Moreover, PPM can be used with a Markov model to construct a compression algorithm. For example, the RAR algorithm, developed by Eugene Roshal and Alexander Roshal, uses PPM and the Lempel–Ziv–Storer–Szymanski algorithm to achieve impressive compression [20].
Smart grids will be key infrastructure considering the rapid developments in IoT technology. This chapter presents data compression techniques, such as combination and compaction, developed for reducing the communication data load in a smart grid. These techniques not only reduce the frequency between instances of transmission but also considerably reduce data volume. Moreover, FC and LC can be used in different situation. FC provides extremely compact ratio for the user who have less bandwidth for transport the meter data. LC can be used when the system requires the raw data of the energy usage and having sufficient network bandwidth. In addition, some well known data compression techniques are also introduce in the chapter. Proposed algorithm can be implement with the compression technique provided above to decrease the volume of the meter data. Also, this chapter explains recent advances in smart grid technology. Readers can build on the aforementioned algorithms to formulate novel contributions of their own.
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