Continuous slowing down range r0 in g cm−2 for electrons of different energies in oxygen, water and muscle tissue [6].
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
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This book covers some advanced aspects in cell culture methodologies. The book has four sections discussing different types of cell culture models, including 3D cell culture techniques, their advantages, and limitations in comparison to traditional 2D culturing; cell viability, autophagy, in vitro toxicity tests and live cell imaging; stem cell culture for cell-based therapeutics; and specific applications and methodologies for hybrid cell lines and cancer models. This book provides a comprehensive overview of some of the advanced cell culture methodologies and applications. 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She is a member in the Tissue Engineering and Regenerative Medicine International Society (TERMIS), Tissue Engineering and Regenerative Medicine Egyptian Society and Egyptian Association of Advancement of Medical Basic Sciences (EAMBS). Dr. Radwa has a number of publications in international peer-reviewed journals in the fields of stem cells and cell culture and is a reviewer in many international peer-reviewed journals.",institutionString:"Alexandria University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Alexandria University",institutionURL:null,country:{name:"Egypt"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"47",title:"Cell Biology",slug:"biochemistry-genetics-and-molecular-biology-cell-biology"}],chapters:[{id:"63158",title:"2D vs. 3D Cell Culture Models for In Vitro Topical (Dermatological) Medication Testing",slug:"2d-vs-3d-cell-culture-models-for-in-vitro-topical-dermatological-medication-testing",totalDownloads:1298,totalCrossrefCites:1,authors:[null]},{id:"64565",title:"Two-Dimensional (2D) and Three-Dimensional (3D) Cell Culturing in Drug Discovery",slug:"two-dimensional-2d-and-three-dimensional-3d-cell-culturing-in-drug-discovery",totalDownloads:2368,totalCrossrefCites:5,authors:[null]},{id:"64047",title:"Time-Lapse Microscopy",slug:"time-lapse-microscopy",totalDownloads:801,totalCrossrefCites:0,authors:[null]},{id:"63703",title:"Cell-Based Assays for Evaluation of Autophagy in Cancers",slug:"cell-based-assays-for-evaluation-of-autophagy-in-cancers",totalDownloads:724,totalCrossrefCites:0,authors:[null]},{id:"63968",title:"In Vitro Toxicity Testing of Nanomaterials",slug:"in-vitro-toxicity-testing-of-nanomaterials",totalDownloads:644,totalCrossrefCites:0,authors:[null]},{id:"63496",title:"Culturing Adult Stem Cells for Cell-Based Therapeutics: Neuroimmune Applications",slug:"culturing-adult-stem-cells-for-cell-based-therapeutics-neuroimmune-applications",totalDownloads:817,totalCrossrefCites:1,authors:[null]},{id:"63877",title:"Morphological Comparison of Stem Cells Using Two- Dimensional Culture and Spheroid Culture",slug:"morphological-comparison-of-stem-cells-using-two-dimensional-culture-and-spheroid-culture",totalDownloads:548,totalCrossrefCites:0,authors:[null]},{id:"63598",title:"Authenticating Hybrid Cell Lines",slug:"authenticating-hybrid-cell-lines",totalDownloads:539,totalCrossrefCites:0,authors:[null]},{id:"62466",title:"Air Pouch Model: An Alternative Method for Cancer Drug Discovery",slug:"air-pouch-model-an-alternative-method-for-cancer-drug-discovery",totalDownloads:758,totalCrossrefCites:0,authors:[null]},{id:"62823",title:"Optimization of the Self-Assembly Method for the Production of Psoriatic Skin Substitutes",slug:"optimization-of-the-self-assembly-method-for-the-production-of-psoriatic-skin-substitutes",totalDownloads:541,totalCrossrefCites:0,authors:[null]},{id:"60390",title:"Monolayers of Carbohydrate-Containing Lipids at the Water- Air Interface",slug:"monolayers-of-carbohydrate-containing-lipids-at-the-water-air-interface",totalDownloads:584,totalCrossrefCites:0,authors:[null]},{id:"63327",title:"Erythropoiesis and Megakaryopoiesis in a Dish",slug:"erythropoiesis-and-megakaryopoiesis-in-a-dish",totalDownloads:1042,totalCrossrefCites:0,authors:[null]}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"205697",firstName:"Kristina",lastName:"Kardum Cvitan",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/205697/images/5186_n.jpg",email:"kristina.k@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Subba Tata",coverURL:"https://cdn.intechopen.com/books/images_new/7999.jpg",editedByType:"Edited by",editors:[{id:"187859",title:"Prof.",name:"Kusal",surname:"Das",slug:"kusal-das",fullName:"Kusal Das"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6986",title:"Telomerase and non-Telomerase Mechanisms of Telomere Maintenance",subtitle:null,isOpenForSubmission:!1,hash:"79b7d4e97e1e0722f4ce1309a2088be3",slug:"telomerase-and-non-telomerase-mechanisms-of-telomere-maintenance",bookSignature:"Tammy A. Morrish",coverURL:"https://cdn.intechopen.com/books/images_new/6986.jpg",editedByType:"Edited by",editors:[{id:"275021",title:"Dr.",name:"Tammy A.",surname:"Morrish",slug:"tammy-a.-morrish",fullName:"Tammy A. Morrish"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"67932",title:"The Secondary Photoelectron Effect: Gamma Ray Ionisation Enhancement in Tissues from High Atomic Number Elements",doi:"10.5772/intechopen.86779",slug:"the-secondary-photoelectron-effect-gamma-ray-ionisation-enhancement-in-tissues-from-high-atomic-numb",body:'\nGamma is a high photon energy electromagnetic radiation which is absorbed by material with a number of different physical consequences. Its absorption results in the generation of fast electron tracks capable of breaking chemical bonds in living tissue with the generation of reactive ionic species and free radicals. These energetic fragments can then, themselves, migrate away from the ionisation track to react with other stable molecules and ions. The overall processes result in damage to living cells, either by direct interaction with a molecule or by indirect effects from the ionised or reactive species, and this can result either in cell death or in downstream genetic and genomic effects which are harmful to the health of the exposed individual. The mechanisms of genetic and genomic biological damage which follow from gamma ray exposure and X-ray exposures are described in the literature and are accepted by all the radiation risk agencies [1, 2, 3]. In this chapter, I will write
It is generally accepted now that the biological effects of exposure are a consequence of either direct damage to cellular DNA or due to induction of instability in cellular DNA through a mechanism involving the detection of ionisation, expressed as an increased concentration of reactive oxygen species (ROS), generated by gamma ray interaction with water. Either way, the essential biological effective target for gamma ray (and indeed all ionising radiation) absorption is not primarily water but is the cellular DNA. Historically, the method developed for assessing exposure after 1950 involved defining quantities based on the absorption of energy per unit mass of material exposed to these high-energy photon radiations. Since the detection and quantification of gamma radiation (and X-rays) became most easily based on the ionisation of gases (Geiger Muller counters, proportional counters and ionisation chambers and, later, scintillation counters), it was a simple step to quantify absorption by living tissue in the same way. Thus, for ionising radiation, the quantity
Clearly, from the outline above, it is the ionisation density at the DNA which is the key factor defining radiation risk. But
The calculation of absorbed dose assumes that the tissue in which the energy is dissipated is water or its tissue-equivalent substitute. Since all photon energy absorption from
Gamma radiation and matter interact mainly by three different mechanisms, Compton scattering, pair production and the photoelectric effect. The different contributions of these to absorption depend on the absorbing material, principally its atomic number Z and the quantum energy
In the photoelectric effect, incident photon energy causes the emission of an electron from the absorbing element. The electron has the energy of the absorbed photon minus the binding energy of the electron. For gamma radiation the binding energies are second order, and the emission electron carries almost all the initial gamma energy. Electrons may also lose energy in secondary processes occurring within the atom. For energies below 1 MeV, the photoelectric effect largely predominates. \nFigure 1\n illustrates the effects by incident gamma energy.
\nRelative contributions of the main different types of energy conversion in materials following the absorption of gamma ray photons. The specific curves differ considerably for different elements, driven by the electronic structure of the element. Note that the attenuation coefficient is normally given in cm2 g−1 and thus incorporates the density of the element.
Thus, for energies below 1 MeV, the photoelectric effect predominates. The cross section for the photoelectric effect is approximately proportional to the atomic number Z to the power of five and to the incident photon energy to the power of −7/2 [5]. The sharp dependence of photoelectron generation on Z immediately raises interest in the resulting wide variation in absorption of gamma rays by high atomic number atoms and molecules in tissue. This concern is related to the range of the photoelectrons and their deposition of ionisation effects close to the atom. For low-energy photoelectrons generated by low-energy gamma and X-ray photons, the effects will be increasingly local to the atom, and if the atom is local to DNA, there will be an enhancement of radiobiological effectiveness of the absorbed energy. This may be termed the secondary photoelectron effect. The SPE will also occur in the vicinity of internal particles of high-Z elements and in the vicinity of metal prosthetic structures.
\nThe starting point for examining this issue is the electron range in tissue by electron energy. This can be calculated on the basis of the continuous slowing down approximation (CSDA), and results for the lower energies for muscle tissue are given in \nTable 1\n [6]. In the lower-energy regions, the ranges of electrons in tissue are shown in \nFigure 2\n.
\nE (keV) | \nOxygen (8) | \nWater | \nMuscle (striated) | \n
---|---|---|---|
10 | \n2.950E−4 | \n2.515E−4 | \n2.536E−4 | \n
50 | \n4.992E−3 | \n4.320E−3 | \n4.356E−3 | \n
100 | \n1.647E−2 | \n1.431E−2 | \n1.443E−2 | \n
150 | \n3.325E−2 | \n2.817E−2 | \n2.841E−2 | \n
500 | \n2.018E−1 | \n1.766E−1 | \n1.781E−1 | \n
Continuous slowing down range r0 in g cm−2 for electrons of different energies in oxygen, water and muscle tissue [6].
Gamma ray absorption cross sections for oxygen (Z = 8) and gold (Z = 79).
For electrons of energy <500 eV, the range in tissue is in the order of 1–10 nm [7]. This is of the order of the dimensions of the DNA molecule.
\nThe photoionisation cross sections with photon energy of low Z (oxygen 8) and high Z (Gold 79) are shown in \nFigure 2\n. From \nTable 1\n we can see that oxygen may be used to approximate tissue absorption. In the low-energy region around 100 keV, it is clear from \nFigure 2\n that the absorption (and thus photoelectron production) of gold is several orders of magnitude greater than tissue. \nTable 2\n gives the photoionisation cross sections for a section of elements of interest [8].
\nZ | \nElement | \n10 keV | \n50 keV | \n100 keV | \n150 keV | \n
---|---|---|---|---|---|
1 | \nHydrogen | \n4.5E−3 | \n1.8E−5 | \n1.6E−6 | \n4.1E−7 | \n
6 | \nCarbon | \n4.1E+1 | \n2.0E−1 | \n2.0E−2 | \n5.4E−3 | \n
8 | \nOxygen | \n1.5E+2 | \n8.1E−1 | \n8.2E−2 | \n2.2E−2 | \n
11 | \nSodium | \n5.7E+2 | \n3.6E00 | \n3.7E−1 | \n1.0E−1 | \n
15 | \nPhosphorus | \n2.0E+3 | \n1.5E+1 | \n1.6E00 | \n4.4E−1 | \n
16 | \nSulphur | \n2.6E+3 | \n1.9E+1 | \n2.2E00 | \n5.9E−1 | \n
17 | \nChlorine | \n3.3E+3 | \n2.5E+1 | \n2.8E00 | \n7.8E−1 | \n
19 | \nPotassium | \n4.1E+3 | \n3.3E+1 | \n3.7E00 | \n1.0E00 | \n
20 | \nCalcium | \n6.2E+3 | \n5.2E+1 | \n5.9E00 | \n1.7E00 | \n
26 | \nIron | \n1.6E+4 | \n1.6E+2 | \n1.9E+1 | \n5.4E00 | \n
53 | \nIodine | \n3.4E+4 | \n2.5E+3 | \n3.6E+2 | \n1.1E+2 | \n
74 | \nTungsten | \n2.8E+4 | \n1.6E+3 | \n1.3E+3 | \n4.3E+2 | \n
78 | \nPlatinum | \n3.5E+4 | \n2.0E+3 | \n1.5E+3 | \n5.1E+2 | \n
79 | \nGold | \n3.7E+4 | \n2.1E+3 | \n1.6E+3 | \n5.4E+2 | \n
80 | \nMercury | \n3.9E+4 | \n2.3E+3 | \n1.7E+3 | \n5.7E+2 | \n
82 | \nLead | \n4.3E+4 | \n2.5E+3 | \n1.8E+3 | \n6.2E+2 | \n
92 | \nUranium | \n6.9E+4 | \n4.0E+3 | \n6.4E+2 | \n9.4E+2 | \n
Photoionisation cross sections for a selection of elements of interest at different incident energies in the natural background low-energy region (barns) (Hartree-Fock approximation) [8].
If the absorption of gamma ray photons by chemical elements varies so widely, with such an increased cross section for the higher Z elements, it seems clear that the incorporation of high-Z elements in living tissue would be essentially harmful. There is evidence from evolution to support this idea, and this will be discussed below. Apart from contamination issues due to anthropogenic sources and the question of medical procedures, the problem arises because of the continuous irradiation of living creatures by natural background radiation (NBR). The gamma spectrum of NBR increases rapidly to lower energies, roughly as the −7/2 power of the energy. From \nTable 2\n, it is clear that the absorption of photon energy in the NBR region (50 keV) from iodine is about 3000 times that from oxygen or water/tissue. It has been suggested that this may explain the radiosensitivity of the thyroid gland [9]. It should be noted in passing that the absorption coefficients at the energies tabulated do not generally reflect the overall absorption differences between the low-Z and high-Z elements over the whole-energy spectrum because of discontinuities in the absorption by the d- and f-orbital electrons in the heavier elements like gold and uranium. These discontinuities for gold are clear in \nFigure 2\n. For gold, the enhancement factor relative to water at the four energies tabulated (10, 50, 100 and 150 keV) are 246, 2592, 19,500 and 24,545. Similar variations in enhanced photon cross section are apparent for uranium which has 45,000 times the photoelectron cross section at 150 keV than the oxygen in water.
\nIt is clear from this approach that the determining absorption of living tissue is defined not by water but by the higher Z elements present. This is starkly true for iron and iodine which must form centres for photon absorption and photoelectron production. It may therefore be plausible to argue that this is why that the main cancers associated with external radiation exposures are leukaemia and thyroid cancer.
\nSince secondary photoelectrons will be generated from all exposures to gamma radiation and since the local ionisation density near the absorbing atom, particle or metal prosthesis is the quantity of interest, it is clear that the energy spectrum of gamma NBR is an important component of any assessment. External gamma radiation degrades in energy as it passes through tissue as a result of the various processes which occur. Energy is lost by Compton scattering resulting in the production of a Compton photon of lower energy than the initial energy. Electrons generated by the photoelectric effect lose energy through collisions and the generation of Bremsstrahlung photons of low energy and so forth. Thus, the further the initial photon travels in tissue, the greater the number of low-energy photons there are in the medium. The natural background radiation spectrum in Burnham-on-Sea, Somerset, UK, is reproduced in \nFigure 3\n.
\nGamma ray spectrum obtained on beach at Burnham-on-Sea using a 2-in. NaI (Tl) Scionix detector. Note rollover at about 60 keV.
Note the sharp increase in the number of photons at low energy: the cut-off is a result of absorption by the shielding of the thallium-doped sodium iodide scintillation detector. The degradation of photon energy inside the human body can be examined by placing an insulated scintillation detector inside a water-filled container and comparing the spectrum with that obtained in air. The spectrum obtained in this way, which compares well with that employed by Pattison et al. (who attempted to model the photoelectron effects in uranium particles [10]), is shown in \nFigure 4\n. The cut-off at low energy 15 cm inside the water jacket is due to the absorption of the low-energy short-range photons. By subtraction it is possible to show that the number of photons of low energy increases inside the water sphere of 30 cm diameter (used to approximate the body). Thus, the dispersion curve shifts to lower energy. The enhancement of photon numbers by energy is shown in \nFigure 5\n.
\nEnergy dispersion in the low-energy region 0–500 keV of the natural background gamma photons at 15 cm depth inside a human body. Based on Pattison et al.,
Enhancement of photon energy at different energies on passage through 15 cm water. Internal photon fluence divided by external photon fluence. Unpublished measurements.
What is clear from these results is that NBR delivers mainly low-energy photons. It turns out that 60% of in-air NBR photons have energy below 150 keV and the peak in photon numbers increases to low energy below 50 keV. Photoelectrons of this energy have a mean CSDA range (\nTable 1\n) which is comparable with the dimensions of a single cell or cell nucleus. Therefore, a high-Z atom in a cell will be continuously amplifying NBR in proportion to the photoionisation cross section shown in \nTable 2\n and delivering enhanced ionisation to that cell or cell nucleus relative to that calculated using the concept of absorbed dose which is based on the assumption that the absorber is effectively water (i.e. oxygen). Further, the biological effectiveness of NBR, its damage to tissues, will be defined by the highest Z atoms in the tissue. This will also be true for other exposures, for X-rays, medical examinations and exposures to anthropogenic sources, indeed the entire range of exposures which are regulated by the law on the basis of the current risk models. It will be the location in the body of a high-Z atom or particle relative to the target DNA which will be the determinator of biological risk. This is a phantom radioactivity: the atom is radioactive by virtue of its high atomic number and its amplification of NBR gamma radiation through photoelectron emission.
\nThe radiobiological issue of photoelectron emission by internal high atomic number particles was raised in 2005 by Busby in connection with depleted uranium weapons which create respirable submicron particles on impact [11]. Research in Iraq, where DU weapons were deployed in 1991 and later in 2003, were shown to have caused high levels of congenital effects and cancer in a number of studies both of civilians in Iraq and of military veterans [12, 13, 14]. The concerns about the genotoxicity of DU particles led to research by a number of groups in the early 2000s. The laboratory researches demonstrated that both uranium and uranium particles were capable of causing measurable genetic effects, chromosome breakages and so forth [15, 16, 17]. In one study with mice, both embedded uranium and tungsten particles caused local cancer effects [18]. These findings have been reviewed in Busby [19, 20] and will not be rehearsed here. What will be presented here are some results from nanoparticle mathematical modelling studies carried out at the University of Ulster between 2009 and 2012 which looked at photoelectron production from water, gold and uranium spheres [21, 22].
\nPhotoelectron emission from nanoparticles of water, gold and uranium was investigated by Elsaessar, Busby and Howard from 2009 to 2012. Preliminary results were presented at a conference [21], and the studies contributed to a PhD thesis [22]. The CERN FLUKA code was employed. The beam geometry is shown in \nFigure 6\n, and in \nFigure 7\n results are given for 10 nm particles of water, gold and uranium. Referring to the numbering in \nFigure 7\n, which is from the conference presentation [21], the top row of \nFigure 2a–c\n shows photoelectron tracks induced by an incident photon beam of 150 keV involving 1000 photons in the cases of 10 nm diameter gold and uranium particles, whilst for the water particle, the number of photons was 10,000. Thus, it is clear that the photoelectron tracks of various energies (lengths) induced in the particles of the high atomic number elements gold and uranium are orders of magnitude greater than those in water. The emission of secondary photoelectron tracks from the three materials is roughly in agreement with a fourth or fifth power law. \nFigure 2d–f\n shows the energy deposition in the particles on a coloured scale given also in the picture. It is immediately clear from \nFigure 7\n how the internal particles of high-Z elements result in increased absorption of background radiation and its re-emission by photoelectrons and associated enhanced biological damage relative to the absorption by tissue (water). Due to self-absorption of the induced photoelectrons, the danger exists mainly from smaller particles. Results for different sizes of particles of gold and three different photon energies are shown in \nFigure 8\n. This shows the variation secondary photoelectron production with photon energy (100 keV, 250 keV, 500 keV and 1 MeV) in a gold target. Photon penetration depth decreases as energy decreases, but the number of electrons escaping the target increases.
\nBeam and target geometry for FLUKA calculations. A photon beam of cross-sectional diameter equal to that of a particle of water, gold (Z = 79) and uranium (Z = 92) [
Secondary escaping photoelectron production (seen in two dimensions following incident 100 keV photon beam into 10 nm particles of water (Z = 7.5) [
Upper: secondary electrons/primary photons in gold particles of different diameters and photon energies 2, 10 and 100 keV. Lower: electrons per target volume/photons per beam projection for gold particles of different diameters and photon energies of 2, 10 and 100 keV [
To examine the deposition of photoelectron energy into the tissue surrounding the particles examined in the analysis presented in \nFigures 7\n and \n8\n, particles were modelled surrounded by water spheres, and the deposition of energy into the spheres was obtained. In \nFigure 9\n, results for different photon energies of 100, 250, 500 and 1000 keV are presented. As the photon energy was decreased, the penetration also decreased, as expected, but the photoelectron density in the local volume near the particle increased. This is not unexpected since the photoelectron range would be shorter with the low-energy photoelectrons.
\nThe variation of secondary photoelectron production with photon energy (100 keV, 250 keV, 500 keV and 1 MeV) in a gold target. Photon penetration depth decreases as energy decreases, but the number of electrons escaping the target increases [
The Ulster results can be used to obtain enhancement factors for photoelectron production from 10 nm diameter gold and uranium particles relative to a water particle of the same size. This enhancement factor is compared with a fourth-power law comparison in \nTable 3\n [19].
\nCalculation | \nWater Z = 7.5 | \nGold Z = 79 | \nUranium Z = 92 | \n
---|---|---|---|
Elsaessar et al. [21] | \n1 | \n12,900 | \n29,200 | \n
Z4\n | \n1 | \n12,300 | \n22,600 | \n
Number of photoelectrons emitted following exposure of a 10 nm particle of water, gold and uranium to 100 keV photons.
Ratio of gold and uranium photoelectron numbers to water photoelectron numbers. Also shown is the Z4 predicted ratio [19].
The range of the photoelectrons increases as the photon energy increases, but the number of photons increases at low energy for natural background radiation as has been discussed above. The trade-off is shown in \nFigure 10\n. Dose enhancement (energy per unit mass) falls off rapidly with distance from the high-Z particle but is significant in the micron region. Results for a 400 nm uranium particle are given in \nFigure 11\n [19].
\nPercentage of all photoelectrons with energies equal to natural background radiation photons (blue diamonds) and range in tissue in microns (red triangles) (from results presented in
Dose enhancement (energy per unit mass of tissue) by distance in nm from a 400 nm uranium particle.
\n\nFigure 11\n shows enhancement of dose close to a 400 nm uranium particle embedded in tissue and exposed to natural background radiation. For the method of obtaining this, see [19].
\nBecause of the use in the battlefield of uranium weapons and the fact that there are other sources of uranium particles (which will be discussed below), there is considerable financial and military investment in showing that these photoelectron effects are not biologically important. The author was a member of the UK Ministry of Defence Depleted Uranium Oversight Board [23] from 2001 to 2005 and also the UK Committee Examining Radiation Risks from Internal Emitters (CERRIE) [24]. He also gave evidence to the Royal Society Committee on Depleted Uranium in 2001. In 2009 a paper describing the secondary photoelectron effect entitled “Phantom Radioactivity of Uranium” was sent by him to the chair of the Royal Society Committee which had published reports on the issue in 2001 and 2002. These reports argued that DU could have no adverse health effects as the absorbed doses from the particles were too low [25]. At the suggestion of the chair, Brian Spratt, the photoelectron paper was submitted to the
Pattison et al. carried out Monte Carlo modelling using a different code to that employed by Elsaessar, EGSnrc [10]. They modelled two sizes of cylindrical particles and hollow cylindrical particles of 10 μ diameter and length. Using input photons of 200 keV, they concluded that the enhancement of dose was significant and of the order of one to tenfold. Apart from the fact that the particles they modelled were too large to represent the respirable DU particles found in Iraq, and the input photons too energetic, the key to dismissing their approach was their finding that the dose enhancement was largest for the larger particles, the opposite result to that obtained at Ulster. This was because their method was to fix the spherical volume into which the photoelectrons were emitted and calculate energy per unit mass in the annular water shell. Clearly as the particle diameter approached the water shell diameter, the dose would become infinite, showing that the method was nonsensical, and it is hard to see how the paper passed the reviewers.
\nEakins et al. study was carried out by employees of the UK National Radiological Protection Board (NRPB) [27]. They used the computer code MCNP5 to model an arrangement consisting of concentric spheres with the particle at the centre and tissue shells surrounding the particle as had the Ulster modelling. However, like Pattison et al., Eakins et al. fixed the volume into which the photoelectron energy was converted into absorbed dose. The authors did, however, model a range of uranium particles, obtaining enhancements of 3-fold at 100 nm diameter and 20-fold for the 2.5 nm diameter particles. Like the Pattison et al. study, this was an absurd analysis since having a fixed volume for the dose absorption but increasing the particle size, the enhancement factor eventually becomes infinite.
\nThe augmentation of dose due to secondary photoelectron emission from high-Z elements is not a new concept; it is just that it has been ignored for the purposes of radioprotection. The idea of employing high-Z elements and their photoelectron emission to augment radiotherapy doses was advanced by Matsudeira et al. who measured the radio-enhancing effect of iodine on cell cultures [28]. Nath et al. incorporated iodine into cellular DNA with iododeoxyuridine in vitro and found a radiation enhancement of about 3-fold [29]. Herold et al. injected gold particles directly into a tumour followed by irradiation and found that the excised cells had reduced plating efficiency [30]. Mello et al. found that direct tumour injection with iodine contrast medium followed by 100 kVp X-rays completely suppressed growth of 80% of tumours in mice [31]. Norman et al. modified a CT scanner to deliver X-rays to spontaneous brain tumours in dogs after iodine injection and found a 53% longer survival [32]. Synchrotron radiation was used in combination with the tumour injected drug cisplatin to treat brain tumours in rats [33]. The issue of the mechanism of cisplatin is revisited below.
\nThe photoelectron enhancement by high-Z nanoparticles was exploited in cancer radiotherapy by Hainfeld et al. who attempted to increase the dose delivered to tumours by injecting 1.9 nm gold nanoparticles into mice [34]. The authors also made the method the subject of a patent.
\nIt is curious that historically photoelectron emission by internal high-Z elements in living systems has received very little attention. The issue of enhanced doses near bones, due to the higher concentration of calcium in the bone, was addressed as long ago as 1949 by Spiers [35], and more recent work has also looked at photoelectron emission near the bone [36]. In 1988 Castillo reported burns and necrosis around reconstructive wires in mandibular cancer patients [37], and Regulla et al. employed a very sophisticated measuring apparatus to show a physical dose enhancement of about 100-fold and a biological enhancement into tissue of 50-fold within a range of 10μ from gold foil [38]. Despite work on enhancing radiotherapy which has been carried out, no authors appear to have related the question of photoelectron enhancement to health effects. One obvious question must be about the enhanced photoelectron doses near metal prosthetic structures containing zirconium (Z = 40). The element has a photoelectron cross section of 3.5E+3 at 150 keV compared with iron (Z = 26) at 5.4 and so would produce some 650 more photoelectrons.
\nThe main question that has to be focused on is the enhancement of dose to the DNA from high-Z atoms or molecules which are attached to the DNA by chemical affinity. If a high-Z atom, ion or molecule were attached to the DNA, then it is easily predicted that this would cause enhanced genetic damage, measurable as downstream effects like cancer and congenital disease but also chromosome breakages and chromosome aberrations. The obvious candidate is uranium, which as the uranyl ion has been known to bind strongly to DNA since the 1960s when it began to be employed as a chromosome stain. The genotoxic effects of uranium exposure are by now well established both in human populations and in in vitro studies [12, 13, 14, 15, 16, 17, 18, 19, 20]. They cannot be explained by the intrinsic alpha activity, and indeed one experiment has revealed genetic effects in the absence of alpha decays [20]. The affinity of uranyl ion for DNA has been measured, and it is significant. So uranium (Z = 92) effects are one clear piece of evidence for the effects of secondary photoelectrons. But there is another one.
\nThere is further evidence from the anticancer agent cisplatin, cis-diamine-dichloro-platinum (II). Cisplatin has been a chemotherapeutic agent of choice since 1978 and is given to more than half of all cancer patients. Its mode of action has been variously described as “damaging nuclear DNA and arresting cell division”. A recent review states: “Almost 30 years after its clinical benefits were first recognised, studies still continue in an effort to understand exactly how cisplatin works” [39].
\nCisplatin also augments radiotherapy, that is to say, the combination of cisplatin and radiotherapy results in much higher cancer therapeutic effects than either agent on its own. This is, of course, a pointer to the mechanism [33, 39]. It is suggested here, based on what has been written above, that cisplatin, a simple diamine-dichloro-square planar complex of platinum (II), merely fixes the platinum atom (Z = 78) at the centre of the nuclear DNA where the secondary photoelectron doses are sufficient to fatally damage the DNA either from natural background radiation or in the case of the radiotherapy, from the induced photoelectrons. If this is the mechanism, then two suggestions are obvious: first, uranium as uranyl acetate, for example, also will act as a chemotherapeutic agent for cancer and will augment radiotherapy in the same way. Since it is suggested that it is the high-Z aspect of cisplatin that is the reason for its action, other high-Z molecular agents could be searched for or synthesised to act as DNA-seeking chemotherapeutic agents.
\nThe question of the spectrum of elements utilised by evolution of life on earth has been generally approached from the point of view of physical chemistry and more specifically redox equilibria [40]. There may be a separate or additional explanation for the reason why elements of high atomic number (e.g. mercury, bismuth, lead, uranium) although often commonly available on earth are not used by living creatures. As has been shown, chemical elements absorb gamma and X-rays of energy below about 250 keV approximately in proportion to the fourth power of their atomic number Z, and the energy is converted mainly to photoelectrons and local Auger recoil electrons resulting from internal rearrangements in the case of high-Z elements. For elements immobilised inside living tissue, this results in higher doses to components near high-Z atoms or nanoparticles than would be experienced by the same tissue in the absence of the contaminant. Thus, high-Z elements, inside the body, act as devices for focusing and enhancing the doses from natural background radiation and should be seen as phantom radioactivity sources.
\nIf the phenomenon is significant, then it would seem reasonable that the contemporary spectrum of chemical elements employed by living systems will have been produced by evolutionary selection forces responding to such potentially critical damage.
\nIt is a well-known fact that the effects of ionising radiation on living systems are mediated by genotoxicity. The damage can be seen as a consequence of both single- and double-strand breaks in DNA; the dose (D) response (E) can be written as [41]
\nBut for the photoelectron effect being considered, dose (i.e. local dose at the DNA) can be written in terms of the atomic number Z or the elements:
\nand thus
\n(a, b, c, α and d being arbitrary constants). For evolution it can be assumed that any stress S which prevents an individual from reproducing will represent an inhibitory effect of the survival probability of the species. S can be written in terms of the concentration C of the element in the individual and the radiation effect on the DNA from the element:
\nThus,
\nIf the log of the concentration of all elements found in living systems is plotted against the log of the atomic number Z, the theory predicts an approximately linear relation with slope of between −4 and −8 depending on the contributions of single- and double-strand breaks in DNA to the overall photoelectron and recoil genotoxicity. Of course, the proposed relation is for non-radioactive or weakly radioactive elements and assumes that only photoelectron and Auger effects contribute.
\n\n\nFigure 12\n shows a log-log plot of concentration of elements vs. atomic number Z for standard man. Data were from the International Commission on Radiological Protection [42].
\nPlot of log(C) vs. log(Z); investigating the relationship between concentration of elements in humans and the atomic number Z. Note H, Li, Be and B are significant outliers from a relation for which the slope of log(Z) is −5.6 (R2 = 0.514, F-statistic = 65.23 on 1 and 41 degrees of freedom; p < 10−10).
Results (\nFigure 12\n) for elements of Z > 5 seem to support the idea that the photoelectric conversion of natural background radiation has been a significant effect in evolution. The slope of the log correlation is −5.6, between −4 and −8 as predicted, suggesting that a significant component of the effect involved double-strand breaks of DNA and thus ionisation which is very local to the elements. Indeed, it is curious how very few of the elements available to life have been employed by biological processes: evolutionary niches are generally found to be occupied but clearly not ones that involve utilising elements of high atomic number. This is not because these elements are scarce. The crustal concentrations of uranium are quite high; there is a significant quantity of uranium in seawater, yet the transfer coefficient for the gut (in mammals) ensures that the element is excluded quite efficiently. The same is true for many other high-Z elements that have been excluded from biological systems.
\nIt is of interest that the elements lithium, beryllium and boron are significant outliers from the relation, and this needs addressing from within the general concept. One reasonable explanation is that all three elements are associated with neutron conversion effects, either the absorption of a neutron in a reaction that produces an alpha particle (boron, 10B(n, α); i.e. 10B + n = 7Li + α; lithium, 6Li(n, α)) or the absorption of an alpha particle in a reaction which produces a neutron (e.g. beryllium, Be(α, n); 4He + 9Be = 12C + n). Both alpha particles and neutrons are densely ionising and carry weightings of between 5 and 20 for radiobiological effectiveness in models which assess risk [41]. The thermal neutron cross sections of these three elements (in Barns, 10Be = 3840, 6Li = 9400 and 7Be = 39,000) are significantly higher than other higher Z elements (238U = 2.7). The neutron cross section of hydrogen is modest (0.2), but the atomic concentration of the element in water ensures significant neutron absorption and the production of energetic protons by recoil. The natural background neutron fluence at ground level, produced by cosmic rays, has been measured at 46 cm−2 h−1 equivalent to a dose of 10 nSv/h about 10% of the overall background dose [43]. Thus, the displacement of the “radiotoxicity relation” to the left by about one order of magnitude corresponds to the mean relative biological effectiveness of neutrons and alpha particles. It is therefore unsurprising that these elements are outliers in the general linear correlation of the log terms and this may be interpreted as a consequence of the existence of a natural background of these neutron radiations.
\nSo, in general high-Z elements are not employed by life. Why then is there the utilisation by mammals of the element iodine (Z = 53)? The iodine-containing systems (blood, thyroid) are those which are clinically most sensitive to radiation exposure (for reasons which are clear from the discussions above). It was suggested that the reason why iodine was employed is that the element is being exploited for its radiation detection quality and that the thyroid mediates an induced radiation damage address system through upregulation of genes associated with cellular surveillance and repair [9].
\nFinally, the relationships discussed here also obtain for plants. Plants are unable to move to avoid radiation exposure and might be expected to reflect responses to evolutionary stresses. The relationship between atomic number and the optimum concentration of elements for plants to thrive has been shown to conform to the same relationship [9]. The correlation is given in \nFigure 13\n.
\nMinimum concentrations of mineral elements essential for plants required for optimum growth as a function of the fourth power of the atomic number Z. The uranium data point is based upon detection of uranium in a wide range of plants [
The secondary photoelectron amplification of gamma radiation by different elements in living systems has importance in radiation dosimetry. For some inexplicable reason, elemental absorption has been entirely omitted from the calculations of absorbed dose published by radiation risk agencies like the International Commission on Radiological Protection (ICRP) which bases its recommendations of external dose limits on water- and tissue-equivalent phantoms. Furthermore, the phantom photoelectron radioactivity from this effect has considerable application to the element uranium which had been shown in a very large number of publications to have significant genotoxicity. This is particularly the case for internal uranium particles, generated from weapon use, from nuclear power station stacks, from global nuclear atmospheric testing, from nuclear fuel reprocessing and from uranium fuel manufacture. All the official risk agencies model uranium on the basis of its very low intrinsic alpha radioactivity and conclude that it cannot pose the risk that it clearly does.
\nThe basis for the current radiation risk model is the lifespan study of the Japanese A-Bomb survivors, the LSS. One major confounding exposure to the LSS cohorts, upon which the current risk model depends, was the post detonation black rain, which consisted of uranium particles from the weapons [44, 45]. On the basis of the arguments and evidence submitted in this chapter, the uranium particle exposures of all the different dose groups that have been used to construct a linear dose response make any attempt to use these data to define radiation risk unsafe. The unusual cancer results which emerged as soon as 1970 resulted in the researchers deciding to discard the not-in-city unexposed groups that are anomalously healthy. This was an error since these were the only groups not exposed to the black rain, although no doubt, the residual contamination will have caused inhalation exposures after they entered the cities, some months and years after the detonation. The issue was raised by Busby 2017 [45]. Studies of the LSS groups based on truly unexposed control groups in neighbouring prefectures carried out in 2009 showed that the cancer rates in all groups, especially the low-dose groups in the LSS cohorts, were significantly high [46].
\nWhat is being suggested here is that the entire understanding of gamma ray interaction with living tissue needs to be rethought. Research must be carried out to quantify the extent to which certain elements with high gamma and X-ray absorption coefficients bind to DNA and the extent to which this causes genetic and genomic damage at background levels and during radiotherapy or other external radiation situations. It is astonishing that no one has questioned the method that has been developed to assess harm from external photon radiations, the simplistic physics-based dilution of energy into water phantoms. It is not as if there was no evidence that this might be an unsafe approach. The radiosensitivity of the iodine-rich thyroid gland should have supplied clues. The mechanism of the anticancer agent cisplatin should have supplied clues.
\nHigh atomic number particles have increased in the environment in the last 50 years or more. Platinum particles emerge from catalytic converters, thorium particles emerge from gas light filaments and uranium particles are released from nuclear power stacks, reprocessing plants and many other sources. The high-Z secondary photoelectron effect is used in cancer therapy. There is a whole field of development here where anticancer agents may be synthesised to bind to DNA and carry a high-Z warhead.
\nFinally, it is suggested that there is a simple experiment which will demonstrate and quantify this effect. It is to contaminate a system in which genetic damage may be measured with a uranyl salt, so that the DNA is contaminated with uranium, and then to irradiate the system with different doses of X-rays or gamma rays and then measure the genetic damage. To exclude alpha particle effects, the agent cisplatin could also be employed in a similar experiment.
\nAlthough the sharp dependence of the gamma- and X-ray-induced photoelectron yield of elements on atomic number has been known for more than 100 years, the implications for radiobiology have been hardly addressed. This chapter aims to open up this issue and call for more research attention. First, it can be concluded that high-Z elements, when inside living tissue, represent a focus for absorption of photon radiation and that the resulting ionisation density close to the element is much higher than what is calculated using conventional dosimetry such as that employed in current radiation protection, as in, e.g. [41]. This effect, the secondary photoelectron effect (SET), is most relevant to elements which also have affinity for DNA, the target for radiation-induced genotoxicity. The intrinsic radioactivity of such elements is not relevant, as can be seen by the genotoxicity and cancer therapy effect of the drug cisplatin. Results of Monte Carlo modelling carried out at the University of Ulster show that internalised high atomic number nanoparticles are likely to cause high local ionisation in living tissue. These effects are greatest for low-energy photons such as those in the natural background radiation spectrum. It is suggested that this may be one explanation for the anomalous genotoxicity of uranium particles found in many studies but hitherto dismissed as radiation effects on the basis of conventional dosimetry. Finally, an examination of the spectrum of elements employed by living systems reveals an interesting relationship which correlates the elemental composition adopted by life itself with the photoelectron cross section of the elements available to evolution. This relationship, which follows the photoelectron cross section and is highly statistically significant, suggests that living systems are exquisitely and critically sensitive to ionising radiation and have had to develop throughout evolution in such a way as to minimise the ionisation damage induced by background radiation. There are many important consequences of this approach, but the main ones are in the area of radiation risk assessment and in cancer therapy. Some approaches and experiments are suggested.
\nCertain microorganisms have the unique ability to populate the human gastrointestinal tract and thus generally referred as gut microbiota. Gut microbiota is always non-pathological, and hence, the immune system is not triggered because of their presence. Humans co-evolved with a huge number of intestinal microbial species that offer to the host certain benefits by playing an important role in preventing them from pathogenic activities [1]. In addition to metabolic benefits, symbiotic bacteria benefit the host with various functions like boosting the immune homeostasis and inhibiting the colonization by other pathogenic microorganisms. The ability of symbiotic bacteria to inhibit pathogen colonization particularly in the gut is mediated via several mechanisms including direct killing of pathogen, competition for limited nutrients, and enhancement of immune responses [2]. The intestinal microorganisms also co-evolved and have strong affiliations and association towards each other. In this evolutionary process, the persistent and enduring members of this microflora become more competent during unsettling influences and thereby become essential for human health [3]. Definite composition of human microbiome varies between individuals [4] particularly among lean and obese people. The microbiome is also affected by the dietary modifications adapted for the weight loss [5]. Examination of metabolic profiles of human infant microbiota revealed that ingestion, storage and digestion of dietary lipids were explicitly regulated by the microbiome [6, 7].
\nThe human gut microbial communities are a mixture of microorganisms. The classes of microbes that constitute the gut microbiome communities differ between hosts. The difference is attributed to factors such as, inability of a microorganism to migrate between different hosts, intense environmental conditions inside and outside host’s gut and host inconsistency in terms of genotype, diet, and colonization history [8]. The co-evolution of humans and their symbiotic microorganism has created bilateral interactions which are important for the health of humans, and any genetic or ecological change in this bilateral interaction can result in pathological conditions like infection [8]. Gut microbial communities are important for diverse host functions, including metabolism, fertility, development, immunity, and even antioxidant activities which promote health and fitness of the host [9, 10, 11, 12]. The gut microbiome has a much larger genetic variety compared to the genome of the host, e.g., human genome is comprised of 20-25,000 genes whereas microbiome inhabiting the body is estimated to be in trillions. Almost 1010 microorganisms enter the human body daily and with the progress of co-evolution of gut microbes in humans, the capability of microbes to exchange their genes and associated functions with the environment are some of the main factors leading to host adaptation. Therefore, the “hologenome” model appraises the host and its microbes genomes as one unit under assortment [13, 14]. It is acknowledged that host-symbiont co-evolution is accountable for basic biological aspects. In this chapter we aim to discuss the importance of gut microbiomes as a new organ system because of its association with the genetics and its role in the disease and health condition of the host. Moreover, the involvement of these microbiomes in shaping the overall health and constructing a symbiotic relationship with their host species is discussed as well as the co-evolution of gut microbes with the human body.
\nA microbiome is the community of microbes dwelling collectively in a selected habitat. Humans, animals, vegetation, soils, oceans or even buildings have their own specific microbiome [15].
\nThe human gut environment is extremely complex with a unique ecology which comprises of trillion of microbiota with approximately 1.5 kg in mass. By using genetic techniques like 16S sequencing, 1000 microorganisms have been identified within the gut, with approx. 200 (0.5%) defining the core of the intestine microbiome [16]. These bacteria protect the gut epithelial cells against external pathogens. They also help the breakdown of indigestible dietary polysaccharides in the gut and thus supply a quick chain of fatty acids, including acetate, butyrate, and propionate, which serve as vital metabolites for direct energy source of intestinal epithelial cells, prevention of insulin resistance and modulators of insulin secretion [17] (Figure 1).
\nCore human microbiome.
The genetic makeup of humans is virtually identical, yet the small differences in DNA give rise to remarkable phenotypic assortment across the human population. The trillions of microbes inhabit our bodies and create complex, body-habitat-specific, adaptive ecosystems that are finely tuned to frequently changing host physiology [18]. A healthy “functional core” is actually a complement of metabolic and other molecular functions that are performed by the microbiome within a particular habitat but are not necessarily provided by the same organisms in different people [19].
\nThe gastrointestinal tract (GIT) of humans is colonized by a vast variety of microbial population that can be understood as a complex and polygenetic trait which has been interacting and co-evolved with their host genetic environment [20, 21, 22]. It was previously considered that fetus lives in a germ free environment in the mother womb and the gut microbiota are transferred to the baby from mother’s birth canal and body via horizontal transmission only [23]. But advanced researches have revealed that microbiota are also vertically transmitted to the infants from their mothers [24]. Presence of microbes in the meconium of the babies born by cesarean section clearly demonstrates that the gut microbes are not only derived after the birth [25, 26]. Moreover, presence of many microbes in the umbilical cord blood of the preterm babies and in the amniotic fluid substantiate the findings that the fetus in the mother womb is not totally sterile [27, 28]. Many gut bacterial genera are shared among the mammal species. The microbiomes of mice show strong fidelity throughout the generations and reiterate the intrinsic significance of these microorganisms in health.
\nAs mentioned above human intestinal microbiome composition is shaped by multiple factors like genetics, diet, environment and lifestyle. Several studies point towards stronger contribution by the environmental factors in shaping the gut microbial composition compared to the genetic factor [29]. It has also been speculated that gut microbial diversity affects the prediction accuracy for certain human traits including glucose and obesity problems, as compared to different animal models that use only host genetic and environmental factors [30].
\nHorizontal gene transfer (HGT), genomic and metagenomics are possible approaches to identify drug targets that may also be considered as an evidence of co-evolution of hosts and their symbionts. Symbionts have the capacity to perform many metabolic activities including fermentation of dietary carbohydrates, drug metabolism, antimicrobial protection and immunomodulation, which is primarily due to the presence of genes in their genome which are missing in mammalian genomes. Therefore, horizontal gene transfer mechanisms are potential targets for drug discovery that become more evident with the use of gnotobiotics (germ free animal) in experimental trial to unveil the microbial function in the complex GIT microenvironment, and to investigate how orally administered drugs impact the gut microbial ecology in long term. HGT has gained immense interest in medical field as it contributes to the spreading of antibiotic resistance genes as well as it may cause closely related microbial strains to differ drastically in terms of clinical parameters [31]. Genetic variation in intestinal microbes may trigger the production of metabolites, but it may also generate changes in host’s genome that may increase metabolite uptake or prevent their further synthesis. Co-evolution may lead to co-differentiation since permanent association of host and symbiont lineage can result in diversification [32]. The co-differentiation correlate resemblances in the microbial symbiont and the host [33, 34] which can be extended to an entire microbial community that passes vertically from host to offspring. Over the course of speciation, the microbial communities differentiate as a mirror to host phylogeny (such situation would be expected in hosts where parents immunize their offspring with microbial clique, e.g., Koala bear mother inoculate “pap” with dropping to shift young one from milk to eucalyptus leaves diet) [35]. Fecal microbiome from healthy humans is a mirror of distal gut microbiome which is highly rich in genes involved in the vitamin synthesis, breakdown of nutrients, and metabolism of xenobiotics as compared to already sequenced human genome and microbes genome [4]. The presence of conjugate transposons in gut microbiome is another important source of horizontal gene transfer in bacteria [36]. The HGT is involved not only in spreading antibiotic resistance genes, but also as a source of clinical response of closely related microbial strains of
Novel strategies in drug discovery are being pursued by targeting horizontal gene transfer involved in the resistance to antibiotic [39] as well as virulence [40]. Targeting virulence factors with Salmonellosis inhibitors causes less damage to indigenous microbes compared to traditional antibiotic therapy, less selective pressure for evolution and transfer of resistance and may be more effective against divergent organisms that have acquired a particular virulence factor by HGT. Genomic islands which are a good source of genes and gene transfer systems are also being targeted with small molecule inhibitors that are co-administered with antibiotics to prevent resistance factors by targeted pathogenesis during the therapy [41].
\nIt has been established that the majority of molecules possessing physiological or pharmacological features are either transported into and or out of the cells by transporting proteins rather than by a passive transport mechanism where drug molecules cross cell membranes through solute transporters that are already involved in the movement of different metabolic intermediary molecules through channels. More than 1000 different types of transporting proteins (transporters) are present in humans [42] comprising solute carriers (SLC) and ATP binding cassettes (ABC) transporters involved in the transport of a broad range of substrates [43].
\nHuman intestinal peptide transporter 1 (hPepT1) belonging to the proton-coupled oligopeptide transporter (POT) family which is also known as solute carrier 15A (SLC15A) is present in the enterocytes, the PepT2 (oligopeptide transporter 2, SLC15A2) in kidney, the PHT1 (peptide histidine transporter 1, SLC15A4) in brain and the PHT2 (peptide histidine transporter 2, SLC15A3) located in spleen, lungs and thymus. Both hPepT1 and PepT2 mediate the transport of di−/tri-peptides and a broad range of peptidomimetics in the organisms, whereas PHT1 and PHT2 mediate the translocation of histidine and with a few selected di- and tri-peptides [44]. The hPepT1, an oligopeptide transporter 1 located in the enterocystes of the small intestine, has low affinity and high capacity transporter protein to transport 400–800 different dipeptides and tripeptides and drugs like ACE’1 (Enalapril) and antiviral (acyclovir) [45]. The hPepT1 is also found in microbes like
Passive diffusion and secondary transport mechanisms in bacteria may involve uptake of drug into bacterial cytoplasm [52, 53]. In the inner membrane of
As described above microorganisms present in the gut of the living organisms contribute to health or cause disease of these organisms by interplay with their immune system. Microbiome is developed at birth according to host interaction but later it is evolved and modified by surrounding factors like environmental and diet. The variation in genetic expression of different individuals is thought to be linked with different microbial composition [57]. Genotype of the host affects the composition of gut microbes. Even mutation of a single gene can cause modification in the structure of gut microbiota. The exact mechanism of association between the gut microbes and the genotype of host is still unknown. Bifidobacteria are highly prevalent beneficial bacteria in gut microbiome and are associated with lactase non-persistent genotype. This genotype is responsible for the synthesis of lactase enzyme which helps to digest the lactose, present in the milk. Absence of this enzyme leads to lactose intolerance in different organisms. So it is important to investigate susceptibility of different underlying pathological conditions by studying microbiomes association with genotype and environmental factors that vary among different human populations [58].
\nDifferent studies showed that metabolic disorders are largely congenital and are associated with different microbiomes. For example, gut microbiomes have been linked to metabolic disorders and obesity [59].
\nIn gut microbiome, dysbiosis (imbalance of microbial flora) can be induced by host factors and/or external factors such as the intake of antibiotics, mental and physical stress, and nutrients in the diet. Dysbiosis is likely to impair the regular gut microbiota and the appearance of pathobionts and the production of metabolites which may be dangerous to the host or may deregulate beneficial microbial-derived metabolites. The microbial symbiosis has a significant role in the development of many diseases [60] such as the gastrointestinal diseases [61, 62], infections [63], metabolic disorders, liver diseases [64], autoimmune diseases [65], mental or psychological diseases [66] and respiratory diseases [67].
\nThe inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), has for quite some time been suspected to be a host reaction to its gut microbiota. CD represents the chronic inflammation of the GIT (involving any part from mouth to anus) with idiopathic etiology while UC is the chronic inflammation of the large bowel of the GIT with no known cause. Numerous aspects of the microbiota’s association in IBD have been inspected in recent years. About 10–20% of adults and adolescents worldwide are affected by IBD [68]. The precise cause of IBD is unidentified, but it is believed to be a multifactorial disease. Inflammation, infection, visceral hypersensitivity, immunity, genetic factors, motor dysfunction of the GIT as well as psychopathological factors are suspected to play a role in its development [69]. Moreover, abnormal gut microbiota has been noticed in the IBD patients and in animals with intestinal inflammatory disease [70, 71, 72, 73]. Some of the metabolically active anaerobic bacteria in the colon and terminal part of ileum interact with the immune system of epithelium and mucosal layer of the host intestine. Continuous stimulation of these microbial antigens promote pathogenic immune responses and may cause defects in the barrier functions of mucous layer by killing some beneficial bacteria or by immune dysregulation, consequently resulting in UC and CD. Moreover, disrupted microbiota structure and function in inflammatory bowel disease intensify the immune response of the host causing dysfunction of epithelium and increased permeability of the mucous layer of the intestine [74].
\nIt is difficult to identify a single factor responsible of IBD; however, several observations have demonstrated a change in the gut microbial composition in IBD patients, both CD and UC [70]. Even though the gut microbiota has been recognized as responsible for the IBD establishment in non-predisposed hosts, numerous researches have revealed a high rate of pathogenic
For gastric cancer,
Worldwide, the colorectal cancer (CRC) is the fourth most common cause of death associated with cancer [81]. Like other cancers, the CRC is a complex disease related to environmental and genetic factors. Ongoing research has proposed that gut microbiota assumes a role in the convergence of these factors, likely through forming a tumor-advancing environment.
\nIn certain studies, by using a germ-free mice model of adenomatous polyposis coli (APC), a markedly reduced incidence of colonic tumor and a lower tumor load was revealed when compared to normally raised mice. Further other distinct CRC phenotypes such as bleeding from rectum and iron deficiency has also been shown with an invasion of inflammatory cells emerging from an intestinal epithelial barrier dysfunction. Therefore, it seems that the microbiome and host factors (for example, age and genetic predisposition) are important to the CRC growth and progression [82].
\nCardiovascular and metabolic disorders are collectively known as cardiometabolic diseases and are associated with high morbidity and mortality along with significant health care expenditures [83]. The gut-derived and endogenously produced endotoxins including indoxyl sulfate,
The gastrointestinal (GI) system and skin are highly vascularized and densely innervated organs with crucial neuroendocrine and immune roles which are uniquely related to the normal function of skin [90]. Evidence of bidirectional and intimate connection between the gut and skin health as well as a close link between GI health to skin allostasis and homeostasis has been established [91]. GI disturbances resulted often in cutaneous manifestations and the GI system, especially the gut microbiota, appears to participate in the pathophysiology of many inflammatory diseases, i.e., acne, atopic dermatitis and psoriasis [92, 93].
\nThe mechanism by which GI flora exert their effect on skin homeostasis is still unknown; however it is postulated that probably such effect may be related to the modulatory influence of gut commensals on the systemic immunity [94]. Certain gut microbiota and their metabolites, i.e., polysaccharide A, retinoic acid from
In cases of disturbance in intestinal barriers, it was found that intestinal bacteria and their metabolites may have the propensity to accumulate in the skin and have also access to the bloodstream which ultimately disrupts skin homeostasis. In fact, DNA of intestinal microbes has been separated from the plasma of psoriatic patients, thus showing a direct connection between the gut microbiota and skin homeostasis [90]. The short chain fatty acids (SCFAs), i.e., acetate, butyrate and propionate resulting from the fermentation of the fibers in GIT are believed to play an important role in the maintenance of certain skin microbiota which consequently affect cutaneous immune defense system. For example, propionic acid has an antimicrobial effect against the most common community-acquired methicillin-resistant
Intestinal dysbiosis may have the negative potential to affect the skin function since gut microbial flora has a huge potential to produce molecules, both harmful and beneficial, that could then reach the circulation and influence skin. Metabolic products of aromatic amino acids, i.e.,
Infectious diseases of the respiratory tract including pneumonia and influenza result in deaths of approximately 3.25 million people annually [99]. The majority of the therapies being used currently are suboptimal because the problems of efficiency, toxicity and antibiotic resistance are difficult to overcome [100]. Most of the respiratory tract infections represent failure of host’s immune defense. Recently, it was suggested that gut microbiota plays a crucial role in the initiation and adaptation of the immune response in other distal mucosal sites including lungs. Therefore, it is of interest to understand the underlying mechanisms that regulate the interplay between lung defense and gastrointestinal tract and how this interaction aids in achieving optimal lung health.
\nAn abnormal T-helper type 2 (Th2) cell responses is often associated with asthma and allergies. The Th2 cells are recognized by their ability to synthesize inflammatory cytokines including IL-13, IL-9, IL-5 and IL-4 [101] Evidence suggests that the development of allergic diseases in lung is directly affected by alteration in gut immune response [65]. In fact, a single oral dose of
Gut microbiota also plays a critical role in the immune response to respiratory tract viral infections like influenza. In infected mice, the CD8 and CD4 T cell subpopulations are directly influenced by the intestinal microbiota [103]. It has also been suggested that an intact intestinal microbiota is necessary for the expression of pro-inflammatory cytokines including pro-IL-18 and pro-IL-1β, which are essential for clearance of influenza [104]. This indicates that microbial signals are provided by gut microbiota which are crucial for the shaping and priming the immune response to viral pneumonia.
\nSimilar findings regarding the role of gut microbiome in immune response to respiratory bacterial infections have also been observed in germ-free mice. These mice were found to be more susceptible to pulmonary infection caused by bacterial pathogen
All systems of the body including maternal microbiome are affected by pregnancy. Changes in gut and vaginal microbiome during gestation are of particular significance because during vaginal delivery there is vertical transmission of microbes to the newborn [106, 107, 108]. During pregnancy the vaginal microbiota composition changes throughout the gestation period. In addition to vaginal microbiome, the maternal intestinal microbiome also undergoes change during pregnancy. It has been reported that bacterial diversity decreases in women as the pregnancy progresses [107]. Particularly, the ratio of pro-inflammatory
The consequences of changes in maternal vaginal and gut microbiota on mother health are not clear; however, the gestational changes in fecal and vaginal microbiota are considered to be important for the adaptive response necessary for protection as well as to promote the fetus health. These changes also help in providing a particular microbial inoculum to the newborn at birth before its exposure to other environmental microbes. Also the microbial communities’ composition in maternal vagina and gut are not independent of each other. In fact, in pregnant women of 35–37 weeks of gestation most of bacteria, including species of
Some research studies reported that shift in gut microbiota of mother during pregnancy may be an adaptive response for the mother and newborn health. In mice, an increase in the gut bacteria associated with gestational age, promotes body weight gain indicating a co-evolution of these microbes with their hosts during pregnancy [107]. Moreover, during vaginal delivery, the vertical transmission of these maternal gut microbiomes to the neonate may help the newborn to get an immediate access to microbiota at birth [107, 111].
\nBoth extrinsic and intrinsic factors play an important role to regulate the development and maturation of the central nervous system (CNS) in humans. In germ-free and antibiotic-treated animals the physiology of the CNS can be affected by neurochemistry as well as by specific microbiota [112]. Evidences for interaction between neuropsychiatric and gastrointestinal pathology in humans have been reported in different psychiatric conditions including autism, depression and anxiety [113].
\nThe role of gut-brain interaction in the nervous system development is also recognized. Gut-brain axis actually establishes a relationship between gut-microbiota and their interaction with brain leading to changes in the status of the CNS. The dysbiosis in microbial species of the gut may lead to induce imbalance in host homeostasis, atypical immune signaling and ultimately progression of CNS diseases [114].
\nThe permeable blood brain barrier (BBB) and functional lymphatic vessels residing in dura meningeal membrane may serve as a gateway for transmission of signals [115]. The exposure to several environmental factors can affect the generation of neurons during the development of the CNS [113]. It has been suggested that maternal-fetal interface permeability permits regulatory factors from the gut microbiota to stimulate Toll-like receptor 2 (TLR2) that helps to promote neural development of fetus and also impart its effects on cognitive function during adulthood [116].
\nThe combination of microbial strains (especially the probiotic) can actively counteract the deficient neurogenesis which further strengthen the developmental link of microbiome to the hippocampal neuronal generation [117]. The brain-blood barrier (BBB) is a highly selective and semipermeable barricade that permits the passage of neutral, low molecular weight and lipidic soluble molecules [118]. In the development of the structural components and growth of vasculature, BBB requires arachidonic acid (AA) and decohexaenoic acid (DHA) which are provided as polyunsaturated fatty acids (PUFA) by gut microbiome [119]. It has been demonstrated that the restoration of BBB is possible in germ-free mice by colonization of
The most important environmental factors that may lead to dysbiosis include (i) Physical or psychological stress, (ii) use of antibiotics, and (iii) diet (Figure 2).
\nEnvironmental factors influencing gut microbiota.
Stress is usually defined as homeostasis disruption due to physical, psychological or environmental stimuli known as stressors leading to adaptive behavioral and physiological response in order to restore homeostasis [121]. The effect of both psychological and physical stress on gut microbiome is widely recognized and has been observed in both humans as well as animals [122]. Some research conducted in mice has shown that the microbial composition in the cecum was altered in response to the exposure of a social stressor by placing an aggressive male mouse into the cages of non-aggressive mice. Furthermore, the plasma concentration of stress hormones such as adrenocorticotropic hormone (ACTH) and corticosterone was found to be significantly higher in germ-free mice as compared to specific pathogen-free mice. In addition, several stressors including acoustic stress, self-control conditions and food deprivation have a negative impact on the gut microbiome resulting in the impairment of the immune system [123, 124].
\nIt has been observed in both humans and animals that the treatment with antibiotics can result in a decreased population of beneficial bacteria including
Food is metabolized by the gut microbial species to extract nutrients, but some microbial species are more efficient in extracting nutrients from food as compared to other species. As different individuals have slightly different microbial populations, it is probable that more nutrients are harvested by some people’s gut microbes making them perhaps more prone to become overweight. A high percentage of
The human body is a super-organism consisting of 10 times more microbial cells than our own body cells. The body’s assortment of microorganisms is mainly in gastrointestinal tract, collectively called the gut microbiota. It can be comparable to an organ in because it performs functions necessary for our survival by contributing directly and/or indirectly in various physiological processes. For the past decade, human gut microbiota has been extensively studied as many scientists believe that human health mainly depends on microbes that are living on or in our body apart from our own genome. Recently, research findings have suggested that gut microbiome is evolving as a new organ system mainly due to its specific biochemical interaction with its host which affirm its systemic integration into the host physiology as gut bacteria are not only critical for regulating gut metabolism, but also important for other systems of host including immune system. The focus of this chapter was to highlight the importance of gut microorganisms as a new organ system and their possible involvement with host systems as well as the metabolism of different drugs and nutrients in the gut by these microbes. So, in this chapter, we have reviewed opinions of different researchers about the role of gut microbiota in maintaining health as well as its contributory role in different ailments. However, literature revealed that the involvement of gut microbiota in altering host genetics effecting disease progression needs further investigations.
\n"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges".
\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.
",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\\n\\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\\n\\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\\n\\nOAI-PMH
\\n\\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\\n\\nLicense
\\n\\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\\n\\nPeer Review Policies
\\n\\nAll scientific works are Peer Reviewed prior to publishing. Read more
\\n\\nOA Publishing Fees
\\n\\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\\n\\nDigital Archiving Policy
\\n\\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\\n"}]'},components:[{type:"htmlEditorComponent",content:'The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
\n\nPeer Review Policies
\n\nAll scientific works are Peer Reviewed prior to publishing. Read more
\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. I have served as the editor for many books, been a member of the editorial board in science journals, have published many papers and hold many patents.",institutionString:null,institution:{name:"Sheffield Hallam University",country:{name:"United Kingdom"}}},{id:"54525",title:"Prof.",name:"Abdul Latif",middleName:null,surname:"Ahmad",slug:"abdul-latif-ahmad",fullName:"Abdul Latif Ahmad",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"20567",title:"Prof.",name:"Ado",middleName:null,surname:"Jorio",slug:"ado-jorio",fullName:"Ado Jorio",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universidade Federal de Minas Gerais",country:{name:"Brazil"}}},{id:"47940",title:"Dr.",name:"Alberto",middleName:null,surname:"Mantovani",slug:"alberto-mantovani",fullName:"Alberto Mantovani",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"12392",title:"Mr.",name:"Alex",middleName:null,surname:"Lazinica",slug:"alex-lazinica",fullName:"Alex Lazinica",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/12392/images/7282_n.png",biography:"Alex Lazinica is the founder and CEO of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his PhD studies in Robotics at the Vienna University of Technology. Here he worked as a robotic researcher with the university's Intelligent Manufacturing Systems Group as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and most importantly he co-founded and built the International Journal of Advanced Robotic Systems- world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career, since it was a pathway to founding IntechOpen - Open Access publisher focused on addressing academic researchers needs. Alex is a personification of IntechOpen key values being trusted, open and entrepreneurial. Today his focus is on defining the growth and development strategy for the company.",institutionString:null,institution:{name:"TU Wien",country:{name:"Austria"}}},{id:"19816",title:"Prof.",name:"Alexander",middleName:null,surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/19816/images/1607_n.jpg",biography:"Alexander I. Kokorin: born: 1947, Moscow; DSc., PhD; Principal Research Fellow (Research Professor) of Department of Kinetics and Catalysis, N. Semenov Institute of Chemical Physics, Russian Academy of Sciences, Moscow.\r\nArea of research interests: physical chemistry of complex-organized molecular and nanosized systems, including polymer-metal complexes; the surface of doped oxide semiconductors. He is an expert in structural, absorptive, catalytic and photocatalytic properties, in structural organization and dynamic features of ionic liquids, in magnetic interactions between paramagnetic centers. The author or co-author of 3 books, over 200 articles and reviews in scientific journals and books. He is an actual member of the International EPR/ESR Society, European Society on Quantum Solar Energy Conversion, Moscow House of Scientists, of the Board of Moscow Physical Society.",institutionString:null,institution:{name:"Semenov Institute of Chemical Physics",country:{name:"Russia"}}},{id:"62389",title:"PhD.",name:"Ali Demir",middleName:null,surname:"Sezer",slug:"ali-demir-sezer",fullName:"Ali Demir Sezer",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62389/images/3413_n.jpg",biography:"Dr. Ali Demir Sezer has a Ph.D. from Pharmaceutical Biotechnology at the Faculty of Pharmacy, University of Marmara (Turkey). 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I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). I am a Reviewer for several refereed journals and international conferences, such as IEEE Transactions on Biomedical Engineering, IEEE Transactions on Industrial Electronics, Optic Letters, Measurement Science Review, and also a member of the International Advisory Committee for 2012 IEEE Business Engineering and Industrial Applications and 2012 IEEE Symposium on Business, Engineering and Industrial Applications.",institutionString:null,institution:{name:"Joseph Fourier University",country:{name:"France"}}},{id:"55578",title:"Dr.",name:"Antonio",middleName:null,surname:"Jurado-Navas",slug:"antonio-jurado-navas",fullName:"Antonio Jurado-Navas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/55578/images/4574_n.png",biography:"Antonio Jurado-Navas received the M.S. degree (2002) and the Ph.D. degree (2009) in Telecommunication Engineering, both from the University of Málaga (Spain). He first worked as a consultant at Vodafone-Spain. From 2004 to 2011, he was a Research Assistant with the Communications Engineering Department at the University of Málaga. In 2011, he became an Assistant Professor in the same department. From 2012 to 2015, he was with Ericsson Spain, where he was working on geo-location\ntools for third generation mobile networks. Since 2015, he is a Marie-Curie fellow at the Denmark Technical University. 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