Comparison of typical commercial satellites and HTS.
\\n\\n
IntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\\n\\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\\n\\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\\n\\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\\n\\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\\n\\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\\n\\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\\n\\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\\n\\nFeel free to share this news on social media and help us mark this memorable moment!
\\n\\n\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/237"}},components:[{type:"htmlEditorComponent",content:'
After years of being acknowledged as the world's leading publisher of Open Access books, today, we are proud to announce we’ve successfully launched a portfolio of Open Science journals covering rapidly expanding areas of interdisciplinary research.
\n\n\n\nIntechOpen was founded by scientists, for scientists, in order to make book publishing accessible around the globe. Over the last two decades, this has driven Open Access (OA) book publishing whilst levelling the playing field for global academics. Through our innovative publishing model and the support of the research community, we have now published over 5,700 Open Access books and are visited online by over three million academics every month. These researchers are increasingly working in broad technology-based subjects, driving multidisciplinary academic endeavours into human health, environment, and technology.
\n\nBy listening to our community, and in order to serve these rapidly growing areas which lie at the core of IntechOpen's expertise, we are launching a portfolio of Open Science journals:
\n\nAll three journals will publish under an Open Access model and embrace Open Science policies to help support the changing needs of academics in these fast-moving research areas. There will be direct links to preprint servers and data repositories, allowing full reproducibility and rapid dissemination of published papers to help accelerate the pace of research. Each journal has renowned Editors in Chief who will work alongside a global Editorial Board, delivering robust single-blind peer review. Supported by our internal editorial teams, this will ensure our authors will receive a quick, user-friendly, and personalised publishing experience.
\n\n"By launching our journals portfolio we are introducing new, dedicated homes for interdisciplinary technology-focused researchers to publish their work, whilst embracing Open Science and creating a unique global home for academics to disseminate their work. We are taking a leap toward Open Science continuing and expanding our fundamental commitment to openly sharing scientific research across the world, making it available for the benefit of all." Dr. Sara Uhac, IntechOpen CEO
\n\n"Our aim is to promote and create better science for a better world by increasing access to information and the latest scientific developments to all scientists, innovators, entrepreneurs and students and give them the opportunity to learn, observe and contribute to knowledge creation. Open Science promotes a swifter path from research to innovation to produce new products and services." Alex Lazinica, IntechOpen founder
\n\nIn conclusion, Natalia Reinic Babic, Head of Journal Publishing and Open Science at IntechOpen adds:
\n\n“On behalf of the journal team I’d like to thank all our Editors in Chief, Editorial Boards, internal supporting teams, and our scientific community for their continuous support in making this portfolio a reality - we couldn’t have done it without you! With your support in place, we are confident these journals will become as impactful and successful as our book publishing program and bring us closer to a more open (science) future.”
\n\nWe invite you to visit the journals homepage and learn more about the journal’s Editorial Boards, scope and vision as all three journals are now open for submissions.
\n\nFeel free to share this news on social media and help us mark this memorable moment!
\n\n\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"2387",leadTitle:null,fullTitle:"New Approach of Indoor and Outdoor Localization Systems",title:"New Approach of Indoor and Outdoor Localization Systems",subtitle:null,reviewType:"peer-reviewed",abstract:"Accurate determination of the mobile position constitutes the basis of many new applications. 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The innate response is characterized by the recognition of molecular patterns associated with damage and pathogens, whose molecules and receptors are fixed in the DNA of the germ line. Adaptive immunity is an antigen-specific response which is relatively slow, since it requires a genetic rearrangement [1]. The main objective of the immune system is the defense against pathogens through these innate and adaptive mechanisms [2, 3]. However, dysfunction or deficiency of the immune system can lead to tissue injuries and diseases. On the one hand, there are hypersensitivity diseases, which are characterized by excessive and undesirable reactions, produced by the immune system [4]. On the other hand, autoimmune diseases refer to the failure of the immunological tolerance mechanisms, causing reactions against own cells and tissues [5].
\nThe innate immune system is the first line of defense against invading pathogens. It has a double role to provide initial control of the infection and initiate an adaptive immune response. The innate immune system consists of physical barriers such as epithelial layers and mucus, soluble factors such as the complement system, soluble mediators, cytokines and cells such as neutrophils, macrophages and dendritic cells [6]. These immune cells detected pathogens based on their molecules or pathogen-associated molecular patterns (PAMPs) that are recognized by multiple classes of pattern-recognition receptors (PRRs) that initiate inflammatory responses [7]. PRRs can also recognize host molecules containing damage-associated molecular patterns (DAMPs), molecules that are released from cells damaged [8]. Then, these PRRs respond by producing several soluble mediators such as the complement system and proinflammatory cytokines to kill microbes or infected cells [1].
\nThe cells of the innate immune system have several functions that are essential for the defense of the organism. These cells respond by producing inflammatory cytokines and some of them are responsible for removing foreign substances, pathogens or infected cells. Some of the innate immune cells include macrophages, dendritic cells, neutrophils, mast cells, basophils and eosinophils.
\nMacrophages function as cells that capture and degrade agents that are not recognized as belonging to the organism, in addition to being antigen-presenting cells; therefore, they are essential in both types of immunity (innate and adaptive) [9]. Macrophages are formed in the bone marrow from myeloid progenitor cells, which when stimulated by the granulocyte-macrophage colony-stimulating factor (GM-CSF) are converted into monocytes, immature cells that are released into the bloodstream. Monocytes mature when stimulated by chemotactic substances, making them migrate to tissues as mature cells, establishing themselves for a lifetime of weeks to months. This cell type is directly related to the inflammatory response, since phagocytosis uses harmful substances that can cause acute cell injury and promote apoptosis, including reactive oxygen species (ROS), high amounts of nitric oxide and halogenating radicals. Other mechanisms that promote inflammation are through the production of cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α. However, it has also been seen that macrophages modulate inflammation through the release of anti-inflammatory cytokines and growth factors such as IL-10, vascular endothelial growth factor (VEGF)-α, transforming growth factor (TGF)-β and Wnt proteins [10, 11]. Then, the macrophages can be divided into two general classes, depending on their phenotype, M1 that promote inflammation and M2 that release anti-inflammatory and pro-regenerative cytokines [12, 13].
\nThe process of formation of dendritic cells (DCs) is like macrophages, being monocytes in their more immature stage. However, these cells are directed to epithelia even as immature cells and remain there for long periods (weeks or months). When they capture microorganisms or antigenic agents, they eliminate them by phagocytosis, going through the lymph to the lymph nodes, where they will perform their specialized function as antigen-presenting cells [14]. The DCs present antigens to the T lymphocytes; however, it has been proven that they are also capable of activating B lymphocytes, natural killer (NK) cells, macrophages and eosinophils. DCs participate in innate immunity; however, they regulate the adaptive immune response and are fundamental for the development of immunological memory and tolerance [15]. There are mainly two DCs subpopulations: classical and plasmacytoid DCs. On the one hand, classical DCs are specialized cells in the antigen processing and presentation, which have both high phagocytic activity and capacity for cytokine production [16]. On the other hand, plasmacytoid DCs are long-lived cells [17], which are present in the bone marrow and in all peripheral organs and are specialized to respond to viral infection with mass production of type I interferons (IFN). However, these DCs can also act as antigen-presenting cells and control the responses of T cells [18].
\nNeutrophils are phagocytes that are derived from myeloid cells as well as monocytes and dendritic cells. Its morphology is very characteristic, since they present nuclear lobes of different morphologies and they are known as polymorphonuclear (PMN). It is the most abundant leukocyte in the blood (up to 70% of the total of leukocytes) and unlike the other phagocytes, neutrophils are released into the blood as mature cells; however, they have a short life time (from hours to maximum 2 days). They are the first cells of the immune system to reach the focus of infection and their function is practically phagocytosis. Although its short life has been identified that neutrophils are also involved in adaptive immunity, previously, it was known that neutrophils participated in the elimination of foreign agents by phagocytosis, dying in their function; however, it has been found that neutrophils have the ability to return to the bloodstream as antigen-presenting cells, interacting with dendritic cells, NK cells, T and B lymphocytes [19, 20].
\nMast cells are derived from mesenchymal precursor cells (MCPs) in bone marrow but mature in peripheral tissues. They are distributed mainly in tissues close to the external environment such as the skin, mucous membranes, digestive tract and respiratory tract. Activation of mast cells is practically due to the binding of immunoglobulin (Ig)-E antibodies to the high-affinity receptors for the Fc region of IgE (FcεRI) found in their plasma membrane, triggering the release of their granules containing high concentrations of histamine, tryptase, chymase, carboxypeptidase and heparin [21]. Activation of mast cells causes the activation of phospholipase A2 and breaks down membrane lipids to produce arachidonic acid, which can be metabolized in two ways: (1) the cyclooxygenase (COX) pathway, producing prostaglandins and (2) the lipoxygenase pathway (LOX), producing leukotrienes. Both prostaglandins and leukotrienes have pro-inflammatory effects, increasing vascular permeability. The mast cells boost the immune response, increasing the recruitment of specific cells against pathogens, activating different types of immune cells such as macrophages, eosinophils and lymphocytes that eliminate bacteria, fungi, some parasites and cells infected by viruses. Mast cells activate other cells of the immune system by releasing TNF-α, TGF-β, IL-4, IL-5, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), VEGF and fibroblast growth factor (FGF)-2 [22].
\nBasophils are granulocytes derived from myeloid cells. They are the least abundant (0.5% of leukocytes) and have a nucleus in the form of S, lobed (1–3 lobes). They have many granules containing histamine, heparin, serotonin and high amounts of leukotrienes. Like mast cells, they contain histamine in their granules, being responsible for most of the early symptoms of IgE-dependent and non-dependent allergy (sneezing, pruritus, bronchospasm and edema). Basophils migrate to the site of inflammation and secrete proteases and various inflammatory mediators such as IL-4 to activate cells such as macrophages, innate lymphoid cells, fibroblasts and endothelial cells, aggravating the allergic inflammatory response [23, 24].
\nEosinophils are bilobed granulocytes originating from the bone marrow from myeloid cells, being released into the bloodstream in a mature manner and at low concentrations (3% of the total of granulocytes). An important characteristic of eosinophils is their high quantity of granules, which have different components, among which are high concentrations of leukotrienes, ROS, IL-4, IL-5, neurotoxins (EDN), main basic protein (MBP), eosinophilic cationic protein (ECP) and eosinophilic peroxidase (EPO) [25, 26]. Eosinophils play an important role in hypersensitivity since they are stimulated by IL-5 produced by mast cells and Th2 cells. Also, fibroblasts when stimulated by IL-4, release eotaxins, molecules that stimulate the function of eosinophils [27].
\nInnate immune cells are capable of recognizing pathogens and endogenous molecules of proteins known as PRRs. These receptors recognize highly conserved motifs known as PAMPs or DAMPs. PRRs dictate the initiation of an adequate and effective innate immune response, as well as the activation of the adaptive immune response to infection or inflammation [28]. These PRRs include Toll-like receptors (TLRs), nucleotide-binding domain and leucine-rich repeat-containing receptors (NLRs) and RIG-I-like receptors (RLRs) [29].
\nThe TLRs family, was originally identified in Drosophila, as important genes for its ontogeny and the innate immune response in Drosophila adults [30]. The TLRs family consists of 10 highly conserved transmembrane glycoproteins in humans, which recognize a wide range of pathogens [31]. TLR-1, TLR-2, TLR-4, TLR-5, and TLR-6 are expressed on the cell surface, while TL-3, TLR-7, TLR-8, and TLR-9 are found intracellularly in endosomes [32]. The extracellular leucine-rich repeat (LRR) regions in the TLRs mediate protein-protein or PAMP-protein interactions, while their intracellular tails mediate proinflammatory signaling through the myeloid differentiation primary response protein (MYD88) and TIR domain-containing adapter molecule 1 (TRIF; also known as TICAM1) pathways [33]. They are expressed in a wide variety of cells such as innate immune cells, T and B cells, epithelial cells, fibroblasts, and endothelial cells; however, not all cell types express every TLR [34]. Different TLRs specifically recognize distinct PAMPs and DAMPs [35]. For example, TLR2 recognizes lipoarabinomannan from mycobacteria [36]. Some TLRs detect different nucleic acids; TLR3 detects viral double-stranded RNA (dsRNA) formed during the replication of positive stranded viral RNA in the cytosol [37]; TLR7 and TLR8 both recognize viral single-stranded RNA (ssRNA) [38, 39] and TLR9 recognizes bacterial DNA [40]. TLR4 together with myeloid differentiation factor (MD)-2 recognizes lipopolysaccharide (LPS), which comes from Gram-negative bacteria [41]. Further, TLR4 is also involved in antiviral innate immunity [42, 43]. TLR5 is highly expressed DCs and detects bacterial flagellin [44, 45]. Plasmacytoid DCs express TLR7 and TLR9, and both are implicated in recognition of viral and bacterial nucleic acids [46]. TLR10 has been implicated in the recognition of
The NLR family comprises 22 members in humans. Most NLRs share common structural characteristics including a C-terminal leucine-rich repeat (LRR) domain, often involved in ligand recognition, a central NOD, and a variable N-terminal effector domain [49]. Based on the type of effector domains that is either a caspase recruitment domain (CARD), a pyrin domain (PYD), or a baculoviral inhibitor of apoptosis protein repeat (BIR) domain [50], the NLR family can be categorized structurally into five subsets based on their N-terminal effector domain: NLRA, NLRB, NLRC, NLRP and NLRX [29]. The most well-defined sensors of peptidoglycan are the cytosolic NOD-like receptors (NLRs), NOD1 and NOD2, which are expressed by diverse cell types, including myeloid phagocytes and epithelial cells [51], which recognize specific ligands from various pathogens. This family is involved in increasing the proinflammatory events caused by cell death and several more proinflammatory processes [52].
\nThe RIG-I-like receptor family consists of RNA-binding proteins that are expressed in almost all cells. Family members include RIG-1, melanoma differentiation-associated gene (MDA)-5, and laboratory of genetics and physiology (LGP)-2 [34]. They act as sensors for viral replication within human host cells necessary to mediate antiviral responses [53].
\nCytokines are secreted proteins that can be delineated as a distinct class of signaling molecules from hormones based on two key factors. First, the kinetics of cytokine secretion (rapid and dramatic induction following specific extracellular stimuli), which is often prolonged at less dramatic concentrations to affect physiological changes. Second, cytokines can be signaling autocrine, paracrine and endocrine fashions [54, 55]. Cytokines are involved in regulating the homeostasis of the organism, but when its production or its signaling pathway in the cell is not regulated, this homeostasis is altered, which can trigger in a pathology [56, 57].
\nCytokines can be classified into five groups [57]: (1) IL-1 superfamily, there are 10 members of the IL-1 family of receptors (IL-1R1–ILR10) [58] and 11 members of the IL-1 family of cytokines (IL-1α, IL-1β, IL-1Ra, IL-18, IL-33, IL-36α, IL-36β, IL-36γ, IL-36Ra, IL-37 and IL-38) [59]. The interleukin-1 superfamily members are closely linked to damaging inflammation; however, the same members also function to increase nonspecific resistance to infection and the development of an immune response to foreign antigens [60]. (2) TNF superfamily is composed of 19 ligands and 29 receptors [61]. This family plays a pivotal role in immunity, inflammation and controlling cell cycle (proliferation, differentiation and apoptosis) [62]. (3) The interleukin (IL)-17 cytokine family is composed of IL-17A and five other members (IL-17B, IL-17C, IL-17D, IL-17E, also referred to as IL-25, and IL17F). IL-17-related cytokines play key roles in defense against extracellular pathogen, autoimmunity. In addition, there is evidence that indicates that some of these molecules are involved in the amplification and perpetuation of pathological processes in many inflammatory diseases, such as psoriasis, rheumatoid arthritis, multiple sclerosis and allergy. However, the same cytokines can exert anti-inflammatory effects in specific settings and play key role in the control of immune homeostasis [63, 64]. (4) IL-6 superfamily is comprised by IL-6, leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), cardiotrophin (CT)-1, IL-11, cardiotrophin-like cytokine factor (CLCF)-1, viral IL-6 (vIL-6), IL-27 and IL-35 [65]. This cytokine family shows some redundant but not uniformly identical biological activity. IL-6 exerts pleiotropic effects on inflammation, immune response and hematopoiesis [66, 67]. IL-6 is produced at the inflammation site by infection or tissue damage, which induces production of acute phase proteins such as C-reactive protein (CRP), serum amyloid A, fibrinogen and hepcidin in liver. IL-6 also plays an important role in acquired immune response to induce differentiation of activated B cells in to antibody (Ab)-producing cells and to prolong survival of plasmablasts [65], while it promotes the development of Th17 cells and follicular helper T cells by naïve T cells and inhibits the differentiation into regulatory T cells (Treg) [68]. But, dysregulated excessive or persistent production of IL-6 plays a pathological role in various kinds of diseases [65]. (5) Type I superfamily, includes the common γ-chain cytokines (IL-2, IL-4, IL-7, IL-9, IL-13, IL-15 and IL-21) [69], common β-chain cytokines (IL-3, IL-5, GM-CSF) [70] and IL-12 subfamilies (IL-12, IL-23, IL-27 and IL-35), as well as similar cytokine products with unique receptor characteristics such as IL-13, IL-14, IL-32, IL-34, granulocyte colony-stimulating factor (G-CSF) and macrophage colony-stimulating factor (M-CSF). (6) Type II superfamily contains the interferons (type I, II and III) and the IL-10 subfamily (IL-10, IL-19, IL-20, IL-22, IL-24 and IL-26) [54].
\nInflammation is a protective response to infection, tissue stress and injury [71]. This inflammatory response is characterized by its clinical signs such as redness, heat, swelling, pain and dysfunction [72]. The inflammatory response is triggered by inducers such as PAMPs derived from bacteria, viruses, fungi and parasites; and DAMPs derived from cell damage, as well as toxic cellular components or any other harmful conditions [73]. Then, these inflammatory inducers are detected by “sensors,” which are present in several immune cells. These sensors are PRRs such as TLRs, NLR and RIG-like receptors [52, 74]. Subsequently, the PRRs induced the synthesis and release of soluble mediators such as cytokines [75]. Cytokines, as optimal protection against pathogens, provide the necessary signals to initiate an inflammatory response, through the differentiation and proliferation of the immune system cells, adapting their effector functions as necessary to promote protective immunity, and once the inducers are eliminated, they suppress the inflammatory response, promoting tissue repair and return to homeostasis [54]. The inflammatory response is characterized by successive phases [76]: (1) silent phase, where cells reside in the damaged tissue releases in the first inflammatory mediators; (2) vascular phase, where vasodilation and increased vascular permeability occur; (3) cellular phase, which is characterized by the infiltration of leukocytes to the site of injury; and (4) resolution of inflammation, which is the process to return tissues to homeostasis [77, 78, 79].
\nPhagocytosis is the physiological process carried out by phagocytic cells to identify, digest and eliminate foreign substances or pathogens (Figure 1). Infection with pathogens is the most common cause to trigger this immune mechanism. The pathogens proliferate releasing small peptides with chemotactic activity, dispersing in the areas of underlying tissue and blood vessels. These chemotactic peptides come into contact with the endothelial cells that form the blood vessels and phagocytes that are found in the invaded tissue (macrophages and/or dendritic cells), as well as those found in the blood (neutrophils and monocytes). Endothelial cells initiate the synthesis of cell adhesion proteins, as do phagocytes found in the blood. The adhesion proteins allow the phagocytes of the blood to bind to the endothelial cells, causing them to roll on the surface until finding an exit between the cell junctions, migrating to the extravascular space by a process known as diapedesis. The phagocytes that were close to the area of infection and those that migrated from the blood move toward the focus of infection attracted by the chemotactic peptides. The microorganisms have structural components (the receptor for IgG (FcR) and PAMPs, among others) that are recognized by PRRs found in phagocytes [80, 81].
\nThe interaction of these surface molecules causes the invagination of the cell membrane and the formation of cellular prolongations that end up involving the foreign pathogens in a phagocytic vacuole or phagosome. The chemical interaction of the molecules on the membrane surface of microorganisms and phagocytes activates diverse receptors, including those of Gq proteins that activate phospholipase C, an enzyme that degrades membrane phospholipids to produce inositol triphosphate (IP3) and diacylglycerol (DAG). The IP3, among many of its functions, is responsible for regulating cell movement by the cytoskeleton through the release of calcium ions by the endoplasmic reticulum. On the other hand, the DAG activates a protein kinase C (PKC), which activates the cytosolic proteins p40, p47 and p67, which, supported by ras-related protein Rap-1A (RAP1A), interact with cytochrome B558, one of the components of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Activated NADPH oxidase promotes the release of ROS, molecules highly toxic to cellular components. NADPH oxidase captures high amounts of oxygen, transforming them into superoxide anions (O2−), which in turn promote the formation of dangerous ROS such as hydrogen peroxide (H2O2), hydroxyl (OH−) and oxygen singlet (1O2). The ROS react with the biomolecules that make up the structures of the microorganisms (lipids, polysaccharides, proteins and nucleic acids), causing their death. Simultaneously, the phagocytes fuse lysosomes to the vacuole in which the microorganism is internalized, forming the phagosome, also releasing many hydrolytic enzymes that favor the digestion of the microorganism components [82].
\nPhagocytosis. (1) Recognition of structural components of pathogens by the PRRs of phagocytes. (2) Invagination of the cellular plasma membrane that causes the internalization of the pathogens, forming the phagosome. (3) Fusion of the lysosomes with the phagosome, promoting the digestion of the pathogens by hydrolytic enzymes. In addition, ROS are released that contribute to the degradation of biomolecules. (4) Destruction of the pathogens. (5) The activation of phospholipase C causes the activation of PKC. (6) PKC activates NADPH oxidase. (6) ROS are produced by NADPH oxidase. (7) ROS are directed to the phagosome, contribute to the degradation of pathogens. (8) Release by exocytosis of the pathogens residual.
Lysosomes contain myeloperoxidase, an enzyme that hydrolyzes hydrogen peroxide for the formation of halogenating radicals such as hypochlorous acid, hypochlorite and hypoiodite, which increase the damage to microorganisms. Finally, cell debris has two purposes: (1) to be eliminated by exocytosis, (debris are evacuated into the bloodstream to be eliminated by renal route); and (2) to transport certain antigenic components to the cell membrane to be presented to T and B cells and be able to give the process of acquired immunity (mainly in the case of dendritic cells and macrophages) [82].
\nThe adaptive immune system has the capacity to generate a wide range of specific antigen receptors, through somatic mechanisms of gene rearrangement. These mechanisms create a random repertoire of receptors that are clonally distributed in T and B lymphocytes. This gives it the advantage of having a wide repertoire of specific antigen receptors, which can be recognized, without these having to be encoded in the host genome, allowing the recognition of almost any antigenic structure. The activation of lymphocytes requires two types of signals: (1) a signal induced by the antigen receptor itself when recognizing its related antigen, and a costimulatory signal by professional antigen-presenting cells (APCs). Therefore, the innate immune system, as already explained earlier, determines the origin of the antigens by means of a non-clonal system of receptors, PRRs, encoded in the germ line, which controls the expression of costimulatory molecules and effector cytokines, while the adaptive immune system does it through antigenic receptors [83, 84].
\nDuring the hematopoiesis that is generated in the bone marrow, it gives rise to the precursors of all the lineages and states of differentiation of the T cells. These precursors, called thymocytes, travel through the peripheral blood and reach the thymus, where they mature in T lymphocytes. Later, they will differentiate into CD4+ T lymphocytes (cooperators) or CD8+ T lymphocytes (cytotoxic). Once they are differentiated, they travel through the blood circulation until they are activated by means of the surface receptor they present, when they encounter a specific antigen. This receptor, known as T cell receptor (TCR), binds to the major histocompatibility complex (MHC), a complex expressed by antigen-presenting cells, in which the antigen is presented in the form of peptides. Depending on the T cell to which the antigen is presented, MHC class I or MHC class II will be used. To present an antigen to the CD4+ T lymphocyte, a presentation through the MHC-II will be required; while for the activation of a CD8+ T lymphocyte, it will be necessary through the MHC-I [84, 85]. T lymphocytes are responsible for cellular adaptive immunity. The activation of CD8+ T lymphocytes allows the destruction of infected cells through the release of perforins, which are proteins responsible for forming pores in the membrane of the target cell that causes the passage of water and ions, inducing an osmotic lysis of the infected cell. Similarly, CD8+ T lymphocytes release toxic enzymes such as the granzyme that passes through the pores formed in the cell membrane, which causes the induction to cell death by fragmenting the DNA of the infected cell. Activation of CD4+ T lymphocytes allows cooperation with other immune cells for their activation. As the case of macrophages, B lymphocytes and other T lymphocytes, through costimulatory molecules and the release of cytokines, this causes a powerful cellular activation and therefore an effective immune response. In addition to this, CD4+ T lymphocytes can differentiate into cellular subpopulations with specific action. Mediated by the secretion of cytokines, they can be differentiated into Th1, Th2, Th9, Th17 and Th22 types [86].
\nIn addition, memory T lymphocytes have a long life, functionally inactive but respond to new exposures of the same antigen quickly and efficiently. There is another population of T lymphocytes, the regulatory T lymphocytes [86]. This cellular population is responsible for eliminating autoreactive T cells that escaped the process of negative selection or central tolerance; with the purpose, to avoid the development of an autoimmune response [87]. Other lymphocytes, such as LTγ/δ, are another very rare cell type that represent about 10% of intraepithelial lymphocytes of the small intestine but increase drastically under certain allergic or inflammatory conditions. In addition, they recognize complete proteins without needing to be processed to be presented through the MHC molecules [88].
\nThe B lymphocytes are originated from the same precursor that gives origin to the T lymphocytes and the NK cells. However, the absence of certain cell membrane receptors in B lymphocytes leads to their differentiation in this cell line, a process that takes place in bone marrow. Up to this point, the B lymphocytes are immature, and it will be until they migrate from the bone marrow into the spleen to undergo positive and negative selection and thus produce a mature B lymphocyte [89]. B lymphocytes can be activated: (1) by a foreign agent through the TCD4+ lymphocytes collaboration; (2) or in specific circumstances independent of CD4+ T lymphocytes. In the case of CD4+ T lymphocytes collaboration, it occurs through the MHC expressed in its cell membrane, which binds to the B cell receptor (BCR), to initiate the antigenic presentation that will end in the synthesis of antibodies [90]. B lymphocytes are cells that participate in humoral adaptive immunity, since once activated they proliferate in response to the antigen and differentiate into plasma cells to produce antibodies against the specific antigen [91]. Likewise, activated B lymphocytes can differentiate into memory cells, acquiring a capacity for survival for long periods of time, up to more than 10 years, approximately [92, 93]. However, various co-stimulatory receptors that are expressed in B cells can induce their proliferation and survival, as well as the regulation of the production of specific antibodies that contribute to a breakdown of immunological tolerance, triggering autoimmune diseases [94].
\nAntibodies, also known as immunoglobulins (Ig) are structurally composed of two heavy polypeptide chains identical to each other and two light chains also identical, joined by one or more disulfide bridges. They have a variable region with two domains (VH, VL) and a constant region with four domains (CL, CH1, CH2 and CH3) [95]. The segments of the variable region originate through a somatic recombination, which allows having the diversity in the repertoire of antibodies, since at least 1026 of different specific antibodies are generated. They have a Fab fragment (fragment antigen binding) and an Fc fragment (crystallizable fraction). The Fab portion is an antigen-binding zone, while the Fc is a constant zone where the interaction with cellular receptors and the effector part of the biological functions presented by the antibodies occurs. Among these biological functions are crossing the placental barrier, activating complement, neutralizing antigens, joining phagocytic cells and acting as opsonin; all to generate protection and eliminate pathogens or elements harmful to the host [96].
\nThere are 5 classes recognized up to the moment of antibodies: IgA, IgG, IgM, IgE and IgD. Most are monomeric, but they can be presented pentameric as IgM and only IgA can be present in both dimeric and monomeric forms. There are 4 subclasses for IgG (IgG1-IgG4) and 2 for IgA (IgA1 and IgA2). This is due to variations in the constant regions, which causes functional differences between the antibodies of the same class [97]. Among the functions of IgG is complement activation, with subclass IgG3 having the greatest effect, whereas IgG4 cannot activate it. It is the antibody in greater amount circulating in the blood and more increases during a secondary immune response. It can cross the placenta and, in the newborn, favors its immunological protection. It helps in phagocytosis through opsonization, as well as in the neutralization of pathogens with great effectiveness [98]. IgA is found in greater concentration due to its location in epithelia, in body secretions such as saliva, tears, colostrum, respiratory, gastrointestinal and genitourinary secretions; which allows it to generate a broad protection against pathogens and allergens. In blood circulation, it is found in a monomeric way; but in mucous, it is found in a dimeric form behaving as secretory IgA [99]. The IgE antibody is found in very small concentrations in the bloodstream. The majority is bound to a surface receptor of mast cells, eosinophils and basophils, which causes it to be involved in allergic reactions in humans, since it induces the release of pro inflammatory cytokines when IgE recognizes specific antigens [100]. It also causes degranulation of the aforementioned cells, causing the release of vasoactive substances such as histamine, causing an inflammatory response. Also, it can increase the production of this antibody by the effect of allergens such as those that can be found in food, some drugs and seasonal allergens, which causes allergic reactions. This immunoglobulin is very effective in the defense against parasitic infections [101]. In the case of IgM, it is the first antibody that appears with immune response reactions. It is the first antibody that is expressed on the surface of B lymphocytes and the one that predominates in primary immune reactions. It is the largest, due to its pentameric formation, which allows it to bind several antigens (approximately, 6 antigens per IgM) and is the main activator of the complement system [102]. Finally, IgD is the immunoglobulin that is also found on the surface of B lymphocytes, being a marker of their maturity. However, at the time of contact with the antigen, IgD is lost during antigenic stimulation. It participates as an antigen receptor and signaling transmitter inside the cell and, in blood circulation, it is found in very small amounts and is not produced by plasma cells [103].
\nThe molecules of the major histocompatibility complex (MHC), also called human leukocyte antigens (HLA) [104, 105], are the product of a set of genes responsible for the lymphocytes rejecting transplanted tissues and detecting foreign elements. These molecules also participate in the induction of the specific immune response, through the presentation of the antigen to the T lymphocytes [104]. In the mammalian genome and, more specifically, in the human genome, the most variable region known forms the MHC that carries a great number of different loci coding for functional genes [106]. The classical MHC encompasses approximately 3.6 megabasepairs (Mb) and is divided into three subregions: the telomeric class I, class III, and the centromeric class II regions [107]. In humans, the MHC region is approximately 4000 kb long, located on the short arm of chromosome 6 [105, 106].
\nMolecular markers, located on the cell surface, help to externalize the intracellular environment and give the individual a specific tissue identity, recognized by their immune system. Under normal conditions, the MHC molecules reach the cell membrane bound to their own elements, so when they are presented to the T lymphocytes, they do not activate them; when by infection or pathological changes of the cell, they emerge, carrying a foreign molecule instead of their own, the T cell is activated and responds immediately [108]. The function of MHC molecules is to bind peptide fragments derived from pathogens and display them on the cell surface for recognition by the appropriate T lymphocyte. The consequences are almost always deleterious to the pathogen—virus-infected cells are killed, macrophages are activated to kill bacteria living in their intracellular vesicles, and B lymphocyte are activated to produce antibodies that eliminate or neutralize extracellular pathogens [105].
\nThe genes, whether expressed, are arranged in three genomic regions or classes. The more distal region corresponds to MHC class I, which carries the genes that code for the classic (1a) class I HLA-A, -B, and -C heavy chains, all nucleated cells express class I molecules on their cell surface [109]. They present cytoplasmic or endogenous antigens (synthesized intracellularly, those of viral or tumoral origin and processed by the proteasome) to the CD8+ T lymphocyte [110]. MHC-I is a molecule made up of an α polypeptide chain, with three domains (α1, α2 and α3) and the β2 microglobulin subunit. In the cleft that is formed between α1 and α2, it is added the antigenic peptide that is going to present [108]. The classical molecules MHC-I (A, B and C) are expressed on the surface of all cells, except those of the trophoblast, erythrocytes and neurons. Its main function is the presentation of antigens to the CD8+ T lymphocyte [111]. The MHC-I is formed in the endoplasmic reticulum and interacts with the chaperone molecules: calnexin and calreticulin, which help it to bind with the β2 microglobulin and confer stability on it. A third molecule, the capsid, helps transporting antigen processing peptides (TAP)-1 and TAP2 to form the channel that allows the passage of the antigenic peptide from the cytoplasm to the endoplasmic reticulum, where it binds to the MHC-I. This complex (MHC-I-antigenic peptide) leaves the endoplasmic reticulum in a vesicle, travels through the cytoplasm and is finally exocytosed. On the cell surface, the MHC molecule and the antigenic peptide that it carries bind to the CD8+ T lymphocyte receptor and it is through this union that the so-called “presentation” is made. If the presented peptide corresponds to a molecule of its own, the lymphocyte does not respond. If the presented peptide is foreign, accessory signals are transmitted through costimulatory molecules such as B7-CD28, CD40-CD40L, etc., which activate CD8+ T lymphocyte. The activated cytotoxic lymphocyte, through the firing of cytolytic enzymes and the induction of apoptosis, destroys the host cell, carrier of endogenous antigens such as viruses or tumor cell elements (Figure 2, right) [108].
\nProcessing and presentation of antigen. In the MHC class I pathway (right), the proteosomes process the protein antigens in the cytoplasm, which are transported to the endoplasmic reticulum (ER), where they bind to the MHC class I molecules. Subsequently, these are presented to the T lymphocytes, to induce a CD8+ phenotype. In the MHC class II pathway (left), the extracellular protein antigens are introduced into the antigen-presenting cell by endocytosis, in vesicles, where the antigens are processed, and the peptides bound to the MHC class II molecules, which are present to the T lymphocytes to induce a CD4+ phenotype.
The MHC class II genes, coding for both chains that will form the functional heterodimer, HLA-DR, HLA-DQ, HLA-DP, HLA-DM, and HLA-DO are in the more centromeric portion of the MHC region [109]. They exhibit restricted expression, being predominantly expressed on antigen-presenting cells (APC), such as macrophages, DCs, Langerhans and Kupffer cells, as well as B lymphocytes [112], also intravesicular or exogenous antigens (synthesized extracellularly and processed by lysosomes) to CD4+ T lymphocyte [110]. CMH-II is composed of two polypeptide chains: α and β, both with two domains. The antigenic peptide binding site it presents is located between α1 and β1 [105, 108]. The antigen, for its presentation, must be processed by the cell that captured it and be reduced to small peptides, since the sites to which it binds both in the MHC and in the T lymphocyte, can only host molecules with a smaller size to 25 amino acids [108]. The classical molecules MHC-II (DP, DQ and DR) are expressed, constitutively, on the surface of the cells participating in the “immune response” (phagocytes and lymphocytes), but by activation with INF-γ, they can be expressed in other cells that, like fibroblasts, keratinocytes, barley and endothelial, also participate in this response [111]. The MHC-II is synthesized in the endoplasmic reticulum and portal a molecule: the invariant chain (Li or CD74) that protects the site that the antigen will occupy, favors its exit of the reticulum and takes it to endosomes where it meets the antigenic peptides. In this place, various cathepsins break the Li chain, which leaves the site corresponding to the antigen free and allows its binding to MHC, the Li residues (CLIP) are removed by the DM molecule. Finally, the antigenic peptide emerges to the surface linked to MHC-II, a molecule through which it makes contact and is presented to the CD4+ T lymphocyte. If the presented molecule is strange, the T-helper cell cytokines are activated and secreted. These cytokines can activate the host cell and lymphocytes and cells surrounding (Th1 predominant response), as well as stimulate the production of antibodies (Th2 predominant response). The class of secreted cytokines and therefore, the function that they do, depends on the type of Th cell that responds. In all cases, there is a regulation that, at the end of the Antigenic stimulus: slows the response, induces apoptosis activated cells, inhibits inflammation and initiates repair (Figure 2, left) [113].
\nThe “immunological tolerance” was established in 1954, as an acquired state learned during the development of the immune system by exposure to antigens in its immediate environment [114]. A single antigen can induce an immune response or tolerance depending on the context in which it occurs. Tolerance is acquired, triggered from the ontogeny of lymphocytes and there are different mechanisms to maintain it. One is carried in the primary lymphoid organs, known as central tolerance. The other is carried in the secondary lymphoid organs and is known as peripheral tolerance [115]. The central tolerance, also known as negative selection, is carried out during the development of the T and B cells, when the newly generated cells test their receptors for the recognition of antigens in their immediate environment. It consists of a clonal elimination in the bone marrow of autoreactive B lymphocytes and self-reactive T lymphocytes in the thymus. It prevents maturation of those lymphocytes capable of recognizing autoantigens through the expression of high affinity receptors and occurs through the recognition of these by the antigen-presenting cells through MHC molecules. On the other hand, peripheral tolerance allows maintenance in the control of effective immune responses against “self” [116].
\nAfter the T and B lymphocytes have passed through the control of negative selection or central tolerance and mature, they are directed by blood circulation to secondary lymphoid organs such as the spleen and lymph nodes. Lymphocytes require secondary signals to activate and generate a positive response against foreign antigens. If the lymphocytes do not generate a positive response against these antigens, the lymphocytes become anergic or die by apoptosis. Similarly, when lymphocytes are activated by antigens inappropriately (autoreactive), regulatory mechanisms are activated that correct such failures through the participation of regulatory T lymphocytes (Tregs) [117].
\nThe tolerance for exogenous antigens is due to the lack of immune response against antigens from food and normal flora, as well as inhaled antigens, to avoid triggering an immune response that affects the integrity of the individual. This type of tolerance occurs mainly on mucous membranes. The participation of IgA immunoglobulin as essential component of mucosal immunity, whose function is the neutralization of antigens or immune complexes, prevents their absorption and progression of active immune response. Dendritic cells are also highly responsible for immunological tolerance toward exogenous antigens. In part, they are responsible for their ability to induce the expression of Tregs FOXP3+ lymphocytes [118].
\nThe immune system is an integral part of human protection against disease, but the normally protective immune mechanisms can sometimes cause detrimental reactions in the host. Hypersensitivity diseases include autoimmune diseases, in which immune responses are directed against self-antigens, and diseases that result from uncontrolled or excessive responses to foreign antigens. Because these reactions tend to occur against antigens that cannot be escaped (i.e., self-antigens) and because of positive feedback systems intrinsic to various aspects of the immune response, hypersensitivity diseases tend to manifest as chronic problems. The traditional classification for hypersensitivity reactions is that of Gell and Coombs and is currently the most commonly known classification system (Figure 3) [119].
\nHypersensitivity reactions. (A) Type I hypersensitivity. The binding of the antigen to preformed IgE antibodies bound to the surface of mast cells or basophils, causes the release of inflammatory mediators such as histamine, cytokines and metabolites of arachidonic acid, which produces clinical manifestations, such as septic shock, rhinitis allergic, allergic asthma and acute allergic reactions to drugs. (B) Type II hypersensitivity. Cytotoxic reactions involve the binding of both IgM and IgG antibodies to antigens bound to cells. The antigen–antibody binding results in the activation of the complement cascade and in the destruction of the cell to which the antigen is bound. (C) Type III hypersensitivity. Immunocomplexes are formed when the antigens bind to the antibodies. They are usually removed from the process by phagocytosis. However, the deposition of these immunocomplexes in the tissues or in the vascular endothelium can produce a tissue aggression mediated by immunocomplexes. (D) Type IV hypersensitivity. These types of reactions are not mediated by antibodies. Delayed hypersensitivity reactions are mediated primarily by T lymphocytes (cell-mediated immunity).
Immediate hypersensitivity reactions are mediated by IgE, but T and B cells play important roles in the development of these antibodies. The allergic reaction first requires sensitization to a specific allergen and occurs in genetically predisposed individuals. The allergen is either inhaled or ingested and is then processed by APC, such as a DCs, macrophage, or B-cell [120]. The APC then migrates to lymph nodes, where they prime
Type II or cytotoxic hypersensitivity [119] depends on the abnormal production of IgG or IgM directed against tissue antigens or a normal reaction to foreign antigens expressed on host cells. There are three main mechanisms of injury in type II reactions: (1) activation of complement followed by complement-mediated lysis or phagocytosis and removal by leukocytes; the IgG or IgM antibody can complex with antigens on the surface of cells or extracellular matrix and this complex then may activate complement. Complement activation will result in formation of the membrane attack complex (MAC) and cause osmotic lysis of the target cell; (2) antibody-dependent cellular cytotoxicity; the second type II reaction is called antibody-dependent cell-mediated cytotoxicity IgG antibodies that can bind FcγRIII on NK cells and macrophages, thus mediating the release of granzymes and perforin and resulting in cell death by apoptosis (ADCC); (3) inactivation of a biologically active molecule; disruption of biologically functional molecules can occur when autoantibodies bind to these molecules (Figure 3B). An example is antibody produced against acetylcholine receptors in myasthenia gravis resulting in increased turnover of the receptor at motor end-plates and subsequent muscular weakness or drug-induced hemolytic anemia [122, 123].
\nDrug-induced immune hemolytic anemia (DIIHA) is rare, and required to provide the optimal serological tests to confirm the diagnosis. The drugs most frequently associated with DIIHA at this time are cefotetan, ceftriaxone and piperacillin. DIIHA is attributed most commonly to drug-dependent antibodies that can only be detected in the presence of drug. The drug affects the immune system, causing production of red blood cell (RBC) autoantibodies; the clinical and laboratory findings are identical to autoimmune hemolytic anemia (AIHA), other than the remission associated with discontinuing the drug. Some of the mechanisms involved in DIIHA are controversial. The most acceptable one involves drugs like penicillin that covalently binds to proteins (e.g., RBC membrane proteins); RBCs become coated with drug in vivo and, a drug antibody (usually IgG) attaches to the drug-coated RBCs that are subsequently cleared by macrophages. The most controversial is the so-called immune complex mechanism, which has been revised to suggest that most drugs are capable of binding to RBC membrane proteins, but not covalently like penicillins. The combined membrane plus drug can create an immunogen; the antibodies formed can be IgM or IgG and often activate complement, leading to acute intravascular lysis and sometimes renal failure; fatalities are more common in this group. It is still unknown why and how some drugs induce RBC autoantibodies, sometimes causing AIHA [124].
\nType III reactions (immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation. An example is serum sickness. Type III hypersensitivity is caused by circulating immunocomplexes and is typified by serum sickness (a drug reaction in which multimeric drug-antibody aggregates form in solution). Preformed immunocomplexes deposit in various vascular beds and cause injury at these sites. Multimeric antigen-antibody complexes are efficient activators of the complement cascade through its classical pathway. The vascular beds in which immunocomplexes are deposited are determined in part by the physical nature of the complexes (their aggregate size, charge, hydrophobicity, etc.), and the specificity of deposition at locations can be surprisingly precise in some diseases (Figure 3C). Typical sites of injury are kidney, skin, and mucous membranes. Type III hypersensitivity is common in systemic lupus erythematosus (SLE) and underlies most of the pathophysiology of this chronic autoimmune disease. Some inflammatory reactions may blend features of type II and III hypersensitivity with the formation of immunocomplexes in situ [125].
\nType IV reactions (delayed hypersensitivity reactions and cell-mediated immunity) are mediated by T cells rather than by antibodies (Figure 3D). An example is contact dermatitis from poison ivy or nickel allergy, tuberculosis, leprosy and sarcoidosis. In tuberculosis, cellular hypersensitivity, the delayed type of allergy, may be defined as an immunological state in which lymphocytes and macrophages are directly or indirectly sensitive to tuberculin, activate macrophages [126], and can passively transfer delayed hypersensitivity to the normal host [127]. Lymphocytes, when exposed to tuberculin merely produce a toxic or irritating product affecting macrophages, whether they sensitize macrophages to tuberculin [128]. In tuberculosis, delayed hypersensitivity is both beneficial and detrimental. In low concentrations, tuberculin stimulates the development of immunity in macrophages. Therefore, the presence of hypersensitivity is an asset in preventing pulmonary tuberculosis for only small units of one to three bacilli that reach the alveolar spaces where the infections begins. In high concentrations, tuberculin kills macrophages and thus is responsible for the liquefaction of caseous foci. This process results in tremendous extracellular multiplication of tubercle bacilli followed by their spread throughout the bronchial tree and to the other people [129].
\nDespite the various immunological mechanisms to maintain tolerance to itself, there are certain individuals who develop autoimmunity. In 1986, the idea was postulated that the T and B cells specific for antigens coming from infecting pathogens, also generate a cross reaction against autoantigens even though the pathogens are eliminated. This type of response is initiated by low affinity T cells that have escaped the central tolerance. In addition, there is a genetic component capable of initiating and causing a persistence of autoimmunity and, therefore, trigger an autoimmune disease. However, epigenetic factors also play an important role in their development. They have been classified as a specific organism or systemic, with the genetic susceptibility in the alleles of class I and class II molecules, a large part of the cause of the occurrence of autoimmune diseases such as systemic lupus erythematosus and type I diabetes mellitus [90]. Thus, the appearance of polymorphisms in more than 50 genes, among which a small number has been identified that affect the expression of molecules involved in the general activation of T cells, causes a high susceptibility to type I diabetes. In the case of the presentation of systemic autoimmune diseases, genetic susceptibility occurs in the general activation of B lymphocytes, affecting the signaling and survival receptors, which allows the autoreactive B cells of higher affinity to escape from the negative selection. Also, the genetic deletion of certain TLRs, such as TLR-9, increases the susceptibility to manifest autoimmune diseases. Depositions of antigen-antibody complexes in tissues, such as kidney, have been an important factor in the manifestation of autoimmune diseases. This is due to the variation in certain genes such as those responsible for synthesizing the components of the complement and its receptors, which can initiate autoimmune pathologies. Another important factor that triggers autoimmunity is the loss of certain immunoregulatory mechanisms. Such is the case of a chronic stimulation of the TCR, by a persistent antigenic exposure that can deregulate the immune response through adaptive tolerance mechanisms. A loss of the anergy of autoreactive T lymphocytes, a failure in cell death by apoptosis of autoreactive T cells, the loss of suppression of these cells due to Tregs lymphocytes, polyclonal activation of autoreactive T lymphocytes, may also occur among other mechanisms that can trigger autoimmunity [130]. Finally, autoimmune diseases can affect a specific cell type, several cells or the entire organism. Its initiation will depend on the pathways by which the immunological tolerance is altered, being of great importance the genetic predisposition that certain individuals present.
\nAutoimmune diseases are a consequence of an immune reaction against an autoantigen. They can affect a single organ or cell type; however, they are usually also systemic, as is the case of the onset of rheumatoid arthritis or systemic lupus erythematosus.
\nSystemic lupus erythematosus (SLE) is a rare disease with a prevalence of 3.3 to 8.8 per 100,000 children. There is a high frequency reported in Asians, African Americans, Hispanics and Native Americans; the age at which it usually manifests is between 11 and 12 years of age and about 80% of adults who have SLE are women [131]. It is a multisystemic autoimmune disorder characterized by extended immunological dysregulation, formation of autoantibodies and immune complexes, resulting in inflammation and potential damage to a wide variety of organs. The clinical manifestation presented is nonspecific, such as the appearance of fever, fatigue, anorexia, alopecia and arthralgias. Symptoms such as generalized inflammation, including lymphadenopathy and hepatosplenomegaly, may manifest during the onset of SLE. However, the hallmark of this disease is the appearance of a butterfly-shaped malar rash. This condition can affect any organ of the system and its diagnosis is given through clinical manifestations and laboratory tests. Such is the case of the search for antibodies such as antinuclear antibodies (ANA), which are present in the serum of almost 98% of patients with SLE; Anti-dsDNA antibodies are present between 61 and 93% of patients with active disease; Anti-Smith antibodies are highly specific, but they can be found only in almost 50% of patients; Antibodies such as anti-Ro, anti-La, anti-U1RNP, anti-histones and rheumatoid factor, can also be used as a diagnosis of SLE. The indicated treatment is according to the activity of the disease and its severity, as well as the organs affected by the SLE. The immunopathogenesis of this disease is mediated by the recruitment of autoreactive T cells and excessive plasma levels of proinflammatory cytokines. In addition, dendritic cells and subpopulations of T cells such as Th1, Th17 and regulatory T cells are significantly altered in function and number. However, the fundamental immunological dysfunction in the appearance of SLE is the loss of tolerance to nuclear antigens. There are defects that promote the presentation of autoantigens and the response to apoptotic residues in an immunogenic form; also, those faults that affect the signaling of the T or B cells, which causes the autoreactive abnormal stimulation of the lymphocytes; as well as those defects that promote the survival of autoreactive lymphocytes. Therefore, the loss of immunological tolerance is a factor that causes the presentation of systemic lupus erythematosus [132].
\nRheumatoid arthritis (RA) is a chronic inflammatory multisystem disease characterized by destructive synovitis, in which all joints can be affected, mainly the small joints of the hands and feet. RA is a chronic progressive disease that results in decreased functional capacity and quality of life. It can manifest in individuals with genetic predisposition; however, it is of unknown etiology. It affects 0.2 to 2% of the worldwide, in a population of 40 years old, although it could happen at any age [133]. The diagnosis of RA occurs through the presentation of clinical manifestations, such as the onset of arthritis of at least 3 joints and morning stiffness of more than 30 minutes, as well as an exacerbated joint inflammation with the presence of pain. Likewise, blood concentrations of C-reactive protein and rheumatoid factor are evaluated, which will be elevated depending on the inflammatory activity of the RA. Another determinant with a high probability for the diagnosis of the disease is the evaluation of anti-CCP antibodies. The immunopathogenesis of RA results from the loss of immunological tolerance, with the consequence of an elevated secretion of proinflammatory cytokines such as IL-6, which is found in some patients, in high quantities in synovial fluid. In addition, the formations of autoantibodies that attack the joints of the entire organism are among the main causes of the presentation of RA [134].
\nThe immune system is characterized by a network of complex mechanisms whose main objective is to protect the body. However, if there is a failure in its regulation, it can generate hypersensitivity and/or autoimmunity. For this reason, it is very important to know how our immune system works and how these pathologies originate. Currently, anaphylactic shock and skin reactions are the most frequent hypersensitivity reactions affecting organs and tissues. There are several mechanisms and factors involved which triggers hypersensitivity reactions. On the other hand, although autoimmune diseases are relatively common and our current knowledge about the mechanisms involved in their pathogenesis is very limited.
\nThanks to the authors who collaborated in the writing of this chapter: Dr. José Luis Muñoz, Dra. Flor Pamela Castro, Dra. Francisca Chávez, Dra. Isabel Chávez, Dr. José Luis Martínez and Dra. Marcela Hernández; as well as the Universities involved: Cuauhtémoc University Aguascalientes, Autonomous University of Durango Campus Zacatecas and Autonomous University of Zacatecas. Thanks for the financial support for chapter publication.
\nWe have no conflict of interest related to this work.
Recently, the space industry has pointed out that in the past 5 years, the commercial market has been driving the advancement of satellite technology. Lockheed Martin is building commercial satellites (e.g., Hellas-sat series) with advanced on-board processing capabilities for the Saudi Arabian [1]. Hellas satellites probably will be the first commercial HTS with a very advanced digital processor on-board. The focus of this chapter will be on commercial satellite systems for communication applications, and a comparison study between commercial HTS and typical satellites systems conducted by Inmarsat will be provided [2].
For communication applications, commercial satellite systems have been categorized as mobile satellite services (MSSs), fixed satellite services (FSSs), broadcast satellite services (BSSs), and high-throughput satellite (HTS) services. Depending on the services, satellite payload architecture will be designed to meet the specified requirements for that service. Basically, satellite payload architecture can be classified into four categories: (1) analog bent-pipe satellite (ABPS); (2) digital bent-pipe satellite (DBPS); (3) advanced digital bent-pipe satellite using digital channelizer and beamformer (AdDBPS-DCB); and (4) advanced regenerative on-board processing satellite (AR-OBPS). This chapter provides an overview of these payload architectures and presents two satellite system architectures using AdBPS-DCBS and AR-OBPS payloads for the fifth-generation cellular phone (5G) applications.
The chapter is organized as follows: Section 2 provides a comparison between commercial HTS and typical satellite systems; Section 3 discusses the typical satellite network topologies; Section 4 presents an overview of legacy ADPS transponder, existing DBPS transponder, AdBPS-DCBS transponder, and AR-OBPS satellite system; Section 5 discusses the use of AdBPS-DCBS transponder and AR-OBPS payloads for the fifth-generation cellular phone (5G) applications; and Section 6 concludes the chapter with a summary and brief discussion of way forward.
Typical and regular commercial satellites are operating in C-band, Ku-band, and Ka-band with downlink frequencies approximately at 4, 12, and 40 GHz, respectively. For C-band, Ku-band, and Ka-band, the spectrum bandwidths available by geostationary orbital position are 500 MHz, 500 MHz, and 3.5 GHz, respectively. Typical antenna types for these regular commercial satellites are pointed antenna type with a single beam. Typical diameters for these pointed antennas are (a) greater than 1.8 m for C-band; (b) 0.9–1.2 m for Ku-band; and (c) 0.6–1.2 m for Ka-band satellite. Figure 1(a) illustrates a typical regular commercial satellite.
Typical commercial satellites and HTS configurations.
Typical HTSs are usually also operating in Ku-band and Ka-band with the same downlink frequencies as the regular satellites except that they employ multiple pointed beam as oppose to a single-pointed beam. Figure 1(b) describes a multiple beam HTS system. The salient feature of multiple beams is the frequency reuse. The frequency reuse is defined as the number of times a satellite can reuse the same spectrum and frequencies. However, high frequency reuse factor can cause potential cochannel interference or an increase in carrier-to-interference power ratio (CIR or C/I). IMMARSAT has reported that a reuse factor of 5–30 is possible with multiple spot beams employed by commercial HTS. Depending on the number of beams implemented on-board of the satellite, the cost for HTS can be twice of the cost for a regular satellite. But, the cost per bit for HTS is much lower than the regular satellite. HTS is a preferred option for point-to-point services, for example, beyond line-of-sight (BLOS) cellular phone services. Table 1 provides a summary of the comparison of HTS and regular commercial satellites [2].
Comparison factor | Typical regular commercial satellite | Typical high-throughput satellite (HTS) | Remark |
---|---|---|---|
Operational frequency band | C-band, Ku-band, Ka-band | Ku-band, Ka-band | It should be noted that for data presented here, all satellites and supply are not equal; various technical, regulatory, and commercial parameters come into play when comparing the two-type satellites. Data collected from IMMARSAT. Source: see [2] |
Throughput capability (Gbps) | ~1–10 | ~5–300+ (with frequency reuse in multiple spot beam) | |
Typical cost including launch (USD) | ~200–300 | ~300–500 (cost can be twice of regular satellite) | |
Advantages | Wide coverage; preferred solution for point-to-multipoint communication | Higher bandwidth/lower cost per bit; preferred option for point-to-point services | |
Disadvantages | Limited supply available; lower spectrum efficiency for an equivalent frequency | Higher upfront costs; difficult to find enough customers to fill each of the beams |
Comparison of typical commercial satellites and HTS.
This section describes the most commonly used satellite network topologies, namely “Star” satellite network (Section 3.1) and “Mesh” satellite network (Section 3.2).
A typical commercial satellite network topology consists of an uplink from a central anchor station (aka satellite Gateway or satellite Hub) to a satellite and a downlink from the satellite to users. Users can be mobile or fixed users. Mobile users can be located in an airplane, a boat, or a car. Fixed users can be located in a building or a cellular base station. The “star” satellite network is derived from a spoke-hub distribution paradigm in computer networks, where one central hub serves as a conduit to transmit messages among network users [3]. Thus, for star satellite networks, all communications will be passed through a satellite gateway. As shown in Figure 2, if Mobile User 1 wants to talk to Mobile User 2, Mobile User 1 needs to send its messages to the satellite gateway (yellow lines), and satellite gateway relays that messages to Mobile User 2 (red lines).
Typical “star” satellite network.
The “mesh” satellite network topology is derived from a local network topology, where the network nodes are corrected to each other directly, dynamically, and nonhierarchically to as many other nodes as possible [4]. In this network topology, the network nodes can cooperate with one another to route data from one user to another user efficiently. Hence, for mesh satellite network, Mobile User 1 can talk to fixed user directly without going through the satellite gateway (solid lines), and Mobile User 2 can also talk to the fixed user directly (dash lines). Any one of the user within the network can send the messages to a terrestrial network through the red lines representing uplink and downlink between the satellite gateway and the satellite (Figure 3).
Typical “mesh” satellite network.
Star satellite network topology does not require advanced satellite payload processing on-board and multiple beam, but mesh satellite network requires advanced on-board processing and multiple beam allowing one user to communicate to another user automatically and effectively. Section 4 discusses various satellite payload architectures used in regular satellite and HTS for star and mesh satellite network applications.
This section presents an overview of legacy, existing, and advanced satellite payload architectures. Section 4.1 presents legacy ABPS payload architecture, Section 4.2 provides a description of a typical existing DBPS payload architecture, Section 4.3 discusses AdDBPS-DCB payload architecture, and Section 4.4 provides an overview of AR-OBPS payload architecture.
A typical legacy ABPS payload architecture is depicted in Figure 4, where the payload has multiple beam antennas (MBAs) using parabolic dishes. For this architecture, the RF signal is received at the satellite payload and amplifies by a low noise amplifier (LNA) for increased received signal-to-noise power ratio (SNR). The RF signal with increased SNR is downconverted (D/C) to an intermediate frequency (IF) and processed by an IF filter to clean up the signal from adjacent interference and out-of-band noise. The clean-up signal is then (a) routed to the proper downlink port by an IF analog switching circuit and upconverted (U/C) to RF, (b) combined by a multiplexer (MUX), and (c) amplified by a high-power amplifier (HPA) for downlink transmission.
Legacy ABPS payload architecture.
As illustrated in Figure 5, there are two options for the D/C, namely Option 1 (see Figure 5(a)) is a double downconverter using two local oscilators (LOs) to downconvert RF signal to IF signal with stable and low phase noise, and Option 2 (see Figure 5(b)) is single downconverter using a LO downconverting RF signal directlty to an IF signal. Option 1 is being used in many legacy, existing, and advanced satellite payloads. Option 2 is mostly used in advanced satellite payloads.
Options for RF downconversion and associated LO’s phase noise.
Figure 5(c) shows commercial-of-the-shelf (COTS) phase noise characteristics for typical LOs operating at X-band, Ku-band, and Ka-band. X-band, Ku-band, and Ka-band illustrated in this figure correspond to 7–11.2, 12–18, and 26.5–40 GHz, respectively. The main advantages of Option 2 using single downconversion are its low cost, small size, and low power consumption (also known as small SWAP-C). This option uses the smallest number of external components as compared to Option 1 using double downconversion, which is also known as super heterodyne receiver [5]. However, Option 2 suffers amplitude and phase imbalances caused by imperfect references associated with I-Q components, direct current (DC) signal due to self-mixing, and flicker noise.1 Option 1 does not suffer from these problems and offers excellent selectivity and sensitivity, that is, better rejection of adjacent interferences. Option 1’s disadvantages are the integration complexity and high SWAP-C.
In satellite electronic communications, MUX is a multiplexer, which is a device that selects several (multiple) analog (or digital) input signals and outputs a single signal. Figure 6(a) describes a functional MUX (aka multiplexer) circuit. On the contrary, Figure 6(b) depicts a DEMUX (aka demultiplexer), which is an electronic device that sends a single input signal to multiple signal outputs.
Functional block diagrams of MUX and DEMUX.
Figure 7 presents an existing DBPS payload architecture using on-board digital channelizer. Similar to analog payload, there are two options for the RF-to-IF downconversion process. Double-downconversion process is typically used for digital bent-pipe payload architecture.
Existing DBPS payload architecture.
Figure 8 depicts typical RF-to-IF (or baseband) downconversion and digitization and sampling processes for a commercial DBPS payload architecture. The RF-to-IF process shown in this figure uses Option 1, double downconversion, and the digitization and sampling process employing bandpass sampling with digital quadrature technology [6]. The RF bandwidth (BW) associated with the RF bandpass filter (BPF) is selected to match with an over channel bandwidth (e.g., a maximum of 500 MHz for Ku-band). The automated gain control (AGC) is designed to maintain a constant power over the specified channel bandwidth. There are several advantages associated with bandpass sampling with digital quadrature techniques, including (a) no phase and amplitude imbalances; (b) digital finite impulse response (FIR) filters are flexible and computational complexity with linear phase introducing a constant group delay; (c) only one A/D converter is required (less weight and power); and (d) when the sampling period is set at one-quarter of the carrier frequency, the reference in-phase and quadrature components reduce to an alternating sequence between I-channel and Q-channel [6].
Typical R/F downconversion and digitization processing approach.
As shown in Figure 9, the key design issue associated with the digitization and sampling processing is the selection of required number of bits of the analog-to-digital (A/D) conversion to (1) achieve optimum loading factor (LF) and (2) minimize the quantization noise. The LF is defined as the root mean square (RMS) of the total input signal voltage-to-A/D converter saturation voltage ratio. The total input signal voltage includes desired signal voltage (S) plus noise voltage (N) plus interference voltage (I). Figure 10 illustrates an optimum LF as a function of number of bit of a typical A/D converter. As an example, for 4-bit, the optimum LF is about 0.4. In conjunction with LF, the number of bit should be selected to maximize the signal-to-quantization noise ratio (SQNR) using the following relationship:2
Existing digitization and sampling processing using bandpass sampling with digital quadrature technique.
Optimum LF as a function of number of bit of A/D converter.
As an example, when
The key feature of DBPS payloads is the flexibility of the digital channelizer. Current digital technologies allow for the implementation of robust and reconfigurable digital channelizer adapting to require the number of users and associated users’ data rates. A typical flexible digital channelizer using polyphase/discrete Fourier transform (DFT) technology is shown in Figure 11.
Typical digital channelizer using polyphase/DFT technology.
As shown in Figure 11, the heart of a typical digital channelizer is a polyphase-filter network (or simply a polyphase network) and a DFT processor. A typical polyphase network with a DFT processor is described in Figure 12. The polyphase network consists of a set of NC digital filters with transfer function H0, H1..., HNc-1, which is obtained by shifting a basic low pass complex filter function along the frequency axis [7]. As an example, for a typical 500 MHz channel bandwidth, assuming for a typical user data rate of 4 MHz and a guardband of 1 MHz, digital channelizer, NC = 500/(4 + 1) = 100, that is, the number of filter is 100, and each has a total of 5 MHz bandwidth. A change in sampling frequency by a factor of NC can be introduced, thus allowing the circuit in different paths of the polyphase network to operate at lower frequency than the original sampling frequency. A practical implementation of a high-throughput low-latency polyphase channelizer can be found in [8, 9].
Typical Polyphase/DFT Technology.
Figure 12 shows an example of five input signals, namely S1, S2, S3, S4, and S5, and the channelizer will select signal interest by filtering out the other signals. As an example, the signal line with the filter transfer function of H0 filters out S2, S3, S4, and S5 and sends S1 as an output signal.
For a typical commercial HTS system architecture, it usually requires on-board multiple beam phase array (PA) antenna with associated adaptive digital beamformer network (DBF) for spot beamforming and frequency reusing of the spot beams when the beams are not located near each other. Figure 13 describes a typical AdDBPS-DCB payload architecture, where the digital channelizer is combined with a DBF to make a “digital channelizer and beamformer” (DCB) [10, 11, 12]. For this payload architecture, the key feature that differentiates this architecture with the ones discussed above is the combined digital channelizer using polyphase network/DFT processor and DBF (PolyN/DFT-DBF).
AdDBPS-DCB payload architecture.
As pointed out in [10, 11, 12], DCB architecture shown in Figure 13 can be designed to (1) form individual beams for each active receive and transmit communication channels; (2) adaptively generate channel beam steering weights to dynamically vary the bandwidth, location, and shape of each beam based on traffic demands and the locations of other, potentially interfering beams avoiding adjacent channel interference; (3) use digital beamforming weight calibration to compensate for the temporal and thermal phase and amplitude response variations inherent in analog multibeam phased array antennas; and (4) adjust the gain of individual receive-and-transmit channel beams automatically to compensate for propagation path and analog payload response variations. In general, there are two possible DCB implementation approaches, namely DCB Approach 1 and DCB Approach 2 [13]. Figure 14 describes the DCB Approach 1 for processing the uplink signals, where the uplink signals are individually processed by the digital channelizer (i.e., PolyN/DFT processing) and DBF independently and separately. DCB Approach 1 requires a larger computational load because each DBF processes all the user link bandwidth (e.g., S1, S2, S3, S4, and S5 in Figure 12) at all times to form multiple beams.
DCB Approach 1: PolyN/DFT and DBFN individual processing.
DCB Approach 2 is shown in Figure 15, where DCB utilizes an unified processing approach with each DBF processes only the bandwidth corresponding to a beam (S1 in Figure 12) at normal times. During anomaly operation condition (e.g., natural disaster event), when the bandwidth has to be reassigned to specific areas, the arithmetic load on DBF can be reduced by implementing multiple DBFs, with each capable of processing a bandwidth narrower than that assigned to a beam (i.e., smaller channel unit). This approach enables a reduction in wasteful arithmetic resource usage on bandwidth.
DCB Approach 2: Unified and combined PolyN/DFT and DBFN individual processing.
If one defines the number of multipliers, D implemented in each Tx/Rx DBF as C/fop, where C is the computational load of a DBF (multiplications/sec), and fop is the operation frequency of the multiplier. Let us compare D calculations between DCB Approach 1 and DCB Approach 2. Let us assume the following parameters:
and that for DCB Approach 2 configuration becomes [13]:
The latter calculation assumes an ideal case in which DBF network (DFBN) processing is performed on a channel-by-channel basis. The complexity of DCB Approach 2 configuration is 10 times less complex than DCB Approach 1.
As pointed out in [12], the DBFN when coupled with a digital channelizer (aka DCB) offered more capabilities with many advantages. Nguyen et al. [14] developed a computer simulation model of a typical DBFN in MATLAB and presented simulation results for X, Ku, and Ka BFNs using 60-element, 104-element, and 149-element, respectively. Figure 16 is an extracted Ka-band BFN result showing the achievable antenna gain of 45.5 dB at 3-dB beamwidth of 0.9°. For practical applications, the DBFN will shape the beam size depending on the coverage area and desired number of beams. Nguyen et al. [14] pointed out that for 2.5° coverage area and the desired number of beams of 7, the minimum 3-dB beamwidth of 1.1° is required. Nguyen et al. [14] also pointed out that DCB can provide a significant increase in frequency reuse, where the frequency reuse is defined as the number of times a satellite can reuse the same spectrum and frequencies. High frequency reuse factor can cause potential cochannel interference (CCI) that results in a decrease in carrier-to-interference power ratio [aka (C/I) CCI]. As pointed out in [14], for dynamic allocation using real-time allocation of beams so that the coverage radius of a cell is equal to the satellite pointing error, assuming satellite pointing error of 0.02 degree pointing error, the (C/I)CCI is about 25 dB for frequency reuse factor 40 [14].
Antenna beamwidth and gain of a notional Ka-band DBFN with 12-bit quantization [
Figure 17 depicts a potential future AR-OBPS payload architecture [10]. The payload includes (1) a typically set of digitized analog multiple beam antenna (MBA) input signals, digitally frequency division demultiplex each input signal to produce single carrier per channel (SCPC) signal data and demodulate and decode individual traffic channels to recover the original information bits transmitted on the uplink; (2) a set of digitized analog multibeam phase array antenna (MB-PAa) input signals, digitally frequency division demultiplex each input signal to produce SCPC signal data and demodulate and decode individual traffic channels to recover the original information bits transmitted on the uplink; and (3) fast packet switches are typically employed at the AR-OBPS payload’s core to realize statistical multiplexing gains by efficiently packing and moving data through the switch and onto the downlink in bursty uplink transmission applications. Moreover, the digital bandwidth (in Hz) through the AR-OBPS switch is at least 25 times less3 than that supported by an equivalent (pre-demodulation) digital baseband switch at the center of a DC- or DCB-based system. AR-OBPS payload can also support digital beamforming, following the frequency division demultiplexing operation, if a phased array is employed in place of the analog MBA. On the secondary (output) side of the switch, each user’s binary information is channel encoded and modulated onto a carrier. The modulated carrier data thus produced are multiplexed, digital-to-analog converted, and passed through an analog reconstruction filter to generate output signals for the transmit portion of the communication payload. The channel codes and modulations employed on the uplink (input) communication channels clearly do not need to be the same as the channel codes and modulations used on the transmitted downlink channels. Hence, an AR-OBPS payload can serve as a “translator” facilitating single-hop communications between terminals employing different link protocols. However, if either the digital multichannel demultiplexer (DMCD), demodulator, decoder, or digital multichannel multiplexer (DMCM) encoder modulator, multiplexer (MCEM2) functions are implemented in ASICs to minimize size-weight-and-power (SWaP), then the AR-OBPS system becomes somewhat inflexible, unable to support either uplink or downlink terminals, respectively, using communication protocols differing from those for which the AR-OBPS was specifically designed. For this reason, AR-OBPS systems are typically employed in support of “private networks” in which the communication satellite service provider only accommodates terminals designed to work on the provider’s network. Iridium and Spaceway are two examples of commercial AR-OBPS-based communication satellite systems.
AR-OBPS payload architecture.
Sections 5.1 and 5.2 present a notional satellite system architecture using AdBPS-DCBS satellite payload and AR-OBPS satellite system architecture for 5G cellular phone applications, respectively.
AdBPS-DCBS satellite payload can be used to support 5G users. There are potentially two satellite system architecture options for using AdBPS-DCBS satellite payload to support 5G mobile user equipment (aka 5G-UE), namely AdBPS-DCBS Option 1 and AdBPS-DCBS Option 2. For AdBPS-DCBS Option 1, the AdBPS-DCBS satellite provides communication services directly to 5G-UEs. While in AdBPS-DCBS Option 2, the satellite provides services to 5G-UEs through the 5G relay nodes (RNs). Figure 18 illustrates the AdBPS-DCBS satellite system architecture for (a) AdBPS-DCBS Option 1 and (b) AdBPS-DCBS Option 2 [15].
AdDBPS-DCB satellite system architectures for supporting 5G users.
Figure 18(a) shows that the AdBPS-DCBS satellite requires new radio (NR) interfaces between (1) AdBPS-DCBS satellite and terrestrial gateway (GW) and (2) AdBPS-DCBS satellite and 5G-UEs. In addition, it is also required a 5G narrow-band (gNB) processing station to process the 5G signals from the next generation core (NGC) network before passing the 5G data to public data network.
Similar to AdBPS-DCBS satellite payload, AR-OBPS satellite payload can also be used to support 5G users. There are also two satellite system architecture options for using AR-OBPS payload to support 5G mobile user equipment, namely AR-OBPS Option 1 and AR-OBPS Option 2. For AR-OBPS Option 1, the AR-OBPS satellite provides communication services directly to 5G-UEs. For AR-OBPS Option 2, the satellite provides services to 5G-UEs through the 5G RNs. Figure 19 describes these two AR-OBPS architecture options, namely (a) for AR-OBPS Option 1 and (b) for AR-OBPS Option 2. For these two system architecture options, the gNB processing is now incorporated into the AR-OBPS satellite payload and no longer required for the ground system. The GW now can pass the 5G data directly to the NGC. The decoding-demodulation and encoding-modulation processing on-board of the satellite will be designed to align with the 5G waveform specifications, including 5G modulation and coding schemes.
AR-OBPS satellite system architectures for supporting 5G users.
Figure 19(a) shows that the AR-OBPS satellite also requires NR interfaces between (1) AR-OBPS satellite and GW and (2) AR-OBPS satellite and 5G-UEs. Similar to AdBPS-DCBS satellite system architecture options, the NR interfaces between the AR-OBPS satellite and 5G-UEs are new. Since the gNB processing is now placed at AR-OBPS satellite payload, the NR interfaces between AR-OBPS satellite and 5G-UEs are not the same as the AdBPS-DCBS satellite and 5G-UEs. To show the differences between the two, Figures 19(a) and (b) use Sat-NG-C and Sat-NG-U to indicate the new radio interface between (1) terrestrial GW-NGC-and-AR-OBPS satellite and (2) AR-OBPS satellite-and-terrestrial GW-NGC, respectively.
This chapter uses a top-down approach for providing an overview of legacy, existing, and future advanced satellite payload architectures for future wireless communication applications. The chapter focuses on the commercial satellite technologies based on the research results presented in [1, 2]. Section 2 provides the comparison results performed by Inmarsat describing the technical characteristics and associated advantages and disadvantages between commercial HTS and typical satellite systems currently available in commercial satellite market. In Section 3, two most commonly satellite network topologies used by existing commercial satellite networks are presented, and the concept of satellite uplink and downlink associated with star satellite network and mesh satellite network is discussed. The satellite network topologies presented lead to Section 4, where four satellite payload architectures are discussed. The legacy analog ABPS payload architecture is shown to be more appropriate for star satellite network than mesh network. Existing digital DBPS and AdDBPS-DCB payload architectures are designed for supporting mesh satellite network with large number of mobile users. Future advanced digital satellite payload architecture, namely AdDBPS-DCB, is also presented in this section. With decoding-demodulating and encoding-modulating processing on-board of the satellite, AR-OBPS allows for packet switching on-board and higher quality of service (QOS) than existing DBPS and AdDBPS-DCB at the expense of higher SWAP-Cost (SWAP-C). Section 4 of the chapter discusses the applications of AdBPS-DCBS and AR-OBPS payloads for supporting 5G users. Four satellite system architecture options are presented for supporting the future 5G users.
The preparation of this chapter was not funded by Gulfstream, and it was done by the author using his own time and resources; thus, it does not represent the Gulfstream’s view on the results presented in this chapter.
The author wishes to thank his wife, Annie Luu-Nguyen, for her immense patience and support.
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Awareness for increased agricultural production is on the increase, arising from the need to feed the ever-increasing human population. Interestingly, almost all agricultural activities generate wastes, which are generated in large quantities in many countries. However, these wastes may constitute a serious threat to human health through environmental pollution and handling them may result in huge economic loss. Unfortunately, in many developing countries where large quantities of these wastes are generated, they are not properly managed because little is known about their potential risks and benefits if properly managed. There are studies that address some of the challenges of agricultural solid wastes as well as suggestions on how they can be properly managed. In this chapter, we intend to explore the major sources of agricultural solid wastes, their potential risks, and how they can be properly managed.",book:{id:"9873",slug:"strategies-of-sustainable-solid-waste-management",title:"Strategies of Sustainable Solid Waste Management",fullTitle:"Strategies of Sustainable Solid Waste Management"},signatures:"Isaac Oluseun Adejumo and Olufemi Adebukola Adebiyi",authors:[{id:"276527",title:"Dr.",name:"Isaac Oluseun",middleName:null,surname:"Adejumo",slug:"isaac-oluseun-adejumo",fullName:"Isaac Oluseun Adejumo"},{id:"328699",title:"Dr.",name:"O.A.",middleName:null,surname:"Adebiyi",slug:"o.a.-adebiyi",fullName:"O.A. 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Through a survey of 312 households, the study analyzed the performance improvement, regulatory policy, and sustainable service delivery of solid waste management in the municipalities. The study found that there were no mechanisms for full cost recovery to include majority of the residents, who patronize communal collection service. The study therefore recommends the adherence to normative standards and agreed rules, adoption, and use of appropriate cost recovery strategies for low-income groups as well as the restructuring of institutional arrangements to ensure user involvement and enforcement of legislation to improve municipal solid waste management in Ghana.",book:{id:"8580",slug:"municipal-solid-waste-management",title:"Municipal Solid Waste Management",fullTitle:"Municipal Solid Waste Management"},signatures:"Richard Kyere, Michael Addaney and Jonas Ayaribilla Akudugu",authors:[{id:"273978",title:"Ph.D. Student",name:"Michael",middleName:null,surname:"Addaney",slug:"michael-addaney",fullName:"Michael Addaney"},{id:"273981",title:"Mr.",name:"Richard",middleName:null,surname:"Kyere",slug:"richard-kyere",fullName:"Richard Kyere"},{id:"273982",title:"Dr.",name:"Jonas Ayaribilla",middleName:null,surname:"Akudugu",slug:"jonas-ayaribilla-akudugu",fullName:"Jonas Ayaribilla Akudugu"}]},{id:"65314",title:"Municipal Solid Waste Disposal in Mangrove Forest: Environmental Implication and Management Strategies in the Niger Delta, Nigeria",slug:"municipal-solid-waste-disposal-in-mangrove-forest-environmental-implication-and-management-strategie",totalDownloads:1031,totalCrossrefCites:2,totalDimensionsCites:4,abstract:"Niger Delta is an oil rich region situated in the southern part of Nigeria. It is made up of nine states which hosts oil industries. There are a handful of businesses (super market, manufacturing companies, etc.) that service the over 40 million people living in the cities. This situation had led to the increase in solid waste in the city. Because of the problem of over population, and poor waste management strategies (e.g., lack of recycling habit and lack of equipment) the mangrove forest had become a dumping ground for waste. This action has impacted the health of aquatic and terrestrial organisms, and has created a public health disaster for citizens because of increase in heavy metal concentration up the food chain. This chapter therefore, identifies poverty, lack of planning, poor behavior and poor technology as key factors affecting effective waste management in the Niger Delta. It suggests that good waste management system can be worked out if there is coordination between research institution and government in the implementation of recommendation by research institutes. Attitudinal change is also necessary on the part of citizens and government to enable a healthy interaction for the purpose of managing waste effectively.",book:{id:"8580",slug:"municipal-solid-waste-management",title:"Municipal Solid Waste Management",fullTitle:"Municipal Solid Waste Management"},signatures:"Aroloye O. Numbere",authors:[{id:"215285",title:"Dr.",name:"Aroloye O.",middleName:null,surname:"Numbere",slug:"aroloye-o.-numbere",fullName:"Aroloye O. 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Nigeria is estimated to have over 178.5 million people and kg/capita/day of 0.26–1.02 MSW, projected to increase with the expansion of the economy which is in need of better articulated MSW management strategies. The enormous natural inland surface and groundwater resources are daily challenged directly and indirectly, through decline in physical, chemical and biological quality. Solid waste disposal along the waterways and leachates from natural activities on materials at dumpsites and landfills was strongly identified and recognized as the source of pollutant inputs. The immediate and projected public health consequences in changes in inland waters were provided for resident aquatic organisms, some of which serves as food for resident human populations that are largely dependent on these water bodies for their daily water requirements.",book:{id:"8580",slug:"municipal-solid-waste-management",title:"Municipal Solid Waste Management",fullTitle:"Municipal Solid Waste Management"},signatures:"Akindayo A. 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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. 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He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. 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He has been a member of the IASTED Technical Committee on Image Processing from 2007 and a member of the IASTED Technical Committee on Artificial Intelligence and Expert Systems from 2011. \n\nHe has held the general chair position for the following: ACM-APPIS (2020, 2021), IEEE-IWOBI (2019, 2020 and 2020), A PPIS (2018, 2019), IEEE-IWOBI (2014, 2015, 2017, 2018), InnoEducaTIC (2014, 2017), IEEE-INES (2013), NoLISP (2011), JRBP (2012), and IEEE-ICCST (2005)\n\nHe is an associate editor of the Computational Intelligence and Neuroscience Journal (Hindawi – Q2 JCR-ISI). He was vice dean from 2004 to 2010 in the Higher Technical School of Telecommunication Engineers at ULPGC and the vice dean of Graduate and Postgraduate Studies from March 2013 to November 2017. 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He has (co)authored more than 150 publications in indexed journals, international conferences and book chapters, 1 book (in Greek), 3 edited books, and 5 journal special issues. His publications have more than 2100 citations with h-index 27 (GoogleScholar). His research interests include computer/machine vision, machine learning, pattern recognition, computational intelligence. \nDr. Papakostas served as a reviewer in numerous journals, as a program\ncommittee member in international conferences and he is a member of the IAENG, MIR Labs, EUCogIII, INSTICC and the Technical Chamber of Greece (TEE).",institutionString:null,institution:{name:"International Hellenic University",institutionURL:null,country:{name:"Greece"}}},editorTwo:null,editorThree:null},{id:"25",title:"Evolutionary Computation",coverUrl:"https://cdn.intechopen.com/series_topics/covers/25.jpg",isOpenForSubmission:!0,editor:{id:"136112",title:"Dr.",name:"Sebastian",middleName:null,surname:"Ventura Soto",slug:"sebastian-ventura-soto",fullName:"Sebastian Ventura Soto",profilePictureURL:"https://mts.intechopen.com/storage/users/136112/images/system/136112.png",biography:"Sebastian Ventura is a Spanish researcher, a full professor with the Department of Computer Science and Numerical Analysis, University of Córdoba. 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In the last five years, he has published more than 60 papers in international journals indexed in the JCR (around 70% of them belonging to first quartile journals) and he has edited some Springer books “Supervised Descriptive Pattern Mining” (2018), “Multiple Instance Learning - Foundations and Algorithms” (2016), and “Pattern Mining with Evolutionary Algorithms” (2016). He has also been involved in more than 20 research projects supported by the Spanish and Andalusian governments and the European Union. He currently belongs to the editorial board of PeerJ Computer Science, Information Fusion and Engineering Applications of Artificial Intelligence journals, being also associate editor of Applied Computational Intelligence and Soft Computing and IEEE Transactions on Cybernetics. Finally, he is editor-in-chief of Progress in Artificial Intelligence. 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He obtained both his M.Sc. and Ph.D. from the University of Liverpool, England, in the field of Intelligent Systems. He is a full professor at the Universidad Autonoma de Queretaro, Mexico, and a member of the National System of Researchers (SNI) since 2009. Dr. Aceves Fernandez has published more than 80 research papers as well as a number of book chapters and congress papers. He has contributed in more than 20 funded research projects, both academic and industrial, in the area of artificial intelligence, ranging from environmental, biomedical, automotive, aviation, consumer, and robotics to other applications. He is also a honorary president at the National Association of Embedded Systems (AMESE), a senior member of the IEEE, and a board member of many institutions. 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Dr. Aydin is currently a Fellow of Higher Education Academy, UK, a member of EPSRC College, a senior member of IEEE and a senior member of ACM. In addition to being a member of advisory committees of many international conferences, he is an Editorial Board Member of various peer-reviewed international journals. 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Carvajal-Gámez, Guillermo Urriolagoitia-Sosa and Alberto J. 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(Eng.) in Telematics from the Universidad de Colima, Mexico. He obtained both his M.Sc. and Ph.D. from the University of Liverpool, England, in the field of Intelligent Systems. He is a full professor at the Universidad Autonoma de Queretaro, Mexico, and a member of the National System of Researchers (SNI) since 2009. Dr. Aceves Fernandez has published more than 80 research papers as well as a number of book chapters and congress papers. He has contributed in more than 20 funded research projects, both academic and industrial, in the area of artificial intelligence, ranging from environmental, biomedical, automotive, aviation, consumer, and robotics to other applications. He is also a honorary president at the National Association of Embedded Systems (AMESE), a senior member of the IEEE, and a board member of many institutions. His research interests include intelligent and embedded systems.",institutionString:"Universidad Autonoma de Queretaro",institution:{name:"Autonomous University of Queretaro",institutionURL:null,country:{name:"Mexico"}}}]},{type:"book",id:"7726",title:"Swarm Intelligence",subtitle:"Recent Advances, New Perspectives and Applications",coverURL:"https://cdn.intechopen.com/books/images_new/7726.jpg",slug:"swarm-intelligence-recent-advances-new-perspectives-and-applications",publishedDate:"December 4th 2019",editedByType:"Edited by",bookSignature:"Javier Del Ser, Esther Villar and Eneko Osaba",hash:"e7ea7e74ce7a7a8e5359629e07c68d31",volumeInSeries:2,fullTitle:"Swarm Intelligence - Recent Advances, New Perspectives and Applications",editors:[{id:"49813",title:"Dr.",name:"Javier",middleName:null,surname:"Del Ser",slug:"javier-del-ser",fullName:"Javier Del Ser",profilePictureURL:"https://mts.intechopen.com/storage/users/49813/images/system/49813.png",biography:"Prof. Dr. Javier Del Ser received his first PhD in Telecommunication Engineering (Cum Laude) from the University of Navarra, Spain, in 2006, and a second PhD in Computational Intelligence (Summa Cum Laude) from the University of Alcala, Spain, in 2013. He is currently a principal researcher in data analytics and optimisation at TECNALIA (Spain), a visiting fellow at the Basque Center for Applied Mathematics (BCAM) and a part-time lecturer at the University of the Basque Country (UPV/EHU). His research interests gravitate on the use of descriptive, prescriptive and predictive algorithms for data mining and optimization in a diverse range of application fields such as Energy, Transport, Telecommunications, Health and Industry, among others. In these fields he has published more than 240 articles, co-supervised 8 Ph.D. theses, edited 6 books, coauthored 7 patents and participated/led more than 40 research projects. 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He is currently a full professor in\nthe Department of Automation and Applied Informatics at the\nsame university. Dr. Voloşencu is the author of ten books, seven\nbook chapters, and more than 160 papers published in journals\nand conference proceedings. He has also edited twelve books and\nhas twenty-seven patents to his name. He is a manager of research grants, editor in\nchief and member of international journal editorial boards, a former plenary speaker, a member of scientific committees, and chair at international conferences. His\nresearch is in the fields of control systems, control of electric drives, fuzzy control\nsystems, neural network applications, fault detection and diagnosis, sensor network\napplications, monitoring of distributed parameter systems, and power ultrasound\napplications. 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Recently, bioinspired systems have been successfully employing biomechanics to develop and improve assistive technology and rehabilitation devices. The research topic "Bioinspired Technology and Biomechanics" welcomes studies reporting recent advances in bioinspired technologies that contribute to individuals\' health, inclusion, and rehabilitation. 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He received his MSc and PhD in Biomedical Engineering respectively from the Federal University of Uberlândia (UFU, Brazil) in 2000 and from the University of Reading (UK) in 2005. He completed a one-year Post-Doctoral Fellowship awarded by the DFAIT (Foreign Affairs and International Trade Canada) at the Institute of Biomedical Engineering of the University of New Brunswick (Canada) in 2010. Currently, he is Professor in the Faculty of Electrical Engineering (UFU). He has authored and co-authored more than 200 peer-reviewed publications in Biomedical Engineering. He has been a researcher of The National Council for Scientific and Technological Development (CNPq-Brazil) since 2009. He has served as an ad-hoc consultant for CNPq, CAPES (Coordination for the Improvement of Higher Education Personnel), FINEP (Brazilian Innovation Agency), and other funding bodies on several occasions. He was the Secretary of the Brazilian Society of Biomedical Engineering (SBEB) from 2015 to 2016, President of SBEB (2017-2018) and Vice-President of SBEB (2019-2020). He was the head of the undergraduate program in Biomedical Engineering of the Federal University of Uberlândia (2015 - June/2019) and the head of the Centre for Innovation and Technology Assessment in Health (NIATS/UFU) since 2010. He is the head of the Postgraduate Program in Biomedical Engineering (UFU, July/2019 - to date). He was the secretary of the Parkinson's Disease Association of Uberlândia (2018-2019). Dr. Andrade's primary area of research is focused towards getting information from the neuromuscular system to understand its strategies of organization, adaptation and controlling in the context of motor neuron diseases. 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