\r\n\tWithin this scenario, special attention needs to be devoted to financial implications, due to their pervasiveness. Nobody would question the key role that finance plays to complement the real sphere of the economy and that has increasingly attracted both academics and practitioners. As a result, traditional pillars – such as financial markets, products, and institutions – have evolved significantly, with financial innovation fueling further progress over time. The global side of the coin features – among others – financially connected markets, international financial exchanges, and financial conglomerates that provide valuable opportunities in terms of international corporate finance. On the other side, recent advances have involved a wider recourse to ESG factors, allowed forward steps towards a more inclusive financial system, and have made digital finance a must, rather than an option, even though much remains to be accomplished, for instance, to facilitate access to formal financial channels in many underdeveloped regions.
\r\n\r\n\t
\r\n\tThis book aims to examine emerging trends, new perspectives, and empirical applications that deal with globalization and sustainability. The goal is to provide a comprehensive overview of these important concepts as valuable support to successfully meet the challenges and take on the opportunities ahead. At the same time, drawing upon empirical evidence can contribute to bridging the gap between theory and practice, which also fits within the scope of this book.
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Osteoarthritis (OA) is a common disease that can affect joints from any part of the body, and it represents a major cause of disability and joint pain worldwide [1, 2]. OA most commonly affects the knee, hip, and shoulder, and it was estimated that more than 25 million people in the USA were affected by some form of OA in the last decade [3]. In addition, OA presents a high susceptibility to affect female gender, elderly people, and obese individuals [4].
The progression of OA leads to cartilage degradation with subchondral bone remodeling, hypertrophy of the joint capsule, and osteophytes formation, causing pain [1, 5, 6]. Although the development of OA is considered a heterogeneous process, which comprises a number of genetic and environmental causes, the presence of local causes, such as trauma and hypermobility of the joint, may worsen OA [2, 7].
The accurate identification of osteoarthritic features has been studied in order to radiographically grade the stages of OA. The Kellgren-Lawrence classification is the most widely used, especially in clinical researches. This classification evaluates the appearance of osteophytes and cysts, joint space loss, and sclerosis, and it grades the severity from 0 to 5 points. The radiological features found in OA joints were graded as follows: (1) formation of osteophytes on joint margins or on tibia spines for knee OA; (2) periarticular ossicles in relation to distal and proximal interphalangeal joints; (3) narrowing of joint cartilage and sclerosis of subchondral bone; (4) pseudocystic areas with sclerotic walls in the subchondral bone; and (5) altered shape of the bone ends [8]. Some of these criteria were adopted by the World Health Organization (WHO) as the standard for studies on OA.
Current options for the treatment of OA focus on reducing pain (non-steroidal anti-inflammatory drugs—NSAIDs) and joint viscosupplementation (intra-articular injections of hyaluronic acid) [1]. Besides presenting a short-term effect, the chronic use of some of these medications, especially NSAIDs, may cause serious adverse events, including toxicity and risk of thromboembolism [9, 10]. In severe cases, surgical procedures, mostly joint replacement, are suggested [1]. Novel alternative therapies, called orthobiologics, have emerged from the need of tissue regeneration. Clinical trials using orthobiologics, which comprise platelet-rich plasma (PRP), bone marrow aspirate concentrate (BMAC), fat graft (Biofat), and expanded mesenchymal stem cells, have shown promising results for the treatments of OA from any origin [11, 12, 13, 14].
Moreover, monoclonal antibody (mAb) therapy represents one of the alternative treatments that aim to control inflammation and slow structural progression [15]. This approach focuses on blocking specific molecules responsible for the maintenance of OA. Preclinical studies with ADAMTS mAbs reported a significant decrease in histological scores after 3 months of treatment [16]. Adalimumab is an anti-TNF-α therapy used in diverse immune-mediated diseases, and it presents a protective role for OA as it reduces the severity of the cartilage lesion and improves the structure of subchondral bone [17]. Since IL-1 family may induces the production of metalloproteinases (MMP), it has also become a target for mAb therapy, and, in a randomized controlled trial with patients who presented knee OA, it was reported great improvement on pain relief [18].
In addition to macroscopic features, several cellular and molecular alterations are present in OA, such as catabolism and anabolism events; hypertrophy and, consequently, death of chondrocytes; and impaired autophagy process [19]. Also, a chronic low-grade inflammation interplayed with immune system has been considered to present a crucial role in the maintenance of OA [1]. This fact is supported by recent progress, which has considerably improved the knowledge regarding factors involved in the OA development and the mechanisms responsible for its progression.
2. Osteoarthritis and immune response
The inflammation observed in OA is believed to involve innate immune response prior to a mild degree of adaptive immunity [20]. During tissue damage, a group of endogenous molecules, called damage-associated molecular pattern (DAMP), signals the immune cells to induce a protective response against the tissue, causing tissue repair. However, a prolonged signaling of DAMP to immune cells leads to an exacerbated cytokine release, which can be destructive to the tissue [21, 22].
Innate immune cells activated by DAMP include macrophages and mast cells, which have shown to present (displayed or demonstrated) a key role in the pathogenesis of OA. Mast cells are considered regulators of vascular permeability, and they may play a crucial role in OA joint inflammation as they facilitate leukocyte infiltration [23].
Macrophages exhibit a functional plasticity based on the environment in which they are located or present [22]. However, their chronic activation can lead to the production of proinflammatory cytokines, which worsen the osteoarthritic joints [24]. In vitro studies of human OA synovium-derived cells showed that macrophage depletion results in diminishing of inflammatory response by decrease of proteolytic enzyme expression, such as metalloproteinases (MMP) This fact is supported by in vitro studies with cell culture suspension of human OA synovium, which reported that, after macrophage depletion, there was a decrease in the production of inflammatory response by less activity of proteolytic enzymes, such as metalloproteinases (MMP) [25]. Although macrophages may also present a protective role, as they are known to secrete transforming growth factor β (TGF-β), which would enhance cartilage repair, intra-articular injection of TGF-β in mice knee led to osteophyte formation and fibrosis [26].
In addition, natural killer (NK) infiltrates are commonly found in synovial tissue from patients who underwent joint replacement surgeries, and a subset of NK cells (CD56bright) was found to be greatly expanded in patients with inflammatory arthritis who have not undergone joint replacement surgeries. However, the effect of these cells on the development of OA has not been elucidated yet [27, 28, 29]. NK cells secrete protease enzymes called granzyme type A and B, which correlate to cytolytic potency. Granzymes can be released during degranulation of cytotoxic cells and, when delivered intracellularly to the target cells, they induce apoptosis. Granzyme A also stimulates the production of tumor necrosis factor (TNF-α), IL-6, and IL-8, while granzyme B may intensify the degradation of extracellular matrix [30, 31]. Tak et al. identified both types of granzymes in synovia from OA and rheumatoid arthritis. However, another study later showed that NK cells within OA synovia were granzyme negative with potential to produce the interferon-γ (IFN-γ) when expanded with IL-2 and stimulated with cytokines known to trigger IFN-γ production in blood NK cells, such as IL-12 and IL-18 [27, 32].
The presence of IFN-γ has a role in the bone resorption and consequently in the osteoclastogenesis process, but the studies have shown controversial results in this regard: in vitro evidence reported that IFN-γ, via TRANCE pathway, strongly suppresses osteoclastogenesis in culture of mononuclear phagocyte cells, which are the osteoclast precursors [33], whereas in culture of peripheral blood it may enhance osteoclast production as IFN-γ increases superoxide generation by neutrophils [34]. In addition, experimental studies in which IFN-γ receptor was silenced suggested a more rapid onset of collagen-induced arthritis [35]. Although IFN-γ plays a key role in angiogenesis, there is no evidence that this cytokine is able to promote angiogenesis in OA.
Proteins from complement system have been found to play a role in OA, especially in early stages, as they were upregulated in both synovial membrane and fluid [23, 36]. Additionally, the deposition of the membrane attack complex (MAC, C5b-9) is correlated with the presence of inflammation on histology of synovial membrane, and it was present in chondrocytes in late OA [36]. MAC can lead to chondrocyte destruction as it stimulates catabolic events through the increase of leukocytes and, consequently, the production of MMP [23]. Also in the studies with experimental knockout models for C5 and C6, the joint damages were attenuated [36].
Cellular infiltrates from adaptive immune response have also been observed in synovial fluid from OA joints. Although the main cell type present in this infiltrate is CD3+ T cells, both CD4+ and CD8+ cells have also been found in OA [37]. Th1 cells, and consequently their secretory cytokines, such as IL-2 and INF-γ, appear to be expressed five times greater than Th2 in most of OA patients [37]. Based on lymphocyte aggregates, there is a suggestion of an active cell-mediated immune response since T-cells in lymphocytic aggregates in OA synovium were shown to bear early (CD69), intermediate (CD25 and CD38), and late (CD45RO) activation markers [38].
3. Inflammatory markers in osteoarthritis
3.1 Cytokines
Inflammatory mediators observed in OA joints are thought to be the downstream effectors of the pathogenesis of the disease. Cytokines are among the most extensively studied mediators of inflammation. Several cytokines have been reported to play a role in the progression of OA, such as TNF, IL-1β, IL-6, IL-15, IL-17, IL-18, IL-4, and IL-10. Although their precise mechanism of action has not been completely elucidated yet, it has been proposed that their presence influences cartilage homeostasis as they induce catabolic events as well as inhibit anabolic processes [21, 39, 40].
3.1.1 IL-1β and TNF
Interleukin (IL)-1β and tumor necrosis factor (TNF) are considered the major mediators in the pathophysiology of OA. They both are secreted not only by immune cells, especially mononuclear cells, but also by chondrocytes and osteoblasts. In OA joints, these cytokines are increased in both synovial fluid and membrane. They are known to drive the inflammatory cascade, and their increased expression induces catabolic events as they enhance MMP [39]. IL-1β and TNF downregulate the synthesis of major extracellular matrix (ECM) components by inhibiting anabolic activities of chondrocytes [40] and reducing type II collagen production [41].
IL-1β is activated through the binding of its specific receptor type I (IL-1RI). Overexpression of IL-1RI in cartilage proximal to the macroscopic injury in OA joints resulting in increased binding of IL-1β was observed [42]. IL-1β has also been reported to be responsible for the catabolic events present in OA: its expression combined with TNF induces the production of MMP-1, -3, and -13 and stimulates the production of aggrecanases (ADAMTS)-4 and -5 in human and bovine chondrocytes [43, 44]. TNF receptor type I (TNFRI) is overexpressed in OA chondrocytes [45]. High levels of TNF-α in cartilage explants seem to inhibit the synthesis of proteoglycan and stimulate resorption [40].
In OA joint, IL-1β and TNF amplify the arthritic condition by inducing the production of proinflammatory cytokines, such as IL-6, IL-8, and monocyte chemoattractant protein 1. In addition, chondrocytes treated with IL-1β and TNF increase the production of nitric oxide (NO), cyclooxygenase 2 (COX-2), and prostaglandin E2 (PGE2), which contribute to articular inflammation and cartilage destruction as they enhance MMP activity, inhibit the production of anabolic products such as collagen and proteoglycan, and induce chondrocyte apoptosis [39].
The catabolic events observed (the catabolic events that occur due to the presence of…) in the presence of IL-1β and TNF are mediated through the activation of signaling pathways, including nuclear factor-κB (NF-κB) signaling. NF-κB pathway induces the expression of the genes related to the inflammatory mediators cited above and also contributes to the induction of MMP-1 and -13 and ADAMTS-4 [46]. However, some signaling pathways are involved in the downregulation of the IL-1β and TNF effects in OA, such as peroxisome proliferator-activated receptor-γ (PPAR-γ). The activation of PPAR-γ seems to reduce the progression of cartilage lesion in experimental models of OA as it assists the downregulation of inflammatory and catabolic responses mediated by IL-1β and TNF [47, 48].
3.1.2 IL-6
IL-6 is a proinflammatory cytokine, whose signaling pathway involves the activation of receptors, such as membrane-bound IL-6 receptor (IL6R), soluble IL-6R (sIL-6R), and gp130, followed by the activation of STAT1 and STAT3 pathways [39]. In physiological conditions, the production of IL-6 by chondrocytes is considerably low. However, the exact mechanism of IL-6 action in OA is unknown, but its production can be stimulated by the number of cytokines and growth factors present in OA, including IL-1β, TGF-β, and PGE2 [25, 49].
Increased levels of IL-6 in synovial fluid and serum have been correlated with the severity of lesions in X-ray imaging [50]. In vitro studies have shown that IL-6, in combination with IL-1β and TNF, upregulates the production of MMP-1 and -13 in human and bovine chondrocytes and induces proteoglycan and type II collagen degradation [51, 52]. The effect of IL-6 in studies with animal models has shown uncertain results. IL-6 knockout mice revealed more advanced degenerative changes compared to wild-type animals [53]. However, when IL-6 was injected in the joint cavity of IL-6-deficient mice, the reduction in the loss of proteoglycans in the acute phase of inflammation was observed [54].
One of the most considered active components in OA is the change in subchondral bone tissue, and IL-6 has been a critical mediator in this regard. Its effect, together with IL-1β and TNF, is based on promoting osteoclast formation and, consequently, bone resorption [55]. In response to IL-6, osteoblasts stimulate the production of receptor activator of NF-κB ligand, IL-1β, and PGE2, which activate osteoclasts [56]. In addition, osteoblasts activated by these cytokines produce MMPs, which adversely affect the surrounding cartilage [57].
3.1.3 IL-15
Despite a better documented involvement in rheumatoid arthritis [58], the knowledge regarding IL-15 and its action in OA is still poor. It acts based on the stimulation and proliferation of T cells and NK cells, and it may also induce the production of MMP [59]. IL-15 levels are elevated in synovial fluid in early stages of OA, and this concentration correlates with pain and severity of lesions seen on X-ray imaging [60, 61].
3.1.4 IL-17
Due to its inflammatory effects, IL-17 family has been implied to play a role in OA [62]. IL-17 is mainly stimulated by CD4+ T cells and mast cells, which are present in the cellular infiltrates observed in OA joints [63]. Within the joints, IL-17 primarily targets chondrocytes and fibroblast-like synoviocytes, which express IL-17 receptor (IL-17R) on their surface [64]. It was reported that IL-17 is able to inhibit proteoglycan synthesis by chondrocytes and increase the production of MMPs [65]. Also, high levels of IL-17 in both serum and synovial fluid were correlated with radiographic lesions in OA [66].
The genetic correlation between IL-17 and OA was suggested: a polymorphism in the gene IL-17A G-197A could be associated with the susceptibility to the development of OA [67]. In addition, IL-17 is produced by a specific T cell lineage called T helper 17, and it is able to cause hypertrophy of synovial membrane as its presence influences the secretion of vascular endothelial growth factor (VEGF), which leads to excessive blood vessel formation [68]. It can also indirectly affect cartilage by inducing the production of cytokines responsible for tissue degradation, such as IL-1β, TNF, IL-6, NO, and PGE2 [64].
3.1.5 IL-18
The active form of IL-18 results from the activation of caspase-1, which has been reported to be elevated in articular cartilage and synovium of OA, leading to great promotion of IL-18 and IL-1β. The production of IL-18 in joints is mainly determined by chondrocytes, osteoblasts, and macrophages [69]. IL-18 affects cartilage by upregulating the production of IL-18Rα on chondrocyte surface and stimulates excessive production of MMP-1, -3, and -13 [70]. Also, IL-18 negatively influences the production of proteoglycans, aggrecan, and type II collagen and may cause morphological changes typically observed in apoptotic processes [71, 72].
The increased concentration of IL-18 observed in synovial fluid, synovium, cartilage, and even blood serum from patients with OA has been correlated with the severity of lesions seen in radiographic imaging [73]. Also, studies have correlated the development of OA and lumbar disc degeneration with polymorphisms in the gene encoding IL-18 and its receptor (IL-18R) [74, 75].
3.1.6 IL-4
Anti-inflammatory cytokines also present a role in the maintenance of OA. IL-4 is associated with chondroprotective effects as it is shown to reduce MMP production and, consequently, inhibit the degradation of proteoglycans in the articular cartilage [76]. However, chondrocytes from OA joints have shown a decreased susceptibility to this IL-4 protective effect, leaving the cartilage unprotected, quickening the degeneration via the action of the proinflammatory cytokines cited above [77]. In addition, a polymorphism in the gene encoding IL-4 and its main receptor (IL-4Rα) could predetermine the development of OA in hand and knee joints [78, 79]. It was also further reported that, when compared with healthy patients, OA patients present an elevated level of soluble IL-4Rα (sIL-4Rα) [80].
The activation of IL-4 depends on intracellular signal transduction by gradual phosphorylation of IL-4Rα, which leads to the expression of several proinflammatory genes [81]. IL-4 production is mainly determined by T cells, especially Th2, which are present in the cellular infiltrates observed in OA [37]. It was reported that IL-4 alone or in combination with IL-10 is able to reduce the production of diverse proinflammatory mediators, such as IL-1β, TNF-α receptors, IL-6, PGE2, and COX-2 [82, 83, 84].
3.1.7 IL-10
Due to its anti-inflammatory features, IL-10 is another cytokine that presents chondroprotective effects, and it is linked to the release of IFN [62]. In vitro studies have shown increased proteoglycan and type II collagen syntheses after the administration of IL-10 in chondrocytes [62]. The protective effects that IL-10 exhibits are likely due to a stimulation of the synthesis of IL-1β antagonist and a tissue inhibition of MMP-1 (TIMP-1) [85]. Also, IL-10, as well as IL-4, reduces apoptotic events in chondrocytes and production of MMP [86, 87].
IL-10 induces the expression of bone morphogenetic protein-2 and -6 (BMP2 and BMP6), which are related to chondrogenesis as they belong to TGF-β family [88]. Together with BMP production, IL-10 activates signaling pathways, such as NKX-3.2/SOX9, that induce the differentiation of mesenchymal stem cells into chondrocytes [89]. Also, by reducing the expression of TNF-α receptors, IL-10 is able to attenuate the effect of TNF-α on synovial fibroblasts. A decrease in COX-2 production was also noted in the same study [90].
The secretion of IL-10 can be influenced by physical exercises. Patients with and without OA had synovial fluid and periarticular tissue harvested from their knee before, during, and after they underwent exercise practice for 3 hours. A significant increase in IL-10 levels was observed in these patients after the exercise. Although it is not clear what exact mechanism led to this result, this observation is likely attributed to an increase in intra-articular pressure and subsequent effects on cellular secretion [91, 92].
3.2 Chemokines
Chemokines comprise small proteins that act as chemoattractants to assist cells to migrate to injured tissue. Diverse chemokines have gained attention in the development of OA. Some of them including their receptors, such as IL-8, CCL5, CCL19, CCR1, CCR2, CCR3, and CCR5, may induce the production of MMP-3 by chondrocytes and increase the breakdown of cartilage matrix components, which trigger the onset of OA [60, 93]. However, some chemokines might present a protective role in OA, such as stromal cell-derived factor-1 (also called CXCL12), whose main function is to recruit mesenchymal stem cells to the injured area in order to promote tissue repair [94].
Several chemokines were reported to be overexpressed in OA, such as IL-8/CXCL-8, GROα/CXCL-1, MCP-1/CCL-2, RANTES/CCL-5, MIP-1α/CCL-3, and MIP-1β/CCL-4. Some of these chemokines are stimulated by IL-1β, which is upregulated in OA, and they induce MMP production upon binding to their ligands, causing tissue degradation [93]. Levels of INF-γ-inducible protein 10 (IP-10), also called as CXCL-10, in plasma and synovial fluid have been correlated with radiographic knee OA. CX3CL1, a serum fractalkine, has also been reported to be significantly elevated in severe knee OA in a study that compared OA patients with healthy patients [95].
To support the role of macrophage in the inflammatory response observed in OA, MCP-1, also known as chemokine ligand-2 (CCL2), has been reported to recruit macrophages into adipose tissue and atherosclerotic lesions [96]. Also, MCP-1 levels in both serum and synovial fluid has been associated with self-reported pain and disability in patients who present knee OA [97]. In addition, it was observed that, in severe knee OA, the levels of macrophage-derived chemokine (MDC) and IP-10 in synovial fluid were elevated, while eotaxin levels, an eosinophil chemotactic protein, were lower when compared with healthy patients [98].
3.3 Adipokines
Adipokines have been associated with the incidence and severity of OA [99]. In vitro studies reported that the presence of adipokines, such as leptin, adiponectin, visfatin, and resistin, increases the production of inflammatory mediators and also induces chondrolysis [99]. Although the exact mechanism of how these cytokines derived from adipose tissue act on arthritic joints has not yet been elucidated, researchers have studied the role of fat pad as a local inflammation mediator in OA, particularly in knee OA due to the infrapatellar fat pad, which has proven to be infiltrated with macrophages, lymphocytes, and granulocytes [100]. These findings support the thought that obesity supports the development of OA more through biochemical pathways rather than biomechanical overload risks on a weight-bearing joint.
3.4 Lipid mediators
The COX-2 enzyme is responsible for the production of lipid mediators, including PGE2 and leukotrienes, and it is also upregulated in OA joints. In addition, the overexpression of COX-2 in OA has been associated with the increased production of IL-1β, TNF, and IL-6 via toll-like receptor-4 (TLR-4) [101]. Besides assisting the production of MMPs and other functions already cited above, PGE2 is also involved in apoptosis and structural changes that characterize arthritic disease [102].
Leukotrienes have also been investigated for their role in OA. These mediators are converted from arachidonic acid, which also produces PGE2 via the activity of the enzyme phospholipase A2 [21]. Leukotrienes, mainly leukotriene B4 (LTB4), are present, to a lesser extent, in OA synovium, bone, and cartilage. Also, LTB4 has been reported to stimulate the production of IL-1β and TNF in arthritic synovium [103].
4. Conclusions
The cumulative evidences over the years have shown that increased expression of proinflammatory cytokines, in particular IL-1β, TNF, and IL-6, in cartilage as well as synovial fluid and membrane, has played a key role in the pathogenesis of OA. Inflammatory processes linked with immune responses have characterized OA as a complex disease and not as a simple age-related cartilage degeneration as it is thought to be. The understanding of individual roles of inflammatory mediators and their compounds is of utmost importance to target new therapies for OA, since the current options are elusive and may be noneffective, invasive, or even capable of presenting serious side effects. Due to advancements in molecular tools, the overall aim would be to dissect the role of each cytokine in the pathophysiology of OA and, together with drug delivery systems, to develop specific anticytokine therapy, given that inflammatory responses contribute substantially to OA maintenance.
Conflict of interest
The authors have no conflict of interest to declare.
\n',keywords:"osteoarthritis, immune response, inflammation, biomarkers, cytokines",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/64798.pdf",chapterXML:"https://mts.intechopen.com/source/xml/64798.xml",downloadPdfUrl:"/chapter/pdf-download/64798",previewPdfUrl:"/chapter/pdf-preview/64798",totalDownloads:1399,totalViews:390,totalCrossrefCites:4,dateSubmitted:"April 27th 2018",dateReviewed:"November 15th 2018",datePrePublished:"January 28th 2019",datePublished:"March 27th 2019",dateFinished:"December 14th 2018",readingETA:"0",abstract:"Osteoarthritis (OA) is the most prevalent joint disease and a common cause of joint pain, functional loss, and disability. In addition to macroscopic features, such as cartilage degradation with subchondral bone remodeling, hypertrophy of the joint capsule, and osteophytes formation, several cellular and molecular alterations are present in OA, which lead to a chronic low-grade inflammation. Inflammatory mediators observed in OA joints are thought to be the downstream effectors of the pathogenesis of the disease. Although cytokines are among the most extensively studied mediators of inflammation, such as IL-1β and TNF, there has been an increase in studies showing the contribution of chemokines and adipokines in OA progression. This fact is supported by recent progress, which has considerably improved knowledge of the factors involved in the development of OA and the mechanisms responsible for its progression. Therefore, the aim of this chapter is to discuss the involvement of the inflammatory response in OA maintenance, focusing on the main inflammatory markers observed in studies with OA.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/64798",risUrl:"/chapter/ris/64798",signatures:"José Fábio dos Santos Duarte Lana and Bruno Lima Rodrigues",book:{id:"7565",type:"book",title:"Osteoarthritis Biomarkers and Treatments",subtitle:null,fullTitle:"Osteoarthritis Biomarkers and Treatments",slug:"osteoarthritis-biomarkers-and-treatments",publishedDate:"March 27th 2019",bookSignature:"Hechmi Toumi and Marija Mazor",coverURL:"https://cdn.intechopen.com/books/images_new/7565.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-78985-738-2",printIsbn:"978-1-78985-737-5",pdfIsbn:"978-1-83962-098-0",isAvailableForWebshopOrdering:!0,editors:[{id:"196403",title:"Prof.",name:"Hechmi",middleName:null,surname:"Toumi",slug:"hechmi-toumi",fullName:"Hechmi Toumi"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Osteoarthritis and immune response",level:"1"},{id:"sec_3",title:"3. Inflammatory markers in osteoarthritis",level:"1"},{id:"sec_3_2",title:"3.1 Cytokines",level:"2"},{id:"sec_4_2",title:"3.1.1 IL-1β and TNF",level:"2"},{id:"sec_5_2",title:"3.1.2 IL-6",level:"2"},{id:"sec_6_2",title:"3.1.3 IL-15",level:"2"},{id:"sec_7_2",title:"3.1.4 IL-17",level:"2"},{id:"sec_8_2",title:"3.1.5 IL-18",level:"2"},{id:"sec_9_2",title:"3.1.6 IL-4",level:"2"},{id:"sec_10_2",title:"3.1.7 IL-10",level:"2"},{id:"sec_11_2",title:"3.2 Chemokines",level:"2"},{id:"sec_12_2",title:"3.3 Adipokines",level:"2"},{id:"sec_13_2",title:"3.4 Lipid mediators",level:"2"},{id:"sec_15",title:"4. Conclusions",level:"1"},{id:"sec_16",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'[Robinson WH, Lepus CM, Wang Q, Raghu H, Mao R, Lindstrom TM, et al. Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis. 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MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. The Journal of Clinical Investigation. 2006;116(6):1494-1505]'},{id:"B97",body:'[Li L, Jiang BE. Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis. Annals of Clinical Biochemistry. 2015;52(2):276-282]'},{id:"B98",body:'[Beekhuizen M, Gierman LM, van Spil WE, Van Osch GJVM, Huizinga TWJ, Saris DBF, et al. An explorative study comparing levels of soluble mediators in control and osteoarthritic synovial fluid. Osteoarthritis and Cartilage. 2013;21(7):918-922]'},{id:"B99",body:'[Conde J, Scotece M, Gómez R, Lopez V, Gómez-Reino JJ, Gualillo O. Adipokines and osteoarthritis: Novel molecules involved in the pathogenesis and progression of disease. Arthritis. 2011;2011:1-8]'},{id:"B100",body:'[Clockaerts S, Bastiaansen-Jenniskens YM, Runhaar J, Van Osch GJVM, Van Offel JF, Verhaar JAN, et al. The infrapatellar fat pad should be considered as an active osteoarthritic joint tissue: A narrative review. Osteoarthritis and Cartilage. 2010;18(7):876-882]'},{id:"B101",body:'[Geng Y, Blanco FJ, Cornelisson M, Lotz M. Regulation of cyclooxygenase-2 expression in normal human articular chondrocytes. Journal of Immunology. 1995;155(2):796-801]'},{id:"B102",body:'[Martel-Pelletier J, Pelletier JP, Fahmi H. Cyclooxygenase-2 and prostaglandins in articular tissues. Seminars in Arthritis and Rheumatism. 2003;33(3):155-167]'},{id:"B103",body:'[Oliveira SHP, Canetti C, Ribeiro RA, Cunha FQ. Neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon TNF-α and IL-1β released by mast cells. Inflammation. 2008;31(1):36-46]'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"José Fábio dos Santos Duarte Lana",address:"josefabiolana@gmail.com",affiliation:'- Institute of Bone and Cartilage, Indaiatuba, Sao Paulo, Brazil
'},{corresp:null,contributorFullName:"Bruno Lima Rodrigues",address:null,affiliation:'- Institute of Bone and Cartilage, Indaiatuba, Sao Paulo, Brazil
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Her postdoctoral fellowship was on T-cell deficiencies and stem cell transplantation at the University of Tubingen and HIV1 infection in macrophages and myeloid cells at the Institut Pasteur in Paris (1981–1985), where for the first time she got interested in vacuolization and prolonged viability as well as persistence of macrophages even under conditions of virus infections. Her next topics were hemophagocytic diseases (hemophagocytic lymphohistiocytosis, HLH) and macrophage activation syndromes (MAS) related to immune dysfunction and chronic virus infections as well as severe sepsis and septic shock. When taking the professorship for Experimental Anesthesiology at Ulm University, Ulm, Germany, in 1998, she concentrated on biomarker analysis combining soluble and membrane-bound characteristics of major inflammatory diseases related to inflammasome activation. Inflammation appears to be a major risk factor for sepsis (systemic inflammation) and also for tumor manifestation. In collaboration with the Department of Neurosurgery in the Ulm University, an intense analysis of autophagy has been initiated to overcome the upregulation of autophagy in type IV glioblastoma with novel chemotherapeutic agents.",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/200898/images/4957_n.jpg",totalCites:0,totalChapterViews:"0",outsideEditionCount:0,totalAuthoredChapters:"1",totalEditedBooks:"0",personalWebsiteURL:null,twitterURL:null,linkedinURL:null,institution:null},booksEdited:[],chaptersAuthored:[{id:"61417",title:"Mitophagy-Related Cell Death Mediated by Vacquinol-1 and TRPM7 Blockade in Glioblastoma IV",slug:"mitophagy-related-cell-death-mediated-by-vacquinol-1-and-trpm7-blockade-in-glioblastoma-iv",abstract:"Glioblastoma IV (GBM) is one of the deadliest malignant diseases in adults and is characterized by a high mutation rate and multiple traits to suppress inborn and acquired immunity. We here approached autophagy-related cell death in newly established GBM cell lines derived from individual tumor isolates. Treatment with a small molecule, termed Vacquinol-1 (Vac) exhibited 100% GBM cell death, which was related to mitochondrial dysfunction, calcium-induced endoplasmic reticulum (ER)-stress, and autophagy. The toxicity of Vac was significantly increased by the inhibition of transient receptor potential cation channel, subfamily M, member 7 (TRPM7). TRPM7 is overexpressed in GBM as well as in many other tumors and thus may be a potential target by the natural compound carvacrol. Of note, at higher concentrations, Vac also induced growth inhibition and cell death in non-transformed cell types. However, in the presence of the TRPM7 inhibitor carvacrol, the tumor-selective effect of Vac was very much increased. Results given in the present study are based on long-term video microscopy using IncuCyteZOOM®, calcium measurements, and 3D ultrastructural analysis using the cryofixed material.",signatures:"Philip Sander, Paul Walther, Barbara Moepps, Michael Hinz,\nHaouraa Mostafa, Patrick Schaefer, Andrej Pala, C. Rainer Wirtz,\nMichael Georgieff and E. Marion Schneider",authors:[{id:"158099",title:"Dr.",name:"Andrej",surname:"Pala",fullName:"Andrej Pala",slug:"andrej-pala",email:"andrej.pala@gmail.com"},{id:"166849",title:"Prof.",name:"Christian Rainer",surname:"Wirtz",fullName:"Christian Rainer Wirtz",slug:"christian-rainer-wirtz",email:"rainer.wirtz@uniklinik-ulm.de"},{id:"200898",title:"Dr.",name:"Elisabeth Marion",surname:"Schneider",fullName:"Elisabeth Marion Schneider",slug:"elisabeth-marion-schneider",email:"marion.schneider@uniklinik-ulm.de"},{id:"236809",title:"M.Sc.",name:"Philip",surname:"Sander",fullName:"Philip Sander",slug:"philip-sander",email:"philip.sander@uni-ulm.de"},{id:"236810",title:"Prof.",name:"Barbara",surname:"Moepps",fullName:"Barbara Moepps",slug:"barbara-moepps",email:"barbara.moepps@uni-ulm.de"},{id:"236811",title:"Prof.",name:"Michael",surname:"Georgieff",fullName:"Michael Georgieff",slug:"michael-georgieff",email:"michael.georgieff@uniklinik-ulm.de"},{id:"245687",title:"Dr.",name:"Paul",surname:"Walther",fullName:"Paul Walther",slug:"paul-walther",email:"paul.walther@uni-ulm.de"},{id:"245688",title:"Dr.",name:"Michael",surname:"Hinz",fullName:"Michael Hinz",slug:"michael-hinz",email:"michael.hinz@frizbiochem.de"},{id:"245689",title:"Dr.",name:"Haouraa",surname:"Mostafa",fullName:"Haouraa Mostafa",slug:"haouraa-mostafa",email:"haouraa-1.mostafa@uni-ulm.de"},{id:"245690",title:"Dr.",name:"Patrick",surname:"Schäfer",fullName:"Patrick Schäfer",slug:"patrick-schafer",email:"SCHAEFERP@EMAIL.CHOP.EDU"}],book:{id:"6700",title:"Glioma",slug:"glioma-contemporary-diagnostic-and-therapeutic-approaches",productType:{id:"1",title:"Edited Volume"}}}],collaborators:[{id:"236240",title:"M.D.",name:"Anastasiya",surname:"Ryabova",slug:"anastasiya-ryabova",fullName:"Anastasiya Ryabova",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Tomsk National Research Medical Center",institutionURL:null,country:{name:"Russia"}}},{id:"237145",title:"Prof.",name:"Ioan Stefan",surname:"Florian",slug:"ioan-stefan-florian",fullName:"Ioan Stefan Florian",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"242903",title:"Prof.",name:"Valery A.",surname:"Novikov",slug:"valery-a.-novikov",fullName:"Valery A. Novikov",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"242904",title:"Dr.",name:"Olga V.",surname:"Gribova",slug:"olga-v.-gribova",fullName:"Olga V. Gribova",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"242905",title:"Prof.",name:"Evgeny L.",surname:"Choynzonov",slug:"evgeny-l.-choynzonov",fullName:"Evgeny L. Choynzonov",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"242906",title:"Dr.",name:"Zhanna A.",surname:"Startseva",slug:"zhanna-a.-startseva",fullName:"Zhanna A. 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\n\nMetadata for all publications is also automatically deposited in IntechOpen's OAI repository, making them available through the Open Access Infrastructure for Research in Europe's (OpenAIRE) search interface further establishing our compliance.
\n\nIn other words, publishing with IntechOpen guarantees compliance.
\n\nRead more about Open Access in Horizon 2020 here.
\n\nWhich scientific publication to choose?
\n\nWhen choosing a publication, Horizon 2020 grant recipients are encouraged to provide open access to various types of scientific publications including monographs, edited books and conference proceedings.
\n\nIntechOpen publishes all of the aforementioned formats in compliance with the requirements and criteria established by the European Commission for the Horizon 2020 Program.
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As this indicates, their removal is insufficient by means of conventional modern water treatment techniques. In the search for a cost-effective solution, advanced oxidation processes have recently gained more attention since they are the most effective available techniques to decompose biorecalcitrant organics. As a main drawback, however, their energy costs are high up to now, preventing their implementation on large scale. For the specific case of water treatment by means of electrical discharge, further optimization is a complex task due to the wide variety in reactor design and materials, discharge types, and operational parameters. In this chapter, an extended overview is given on plasma reactor types, based on their design and materials. Influence of design and materials on energy efficiency is investigated, as well as the influence of operational parameters. The collected data can be used for the optimization of existing reactor types and for development of novel reactors.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Patrick Vanraes, Anton Y. Nikiforov and Christophe Leys",authors:[{id:"49112",title:"Prof.",name:"Christophe",middleName:null,surname:"Leys",slug:"christophe-leys",fullName:"Christophe Leys"},{id:"176861",title:"Dr.",name:"Anton",middleName:null,surname:"Nikiforov",slug:"anton-nikiforov",fullName:"Anton Nikiforov"},{id:"176862",title:"Mr.",name:"Patrick",middleName:null,surname:"Vanraes",slug:"patrick-vanraes",fullName:"Patrick Vanraes"}]},{id:"49562",doi:"10.5772/61784",title:"Laser-Induced Plasma and its Applications",slug:"laser-induced-plasma-and-its-applications",totalDownloads:4641,totalCrossrefCites:11,totalDimensionsCites:25,abstract:"The laser irradiation have shown a range of applications from fabricating, melting, and evaporating nanoparticles to changing their shape, structure, size, and size distribution. Laser induced plasma has used for different diagnostic and technological applications as detection, thin film deposition, and elemental identification. The possible interferences of atomic or molecular species are used to specify organic, inorganic or biological materials which allows critical applications in defense (landmines, explosive, forensic (trace of explosive or organic materials), public health (toxic substances pharmaceutical products), or environment (organic wastes). Laser induced plasma for organic material potentially provide fast sensor systems for explosive trace and pathogen biological agent detection and analysis. The laser ablation process starts with electronic energy absorption (~fs) and ends at particle recondensation (~ms). Then, the ablation process can be governed by thermal, non-thermal processes or a combination of both. There are several types of models, i.e., thermal, mechanical, photophysical, photochemical and defect models, which describe the ablation process by one dominant mechanism only. Plasma ignition process includes bond breaking and plasma shielding during the laser pulse. Bond breaking mechanisms influence the quantity and form of energy (kinetic, ionization and excitation) that atoms and ions can acquire. Plasma expansion depends on the initial mass and energy in the plume. The process is governed by initial plasma properties (electron density, temperature, velocity) after the laser pulse and the expansion medium. During first microsecond after the laser pulse, plume expansion is adiabatic afterwards line radiation becomes the dominant mechanism of energy loss.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Kashif Chaudhary, Syed Zuhaib Haider Rizvi and Jalil Ali",authors:[{id:"176684",title:"Dr.",name:"Kashif Tufail",middleName:null,surname:"Chaudhary",slug:"kashif-tufail-chaudhary",fullName:"Kashif Tufail Chaudhary"},{id:"176867",title:"Dr.",name:"Syed Zuhaib",middleName:null,surname:"Haider Rizivi",slug:"syed-zuhaib-haider-rizivi",fullName:"Syed Zuhaib Haider Rizivi"},{id:"176868",title:"Prof.",name:"Jalil",middleName:null,surname:"Ali",slug:"jalil-ali",fullName:"Jalil Ali"}]},{id:"64351",doi:"10.5772/intechopen.80798",title:"Progress in Plasma-Assisted Catalysis for Carbon Dioxide Reduction",slug:"progress-in-plasma-assisted-catalysis-for-carbon-dioxide-reduction",totalDownloads:1895,totalCrossrefCites:3,totalDimensionsCites:13,abstract:"Production of chemicals and fuels based on CO2 conversion is attracting a special attention nowadays, especially regarding the fast depletion of fossil resources and increase of CO2 emissions into the Earth’s atmosphere. Recently, plasma technology has gained increasing interest as a non-equilibrium medium suitable for CO2 conversion, which provides a promising alternative to the conventional pathway for greenhouse gas conversion. The combination of plasma and catalysis is of great interest for turning plasma chemistry in applications related to pollution and energy issues. In this chapter a short review of the current progress in plasma-assisted catalytic processes for CO2 reduction is given. The most widely used discharges for CO2 conversion are presented and briefly discussed, illustrating how to achieve a better energy and conversion efficiency. The chapter includes the recent status and advances of the most promising candidates (plasma catalysis) to obtain efficient CO2 conversion, along with the future outlook of this plasma-assisted catalytic process for further improvement.",book:{id:"7502",slug:"plasma-chemistry-and-gas-conversion",title:"Plasma Chemistry and Gas Conversion",fullTitle:"Plasma Chemistry and Gas Conversion"},signatures:"Guoxing Chen, Ling Wang, Thomas Godfroid and Rony Snyders",authors:[{id:"199226",title:"Mr.",name:"Guoxing",middleName:null,surname:"Chen",slug:"guoxing-chen",fullName:"Guoxing Chen"}]},{id:"63317",doi:"10.5772/intechopen.80523",title:"Plasma-Enabled Dry Methane Reforming",slug:"plasma-enabled-dry-methane-reforming",totalDownloads:1893,totalCrossrefCites:7,totalDimensionsCites:10,abstract:"Plasma-enabled dry methane reforming is a promising technology for biogas upgrade and shows multiple benefits to provide additional energy and material conversion pathways. This chapter first presents the role of nonthermal plasma as a potential energy supply pathway in the low-temperature methane conversion: an appropriated combination of electrical energy provided by plasma (ΔG) and the low-temperature thermal energy (TΔS) satisfies the overall reaction enthalpy (ΔH) with higher energy conversion efficiency. Moreover, plasma-enabled dry methane reforming could be operated at much lower temperature than thermal catalysis with sufficient material conversion. Three kinds of typical packed-bed plasma reactor were introduced to give a better understanding of the application of plasma and catalyst hybrid system. Subsequently, plasma-enabled dry methane reforming was diagnosed by pulsed reaction spectrometry compared with thermal catalysis, presenting a clear overview of gas component changes and significant promotion in reactant conversion and product yield. The interaction between plasma and catalyst was summarized based on two aspects: catalyst affects plasma, and plasma affects catalyst. We discussed the coke formation behavior of Ni/Al2O3 catalyst in the plasma-enabled and thermal dry methane reforming, followed by the oxidation behavior. The interaction between plasma and catalyst pellets was discussed toward deeper insight into the mechanism.",book:{id:"7502",slug:"plasma-chemistry-and-gas-conversion",title:"Plasma Chemistry and Gas Conversion",fullTitle:"Plasma Chemistry and Gas Conversion"},signatures:"Zunrong Sheng, Seigo Kameshima, Kenta Sakata and Tomohiro Nozaki",authors:null},{id:"49662",doi:"10.5772/62007",title:"Non-thermal Plasma Technology for the Improvement of Scaffolds for Tissue Engineering and Regenerative Medicine - A Review",slug:"non-thermal-plasma-technology-for-the-improvement-of-scaffolds-for-tissue-engineering-and-regenerati",totalDownloads:2204,totalCrossrefCites:4,totalDimensionsCites:10,abstract:"Non-thermal plasma technology is one of those techniques that suffer relatively little from diffusion limits, slow kinetics, and complex geometries compared to more traditional liquid-based chemical surface modification techniques. Combined with a lack of solvents, preservation of the bulk properties, and fast treatment times; it is a well-liked technique for the treatment of materials for biomedical applications. In this book chapter, a review will be given on what the scientific community determined to be essential to obtain appropriate scaffolds for tissue engineering and how plasma scientists have used non-thermal plasma technology to accomplish this. A distinction will be made depending on the scaffold fabrication technique, as each technique has its own set of specific problems that need to be tackled. Fabrication techniques will include traditional fabrication methods, rapid prototyping, and electrospinning. As for the different plasma techniques, both plasma activation and grafting/polymerization will be included in the review and linked to the in-vitro/in-vivo response to these treatments. The literature review itself is preceded by a more general overview on cell communication, giving useful insights on how surface modification strategies should be developed.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Pieter Cools, Rouba Ghobeira, Stijn Van Vrekhem, Nathalie De\nGeyterand and Rino Morent",authors:[{id:"31411",title:"Prof.",name:"Nathalie",middleName:null,surname:"De Geyter",slug:"nathalie-de-geyter",fullName:"Nathalie De Geyter"},{id:"32004",title:"Prof.",name:"Rino",middleName:null,surname:"Morent",slug:"rino-morent",fullName:"Rino Morent"},{id:"171765",title:"Dr.",name:"Pieter",middleName:null,surname:"Cools",slug:"pieter-cools",fullName:"Pieter Cools"},{id:"180883",title:"Mrs.",name:"Rouba",middleName:null,surname:"Ghobeira",slug:"rouba-ghobeira",fullName:"Rouba Ghobeira"},{id:"180884",title:"Mr.",name:"Stijn",middleName:null,surname:"Van Vrekhem",slug:"stijn-van-vrekhem",fullName:"Stijn Van Vrekhem"}]}],mostDownloadedChaptersLast30Days:[{id:"49562",title:"Laser-Induced Plasma and its Applications",slug:"laser-induced-plasma-and-its-applications",totalDownloads:4646,totalCrossrefCites:11,totalDimensionsCites:25,abstract:"The laser irradiation have shown a range of applications from fabricating, melting, and evaporating nanoparticles to changing their shape, structure, size, and size distribution. Laser induced plasma has used for different diagnostic and technological applications as detection, thin film deposition, and elemental identification. The possible interferences of atomic or molecular species are used to specify organic, inorganic or biological materials which allows critical applications in defense (landmines, explosive, forensic (trace of explosive or organic materials), public health (toxic substances pharmaceutical products), or environment (organic wastes). Laser induced plasma for organic material potentially provide fast sensor systems for explosive trace and pathogen biological agent detection and analysis. The laser ablation process starts with electronic energy absorption (~fs) and ends at particle recondensation (~ms). Then, the ablation process can be governed by thermal, non-thermal processes or a combination of both. There are several types of models, i.e., thermal, mechanical, photophysical, photochemical and defect models, which describe the ablation process by one dominant mechanism only. Plasma ignition process includes bond breaking and plasma shielding during the laser pulse. Bond breaking mechanisms influence the quantity and form of energy (kinetic, ionization and excitation) that atoms and ions can acquire. Plasma expansion depends on the initial mass and energy in the plume. The process is governed by initial plasma properties (electron density, temperature, velocity) after the laser pulse and the expansion medium. During first microsecond after the laser pulse, plume expansion is adiabatic afterwards line radiation becomes the dominant mechanism of energy loss.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Kashif Chaudhary, Syed Zuhaib Haider Rizvi and Jalil Ali",authors:[{id:"176684",title:"Dr.",name:"Kashif Tufail",middleName:null,surname:"Chaudhary",slug:"kashif-tufail-chaudhary",fullName:"Kashif Tufail Chaudhary"},{id:"176867",title:"Dr.",name:"Syed Zuhaib",middleName:null,surname:"Haider Rizivi",slug:"syed-zuhaib-haider-rizivi",fullName:"Syed Zuhaib Haider Rizivi"},{id:"176868",title:"Prof.",name:"Jalil",middleName:null,surname:"Ali",slug:"jalil-ali",fullName:"Jalil Ali"}]},{id:"64351",title:"Progress in Plasma-Assisted Catalysis for Carbon Dioxide Reduction",slug:"progress-in-plasma-assisted-catalysis-for-carbon-dioxide-reduction",totalDownloads:1899,totalCrossrefCites:3,totalDimensionsCites:13,abstract:"Production of chemicals and fuels based on CO2 conversion is attracting a special attention nowadays, especially regarding the fast depletion of fossil resources and increase of CO2 emissions into the Earth’s atmosphere. Recently, plasma technology has gained increasing interest as a non-equilibrium medium suitable for CO2 conversion, which provides a promising alternative to the conventional pathway for greenhouse gas conversion. The combination of plasma and catalysis is of great interest for turning plasma chemistry in applications related to pollution and energy issues. In this chapter a short review of the current progress in plasma-assisted catalytic processes for CO2 reduction is given. The most widely used discharges for CO2 conversion are presented and briefly discussed, illustrating how to achieve a better energy and conversion efficiency. The chapter includes the recent status and advances of the most promising candidates (plasma catalysis) to obtain efficient CO2 conversion, along with the future outlook of this plasma-assisted catalytic process for further improvement.",book:{id:"7502",slug:"plasma-chemistry-and-gas-conversion",title:"Plasma Chemistry and Gas Conversion",fullTitle:"Plasma Chemistry and Gas Conversion"},signatures:"Guoxing Chen, Ling Wang, Thomas Godfroid and Rony Snyders",authors:[{id:"199226",title:"Mr.",name:"Guoxing",middleName:null,surname:"Chen",slug:"guoxing-chen",fullName:"Guoxing Chen"}]},{id:"49712",title:"Plasma Nitriding of Titanium Alloys",slug:"plasma-nitriding-of-titanium-alloys",totalDownloads:3418,totalCrossrefCites:2,totalDimensionsCites:10,abstract:"Titanium alloys are found in many applications where weight saving, strength, corrosion resistance, and biocompatibility are important design priorities. However, their poor tribological behavior is a major drawback, and many surface engineering processes have been developed to enhance wear in titanium alloys such as nitriding. Plasma (ion) nitriding, originally developed for ferrous alloys, has been adopted to address wear concerns in titanium alloys. Plasma nitriding improves the wear resistance of titanium alloys by the formation of a thin surface layer composed of TiN and Ti2N titanium nitrides (e.g., compound layer). Nonetheless, plasma nitriding treatments of titanium alloys typically involve high temperatures (700–1100°C) that promote detrimental microstructural changes in titanium substrates, formation of brittle surface layers, and deterioration of mechanical properties especially fatigue strength. This chapter summarizes the previous and ongoing investigations in the field of plasma nitriding of titanium alloys, with particular emphasis on the authors’ recent efforts in optimization of the process to achieve tribological improvements while maintaining mechanical properties. The development of low-temperature plasma nitriding treatments for α + β and near-β titanium alloys and further wear improvements by alteration of near-surface microstructure prior to nitriding are also briefly reviewed.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Afsaneh Edrisy and Khorameh Farokhzadeh",authors:[{id:"176935",title:"Prof.",name:"Afsaneh",middleName:null,surname:"Edrisy",slug:"afsaneh-edrisy",fullName:"Afsaneh Edrisy"},{id:"176962",title:"Dr.",name:"Kora",middleName:null,surname:"Farrokhzadeh",slug:"kora-farrokhzadeh",fullName:"Kora Farrokhzadeh"}]},{id:"49564",title:"Optically Thick Laser-Induced Plasmas in Spectroscopic Analysis",slug:"optically-thick-laser-induced-plasmas-in-spectroscopic-analysis",totalDownloads:2278,totalCrossrefCites:0,totalDimensionsCites:2,abstract:"Studies on the plasma physics has been grown over the past few decades as a major research field. The plasma can be produced by different sources such as acr, spark, electric discharge, laser and so on. The spectral radiation of the plasma which acts as its fingerprint, contains valuable information about plasma features. Characterization of plasmas by spectroscopic measurement is a powerful tool for increasing the knowledge and applications of these kinds of radiation sources. Therefore, the spectral diagnostics methods are proposed which are based on measurement of spectral lines intensity, estimation of continuous and absorption radiation, and as well as determination of shifts and halfwiths of the spectrum [1]. The fundamental characteristic parameters of the plasma, i.e., the number densities of plasma species, electron temperature, and as well as particle transport property at each plasma space can be determined by optical emission spectroscopy and utilizing appropriate methods [2]. For accurate evaluation of plasma parameters, its thickness must be thoroughly considered. Generally, the plasmas can be separated into two categories of thin and thick groups. In thin plasmas, the re-absorption of radiation is negligible. Consequently, in spectroscopic analysis, the non-self-absorbed spectral radiation is evaluated by considering the summation of all spectral emissions along the line of sight. In optically thick plasmas, the radiation trapping happens which leads to the self-absorption phenomenon in spectroscopic analysis that is explained with details in below section.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Fatemeh Rezaei",authors:[{id:"176687",title:"Dr.",name:"Fatemeh",middleName:null,surname:"Rezaei",slug:"fatemeh-rezaei",fullName:"Fatemeh Rezaei"}]},{id:"50056",title:"Plasma-Enhanced Vapor Deposition Process for the Modification of Textile Materials",slug:"plasma-enhanced-vapor-deposition-process-for-the-modification-of-textile-materials",totalDownloads:2659,totalCrossrefCites:1,totalDimensionsCites:8,abstract:"Nowadays many techniques are used for the surface modification of fabrics and textiles. Two fundamental techniques based on vacuum deposition are known as chemical vapor deposition (CVD) and physical vapor deposition (PVD). In this chapter, the effect of plasma-enhanced physical and chemical vapor deposition on textile surfaces is investigated and explained.",book:{id:"5093",slug:"plasma-science-and-technology-progress-in-physical-states-and-chemical-reactions",title:"Plasma Science and Technology",fullTitle:"Plasma Science and Technology - Progress in Physical States and Chemical Reactions"},signatures:"Sheila Shahidi, Jakub Wiener and Mahmood Ghoranneviss",authors:[{id:"58854",title:"Dr.",name:null,middleName:null,surname:"Shahidi",slug:"shahidi",fullName:"Shahidi"},{id:"87913",title:"Prof.",name:"Jakub",middleName:null,surname:"Wiener",slug:"jakub-wiener",fullName:"Jakub Wiener"},{id:"176974",title:"Prof.",name:"Mahmood",middleName:null,surname:"Ghoranneviss",slug:"mahmood-ghoranneviss",fullName:"Mahmood Ghoranneviss"}]}],onlineFirstChaptersFilter:{topicId:"1232",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[],lsSeriesList:[],hsSeriesList:[],sshSeriesList:[],testimonialsList:[]},series:{item:{id:"25",title:"Environmental Sciences",doi:"10.5772/intechopen.100362",issn:"2754-6713",scope:"\r\n\tScientists have long researched to understand the environment and man’s place in it. The search for this knowledge grows in importance as rapid increases in population and economic development intensify humans’ stresses on ecosystems. Fortunately, rapid increases in multiple scientific areas are advancing our understanding of environmental sciences. Breakthroughs in computing, molecular biology, ecology, and sustainability science are enhancing our ability to utilize environmental sciences to address real-world problems.
\r\n\tThe four topics of this book series - Pollution; Environmental Resilience and Management; Ecosystems and Biodiversity; and Water Science - will address important areas of advancement in the environmental sciences. They will represent an excellent initial grouping of published works on these critical topics.
",coverUrl:"https://cdn.intechopen.com/series/covers/25.jpg",latestPublicationDate:"April 13th, 2022",hasOnlineFirst:!1,numberOfPublishedBooks:1,editor:{id:"197485",title:"Dr.",name:"J. Kevin",middleName:null,surname:"Summers",slug:"j.-kevin-summers",fullName:"J. Kevin Summers",profilePictureURL:"https://mts.intechopen.com/storage/users/197485/images/system/197485.jpg",biography:"J. Kevin Summers is a Senior Research Ecologist at the Environmental Protection Agency’s (EPA) Gulf Ecosystem Measurement and Modeling Division. He is currently working with colleagues in the Sustainable and Healthy Communities Program to develop an index of community resilience to natural hazards, an index of human well-being that can be linked to changes in the ecosystem, social and economic services, and a community sustainability tool for communities with populations under 40,000. He leads research efforts for indicator and indices development. Dr. Summers is a systems ecologist and began his career at the EPA in 1989 and has worked in various programs and capacities. This includes leading the National Coastal Assessment in collaboration with the Office of Water which culminated in the award-winning National Coastal Condition Report series (four volumes between 2001 and 2012), and which integrates water quality, sediment quality, habitat, and biological data to assess the ecosystem condition of the United States estuaries. He was acting National Program Director for Ecology for the EPA between 2004 and 2006. He has authored approximately 150 peer-reviewed journal articles, book chapters, and reports and has received many awards for technical accomplishments from the EPA and from outside of the agency. Dr. Summers holds a BA in Zoology and Psychology, an MA in Ecology, and Ph.D. in Systems Ecology/Biology.",institutionString:null,institution:{name:"Environmental Protection Agency",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:0,paginationItems:[]},overviewPageOFChapters:{paginationCount:0,paginationItems:[]},overviewPagePublishedBooks:{paginationCount:0,paginationItems:[]},openForSubmissionBooks:{},onlineFirstChapters:{paginationCount:0,paginationItems:[]},subseriesFiltersForOFChapters:[],publishedBooks:{},subseriesFiltersForPublishedBooks:[],publicationYearFilters:[],authors:{}},subseries:{item:{id:"25",type:"subseries",title:"Evolutionary Computation",keywords:"Genetic Algorithms, Genetic Programming, Evolutionary Programming, Evolution Strategies, Hybrid Algorithms, Bioinspired Metaheuristics, Ant Colony Optimization, Evolutionary Learning, Hyperparameter Optimization",scope:"Evolutionary computing is a paradigm that has grown dramatically in recent years. This group of bio-inspired metaheuristics solves multiple optimization problems by applying the metaphor of natural selection. It so far has solved problems such as resource allocation, routing, schedule planning, and engineering design. Moreover, in the field of machine learning, evolutionary computation has carved out a significant niche both in the generation of learning models and in the automatic design and optimization of hyperparameters in deep learning models. This collection aims to include quality volumes on various topics related to evolutionary algorithms and, alternatively, other metaheuristics of interest inspired by nature. For example, some of the issues of interest could be the following: Advances in evolutionary computation (Genetic algorithms, Genetic programming, Bio-inspired metaheuristics, Hybrid metaheuristics, Parallel ECs); Applications of evolutionary algorithms (Machine learning and Data Mining with EAs, Search-Based Software Engineering, Scheduling, and Planning Applications, Smart Transport Applications, Applications to Games, Image Analysis, Signal Processing and Pattern Recognition, Applications to Sustainability).",coverUrl:"https://cdn.intechopen.com/series_topics/covers/25.jpg",hasOnlineFirst:!1,hasPublishedBooks:!0,annualVolume:11421,editor:{id:"136112",title:"Dr.",name:"Sebastian",middleName:null,surname:"Ventura Soto",slug:"sebastian-ventura-soto",fullName:"Sebastian Ventura Soto",profilePictureURL:"https://mts.intechopen.com/storage/users/136112/images/system/136112.png",biography:"Sebastian Ventura is a Spanish researcher, a full professor with the Department of Computer Science and Numerical Analysis, University of Córdoba. Dr Ventura also holds the positions of Affiliated Professor at Virginia Commonwealth University (Richmond, USA) and Distinguished Adjunct Professor at King Abdulaziz University (Jeddah, Saudi Arabia). Additionally, he is deputy director of the Andalusian Research Institute in Data Science and Computational Intelligence (DaSCI) and heads the Knowledge Discovery and Intelligent Systems Research Laboratory. He has published more than ten books and over 300 articles in journals and scientific conferences. Currently, his work has received over 18,000 citations according to Google Scholar, including more than 2200 citations in 2020. In the last five years, he has published more than 60 papers in international journals indexed in the JCR (around 70% of them belonging to first quartile journals) and he has edited some Springer books “Supervised Descriptive Pattern Mining” (2018), “Multiple Instance Learning - Foundations and Algorithms” (2016), and “Pattern Mining with Evolutionary Algorithms” (2016). He has also been involved in more than 20 research projects supported by the Spanish and Andalusian governments and the European Union. He currently belongs to the editorial board of PeerJ Computer Science, Information Fusion and Engineering Applications of Artificial Intelligence journals, being also associate editor of Applied Computational Intelligence and Soft Computing and IEEE Transactions on Cybernetics. Finally, he is editor-in-chief of Progress in Artificial Intelligence. He is a Senior Member of the IEEE Computer, the IEEE Computational Intelligence, and the IEEE Systems, Man, and Cybernetics Societies, and the Association of Computing Machinery (ACM). Finally, his main research interests include data science, computational intelligence, and their applications.",institutionString:null,institution:{name:"University of Córdoba",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null,series:{id:"14",title:"Artificial Intelligence",doi:"10.5772/intechopen.79920",issn:"2633-1403"},editorialBoard:[{id:"111683",title:"Prof.",name:"Elmer P.",middleName:"P.",surname:"Dadios",slug:"elmer-p.-dadios",fullName:"Elmer P. 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