Current therapeutic targets for arthritis and their effect on neutrophils.
\r\n\tThis book will aim at serving as a complete and updated reference for a broad audience, including, students, orthotics, optometrist and ophthalmologist. The book will describe in detail general myopia features as well the most recent diagnostic techniques (e.g. OCT and visual field) which occupy a more and more relevant position in early myopia complications detection. It will explore the connection between myopia and other, popular disorders such as glaucoma, choroidal neovascularization, and retinal detachment: highly myopic eyes tend to have a retina and choroid thinner than normal and, then, the assessment of myopic eyes is far from being a simple task even with the most advanced imaging techniques. In the light of such observations, the book will give a special mention to pharmacological and surgical treatments currently available along with rehabilitation procedures and optical devices.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"41ca0f616bfa2745783b652b87ebedc3",bookSignature:"Prof. Felicia M. Ferreri",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/8705.jpg",keywords:"Myopia of prematurity, Retinal detachment, Intraocular pressure, Myopia and glaucoma, Myopic macular degeneration, Ocular motility,Visual rehabilitation, Clinical treatment, Retinal sensitivity, Visual Electrophysiology response, Visual Field, Ultrasonic Biometry",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 3rd 2018",dateEndSecondStepPublish:"December 24th 2018",dateEndThirdStepPublish:"February 22nd 2019",dateEndFourthStepPublish:"May 13th 2019",dateEndFifthStepPublish:"July 12th 2019",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"32442",title:"Prof.",name:"Felicia M.",middleName:null,surname:"Ferreri",slug:"felicia-m.-ferreri",fullName:"Felicia M. Ferreri",profilePictureURL:"https://mts.intechopen.com/storage/users/32442/images/system/32442.png",biography:"Felicia M. Ferreri graduated summa cum laude from University of Messina, Italy in 1998 and completed her ophthalmology residency at the Policlinico Universitario, Messina in 2002. She was interned at San Raffaele Hospital in Milan (Corneal Section) and at Hospital Careggi in Florence (pediatric ophthalmology diseases). She spent research periods in Seville ('Virginio del Rocio' hospital), Madrid ('San Carlos' hospital), Manchester ('The 'Bolton Hospital') and Rio de Janiero (Universidade Fluminense).\r\nShe served as co-investigator for many national and international clinical trials. Since 2002, she is an Assistant Professor in Ophthalmology at the University of Messina. Her research interests are in the areas of glaucoma, neuro-ophthalmology, pediatric ophthalmology, and cataract. She authored more than 50 scientific papers.",institutionString:"University of Messina",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of Messina",institutionURL:null,country:{name:"Italy"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"191",title:"Ophthalmology",slug:"medicine-ophthalmology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"280415",firstName:"Josip",lastName:"Knapic",middleName:null,title:"Mr.",imageUrl:"https://mts.intechopen.com/storage/users/280415/images/8050_n.jpg",email:"josip@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copy-editing and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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by",editors:[{id:"157235",title:"Dr.",name:"Artashes",surname:"Zilfyan",slug:"artashes-zilfyan",fullName:"Artashes Zilfyan"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"55356",title:"Neutrophils in Rheumatoid Arthritis: A Target for Discovering New Therapies Based on Natural Products",doi:"10.5772/intechopen.68617",slug:"neutrophils-in-rheumatoid-arthritis-a-target-for-discovering-new-therapies-based-on-natural-products",body:'\nArthritis is an inflammatory joint disorder that can cause edema, pain, and loss of function. The most common types of arthritis are osteoarthritis, gout, and rheumatoid arthritis [1, 2]. Rheumatoid arthritis is a systemic, autoimmune disorder with an important inflammatory component in which genetic and environmental risk factors contribute to disease development. Its prevalence in the world population is between 0.3 and 1%, and it affects three times more women than men [3, 4].
\nThe pathophysiology of RA is complex and appears to be initiated when the adaptive immune system (cellular or humoral) recognizes self-joint antigens as non-self, which triggers a variety of distinct inflammatory effector mechanisms, including the recruitment of leukocytes [5–8].
\nRA is characterized by intense inflammatory processes and joint damage that are mediated by the influx of immune system cells to the synovial space such as neutrophils, macrophages, and lymphocytes [1, 2]. A critical factor that contributes to tissue damage is the excessive production of inflammatory mediators by resident and/or infiltrated cells. Among the primary mediators involved in joint damage are free radicals, enzymes that degrade the matrix, and pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, as well as chemokines such as CXCL-8, lipid mediators, such as leukotriene B4 (LTB4) [9, 10], and endothelin (ET) [11, 12]. Inflamed synovial tissue is invasive and called pannus, which can be formed by synovial cell proliferation, angiogenesis, and the accumulation of macrophages, lymphocytes, and neutrophils [13].
\nNeutrophils are crucial cells that have significant roles in diverse inflammatory diseases, including acute, chronic, autoimmune, infectious, and non-infectious conditions [14]. The most well-known effector function of neutrophils is their role in innate immunity. However, recent studies have identified neutrophils as active cells during adaptive immunity, facilitating the recruitment and activation of antigen-presenting cells or directly interacting with T cells. Neutrophils are the most abundant leukocytes in inflamed joints, and the importance of these cells in the initiation and progression of human RA as well as in murine models has been demonstrated [15–18]. Therefore, neutrophils play an essential role in joint inflammation, and the modulation of neutrophil functions is considered a potential target for pharmacological intervention in arthritis [19–21].
\nThe pharmacologic treatment options for arthritis are diverse. The current treatments are mostly symptomatic and include non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, disease-modifying antirheumatic drugs (DMARDs), and biologic therapies. High costs and an increased risk of malignancies limit the use of these agents, in addition to the potential side effects that all therapies possess. Plant-derived products, such as polyphenols, sesquiterpenes, flavonoids, and tetranortriterpenoids, which are herbal metabolites with anti-inflammatory activity, may provide new therapeutic agents and cost-effective treatments [22, 23]. This chapter focuses on the role of neutrophils in the pathogenesis of arthritis and the action of substances from natural products as putative antirheumatic therapies.
\nNeutrophil recruitment is an important stage in the inflammatory development process, including autoimmune diseases such as RA. Among the circulating cells, neutrophils are the first ones to reach the synovium and are the most abundant cells in the synovial fluid [24]. In this section, we discuss the cascade of events that culminates in neutrophil entry into inflamed joints. The leukocyte recruitment cascade involves the following commonly recognized steps: capture, rolling, firm adhesion, and finally transendothelial migration.
\nNeutrophil release from the bone marrow to the circulating blood occurs immediately after the first signal of inflammation, serving to increase the number of neutrophils available for recruitment into the tissue in response to inflammation [25]. The mobilization of neutrophils from the bone marrow is orchestrated by the hematopoietic cytokine granulocyte colony-stimulating factor (G-CSF). G-CSF mobilizes neutrophils indirectly by shifting the balance between CXCR4 and CXCR2 ligands [26]. In response to the release of inflammatory mediators such as TNF-α and IL-17, the adjacent vascular endothelium becomes activated. Cell surface proteins of the selectin family termed E- and P-selectin and their ligands (L-selectin) mediate this initial neutrophil capture. Neutrophil rolling through the endothelium facilitates their contact with chemotactic factors that promotes neutrophil activation [27]. Chemokines (CXCR-1 or 2 ligands, such as IL-8), the C5a fragment of the complement system, and leukotriene B4 (LTB4) are responsible for neutrophil mobilization to the synovial fluid [28–30].
\nFirm adhesion is mediated by interactions between β2 integrins (LFA-1, CD11a/CD18, and MAC-1, CD11b/CD18) and their ligand (ICAM-1). Integrins are usually in an inactive state on neutrophil and become activated after the triggering of G protein-coupled receptors such as chemokine receptors [31]. The binding of integrins to their ligands activates signaling pathways in neutrophils stabilizing adhesion and initiating cell motility [32, 33]. This signaling also regulates actin polymerization, which controls the direction of neutrophil movement [34, 35]. The final stage in the adhesion cascade is the ultimate migration of the neutrophil from the vasculature into the inflamed tissue. Passage through the endothelial cell layer occurs both paracellularly (between endothelial cells) and by a transcellular route (over the endothelial cell). Paracellular migration of neutrophils is mediated by binding to endothelial proteins that target neutrophils to intercellular junctions and facilitate their passage through them. To reach the inflamed joint, neutrophils must pass over the basal membrane, which occurs through the degradation of extracellular matrix molecules by proteases stored inside the cells, such as matrix metalloproteinases (MMPs) and serine proteases [14].
\nIn inflammatory foci, neutrophils find immune complexes on the synovium that bind to Fcγ receptors on the neutrophil membrane, triggering their degranulation and reactive oxygen species (ROS) production [36]. In RA pathology, oxidative stress is a result of inadequate ROS release by neutrophils [37]. Oxygen radicals cause DNA damage and oxidation of lipids, proteins, and lipoproteins and may be involved in immunoglobulin mutations that lead to rheumatoid factor (RF) formation [38, 39]. Moreover, proteins from neutrophil degranulation are found at high concentrations in the RA synovial fluid and could be responsible for cartilage and tissue damage, activation of cytokines and soluble receptors, inhibition of chondrocyte proliferation and activation of synoviocytes proliferation and invasion [40–43]. In addition, activated neutrophils also generate chemoattractants (such as IL-8 and LTB4) that promote further neutrophil recruitment and amplify the inflammatory response (see Figure 1).
\nOverview of the role of neutrophils in arthritis. Neutrophils leave blood vessels after chemotactic signals from inflamed tissues that promote the firm adhesion of neutrophils to endothelial cells mediated by adhesion molecules, which induce neutrophil activation and actin filament formation followed by transendothelial migration toward the inflammatory foci. Immune complexes and proinflammatory molecules activate neutrophils, which then produce ROS and release enzymes responsible for cartilage destruction. Activated neutrophils communicate with other cells of the immune system through the secretion of cytokines and chemokines and by antigen presentation in conjunction with MHC class II. Neutrophils can undergo a special form of cell death called NETosis. This results in the release of a complex of nuclear and granule molecules called NETs contributing to tissue damage. Activated neutrophils also generate chemoattractants (such as IL-8 and LTB4), forming a positive-feedback loop that promotes further neutrophil recruitment and amplifies the acute inflammatory response. Finally, effective neutrophil apoptosis is required for the resolution of inflammation. However, delayed neutrophil apoptosis occurs in the inflamed joint, which results in persistent inflammation and tissue damage due to the continued release of ROS, granule enzymes, and cytokines.
Neutrophils are key cells in articular inflammation that are abundant in the synovial fluid and pannus of patients with active RA [44], a typical knee joint may have 2 × 109 cells, of which 90% are neutrophils [24]. These cells are mobilized to synovial tissue by chemoattractant mediators, such as CXCL1, CXCL2, endothelin (ET)-1, and leukotriene B4, a process in which resident macrophages play a central role [11, 45, 46].
\nFor many years, the major contribution of neutrophils to the pathology of RA was thought to be their cytotoxic potential, since neutrophils participate in the pathogenesis of arthritis by promoting the inflammatory process and cartilage degradation, as well as bone resorption. However, neutrophils are now recognized to have an active role in orchestrating the progression of inflammation through regulating the functions of other immune cells [47, 48], and current research has shown that these cells are involved in RA onset [49, 50].
\nIn the synovial cavity, activated neutrophils exhibit an increased expression of plasma membrane receptors such as major histocompatibility complex (MHC) class II molecules and present antigens to T lymphocytes, an immune function that they share with macrophages and dendritic cells (DCs) [51]. In addition, the interaction of neutrophils with other cells induces the secretion of MMP-8 and MMP-9, and a repertoire of cytokines (IL-1β, IL-12, IL-18, IL-23, and TNF-α) and chemokines (CCL-2, CCL-4, CCL-5, and CXCL-8), including TNF ligand superfamily member (RANKL) [52, 53] and TNFSF13B (also known as BLyS or BAFF) [54], which are implicated in the activation of osteoclasts and B lymphocytes, respectively, regulate the function of other immune cells [48, 55–57].
\nNeutrophils from patients with RA are functionally very different from those isolated from healthy individuals. RA blood neutrophils are already primed for ROS production [58] and striking differences in gene and protein expression exist between peripheral blood neutrophils from patients with RA and their healthy counterparts [18], including higher levels of membrane-expressed TNF and myeloblastin (also known as PR-3 or cANCA antigen) in RA [59].
\nIn RA patients, neutrophils can be activated by immune complexes, such as RF or anti-citrullinated protein antibodies (ACPAs), both within the synovial fluid and deposited on the articular cartilage surface [60]. These complexes engage Fcγ receptors and thereby trigger neutrophil activation, which release ROS and RNS [61, 62], collagenases, gelatinases, neutrophil myeloperoxidase (MPO), elastase, and cathepsin G into the synovial fluid and joints [14, 55, 56, 63] due to frustrated phagocytosis [60].
\nOne of the most prevalent symptoms of RA is the increase in sensitivity to joint pain (hyperalgesia), which causes movement limitations. Despite its clinical relevance, strategies for the treatment of arthralgia remain limited. In animal models, hyperalgesia (inflammatory pain) is defined as hypernociception (a decreased nociceptive threshold) [64]. It is broadly accepted that articular hypernociception results mainly from the direct and indirect effects of inflammatory mediators on the sensitization (increased excitability) of primary nociceptive fibers that innervate the inflamed joints [65–67]. Prostaglandins and sympathetic amines are the key mediators of this process. Furthermore, other mediators, such as the cytokines TNF-α, IL-1β, IL-6, and IL-17 play a crucial role in the pathogenesis of arthritis, increasing the recruitment of neutrophils into the joint and driving the enhanced production of chemokines and degradative enzymes [68–70]. In addition, endothelin-1 (ET-1), acting directly or indirectly, also sensitizes primary nociceptive neurons [71–74].
\nDuring the inflammatory process, the migrating neutrophils participate in the cascade of events leading to mechanical hypernociception, by mediating the release of hyperalgesic molecules (such as MPO, MMPs, hypochlorite, superoxide anion, and PGE2) capable of activating nociceptive neurons and causing pain [17, 75–78].
\nIndeed, decreased inflammation and joint destruction have been directly correlated with reduced neutrophil influx into the joints, as observed in mouse models by means of antibody blockade or the gene deletion of chemoattractant receptors such as CXCR1, CXCR2, and BLT1 (LTB4 receptor) [15, 79]. Therefore, the blockade of neutrophil migration could be a target in the development of new analgesic drugs [77].
\nCitrullination is the natural posttranslational conversion of arginine to citrulline mediated by peptidyl arginine deiminases (PADs), enzymes present in macrophages, dendritic cells, and neutrophils. Experimental evidence indicates that citrullination is involved in the breakdown of immune tolerance and may generate neoantigens (neoAgs) that become additional targets during epitope spreading [80]. Citrullinated residues stimulate the production of anti-citrullinated protein antibodies (ACPAs) in predisposed individuals. It has been observed that ACPAs can be present for several years before any clinical signs of arthritis appear [81–83]. A substantial increase in the number and titer of many antibodies against posttranslationally modified proteins is also seen shortly before the onset of arthritis. Citrullinated Ags have increased immunogenicity and arthritogenicity, and their presence in arthritic joints correlates with disease severity [80, 84–86].
\nOsteoclasts are dependent on citrullinating enzymes for their normal maturation and display citrullinated antigens on their cell surface in a non-inflamed state. In humans, the binding of ACPAs to osteoclasts in the bone compartment induces IL-8 secretion. In turn, IL-8 sensitizes and/or activates sensory neurons by binding to CXC chemokine receptor (CXCR) 1 and CXCR2 on peripheral nociceptors [87–90], producing IL 8 dependent joint pain that is associated with ACPA-mediated bone loss.
\nIL-8 release contributes to the chemoattraction of neutrophils [49], which play critical roles in initiating and maintaining joint-inflammatory processes that have been described in experimental arthritis [36, 91]. However, the exact roles that neutrophils play in the posttranslational modification of proteins and disease initiation and progression in RA remain unclear. Recent evidence suggests that, among the various mechanisms by which neutrophils cause tissue damage and promote autoimmunity, aberrant formation of neutrophil extracellular traps (NETs) could play important roles in the pathogenesis of RA [50].
\nNETs are released during a process of cellular death named NETosis. NETosis occurs with neutrophils upon contact with bacteria, fungi [92], or under several inflammatory stimuli. This process is associated with changes in the morphology of the cells, which eventually lead to cell death with extrusion of NETs [93, 94]. This process requires calcium mobilization, reactive oxygen species (ROS) produced by NADPH oxidase, neutrophil chromatin decondensation mediated by neutrophil elastase (NE) and myeloperoxidase (MPO), and chromatin modification via the citrullination of histones by peptidyl arginine deiminase 4 (PAD4) [95–99]. NETs are a network of extracellular fibers, which contain nuclear compounds as DNA and histones and that are covered with antimicrobial enzymes and granular components, such as MPO, NE, cathepsin G, and other microbicidal peptides [93, 94]. In the extracellular environment, NET fibers entrap microorganisms, and their enzymes and granular substances reach locally high concentrations and are thus able to cleave virulence factors and kill microorganisms [95, 100, 101].
\nAlthough NETs play a key role in the defense against pathogens, they may cause undesirable effects to the host, which has increased the interest in the role of neutrophils and NETs in autoimmunity. Augmented NET formation was first described in preeclampsia and ANCA-associated vasculitis and followed by the description in a series of autoimmune conditions, including psoriasis, systemic lupus erythematosus (SLE), antiphospholipid antibody syndrome (APS), and RA [50, 100, 102–105]. Neutrophil extracellular traps are an obvious source of nuclear material. Among these are a range of cytoplasmic and extracellular citrullinated antigens, well-established targets of the ACPAs found in RA [50, 100]. The protein contents of NETs not only serve as targets for autoantibody and immune complex formation but also induce further NETosis, resulting in a harmful positive-feedback loop. These factors form an inflammatory microenvironment that may trigger a strong autoimmune response in individuals with the corresponding susceptibility [106, 107]. Pro-inflammatory cytokines, such as TNF-α and IL-17, as well as autoantibodies stimulate the formation of NETs and affect their protein composition [50]. Additionally, NETs have been shown to stimulate autoimmunity via the production of interferons and activation of the complement cascade. Interferons activate both the innate and adaptive immune systems, inducing a Th1 immune response and stimulating B cells toward the generation of autoantibodies [108]. The deposition of NETs observed in various inflammatory pathologies is associated with the circulating cell-free DNA (cfDNA) levels in biological fluids, such as plasma and serum, from patients [100, 101, 109]. Therefore, circulatory cfDNA could eventually be utilized as a marker of NETs in these pathologies, while the determination of the DNA levels might facilitate the monitoring of disease activity and assessment of the effectiveness of a selected therapeutic strategy.
\nNeutrophils have been traditionally viewed as short-lived cells that die at sites of inflammation; however, some evidence suggests that they can prolong their life span upon specific stimuli and transmigrate away from inflammatory loci [48, 110, 111]. Conditions within the synovial joint, such as hypoxia [112] and the presence of antiapoptotic cytokines (including TNF, granulocyte-macrophage colony-stimulating factor (GM CSF), and IL 8) [113, 114], can increase neutrophil survival for up to several days [115, 116], which contributes to enhanced tissue damage.
\nAs described above, neutrophils play an essential role on innate and adaptive immunity in RA physiopathology, contributing to tissue lesions in RA, and therefore represent a promising pharmacological target in RA. Pharmacological strategies that inhibit or reduce neutrophil mobilization or activation could be successful in RA treatment.
\nAnimal models have been extensively used in studies of RA pathogenesis. Despite the inherent limitations of all animal models, several rodent models have greatly contributed to the overall knowledge of important processes/mediators in the generation of inflammation, cartilage destruction, and bone resorption. In addition, the pharmaceutical industry has used these models for testing potential anti-arthritic agents, leading to important advances in therapeutic interventions for this destructive disease [117]. Such models include collagen-induced arthritis, collagen antibody-induced arthritis, zymosan-induced arthritis, the methylated BSA model, and genetically manipulated or spontaneous arthritis models such as the TNF-α-transgenic mouse, K/BxN mouse, and Skg mouse [118]. Many of these models show that neutrophils are the first immune cells to enter the arthritic joint, and that early measures of joint inflammation correlate with neutrophil infiltration [45, 119, 120]. In this section, we highlight pharmacological approaches targeting neutrophil recruitment and activity, which present a therapeutic benefit to patients with RA.
\nThe current treatments available to RA patients include glucocorticoids, non-steroidal anti-inflammatory drugs, and disease-modifying antirheumatic drugs. Only disease-modifying agents—and to some extent glucocorticoids—can impede or halt the inflammatory and destructive disease processes [121]. With a more complete understanding of the immune-inflammatory events that occur in the pathogenesis of RA, scientists have developed therapeutic strategies that include monoclonal antibodies and receptor constructs, which target specific soluble or cell-surface molecules of interest. Biological agents such as monoclonal antibodies and recombinant proteins that target TNF-α, CD20, CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), and the IL-1 receptor as well as therapies based on the blockade of T-cell and B-cell functions have shown efficacy in controlling the physical signs and pain associated with RA [122, 123].
\nMany interventions used to treat RA exert inhibitory effects on neutrophil responses in inflammation. However, non-steroid anti-inflammatory drugs (NSAIDS), DMARDs, and biologics do not specifically target neutrophil function [124].
\nMost NSAIDs inhibit the action of the cyclo-oxygenase-1 and -2 (COX-1 and -2) enzymes, which metabolize arachidonic acid into inflammatory mediators of the prostaglandin family. NSAIDs have been shown to inhibit neutrophil adherence, decrease degranulation and oxidant production, inhibit neutrophil elastase activity, and induce neutrophil apoptosis [125–127]. Corticosteroids induce anti-inflammatory signals by several mechanisms; a major one may be to reduce the expression of cytokine-induced genes. They enter all cells and bind to the cytoplasmic steroid receptor, and then this complex translocates to the nucleus where it is recognized by specific DNA sequences. The major effect of binding to DNA is the suppression of transcription by opposing the activation of the transcription factors AP-1 and NF-κB [128]. Corticosteroids have been shown to inhibit neutrophil degranulation and ROS production, decrease production of inflammatory mediators, and prevent neutrophil adhesion and migration into RA joints [44, 129–131]. The most widely used DMARD in clinic settings is methotrexate, a compound that blocks folic acid metabolism. Its benefits in RA include the stimulation of neutrophil apoptosis [116], inhibition of the NF-κB pathway [132], and reduced adhesion molecule expression and LTB4 production [133], consequently decreasing neutrophil recruitment and ROS production [134].
\nAnti-TNF-α therapies are also widely used for the treatment of RA patients. TNF primes the neutrophil respiratory burst, upregulates the expression of adhesion molecules, cytokines and chemokines, and at high local concentrations can stimulate ROS production in adherent neutrophils [135–138]. Three different TNF inhibitors are available for RA patients who fail to respond adequately to standard DMARD therapy. Infliximab and adalimumab are monoclonal antibodies against TNF, whereas etanercept is a TNFRII fusion protein. All three drugs sequester soluble TNF [139]. Reports regarding the direct effect of anti-TNF agents on neutrophils have been published, and these drugs have been shown to decrease the mobilization of neutrophils from the peripheral blood to inflamed joints [140], decrease ex vivo neutrophil ROS production [20], and reduce neutrophil chemotactic and adhesive properties [141].
\nTocilizumab, a monoclonal antibody that blocks the soluble and tissue-expressed IL-6 receptor, is also proving to be a highly effective biologic agent in RA treatment [142]. Neutrophils are a major source of soluble IL-6 receptors, which they shed in large quantities when activated, and their accumulation in high numbers within the synovial joint could contribute significantly to IL-6 signaling within the synovium through trans-signaling [143]. In vivo therapeutic blockade of IL-6 with tocilizumab induces transient neutropenia caused by apoptosis or phagocytosis of apoptotic neutrophils but does not impair antibacterial neutrophil functions [144].
\nDespite the clinical efficacy of these therapies, many patients do not exhibit significant responses or discontinue treatment because of adverse effects. In addition, the limited availability of biological agents in developing countries, the need for parenteral administration of these products, and the high cost restrict access to such therapies for many RA patients worldwide, and this promotes a continuous search for new therapeutic targets and the development of new drugs [145]. Due to these limitations, interest has grown in the use of alternative treatments and herbal therapies for arthritis patients [146, 147] (Table 1).
\nTherapy | \nEffect on neutrophil response | \nReference |
---|---|---|
Non-steroidal anti-inflammatory drugs (NSAIDS) | \nInhibit neutrophil adherence, decrease neutrophil degranulation and ROS production, inhibit neutrophil elastase activity, and induce neutrophil apoptosis | \n[125–127] |
Corticosteroids | \nInhibit neutrophil degranulation and ROS production, decrease the production of inflammatory mediators, and prevent neutrophil adhesion and migration into RA joints | \n[44, 129–131] |
Disease-modifying antirheumatic drugs (DMARDs) | \nStimulate neutrophil apoptosis, inhibit the NF-κB pathway, and reduce adhesion molecule expression, LTB4 production, neutrophil recruitment, and ROS production | \n[116, 132–134] |
TNF-α inhibitors | \nDecrease neutrophil mobilization from the peripheral blood to inflamed joints and reduce ex vivo neutrophil ROS production and neutrophil chemotactic and adhesive properties | \n[20, 140, 141] |
IL-6 inhibitor | \nInduce transient neutropenia caused by apoptosis or phagocytosis of apoptotic neutrophils but not impair antibacterial neutrophil functions | \n[144] |
Current therapeutic targets for arthritis and their effect on neutrophils.
Current arthritis treatments result in unwanted side effects and tend to be expensive, and natural products devoid of such disadvantages offer a novel opportunity. The use of natural products represents a promising alternative to treat rheumatic diseases, in particular by acting as therapeutic adjuvants to reduce the daily doses of conventional drugs that RA patients administer [148–150]. In this section, we highlight future perspectives in the treatment of RA with natural compounds, mainly herbal compounds, to minimize the harmful effects of the over-activation of neutrophils.
\nDecreased inflammation and joint destruction have been directly correlated with reduced neutrophil influx into the joints, as observed in mouse models by means of antibody blockade or the gene deletion of chemoattractant receptors such as CXCR1, CXCR2, and BLT1 (LTB4 receptor) [15, 79]. The prospect of new drugs obtained from herbal products (or from structures of herbal products) plays a compelling role in drug discovery and development [151].
\nAs previously mentioned, pharmacologic treatment options for arthritis are diverse and present several side effects. Furthermore, the high costs and increased risk of malignancies limit the use of such agents. Because of these limitations, there is a growing interest in the use of natural products as therapies or adjunct therapies [22]. Plant-derived products such as polyphenols, sesquiterpenes, flavonoids, and tetranortriterpenoids, which are herbal metabolites, are considered to have potential activity to block inflammation, and they may provide new therapeutic agents and cost-effective treatments [22, 23]. These natural products have attracted considerable interest over the past decade because of their multiple beneficial effects, such as their antioxidant, anti-inflammatory, antiproliferative, and immunomodulatory properties. In this section, we discuss the plant-derived products that have been most studied in RA experimental models and/or clinical trials (Table 2).
\nQuercetin (Figure 2a) is the major dietary flavonol found in fruits, vegetables, and beverages, such as tea and red wine [152]. Several epidemiological and experimental studies support the antioxidant, anti-inflammatory, antiangiogenic, antiproliferative, and proapoptotic effects of this molecule [153–155]. Preclinical studies on primary cells and animal models, as well as clinical studies, suggest an inhibitory action of quercetin in RA. Quercetin has been reported to lower the levels of IL-1β, C-reactive protein, and monocyte chemotactic protein-1 (MCP-1), and restore plasma antioxidant capacity. In addition, quercetin increased the expression of hemeoxygenase-1 in the joints of arthritic rats. Finally, quercetin inhibited the twofold increase in NF-κB activity observed in joints after arthritis induction [156].
\nChemical structure of (a) quercetin, (b) methyl gallate, (c) gedunin, (d) epigallocatechin gallate, and (e) curcumin.
Compound | \nChemical class | \nArthritis experimental model | \nReference |
---|---|---|---|
Quercetin | \nFlavonoid | \nAdjuvant-induced arthritis | \n[156] |
Methyl gallate | \nPolyphenol | \nZymosan-induced arthritis | \n[171] |
Gedunin | \nTetranortriterpenoid | \nZymosan-induced arthritis | \n[176] |
Epigallocatechin gallate | \nPolyphenol | \nCollagen-induced arthritis | \n[179] |
Curcumin | \nPolyphenol | \nCollagen-induced arthritis | \n[191] |
Herbal products that exhibit anti-arthritic potential in animal models.
There are divergent data on the effect of quercetin in neutrophils. For instance, in vitro, quercetin inhibited myeloperoxidase activity [157] but had no effect on lipopolysaccharide-induced neutrophil surface expression of the adhesion molecules L-selectin (CD62L) and β2 integrin (CD11b/Mac1), [158] which are related to rolling and firm adhesion, respectively [159]. In paw edema induced by carrageen, quercetin did not inhibit the increase in myeloperoxidase, which is used as a marker of neutrophil recruitment [160]. Therefore, it seems unlikely that quercetin would inhibit neutrophil recruitment [158]. On the other hand, quercetin inhibits the fMLP-induced increase in intracellular calcium, [158] which is necessary for actin polymerization and consequently neutrophil migration [159]. In addition, in vitro, quercetin blocked human neutrophil mobilization through the inhibition of the cellular signaling responsible for actin polymerization in association with the down-regulation of adhesion molecules [161], indicating that treatment with this flavonoid is a conceivable approach to control excessive neutrophil recruitment during inflammation and to prevent neutrophil-mediated tissue lesions [162] (Table 3).
\nCompound | \nMolecular targets/mechanisms | \nReference |
---|---|---|
Quercetin | \nInhibits IL-1β, C-reactive protein, and MCP-1 levels. Restores plasma antioxidant capacity, increases HO-1 expression, and inhibits NF-κB activity in joints Inhibits myeloperoxidase activity in neutrophils and blocks neutrophil mobilization | \n[156, 157, 161] |
Methyl gallate | \nReduces edema formation, total leukocyte accumulation, neutrophil migration and IL-6, TNF-α, CXCL-1, IL-1β, LTB4, and PGE2 production in zymosan-induced arthritis. Impairs neutrophil chemotaxis and adhesion | \n[171] |
Gedunin | \nAttenuates zymosan-induced articular edema, neutrophil migration, hypernociception, and the production of IL-6, TNF-α, LTB4, and PGE2 and prevents increases in lipid bodies. Decreases neutrophil shape changes, chemotaxis, and lipid body formation | \n[176] |
Epigallocatechin gallate | \nAmeliorates the severity of arthritis and regulates the expression of cytokines, chemokines, MMPs, ROS, NO, COX-2, and PGE2. Affects neutrophil functionality and inhibits IL-8 and MIP-3α expression | \n[179–184, 186–189] |
Curcumin | \nSuppresses collagen-induced arthritis by reducing cellular infiltration, synovial hyperplasia, cartilage destruction, and bone erosion. Blocks neutrophil recruitment | \n[191, 193] |
Major molecular targets and anti-arthritic mechanisms of herbal products.
S. terebinthifolius Raddi (Anacardiaceae) is a native plant from South America. It has been used in folk medicine as teas, infusions, or tinctures, as an anti-inflammatory, febrifuge, analgesic, and depurative agent and to treat urogenital system illnesses [163]. Scientific reports demonstrated that S. terebinthifolius extracts and fractions are rich in polyphenols and display antioxidant, antibacterial, and antiallergic properties in different experimental models [164–166]. The HPLH chromatograms of hydroalcoholic extracts from S. terebinthifolius leaves (ST-70) reveal that methyl gallate (MG, Figure 2b) is one of the major polyphenol components of the ST-70 extract [167]. Methyl gallate has been extensively studied because of its antioxidant, antitumor, and antimicrobial activities [168–170]. Pharmacological studies have shown that ST-70 and MG also have an anti-inflammatory effect and may have potential activity against arthritis. Pretreatment with ST-70 or MG markedly reduced knee-joint thickness, total leukocyte (mainly neutrophil) infiltration, and reduced the production of inflammatory mediators associated with arthritis such as CXCL-1/KC, IL-6, TNF-α, IL-1β, LTB4, and PGE2. ST-70 and MG also inhibited murine neutrophil chemotaxis induced by CXCL-1/KC in vitro, and MG impaired the adhesion of these cells to TNF-α-primed endothelial cells [167, 171]. These results provide some evidence that MG inhibits neutrophil activation and adhesion molecules expression and consequently prevents the neutrophil entry into inflammatory sites (Table 3).
\nMoreover, unlike potassium diclofenac, the long-term oral administration of ST-70 does not induce lethality or gastric damage in mice, which suggests that ST-70 could be used to treat inflammatory conditions such as arthritis with less toxicity [167].
\nC. guianensis Aublet is a member of the Meliaceae family that is widely used in folk medicine in Brazil and other countries surrounding the Amazon rainforest [172]. Anti-inflammatory and analgesic activities are among the most remarkable properties attributed by ethnopharmacological research to the oil extracted from C. guianensis seeds, mainly for rheumatic pain and arthritis [172, 173]. C. guianensis oil and six different tetranortriterpenoids (TNTP) isolated from the oil were able to significantly inhibit zymosan-induced knee joint edema formation and protein extravasation. TNTP pretreatment inhibited the increase in total leukocyte and neutrophil numbers in the synovial fluid. TNTP also impaired the production of TNF-α, IL-1β, and CXCL-8/IL-8, and significantly inhibited the expression of the NF-κB p65 subunit [174].
\nGedunin (Figure 2c) is a natural tetranortriterpenoid isolated from vegetal species of the Meliaceae family and is known to inhibit the stress-induced chaperone heat shock protein (Hsp) 90 [175]. Mouse pretreatment and posttreatment with gedunin impaired zymosan-induced edema formation and total leukocyte influx mainly due to the inhibition of neutrophil migration and reduced articular hypernociception. Gedunin also reduced the in situ expression of preproET-1 mRNA and IL-6, TNF-α, LTB4 and PGE2 production and prevented increases in the number of lipid bodies in synovial leukocytes [176]. Lipid bodies are important sites for the synthesis and storage of lipid mediators and they increase in number during inflammatory responses [177]. In neutrophils, gedunin impaired ET-1-induced shape changes, blocked ET-1- and LTB4-induced chemotaxis, decreased ET-1-induced lipid body formation and impaired neutrophil adhesion to TNF-α-primed endothelial cells [176]. The combined in vitro and in vivo effects of gedunin reveal its potential as an anti-arthritic candidate, especially its direct effect on key cells involved in articular inflammation such as neutrophils (Table 3).
\nEpigallocatechin gallate (EGCG, Figure 2d) is one of the main components of green tea [178]. It has antioxidative, anti-inflammatory, antitumor, and chemopreventive properties. The potential disease-modifying effects of green tea on arthritis have been reported; for example, in a mouse model of RA, the induction and severity of arthritis was ameliorated by the prophylactic administration of green tea polyphenols [179]. Subsequent studies suggested that EGCG possesses remarkable potential to prevent chronic diseases like OA and RA [180–184]. The anti-inflammatory and anti-arthritic effects of EGCG are supported by in vitro and in vivo data indicating that EGCG can regulate the expression of cytokines, chemokines, MMPs, ROS, nitric oxide (NO), COX-2, and PGE2 in cell types relevant to the pathogenesis of RA [179–184]. In in vivo studies, EGCG was found to inhibit inflammation in mouse models by affecting the functioning of T cells and neutrophils [185, 186]. IL-8 is the most powerful chemo-attractant for neutrophils in the target tissue. EGCG is a very effective inhibitor of IL-1β and of TNF-α-induced IL-8 and macrophage-inflammatory protein-3α (MIP-3α) expression in different cell types [187–189]. These in vitro and in vivo observations indicated the efficacy of EGCG and demonstrate that it can modulate multiple signal transduction pathways in a fashion that suppresses the expression of inflammatory mediators that play a role in the pathogenesis of arthritis (Table 3).
\nCurcumin (Figure 2e) is a yellow-colored polyphenol found in the rhizome of turmeric. It has antioxidant, anti-inflammatory, antiapoptotic, and anticarcinogenic properties [190]. Oral administration of curcumin suppressed type II collagen-induced arthritis (CIA) in mice by reducing cellular infiltration, synovial hyperplasia, cartilage destruction, and bone erosion. Moreover, the production of MMP-1 and MMP-3 was inhibited by curcumin in CIA and in TNF-α-stimulated RA fibroblast-like synoviocytes (RA-FLS) and chondrocytes [191].
\nIn vitro, it has been reported that curcumin decreases IL-1β-induced expression of the pro-inflammatory cytokine IL-6 and vascular endothelial growth factor (VEGF) in RA-FLS [192]. In addition, curcumin blocks neutrophil recruitment through the inhibition of cellular signaling responsible for actin polymerization in association with the down-regulation of adhesion molecules [193]. It has also been shown to induce apoptosis of RA-FLS (which are resistant to apoptosis) by increasing the expression of the proapoptotic protein Bax and down-regulating the expression of the antiapoptotic protein Bcl-2 [190]. Some molecular mechanisms related to curcumin have been identified. In a human synovial fibroblast cell line (MH7A) stimulated with IL-1β, curcumin blocked the activation of the NF-κB pathway and induced deactivation of the ERK-1/2 pathway [192]. In addition, this polyphenol inhibited activating phosphorylation of protein kinase Cδ (PKCδ) in CIA, RA-FLS, and chondrocytes. Curcumin also suppressed JNK and c-Jun activation in those cells [191].
\nIn a clinical trial with RA patients, curcumin reduced reported pain, tenderness, and swelling of joints [194]. A curcumin-based medicine, Meriva®, demonstrated efficacy in clinical trials with patients with osteoarthritis by reducing reported pain [195]. In another clinical trial, treatment with Meriva® reduced stiffness and physical signs of RA (treadmill test) along with IL-1, IL-6, and VCAM-1 production [196] (Table 3).
\nIn RA, neutrophils are key cells that are recognized to play an active role in orchestrating the progress of inflammation, through the release of pro-inflammatory cytokines, ROS, RNS, and NETs, which potentially affect the activities of both neutrophils and other cell types, such as resident mononuclear cells and chondrocytes. In addition, neutrophils participate in the cascade of events leading to mechanical hypernociception. Therefore, neutrophils participate in the pathogenesis of arthritis by promoting the inflammatory process, degradation of cartilage, and bone resorption. The modulation of neutrophil migration and functions in RA can be considered a potential target for pharmacological intervention in arthritis. The pharmacologic treatment options for arthritis are diverse. High costs and an increased risk of malignancies limit the use of these agents, in addition to the potential for side effects that all therapies possess. Nevertheless, herbal metabolites with anti-inflammatory activity and inhibitory action in neutrophils may provide new therapeutic agents and cost-effective treatments.
\nThis work was supported by Brazilian grants from Coordenadoria de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), and Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ). L. B. Correa is a student of the post-graduation Program in Cellular and Molecular Biology from Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil.
\nMonsoon region of South Asia remains one of the important worries with respect to frequency and magnitude of drought in the contemporary scenario of climate change [1]. About 23 million hectares of Asian rice producing areas experience frequent yield loss due to drought [2]. Afghanistan, India, Pakistan and Sri Lanka have reported droughts at least once in every 3 year over the past 5 decades [3]. In India the net sown area is about 140 Mha, out of which as much as 50% area is considered as severely drought prone [4]. Therefore, a comprehensive assessment of drought is needful for monsoon based agro-economy of India.
Gangetic West Bengal (GWB), the leading agricultural hubs of Eastern India, severely experienced the effect of climate change over the last few years [5]. Late monsoon arrival has been observed with less intensity, duration of summer has become longer and drought has become more frequent [6, 7, 8, 9, 10]. Moreover, this region is less experienced of coping with droughts resulting in poor preparedness. Growing population, lacking water resource management initiatives etc. further compounded the problem. Therefore, we need to improve our knowledge on drought jeopardy in this densely populated tract with vast agricultural expanse. The present chapter is an attempt in this regard to ensure two folds objectives—i. to portray a comprehensive and holistic picture of droughts over GWB-its intensity-duration-frequency and trend and ii. to identify areas exposed to drought.
The study focuses on the southern half of West Bengal below Farakka barrage (Figure 1) located between latitudes 21°32′23″N to 24°51′20″N and longitudes 85°49′49″ E to 89°8′48″ E (area: 63,879 km2, elevation range: 0–677 m) surrounded by Jharkhand in the West, Odisha in the Southwest and Bangladesh in the East. Physiographically, GWB forms the transitional zones between Chhotanagpur plateau in the West and Ganga-Brahmaputra delta in the southern and eastern section. River Bhagirathi and its tributaries/distributaries drain this region [11]. The climate is typical sub-tropical monsoon type having four main seasons namely, winter (Jan-Feb); Pre-Monsoon (Mar-May); Monsoon (Jun-Sep) and Post-Monsoon (Oct-Dec) [12]. Out of the total annual rainfall, about 70–80% occurs during the monsoon and contributing as much as 90% to the discharge of the rivers.
Reference map of the Gangetic West Bengal showing elevations, district boundaries, physiographic divisions and location of the weather stations used in the analysis.
GWB is a densely populated (1051 person/km−2) tract, coupled with vast stretch of fertile alluvial soil and is the heart of rice and jute cultivation as well as freshwater fish production of eastern India, the gross cropped area and cropping intensity of this region count about 112 and 184% respectively [13]. Agriculture in this region is mainly rain-fed and rainfall extremities put heavy stress on not merely agricultural activities but also other economic activities. Average water demand in this region varies from about 0.9 to 1.8mm3 per km−2 in compare to the average water availability of 0.5 to 1.0mm3 per km−2 [14]. These demonstrate sensitiveness to drought of this region.
According to the study of Ghosh [9] there is a considerable decrease in rainfall during early monsoonal month June and mid monsoonal month August in this tract. In the year 2010 10 districts of GWB have received <33% of the normal monsoon rainfall, which severely affected the sowing of paddy [15]. In the northern Rarh and moribund delta there are significant decreasing trend of rainfall (Figure 2) which is a sign of strengthening of drier condition of these two regions. Nath et al. [16], WBSAPCC [6], RPAPCC [8] etc. have roughly addressed the way for drought management of the state. Nevertheless, comprehensive assessment of drought jeopardy of this region in prime prerequisite before chalking out the management plan and the present chapter opt to do so.
Site (meteorological station) specific annual rainfall trend during 1901–2002.
For the present study continuous time series rainfall data [
Over a geographic area deficit of rainfall from normal during a period is broadly accepted as drought. In this study standardized precipitation index (SPI) has been used to detail the geographical variations of drought at multiple time steps. Different dimensions of drought (like- drought intensity, duration, frequency etc.) following Dracup et al. [17] have been captured for the holistic appraisal.
SPI, developed by McKee et al. [18, 19] is a simple but flexible tool to monitor drought at multiple time step. SPI is recommended by the WMO as a standard drought monitoring index [20] and is calculated by taking the difference of the precipitation, Xi from the mean,
SPI is used to monitor both dry and wet conditions [22]. Negative values indicate dry and positive values indicate wet periods [23]. As SPI becomes more negative or positive, the conditions become more severely dry or wet (Table 1).
SPI values | Draught severity class | D-scale |
---|---|---|
2.0+ | Extremely wet | W3 |
1.5 to 1.99 | Very wet | W2 |
1.0 to 1.49 | Moderately wet | W1 |
−.99 to .99 | Near normal | N |
−1.0 to −1.49 | Moderately dry | D1 |
−1.5 to −1.99 | Severely dry | D2 |
−2 and less | Extremely dry | D3 |
Precipitation excess (wet) or deficit (dry) severity class according to SPI values.
Source:
McKee et al. [18] originally calculated the SPI for 3-, 6-, 12-, 24- and 48-month timescales. For the present case, typically SPI for 3- and 12-months step SPI are calculated to explore the drought variation at inter-seasonal and inter-annual time scales.
Drought intensity (ID): ID annotates departure of a climate index from its normal value [24]. According to McKee et al. [18] a drought event is defined as a period in which the SPI is continuously negative and SPI reaches a value of −1.0 or less. Hence, ID indicates the absolute value of SPI less than −1.0. Lesser the value more will be the drought intensity.
Drought duration (DD): DD equals the number of months between its start and end [25]. A drought event starts when the SPI is continuously negative and reaches an intensity of −1.0 or less while, the event ends when the SPI becomes positive.
Drought magnitude (MD) and mean intensity, (MID): MD corresponds to the cumulative water deficit over a drought period [26] and the average of this cumulative water deficit over the drought period is MID. Thus, MD is the absolute value of the sum of all SPI values during a drought event and MID refers to magnitude divided by duration.
Drought frequency (FD): FD is used to assess the drought liability during a study period [27]. The number of droughts per 100 years was calculated as:
where FDi,100 is the frequency of droughts for timescale i in 100 years; Ni is the number of months with droughts for timescale i in the n-year set; i is timescale (3-, 6-, 12-, 24-months); n is the number of years in the data set.
Trend analysis: The rank-based nonparametric Mann-Kendall test [28, 29] is applied to the long-term data in this study to detect statistically significant trends. Sen’s nonparametric method [30] is used to estimate the trends slope in the time series data.
Return period or recurrence interval (Tr): Bonaccorso et al. [31] expressed Tr as a function of the statistical characteristics of historical long records of precipitation and of a threshold parameter. In the present study the original concept of the return period [32] is used, i.e. the average number of years between events above a threshold magnitude.
Rainfall threshold/critical rainfall (TRD): To calculate the threshold rainfall, first we have to calculate the
The complete set of raw data for the said period (Jan 1901 to Dec 2002) in the current study have been tested to check if there are any missing data or irregularities in the data series. SPI is then calculated for different time steps using ‘SPI Calculator’ of the National Drought Mitigation Centre (NDMC) as recommended by WMO [20]. Afterwards drought-related indicators as indicated in Section 6.2.2 are calculated. SPSS 14.0 and XLSTAT 2015 Excel plug-in have been used for the MK test and Sen’s slope. For the purpose of revealing the spatial variation over GWB Choropleth maps are then prepared using GIS software.
On 12-month time lag 10 significant droughts have occurred during 1901–2002 (Figure 3a) among which, 1966–1967 is the most significant with DD of 14 months; PID of −2.82 and a MID of −2.06. On 48-month time step the last century roughly exhibit some consecutive surplus and deficit phase (Figure 3b): (i) slight deficit (1901–1917), (ii) short surplus (1918–1922); (iii) oscillating or near normal (1923–1940); (iv) short surplus (1941–1953); (v) longest and peak deficit (1954–1970); (vi) peak surplus (1971–1982); (vii) short deficit (1983–1986) and (viii) longest surplus (1987–2001). Noticeably, at the longer time scales, droughts become less frequent but their duration increases (Figure 3b) and after 1950s the extremities of surplus and deficit as well as duration have increased substantially. Most of the drought event reaches to its maximum intensity during the pre-monsoon months of March to May (Table 2).
SPI time series (1901-2002) for GWB for (a) 12- and (b) 48- month time scales.
Lag time | Observed peak intensity (PID) during 1901–2002 | Mean intensity (MID) | ||
---|---|---|---|---|
SPI | Year | Month | ||
3-Month | −3.72 | 1999 | April | −2.68 (gross avg. −0.81) |
6-Month | −3.65 | 1922 | March | −2.64 (gross avg. −0.77) |
12-Month | −2.83 | 1939 | June | −1.68 (gross avg. −0.77) |
24-Month | −2.62 | 1968 | January | −2.13 (gross avg. −0.81) |
48-Month | −2.43 | 1968 | May | −1.49 (gross avg. −0.79) |
Drought intensity at different time scale for GWB during 1901–2002.
During the 102 year time span the MID at the 3- and 12-month time step was −0.81 and − 0.77 respectively. MID for most stations (69.44%) at all the time scale were ≥−0.8 but did not cross the limit of mild drought (i.e. 0 to −0.99). Regional MID varies between −0.75 (Krishnanagar) and −0.86 (Purulia). Spatially (Figure 4a and b), average drought intensity is the greatest in the degraded plateau region and western fringe of the Rarh region; it is less in the mature & active delta region and eastern fringe of the Rarh plain. Roughly the drought intensity gradually decreases from West to East and South East.
Iso-mean intensity drought map for (a) 3-, (b) 12- month SPI.
At the 3-month step observed peak intensities are maximum in the mature delta region (Figure 5a and b). At the 12-month step it was greatest in the western degraded plateau region, extreme northern part of moribund delta and Rarh plain region. Thus the western degraded plateau region is more sensitive to long-duration droughts.
Observed maximum intensity drought map at (a) 3-month and (b) 12-month time scale.
During 1901–2002, average drought duration identified by SPI on 12-month scale for most stations (>90.0%) was 4–6 months (Table 3) and the regional average value was 4.18. The maximum drought duration at all the stations was more than 20 months (Table 3) and the regional average of the most intense drought was 7 month. The average magnitude of the longest drought and the most intense drought event on 12 month scale is about −29 and −16 respectively with their mean intensity of −1.37 and −2.29.
Weather station | Longest duration (≤ − 1.0 for consecutive months) | Most intense duration (≤ − 2.0 for consecutive months) | DDA(M) | ||||
---|---|---|---|---|---|---|---|
DDL(M) | Year | MD | DDL(M) | Year | MD | ||
Berhampore | 24 | Sept, 2000 to Aug, 2002 | −32.18 | 11 | July, 1982 to May, 1983 | −27.87 | 4.57 |
Krishnanagar | 23 | July, 1966 to May, 1968 | −42.33 | 8 | Sept, 1982 to April, 1983 | −18.09 | 4.19 |
Chinsurah | 21 | Sept, 1957 to May, 1959 | −28.13 | 7 | Oct, 1935 to April, 1936 | −15.53 | 3.93 |
Uluberia | 20 | Oct, 1957 to May, 1959 | 26.05 | 8 | Oct, 1935 to May, 1936 | −19.97 | 4.46 |
Alipore | 21 | Sept, 1957 to May, 1959 | −28.28 | 7 | Oct, 1935 to April, 1936 | −16.72 | 3.98 |
Basirhat | 23 | Sept, 1957 to July, 1959 | −37.63 | 8 | Oct, 1935 to May, 1936 | −21.02 | 4.55 |
Purulia | 25 | Aug, 2000 to Aug, 2002 | −46.23 | 12 | July, 1966 to June, 1967 | −33.34 | 5.17 |
Bankura | 23 | Sept, 2000 to July, 2002 | −36.58 | 12 | July, 1966 to June, 1967 | −31.59 | 5.08 |
Sriniketan | 23 | Sept, 2000 to July, 2002 | −34.06 | 7 | Aug, 1966 to Feb, 1967 | −16.15 | 5.15 |
Burdwan | 23 | Sept, 2000 to July, 2002 | −31.73 | 8 | Aug, 1966 to Mar, 1967 | −19.4 | 4.55 |
Midnapore | 20 | Sept, 1957 to April, 1959 | −25.75 | 8 | Sept, 1935 to April, 1936 | −20.55 | 5.07 |
Sagar Island | 20 | Oct, 1957 to May, 1959 | −24.52 | 9 | Sept, 1935 to May, 1936 | −29.43 | 4.17 |
GWB | 21 | Sept, 1957 to May, 1959 | −28.76 | 7 | Sept, 1966 to Mar, 1967 | −16.05 | 4.18 |
Drought duration and magnitude at 12 month time scale for different weather stations of the GWB during 1901–2002.
Note: DD(M): duration (month); DDL(M): observed longest duration (month); DDI(M): observed most intense duration (month); DDA(M): average duration (month); MD: magnitude.
Spatially at the shorter time span (3-month lag) the coastal plain followed by the southern Rarh and parts of the lower Ganga plain are sensitive to relatively longer drought duration (Figure 6a). At the 12-month lag, it was relatively longer in the degraded plateau and plateau fringe fans of the Rarh Bengal (Figure 6b). Noticeably the area suffered from lengthier drought, magnitude was also counted high there (Figure 7).
(a) Average duration of drought events for (a) 3-, (b) 12-month time scale.
Magnitude for (a) longest and (b) most most-intense duration draughts on 12-month time step.
Percentage frequencies of drought occurrences of varying drought categories at different time steps have been outlined in Table 4. At all the time steps, more or less 16% years (i.e. once in every 6 year) have recorded drought of all categories.
Draught severity class | SPI values | 3-M lag | 12-M lag | 24-M lag | 48-M lag |
---|---|---|---|---|---|
Moderately dry | (−1.0 to −1.49) | 8.76 | 10.80 | 7.83 | 13.08 |
Severely dry | (−1.5 to −1.99) | 4.09 | 4.20 | 5.66 | 3.91 |
Extremely dry | (−2 and less) | 3.11 | 1.24 | 2.66 | 1.10 |
Total (%) of all categories drought | 15.96 | 16.24 | 16.15 | 18.10 |
Frequency of drought occurrences (%) in GWB at different time steps.
At the 12-month time steps the moribund delta followed by parts of northern as well as southern Rarh has experienced higher occurrence severe droughts (Figure 8a). Extreme drought occurrences, on the other hand, are more pronounced in the western degraded plateau region (Figure 8b). This means that the western degraded plateau suffers from extreme drought condition frequently while parts of Rarh Bengal and northern extreme of the deltaic Bengal suffer from frequent severe drought conditions.
(a) Severe and (c) extreme drought occurrences at 12-month time steps.
To evaluate the Phase-wise change of drought variables during 1901–2002, the annual rainfall data series have been fitted with LOWESS or locally weighted regression curves [33, 34] to identify the patterns over time (Figure 9) and thereby to divide the entire time span into some clearly distinct phases (Table 5).
Locally weighted regression (LOWESS) and scatter plots of the average annual rainfall in GWB for the period 1901–2002.
Drought indicators | Phase-I: 1901–1933 | Phase-II: 1934–1964 | Phase-III: 1965–2002 | 1901–2002 |
---|---|---|---|---|
Average drought intensity (MID) | −0.71 | −0.82 | −0.77 | −0.77 |
Maximum drought intensity (PID) | −1.98, 1903, July | −2.83, 1939, June | −2.82, 1967, June | −2.83, 1939, June |
Average drought duration (DDA(M)) (SPI: ≤ −1.0 for consecutive months) | 2.61 | 5.54 | 4.39 | 4.18 month |
Maximum drought duration (DDL(M)) (SPI: ≤ −1.0 for consecutive months) | 10 month (August, 1927 to May, 1928) | 21 month (Sept, 1957 to May, 1959) | 14 month (July, 1966 to August, 1967) | 21 month (Sept, 1957 to May, 1959) |
Most intense duration (DDI(M)) (SPI: ≤ −2.0 for consecutive months) | 8 month (July, 1903 to Feb, 1904). Mean intensity: −1.46 | 11 month (Sept, 1938 to July, 1939). Mean intensity: −1.68 | 7 month (Sept, 1966 to March, 1967). Mean intensity: −2.06 | 7 month (Sept, 1966 to March, 1967): Mean intensity: −2.06 |
Moderate drought frequency (%) | 10.65 | 10.65 | 12.73 | 10.80 |
Severe drought frequency (%) | 2.69 | 6.72 | 4.30 | 4.20 |
Extreme drought frequency (%) | 0 | 1.32 | 1.97 | 1.24 |
Regional intensity, duration and frequency of drought events identified from SPI values at a 12-month scale for different periods in GWB.
Regional average as well as peak drought intensity has increased significantly during first two consecutive phases. Meanwhile, there is no obvious change in average and maximum drought intensity between phase-II and Phase-III. The average drought duration has increased from 2.6 months in the phase-I to 5.5 month in the Phase-II and again has decreased to 4.4 months in the phase-III. Meanwhile, the most intense duration has increased from 8 month (Phase-I) to 11 month (Phase-II) again has equalized to 7 months in Phase-III. This may seem to be a good sign, but there is significant increase in mean intensity in the most intense duration drought from −1.46 in phase-I to as maximum as −2.06 in phase-III. This signifies that extreme drought events become short duration but its intensity is escalating as a signature of climate change. The regional extreme drought frequency during 1965–2002 compared to 1901–1933 has increased from 0 to about 2%.
The MK test has been used to identify trend of drought intensity (Table 6). Here, in case of drought analysis, positive trend will indicate intensification of wet condition and negative change will indicate amplification of dry condition because trend of drought intensity is inversely related to the rainfall trend i.e. if rainfall declines drought event will amplify.
Weather stations | SPI-3 | SPI-12 | SPI-24 | ||||||
---|---|---|---|---|---|---|---|---|---|
Z | Q | Tr | Z | Q | Tr | Z | Q | Tr | |
Berhampore | −1.30* | −0.21 | In* | −2.05* | −0.49 | In* | −1.87+ | −0.59 | In+ |
Krishnanagar | 0.44 | 0.07 | De | 0.94 | 0.22 | De | 1.49 | 0.39 | De |
Chinsurah | 1.17 | 0.17 | De | 1.86 | 0.48 | De | 2.52+ | 0.75 | De+ |
Uluberia | 1.75+ | 0.24 | De+ | 2.77+ | 0.71 | De+ | 3.23* | 0.99 | De* |
Alipore | 1.46+ | 0.22 | De+ | 2.40+ | 0.61 | De+ | 2.98* | 0.91 | De* |
Basirhat | 1.98* | 0.32 | De* | 3.27* | 0.81 | De* | 3.88* | 0.15 | De* |
Purulia | −1.26 | −0.18 | In+ | −1.79+ | −0.44 | In+ | −1.95+ | −0.60 | In+ |
Bankura | −0.53 | −0.10 | In | −0.80 | −0.18 | In | −0.63 | −0.20 | In |
Sriniketan | −1.49* | −0.24 | In* | −2.53* | −0.63 | In* | −2.77* | −0.85 | In* |
Burdwan | −0.45 | −0.06 | In | −0.81 | −0.18 | In | −0.61 | −0.16 | In |
Midnapore | 1.33 | 0.20 | De | 2.22 | 0.55 | De | 2.81+ | 0.80 | De+ |
Sagar Island | 2.17* | 0.34 | De* | 3.48* | 0.89 | De* | 4.00* | 0.25 | De* |
GWB Avg. | 0.53 | 0.08 | De | 0.92 | 0.24 | De | 1.56 | 0.44 | De |
Result of MK test, Sen’s slope and trend of drought (1901–2002) over GWB.
Significant trend at 0.05 level of significance.
Significant trend at 0.1 level of significance.
Note: Z: standardized test statistics of MK test; Q: Sen’s slope estimate; Tr: trend of drought; In: increasing and De: decreasing trend of dry condition.
At all the time steps, stations Berhampore, Purulia, Bankura, Sriniketan and Burdwan, irrespective of their level of significance, have experienced amplification of dry condition over the assessed period. For the 3-month step, significant positive trends (on 95% sig. level) have been detected at Berhampore, Sriniketan and Purulia of the Moribund delta, northern Rarh and western degraded plateau respectively (Figure 10a). For the station Sriniketan and Purulia the trend remains analogous for the 12- and 24-month time series also (Figure 10b and Table 6). However, on longer time span of 24-month scale, station Berhampore of the Moribund deltaic Bengal has experienced insignificant growth on 95% level of significance unlike the 3- and 12-month scale (Table 6).
Single-site trend of drought intensity for SPI at different time scales.
In case of mod drought, the return periods are lesser in parts of deltaic Bengal and Rarh plain (Figure 11a). However, the circumstances roughly reversed in case of the extreme drought (Figure 11b) and the western degraded plateau and some parts of the plateau fringe fans and moribund delta part return periods count lesser. Thus, on entire regional scale the deltaic Bengal & Rarh plain are more sensitive to frequent attack of severe drought but extreme drought attack more recurrently in the western degraded plateau and some adjacent parts of the Rarh plain.
Return period of (a) severe drought (SPI < −1.5 to −1.99) and (b) extreme drought (SPI < −2.0) on 12-month time steps.
Critical rainfall is the least amount of rainfall below which can initiate drought. The critical rainfall demands for no-drought occurrences roughly increases from West to East and South-east (Figure 12a and b). Therefore, it is likely that the interior region immediately after the coastal and lower Ganga delta will be more exposed to droughts particularly the non-irrigated croplands due to relatively more demand of water.
Critical rainfall values for (a) 3-months and (b) 12-month time lag.
This chapter has provided results on the assessment meteorological drought condition for the Gangetic West Bengal of Eastern India over the last century in the context of climate change. The patterns of drought frequency, magnitude, trend etc. portrayed through statistical assessment, visually interpretive maps and geographic description so as to improve our understanding of drought jeopardy of this region.
The study confirmed that, the last century exhibits some consecutive deficit and surplus phases and after 1950s extremity of surplus and deficit as well as duration have been increased substantially. Stepping up of the maximum drought intensity; mean intensity of the most intense drought event; average drought duration; severe and extreme drought frequency from 1940s in this agricultural tract are some alarming events to think over. At the intra-regional scale, average drought intensity as well as duration was the greatest in the western degraded plateau and Rarh region and are also sensitive to extreme droughts. The impact of drought is expected to be rigorous at or adjacent areas of the western degraded plateau, particularly the northern Rarh and moribund delta where the drought intensities are tend to increase while the rainfall as well as recurrence interval of drought are tend to lessen. The western degraded plateau is widely known for its drought proneness [35]. But, this work provides evidences demonstrating the extension and intensification of dryness at and in the adjacent areas of this traditional drought prone region namely, towards the northern Rarh plain and moribund delta. All of these indicate potential threat to the rain-fed agriculture, food security and socio-economic vulnerability to drought of this region. Therefore, a more detailed study to explore the drought risk as well as trend and pattern of other hydro-climatic variables is essential. Work related to this issue is in progress and will be reported elsewhere.
The author is like to express his sincere thanks to Prof. Sutapa Mukhopadhyay of the Department of Geography, Visva-Bharati University, Santiniketan and Dr. Swades Pal of the Gour Banga University, Malda for their fair and priceless assistance in upgrading the present piece of writing. The author is also appreciative to the India Meteorological Department for providing the data.
The author states that there is no conflict of interest.
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",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"54525",title:"Prof.",name:"Abdul Latif",middleName:null,surname:"Ahmad",slug:"abdul-latif-ahmad",fullName:"Abdul Latif Ahmad",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"20567",title:"Prof.",name:"Ado",middleName:null,surname:"Jorio",slug:"ado-jorio",fullName:"Ado Jorio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universidade Federal de Minas Gerais",country:{name:"Brazil"}}},{id:"47940",title:"Dr.",name:"Alberto",middleName:null,surname:"Mantovani",slug:"alberto-mantovani",fullName:"Alberto Mantovani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,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,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). He is the member of many Pharmaceutical Associations and acts as a reviewer of scientific journals and European projects under different research areas such as: drug delivery systems, nanotechnology and pharmaceutical biotechnology. Dr. Sezer is the author of many scientific publications in peer-reviewed journals and poster communications. Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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