Types and frequency range of oscillations in Hall thrusters.
\r\n\tSmart cities, the intelligent transportation system (ITS), AI cloud computing, and wireless intelligence (in 6G) require high-speed, low latency, and high bandwidth networks. With RF band limitations in the existing wireless world to meet the rise of big data traffic, exploring new bands is a common trend. Fortunately, the THz band is considered a promising candidate to combat these limitations. THz is an underdeveloped ultra-wideband zone between microwave and infrared, therefore it benefits from both advantages of electronics and optics.
\r\n\tIntelligent electronics could shape the future smart world and promote initiatives on exploring brand-new integrated circuits, high-effective intelligent reconfigurable surface, nondestructive evaluation, SWIPT, ITS, 6G, medical imaging, and signal processing.
\r\n\tThis book volume aims at exploiting the mainstream principles, circuitry architectures, and development roadmap for intelligent electronic systems. The intention of this book is to acquaint the Science and Engineering Community with a thoughtful and comprehensive understanding of the state of the art in intelligent electronics as well as novel technologies that promote contemporary THz, IRS systems, and beyond. Related new research directions across different disciplines will also be covered in this volume: from theoretical basis to materials characteristics, and from featured architectures to practical applications.
",isbn:"978-1-80355-001-5",printIsbn:"978-1-80355-000-8",pdfIsbn:"978-1-80355-002-2",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,isSalesforceBook:!1,isNomenclature:!1,hash:"23cc72ecaa024d12b2abd7aaf61405be",bookSignature:"Dr. Mingbo Niu",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10963.jpg",keywords:"Beam Forming, Machine Learning, Non-Orthogonal Multiple Access, Multi-User System, Imaging and Signal Processing, Nano Technology, Automatic Incident Detection, Smart Driving, Vehicle-to-Anything, Energy Harvesting, Sustainable Electronics and Optics, Clean Energy Based Smart Grid",numberOfDownloads:336,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"June 9th 2021",dateEndSecondStepPublish:"August 5th 2021",dateEndThirdStepPublish:"October 4th 2021",dateEndFourthStepPublish:"December 23rd 2021",dateEndFifthStepPublish:"February 21st 2022",dateConfirmationOfParticipation:null,remainingDaysToSecondStep:"a year",secondStepPassed:!0,areRegistrationsClosed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:"Dr. Niu was the recipient of numerous scholarships during his undergraduate and graduate studies, which included a Chinese Government Award, two University of British Columbia University Graduate Fellowships (UGFs), and a Huawei Tech. Ltd Special Fellowship. He is a licensed Professional Engineer in British Columbia.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"141595",title:"Dr.",name:"Mingbo",middleName:null,surname:"Niu",slug:"mingbo-niu",fullName:"Mingbo Niu",profilePictureURL:"https://mts.intechopen.com/storage/users/141595/images/system/141595.jpg",biography:"Mingbo Niu received a B. Eng. degree in Electronic Engineering from Northwestern Polytechnical University in China, and an M. Sc. (Eng.) degree (first-class) major in Communication and Information Systems from the same university. Prior to his Ph.D., he worked at a National Key Laboratory on Information and Signal Processing. He received his Ph.D. degree in Electrical and Computer Engineering from the University of British Columbia, Canada in 2013. From 2008 to 2012, he was a Research Assistant at Optical Wireless Communications Laboratory and Integrated Optics Laboratory where he contributed to the development of ultra-high speed optical data transmission links. Dr. Niu held a postdoctoral fellowship at Queen’s University from 2013 to 2015. He also worked for Defence Research and Development Canada (DRDC) at Calian Tech. Ltd where he contributed to statistical evaluation models of MIMO compressive sensing projects. He is now a Professor of Electrical Engineering at Okanagan College, Canada. Dr. Niu has co-authored more than 20 IEEE and OSA papers and supervised a number of students’ projects. Currently, he serves as a Lead Guest Editor for the journal Wireless Communications and Mobile Computing (IF: 1.899) and an Editor for InTech book projects on \\Advanced Analog/Digital Circuits\\. Dr. Niu was the recipient of numerous scholarships during his undergraduate and graduate studies, which included a Chinese Government Award, two University of British Columbia University Graduate Fellowships (UGFs), and a HuaWei Tech. Ltd Special Fellowship. His current research and teaching interests include digital communications, microcontrollers, MIMO, DSP, energy harvesting, electronic circuit theory, and ICs for data communication networks. 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The etiology is very complex and heterogeneous, with numerous causes described, and includes genetic, epigenetic, or environmental factors in isolation or associated. It aggregates in families with the heritability being estimated at 0.50, but the individual risk and to what extent this is caused by genetic factors or environmental factors remains unresolved. These factors probably interact at least in the majority of cases, and thus the assessment of individuals and genetic counseling is further complicated [124].
Valuable information is been gained through the identification of candidate genes, though case-control and association studies and more recently by comparative genomic hybridization and whole exome and genome sequencing. In the epigenetic area, mechanisms such as genomic imprinting, epimutations and methylation have been identified [133]. Copy number variations (CNVs) have gained prominence on the stage of the discovery of the causes of autism. The
One other issue that has emerged recently is that a significant number of synaptic proteins directly or indirectly affect the structure and function of neurons, dendrites and synapses. Subtle changes in the dendritic and synaptic structures can lead to huge changes in information processing. Dendritic branches and spines are essential for the formation and plasticity of neuronal circuits but are interrupted in many neurologic disorders, such as autism. In many cases the same mutations are observed in unaffected relatives. This suggests the existence of a compensatory mechanism or other genetic or non-genetic causes [140].
New findings on the genetic etiology of autism have pointed to the participation of regulatory regions of transcription factors, the microRNAs (miRNAs), a class of noncoding RNAs of ~22 nucleotides that suppress translation by pairing with miRNA recognition elements present in the 3\'untranslated region (3\'UTR) of target mRNAs. Candidate genes and sites of miRNA targets have been identified from these. It is known that the expression of many genes involved in autism is regulated by miRNAs. Single nucleotide polymorphisms (SNPs) have been described as modulators or creators of new recognition elements of miRNAs. Therefore, there is a hypothesis that SNPs disrupting the interaction between miRNA and genes can lead to the aberrant expressions of genes implicated in autism, resulting in susceptibility to disease or pathogenesis in at least one subpopulation of affected individuals [149].
Although the involvement of genetic abnormalities in autism is well accepted, recent studies have indicated that there is a similar contribution of environmental factors. However, studies related to the environment, especially those regarding toxic products, have not been systematically reviewed yet, as many studies have limitations, including a lack of reproducibility, small sample size, retrospective design, bias between cases and controls and non-use of an appropriate autism diagnostic tool. Thus, in general, there is a potential involvement of some toxic products in complex genetic-environmental interactions which act synergistically or in parallel on the brain in a way that increases the likelihood of developing autism.
Moreover, although some studies suggest that autistic characteristics are due to central nervous system (CNS) dysfunction, there is evidence of autism-related abnormalities that are not related to the CNS, at least in some individuals. Hence, the metabolic system, immune system dysregulation and oxidative stress have also been implicated in the etiology [107].
Furthermore, other new lines of research also point to the importance of the so-called "brain-gut axis" revealing the central role of the intestinal microbiota in postnatal development and maturation of the immune and endocrine systems that, in turn, control CNS signaling, brain function and behavior [151]. But studies on this line must be carefully analyzed.
The low recurrence related to any one cause is one of the most intriguing aspects of the etiology, as is the difference in the proportion of affected between the genders, because men are four times more affected by ASD than women [27]. Additionally, there is an association between increased paternal age and risk for ASD. This finding may indicate that
Investigating and understanding the etiology of autism is extremely important for families because it allows a determination of the recurrence risk, the possibility of detecting other associated medical problems, an assessment of the molecular nature and cellular pathophysiology, and potential therapeutic approaches. In this context, the aim of this chapter is to provide the reader with an overview of these possible causes and others that may contribute to autistic behavior.
In addition to well-established genic syndromes, a lot of cases of ASD present with numerical or structural chromosomal alterations visible by conventional cytogenetic techniques [164]. Due to the high number of cases and the type and location of the genes described, the association of some chromosomal regions is well established in autism including: 1q21, 2q37, 7q11.23, 15q11-13, 16p11.2, 17p11.2, 22q11.2 and 22q13. Rearrangements involving these regions are detected by GTG banding however more sophisticated molecular techniques are recommended. High-resolution whole-genome analysis with array-based technologies have revealed genomic imbalances in at least 10% of cases [170].
Chromosome 15 is reportedly the most common site of autosomal abnormalities in autism with the duplication of 15q11-q13 being the most frequently reported alteration. This region contains at least 30 genes, several of which have been associated to ASD, neurobehavioral disorders, cognitive deficits, hypotonia, language delay and seizures [141, 154].This region, known for its genetic instability, contains many low copy repeats and segmental duplications. It is known as a critical region for Prader-Willi/Angelman syndrome and has a complex pattern of paternal and maternal imprinting; it contains at least five paternally expressed genes (
The phenotype involving recurrent ∼600 kb microdeletions and microduplications in the 16p11.2 region is characterized by a spectrum of neurodevelopmental impairments including developmental delay and intellectual disability, epilepsy, autism and other psychiatric disorders which are all subject to incomplete penetrance and variable expressivity. This deletion is observed in ~0.5% of autism patients, making this the second most common abnormality in this disorder [48, 156]. Losses in candidate genes in this region, such as
The 22q11.2 deletion is one of the most commonly known interstitial deletions identified in humans, and with a frequency of around 1:4,000 live births in the general population, it is related to DiGeorge Sequence/Velocardiofacial syndrome [98, 132]. Recent studies suggest that the high prevalence of autistic behaviors in children with 22q11.2 deletions should not be viewed only as ASD but as prodromal symptoms preceding the onset of schizophrenia [9, 132, 153]. Individuals with hemizygosity of the 22q11.2 deletion represent genetically identifiable cases of ASD. However, the 22q11.2 gene(s) responsible for ASD have not been identified yet.
Several large chromosomal microarray studies have reported the prevalence of CNV variants in people with particular features (e.g., autism, schizophrenia, and epilepsy) but few studies have investigated the prevalence in the general population. In a screening of 6,813 consecutive cord blood samples from a predominantly French–Canadian population to assess genomic CNVs, 23 children were identified with alterations in 15q11-q13, 16p11.2 or 22q11.2. Longitudinal follow-up studies are needed to determine the clinical consequences of CNVs identified at birth [146]. Anyway, considering the important implications for genetic counseling, these regions must be evaluated in ASD patients.
Dysregulation of gene expression of several genes/loci converging on the same networks (overlay) and/or combinatorial effects of different deleterious genetic variations appear to exceed a threshold and result in the autistic phenotype. In support of these ideas, strategies based on bioinformatics have identified many candidate genes, showing that ASD can be triggered by different types of genetic variations in many different genes, a phenomenon known as non-allelic genetic heterogeneity [74, 138, 105]. This model is more accepted; combines both common and rare variations posing risk for ASD, particularly those involving synaptic genes and genes involved in neurogenesis [138]. Thus it is assumed that people with ASD have a set of genetic variants that predispose them to abnormal development of brain structures involved in processing social information (the "social brain"). But it is known that there is no common pathophysiology in ASD. This may result from mutations in many different genes involved in different functions [138]. The kinds of variants that incline to autism and can involve several genes at the same time are the CNVs.
CNVs are microduplications or microdeletions resulting from insertions, deletions or translocations in the human genome that are observed in the general population and commonly found in genic regions in individuals with neuropsychiatric disorders. They can be inherited or
Although structural variations, such as CNVs, play an important etiologic role in the development of ASD as has been proposed by several authors since 2006, most of the results of different studies are not considered in the clinical evaluation of children with ASD, probably due to the rarity of individual variants, the lack of coverage of probes in clinical microarrays, the lack of reproducibility of studies that present different findings and the difficulty to understand the biology corresponding to some variants even when they are significantly associated with ASD. Nevertheless, clinical guidelines suggest that microarray-based tests are the first step in the genetic analysis of children with ASD [128, 68]; however this is not feasible in most cases of low-income countries due to the high cost of these tests.
While the majority of genetic mutations currently linked to autism are rare variants that change the protein-coding sequence of synaptic candidate genes, regulatory polymorphisms affecting constitutive and alternative splicing have emerged as risk factors in other diseases, accounting for an estimated 40-60% of general disease risk [131].
Neurons communicate via synapses, mainly mediated by precisely controlled intercellular interactions. Interactions between presynaptic and postsynaptic cellular adhesion molecules (CAMs) drive synapse maturation during development. CAMs provide "bridges", that is, cell-to-cell connectivity between pre and postsynaptic sites. These transsynaptic interactions are regulated by alternative splicing of CAMs RNAs, which ultimately determines neurotransmitter phenotype. Failure to generate the appropriate CAMs can result in loss of activity-dependent neuronal plasticity, and risk for developmental disorders, including autism. However, it remains unclear as to how many and which proteins are involved in the synaptogenesis process [161]. The postsynaptic proteome of excitatory synapses of a mammalian brain contains over 1,000 proteins, indicating complex protein-protein interactions that occur both within and between synapses [15, 30, 32, 47].
Typically, CAMs are located at the center of synapse and contain three domains: an intracellular domain that interacts with the intracellular scaffolding protein, a transmembrane domain and an extracellular domain which interacts with other CAMs [101]. Intercellular interactions in synapses mediated by protein-protein CAMs are involved in recognition and alignment of pre and postsynaptic sites, transsynaptic signaling, the exact location of neurotransmitter receptors and release of synaptic vesicles. There are several families of CAMs that have already been recognized, including neurexins (Nrxs) and neuroligins (NLS), neuronal transmembrane proteins rich in leucine (LRRTMs), N-cadherin/β-catenin, ephrins and Eph, SynCAM receptors and integrins [161].
The Nrxs and NLS contain an extracellular domain that participates in the pre and postsynaptic interaction and an intracellular domain that is involved in multiple functional interactions and regulatory processes. They interact with high affinity via their extracellular regions [135, 136]. Nrxs create extracellular protein-protein interactions with the intracellular signaling cascade. NLS binds to areas of postsynaptic density (PSD), proteins which are supported by glutamatergic synapses. In postsynaptic sites, the NLS/Nrxs interactions cause an increase in the PSD agglomeration recruitment of postsynaptic N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). Thus, the binding of Nrxs and NLS helps to align presynaptic and postsynaptic receptor release (Budreck et al., 2013; Mondin, Tessier, Thoumine, 2013).
LRRTM proteins are a group of type I transmembrane proteins containing extracellular leucine-rich repeats and a short cytoplasmic tail. They play a key role in the development and maturation of synapses, but are also directly involved in synaptic transmission and more complex behavior [87]. Contactins (CNTNs) provide a set of glycan phosphatidyl-inositol (GPI) Ig-CAM links containing six N-terminal Ig-like domains and four Fibronectin Type III domains. CNTNs play an important role in the formation of axon connections in the developing nervous system. For example, Cntn-1 and Cntn-2 are involved in axon growth and guidance, and Cntn-6 is expressed in the presynaptic region in the developing nervous system [169].
As most neurological diseases originate as a dysfunction of neural circuits whose function is highly dependent on the accuracy of cell-cell adhesions, there is increasing evidence connecting several neurological disorders with mutations or altered expressions of CAMs. For example, mutations in the
Alterations in neurotransmission and its components, such as synaptic vesicles seem to be one of the keys in neurological disorders. Abnormalities in synaptic vesicle endocytosis and recycling may contribute with this type of disorder. Exoendocytic cycling of synaptic vesicles, which are organelles of 40 nm in diameter, is involved in neurotransmitter release. Hundreds of synaptic vesicles, filled with neurotransmitters are found in each presynaptic nerve terminal. When presynaptic plasma membranes depolarize, Ca2þ-channels open and calcium flows into the nerve terminal, triggering the exocytosis of synaptic vesicles and releasing their neurotransmitters into the synaptic cleft. Calcium binds to synaptotagmin, and after exocytosis, vesicles are re-endocytosed, recycled, and refilled with neurotransmitters. Recycling can occur by multiple parallel pathways, either by fast recycling via local reuse of vesicles, or by slower recycling through an intermediate endosomal [137]. Also, a critical step in presynaptic differentiation is the clustering of synaptic vesicles near neurotransmitter release sites, the active zone, where vesicle fusion and exocytosis of neurotransmitters occur. Synaptic vesicles at presynaptic terminals store neurotransmitters from presynaptic neurons such as gamma-aminobutyric acid (GABA) and glutamate [133].
Many presynaptic molecules are involved in the regulation of synaptic vesicle release, including CAMs. The family of adaptor protein (AP) complexes, AP-1, AP-2, AP-3 and AP-4 mediates various types of vesicle formation and selection of cargo molecules for inclusion in these vesicles. The synaptic vesicle process involves AP-2/clathrin-mediated endocytosis [133]. The structural composition of synapses may be altered by mutations or deletions in other scaffold proteins, such as those of the Shank family, neurexin and NLS. These changes may result in an altered number of receptors such as mGluR receptors or changes in the composition of NMDA and AMPA, and affect component signaling in PSD. Dysregulation in the synapse morphology induced by structural alterations and disturbed signaling might converge and lead to disrupted long-term potentiation (LTP) formation and plasticity, and a specific decrease in excitatory signaling by various genetic mutations, environmental factors, or immune system alterations, which would lead to an imbalance in inhibition and excitation as a likely cause of autism [26].
The main excitatory neurotransmitter in the brain, glutamate, modulates the neuronal formation and synaptic strength in the early phases of development due to its role in neuronal plasticity and cognitive functioning [88]. Glutamate receptors are diffused throughout the brain, in the cerebellum and hippocampus, regions implicated in ASD pathogenesis [25]. Genetic alterations in glutamate signaling have been found in association with ASD through candidate gene screening and genetic association studies and an imbalance in excitation and inhibition with glutamate signaling is proposed as a mechanism involved in ASD during the early development stages, between one and three years of age [112].
There are two types of glutamate receptors, metabotropic and ionotropic. Metabotropic glutamate receptors (mGluR) are G-protein coupled receptors involved in intracellular signal transduction and can be divided into three groups: Groups I (mGluR1 and mGluR5), II (mGluR2 and mGluR3) and III (mGluR4, mGluR6, mGluR7 and mGluR8). Group I receptors activate phospholipase C. Groups II and III are negatively linked to cyclic adenosine 3′,5′-monophosphate (AMP) production, but they differ in agonist selectivity. Two Group III receptors, mGluR7 and mGluR8, are located within the presynaptic grid, whereas mGluR3 and mGluR2 are located on the preterminal axons. Ionotropic glutamate receptors form ligand-gated ion channels (LGICs) and are labeled according to their prototypical agonists: NMDA, AMPA and kainate [25].
Some studies have focused on the endocytosis, docking, priming, fusion and recycling processes that may play a role in intellectual disability and ASD, but the functions of several vesicle components remain unidentified and more studies are needed to understand these processes [133].
The cytoskeleton forms the backbone of neuronal architecture and is essential for axon growth and synapse formation. The microtubule cytoskeleton has an active role during different phases of neuronal polarization; microtubules and their stability determine axon formation, they maintain the identity of axons and they regulate the dynamics of dendritic spines. Once the synapses have been formed, the neuronal cytoskeleton supports maturation and maintenance, and so the synaptic cytoskeleton is essential for the stabilization and remodeling of synaptic connections [40]. Actin filaments are the predominant component of the cytoskeleton in dendritic spines [20]. Changes in these key molecules mediating that bind to actin and members of the Rho family of small GTPases, such as RhoA, Rac and Cdc42 can disrupt this process [69]. These proteins play important roles in synaptic functions, dendritic branching, the formation and maintenance of dendritic spines and the growth and differentiation of neurites [133]. Their genes include
It is known that genetic alterations in the pathways controlling local protein synthesis in neurons contribute to diverse intellectual disabilities and ASD. A set of cytoskeletal proteins has been reported as mutated in these individuals. The resulting disorders are called synaptopathies with dysgenesis of dendritic spines being a recurrent anatomical feature. These include factors that regulate the dynamics of the actin cytoskeleton, such as GAPs and guanosine factors [12]. Mutations in the tumor suppressor genes,
New research has revealed many interactions associated with brain disorders, opening up new perspectives to define regulatory pathways shared by neurological disabilities characterized by dendritic spine dysmorphogenesis.
It has been seen that many synaptic proteins are critical to the formation and maintenance of proper synaptic function. The expression level of many of these proteins may be tightly controlled by the balance between translation and turnover. The growing number of developmental cognitive diseases, whose underlying cause is a defect in the regulation of either translation or turnover, suggests that the equilibrium between these opposing processes is a sensitive point in establishing normal cognition and behavior [36].
Ubiquitination, the covalent attachment of ubiquitin to a target protein, regulates most cellular processes and is involved in several neurological disorders. Many genes in the ubiquitin pathway and neuronal proteins that are targeted by the ubiquitin-proteasome system have been linked to cognitive deficits [57, 82].
Studies have highlighted an important role for protein degradation by the ubiquitin proteasome system (UPS) in synaptic plasticity [126, 91]. These observations suggest that changes in synaptic transmission involve extensive regulation of the synaptic proteome. The synaptic proteome is also affected by nonsense-mediated mRNA decay (NMD) that provides a quality control linked to translation. NMD has a role in degradation of aberrant mRNAs with a premature termination codon and the regulation of the transcriptome [109]. CNVs and mutations in several genes associated to NMD such as
UPS consists of a group of enzymes, an ubiquitin activating enzyme (E1), an ubiquitin conjugating enzyme (E2) and an ubiquitin ligase (E3), which are associated with ubiquitin ligases and proteasomes to mediate protein degradation. The ubiquitinated target protein is subsequently shuttled to a protease complex known as the 26S proteasome and subjected to degradative proteolysis. They also play a role in the regulation of cell signaling and cell cycle progression, and are associated with cytoskeletal elements. Thus, posttranslational ubiquitination modifies protein function and triggers the subsequent degradation of ubiquitinated proteins by the 26S proteasome. Several components of the UPS are required for proper brain development, axon guidance, and the development and plasticity of synapses. It has been shown that protein degradation via the UPS controls the appropriate synaptic balance, maintaining optimum levels of the protein, thereby promoting functional balance [23].
Several studies have shown a crucial role of UPS in neuronal transmission. For example, mutations in
As previously reported, CNVs are recognized as important genetic factors in ASD, with a high prevalence of
A few studies have investigated the transcriptome in ASD samples of postmortem brains and some of them used mRNA from peripheral blood of patients [1, 54, 71, 110]. More recently, disruption of miRNA expression has been repeatedly reported in microarray studies and it is believed to be linked to the pathogenesis of autism (Sarachana et al., 2010; [28, 55]. However, lymphoblastoid cells are not representative of neural tissue and very few miRNAs exhibit consistent deregulation between studies.
According to [93], miRNA loci are underrepresented in highly polymorphic and well-validated CNV regions. One study investigated the pathogenic role of miRNAs in autism by checking associations with
The
On the other hand, dysfunction of neuronal miRNAs can result in a number of neuropathological conditions. It has been reported that neural miRNAs and their target mRNAs are co-expressed, suggesting their participation in feedback mechanisms to connect the transcriptional activation with the control of local dendritic protein synthesis [145]. Interestingly, the functions attributed to miRNAs overlap with growth abnormalities, delays and the disruption of neuronal maturation observed in the brains of autistic individuals. Aberrations in the translational control of multiple mRNAs mediated by targets of each miRNA may lead to the difference in phenotypes observed in ASD. Moreover, multiple miRNAs may target the same mRNA leading to phenotypes resulting from the converging of several loci in CNVs. Thus, a change in expression or level of miRNA will affect the expression of target genes and might have a pleiotropic effect that would produce a more severe autistic phenotype. However, one can not underestimate the clinical relevance of the deregulation of a single or a subset of CNV-miRNAs. Based on this, it is clear that the characterization of this relationship may illustrate the complexity of the underlying neuronal development, function and dysfunction that will eventually help in the understanding and treatment of autism [150].
Chromatin is defined simply and collectively as genomic DNA associated to proteins within the nucleus. There is a vast assortment of chromatin factors dedicated to the DNA packaging and the enzymatic functions involved in changing chromatin states. Nucleosomes are the primary unit of chromatin organization with a histone core (H2A/B, H3, and H4) and linking subunit H1. They keep DNA condensed and regulated by only releasing genes into the open conformation when their accessibility is needed [81]. Interestingly, disruptions in chromatin regulator genes are frequently the cause of neurodevelopmental and neuropsychiatric disorders. Chromatin regulators are widely expressed in the brain, yet symptoms suggest that specific circuits are altered when they mutate [143]
Chromatin regulator genes are also altered by
Methylation of the genome in certain areas appears to remodel chromatin and consequently the genes that are in this region. The regulation of each histone modification requires specific enzymes that add or remove the methyl or acetyl group. Several mutated genes associated to ASD encode histone demethylases, including
Epigenetic is a term used to refer to features of organisms, such as DNA and chromatin modifications, that do not involve changes in DNA sequence. The effects of environment on the phenotype are generally mediated through epigenetic mechanisms. These mechanisms, such as DNA methylation, can become programmed (e.g. imprinted). Genomic imprinting is a unique phenomenon wherein genes are expressed in a monoallelic way, and the choice of which allele is expressed is determined by the parental origin of the allele. Disruptions of the epigenome are called epimutations. Some of these appear to be corrected by normal germline-specific epigenetic reprogramming and are therefore not transmitted transgenerationally, but others are not corrected and are transmitted over multiple subsequent generations [97].
Epigenetic mechanisms act on chromatin accessibility to transcriptional regulation. Then, they regulate DNA structure and gene expression that can be influenced by exposure to environmental factors. The most studied are the methylation of genes and modification of histones. Interestingly, epigenetic abnormalities are associated with several neurodevelopmental diseases. The connection between ASD and epigenetic comes from the identification of genetic mutations in imprinted regions and genes that control epigenetic processes. As cited before, among the most common chromosomal alterations in ASD are duplications of the imprinted region 15q11–13, which is maternally inheritable [96].
There are several possible explanations for the involvement of imprinted genes in autism. The imprinted brain theory of autism suggests that autism is a disorder of the extreme imprinted brain and would be caused by imbalances that involve increased effects of the ‘paternal brain’ relative to the ‘maternal brain’. Imprinting has been hypothesized to explain the gender difference through the proposed action of unknown paternally imprinted loci on the X chromosome. Also, as mentioned, autism has been strongly associated with chromosomal abnormalities in the imprinted region of chromosome 15q. This includes the Angelman and Prader-Willi syndromes, as well the 15q duplication syndrome, which occurs in up to 5% of individuals with ASD. Imprinted genes may also contribute to autism indirectly as targets of other genes such a regulatory connection between
The imprinted genes are expressed in several types of tissues but are highly expressed in the brain. Human neurons require extensive methyl modifications throughout development and postnatal life. Several important posttranslational modifications of histone core subunits within nucleosomes involve methylation, an epigenetic mechanism. Recent unbiased genome-wide analyses have turned up a multitude of novel candidate genes that encode nuclear factors implicated in chromatin remodeling, histone demethylation, histone variants, and the recognition of DNA methylation. Both histone and DNA methylation patterns are highly dynamic processes in the early development phase that correlate with dynamic changes in cell lineage and differentiation events. Interestingly, mutations in autism have been found in several genes encoding proteins involved in demethylase reactions, that is, reactions that remove methyl groups from histones or DNA [81].
The mechanism of action of the
[75] reported that mothers of autistic children show significantly lower levels of methylfolate and methionine, two essential precursors for methylation in DNA compared to a control group, but methylation-inhibiting protein levels and S-adenosylmethionine (SAM), adenosine, and homocysteine were elevated. SAM has a role in the DNA methyltransferase reaction, which produces S-adenosylhomocysteine (SAH) and methylated DNA. The SAM/SAH ratio is considered to be an indicator of DNA methylation potential.
Additionally, oxidative stress in brain cells caused by environmental and genetic factors leads to decreased activity of the methionine synthase enzyme which participates in DNA methylation processes. When the activity of this enzyme is impaired, affected individuals can exhibit attention deficits and other signs, including autistic behavior symptoms due to defects in the expression of genes controlled by this epigenetic mechanism [42, 104]. Therefore, environmental factors may also activate intracellular pathways during embryonic development, causing epigenetic changes in neural function that would explain the relationship between environmental signals and the genome in the regulation of individual differences in behavior [166].
A study in Sweden with 208 autistic children showed an association between advanced paternal age and an increasing risk for ASD in offspring. Autistic-like traits in the normal population are associated to both young and advancing paternal age and the autistic similarity in twins seems to increase with advancing paternal age. Exposure to toxic agents during life,
Thus, epigenetic alterations may be the biological targets through which environmental factors can cause autism. Imprinted genes may be associated with autism because they are involved in brain development and also because they may be more vulnerable to genetic or epigenetic mutations. Some features of ASD are highly consistent with epigenetic dysregulation such as the discordance between monozygotic twins, parental origin and the gender-dependent effects of some alterations. The cause of autism is not just by congenital genetic defects but can also be caused by environmental factors via epigenetic factors, with epigenetic modifications being affected by environmental factors including fetal exposure to drugs.
Although the involvement of genetic alterations in ASD is clearly accepted, new studies point to a similar or even greater contribution by environmental factors, particularly environmental toxicants. Toxic chemicals cause dysregulation of the developing human brain by interacting with the genome or through direct toxicity.
The developing human brain is exceptionally sensitive to injury caused by toxic chemical exposure with several developmental processes being highly vulnerable. The dissemination of chemical industrial agents in the environment is important contributor to the call “global silent pandemic of neurodevelopmental toxicity” [63]. An estimative by U.S. National Academy of Sciences (NAS) shows that 3% of all neurobehavioral disorders including ASD, attention-deficit hyperactivity disorder and dyslexia are caused directly by exposure to environmental toxics and that another 25% are caused by interactions between environmental factors and inherited susceptibility [103].
About 80,000 new synthetic chemicals have been developed in the past 50 years, but only about 20% was screened for potential toxicity in early neurodevelopment. The human fetus is susceptible and not well protected against industrial chemicals, because the placenta does not block the passage of all toxicants from the maternal to fetal circulation. The individual’s brain is unique and individual variability in genetic susceptibility can influence responses to environmental toxicants [62, 79, 106].
Exposure to many environmental toxicants has been correlated to autism including pesticides, polychlorinated biphenyls, solvents, toluene, toxic waste, and heavy metals such as mercury, lead and arsenic, besides exposure to automotive air pollution [115, 132, 152]. On the other hand, there was a false indicative association between these disorders and vaccines such as the measles, mumps, rubella vaccine and thimerosal-containing vaccines against diphtheria, tetanus and pertussis vaccine. One meta-analysis, combining the results of five previous studies involving 1,256,407 children with five case-controlled studies with a further 9,920 children show that there was no relationship between vaccination and autism [144].
There is thus strong evidence that the relation between environmental and genetic factors may converge to neurotoxic mechanisms that could lead to behavior disorders. But what kind of biological mechanisms would be involved in the causation of autism due to toxic agents? Epigenetic mechanisms are known to affect the subsequent gene expression in the brain as has already been described in this chapter. Toxics can lead to a modification in epigenetic gene expression, resulting in methylation, histone modification or changes in non-protein-coding RNA [60]. However, possible individual susceptibilities to toxicants implicated in ASD, including altered detoxification, genetic factors, oxidative stress, altered neuronal development, epigenetic mechanisms, synaptic function, hormonal factors, etc., may amplify the effects of toxicants during the prenatal and early postnatal periods [123]. The susceptibility to effects of environmental toxicants needs more attention and studies.
ASD also can be characterized by some physiological abnormalities, such as oxidative stress and immune dysregulation/inflammation. Many of the behavioral and cognitive features of ASD appear to arise from dysfunctions of the brain but studies have documented physiological abnormalities in organs other than the brain [122].
Many studies have reported genetic variations in glutathione-related pathways associated with autism, such as lower concentrations of reduced glutathione (GSH), higher levels of oxidized glutathione (GSSG) and a decrease in the GSH/GSSG redox ratio, along with a lower mitochondrial GSH reserve in individuals with ASD compared to controls [19, 2952, 65, 75 ,121]. Moreover, ASD severity has been correlated with lower GSH levels and markers of increased oxidative stress [2, 56, 123]. Oxidative stress studied in postmortem brain samples from individuals with ASD demonstrated low levels of GSH, the major cellular antioxidant, oxidative damage to proteins, lipids and deoxyribonucleic acid (DNA) as well as alterations in the activity of enzymes important for redox metabolism [123, 142].
Adaptive responses to oxidative stress were shown by [102], when significantly lower methionine synthase mRNA levels and lower homocysteine and cystathionine concentrations were observed in the frontal cortex of the brains of ten individuals with autism compared to ten controls.
Also it is possible that the reduced transportation of folate into the brain as a consequence of the folate receptor alpha autoantibody or mitochondrial dysfunction could reduce the methylation process and glutathione metabolism. Many findings reported for the brain (oxidative damage to lipids, protein and DNA, glutathione abnormalities and reduced function of enzymes essential in oxidative stress regulation) have been found in the blood, immune cells and cell lines from individuals with ASD, raising the question of whether these findings are specific to the brain or whether they represent a more general process [53, 123].
Dysfunctional immune activity, both innate and adaptive, can impact neurodevelopment, cognitive function and behavior, suggesting a profound effect on neurodevelopment. Some studies in individuals with ASD have reported evidence of immune dysregulation and inflammation related to ASD, including disruption of genes of the immune system with elevations of tumor necrosis factor-alpha (TNF-α) in lymphocytes and amniotic fluid, alterations of immune proteins, and increased levels of cytokines, expression in genes related to immunity and microglial cell activation in brain tissue [113]. The expression of inflammatory genes in brain tissue was studied by [163], who reported that nuclear factor-kappa β expression in the orbitofrontal cortex was increased in individuals with autism compared to controls.
Microglias, a type of glial cell, are the resident macrophages of the brain and spinal cord. They therefore act as the first and main line of active immune defense of the CNS and participate in immune surveillance of the CNS and synaptic pruning in normal neurodevelopment. They are activated to eliminate some agents and damaged cells via phagocytosis, but, they may increase inflammation if chronically activated by releasing proinflammatory cytokines and free radicals [41]. Changes in microglial morphology and gene expression are seen in many psychiatric disorders and neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, Multiple Sclerosis and autism. [100] and [165] reported that microglias in the dorsolateral prefrontal cortex were frequently located closer to neurons in ASD individuals compared to controls. Another study with autism showed microglial activation in the cerebellum, brainstem, corpus callosum, fusiform gyri, superior temporal gyri, anterior cingulate, orbitofrontal, and parietal lobes [139].
Proteomic analysis indicates that the levels of many immune proteins in plasma, such as cytokines, chemokines, complement proteins, adhesion molecules and growth factors are altered in ASD [113]. Increases in plasma levels of pro-inflammatory cytokines [interleukin (IL)-1β, IL-6, IL-8 and IL-12p40] as well as macrophage migration inhibitory factor (MIF) and platelet-derived growth factor (PDGF), have been reported in ASD [11, 64].
Alterations in immune mediators can occur at an early stage of development and might alter NMDA and NMD receptor-mediated excitatory synaptic transmission and plasticity, which is relevant to ASD (Escobar et al., 2011). These immune mediators may be related in LTP which is involved in synaptic plasticity in learning and memory processes. IL-1 influences many molecular components of LTP, such as NMDA and AMPA receptor signaling and glutamate release. IL-6 is involved in the generation of LTP and an increase in IL-6 leads to a reduction of insulin-like growth factor (IGF)-binding protein 3 and IGF1 [43, 117]. Furthermore, other cytokines, such as IL-18, IL-1b, and TNF-α, act on AMPA and NMDA receptors in different ways [25].
Increases of pro-inflammatory cytokines (including TNF-α, IL-6 and granulocyte-macrophage colony-stimulating factor), a T helper cell type 1 cytokine (interferon gamma) and a chemokine (IL-8) were reported in postmortem frontal cortex brain samples of autistic individuals, but no significant differences in T helper cell type 2 cytokines were identified (IL-4, IL-5, and IL-10) [86]. The cytokines IL-2 and IL-4 have been shown to influence repetitive and cognitive behaviors. Mice treated with IL-2 showed an increased “climbing behavior” that is thought to denote repetitive behavior, a pattern of behavior that is characteristic of ASD.
There is evidence suggesting a role of immune dysfunction in ASD symptoms, but further investigations should be carried out to clarify these findings because it is still unknown whether these changes are a primary cause or a secondary consequence of neuronal deficits.
Gastrointestinal (GI) disorders are a comorbidity of autism and interestingly have a strong correlation with disease severity [7, 16]. Thus, a growing number of papers point to the importance of the so-called "brain-gut axis", revealing the central role of the intestinal microbiota (the new name of "microflora") in postnatal development and maturation of the immune and endocrine systems for control signaling in the CNS, brain function, and behavior [51; 158].
Individuals with ASD often suffer from GI illnesses, e.g., diarrhea, constipation, bloating, and gastroesophageal reflux [22, 3]. The composition of the microbiota is influenced primarily by genetic factors, age and diet [80, 168], although the interactions between these are multifactorial and not well defined yet [21].
Thus, several studies have been conducted in an attempt to profile the microbiota in ASD compared with healthy siblings and controls [4, 51, 59]. While some authors have reported little or no differences in the composition of the intestinal flora between children with ASD and their unaffected siblings, the imbalance in the intestinal microbial composition in samples of ASD has been identified, especially when compared to controls [49, 50].
Analyses of the feces of patients with ASD have revealed that the microbiome of ASD is significantly different to controls and consists in over 1,000 different species compared to unaffected children. Of the phyla, patients with autism have underrepresented
Interestingly, non-autistic siblings often presented intermediate microbiota profiles between ASD and controls [49, 155], possibly due to genetic factors, but also as a reflection of shared environmental conditions. These studies are complicated by the fact that autistic individuals often receive medications such as antibiotics and are often on special diets or have repetitive eating habits, both of which can alter the composition of the microbiota [89].
Interestingly, although
Few studies have considered a deregulated metabolism of fecal levels free of amino acids in autism. Certain amino acids, in particular glutamic acid (Glu), act as neurotransmitters in the center of the CNS. An excess of Glu leads to neuronal cell death and plays an important role in the pathophysiology of several neuropsychiatric disorders [127]. High levels of Glu were found in fecal samples of autistic children [37]. As it has a role in brain development, the findings support the hypothesis that glutamatergic neurotransmission is involved in ASD [130].
The microbiota might also be involved in the etiology of the disease via interactions with the immune system. Some of the possible mechanisms described above are likely to involve changes in the global balance of the entire microbial community, while others may be exercised by certain bacteria. More studies are needed to clarify whether the gut microbiota in fact plays a role in ASD. These include prospective studies to address the issue of cause and consequence, and intervention studies aimed at modulating the microbiota with probiotics or dietary interventions. The right profile, the categorization of patients and control groups, with the application of molecular techniques to verify the profile of fecal microbiota and urinary metabolome will corroborate the underlying relationship between gut microbes and the host [34].
Some authors believe that the action of microbiota may have much wider effects on the physiology of the host than originally thought, and emerging evidence shows that it may include modulation of brain activity and behavior. Differences in the composition of the microbiota between individuals with ASD and healthy controls were identified in several studies, both based on bacterial cultures and on molecular methods [18]. However, changes in bacterial diversity that were reported in one study [51] were not confirmed by another [158]. The direct comparison between studies is complicated because different methodologies are employed and study groups may not be directly comparable due to the heterogeneous nature of ASD [89]. However, if the differences in gut microbiota between autistic children and controls are one of the causes of the disorder or the result, could have implications on the diagnosis, treatment and prevention [37].
Nevertheless, despite the substantial amount of data, it is not possible to clarify whether the results represent the presence of a causative agent, or reflect a consequence of treatment, or whether they are nothing more than confounders. This has to be considered and caution is needed before recommending "miracle diets" to the child and family that may only increase the anxiety in respect to symptom improvement.
It is well known that ASD affects more males at a ratio of 4 boys:1 girl. Some studies suggest that gender differences in phenotypic presentation, including less severe manifestations of restricted and repetitive behaviors in girls, seem to affect this ratio. Genetic studies show that girls seem to be more "protected" from the effects of inherited and
Despite the fact that ASD is more prevalent in boys
Although neurodevelopmental systems evolved to be robust, they can be vulnerable to disturbances in a specific subset of genes called phenotypic capacitors [85]. Phenotypic capacitors are genes that act against disturbances and thus contribute to the robustness of the phenotype. Thus, phenotypic capacitors, when operating normally, can prevent the development of diseases such as ASD, even in patients exposed to genetic and environmental risks. This means that girls are less likely to develop ASD, but when they have, they tend to have a more severe phenotype [138].
There seems to be unknown factors that "protect" females from ASD [157]. Recent genome studies showed that, on average, women with ASD have more mutations than men, including single nucleotide variants (SNVs) and CNVs [74, 84, 105]. Furthermore,
Moreover, not all genes in the inactive X chromosome are inactivated, and the genes that escape X inactivation in females are revealing some interesting insights into gender differences related to chromatin.
Recently, gender-specific gene expression obtained from the transcriptome of normal human brain development using a bioinformatics approach suggested that male-biased genes are enriched for the processes of extracellular matrix formation/glycoproteins, immune response, chromatin, and cell cytoskeleton. These pathways have been repeatedly implicated in autism and demonstrate that autism candidate genes are also enriched for these pathways. Furthermore, the development of the male brain may be naturally more susceptible to environmental factors as its normal development is more strictly dependent on the immune system [167].
A gender-dependent difference in the incidence of neural tube defects has been described. It was speculated that these defects are due to a synergistic effect between the gene expression of
On the other hand, altered behaviors in ASD are often related to a “more masculine” pattern of behavior linked to testosterone. However, although current levels of steroid hormones appear to be altered in patients with autism, the data indicate that prenatal testosterone by itself does not seem to be sufficient for the disorder to develop [125].
Differences between individuals with an atypical karyotype (monosomy X or Y or X-polysomy) and those with a typical karyotype are often interpreted as being significant for the difference in susceptibility between genders. However, it is likely that many of the differences arise because of hyperexpression or hypoexpression of genes in pseudo autosomal regions that escape X inactivation, thereby being similarly expressed in men and women with a typical karyotype. The addition or loss of an X or Y chromosome, which leads to altered protein levels that are atypical or typical for both men and women, cannot explain the gender difference in ASD. However, some genes on the X chromosome are not in these regions and have no corresponding functional alleles on the Y chromosome, and escape X inactivation in some circumstances [125].
Moreover, the
Another factor that may contribute to the skewed gender ratio in ASD is parental age. Increased parental age is known to increase the risk of a child with ASD [45] and there are some indications that parental age affects the gender ratio of children diagnosed with ASD [125]. The male-female ratio dropped from 6.2:1 in under 30-year-old parents to 1.2:1 in parents older than 44 years old [8]. This finding may be related to the higher frequency of
Thus, considering all that has been studied about ASD, it is difficult to conduct a comprehensive analysis about the etiologic complexity, without running the risk of over or under estimating some factors. On consulting the available literature on ASD, there is an impression that all can cause autism. The truth is that everything that affects the CNS system can interfere with mental health and this opens up a universe of possibilities. The gene expression, immune susceptibility and environmental stressors, even those that affect men more than women, need to be organized using a multidisciplinary approach in order to explain what actually happens in normal CNS development within the first three years of life. From there, the goal is to have a method of comprehensively analyzing each particular case to try to obtain specific treatment. While this is not available, it is interesting to investigate the most common risk factors and give support to the patients and families in order to improve their quality of life.
This study was supported by grant nº2013/14919-6, São Paulo Research Foundation (FAPESP) and Faculdade de Medicina de São José do Rio Preto (BAP-FAMERP)
In the past few years, electric propulsion has received widespread attention as an alternative to chemical propulsion for spacecraft. A chemical thruster is capable of producing high thrust, but it provides a relatively low specific impulse. This limitation of chemical thrusters opens up discussion of the use of electric thrusters, which provide much higher specific impulses. A high specific impulse allows the spacecraft to reach the same speed with lower propellant consumption than chemical ones or travel faster with the same propellant mass [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]. In addition, the use of a high specific impulse, electric thruster permits a significant reduction in propellant mass on spacecraft, which helps reduce launching cost, extending mission lifetime or increase the payload mass on the spacecraft [2]. Therefore, the benefits that electric thrusters provide make them the best choice for in-space propulsion of spacecraft.
To date, several different types of electric propulsion thrusters have been developed, of which Hall thrusters are the most reliable and widely used. Hall thrusters are simple in design, consisting of an annular discharge channel, an anode, a cathode and a radial magnetic field across the channel [1]. A propellant, usually Xenon, is injected to channel through the hollow anode and a high potential difference is applied between the anode and cathode. The electrons emitted from the cathode and start moving towards the anode due to the potential difference. As they enter the discharge channel, they get trapped in the radial magnetic field generated by electromagnetic coils (or permanent magnets) and start drifting in the azimuthal direction (E x B). Due to this trapping, the residence time of electrons in the discharge channel increases and they move very slowly towards the anode. Electrons, then collide with neutral propellant atoms entering the discharge channel and ionize them. Then, these generated ions are accelerated to high velocity towards the thruster exhaust by the electric field to generate thrust. On the thruster exterior, the ion beam is neutralized by electrons from the virtual cathode so that no charge builds up on the spacecraft’s surface [2]. More details on Hall thruster operation and fundamentals can be found in [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13].
Hall thrusters offer several benefits like simple design, high thrust-to-power ratio, high efficiency, improved performance, etc., which give them a clear advantage over other electric thrusters. For an input power range of 0.1 kW–20 kW, they can produce a few mN to 1 N of thrust and offers a specific impulse in the range of 1000s–3000s with more than 50% efficiency [14]. Hall thrusters can also adjust their thrust level and specific impulse by varying the discharge voltage and propellant mass flow rate, which makes them suitable for applications such as precision maneuvering, attitude control, station keeping and orbital raising [15]. In addition, plasma in a Hall thruster remains quasi-neutral, which eliminates the issue of space charge, allowing the Hall thruster to achieve higher thrust densities. Because of all these characteristics, the space community has shown great interest in Hall thrusters and they have been used successfully on many spacecraft for space missions and maneuvers.
Thrust is caused by a change in a substance’s momentum as a result of a chemical reaction or an electrical principle. The thrust indicates how much force, in newtons (N), the propulsion system exert on the vehicle. Let us denote
The performance of thrusters is usually determined by thrust
Tsiolkovsky rocket Eq. (1) can be read as
The above Rocket equation defines the change in velocity of a spacecraft. It is clear that a higher
We can now say that Isp plays a key role in the design of a space mission propulsion system.
This description of the Hall thruster is shown in Figure 1. The anode and cathode set up an axial electric field and magnetic coils create a radial magnetic field. First cathode starts producing a stream of electrons and these electrons are attracted by positive anode. When electrons are moving to anode, then at the channel exit they face of perpendicular electric and magnetic fields, these fields are more strong at channel exit. Due to these perpendicular fields, electrons trapped in an ExB drift and formed Hall current [1]. At this time Xenon gas is released from the anode, when neutral atom of gas reached at the channel exit, then electron collides with neutral atoms and ionized them. These ions are accelerated out of channel by electric field at the channel exit and this motion of ions imparts a reaction force on the thruster in reverse direction. The cathode is also used to neutral the ions charge so it produce a stream of electron to neutral the ions [1, 2, 3, 4, 5, 6, 7, 8, 9, 10].
Schematic diagram of a typical Hall plasma thruster.
The wall material of this type of thruster is dielectric like borosil (BN-SiO2), boron nitride (BN) and alumina. This type of material has low secondary electron emission coefficient with Xenon ion interaction. Most of SPT use Xenon as a propellant because of its higher mass (131.3 amu), lower first ionization potential, less toxicity, ionization cross section of (∼2.3 10−6 cm2) and of its desirable thermodynamics properties [1, 10].
These types of thruster has metallic conducting walls and has narrow acceleration zone associated with the narrow electric field region near the anode. The ratio of channel width and channel depth in these thruster is 2:1. The conducting channel wall is negatively biased and it is a part of magnetic circuit so it prevent electron to move in direction of wall and repel them to ionization region and reduce electron power losses [1, 2, 3, 4, 5, 6, 7, 8, 9, 10].
The main components of a Hall thruster are body, magnetic coils, discharge channel, anode and cathode. The body of the Hall thruster provides better shape of external magnetic field, so it is normally made up of iron (steel). In this thruster a single thick disk shape annular discharge channel exist on the front face. To create better shape of magnetic field two type of magnetic coils are situated in the thruster channel. The inner coil is made of single reel and located radially inward in the channel and the outer coil is made of multiple reels and located radially outward in the channel. The magnetic coils and iron body made a magnetic circuit. The magnetic iron body of the thruster is separated from thruster discharge channel by walls and the material of these walls is metal or ceramic. The material of the anode is normally stainless steel, which avoids magnetic interaction and supply hardiness [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]. To set up an axial electric field in discharge channel of thruster a cathode is required and this cathode is normally hollow cathode with lanthanum hexaboride or barium oxide. The cathode completes the discharge circuit and work like an electron source. This description of the Hall thruster provides knowledge about the structure of thruster.
As discussed earlier, there is an azimuthal electron drift in a Hall thruster channel, which is normal to both the applied electric field and generates a Hall current [1, 10]. Because of the collisions of the electrons with neutrals, electrons, ions and potential fluctuations in the plasma, generate the axial electron current density. The azimuthal E X B drift is given by
The Hall current may be approximated by integrating the magnitude of
Here,
The ratio of electric and magnetic field is such that the ion’s gyro radius is much larger than electron’s gyro radius, so that ions are not magnetized inside the channel. The channel length is calculated by determining the Larmor radius of both the plasma species [10]. The motion of the moving charged particle under the electromagnetic fields defined as follows
This gives the radius of gyration
Here,
This implies to
These above equations gives the larmor radius in terms of the applied potential
The magnitudes of the fields are such that
Despite many successful applications of Hall thrusters, some aspects of their operation are still poorly understood. One notable problem is the anomalous electron mobility [16, 17] and plasma sheath, which is far above the classical collisional values. It has been established that the inhomogeneous plasma under the electromagnetic fields is not in the thermodynamically equilibrium state [17, 18, 19, 20]. The equilibrium E × B electron drift, ion flow rate, plasma and magnetic field gradients are all sources of plasma instabilities in Hall plasmas. Hall plasmas devices with ExB electron drift demonstrate wide range of turbulent fluctuations. These fluctuations are probably the reason of the observed anomaly in the electron transport across the magnetic field [21, 22, 23] and other nonlinear phenomena (coherent rotating spoke) [24, 25, 26]. Understanding of the mechanisms of the coherent structures and anomalous transport requires the detailed study of linear instabilities in Hall plasma devices. These instabilities are also considered to be a principal source of anomalous transport in toroidal magnetic confinement devices [2].
If free energy is available in the system and even though system is in equilibrium in the sense that all the forces are in balance, then these oscillations can grow at the cost of free energy and hence instabilities can take place. There are different types of instabilities that depend on different conditions. For proper description of a particular instability, one should be able to define the mode of the growing wave, the nature of the growth and the source of the free energy. Instabilities are mainly classified into four groups, namely streaming instabilities, Rayleigh–Taylor instabilities, universal instabilities and kinetic instabilities.
When there is any kind of perturbation, the free energy available excites the waves and the plasma waves no longer remains in thermal equilibrium. Even though there exist an equilibrium because all the forces are balanced and there is no net force and it is possible to find a time independent solution to the wave. Perturbation makes the plasma waves unstable, which is always a motion that brings the plasma closer to true thermodynamic equilibrium by decreasing the free energy. Instabilities may be classified according to the type of free energy available to drive them. Few of them has been explained below.
This type of instability occurs, when either a current or a beam of energetic particles is driven through plasma so that the different species of particles have drifts relative to one another. This drift energy attempt to excite waves and oscillation. This energy is acquired at the loss of the drift energy, which is in the unperturbed state.
In this kind of instability, the plasma has a sharp boundary or a density gradient, so that it does not remain uniform. In addition to this, an external, non-electromagnetic force is applied into the plasma. This force is responsible for driving the instability in plasma. This analogy can be realized in an inverted glass of water. Though the plane interface between the air and the water is in the state of equilibrium, where the air pressure support the weight of the water. Any ripple arising in the surface of water tend to grow at the loss of potential energy in the influence of gravitational field. Whenever a light fluid supports a heavy fluid this things happen, which is quite known in the field of hydrodynamics [1].
A plasma is hardly present in perfect thermodynamic equilibrium, when it is confined by gravitational field or an electric field (driving forces). The plasma is expanded by plasma pressure and an instability is driven by the expansion energy. Any finite plasma always contains this type of free energy and the waves, which comes out as a result are called universal instabilities.
Generally, the velocity distributions are assumed to be Maxwell-Boltzmann in fluid theory. If there is a case, where distributions are not Maxwell-Boltzmann, then there may be a departure from thermodynamic equilibrium and this anisotropy of the velocity distribution drive the kinetic instabilities.
These kind of instabilities occur, when the plasma particles streams with their relative drift, which may be driven due to the travel of charge particle beam or internal driven current. For example, the two stream instability is due to the relative drift of ion and electron streams.
These instabilities have been investigated in various positions of the acceleration channel of the thruster. The effect of radial magnetic field, thermal motions of plasma particles and electron collisions can induce time varying fields in the discharge oscillations. This can prompt an electromagnetic resistive instability in the Hall thruster. In this chapter, we derive the dispersion relation for the electromagnetic instabilities in a Hall thruster and conditions for the instability.
There are numerous types of oscillation found in thrusters which propagates in azimuthally and axially direction ranging from a few kHz to tens of MHz [1, 10]. These oscillations may reduce the specific impulse and the efficiency of a Hall thruster. These disturbances can also limit the operating life of a Hall thruster and therefore, suppression of this oscillation has become an essential task for Hall thrusters. These fluctuations are responsible for electron transport across magnetic field lines, performance and ionization of propellant [27, 28, 29, 30]. The magnitude of these oscillations strongly depend on the magnetic field, location of the cathodes, the discharge voltage and the mass flow rate.
Low frequency oscillation, frequently referred to as the breathing mode, is intimately tied to the details of propellant ionization and eventual ion acceleration and manifests itself as a strong 10–30 kHz oscillation in the thruster discharge current. Breathing mode models suggest the presence of a propagating ionization front traversing the channel of the thrusters [31]. Benítez and Ahedo investigated the axial-azimuthal instabilities in the global discharge region of a Hall-thruster to identify dominant mode (develops in the near plume at 1–5 MHz) and subdominant mode (develops near the anode100–300 kHz) [32]. Lafleur
At small amplitudes, the oscillations can be considered a part of normal operation with no significant effect on operation. At large amplitudes, the oscillations can severely and adversely affect operation. The details of these oscillation are given in Table 1.
Type | Description | Ranges of frequencies |
---|---|---|
Spoke type | Spoke type oscillations are propagating in the azimuthal direction at low discharge voltages [47, 48]. | 15–35 kHz |
Breathing mode | Discharge-current low-frequency oscillations [49] | Range of 10–100 kHz |
Contour oscillations | These are longitudinal oscillations connected with an instability in the location of the ionization region and can have very large amplitude [50, 51, 52, 53]. Contour oscillations depend on the parameters of the discharge power supply circuit. | 1–30 kHz (correspond to the transit time for a neutral propellant atom) |
Ionization oscillations | These oscillations are caused from the ionization front propagating irregularly around the circumference of the discharge channel [47, 52]. | 10–100 kHz. |
Flight oscillations | These oscillations are also called ionization flight oscillations, because they are determined by the change of ionization rate due to the delay of particle appearance, from one region to another. The analysis is based on the concept that plasma particles are delayed in being transferred from one region to other [54]. | 100 kHz up to 10 MHz (correspond with the transit time for an ion) |
High frequency oscillations | The amplitude of these oscillations is smaller and these are azimuthal waves generated near the exit part of the thruster [55]. | 1–100 MHz |
Super high frequency oscillations | These oscillations are connected with the development of electron layers in the plasma and the formation of flows of fast overheated electrons and have the smallest amplitude [55]. | Few GHz |
Types and frequency range of oscillations in Hall thrusters.
Lakhin
Magnetic field is an important parameter, which affect the performance and operation of Hall thruster. The erosion on the channel walls and on the electrodes can be minimized by accelerated beam of ions to a narrower beam width and by use of appropriate profile of magnetic field. The radial magnetic field causes the erosions of the walls, so new topology of magnetic field ‘lens’ is proposed by Morozov [69]. By using magnetic shielding technique, the discharge chamber erosion rate can be reduced by orders of magnitude [70]. Morozov and Lebedev proposed a magnetic field lens to focus the plasma beam [71]. Morozov et al. have designed a lens-type magnetic field with a zero magnetic point to make the plume divergence half angle only 10° in SPT-ATON Hall thruster [72]. Hofer et al. showed that the performance of the Hall thruster can be enhanced by reducing the divergence of the plume that could damage the solar panels and other parts of the satellite [73]. Hofer et al. used magnetic field to control the unmagnetized ion beam that formed in Hall thruster. By controlling ion beam the wall erosion was reduced to 2–3 order by ion bombardment [74]. Huang et al. studied the effect of background pressure on performance and plume of NASA’s High Voltage Hall Accelerator Hall thruster [75]. Their result shows that discharge current and thrust are increases with pressure and ion beam current, ion energy per charge, plum divergence decreases with increasing background pressure.
Liu et al. studied the effect of azimuthally electron drift on sheath profile and anomalous erosion in thrusters. Their results show that azimuthally electron drift induce sheath oscillations and it can produce an asymmetric sheath structure. To simulate the azimuthally erosion evolution, an erosion modal is used and it has been concluded that the azimuthally asymmetric ion sputtering is responsible for an asymmetric erosion profile [76]. Kim studied the ionization processes and ion dynamics in the accelerating channel to determine the stationary plasma thrusters performance levels [54]. Choueiri theoretically studied the difference between stationary plasma thruster and thruster with anode layer by measuring the temperature of secondary electron emission from the walls of thruster [77]. Hong et al. studied the effect of wall grooves on Hall thruster discharge to improve the performance of Hall thruster. If wall grooves are present in ionization region it increases near wall conductivity and decrease electron transient time, thrust and efficiency [78]. Ding et al. studied the discharge current and stability in graphite walls and BN-SiO2 walls for magnetic shielded and unshielded thruster. Their result shows that magnetic shielded thruster does not show change in stability and discharge current but 25% discharge current increases in unshielded thruster [79]. Experimental results and PIC simulation show that oblique channel’s specific impulse, anode efficiency, thrust, propellant utilization and ionization in plume region is improved 20% rather than the straight channel thruster [80]. Olano et al. studied the effect of magnetic field configuration on thruster performance and plasma discharge by proposing three types of configurations: (A) nominal, (B) orthogonal magnetic field and (C) high magnetic field [80, 81]. Garrigues et al. did PIC simulations and shows that in a Hall thruster electric discharge produce due to wall-plasma interaction and wall of thruster channel is reduced due to interaction with ions [82]. The electrostatic and magnetic probes are used to investigate the electromagnetic fluctuations and coherent magnetohydrodynamic azimuthal modes in thruster [68].
The resistive instability is driven by coupling to a dissipative process. Due to the collisions between the electrons and neutral particles, resistive instability can occur in the acceleration channel of the Hall thruster. This instability occurs due to the interaction of the wave with the electrons’ flow in the presence of electron collisions. The two major problems in plasma confinement are equilibrium and stability of plasma. The system in an equilibrium state if all the forces, which act on a system are balanced but stability and instability of the equilibrium can be assured by giving some perturbations to the equilibrium state. The stable and unstable state of equilibrium depend on small perturbation whether the perturbations are damped or amplified. For small perturbations, equilibrium is non- linear but stability can be linearized.
For the case of small amplitude perturbations and wavelengths much smaller than the scale lengths of inhomogeneities, the analysis of linearization can be applied. In the simplest approach, we consider the x
where
To linearize all the equations, let us write
The linearizations of the above eqation leads to
We take the variation of oscillating quantities in azimuthal direction as ∼
From Eq. (15)
The x-component of the perturbed current density
and the y-component of the perturbed current density
From the Maxwell’s equation, we have
or
Faraday’s law gives the relationship between changing electric and magnetic field as
For a plane electromagnetic wave
Where
or
From Maxwell’s equations, we get
which on expansion will give
Then permittivity tensor will be
In general
But for a pure dielectric medium
Then, the Maxwell’s equations are used in view of the perturbed electric and magnetic fields of the electromagnetic wave, and the plasma dielectric tensor
Finally, the wave equation
Where, the components of the dielectric tensor are obtained from Eq. (34) with the help of the Eqs. (24) and (25)
By substituting these components into Eq. (35) we get the following cumbersome analytical expression of the dispersion relation of electromagnetic waves propagating in magnetized plasma [40].
The values and ranges of some typical parameters are given in Table 2.
Property | Typical value | Property | Typical value |
---|---|---|---|
Inner diameter | Neutral velocity | ||
Outer diameter | Electron temperature | ||
Plasma density | Ion temperature | ||
Neutral density | Neutral temperature | ||
Ion velocity | Debye length | ||
Collision mean free path |
Typical values of parameters used in Hall thruster.
We solve the dispersion Eq. (40) to find out complex root by using typical values of the magnetic field, azimuthal wave number, collision frequency, electron drift velocity, ion drift velocity and electron temperature. Then the effect of these parameters on the growth
Figure 2 shows that the growth rate of the wave get enhanced for the larger values of the drift velocity of the electrons [64]. Since the drift velocity can be correlated with the discharge voltage, so it can be said that the growth rate is increased with the discharge voltage. Esipchuk and Tilinin [83] also reported the proportionality of the frequency of drift instability to the discharge voltage. The increase in the growth rate may be attributed to the strong coupling between the electric field and electron current [84].
The dependence of growth rate with electron drift velocity.
Figure 3 shows the variation of growth rate under the effect of collisional frequency. It is seen that the wave grows at a faster rate in the presence of more electron collisions. Since the stronger resistive coupling of the oscillations to the electrons’ closed drift requires the electron collisions, it is obvious that this instability grow faster in the presence of higher collision frequency. Similar results were also reported in the simulation studies of resistive instability by Fernandez
Variation of growth rate with collision frequency.
The dependence of growth rate on the magnetic field is shown in Figure 4, where it is observed that the wave grows faster in the presence of strong magnetic field. The growth rate of the wave gets suppressed under the larger drift of the ions as shown in the Figure 5. Since in the presence of their large drift, the ions try to diminish the transverse oscillations of the electrons in the x-direction.
Variation of growth rate with magnetic field.
Dependence of growth on ion drift velocity.
The different aspects of the Hall thrusters have been reviewed in this chapter along with future challenges related to the performance and efficiency. The different types of turbulence and oscillation with frequency ranges are also summarized. Hall thruster Plasma support electrostatic and electromagnetic waves under the influence of resistive effects. Therefore the waves (electrostatic and electromagnetic) propagating in azimuthal direction in a Hall thruster channel are found to be unstable due to the resistive coupling to the electrons’ closed drift in the presence of collisions. The theoretical model for the propagation of electromagnetic instability is derived in a Hall thrusters. The dispersion relation for the electromagnetic instability is derived analytically. The dispersion relation is solved numerically with the help of MATLAB to study the growing and propagating modes. The dominated modes are plotted to observe the behaviors of the instability.
The University Grants Commission (UGC), New Delhi, India is thankfully acknowledged for providing the startup Grant (No. F. 30-356/2017/BSR).
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\n\nThe significance of Peer Review cannot be overstated when it comes to defining, in our terms, what constitutes a published scientific work. Peer Review is widely considered to be the cornerstone of modern publishing processes and the key value-adding contribution to a scholarly manuscript that a publisher can make.
\n\nOther than the issue of originality, research misconduct is another major issue that all publishers have to address. IntechOpen’s Retraction & Correction Policy and various publication ethics guidelines identify both redundant publication and (self)plagiarism to fall within the definition of research misconduct, thus constituting grounds for rejection or the issue of a Retraction if the work has already been published.
\n\nIn order to facilitate the tracking of a manuscript’s publishing history and its development from its earliest draft to the manuscript submitted, we encourage Authors to disclose any instances of a manuscript’s prior publication, whether it be through a conference presentation, a newspaper article, a working paper publicly available in a repository or a blog post.
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\n\nSome basic information about the editorial treatment of different varieties of prior publication is laid out below:
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\n\nGiven that conference papers and presentations generally pass through some sort of peer or editorial review, we consider them to be published in the accepted scholarly sense, particularly if they are published as a part of conference proceedings.
\n\nAll submitted manuscripts originating from a previously published conference paper must contain at least 50% of new original content to be accepted for review and considered for publication.
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\n\nNewspaper and magazine articles usually do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense. Articles appearing in newspapers and magazines rarely possess the depth and structure characteristic of scholarly articles.
\n\nSubmitted manuscripts stemming from a previous newspaper or magazine article will be accepted for review and considered for publication. However, Authors are strongly advised to report any such publication in an accompanying note to the External Editor.
\n\nAs with the conference papers and presentations, Authors should obtain any necessary permissions from the newspaper or magazine that published the work, and indicate that they have done so in a note to the External Editor.
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\n\nWhite papers, working papers, technical reports and all other forms of papers which fall within the scope of the ‘Luxembourg definition’ of grey literature do not pass through any extensive peer or editorial review and we do not consider them to be published in the scholarly sense.
\n\nAlthough such papers are regularly made publicly available via personal websites and institutional repositories, their general purpose is to gather comments and feedback from Authors’ colleagues in order to further improve a manuscript intended for future publication.
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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. On September, 29th 2006 he has won a post PhD fellowship from the university of Bologna (from October 2006 to October 2008), at the competitive examination he was ranked first in the industrial engineering area. He extensively served as referee for several international journals. He is author/coauthor of more than 100 research papers. He has been involved in some projects supported by MURST and European Community. His research interests include pattern recognition, bioinformatics, and biometric systems (fingerprint classification and recognition, signature verification, face recognition).",institutionString:null,institution:null},{id:"496",title:"Dr.",name:"Carlos",middleName:null,surname:"Leon",slug:"carlos-leon",fullName:"Carlos Leon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Seville",country:{name:"Spain"}}},{id:"512",title:"Dr.",name:"Dayang",middleName:null,surname:"Jawawi",slug:"dayang-jawawi",fullName:"Dayang Jawawi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Technology Malaysia",country:{name:"Malaysia"}}},{id:"528",title:"Dr.",name:"Kresimir",middleName:null,surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/528/images/system/528.jpg",biography:"K. 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. His current research interests are in the fields of intelligent control and robotics.",institutionString:null,institution:{name:"Technical University of Sofia",country:{name:"Bulgaria"}}},{id:"585",title:"Prof.",name:"Munir",middleName:null,surname:"Merdan",slug:"munir-merdan",fullName:"Munir Merdan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/585/images/system/585.jpg",biography:"Munir Merdan received the M.Sc. degree in mechanical engineering from the Technical University of Sarajevo, Bosnia and Herzegovina, in 2001, and the Ph.D. degree in electrical engineering from the Vienna University of Technology, Vienna, Austria, in 2009.Since 2005, he has been at the Automation and Control Institute, Vienna University of Technology, where he is currently a Senior Researcher. His research interests include the application of agent technology for achieving agile control in the manufacturing environment.",institutionString:null,institution:null},{id:"605",title:"Prof",name:"Dil",middleName:null,surname:"Hussain",slug:"dil-hussain",fullName:"Dil Hussain",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/605/images/system/605.jpg",biography:"Dr. Dil Muhammad Akbar Hussain is a professor of Electronics Engineering & Computer Science at the Department of Energy Technology, Aalborg University Denmark. Professor Akbar has a Master degree in Digital Electronics from Govt. College University, Lahore Pakistan and a P-hD degree in Control Engineering from the School of Engineering and Applied Sciences, University of Sussex United Kingdom. Aalborg University has Two Satellite Campuses, one in Copenhagen (Aalborg University Copenhagen) and the other in Esbjerg (Aalborg University Esbjerg).\n· He is a member of prestigious IEEE (Institute of Electrical and Electronics Engineers), and IAENG (International Association of Engineers) organizations. \n· He is the chief Editor of the Journal of Software Engineering.\n· He is the member of the Editorial Board of International Journal of Computer Science and Software Technology (IJCSST) and International Journal of Computer Engineering and Information Technology. \n· He is also the Editor of Communication in Computer and Information Science CCIS-20 by Springer.\n· Reviewer For Many Conferences\nHe is the lead person in making collaboration agreements between Aalborg University and many universities of Pakistan, for which the MOU’s (Memorandum of Understanding) have been signed.\nProfessor Akbar is working in Academia since 1990, he started his career as a Lab demonstrator/TA at the University of Sussex. 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. In the Engineering side, Digital Signal Processing, Computer Architecture, Electronics Devices, Digital Filtering and Engineering Management.\nApart from his Academic Interest and activities he loves sport especially, Cricket, Football, Snooker and Squash. He plays cricket for Esbjerg city in the second division team as an opener wicket keeper batsman. 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Therefore, the equations of the mathematical model on which the vector control system is based are compiled with the assumption of the sinusoidality of the processes occurring in the control object. Comparative results of the analysis of dynamic of VFD with two types of sensorless control, vector and scalar, show the problems that these assumptions lead to.. For identification of nonlinearities, dynamic formulas of transfer functions of torque generator in VFD are proposed, taking into account slip and stator voltage frequency The nonlinear transfer functions obtained in this work made it possible to substantiate structural solutions that linearize the VFD and substantially increase their efficiency. The use of dynamic feedback on the stator current allowed to significantly increase the dynamics and efficiency of a more stable scalar control.",book:{id:"9287",slug:"control-theory-in-engineering",title:"Control Theory in Engineering",fullTitle:"Control Theory in Engineering"},signatures:"Vladimir L. Kodkin, Alexandr S. Anikin and Alexandr A. Baldenkov",authors:null},{id:"54865",title:"An Assessment on the Non-Invasive Methods for Condition Monitoring of Induction Motors",slug:"an-assessment-on-the-non-invasive-methods-for-condition-monitoring-of-induction-motors",totalDownloads:2161,totalCrossrefCites:8,totalDimensionsCites:11,abstract:"The ability to forecast motor mechanical faults at incipient stages is vital to reducing maintenance costs, operation downtime and safety hazards. This paper synthesized the progress in the research and development in condition monitoring and fault diagnosis of induction motors. The motor condition monitoring techniques are mainly classified into two categories that are invasive and non-invasive techniques. The invasive techniques are very basic, but they have some implementation difficulties and high cost. The non-invasive methods, namely MCSA, PVA and IPA, overcome the disadvantages associated to invasive methods. This book chapter reviews the various non-invasive condition monitoring methods for diagnosis of mechanical faults in induction motor and concludes that the instantaneous power analysis (IPA) and Park vector analysis (PVA) methods are best suitable for the diagnosis of small fault signatures associated to mechanical faults. Recommendations for the future research in these areas are also presented.",book:{id:"5496",slug:"fault-diagnosis-and-detection",title:"Fault Diagnosis and Detection",fullTitle:"Fault Diagnosis and Detection"},signatures:"Muhammad Irfan, Nordin Saad, Rosdiazli Ibrahim, Vijanth S.\nAsirvadam, Abdullah S. Alwadie and Muhammad Aman Sheikh",authors:[{id:"9739",title:"Dr.",name:"Nordin",middleName:"Bin",surname:"Saad",slug:"nordin-saad",fullName:"Nordin Saad"},{id:"174671",title:"Dr.",name:"Rosdiazli B. Ibrahim",middleName:null,surname:"Ibrahim",slug:"rosdiazli-b.-ibrahim-ibrahim",fullName:"Rosdiazli B. 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Inside a planetary gearbox, there are multiple vibration sources as several sun-planet gear pairs, and several ring-planet gear pairs are meshing simultaneously. In addition, due to the rotation of the carrier, distance varies between vibration sources and a transducer installed on the planetary gearbox housing. Dynamics-based vibration signal modeling techniques can simulate the vibration signals of a planetary gearbox and reveal the signal generation mechanism and fault features effectively. However, these techniques are basically in the theoretical development stage. Comprehensive experimental validations are required for their future applications in real systems. This chapter describes the methodologies related to vibration signal modeling of a planetary gear set for gear tooth damage diagnosis. The main contents include gear mesh stiffness evaluation, gear tooth crack modeling, dynamic modeling of a planetary gear set, vibration source modeling, modeling of transmission path effect due to the rotation of the carrier, sensor perceived vibration signal modeling, and vibration signal decomposition techniques. The methods presented in this chapter can help understand the vibration properties of planetary gearboxes and give insights into developing new signal processing methods for gear tooth damage diagnosis.",book:{id:"5496",slug:"fault-diagnosis-and-detection",title:"Fault Diagnosis and Detection",fullTitle:"Fault Diagnosis and Detection"},signatures:"Xihui Liang, Ming J. Zuo and Wenhua Chen",authors:[{id:"191577",title:"Dr.",name:"Xihui",middleName:null,surname:"Liang",slug:"xihui-liang",fullName:"Xihui Liang"}]},{id:"64980",title:"Power Balance Mode Control for Boost-Type DC-DC Converter",slug:"power-balance-mode-control-for-boost-type-dc-dc-converter",totalDownloads:1084,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"In recent years, the demand for switching converters has steadily increased. The desired converters need to be small and have high power density, good efficiency, good responsiveness, and good robustness. High responsiveness and high robustness are required for the control systems of switching converters. Some studies suggest that responsiveness and robustness can be improved using current mode control. However, it is difficult to improve the control performance of boost-type DC-DC converters significantly only by using these technologies. The power balance mode control approach can be used for solving various problems. In this approach, control is exerted to eliminate the difference between the input power and the output power. As a result, responsiveness and robustness can be improved when compared to the conventional control method. In this study, the effectiveness of the power balance mode control is confirmed using a circuit simulator.",book:{id:"9287",slug:"control-theory-in-engineering",title:"Control Theory in Engineering",fullTitle:"Control Theory in Engineering"},signatures:"Taichi Kawakami",authors:null}],onlineFirstChaptersFilter:{topicId:"717",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:31,numberOfPublishedChapters:314,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:11,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:105,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:17,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:14,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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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. 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She has run and participated in several funded and non-funded projects on the teaching of Science, Social Sciences, and ICT in education. She also has the experience of participating in five Erasmus+ projects.",institutionString:"University of Crete",institution:{name:"University of Crete",institutionURL:null,country:{name:"Greece"}}},editorThree:null},{id:"90",title:"Human Development",coverUrl:"https://cdn.intechopen.com/series_topics/covers/90.jpg",isOpenForSubmission:!0,editor:{id:"191040",title:"Dr.",name:"Tal",middleName:null,surname:"Dotan Ben-Soussan",slug:"tal-dotan-ben-soussan",fullName:"Tal Dotan Ben-Soussan",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSBf1QAG/Profile_Picture_2022-03-18T07:56:11.jpg",biography:"Tal Dotan Ben-Soussan, Ph.D., is the director of the Research Institute for Neuroscience, Education and Didactics (RINED) – Paoletti Foundation. 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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. 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. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). 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. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). 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. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:null},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. 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). 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Thus proteomics, an area of research that detects all protein forms expressed in an organism, including splice isoforms and post-translational modifications, is more suitable than genomics for a comprehensive understanding of the biochemical processes that govern life. The most common proteomics applications are currently in the clinical field for the identification, in a variety of biological matrices, of biomarkers for diagnosis and therapeutic intervention of disorders. From the comparison of proteomic profiles of control and disease or different physiological states, which may emerge, changes in protein expression can provide new insights into the roles played by some proteins in human pathologies. Understanding how proteins function and interact with each other is another goal of proteomics that makes this approach even more intriguing. Specialized technology and expertise are required to assess the proteome of any biological sample. Currently, proteomics relies mainly on mass spectrometry (MS) combined with electrophoretic (1 or 2-DE-MS) and/or chromatographic techniques (LC-MS/MS). MS is an excellent tool that has gained popularity in proteomics because of its ability to gather a complex body of information such as cataloging protein expression, identifying protein modification sites, and defining protein interactions. 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