Representative non-syndromic and syndromic ichthyosis with causative genes. Modified citation from Ref. [3].
Keratinocytes are the principal epidermal cells constituting the outermost layer of the skin—the external and largest organ of the human body. They are immunologically active in that they produce various cytokines and chemokines, stimulating dendritic cells and lymphocytes to trigger inflammatory skin diseases, as well as they respond to cytokines produced from immune cells to establish skin lesions of inflammatory skin diseases, such as psoriasis and atopic dermatitis. They are also very efficient in avoiding harsh environmental assaults, such as chemical, mechanical, radiological, and microbial insults. The keratinocytes protect the dermal homeostasis by having a constant turnover whereby the basal (inner) layer differentiates into the cornified (outer) layer. Thus, they form a constant and perfect outer barrier to the inner dermal layers and the body. They also form a rigid mechanical barrier by cornification—constructing a brick-and-mortar type of structure with cornified cells and lipids, the defects in either of which cause hereditary skin disorders upon mutation. They also secrete various antimicrobial peptides, such as cathelicidin, psoriasin, defensin, and many S100 proteins, to protect the skin from infection. The nuclei of keratinocytes contain various alarmins, such as HMGB1, IL-33, and IL-1alpha, which can induce rapid and strong inflammation upon injury, but also can get promptly inactivated by the enzymes present in the inflammatory environment. However, malfunctioning of the keratinocytes at its immunological level or at a genetic/protein level can lead to pathological conditions such as psoriasis, atopic dermatitis, and hereditary skin disorders.
Keratinocytes, as the main component of outermost epidermal layer, should provoke and at the same time stop inflammation at appropriate time points to maintain a stable and healthy condition of not only the skin, but also the entire body. Keratinocytes harbor anti-inflammatory properties more than other types of cells do, such as lymphocytes, macrophages, and dendritic cells, as keratinocytes are always exposed to environmental insults. The mechanism of developing inflammatory conditions has been intensely investigated; however, the mechanism of ceasing inflammation has not been fully investigated. I speculate that a novel approach to maintaining healthy conditions would be unraveled when the mechanism of sequestrating inflammation is investigated and that epidermal keratinocytes are good candidates to investigate these mechanisms because they present pro- and anti-inflammatory properties in vivo and in vitro.
In this chapter, various cutaneous disorders have been discussed with emphasis on keratinocyte function and roles in pathogenesis. We have surveyed PubMed with each disease name, picked up the original literature with pivotal findings, reviewed articles covering the related area of interest, and wrote this chapter.
Epidermal keratinocytes form a stratified epithelium, consisting of basal, spinous, granular, and cornified layers starting from the dermal side. Epidermal keratinocytes exert their functions through structural components such as actin, microtubules, keratin filaments, desmosomes, hemidesmosomes, tight junctions, and adherence junctions; their motility, proliferation, and cytokine production being controlled by these structural proteins. Epidermal keratinocytes gradually differentiate through the layers—from the basal, spinous, and granular, ultimately to the cornified cell layer. They demonstrate various characteristic features owing to their differential function and according to their differentiation state, which are sometimes more complex than those of simple epithelial cells constituting the digestive tract and glands [1].
The primary and most important function of epidermal keratinocytes is their role as a physical barrier of the skin, in addition to their role as a responder to the external stimuli. The cornified cells, together with inter-cornified cell lipids, form cornified cell barriers to protect the inner body from harsh external environmental stimuli. The cornified cells, upon catalysis by transglutaminase 1, form a cornified cell envelope—a strong structure composed of filaggrin that aggregates keratin filaments, with various protein components such as involucrin, loricrin, SPR, and desmosomal proteins. Defects in the enzymes and protein components essential in forming cornified cell envelopes cause skin barrier dysfunction, resulting in skin disorders [2, 3].
Recent findings have revealed that some patients with atopic dermatitis (AD) harbor loss-of-function mutations in the filaggrin gene, resulting in severe skin barrier defects. Ichthyosis vulgaris (IV) is also caused by mutations in the filaggrin gene, but patients with this mutation develop either AD, IV, or both, indicating that mutations in the filaggrin gene alone are not enough to determine the phenotypes [4, 5, 6, 7]. Mutations in the transglutaminase 1 gene and other genes important in the cornification processes, such as ATP-binding cassette subfamily A member 12 (ABCA12), and arachidonate 12-lipoxygenase 12 s type (ALOX12), cause hereditary ichthyosis, also known as acquired recessive congenital ichthyosis [8]. Connexin is a component of the gap junction, and mutation in gap junction protein beta 3 (GJB3) gene, which encodes connexin (Cx31) causes erythrokeratodermia variabilis, in which inflammatory erythematous eruptions with hyperkeratinization gradually changes its form [9]. Mutations in the loricrin gene cause loricrin keratoderma, with characteristic finger constriction ring formation or congenital ichthyosiform erythroderma [10, 11].
Steroid sulfatase is an enzyme that catalyzes the degradation of cholesterol sulfate, a molecule that functions in the attachment of cornified cells. The mutation in its gene causes X-lined ichthyosis, with retarded detachment of cornified cells, termed as retention hyperkeratosis. Point mutations result in typical skin manifestations; whereas, mutations spanning bigger lengths of this gene involving the surrounding genomic region are accompanied by other syndromic symptoms, such as mental retardation, short stature, and epilepsy [12].
Some hereditary keratinizing disorders are accompanied by syndromic symptoms other than skin manifestations. Mutations in GJB2 gene, encoding Cx26, cause KID syndrome—with keratitis, ichthyosis, and deafness as triads, exhibiting papillomatous and spinous keratotic eruptions on the face and extremities, and with palmoplantar keratoderma and alopecia [13]. Mutation in the serine protease inhibitor SPINK5 causes Netherton syndrome, with atopic dermatitis-like skin eruptions, characteristic ichthyosis linearis circumflexa and bamboo hair [14]. Sjogren-Larsson syndrome is caused by a mutation in the fatty aldehyde dehydrogenase (ALDH3A2) gene, with clinical symptoms including ichthyosis, spastic limb paralysis, and mental retardation [15]. Figures 1 and 2 shows skin manifestations of several hereditary skin disorders. Table 1 shows a summary of the types of ichthyosis and their accompanying gene mutations.
Characteristic skin manifestation in hereditary skin disorders with mutation in genes expressed in keratinocytes. a) Bulla formation on the foot of a child having epidermolysis bullosa simplex (EBS) and with mutation in the
Ichthyosis vulgaris | AD | FLG | |
X-linked ichthyosis | XR | STS | |
Harlequin ichthyosis | AR | ABCA12 | |
Lamellar ichthyosis | AR | TGM1; NIPAL4; ALOX12B; ABCA12 | |
Congenital ichthyosiform erythroderma | AR | ALOXE3; ALOX12B; ABCA12; NIPAL4; TGM1 CYP4F22 | |
Epidermolytic ichthyosis | AD | KRT1; KRT10 | |
Superficial epidermolytic ichthyosis | AD | KRT2 | |
Loricrin keratoderma | AD | LOR | |
X-linked ichthyosis syndromic presentation | XR | STS and others | |
FPAP syndrome | XR | MBTPS2 | |
Netherton syndrome | AR | SPINK5 | |
Sjogren Larsson syndrome | AR | ALDH3A2 | |
Refsum syndrome | AR | PHYH; PEX7 | |
Gaucher syndrome II | AR | GBA | |
KID syndrome | AD | GJB2; GJB6 |
Representative non-syndromic and syndromic ichthyosis with causative genes. Modified citation from Ref. [3].
Keratins are the main intermediate filaments of epidermal keratinocytes. The keratin family consists of more than 50 members; acidic keratin and basic keratin monomers pair to form heterodimers, which are then organized into tetramers with an anti-parallel alignment. Tetramers of keratins are stored at the peripheral boundaries of cells for filament formation when needed. Lateral and longitudinal aggregations of these tetramers and octamers form keratin filaments. Local pH, osmotic conditions, and phosphorylation status are thought to be the driving forces of filament formation [16].
Simple epithelia consist of simple epithelial keratins, such as K8, K18, and K19. Basal cells of the simple and stratified epithelia express K5 and K14, while the suprabasal cells express K1 and K10 in the interfollicular epidermis, K3 and K12 in the corneal epithelium, K4 and K13 in the esophageal epithelium, and K6 and K16 in the oral epithelium. The follicular epidermis and palmoplantar epidermis express K6, K16, and K17. Their expression is tightly controlled by transcription factors in a differentiation- and localization-dependent manner.
Mutations in keratin genes cause various hereditary skin disorders [17]. Mutations either in
Characteristic skin manifestation and electron microscopic findings of genetic skin disorders. a) Clinical manifestation of X-liked ichthyosis (XI) patient, b) histopathology with hematoxylin and eosin staining, c) electron microscopic features in patients with XI and deletion in
Adherence machinery is indispensable for controlling keratinocyte cell motility, proliferation, and viability, as well as the epidermal barrier function by controlling cell attachment and cell tension. Keratinocytes have six major adherence mechanisms [23, 24]: 1) Hemidesmosomes, which connect basal keratinocytes to the dermal component, with cytoskeletal molecules such as keratins, 2) desmosomes, which connect neighboring keratinocytes, sustain the epidermal sheet structure and maintain tension by connecting to cytoskeletal molecules, such as keratins, 3) Adherence junctions, which control keratinocyte motility by connecting intracellular actin to E-cadherin in the adherence junctions to neighboring keratinocytes [25], 4) Gap junctions, which also have ion-transporter functions, indirectly control keratinocyte barrier function, 5) Tight junctions, which control the liquid interface in epithelia and consist of claudins and occludins [26], and 6) Focal adhesion—attachment of plaques connecting cells to the extracellular matrix, thereby, making connections to scaffolds to maintain the keratinocyte motility, proliferation, and viability.
Hemidesmosomal proteins are indispensable for maintaining normal dermal-epidermal structures (Figure 3) [27, 28]. Mutations in hemidesmosomal protein genes, such as integrin alpha 6 or beta 4, cause junctional epidermolysis bullosa [29]. Mutations in plectin, a constituent of desmosomes and hemidesmosomes, cause junctional type epidermolysis bullosa with pyloric atresia [30]. Collagen type VII localizes from just beneath lamina densa to support attachment of lamina densa to the dermal structure. Mutations in the collagen type VII gene cause dystrophic epidermolysis bullosa with prominent skin ulcer and scar formation [31, 32]. These severe EBs usually occur in patients with homozygous mutation or compound heterozygous mutations. A heterozygous mutation, the same mutation but which harbors on only one allele of the gene, causes a milder form of EB, leading to the development of nodular prurigo-like lesions or scar formations in autosomal dominant type dystrophic EB or development of palmoplantar keratoderma with alopecia and dental deformation in autosomal dominant type junctional EB. A recent study revealed that mutations in desmoplakin cause lethal acantholytic epidermolysis bullosa [33].
The structure of hemidesmosome. a) Electron microscopy of hemidesmosomes and basal lamina of a normal human subject. b) Schematic view of a hemidesmosome structure. Plectin forms a platform where keratin filaments and hemidesmosomal proteins bind, crosslinking keratin filaments with integrin beta4. Transmembrane protein bullous pemphigoid antigen 1 (BP180) connects hemidesmosomes to laminin 332, a component of the lamina densa. Bullous pemphigoid antigen 2 (BP230) is an intra-cytoplasmic protein that composes the hemidesmosome from inside the cells.
Atopic dermatitis patients present decreased filaggrin and ceramide contents in their cornified layers, along with decreased skin barrier function [34]. This dysfunctional barrier allows allergens to penetrate the skin, thus, resulting in sensitization to environmental allergens [35]. Peanut allergies are often observed in infants of families that consume large amounts of peanut and have detectable levels of peanut debris in the surrounding environment [36]. Exercise-induced food allergy also develops in relation to filaggrin mutation [37]. A previous study has shown that infants with frequent emollient hydration of skin showed a lower rate of bronchial asthma development compared to babies without emollient hydration of skin, indicating the importance of the skin barrier functioning in maintaining overall health and stable homeostasis [38]. Figure 4 illustrates the epidermal structure with barrier proteins.
Mutations in filaggrin and protease inhibitors can cause atopic dermatitis. Netherton syndrome is caused by a mutation in the serine protease inhibitor KAZAL type5 (
Lipid abnormalities could be another cause of atopic dermatitis, demonstrating the skin barrier dysfunction. A decrease in ceramide content of the cornified layer has been demonstrated in patients with atopic dermatitis, which is another cause of skin barrier dysfunction [42]. Ceramide constitutes almost 50% of the lipids in the corneal layer and is indispensable for skin barrier function. Mutations in genes involved in lipid metabolism are not known in atopic dermatitis, but gene metabolic diseases, such as Gauche disease and Nieman-Pick disease that are characterized by mutations in the glucocerebrosidase and sphingomyelin phosphodiesterase 1 gene, respectively, which are indispensable in ceramide synthesis, resulting in development of atopic dermatitis-like skin eruptions from early childhood. Abnormalities in lipid metabolism could be another cause of atopic dermatitis, which requires further investigation [43].
Skin barrier function is affected not only by genetic conditions but also by ordinary routines of daily life. People who often scrub too much during bathing, bathe for a long time period or very frequently, and especially those who scrub their skin with nylon towels or scrubbing brushes show very dry skin with small scales all over the body. These individuals often complain of severe itching, especially after bathing, often resulting in eczema development. Excessive use of detergent also causes barrier disruption by increasing the pH of the skin, resulting in enhanced enzymatic activity of proteinases in the cornified layers [44]. These lifestyle routines would exacerbate eczematous changes in individuals having a genetic predisposition that makes them more susceptible to barrier disruption.
Keratinocytes form not only mechanical barriers but also chemical or immunological barriers for humans. They express several antimicrobial peptides, such as cathelicidin, defensin, psoriasin, and various S100 proteins. These antimicrobial peptides prevent pathogenic microbes from colonizing the skin surface, thus conferring resistance to microbial infections [45]. Certain conditions such as atopic dermatitis have decreased production of antimicrobial peptides, leaving the individuals more susceptible to bacterial or viral infections through the skin [46, 47]. Filaggrin mutations are at times the direct cause of barrier disruption, but T helper (Th)2-skewed immune conditions can be another cause too, as Th2 type cytokines cause a less differentiated state of keratinocytes thus resulting in lower production of antimicrobial molecules and barrier proteins [48]. Mutations in filaggrin also cause ichthyosis vulgaris, which often co-exists in atopic dermatitis patients. However, not all patients with atopic dermatitis have ichthyosis vulgaris and vice versa, even in the presence of filaggrin gene mutations [7]. Thus, the filaggrin mutation alone cannot explain the pathogenesis of atopic dermatitis.
The structure of epidermis and its adhesion molecules. a) Schematic view of epidermis structure and its adhesion molecules. Basal keratinocytes attach to basement membrane through hemidesmosomes, having keratins such as
Psoriasis is another major inflammatory skin disorder that shows hyperproduction of antimicrobial peptides in the epidermis induced by skewed Th17 populations thus making patients resistant to skin infections [49, 50]. Cathelicidin—one of the antimicrobial peptides, complexes with self RNA or DNA to induce the activation of myeloid dendritic cells and plasmacytoid dendritic cells, respectively. This activation further triggers psoriatic inflammation, thus creating a positive feedback loop in pathogenesis of psoriasis [51, 52]. Recent advancements in translational research produced many “biologics”, which target inflammatory cytokines, such as IL-17, TNF, and IL-23, as a treatment option for psoriasis. These include anti-TNF antibodies (adalimumab [53], infliximab [54], certolizumab-pegol [55]), anti-IL-17 antibodies (secukinumab [56, 57], ixekizumab [58], brodalumab [59], bimekizumab [60]), anti-IL-12/23p40 antibody (ustekinumab [61, 62]), and anti-IL-23p19 antibodies (guselkumab [63], risankizumab [64, 65], thildrakizumab [66, 67, 68, 69]). Janus kinases (JAKs) are important intracellular signaling molecules downstream of cytokine receptors [70]. They are also deeply involved in inflammation in psoriasis, and JAK inhibitors have been developed as therapeutic options in psoriasis [71, 72, 73, 74, 75, 76].
Ichthyosis has also been shown to have a Th17-skewed immune balance [77], and Th17 is a potent inducer of antifungal immunity. However, ichthyosis patients often develop cutaneous superficial fungal infections [78, 79]. Taken together, this suggests that the immune imbalance by itself cannot explain the susceptibility to fungal infections, meanwhile also implicating the importance of proper functioning of the skin barrier to avoid superficial fungal infections.
As a barrier, keratinocytes respond to emergency conditions by releasing danger-associated molecular patterns (DAMPs) when acutely injured. IL-33 is one such emergency molecule, which resides in the nucleus in a steady-state, but is released when cells undergo necrosis to stimulate immune reactions [80]. IL-33 is a relatively recently identified member of the IL-1 family and functions mainly as a pro-inflammatory molecule, although under certain conditions, it can also work as an anti-inflammatory molecule. IL-1 alpha—the prototype of IL-1 family members, was identified as an alarmin several decades ago. The Koebner phenomenon in psoriasis is attributed to the release of IL-1 alpha from damaged keratinocytes, which induces psoriasis in regions after skin injury [81]. IL-1 alpha is an interesting cytokine that mainly functions as a soluble cytokine, but also shows a nuclear presence. It has been reported that IL-1 alpha repeatedly travels between the cytoplasm and nucleus, and is released into the extracellular space upon cell damage to provoke inflammation [82]. IL-33 has similar characteristics in that it resides in the nucleus too, is released during cell necrosis, and induces inflammation. IL-33, similar to IL-1 beta, is produced as a full-length pro-form. IL-33 pro-form is active, but even more, activated when digested by neutrophil elastases or cathepsin. It is, however, inactivated when digested by caspases, unlike IL-1 beta, which is activated by caspases during activation of NRLP3 inflammasomes. ST2L—a receptor of IL-33, is expressed on Th2 cells, group 2 innate lymphoid cells, and regulatory T cells, and its soluble form—sST2, blocks the interaction of IL-33 with ST2L [83].
IL-33 exhibits both pro-inflammatory and anti-inflammatory roles. As a Th2 cytokine, it stimulates ST2L-expressing cells, including mast cells, Th2, and ILC2 cells. This enhances Th2 type inflammation by inducing expression of Th2 type cytokines, such as IL-5 and IL-13. However, upon Th1 or Th17 activation, IL-33 may attenuate pathological conditions by skewing Th2 type inflammation. The graft versus host disease (GVHD) reaction [84] was reported to be attenuated by IL-33, and experimental autoimmune encephalomyelitis showed reduction in response to IL-33 action [85]. Graft rejection in heart transplantation was reported to be attenuated by treatment with IL-33 [86]. IL-33, by inducing regulatory T cell function, was shown to induce immunosuppression [87]. UVB-induced immunosuppression too has been shown to be attributed with IL-33 [87]. Immune dysregulation in coronavirus infection is hypothesized to be caused by the IL-1 family member of cytokines [88]. IL-33 has also been shown to induce neutrophilic infiltration in several animal models and disease conditions, which may be interpreted as a pro-inflammatory effect [89].
IL-33 has dual nuclear and soluble cytokine forms. Nuclear IL-33 functions as a transcriptional regulator. In acute wound healing processes, IL-33 functions by attenuating inflammation by affecting the NF kappa B activity and enhancing wound healing [90]. On the other hand, IL-33 as a cytokine enhances immune reactions in decubitus ulcer models (unpublished). Both IL-33 and IL-1 alpha, when in the nucleus, bind to chromatin and are not released easily, thus, forming a reservoir for inflammatory signals. The regulation of nuclear or cytoplasmic localization of IL-33 is not clear but maybe dependent on its nuclear localization signal. Tsuda et al. [91] revealed that there are several different forms of splice variants of naturally occurring IL-33, of which expression is regulated by distinct promoters [92]. These splice variants should have distinct roles, which could regulate the pro- or anti-inflammatory properties of IL-33.
In the steady-state, keratinocytes should remain silent as a constitutively active state could result in excessive inflammation, which in turn can harm the overall human health. Cultured keratinocytes usually require higher concentrations of cytokines to provoke inflammatory signals; for example, keratinocytes need TNF in the range of several ng/ml to produce inflammatory cytokines, while dendritic cells or lymphocytes require only several pg/ml of the same cytokine to produce an inflammatory effect to the same or even a greater extent [93, 94]. Keratinocytes by differentiating to cornified cells become resistant to environmental stimuli, such as UVB; i.e., they usually respond sensitively to UVB in monolayer culture, but they become resistant to UVB stimulation when they differentiate in 3D-culture [95]. Some chemokines, such as MIP3 alpha/CCL20 are produced more in suprabasal cells than from basal cells [96], but production of IL-1 receptor antagonist is enhanced when keratinocytes are differentiated [97], which may result in attenuation of inflammatory response in differentiated keratinocytes. IL-33 and IL-1 alpha, more clearly expressed in suprabasal cells [98], when in the nucleus bind to chromatin not to be released easily, thus forming the reservoir for inflammatory signals.
Epidermal keratinocytes protect humans from the outer environment by forming an efficient mechanical, chemical, and antimicrobial barrier. Mutations in various molecules present in the keratinocyte can cause hereditary disorders. The keratinocyte structure is maintained by many structural molecules, including keratins, actin, microtubules, and associated proteins and adhesion molecules. The barrier function depends on these structural molecules, as well as other antimicrobial and immunological components, such as infiltrating or resident immune cells, such as lymphocytes, dendritic cells, and macrophages. At the same time, keratinocytes are resistant to stimulation in comparison to other cell types, such as lymphocytes and dendritic cells, as shown in some pieces of literature that they respond to the same stimuli with much fewer attitudes compared to immune cells. IL-33, an alarmin released during insults into the skin, works as an alarmin to provoke inflammation, but at the same time often attenuates inflammation by activating regulatory T cells and skewing Th2 mediated inflammation. This relative unresponsiveness and dual-faced character with pro- and anti-inflammatory properties would be the characteristics of keratinocytes, which cover the entire body by facing environmental stimuli all the time. Thus, the differentiation and structural characteristics of epidermal keratinocytes prevent the skin from hypersensitivity to environmental stimuli.
The mechanism of developing inflammatory conditions has been intensively investigated, but the mechanism by which the inflammation status returns to the steady-state, or how inflammatory status remains under control to prevent excessive inflammation in healthy humans has not been fully investigated.
A novel approach to maintaining healthy conditions would be unraveled when the mechanism of sequestrating inflammation and returning to normal steady-state condition is investigated. Epidermal keratinocytes are good candidates to investigate these mechanisms because they present both pro- and anti-inflammatory properties in vivo and in vitro.
I thank all the members of our department for participating in clinical and basic research on patients.
The authors declare no conflict of interest.
"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.
",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)
\\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:
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\\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
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\\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
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\\n\\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\\n\\nDigital Archiving Policy
\\n\\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\\n\\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\\n\\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\\n\\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\\n\\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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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.
\n\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\n\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\n\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\n\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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Among different technologies for hydrogen production, oxygenic natural and artificial photosynthesis using direct photochemistry in synthetic complexes have a great potential to produce hydrogen as both use clean and cheap sources - water and solar energy. Photosynthetic organisms capture sunlight very efficiently and convert it into organic molecules. Artificial photosynthesis is one way to produce hydrogen from water using sunlight by employing biomimetic complexes. However, splitting of water into protons and oxygen is energetically demanding and chemically difficult. In oxygenic photosynthetic microorganisms water is splitted into electrons and protons during primary photosynthetic processes. The electrons and protons are redirected through the photosynthetic electron transport chain to the hydrogen-producing enzymes-hydrogenase or nitrogenase. By these enzymes, e- and H+ recombine and form gaseous hydrogen. Biohydrogen activity of hydrogenase can be very high but it is extremely sensitive to photosynthetic O2. At the moment, the efficiency of biohydrogen production is low. However, theoretical expectations suggest that the rates of photon conversion efficiency for H2 bioproduction can be high enough (> 10%). Our review examines the main pathways of H2 photoproduction using photosynthetic organisms and biomimetic photosynthetic systems and focuses on developing new technologies based on the effective principles of photosynthesis.",book:{id:"3587",slug:"biomimetics-learning-from-nature",title:"Biomimetics",fullTitle:"Biomimetics Learning from Nature"},signatures:"Suleyman I. Allakhverdiev, Vladimir D. Kreslavski, Velmurugan Thavasi, Sergei K. Zharmukhamedov, Vyacheslav V. 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It performs very complex tasks while occupying about 2 liters of volume and consuming very little energy. The computation tasks are performed by special cells in the brain called neurons. They compute using electrical pulses and exchange information between them through chemicals called neurotransmitters. With this as inspiration, there are several compute models which exist today trying to exploit the inherent efficiencies demonstrated by nature. The compute models representing spiking neural networks (SNNs) are biologically plausible, hence are used to study and understand the workings of brain and nervous system. More importantly, they are used to solve a wide variety of problems in the field of artificial intelligence (AI). They are uniquely suited to model temporal and spatio-temporal data paradigms. 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Finally, applications on the chaotic time series prediction and the video frame recognition will be demonstrated.",book:{id:"6875",slug:"bio-inspired-technology",title:"Bio-Inspired Technology",fullTitle:"Bio-Inspired Technology"},signatures:"Kangjun Bai and Yang Yi",authors:[{id:"239041",title:"Prof.",name:"Yang",middleName:null,surname:"Yi",slug:"yang-yi",fullName:"Yang Yi"},{id:"245542",title:"Mr.",name:"Kangjun",middleName:null,surname:"Bai",slug:"kangjun-bai",fullName:"Kangjun Bai"}]},{id:"58622",title:"Bio-inspired Adaptable Facade Control Reflecting User's Behavior",slug:"bio-inspired-adaptable-facade-control-reflecting-user-s-behavior",totalDownloads:1619,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"The purpose of this research is to develop the process of methodology in designing adaptable façade. This study focuses on the processes of façade operation control for each resident’s unit according to the user’s lifestyle. 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His research focuses on biochemistry, biophysics, genetics, molecular biology, and molecular medicine with specialization in the fields of drug design, protein structure-function, protein folding, prions, microRNA, pseudogenes, molecular cancer, epigenetics, metabolites, proteomics, genomics, protein expression, and characterization by spectroscopic and calorimetric methods.",institutionString:"University of Health Sciences",institution:null},{id:"180528",title:"Dr.",name:"Hiroyuki",middleName:null,surname:"Kagechika",slug:"hiroyuki-kagechika",fullName:"Hiroyuki Kagechika",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180528/images/system/180528.jpg",biography:"Hiroyuki Kagechika received his bachelor’s degree and Ph.D. in Pharmaceutical Sciences from the University of Tokyo, Japan, where he served as an associate professor until 2004. He is currently a professor at the Institute of Biomaterials and Bioengineering (IBB), Tokyo Medical and Dental University (TMDU). From 2010 to 2012, he was the dean of the Graduate School of Biomedical Science. Since 2012, he has served as the vice dean of the Graduate School of Medical and Dental Sciences. He has been the director of the IBB since 2020. Dr. Kagechika’s major research interests are the medicinal chemistry of retinoids, vitamins D/K, and nuclear receptors. 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Then, he was appointed as an Assistant Professor of Neurology, UTHSC in 2005. He moved to the Cleveland Clinic in USA as a Project Scientist/Staff in 2006 where he focused on the studies of eye disease proteomics and biomarkers. He returned to UTHSC as an Assistant Professor of Neurology in the end of 2007, engaging in proteomics and biomarker studies of lung diseases and brain tumors, and initiating the studies of predictive, preventive, and personalized medicine (PPPM) in cancer. In 2010, he was promoted to Associate Professor of Neurology, UTHSC. Currently, he is a Professor at Xiangya Hospital of Central South University in China, Fellow of Royal Society of Medicine (FRSM), the European EPMA National Representative in China, Regular Member of American Association for the Advancement of Science (AAAS), European Cooperation of Science and Technology (e-COST) grant evaluator, Associate Editors of BMC Genomics, BMC Medical Genomics, EPMA Journal, and Frontiers in Endocrinology, Executive Editor-in-Chief of Med One. He has\npublished 116 peer-reviewed research articles, 16 book chapters, 2 books, and 2 US patents. 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He has published several articles in peer-reviewed journals, chapters, and edited books. His area of specialization is free radical biochemistry and autoimmune diseases.",institutionString:"Imam Abdulrahman Bin Faisal University",institution:{name:"Imam Abdulrahman Bin Faisal University",country:{name:"Saudi Arabia"}}},{id:"41865",title:"Prof.",name:"Farid A.",middleName:null,surname:"Badria",slug:"farid-a.-badria",fullName:"Farid A. Badria",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/41865/images/system/41865.jpg",biography:"Farid A. Badria, Ph.D., is the recipient of several awards, including The World Academy of Sciences (TWAS) Prize for Public Understanding of Science; the World Intellectual Property Organization (WIPO) Gold Medal for best invention; Outstanding Arab Scholar, Kuwait; and the Khwarizmi International Award, Iran. He has 250 publications, 12 books, 20 patents, and several marketed pharmaceutical products to his credit. He continues to lead research projects on developing new therapies for liver, skin disorders, and cancer. Dr. Badria was listed among the world’s top 2% of scientists in medicinal and biomolecular chemistry in 2019 and 2020. He is a member of the Arab Development Fund, Kuwait; International Cell Research Organization–United Nations Educational, Scientific and Cultural Organization (ICRO–UNESCO), Chile; and UNESCO Biotechnology France",institutionString:"Mansoura University",institution:{name:"Mansoura University",country:{name:"Egypt"}}},{id:"329385",title:"Dr.",name:"Rajesh K.",middleName:"Kumar",surname:"Singh",slug:"rajesh-k.-singh",fullName:"Rajesh K. Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/329385/images/system/329385.png",biography:"Dr. Singh received a BPharm (2003) and MPharm (2005) from Panjab University, Chandigarh, India, and a Ph.D. (2013) from Punjab Technical University (PTU), Jalandhar, India. He has more than sixteen years of teaching experience and has supervised numerous postgraduate and Ph.D. students. He has to his credit more than seventy papers in SCI- and SCOPUS-indexed journals, fifty-five conference proceedings, four books, six Best Paper Awards, and five projects from different government agencies. He is currently an editorial board member of eight international journals and a reviewer for more than fifty scientific journals. He received Top Reviewer and Excellent Peer Reviewer Awards from Publons in 2016 and 2017, respectively. He is also on the panel of The International Reviewer for reviewing research proposals for grants from the Royal Society. He also serves as a Publons Academy mentor and Bentham brand ambassador.",institutionString:"Punjab Technical University",institution:{name:"Punjab Technical University",country:{name:"India"}}},{id:"142388",title:"Dr.",name:"Thiago",middleName:"Gomes",surname:"Gomes Heck",slug:"thiago-gomes-heck",fullName:"Thiago Gomes Heck",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/142388/images/7259_n.jpg",biography:null,institutionString:null,institution:{name:"Universidade Regional do Noroeste do Estado do Rio Grande do Sul",country:{name:"Brazil"}}},{id:"336273",title:"Assistant Prof.",name:"Janja",middleName:null,surname:"Zupan",slug:"janja-zupan",fullName:"Janja Zupan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/336273/images/14853_n.jpeg",biography:"Janja Zupan graduated in 2005 at the Department of Clinical Biochemistry (superviser prof. dr. Janja Marc) in the field of genetics of osteoporosis. Since November 2009 she is working as a Teaching Assistant at the Faculty of Pharmacy, Department of Clinical Biochemistry. In 2011 she completed part of her research and PhD work at Institute of Genetics and Molecular Medicine, University of Edinburgh. She finished her PhD entitled The influence of the proinflammatory cytokines on the RANK/RANKL/OPG in bone tissue of osteoporotic and osteoarthritic patients in 2012. From 2014-2016 she worked at the Institute of Biomedical Sciences, University of Aberdeen as a postdoctoral research fellow on UK Arthritis research project where she gained knowledge in mesenchymal stem cells and regenerative medicine. She returned back to University of Ljubljana, Faculty of Pharmacy in 2016. She is currently leading project entitled Mesenchymal stem cells-the keepers of tissue endogenous regenerative capacity facing up to aging of the musculoskeletal system funded by Slovenian Research Agency.",institutionString:null,institution:{name:"University of Ljubljana",country:{name:"Slovenia"}}},{id:"357453",title:"Dr.",name:"Radheshyam",middleName:null,surname:"Maurya",slug:"radheshyam-maurya",fullName:"Radheshyam Maurya",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/357453/images/16535_n.jpg",biography:null,institutionString:null,institution:{name:"University of Hyderabad",country:{name:"India"}}},{id:"418340",title:"Dr.",name:"Jyotirmoi",middleName:null,surname:"Aich",slug:"jyotirmoi-aich",fullName:"Jyotirmoi Aich",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000038Ugi5QAC/Profile_Picture_2022-04-15T07:48:28.png",biography:"Biotechnologist with 15 years of research including 6 years of teaching experience. Demonstrated record of scientific achievements through consistent publication record (H index = 13, with 874 citations) in high impact journals such as Nature Communications, Oncotarget, Annals of Oncology, PNAS, and AJRCCM, etc. Strong research professional with a post-doctorate from ACTREC where I gained experimental oncology experience in clinical settings and a doctorate from IGIB where I gained expertise in asthma pathophysiology. A well-trained biotechnologist with diverse experience on the bench across different research themes ranging from asthma to cancer and other infectious diseases. An individual with a strong commitment and innovative mindset. Have the ability to work on diverse projects such as regenerative and molecular medicine with an overall mindset of improving healthcare.",institutionString:"DY Patil Deemed to Be University",institution:null},{id:"349288",title:"Prof.",name:"Soumya",middleName:null,surname:"Basu",slug:"soumya-basu",fullName:"Soumya Basu",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000035QxIDQA0/Profile_Picture_2022-04-15T07:47:01.jpg",biography:"Soumya Basu, Ph.D., is currently working as an Associate Professor at Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India. With 16+ years of trans-disciplinary research experience in Drug Design, development, and pre-clinical validation; 20+ research article publications in journals of repute, 9+ years of teaching experience, trained with cross-disciplinary education, Dr. Basu is a life-long learner and always thrives for new challenges.\r\nHer research area is the design and synthesis of small molecule partial agonists of PPAR-γ in lung cancer. She is also using artificial intelligence and deep learning methods to understand the exosomal miRNA’s role in cancer metastasis. Dr. Basu is the recipient of many awards including the Early Career Research Award from the Department of Science and Technology, Govt. of India. She is a reviewer of many journals like Molecular Biology Reports, Frontiers in Oncology, RSC Advances, PLOS ONE, Journal of Biomolecular Structure & Dynamics, Journal of Molecular Graphics and Modelling, etc. She has edited and authored/co-authored 21 journal papers, 3 book chapters, and 15 abstracts. She is a Board of Studies member at her university. She is a life member of 'The Cytometry Society”-in India and 'All India Cell Biology Society”- in India.",institutionString:"Dr. D.Y. Patil Vidyapeeth, Pune",institution:{name:"Dr. D.Y. Patil Vidyapeeth, Pune",country:{name:"India"}}},{id:"354817",title:"Dr.",name:"Anubhab",middleName:null,surname:"Mukherjee",slug:"anubhab-mukherjee",fullName:"Anubhab Mukherjee",position:null,profilePictureURL:"https://intech-files.s3.amazonaws.com/0033Y0000365PbRQAU/ProfilePicture%202022-04-15%2005%3A11%3A18.480",biography:"A former member of Laboratory of Nanomedicine, Brigham and Women’s Hospital, Harvard University, Boston, USA, Dr. Anubhab Mukherjee is an ardent votary of science who strives to make an impact in the lives of those afflicted with cancer and other chronic/acute ailments. He completed his Ph.D. from CSIR-Indian Institute of Chemical Technology, Hyderabad, India, having been skilled with RNAi, liposomal drug delivery, preclinical cell and animal studies. He pursued post-doctoral research at College of Pharmacy, Health Science Center, Texas A & M University and was involved in another postdoctoral research at Department of Translational Neurosciences and Neurotherapeutics, John Wayne Cancer Institute, Santa Monica, California. In 2015, he worked in Harvard-MIT Health Sciences & Technology as a visiting scientist. He has substantial experience in nanotechnology-based formulation development and successfully served various Indian organizations to develop pharmaceuticals and nutraceutical products. He is an inventor in many US patents and an author in many peer-reviewed articles, book chapters and books published in various media of international repute. Dr. Mukherjee is currently serving as Principal Scientist, R&D at Esperer Onco Nutrition (EON) Pvt. Ltd. and heads the Hyderabad R&D center of the organization.",institutionString:"Esperer Onco Nutrition Pvt Ltd.",institution:null},{id:"319365",title:"Assistant Prof.",name:"Manash K.",middleName:null,surname:"Paul",slug:"manash-k.-paul",fullName:"Manash K. Paul",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/319365/images/system/319365.png",biography:"Manash K. Paul is a Principal Investigator and Scientist at the University of California Los Angeles. He has contributed significantly to the fields of stem cell biology, regenerative medicine, and lung cancer. His research focuses on various signaling processes involved in maintaining stem cell homeostasis during the injury-repair process, deciphering lung stem cell niche, pulmonary disease modeling, immuno-oncology, and drug discovery. He is currently investigating the role of extracellular vesicles in premalignant lung cell migration and detecting the metastatic phenotype of lung cancer via machine-learning-based analyses of exosomal signatures. Dr. Paul has published in more than fifty peer-reviewed international journals and is highly cited. He is the recipient of many awards, including the UCLA Vice Chancellor’s award, a senior member of the Institute of Electrical and Electronics Engineers (IEEE), and an editorial board member for several international journals.",institutionString:"University of California Los Angeles",institution:{name:"University of California Los Angeles",country:{name:"United States of America"}}},{id:"311457",title:"Dr.",name:"Júlia",middleName:null,surname:"Scherer Santos",slug:"julia-scherer-santos",fullName:"Júlia Scherer Santos",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/311457/images/system/311457.jpg",biography:"Dr. Júlia Scherer Santos works in the areas of cosmetology, nanotechnology, pharmaceutical technology, beauty, and aesthetics. Dr. Santos also has experience as a professor of graduate courses. Graduated in Pharmacy, specialization in Cosmetology and Cosmeceuticals applied to aesthetics, specialization in Aesthetic and Cosmetic Health, and a doctorate in Pharmaceutical Nanotechnology. Teaching experience in Pharmacy and Aesthetics and Cosmetics courses. She works mainly on the following subjects: nanotechnology, cosmetology, pharmaceutical technology, aesthetics.",institutionString:"Universidade Federal de Juiz de Fora",institution:{name:"Universidade Federal de Juiz de Fora",country:{name:"Brazil"}}},{id:"219081",title:"Dr.",name:"Abdulsamed",middleName:null,surname:"Kükürt",slug:"abdulsamed-kukurt",fullName:"Abdulsamed Kükürt",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/219081/images/system/219081.png",biography:"Dr. Kükürt graduated from Uludağ University in Turkey. He started his academic career as a Research Assistant in the Department of Biochemistry at Kafkas University. In 2019, he completed his Ph.D. program in the Department of Biochemistry at the Institute of Health Sciences. He is currently working at the Department of Biochemistry, Kafkas University. He has 27 published research articles in academic journals, 11 book chapters, and 37 papers. He took part in 10 academic projects. He served as a reviewer for many articles. He still serves as a member of the review board in many academic journals.",institutionString:"Kafkas University",institution:{name:"Kafkas University",country:{name:"Turkey"}}},{id:"178366",title:"Associate Prof.",name:"Volkan",middleName:null,surname:"Gelen",slug:"volkan-gelen",fullName:"Volkan Gelen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/178366/images/system/178366.jpg",biography:"Volkan Gelen is a Physiology specialist who received his veterinary degree from Kafkas University in 2011. Between 2011-2015, he worked as an assistant at Atatürk University, Faculty of Veterinary Medicine, Department of Physiology. In 2016, he joined Kafkas University, Faculty of Veterinary Medicine, Department of Physiology as an assistant professor. Dr. Gelen has been engaged in various academic activities at Kafkas University since 2016. There he completed 5 projects and has 3 ongoing projects. He has 60 articles published in scientific journals and 20 poster presentations in scientific congresses. His research interests include physiology, endocrine system, cancer, diabetes, cardiovascular system diseases, and isolated organ bath system studies.",institutionString:"Kafkas University",institution:{name:"Kafkas University",country:{name:"Turkey"}}},{id:"418963",title:"Dr.",name:"Augustine Ododo",middleName:"Augustine",surname:"Osagie",slug:"augustine-ododo-osagie",fullName:"Augustine Ododo Osagie",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/418963/images/16900_n.jpg",biography:"Born into the family of Osagie, a prince of the Benin Kingdom. I am currently an academic in the Department of Medical Biochemistry, University of Benin. Part of the duties are to teach undergraduate students and conduct academic research.",institutionString:null,institution:{name:"University of Benin",country:{name:"Nigeria"}}},{id:"192992",title:"Prof.",name:"Shagufta",middleName:null,surname:"Perveen",slug:"shagufta-perveen",fullName:"Shagufta Perveen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/192992/images/system/192992.png",biography:"Prof. Shagufta Perveen is a Distinguish Professor in the Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia. Dr. Perveen has acted as the principal investigator of major research projects funded by the research unit of King Saud University. She has more than ninety original research papers in peer-reviewed journals of international repute to her credit. She is a fellow member of the Royal Society of Chemistry UK and the American Chemical Society of the United States.",institutionString:"King Saud University",institution:{name:"King Saud University",country:{name:"Saudi Arabia"}}},{id:"49848",title:"Dr.",name:"Wen-Long",middleName:null,surname:"Hu",slug:"wen-long-hu",fullName:"Wen-Long Hu",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/49848/images/system/49848.jpg",biography:"Wen-Long Hu is Chief of the Division of Acupuncture, Department of Chinese Medicine at Kaohsiung Chang Gung Memorial Hospital, as well as an adjunct associate professor at Fooyin University and Kaohsiung Medical University. Wen-Long is President of Taiwan Traditional Chinese Medicine Medical Association. He has 28 years of experience in clinical practice in laser acupuncture therapy and 34 years in acupuncture. He is an invited speaker for lectures and workshops in laser acupuncture at many symposiums held by medical associations. He owns the patent for herbal preparation and producing, and for the supercritical fluid-treated needle. Dr. Hu has published three books, 12 book chapters, and more than 30 papers in reputed journals, besides serving as an editorial board member of repute.",institutionString:"Kaohsiung Chang Gung Memorial Hospital",institution:{name:"Kaohsiung Chang Gung Memorial Hospital",country:{name:"Taiwan"}}},{id:"298472",title:"Prof.",name:"Andrey V.",middleName:null,surname:"Grechko",slug:"andrey-v.-grechko",fullName:"Andrey V. Grechko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/298472/images/system/298472.png",biography:"Andrey Vyacheslavovich Grechko, Ph.D., Professor, is a Corresponding Member of the Russian Academy of Sciences. He graduated from the Semashko Moscow Medical Institute (Semashko National Research Institute of Public Health) with a degree in Medicine (1998), the Clinical Department of Dermatovenerology (2000), and received a second higher education in Psychology (2009). Professor A.V. Grechko held the position of Сhief Physician of the Central Clinical Hospital in Moscow. He worked as a professor at the faculty and was engaged in scientific research at the Medical University. Starting in 2013, he has been the initiator of the creation of the Federal Scientific and Clinical Center for Intensive Care and Rehabilitology, Moscow, Russian Federation, where he also serves as Director since 2015. He has many years of experience in research and teaching in various fields of medicine, is an author/co-author of more than 200 scientific publications, 13 patents, 15 medical books/chapters, including Chapter in Book «Metabolomics», IntechOpen, 2020 «Metabolomic Discovery of Microbiota Dysfunction as the Cause of Pathology».",institutionString:"Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology",institution:null},{id:"199461",title:"Prof.",name:"Natalia V.",middleName:null,surname:"Beloborodova",slug:"natalia-v.-beloborodova",fullName:"Natalia V. Beloborodova",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/199461/images/system/199461.jpg",biography:'Natalia Vladimirovna Beloborodova was educated at the Pirogov Russian National Research Medical University, with a degree in pediatrics in 1980, a Ph.D. in 1987, and a specialization in Clinical Microbiology from First Moscow State Medical University in 2004. She has been a Professor since 1996. Currently, she is the Head of the Laboratory of Metabolism, a division of the Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russian Federation. N.V. Beloborodova has many years of clinical experience in the field of intensive care and surgery. She studies infectious complications and sepsis. She initiated a series of interdisciplinary clinical and experimental studies based on the concept of integrating human metabolism and its microbiota. Her scientific achievements are widely known: she is the recipient of the Marie E. Coates Award \\"Best lecturer-scientist\\" Gustafsson Fund, Karolinska Institutes, Stockholm, Sweden, and the International Sepsis Forum Award, Pasteur Institute, Paris, France (2014), etc. Professor N.V. Beloborodova wrote 210 papers, five books, 10 chapters and has edited four books.',institutionString:"Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology",institution:null},{id:"354260",title:"Ph.D.",name:"Tércio Elyan",middleName:"Azevedo",surname:"Azevedo Martins",slug:"tercio-elyan-azevedo-martins",fullName:"Tércio Elyan Azevedo Martins",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/354260/images/16241_n.jpg",biography:"Graduated in Pharmacy from the Federal University of Ceará with the modality in Industrial Pharmacy, Specialist in Production and Control of Medicines from the University of São Paulo (USP), Master in Pharmaceuticals and Medicines from the University of São Paulo (USP) and Doctor of Science in the program of Pharmaceuticals and Medicines by the University of São Paulo. Professor at Universidade Paulista (UNIP) in the areas of chemistry, cosmetology and trichology. Assistant Coordinator of the Higher Course in Aesthetic and Cosmetic Technology at Universidade Paulista Campus Chácara Santo Antônio. Experience in the Pharmacy area, with emphasis on Pharmacotechnics, Pharmaceutical Technology, Research and Development of Cosmetics, acting mainly on topics such as cosmetology, antioxidant activity, aesthetics, photoprotection, cyclodextrin and thermal analysis.",institutionString:null,institution:{name:"University of Sao Paulo",country:{name:"Brazil"}}},{id:"334285",title:"Ph.D. Student",name:"Sameer",middleName:"Kumar",surname:"Jagirdar",slug:"sameer-jagirdar",fullName:"Sameer Jagirdar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334285/images/14691_n.jpg",biography:"I\\'m a graduate student at the center for biosystems science and engineering at the Indian Institute of Science, Bangalore, India. I am interested in studying host-pathogen interactions at the biomaterial interface.",institutionString:null,institution:{name:"Indian Institute of Science Bangalore",country:{name:"India"}}},{id:"329248",title:"Dr.",name:"Md. Faheem",middleName:null,surname:"Haider",slug:"md.-faheem-haider",fullName:"Md. Faheem Haider",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/329248/images/system/329248.jpg",biography:"Dr. Md. Faheem Haider completed his BPharm in 2012 at Integral University, Lucknow, India. In 2014, he completed his MPharm with specialization in Pharmaceutics at Babasaheb Bhimrao Ambedkar University, Lucknow, India. He received his Ph.D. degree from Jamia Hamdard University, New Delhi, India, in 2018. He was selected for the GPAT six times and his best All India Rank was 34. Currently, he is an assistant professor at Integral University. Previously he was an assistant professor at IIMT University, Meerut, India. He has experience teaching DPharm, Pharm.D, BPharm, and MPharm students. He has more than five publications in reputed journals to his credit. Dr. Faheem’s research area is the development and characterization of nanoformulation for the delivery of drugs to various organs.",institutionString:"Integral University",institution:{name:"Integral University",country:{name:"India"}}},{id:"329795",title:"Dr.",name:"Mohd Aftab",middleName:"Aftab",surname:"Siddiqui",slug:"mohd-aftab-siddiqui",fullName:"Mohd Aftab Siddiqui",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/329795/images/15648_n.jpg",biography:"Dr. Mohd Aftab Siddiqui is currently working as Assistant Professor in the Faculty of Pharmacy, Integral University, Lucknow for the last 6 years. He has completed his Doctor in Philosophy (Pharmacology) in 2020 from Integral University, Lucknow. He completed his Bachelor in Pharmacy in 2013 and Master in Pharmacy (Pharmacology) in 2015 from Integral University, Lucknow. He is the gold medalist in Bachelor and Master degree. He qualified GPAT -2013, GPAT -2014, and GPAT 2015. His area of research is Pharmacological screening of herbal drugs/ natural products in liver and cardiac diseases. He has guided many M. Pharm. research projects. He has many national and international publications.",institutionString:"Integral University",institution:null},{id:"333824",title:"Dr.",name:"Ahmad Farouk",middleName:null,surname:"Musa",slug:"ahmad-farouk-musa",fullName:"Ahmad Farouk Musa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333824/images/22684_n.jpg",biography:"Dato’ Dr Ahmad Farouk Musa\nMD, MMED (Surgery) (Mal), Fellowship in Cardiothoracic Surgery (Monash Health, Aust), Graduate Certificate in Higher Education (Aust), Academy of Medicine (Mal)\n\n\n\nDato’ Dr Ahmad Farouk Musa obtained his Doctor of Medicine from USM in 1992. He then obtained his Master of Medicine in Surgery from the same university in the year 2000 before subspecialising in Cardiothoracic Surgery at Institut Jantung Negara (IJN), Kuala Lumpur from 2002 until 2005. He then completed his Fellowship in Cardiothoracic Surgery at Monash Health, Melbourne, Australia in 2008. He has served in the Malaysian army as a Medical Officer with the rank of Captain upon completing his Internship before joining USM as a trainee lecturer. He is now serving as an academic and researcher at Monash University Malaysia. He is a life-member of the Malaysian Association of Thoracic & Cardiovascular Surgery (MATCVS) and a committee member of the MATCVS Database. He is also a life-member of the College of Surgeons, Academy of Medicine of Malaysia; a life-member of Malaysian Medical Association (MMA), and a life-member of Islamic Medical Association of Malaysia (IMAM). Recently he was appointed as an Interim Chairperson of Examination & Assessment Subcommittee of the UiTM-IJN Cardiothoracic Surgery Postgraduate Program. As an academic, he has published numerous research papers and book chapters. He has also been appointed to review many scientific manuscripts by established journals such as the British Medical Journal (BMJ). He has presented his research works at numerous local and international conferences such as the European Association for Cardiothoracic Surgery (EACTS) and the European Society of Cardiovascular Surgery (ESCVS), to name a few. He has also won many awards for his research presentations at meetings and conferences like the prestigious International Invention, Innovation & Technology Exhibition (ITEX); Design, Research and Innovation Exhibition, the National Conference on Medical Sciences and the Annual Scientific Meetings of the Malaysian Association for Thoracic and Cardiovascular Surgery. He was awarded the Darjah Setia Pangkuan Negeri (DSPN) by the Governor of Penang in July, 2015.",institutionString:null,institution:{name:"Monash University Malaysia",country:{name:"Malaysia"}}},{id:"30568",title:"Prof.",name:"Madhu",middleName:null,surname:"Khullar",slug:"madhu-khullar",fullName:"Madhu Khullar",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/30568/images/system/30568.jpg",biography:"Dr. Madhu Khullar is a Professor of Experimental Medicine and Biotechnology at the Post Graduate Institute of Medical Education and Research, Chandigarh, India. She completed her Post Doctorate in hypertension research at the Henry Ford Hospital, Detroit, USA in 1985. She is an editor and reviewer of several international journals, and a fellow and member of several cardiovascular research societies. Dr. Khullar has a keen research interest in genetics of hypertension, and is currently studying pharmacogenetics of hypertension.",institutionString:"Post Graduate Institute of Medical Education and Research",institution:{name:"Post Graduate Institute of Medical Education and Research",country:{name:"India"}}},{id:"223233",title:"Prof.",name:"Xianquan",middleName:null,surname:"Zhan",slug:"xianquan-zhan",fullName:"Xianquan Zhan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/223233/images/system/223233.png",biography:"Xianquan Zhan received his MD and Ph.D. in Preventive Medicine at West China University of Medical Sciences. He received his post-doctoral training in oncology and cancer proteomics at the Central South University, China, and the University of Tennessee Health Science Center (UTHSC), USA. He worked at UTHSC and the Cleveland Clinic in 2001–2012 and achieved the rank of associate professor at UTHSC. Currently, he is a full professor at Central South University and Shandong First Medical University, and an advisor to MS/PhD students and postdoctoral fellows. He is also a fellow of the Royal Society of Medicine and European Association for Predictive Preventive Personalized Medicine (EPMA), a national representative of EPMA, and a member of the American Society of Clinical Oncology (ASCO) and the American Association for the Advancement of Sciences (AAAS). He is also the editor in chief of International Journal of Chronic Diseases & Therapy, an associate editor of EPMA Journal, Frontiers in Endocrinology, and BMC Medical Genomics, and a guest editor of Mass Spectrometry Reviews, Frontiers in Endocrinology, EPMA Journal, and Oxidative Medicine and Cellular Longevity. He has published more than 148 articles, 28 book chapters, 6 books, and 2 US patents in the field of clinical proteomics and biomarkers.",institutionString:"Shandong First Medical University",institution:{name:"Affiliated Hospital of Shandong Academy of Medical Sciences",country:{name:"China"}}},{id:"297507",title:"Dr.",name:"Charles",middleName:"Elias",surname:"Assmann",slug:"charles-assmann",fullName:"Charles Assmann",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/297507/images/system/297507.jpg",biography:"Charles Elias Assmann is a biologist from Federal University of Santa Maria (UFSM, Brazil), who spent some time abroad at the Ludwig-Maximilians-Universität München (LMU, Germany). He has Masters Degree in Biochemistry (UFSM), and is currently a PhD student at Biochemistry at the Department of Biochemistry and Molecular Biology of the UFSM. His areas of expertise include: Biochemistry, Molecular Biology, Enzymology, Genetics and Toxicology. He is currently working on the following subjects: Aluminium toxicity, Neuroinflammation, Oxidative stress and Purinergic system. Since 2011 he has presented more than 80 abstracts in scientific proceedings of national and international meetings. Since 2014, he has published more than 20 peer reviewed papers (including 4 reviews, 3 in Portuguese) and 2 book chapters. He has also been a reviewer of international journals and ad hoc reviewer of scientific committees from Brazilian Universities.",institutionString:"Universidade Federal de Santa Maria",institution:{name:"Universidade Federal de Santa Maria",country:{name:"Brazil"}}},{id:"217850",title:"Dr.",name:"Margarete Dulce",middleName:null,surname:"Bagatini",slug:"margarete-dulce-bagatini",fullName:"Margarete Dulce Bagatini",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/217850/images/system/217850.jpeg",biography:"Dr. Margarete Dulce Bagatini is an associate professor at the Federal University of Fronteira Sul/Brazil. She has a degree in Pharmacy and a PhD in Biological Sciences: Toxicological Biochemistry. She is a member of the UFFS Research Advisory Committee\nand a member of the Biovitta Research Institute. She is currently:\nthe leader of the research group: Biological and Clinical Studies\nin Human Pathologies, professor of postgraduate program in\nBiochemistry at UFSC and postgraduate program in Science and Food Technology at\nUFFS. She has experience in the area of pharmacy and clinical analysis, acting mainly\non the following topics: oxidative stress, the purinergic system and human pathologies, being a reviewer of several international journals and books.",institutionString:"Universidade Federal da Fronteira Sul",institution:{name:"Universidade Federal da Fronteira Sul",country:{name:"Brazil"}}}]}},subseries:{item:{id:"38",type:"subseries",title:"Pollution",keywords:"Human activity, Pollutants, Reduced risks, Population growth, Waste disposal, Remediation, Clean environment",scope:"
\r\n\tPollution is caused by a wide variety of human activities and occurs in diverse forms, for example biological, chemical, et cetera. In recent years, significant efforts have been made to ensure that the environment is clean, that rigorous rules are implemented, and old laws are updated to reduce the risks towards humans and ecosystems. However, rapid industrialization and the need for more cultivable sources or habitable lands, for an increasing population, as well as fewer alternatives for waste disposal, make the pollution control tasks more challenging. Therefore, this topic will focus on assessing and managing environmental pollution. It will cover various subjects, including risk assessment due to the pollution of ecosystems, transport and fate of pollutants, restoration or remediation of polluted matrices, and efforts towards sustainable solutions to minimize environmental pollution.
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Dr. Rahman was also adjunctly attached with Kanazawa University, Japan (Visiting Research Professor, Dec 2014 to Mar 2015; JSPS Postdoctoral Research Fellow, Apr 2012 to Mar 2014), and Tokyo Institute of Technology, Japan (TokyoTech-UNESCO Research Fellow, Oct 2004–Sep 2005). \nHe received his Ph.D. degree in Environmental Analytical Chemistry from Kanazawa University, Japan (2011). He also achieved a Diploma in Environment from the Tokyo Institute of Technology, Japan (2005). Besides, he has an M.Sc. degree in Applied Chemistry and a B.Sc. degree in Chemistry, all from the University of Chittagong, Bangladesh. \nDr. Rahman’s research interest includes the study of the fate and behavior of environmental pollutants in the biosphere; design of low energy and low burden environmental improvement (remediation) technology; implementation of sustainable waste management practices for treatment, handling, reuse, and ultimate residual disposition of solid wastes; nature and type of interactions in organic liquid mixtures for process engineering design applications.",institutionString:null,institution:{name:"Fukushima University",institutionURL:null,country:{name:"Japan"}}},editorTwo:{id:"201020",title:"Dr.",name:"Zinnat Ara",middleName:null,surname:"Begum",slug:"zinnat-ara-begum",fullName:"Zinnat Ara Begum",profilePictureURL:"https://mts.intechopen.com/storage/users/201020/images/system/201020.jpeg",biography:"Zinnat A. 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