\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:{caption:"Highly Cited",originalUrl:"/media/original/117"}},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"2575",leadTitle:null,fullTitle:"Prolactin",title:"Prolactin",subtitle:null,reviewType:"peer-reviewed",abstract:"Prolactin is a polypeptide hormone that is synthesized in and secreted from the lactotrophs of the anterior pituitary gland. We are now aware that synthesis and secretion of prolactin is not restricted to the anterior lobe of the pituitary gland, but other organs and individual cells can also produce it. This book provides the headlines to follow a course of cumulated knowledge on prolactin research during the last two-three decades and it may also help us understand some of the concerns that we face today.",isbn:null,printIsbn:"978-953-51-0943-3",pdfIsbn:"978-953-51-7073-0",doi:"10.5772/2950",price:119,priceEur:129,priceUsd:155,slug:"prolactin",numberOfPages:246,isOpenForSubmission:!1,isInWos:null,isInBkci:!1,hash:"338ea99a4e29b28d7463a976a301711b",bookSignature:"György M. Nagy and Bela E. Toth",publishedDate:"January 23rd 2013",coverURL:"https://cdn.intechopen.com/books/images_new/2575.jpg",numberOfDownloads:41769,numberOfWosCitations:29,numberOfCrossrefCitations:20,numberOfCrossrefCitationsByBook:0,numberOfDimensionsCitations:49,numberOfDimensionsCitationsByBook:0,hasAltmetrics:1,numberOfTotalCitations:98,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 1st 2011",dateEndSecondStepPublish:"December 22nd 2011",dateEndThirdStepPublish:"April 30th 2012",dateEndFourthStepPublish:"June 25th 2012",dateEndFifthStepPublish:"July 25th 2012",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"145362",title:"Prof.",name:"György M.",middleName:null,surname:"Nagy",slug:"gyorgy-m.-nagy",fullName:"György M. Nagy",profilePictureURL:"https://mts.intechopen.com/storage/users/145362/images/3683_n.jpg",biography:"György M. Nagy, MD, PhD, DSc graduated from the Medical University in Pécs in 1974. He started his work at the Semmelweis University in 1974 at the 2nd Department of Anatomy led by Prof. Béla Halász. He obtained his PhD in Neuroendocrinology in 1992 and his Doctor of Science Degree in 1995. He worked in Birmingham (University of Alabama at Birmingham, USA) as a Research Fellow from 1984 to 1987 in the laboratory of Jimmy D. Neill. He also spent two years (from 1989 till 1991) as a visiting professor in Charleston, SC at the Medical University of South Carolina, USA, in the laboratory of Steve L. Frawley and one year (between 1997-1998) at the Florida State University, Tallahassee, FL, USA in Marc E. Freeman’s laboratory. At present, he is a Professor of The Ross University, Department of Anatomy, Commonwealth of Dominica. His main interests are the hypothalamic regulation of pituitary prolactin secretion and the molecular aspects of the function of mammotrope cells. The title of his best cited article is “Prolactin: Structure, function and regulation of secretion”, written by Freeman ME, Kanyicska B, Lerant A, and Nagy GM (Physiological Reviews 80: 1523-1631, 2000)",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Semmelweis University",institutionURL:null,country:{name:"Hungary"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:{id:"164305",title:"Dr.",name:"Bela E.",middleName:null,surname:"Toth",slug:"bela-e.-toth",fullName:"Bela E. Toth",profilePictureURL:"https://mts.intechopen.com/storage/users/164305/images/4963_n.jpg",biography:"Bela Ernest Toth Dipl. Eng, MD, PhD started his education with School of Engineering, (Dipl. Eng), graduated as a Medical Doctor (MD), and completed PhD in Neuroscience. He worked as a lecturer for graduate and postgraduate education at Medical School and also at Faculties of Bioengineering and Healthcare Sciences. His scientific background is based on\nuniversity appointments and academic collaborations (Semmelweis University Budapest, Neuroendocrine Research Group Hungarian Academy of Sciences, Rudolph Magnus Institute of Pharmacology, University of Utrecht; Dept. of Molecular and Cell Biology Penn State University, USA; University of Veterinary Sciences, Hungary). Dr. Toth’s research interest on circadian rhythms of PRL secretion started during the university years. He later continued to focus on biology of nutrition, development and regulation of immune cell response, and function of DA in neuroendocrine regulation. Lately, his interests are involving pre-clinical research. 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Emerging Trends and Future Perspectives",slug:"transgenic-crops-emerging-trends-and-future-perspectives",publishedDate:"October 23rd 2019",bookSignature:"Muhammad Sarwar Khan and Kauser Abdulla Malik",coverURL:"https://cdn.intechopen.com/books/images_new/6976.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"212511",title:"Prof.",name:"Muhammad Sarwar",middleName:null,surname:"Khan",slug:"muhammad-sarwar-khan",fullName:"Muhammad Sarwar Khan"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"211046",title:"Dr.",name:"Ghulam",middleName:null,surname:"Mustafa",fullName:"Ghulam Mustafa",slug:"ghulam-mustafa",email:"drmustafa8@gmail.com",position:null,institution:{name:"University of Agriculture Faisalabad",institutionURL:null,country:{name:"Pakistan"}}},{id:"212508",title:"Dr.",name:"Faiz",middleName:null,surname:"Ahmad",fullName:"Faiz Ahmad",slug:"faiz-ahmad",email:"faizahmad1980@gmail.com",position:null,institution:null},{id:"212511",title:"Prof.",name:"Muhammad Sarwar",middleName:null,surname:"Khan",fullName:"Muhammad Sarwar Khan",slug:"muhammad-sarwar-khan",email:"sarwarkhan_40@hotmail.com",position:null,institution:{name:"University of Agriculture Faisalabad",institutionURL:null,country:{name:"Pakistan"}}}]},book:{id:"6976",title:"Transgenic Crops",subtitle:"Emerging Trends and Future Perspectives",fullTitle:"Transgenic Crops - Emerging Trends and Future Perspectives",slug:"transgenic-crops-emerging-trends-and-future-perspectives",publishedDate:"October 23rd 2019",bookSignature:"Muhammad Sarwar Khan and Kauser Abdulla Malik",coverURL:"https://cdn.intechopen.com/books/images_new/6976.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"212511",title:"Prof.",name:"Muhammad Sarwar",middleName:null,surname:"Khan",slug:"muhammad-sarwar-khan",fullName:"Muhammad Sarwar Khan"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},ofsBook:{item:{type:"book",id:"11513",leadTitle:null,title:"Gas Sensors",subtitle:null,reviewType:"peer-reviewed",abstract:"\r\n\tWe are living in a society where automation in each electrical appliance/instrument is a great demand. We wish to have automatic devices/gadgets/instruments with no or minimal intervention from humans in their daily operation. Then only, these devices can qualify to call it is smart instruments. To fulfill this, one of the major requirements is to come up with highly sensitive, long-lasting, low-cost smart sensors. On the other hand, the healthcare industry demands low-cost, Lab-on-chip type biosensors for simple and rapid detection of various biomolecules or biogases. A sensor is an analytical device that detects the change in the environment and responds to some output in terms of a measurable analog resistance/voltage/current converted into a human-readable display or transmitted for further processing. In the last two decades, a significant amount of research has been devoted to the development of various types of gas sensors using different nanomaterials in the electronic and healthcare industry.
\r\n\r\n\tThis book aims to provide the reader (research scholars, scientists, and engineers working in the field of sensors) an overview of the recent advances made in the development of various gas sensors for the electronic and healthcare industries for the betterment of the human lifestyle. Also, this book will intend to address existing challenges and a few future directions of research for easy integration and cost-effective fast sensing of such
\r\n\tgas sensors.
Alzheimer’s disease (AD) is kind of neurodegenerative disease, which affects elder’s health and living quality. There are some hypotheses raised up for the pathogenesis of the disease, such as amyloid cascade and tau hyperphosphorylation. Besides, neuroinflammation induced by neurotoxic amyloid β (Aβ) peptide is also considered contribute to the development of AD. Inteleukin-1 receptor (IL-1R) is one of the inflammation-related surface receptors that are distributed widely in various tissues and cells in the body. Evidence has been shown that IL-1R-mediated neuroinflammation may be closely related to pathogenesis and development of AD. In the current chapter, AD-related neuroinflammation and the participation of IL-1R in such progress would be reviewed and discussed in detail.
As a kind of chronic neurodegenerative disease, AD usually starts slowly and gets worse over comparatively longer time. The initial symptoms of AD are often mistaken with normal aging. The most common early symptom for AD is the difficulty in remembering recent events (short-term memory loss). As the disease advances, symptoms may include problems with language, disorientation (easily getting lost), mood swings, loss of motivation, not managing self-care, and behavioral issues. AD patients may suffer from the disease symptoms for years and especially at the later stage of the progress.
AD is currently supposed to be the cause of approximately 60–70% of total dementia cases. There is a large amount of data about potential risk factors for AD, including age [1], genetics [2], and injury [3]. Many treatable medical conditions are also associated with an increased risk of AD, including stroke [4], diabetes [5], midlife hypertension [6], and hypercholesterolemia [7, 8].
The early identification of molecular pathological description of AD was the functional reduction of cholinergic nerve system in the cerebral cortex, like the remarkable reduction in choline acetyltransferase (ChAT) [9]. Later, senile plaques and neurofibrillary tangles (NFTs), two typical protein depositions, were confirmed related to AD [10]. The main component of senile plaques is Aβ peptide; while NFTs are made from abnormal tau proteins [11]. A 42-amino acid long form of Aβ (Aβ42) was found as the main content in fibrillar Aβ peptides [12]. Aβ40, which is also found in the plaque, although is normally more abundantly produced by cells, contributes to the lower portion of the plaque [13]. Compared to Aβ40, Aβ42 is the more hydrophobic form that aggregates more easily and quickly [14]. NFTs are formed by hyperphosphorylated tau protein. As the raise of Aβ concentration, tau protein happens to be more easily phosphorylated, leading to an imbalance of various kinases and phosphatases [15]. Consequently, mass transport and impaired impulse occurs in neurons, followed by severe neuronal dysfunction.
Thus, the amyloid hypothesis puts Aβ accumulation at the core of AD pathogenesis. Aβ is the sequential proteolytic product of its precursor amyloid precursor protein (APP). APP is a type I transmembrane protein, consisted of a large N-terminal ectodomain, a transmembrane domain, and a short cytoplasmic domain. The Aβ peptide generation is supposed to be influenced by the pattern of cleavage from APP by α, β, and γ-secretases [16]. APP can be processed in two different pathways, the amyloid, and non-amyloid pathway. In the amyloid pathway, APP can be cleaved by β-secretase (BACE1), releasing the soluble APP β fragment (sAPPβ); and the C-terminal fragment (CTF) is still in the membrane and can be cleaved by γ-secretase (presenilin1, PS1) to release Aβ [17]. This process leads to Aβ generation, aggregation, and deposit. In the other non-amyloid pathway, APP can be cleaved by α-secretase (ADAM10/17), releasing soluble APP α fragment (sAPPα). The cleavage site of α-secretase is between the sites of β- and γ-secretase. So the non-amyloid pathway can reduce the damage induced by Aβ on neurons.
Consider to the crucial role of Aβ in the amyloid cascade, therapeutic approaches related to APP metabolic pathways were always under careful and detail research and develop [18]. Those therapeutic approaches include inhibition of Aβ monomers developing into toxic oligomers or enhancement of clearance and disaggregation of fibrillar aggregates from cerebral cortex [19]; modulation of the fate and toxicity of Aβ using antibodies against Aβ [20]. However, the only clinical effective therapeutic approach so far is the treatment and enhancement of the functions of cholinergic neurons. Acetylcholinesterase (AChE) inhibitors, galantamine, and rivastigmine were thought to improve cognition and indirectly help function and behavior in patients with AD [21–23]. Such treatments for AD have been widely available since the mid-1990s, but these drugs do not treat the underlying mechanism, so the effects are limited.
As described above, the amyloid hypothesis was raised up as the most popular and acceptable pathogenesis mechanism for AD. The initial changes of the cascade happen to Aβ metabolism. The Aβ balance in favor of Aβ42 followed by the formation of diffuse plaques can induce the toxic effect to neurons to different extends. The diffuse Aβ plaques can then convert to more toxic Aβ deposit fibrillars. Aβ triggers the activation of the cellular signaling cascade, the induction of inflammatory enzyme systems in a vicious cycle and finally the expression and secretion of proinflammatory cytokines. The activation of microglial and astrocyte, together with the corresponding inflammatory reactions, is another important event in AD pathogenesis. Both aggregated amyloid fibrils and inflammatory mediators secreted by microglia contribute to neuronal dystrophy. NFTs occur under such condition, which enhances neuronal dysfunction and death. The widespread neuronal dysfunction is regarded as the immediate cause of the disease [18, 24]. On the basis of these observations, Aβ has become a major pharmacological target for the treatment of the disease. However, such trails of treatment have not reached a satisfactory outcome. Thus, the AD-related neuroinflammation starts to sneak into current research attention.
In parallel, neuroinflammation has been implicated in contributing to the etiology of AD. Epidemiological and prospective population-based studies show an association between suppression of inflammation and reduced risk for AD [25, 26]. The protective effects of non-steroidal anti-inflammatory drugs (NSAIDs) against AD development [27] further support the neuroinflammation hypothesis. In animals, the beneficial effects of NSAIDs have also been confirmed, including behavioral improvement and reductions in glial activation, Aβ levels, and plaque size [28]. Inflammatory responses to amyloidosis have also been observed in animal models overexpressing Aβ [29, 30]. Proinflammatory cytokines, such as (interleukin-1) IL-1, IL-6, and tumor necrosis factor α (TNFα), are elevated in the plasma, brains, and cerebrospinal fluid of patients with AD or mild cognitive impairment, whereas anti-inflammatory cytokines are decreased [31, 32]. Besides, inhibition of TNFα signaling has been shown to attenuate AD-like pathology and cognitive impairments in transgenic mouse models, as well as in AD patients [33, 34].
Inflammation is a complex cellular and molecular response to insults (stress, injury or infection), an attempt to defend against these insults. AD-associated inflammation is generally considered as a secondary response to the pathological lesions evoked by Aβ [35, 36]. AD-related inflammatory response is supposed to be driven mainly by activated microglia [37, 38].
The activation of migrolia has been reported in both AD patients and animal models [39], accompanied by increased levels of specific chemokines and cytokines [40]. Microglia surrounding plaques stain positive for activation markers and proinflammatory mediators, including cyclooxygenase-2 (Cox-2), monocyte chemotactic protein 1 (MCP-1), TNFα, transforming growth factor-β (TGFβ), IL-1α, IL-1β, and IL-6 [41–43]. Aβ and its fibrils can induce self-defense, inflammatory responses via pattern recognition receptors (PRRs), such as toll-like receptors (TLRs) [44, 45]. Aβ aggregates interact with microglial receptors like TLR4, CD14, CD36, CD47, the receptor for advanced glycation end products (RAGE), and some integrins [46–50]. More recently, it has been reported that Aβ activates microglia through its interaction with the APP present in the membrane of these cells [51], which defines a novel function of APP in microglial regulation of the inflammatory response in AD.
Microglial activation seems to be the comparative early event in AD pathological development. Imaging study results showed that reactive microglia can be detected at the very early clinical stage of the disease [39]. In AD mouse model, microglial activation was observed before amyloid plaque formation [52]. Once activated, microglia can produce several proinflammatory signal molecules, including cytokines, growth factors, chemokines, and cell adhesion molecules. Besides, Microglia may also play a role in plaque evolution by phagocytosing and/or degrade deposited Aβ. Many different laboratories have shown that microglia, both
IL-1R family belongs to one category of TIR domain-containing receptor superfamily. The TIR domain-containing receptors are a large family of molecules involved in the activation of innate immunity [55]. The TIR superfamily can be broadly divided into two main groups: the immunoglobulin (Ig) domain-bearing receptors and the receptors with a leucine-rich repeat (LRR) domain [56, 57]. The Ig domain subgroup of TIR receptors includes 10 members of the IL-1R family, whereas the LRR group includes the toll-like receptors (TLR). When an agonist IL-1 family cytokine binds to its specific TIR-containing receptor, the initiation of IL-1R activation signaling occurs [56]. The signaling pathway involves the recruitment of adapter molecule MyD88 and kinase IRAK, followed by interaction with TRAF6. The final step is the phosphorylation of the inhibitory molecule IκB by IκB kinase complex leading to relocalization of transcription factor NF-κB. NF-κB is translocated into the nucleus and intermediates inflammatory immune response [58]. NF-κB is a major inflammatory switch that comprises a family of transcription factors that regulate expression of various proinflammatory cytokines (IL-1, IL-6, IL-8 and TNFα), chemokines, antiapoptotic factors and stress factors [59].
IL-1 family is the typical ligands for IL-1R and its activation. IL-1 family includes a set of cytokines, some of which have been demonstrated to play a critical role in host responses to pathogens and other noxious agents [60]. IL-1α and IL-1β are two most prevalent ligands that are supposed to trigger the activation of IL-1R. IL-1α/β are endogenous pyrogens with activities similar to lipopolysaccharides (LPS), which are the major molecular components of the outer membrane of Gram-negative bacteria [61].
One of IL-1R ligand cytokine IL-1β appears to play an important role in AD. IL-1β level was confirmed obviously in and around the area of Aβ deposit [62, 63]. The inhibition of IL-1 signaling by IL-1R knockout could significantly relief the Aβ burden in transgenic AD mice [64]. And the protective impact by IL-1R knockout was believed to be dependent on attenuated AD-related neuroinflammation [65]. Besides, the inflammation- or IL-1β-induced pathological tau development has also been well documented [66–68]. The inhibition of IL-1 signaling significantly suppressed the activation of cdk5/p25, GSK-3β, and p38-MAPK, all major kinases that phosphorylate tau in neurons. Another study demonstrated a direct effect of IL-1β secreted by microglia on neurons and subsequent activation of p38-MAPK and accumulation of tau phosphorylation [69]. NSAIDs could be repurposed as NLRP3 inflammasome inhibitors that provide neuroprotective impact against AD [70].
Inflammasomes are responsible for the maturation of pro-inflammatory cytokines such as interleukin IL-1, IL-18, and IL-33 and activation of inflammatory cell death, pyroptosis [71]. The inflammasome is a multiprotein oligomer consisting of caspase 1, PYCARD, NALP, and sometimes caspase 5 (also known as caspase 11 or ICH-3). It is expressed in myeloid cells and is a component of the innate immune system. Analogous to the apoptosome, which activates apoptotic cascades, the inflammasome activates an inflammatory cascade. Once active, the inflammasome binds to pro-caspase-1 (the precursor molecule of caspase-1), either homotypically via its own caspase activation and recruitment domain (CARD) or via the adaptor protein ASC. Caspase-1 then assembles into its active form which obtains the peptidase activity. The metabolic process performed by caspase-1 includes the proteolytic cleavage of pro-IL-1β at Asp116 into IL-1β [72] and cleavage of pro-IL-18 into IL-18 to induce IFN-γ secretion and natural killer cell activation [73]. Thus, the inflammasome promotes the maturation of the inflammatory cytokines, interleukin 1β (IL-1β) and interleukin 18 (IL-18) [72]. Thus, IL-1R signaling is considered to play a crucial role in inflammasome activation-induced inflammation.
Nucleotide oligomerization domain (NOD)-like receptor family, pyrin domain 3 (NLRP3) containing inflammasome is an intracellular multiprotein complex, which has been verified to participate in Aβ-induced neuroinflammation [74]. Halle et al. demonstrated that the phagocytosis of fibrillar Aβ activates NALP3 inflammasomes in mouse microglia. The activation of NALP3 was dependent on lysosomal damage and cathepsin B release, as was observed earlier in the crystal-induced NALP3 activation [75, 76]. Then, more evidence was supportive for that Aβ activate the NLRP3 inflammasome in microglial cells
The possible roles of the NLRP3 inflammasome in AD pathogenesis discussed above open a novel investigation of inflammasome signaling pathway for understanding AD. Designing agents for critically controlling the activation of NLRP3 inflammasome at the molecular level might offer considerable promise to tackle neuroinflammation and slow AD progression.
IL-1R is widely distributed in the central nerves system (CNS). Early evidence revealed that IL-1R was detected in high density in the dentate gyrus of the hippocampus, choroid plexus, meninges, and anterior pituitary and is low expressed in the frontoparietal cortex. Both neurons and glial cells were shown to express IL-1R [81]. Later, a pile of data demonstrated that IL-1R could be activated in various cell types in CNS. In cultured human microglia, numerous proinflammatory cytokines such as IL-1, IL-6, and TNFα are produced after IL-1 stimulation. In cultured rat astrocytes, IL-1 could stimulate astrocytes to release nerve growth factor which can mediate neuroprotective effects [82]. In addition, administration of IL-1 in the cerebral ventricle induced COX-2 exclusively in endothelial cells comprising brain blood vessels [83]. As we described in the previous paragraph, IL-1R plays an important role in glial activation-induced neuroinflammation, the participation of IL-1R in neuronal function has not been carefully discussed.
IL-1β has been reported to increase the expression of APP in neuronal culture [69]. The amyloid precursor protein (APP), via stimulation of amyloidogenic processing, undergoes sequential proteolytic cleavage by β-secretase and γ-secretase to generate Aβ. Alternatively, a non-amyloidogenic pathway involving α-secretase activation could reduce Aβ generation, which competitively inhibits activation of the detrimental amyloidogenic pathway. Also, sAPPα is proven to possess neuroprotective and memory-enhancing properties, often being compared to cerebral growth stimulants. Thus, the non-amyloidogenic pathway is supposed to be a suitable therapeutic target for AD.
The identity of α-secretase of APP has been verified to be ADAM10 (a disintegrin and metalloprotease 10) constitutively and ADAM17 regulatively [84]. Different kinds of stimuli have been suggested to increase the secretion of sAPPα under certain conditions via ADAM17, including various cytokine, chemokines, adhesion molecules and growth factors [85]. The two most important ligands for IL-1R, IL-1α [86] and IL-1β [87, 88] were proved to enhance ADAM17 activity in neurons. The detail mechanism research concerning to IL-1 signaling and APP proteolysis revealed that the GC-rich APP mRNA 5’UTR-stem loop structure bears an amyloid-specific CAGA sequence, IL-1 responsive element, and an iron responsive element. IL-1 binding to its responsive element significantly impacts the functioning of APP 5’UTR that affects APP metabolism and thus sAPPα release [89]. Besides, p38/ERK/JNK pathway and PI3K/AKT pathway are believed to participate in IL-1 signaling mediated activity regulation of APP α-secretase ADAM17 [90, 91].
Thus, IL-1R is considered play an important and distinct role in different aspects in the process of AD development. The exact relationship of IL-1R signaling activation between microglial activation-induced neuroinflammation and APP α-shedding in neurons is somehow tricky. The cytokines and growth factors from reactive microglia induced by neurotoxic Aβ may enhance ADAM17 activity in nearby neurons (paracrine), which provides a possible self-protection against Ab-induced neuronal dystrophy.
IL-1R participates in AD-related neuroinflammation by microglial activation and the secretion of various pro-inflammatory cytokines and chemokines. The anti-inflammation treatment has been raised up, including IL-1R antagonist as a potential AD therapeutic approach. However, IL-1R activation in neurons, where exactly APP proteolysis takes place, may enhance the activity of neuroprotective α-secretase. The safety of novel promising therapeutic approaches targeting IL-1R activity regulation has to be evaluated carefully to avoid unexpected side effects.
This work was financially supported by National Natural Science Foundation of China (81302781).
There is a very interesting phenomenon that takes place in solid-state physics when certain metals are cooled below critical temperature of order of few Kelvin. The resistance of these metals completely disappears and they become superconducting. How does this happen? One may guess that maybe at low temperatures there are no phonons. That is not true, as we have low frequency phonons present. Why do we then lose all resistivity? Electrons bind together to form a molecule by phonon-mediated interaction. The essence of this interaction is that electron can pull on the lattice which pulls on another electron. This phonon-mediated bond is not very strong for only few meV, but at low temperatures, this is good enough; we cannot break it with collisions with phonons which only carry \n
This phenomenon whereby many materials exhibit complete loss of electrical resistance when cooled below a characteristic critical temperature [1, 2] is called superconductivity. It was discovered in mercury by Dutch physicist Onnes in 1911. For decades, a fundamental understanding of this phenomenon eluded the many scientists who were working in the field. Then, in the 1950s and 1960s, a remarkably complete and satisfactory theoretical picture of the classic superconductors emerged in terms of the Bardeen-Cooper-Schrieffer (BCS) theory [3]. Before we talk about the BCS theory, let us introduce the notion of local potentials.
\nShown in \nFigure 1\n is a bar of metal. How are electrons in this metal bar? Solid-state physics texts start by putting these electrons in a periodic potential [4, 5, 6]. But that is not the complete story.
\nDepiction of a metallic bar.
Shown in \nFigure 2\n is a periodic array of metal ions. Periodic arrangement divides the region into cells (region bounded by dashed lines in \nFigure 2\n) such that the potential in the
Depiction of the potential due to metal ions. A rapidly varying periodic part
where
Depiction of Fermi gas of electrons in a metal moving in a confining potential.
Coming back to a more realistic estimate of the kinetic energy, electron wave function is confined to length \n
The dispersion curve and energy band for electrons in a periodic potential.
With this energy bandwidth, electrons are all well confined by the confining potential. In fact we do not need a potential of depth 50 eV; to confine the electrons, we can just do it with a depth of ∼10 eV which means a length of around
Depiction of local potentials due to metal ions that locally confine electrons.
In this chapter, we spell out the main ideas of the BCS theory. The BCS theory tells us how to use phonon-mediated interaction to bind electrons together, so that we have big molecule and we call the BCS ground state or the BCS molecule. At low temperatures, phonons do not have energy to break the bonds in the molecule; hence, electrons in the molecule do not scatter phonons. So, let us see how BCS binds these electrons into something big.
\nLet us take two electrons, both at the Fermi surface, one with momentum
(A) Depiction of the Fermi sphere and how electron pair
We proceed into the interaction frame of the natural Hamiltonian (system energies) by transformation
\nThis gives for \n
\n\n
The first integral averages to zero, while the second integral
\nEvaluating it explicitly, we get for our system that second-order integral is
\nwhich couples levels 1 and 3 and drives transition between them at rate \n
Observe \n
How does all this help. Suppose \n
has energy \n
Recall we are interested in studying how a BCS molecule scatters phonons. For this we first understand how a normal electron scatters of a thermal phonon. We also derive electron–phonon interaction (
Consider phonons in a crystalline solid. We first develop the concept of a phonon packet. To fix ideas, we start with the case of one-dimensional lattice potential. Consider a periodic potential with period
where
\nThe potential is shown in \nFigure 7\n.
\nDepiction of the periodic potential in
Now, consider how potential changes when we perturb the lattice sites from their equilibrium position, due to lattice vibrations:
\nFor a phonon mode with wavenumber
we have
\nwhere
Using Fourier series, we can write
\nWe can determine
where \n
We do not worry much about
where \n
Then, we get
\nAt temperature of
\n\n
with \n
We considered one phonon mode. Now, consider a phonon wave packet (which can also be thought of as a mode, localized in space) which takes the form
\nwhere \n
This deformation potential due to phonon wave packet is shown in \nFigure 8\n. The maximum value of the potential is around \n
Depiction of the deformation potential in
Of course phonons have a time dynamics given by their dispersion relation:
\nWith the phonon dispersion relation \n
The deformation potential travels with velocity of sound and collides with an incoming electron. To understand this collision, consider a phonon packet as in Eq. (14) centred at the origin. The packet is like a potential hill. A electron comes along say at velocity \n
Depiction on how an incoming electron goes past the deformation potential (b); if its velocity is sufficient, else it slides back and rebounds as in (a).
In the above, we assumed phonon packet is stationary; however, it moves with velocity \n
Depiction on how an electron and phonon traveling towards each other collide.
In the phonon frame the electron travels towards it with velocity \n
and by conservation of energy, the phonon has lost energy, lowering its temperature.
\nIn the second case, electron and phonon are traveling in the same direction. This is shown in \nFigure 11\n. In the frame of phonon, electron travels towards the phonon with velocity \n
Depiction on how an electron and phonon traveling in same direction collide.
Thus, we have shown that electron and phonon can exchange energy due to collisions. Now, everything is true as in statistical mechanics, and we can go on to derive
All our analysis has been in one dimension. In two or three dimensions, the phonon packets are phonon tides (as in ocean tides). Let us fix ideas with two dimensions, and three dimensions follow directly. Consider a two-dimensional periodic potential with period
Now, consider how potential changes when we perturb the lattice sites from their equilibrium position, due to lattice vibrations:
\nLet us consider phonons propagating along
We have due to \n
where \n
Note
\nUsing Fourier series, we can write
\nWe can determine
which gives us a deformation potential as before:
\nwhich is same along
Depiction of the deformation potential tide as shown in
Since deformation potential is a tide, electron–phonon collisions do not have to be head on; they can happen at oblique angles, as shown in \nFigure 13\n in a top view (looking down). The velocity of electron parallel to tide remains unchanged, while velocity perpendicular to tide gets reflected. If the perpendicular velocity is large enough, the electron can jump over the tide and continue as shown by a dotted line in \nFigure 13\n. Imagining the tide in three dimensions is straightforward. In three dimensions, the deformation potential takes the form a wind gust moving in say
The top view collision of an electron with a deformation potential tide at an angle
We described how a normal electron scatters phonons. Now, let us go back to our discussion on electron-phonon interaction and recall a phonon \n
where
Using \n
Thus, electron-phonon coupling Hamiltonian is of form
\nwhere \n
Using a cosine potential with \n
We just derived an expression for the electron-phonon interaction (
We said there are only two states, \n
it has energy \n
(A) Electron pairs on the fermi surface and (B) electron pairs in an annulus around the fermi surface.
The states do not have to be exactly on a Fermi surface as shown in \nFigure 14A\n; rather, they can be in an annulus around the Fermi sphere as shown in \nFigure 14B\n. When \n
But before we proceed, a note of caution is in order when we use the formula \n
We proceed into the interaction frame of the natural Hamiltonian (system energies) by transformation:
\nThis gives for \n
We evaluate the effective evolution of
Let us calculate \n
Similarly
\nand finally
\nThen, from Eq. (27), we get
\nwhere
\nObserve in the above the term \n
We have been talking about electron waves in this section. Earlier, we spent considerable time showing how electrons are wave packets confined to local potentials. We now look for phonon-mediated interaction between wave packets. A wave packet is built from many k-states (k-points). These states have slightly different energies (frequencies) which make the packet moves. We call these different frequencies
has binding energy \n
The offsets getting averaged by showing wave packets standing in the local potential, bound by phonon-mediated interaction. Offset average so effectively packets are standstill; they do not move.
(A) Packet pairs
The wave packet in a potential well shuttles back and forth, which averages the offsets \n
We saw how two electrons bind to form a Cooper pair. However, for a big molecule, we need to bind many electrons. How this works will be discussed now. The basic idea is with many electrons; we need space for electron wave packets to scatter to. For example, when there was only one packet pair at the Fermi surface, it could scatter into all possible other packet pairs, and we saw how we could then form a superposition of these states. Now, suppose we have 2
Packets at the Fermi surface that has twice the number of k-states as electrons. This means half the packet sites will be empty.
Let \n
Depiction of the Fermi sphere with surface as a thick circle and an annulus of thickness
\n\n
As we will see soon, \n
As shown in last section, the Cooper pair \n
The binding energy of this state is \n
Next, we study how low-frequency thermal phonons try to break the BCS molecule. The electron wave packet collides with the phonon and gets deflected, which means the Cooper pair gets broken. Then, the superconducting state constitutes \n
which gives
\nWhen \n
We now come to interaction of neighboring BCS molecules. In our picture of
Depiction of two BCS ground states in local potential wells separated in a weak link.
If \n
where \n
We talked about two BCS states separated by a thin insulator in a Josephson junction. In an actual superconductor, we have an array (lattice) of such localized BCS states as shown in \nFigure 20\n. Different phases \n
Depiction of array of local BCS states in local potential wells with different phases.
If \n
where \n
What we have now is a new lattice of potential wells as shown in \nFigure 20\n with spacing of
is the ground state of new lattice (Eq. 40). A state like
\nhas a momentum and constitutes the supercurrent. It has energy \n
In the presence of electric field
Now, consider the local BCS states in \nFigure 20\n put in a loop. If we turn on a magnetic field (say in time
where
giving
\nThis is the magnetic quantum flux. When one deals with the superconducting loop or a hole in a bulk superconductor, it turns out that the magnetic flux threading such a hole/loop is quantized [9, 10] as just shown.
\n\n\nFigure 21\n depicts the schematic of a superconducting quantum interference device (SQUID) where two superconductors
Depiction of the schematic of a SQUID where two superconductors
When a superconductor placed in an magnetic field is cooled below its critical
Depiction of the Meissner effect whereby the magnetic field inside a superconductor is expulsed when we cool it below its superconducting temperature
German physicists Walther Meissner and Robert Ochsenfeld discovered this phenomenon in 1933 by measuring the magnetic field distribution outside superconducting tin and lead samples. The samples, in the presence of an applied magnetic field, were cooled below their superconducting transition temperature, whereupon the samples canceled nearly all interior magnetic fields. A superconductor with little or no magnetic field within it is said to be in the Meissner state. The Meissner state breaks down when the applied magnetic field is too large. Superconductors can be divided into two classes according to how this breakdown occurs. In type-I superconductor if the magnetic field is above certain threshold
We talked about how wave packets shuttle back and forth in local potentials and get bound by phonons to form a BCS molecule. In the presence of a magnetic field, they do not shuttle. Instead, they do cyclotron motion with frequency \n
(A) Depiction on how packets shuttle back and forth in local potential and (B) how they execute a cyclotron motion in the presence of a magnetic field.
When we bring two metals in proximity, separated by a thin-insulating barrier, apply a tiny voltage nd then the current will flow in the circuit. There is a thin-insulating barrier, but electrons will tunnel through the barrier. Now, what will happen if these metals are replaced by a superconductor? These are a set of experiments carried out by Norwegian-American physicist Ivar Giaever who shared the Nobel Prize in Physics in 1973 with Leo Esaki and Brian Josephson “for their discoveries regarding tunnelling phenomena in solids”. What he found was that if one of the metals is a superconductor, the electron cannot just come in, as there is an energy barrier of \n
(A) Depiction on how a tiny voltage between two metals separated by an insulating barrier generates current that goes through an insulating barrier through tunneling. (B) If one of the metals is a superconductor, then the applied voltage has to be at least as big as the superconducting gap.
Recall in our discussion of superconducting state that we had 2
Depiction on how upon tunneling an extra electron, shown in dashed lines, enters the superconducting state.
High-temperature superconductors (abbreviated high-
Whereas “ordinary” or metallic superconductors usually have transition temperatures (temperatures below which they are superconductive) below 30 K (243.2°C) and must be cooled using liquid helium in order to achieve superconductivity, HTS have been observed with transition temperatures as high as 138 K (135°C) and can be cooled to superconductivity using liquid nitrogen. Compounds of copper and oxygen (so-called cuprates) are known to have HTS properties, and the term high-temperature superconductor was used interchangeably with cuprate superconductor. Examples are compounds such as lanthanum strontium copper oxide (LASCO) and neodymium cerium copper oxide (NSCO).
\nLet us take lanthanum copper oxide \n
When we hole/electron dope, we remove/add electron to \n
(A) Depiction on how in narrow
The characteristic phase diagram of a high
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His studies in robotics lead him not only to a PhD degree but also inspired him to co-found and build the International Journal of Advanced Robotic Systems - world's first Open Access journal in the field of robotics.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"441",title:"Ph.D.",name:"Jaekyu",middleName:null,surname:"Park",slug:"jaekyu-park",fullName:"Jaekyu Park",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/441/images/1881_n.jpg",biography:null,institutionString:null,institution:{name:"LG Corporation (South Korea)",country:{name:"Korea, South"}}},{id:"465",title:"Dr",name:"Christian",middleName:null,surname:"Martens",slug:"christian-martens",fullName:"Christian Martens",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"479",title:"Dr.",name:"Valentina",middleName:null,surname:"Colla",slug:"valentina-colla",fullName:"Valentina Colla",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/479/images/358_n.jpg",biography:null,institutionString:null,institution:{name:"Sant'Anna School of Advanced Studies",country:{name:"Italy"}}},{id:"494",title:"PhD",name:"Loris",middleName:null,surname:"Nanni",slug:"loris-nanni",fullName:"Loris Nanni",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/494/images/system/494.jpg",biography:"Loris Nanni received his Master Degree cum laude on June-2002 from the University of Bologna, and the April 26th 2006 he received his Ph.D. in Computer Engineering at DEIS, University of Bologna. 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Delac received his B.Sc.E.E. degree in 2003 and is currentlypursuing a Ph.D. degree at the University of Zagreb, Faculty of Electrical Engineering andComputing. His current research interests are digital image analysis, pattern recognition andbiometrics.",institutionString:null,institution:{name:"University of Zagreb",country:{name:"Croatia"}}},{id:"557",title:"Dr.",name:"Andon",middleName:"Venelinov",surname:"Topalov",slug:"andon-topalov",fullName:"Andon Topalov",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/557/images/1927_n.jpg",biography:"Dr. Andon V. Topalov received the MSc degree in Control Engineering from the Faculty of Information Systems, Technologies, and Automation at Moscow State University of Civil Engineering (MGGU) in 1979. He then received his PhD degree in Control Engineering from the Department of Automation and Remote Control at Moscow State Mining University (MGSU), Moscow, in 1984. From 1985 to 1986, he was a Research Fellow in the Research Institute for Electronic Equipment, ZZU AD, Plovdiv, Bulgaria. In 1986, he joined the Department of Control Systems, Technical University of Sofia at the Plovdiv campus, where he is presently a Full Professor. He has held long-term visiting Professor/Scholar positions at various institutions in South Korea, Turkey, Mexico, Greece, Belgium, UK, and Germany. And he has coauthored one book and authored or coauthored more than 80 research papers in conference proceedings and journals. 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After finishing his P. hD degree in 1992, he served in the Industry as a Scientific Officer and continued his academic career as a visiting scholar for a number of educational institutions. In 1996 he joined National University of Science & Technology Pakistan (NUST) as an Associate Professor; NUST is one of the top few universities in Pakistan. In 1999 he joined an International Company Lineo Inc, Canada as Manager Compiler Group, where he headed the group for developing Compiler Tool Chain and Porting of Operating Systems for the BLACKfin processor. The processor development was a joint venture by Intel and Analog Devices. In 2002 Lineo Inc., was taken over by another company, so he joined Aalborg University Denmark as an Assistant Professor.\nProfessor Akbar has truly a multi-disciplined career and he continued his legacy and making progress in many areas of his interests both in teaching and research. He has contributed in stochastic estimation of control area especially, in the Multiple Target Tracking and Interactive Multiple Model (IMM) research, Ball & Beam Control Problem, Robotics, Levitation Control. He has contributed in developing Algorithms for Fingerprint Matching, Computer Vision and Face Recognition. He has been supervising Pattern Recognition, Formal Languages and Distributed Processing projects for several years. He has reviewed many books on Management, Computer Science. Currently, he is an active and permanent reviewer for many international conferences and symposia and the program committee member for many international conferences.\nIn teaching he has taught the core computer science subjects like, Digital Design, Real Time Embedded System Programming, Operating Systems, Software Engineering, Data Structures, Databases, Compiler Construction. 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This change influences one another at various temporal and spatial scales; however, improper land uses are the primary causal factor on climate change. It studies relevant literature and Nepal’s case to assess the relationship between land use and climate change. Similarly focuses on how land-use impacts climate change and vice versa. In recent centuries land-use change significant effects on ecological variables and climate change. Likewise, understanding the research on both topics will help decision-makers and conservation planners manage land and climate.",book:{id:"10754",slug:"the-nature-causes-effects-and-mitigation-of-climate-change-on-the-environment",title:"The Nature, Causes, Effects and Mitigation of Climate Change on the Environment",fullTitle:"The Nature, Causes, Effects and Mitigation of Climate Change on the Environment"},signatures:"Pawan Thapa",authors:[{id:"349566",title:"M.Sc.",name:"Pawan",middleName:null,surname:"Thapa",slug:"pawan-thapa",fullName:"Pawan Thapa"}]},{id:"42926",title:"Disaster Risk Management and Social Impact Assessment: Understanding Preparedness, Response and Recovery in Community Projects",slug:"disaster-risk-management-and-social-impact-assessment-understanding-preparedness-response-and-recove",totalDownloads:10017,totalCrossrefCites:3,totalDimensionsCites:10,abstract:null,book:{id:"3364",slug:"environmental-change-and-sustainability",title:"Environmental Change and Sustainability",fullTitle:"Environmental Change and Sustainability"},signatures:"Raheem A. 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The consequences of greenhouse effect and climate change from rising temperatures, frequent droughts, irregular rainfall, etc. are already evident. Insects and plants are affected by climate change and extreme weather events and the direct impact of anthropogenic climate change has been reported on every continent, in every ocean and in most major taxonomic groups. In the modern period, as a result of natural cycles and anthropogenic activities and their effects on the global climate, plants are typically susceptible to new environmental factors, i.e. higher levels solar radiation, rise in temperatures, greenhouse effect and changes in rainfall patterns over the seasons. Increased temperatures, CO2 and rapid changes in rainfall patterns can dramatically alter the biochemistry of plants and thus plant defence responses. This can have important implications in insect fertility, feeding rates, survival, population size, and dispersal. The relationships between plants and insects are thus changed with significant consequences for food security and natural ecosystems. Similarly, mismatches between plants and insect pollinators are caused by the acceleration of plant phenology by warming. Human nutrition which depends on insect pollination can be affected with reduction in plant reproduction and fitness. Thus, understanding abiotic stress reactions in plants and insects is relevant and challenging in agriculture. In the preparation and implementation of effective strategies for future insect pest management programmes, the impact of climate change on crop production, mediated by changes in the populations of extreme insect pests should be carefully considered.",book:{id:"10754",slug:"the-nature-causes-effects-and-mitigation-of-climate-change-on-the-environment",title:"The Nature, Causes, Effects and Mitigation of Climate Change on the Environment",fullTitle:"The Nature, Causes, Effects and Mitigation of Climate Change on the Environment"},signatures:"Somala Karthik, M.S. Sai Reddy and Gummudala Yashaswini",authors:[{id:"416107",title:"Ph.D. Student",name:"Somala",middleName:null,surname:"Karthik",slug:"somala-karthik",fullName:"Somala Karthik"},{id:"416115",title:"Prof.",name:"M.S.",middleName:null,surname:"Sai Reddy",slug:"m.s.-sai-reddy",fullName:"M.S. 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He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. 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He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. 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She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. 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Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. She is a professor in the Stomatology Faculty, St. Petersburg State University. She has expertise in the development and evaluation of a wide range of live mucosal vaccines against influenza and bacterial complications. Her research interests include immunity against influenza and COVID-19 and the development of immunization schemes for high-risk individuals.",institutionString:'Federal State Budgetary Scientific Institution "Institute of Experimental Medicine"',institution:null},{id:"238958",title:"Mr.",name:"Atamjit",middleName:null,surname:"Singh",slug:"atamjit-singh",fullName:"Atamjit Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/238958/images/6575_n.jpg",biography:null,institutionString:null,institution:null},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:null},{id:"252058",title:"M.Sc.",name:"Juan",middleName:null,surname:"Sulca",slug:"juan-sulca",fullName:"Juan Sulca",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/252058/images/12834_n.jpg",biography:null,institutionString:null,institution:null},{id:"191392",title:"Dr.",name:"Marimuthu",middleName:null,surname:"Govindarajan",slug:"marimuthu-govindarajan",fullName:"Marimuthu Govindarajan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191392/images/5828_n.jpg",biography:"Dr. M. Govindarajan completed his BSc degree in Zoology at Government Arts College (Autonomous), Kumbakonam, and MSc, MPhil, and PhD degrees at Annamalai University, Annamalai Nagar, Tamil Nadu, India. He is serving as an assistant professor at the Department of Zoology, Annamalai University. His research interests include isolation, identification, and characterization of biologically active molecules from plants and microbes. He has identified more than 20 pure compounds with high mosquitocidal activity and also conducted high-quality research on photochemistry and nanosynthesis. He has published more than 150 studies in journals with impact factor and 2 books in Lambert Academic Publishing, Germany. He serves as an editorial board member in various national and international scientific journals.",institutionString:null,institution:null},{id:"274660",title:"Dr.",name:"Damodar",middleName:null,surname:"Paudel",slug:"damodar-paudel",fullName:"Damodar Paudel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/274660/images/8176_n.jpg",biography:"I am DrDamodar Paudel,currently working as consultant Physician in Nepal police Hospital.",institutionString:null,institution:null},{id:"241562",title:"Dr.",name:"Melvin",middleName:null,surname:"Sanicas",slug:"melvin-sanicas",fullName:"Melvin Sanicas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241562/images/6699_n.jpg",biography:null,institutionString:null,institution:null},{id:"337446",title:"Dr.",name:"Maria",middleName:null,surname:"Zavala-Colon",slug:"maria-zavala-colon",fullName:"Maria Zavala-Colon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Puerto Rico, Medical Sciences Campus",country:{name:"United States of America"}}},{id:"338856",title:"Mrs.",name:"Nur Alvira",middleName:null,surname:"Pascawati",slug:"nur-alvira-pascawati",fullName:"Nur Alvira Pascawati",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universitas Respati Yogyakarta",country:{name:"Indonesia"}}},{id:"441116",title:"Dr.",name:"Jovanka M.",middleName:null,surname:"Voyich",slug:"jovanka-m.-voyich",fullName:"Jovanka M. Voyich",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Montana State University",country:{name:"United States of America"}}},{id:"330412",title:"Dr.",name:"Muhammad",middleName:null,surname:"Farhab",slug:"muhammad-farhab",fullName:"Muhammad Farhab",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"349495",title:"Dr.",name:"Muhammad",middleName:null,surname:"Ijaz",slug:"muhammad-ijaz",fullName:"Muhammad Ijaz",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Veterinary and Animal Sciences",country:{name:"Pakistan"}}}]}},subseries:{item:{id:"20",type:"subseries",title:"Animal Nutrition",keywords:"Sustainable Animal Diets, Carbon Footprint, Meta Analyses",scope:"An essential part of animal production is nutrition. Animals need to receive a properly balanced diet. One of the new challenges we are now faced with is sustainable animal diets (STAND) that involve the 3 P’s (People, Planet, and Profitability). We must develop animal feed that does not compete with human food, use antibiotics, and explore new growth promoters options, such as plant extracts or compounds that promote feed efficiency (e.g., monensin, oils, enzymes, probiotics). These new feed options must also be environmentally friendly, reducing the Carbon footprint, CH4, N, and P emissions to the environment, with an adequate formulation of nutrients.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/20.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11416,editor:{id:"175967",title:"Dr.",name:"Manuel",middleName:null,surname:"Gonzalez Ronquillo",slug:"manuel-gonzalez-ronquillo",fullName:"Manuel Gonzalez Ronquillo",profilePictureURL:"https://mts.intechopen.com/storage/users/175967/images/system/175967.png",biography:"Dr. Manuel González Ronquillo obtained his doctorate degree from the University of Zaragoza, Spain, in 2001. He is a research professor at the Faculty of Veterinary Medicine and Animal Husbandry, Autonomous University of the State of Mexico. He is also a level-2 researcher. He received a Fulbright-Garcia Robles fellowship for a postdoctoral stay at the US Dairy Forage Research Center, Madison, Wisconsin, USA in 2008–2009. He received grants from Alianza del Pacifico for a stay at the University of Magallanes, Chile, in 2014, and from Consejo Nacional de Ciencia y Tecnología (CONACyT) to work in the Food and Agriculture Organization’s Animal Production and Health Division (AGA), Rome, Italy, in 2014–2015. He has collaborated with researchers from different countries and published ninety-eight journal articles. He teaches various degree courses in zootechnics, sheep production, and agricultural sciences and natural resources.\n\nDr. Ronquillo’s research focuses on the evaluation of sustainable animal diets (StAnD), using native resources of the region, decreasing carbon footprint, and applying meta-analysis and mathematical models for a better understanding of animal production.",institutionString:null,institution:{name:"Universidad Autónoma del Estado de México",institutionURL:null,country:{name:"Mexico"}}},editorTwo:null,editorThree:null,series:{id:"13",title:"Veterinary Medicine and Science",doi:"10.5772/intechopen.73681",issn:"2632-0517"},editorialBoard:[{id:"175762",title:"Dr.",name:"Alfredo J.",middleName:null,surname:"Escribano",slug:"alfredo-j.-escribano",fullName:"Alfredo J. 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