The results of molecular docking simulation.
\\n\\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\nThank you all for being part of the journey. 5,000 times thank you!
\\n\\nNow with 5,000 titles available Open Access, which one will you read next?
\\n\\nRead, share and download for free: https://www.intechopen.com/books
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\nDr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\n\nThank you all for being part of the journey. 5,000 times thank you!
\n\nNow with 5,000 titles available Open Access, which one will you read next?
\n\nRead, share and download for free: https://www.intechopen.com/books
\n\n\n\n
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\r\n\tElectromagnetic imaging is an emerging biomedical imaging modality, which when matured, might present an effective supplement to current imaging technologies for non-invasive assessment of functional and pathological conditions of tissues. This book aims to provide a state-of-art for the most relevant advancements in the development of electromagnetic sensing and imaging for non-invasive detection, by covering all aspects related to the design, modeling, and experimentation. The authors are welcome to submit original research and review articles reporting recent advances in the application of electromagnetic waves technologies in industry and bioengineering.
\r\n\r\n\tThe scope of this book will be the collection of new and/or review results exploring the use of electromagnetic waves for industrial and biomedical applications with particular focus on inclusion detection and medical treatment as well as a diagnostic tool for disease detection. Potential topics include but are not limited to the following: Electromagnetic sensing and imaging for industry applications, Electromagnetic sensing and imaging for biomedical applications, Microwave sensing and imaging , Non-invasive electromagnetic diagnostic tools, Usage of electromagnetic waves for probing organs and advanced MRI techniques, Theoretical modeling of electromagnetic wave propagation, Application of electromagnetic waves in advanced MRI techniques, RF sensors and coils, Biomaterials for wearable sensors, In vitro and in vivo testing.
",isbn:"978-1-83968-582-8",printIsbn:"978-1-83968-581-1",pdfIsbn:"978-1-83968-583-5",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"e57ef4b5bada0d966637cd303d76278f",bookSignature:"Distinguished Prof. Lulu Wang",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/9878.jpg",keywords:"Electromagnetic Sensing, Imaging, Biomedical Applications, Electromagnetic Measurements, Conductivity, Electromagnetic Induction Tomography, Electric Impedance Imaging, Microwave Imaging, Biomaterials, RF Coils, Electromagnetic Scattering Problems, Integral Equations",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"August 26th 2020",dateEndSecondStepPublish:"November 3rd 2020",dateEndThirdStepPublish:"January 2nd 2021",dateEndFourthStepPublish:"March 23rd 2021",dateEndFifthStepPublish:"May 22nd 2021",remainingDaysToSecondStep:"3 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"With an M.E. (Hons.) and a Ph.D. degree from the Auckland University of Technology, New Zealand, Dr. Wang is the first author of over 60 peer-reviewed publications, received multiple national and international awards from various professional societies and organizations she is a member of (ASME, IEEE, AAAS, PSNZ, and IPENZ ).",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"257388",title:"Distinguished Prof.",name:"Lulu",middleName:null,surname:"Wang",slug:"lulu-wang",fullName:"Lulu Wang",profilePictureURL:"https://mts.intechopen.com/storage/users/257388/images/system/257388.jpg",biography:"Lulu Wang is a Full Professor of Biomedical Engineering at Shenzhen Technology University in China. She received the M.E. (First class Hons.) and Ph.D. degrees from the Auckland University of Technology, New Zealand, in 2009 and 2013, respectively. From 2013 to 2015, she was a Research Fellow with the Institute of Biomedical Technologies, Auckland University of Technology, New Zealand. In 2015, Dr. Wang became an Associate Professor of biomedical engineering with the Hefei University of Technology. In 2019, she became a Full Professor of biomedical engineering with the College of Health Science and Environmental Engineering, Shenzhen Technology University. Her research interests include medical devices, electromagnetic sensing and imaging, and computational mechanics. Over the past five years, Dr. Wang is the first author of 60 peer-reviewed publications, 2 ASME books, 7 book chapters, and 12 innovation patents. She has edited three books and two special issues of international journals. Dr. Wang is a member of ASME, IEEE, AAAS, PSNZ, and IPENZ. She has been an active scientific reviewer for numerous journals and international conferences. She received multiple National and International Awards from various professional societies and organizations.",institutionString:"Shenzhen Technology University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"2",institution:{name:"Shenzhen Technology University",institutionURL:null,country:{name:"China"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"20",title:"Physics",slug:"physics"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"259492",firstName:"Sara",lastName:"Gojević-Zrnić",middleName:null,title:"Mrs.",imageUrl:"https://mts.intechopen.com/storage/users/259492/images/7469_n.png",email:"sara.p@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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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"58078",title:"Bioinformatics Approach to Screening and Developing Drug against Ebola",doi:"10.5772/intechopen.72278",slug:"bioinformatics-approach-to-screening-and-developing-drug-against-ebola",body:'Ebola, previously known as Ebola virus disease, is an acute viral infection causing hemorrhagic fever marked by high mortality rate in human and nonhuman primates [1]. It is a zoonotic disease transmitted by direct contact with mucosal tissue or bodily fluids (blood, feces, and other secreted fluids) of the infected living or dead human and animal [2, 3, 4]. The animal reservoir for this disease is still unknown. Fruit bat (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) which belongs to Pteropodidae family is suspected as the most likely host of Ebola, although the linkage has not been confirmed [5, 6, 7].
Ebola is an enveloped, nonsegmented, negative-sense, single-stranded RNA virus which belongs to Ebolavirus genus, Filoviridae family, and Mononegavirales order [8, 9]. Ebola virus (EBOV), Tai Forest virus (TAFV), Reston virus (RESTV), Sudan virus (SUDV), and Bundibugyo virus (BDBV) are the virus making up the Ebolavirus genus [10]. EBOV and SUDV come as the most frequent outbreak-causing virus which has the case-fatality rate of 76 and 55% (CI 95%), respectively [11]. On the other hand, RESTV causes death in primates such as gorillas and chimpanzees but not known to have caused disease in humans [12, 13].
The Ebola virus genomic RNA is consisted of around 19,000 nucleotides [14]. It encodes seven structural protein, namely, nucleoprotein (NP), glycoprotein (GP), RNA-dependent RNA polymerase (L), matrix protein (VP40), and three nucleocapsid proteins (VP24, VP30, and VP35) [15, 16]. It also encodes one nonstructural protein, the secretory glycoprotein (sGP) [17]. The genome is linearly arranged as follows: 3′-leader-NP-VP35-VP40-GP/sGP-VP30-VP24-L-trailer-5′ [14, 17, 18].
The seven structural proteins and one nonstructural protein have an imperative role in Ebola virus life cycle [16]. NP: viral replication and scaffold for additional viral proteins. GP: binds to receptors on the cell surface and membrane fusion, pathogenicity. sGP: inhibits neutrophil function and adsorbs neutralizing antibodies. L: synthesis of positive-sense RNA. VP40: viral assembly and budding, structural integrity of viral particles, and maturation of the virion. VP24: nucleocapsid formation, encapsulates and shields viral genome from nucleases, viral replication. VP30: viral transcription activator. VP35: multi-virulence functionality, innate immune antagonist, and an RNAi silencing suppressor [16, 17].
The patient who suffers from Ebola shows no symptoms during the initial infection. After the incubation for about 4–10 days, the general symptoms such as fever, myalgia, and malaise and sometimes accompanied by chills appear. These symptoms often confused with dengue or malaria in tropical climates [3, 19]. As the infection progresses, the patient shows flu-like symptoms accompanied by gastrointestinal symptoms. In severe cases, Ebola developed into a conjunctival hemorrhage, epistaxis, melena, hematemesis, coagulation abnormalities, and a range of hematological irregularities. The neurological symptoms such as encephalopathy, convulsions, and delirium may also occur during the late stage of the infection [19, 20]. The patient dies around 6–9 weeks after the symptoms appear [21]. With the nonspecific symptoms, severe morbidity, and high mortality rate, the World Health Organization (WHO) has acknowledged Ebola as one of the most malignant diseases in the world [22].
The first recorded Ebola outbreak emerged in Sudan between June and November 1976. It mainly affected Nzara, Maridi, Tembura, and Juba where 150 of 284 victims died (the mortality rate of 53%) [2, 23]. After the first outbreak, 19 other outbreaks have occurred in Africa with the mean fatality rate of 65.4% [11].
The last and the most extensive Ebola outbreak was announced by the WHO on March 23, 2014. This outbreak appears to have emerged in the Guéckédou district of the southeast region of Republic of Guinea [24, 25, 26]. The WHO announced the epidemic to be a Public Health Emergency of International Concern (PHEIC) on August 8, 2014, due to the severe consequences if Ebola ever spread around the globe. PHEIC was disclosed because of the weak health services of Guinea, Liberia, Sierra Leone, and other neighboring countries at risk in combating Ebola and the continuing transmission with a high fatality rate of Ebola in West Africa [26]. When the outbreak ends in March 2016, Ebola has claimed 1310 lives out of 28,616 reported cases [27, 28]. Even though the damage caused by the last outbreak of Ebola is calamitous, there is still no FDA-approved antiviral drug to treat this disease.
Ebola is considered as one of the neglected tropical diseases because the outbreaks take place in the poor populations with limited resources, mostly in West Africa [29]. The research and drug development for Ebola have been neglected for decades because the drug developers regard it as a commercially unattractive project to invest their resource. The negligence occurs to all tropical diseases by only 13 out of 1393 new approved drugs between 1975 and 1999 that were indicated for tropical disease [30]. However, the frequent outbreaks in the last decade and the massive outbreak which was occurred in 2014 have drawn much attention to drug development for Ebola [16]. Without available treatment or vaccine, paramedic only relied on palliative care for the infected patients and barrier methods to prevent the transmission [31]. Hence, the researchers investigating ways for helping people just infected with Ebola (treatment) and preventing people to get infected when exposed to Ebola (vaccine) [32].
The conventional medical treatment for Ebola is a supportive care with intravenous fluids or oral rehydration with electrolyte solutions. The reason being that the virus interferes with blood clotting and disrupts electrolyte balance. Thus, such intervention can help to keep up the condition of the patient. However, such intervention is not enough for severely ill patients to sustain and recover [21, 32].
Zmapp, a combined humanized monoclonal antibody, was tested as a passive immunotherapy against Ebola. The preclinical test was conducted by Mapp Biopharmaceutical. This monoclonal antibody shows 100% efficacy in preventing lethal disease on cynomolgus macaques when treatment is initiated up to 5 days postinfection of EBOV [31].
Other experimental therapies developed a novel synthetic adenosine analog, BCX4430. This compound shows in vitro and in vivo activity by inhibiting viral RNA polymerase function, acting as a non-obligate RNA chain terminator. BCX4430 protects both mice and guinea pig models from a severe infection of Ebola virus and Marburg virus. In addition, this compound completely protects cynomolgus macaques from Marburg virus infection if administered as late as 48 h after infection [33].
Not only does the research focus on the development of a novel drug, but the research is also conducted to identify potential repurposed therapeutic agents for the treatment of Ebola [34, 35]. Toremifene and clomiphene, the selective estrogen reuptake modulators, are currently known as the drug to treat breast cancer and infertility, respectively. Both drugs inhibit Ebola virus entry into the cell by preventing the late stage membrane fusion. These drugs show an inhibition activity by more than 90% in vitro. Higher dose than the standard clinical range is needed to achieve the therapeutic effect on Ebola. However, a higher dose would increase the risk of serious side effect of toremifene and clomiphene, which are electrolyte derangements and ocular adverse effect, respectively [36].
Other experiments screen amiodarone, a multichannel ion blocker; sertraline, selective serotonin reuptake inhibitor; and bepridil, a calcium channel blocker as a repurposed therapeutic agent targeting Ebola. Amiodarone works by the induction of Niemann-Pick C-like phenotype that inhibits late endosomal entry of Ebola virus [37]. Sertraline and bepridil work in a similar fashion to amiodarone. Both drugs show inhibition activity in an in vitro test by more than 90% [35].
Several vaccines have also been developed to prevent the Ebola. ChAd3-ZEBOV, which has developed by GlaxoSmithKline in collaboration with the US National Institute of Allergy and Infectious Diseases, is a chimpanzee-derived adenovirus vector with an Ebola virus gene inserted. This vaccine induced uniform protection against acute lethal Ebola virus in cynomolgus macaques. However, the protection of this vaccine declines over several months [38].
The other vaccine, which is developed by the Public Health Agency of Canada in Winnipeg, is rVSV-ZEBOV. It uses an attenuated vesicular stomatitis virus which has been genetically modified to express glycoprotein of Ebola virus. The rVSV-ZEBOV has undergone a ring vaccination phase 3 efficacy trial which assesses the protective activity of rVSV-ZEBOV against Ebola virus in human beings. The result shows that rVSV-ZEBOV offers substantial protection against Ebola virus infection. Both randomized and a non-randomized clusters of vaccinated individuals show no disease development from the challenge performed 10 days postvaccination [39].
The Center for Disease Control and Prevention considered Ebola virus as a tier 1 select agent because it possesses a considerable risk of intentional misuse with a severe threat to public health and safety [40]. Researchers need to fill the APHIS/CDC Form 1 in order to register for possession, use, and transfer of Ebola virus. All requirements including the availability of Biosafety Level (BSL) 4 laboratory and certified personnel are needed to get access to Ebola virus sample [41]. Thus, to get a suitable sample, researchers tend to move their experiments on the genetically modified virus that can express part of known Ebola virus genome because it is not subjected to select agent [42].
Genomic and proteomic data of Ebola virus has been collected each time the outbreak occurred and stored in the open source database. Also, the Ebola virus protein interaction with the corresponding drug lead through in vitro test has also been increased in the past decades. To date, the protein three-dimensional (3D) structure of Ebola virus NP, VP35, VP40, GP, VP30, and VP24 has been available in Protein Databank (PDB). In addition, the active site residues of each protein have also been identified, except for NP. L is the only Ebola virus protein with unavailable 3D structure and unidentified active site [16]. Thus, researchers use a bioinformatics approach to utilize the readily available genomic and proteomic data to research drug design and discovery.
Computer-aided drug discovery and development (CADDD) is employed to accelerate hit identification, hit-to-lead selection, enhance absorption, distribution, metabolism, excretion, and toxicity (ADMET) profile and avoid another safety issue [43]. This approach is currently growing and adapted quickly by pharmaceutical industry and academia because it reduces the time and cost of drug research [44, 45]. Currently, 16 compounds (Aliskiren, Boceprevir, Captopril, Dorzolamide, Indinavir, LY-517717, Nolatrexed, NVP-AUY922, Oseltamivir, Raltegravir, Ritonavir, Rupintrivir, Saquinavir, TMI-005, Tirofiban, and Zanamivir) are in clinical trial or have been approved for therapeutic use. These compounds are the examples of successful application of CADDD [46, 47]. Through CADDD, the hit rate of the novel and repurposed drug for Ebola therapy could be improved.
A consistently effective treatment for Ebola is currently not yet available. Present therapeutic options are directed at palliative and supportive care to maintain and prolong the patient life. The majority of treatment, novel or repurposed drug, have been developed, but none of them are entirely satisfactory. In attempts to find a drug in the treatment of Ebola, inhibitors targeting EBOV VP35 have received little attention even though it has a critical function in host immune evasion and viral RNA synthesis. Our objective is to find the optimal in silico Ebola therapeutic agents which later will be implemented in the wet laboratory.
In this chapter, we will discuss the result of our in silico approach against EBOV VP35, one of the viral protein of EBOV which is responsible for the viral RNA synthesis and as the RNAi silencing suppressor agents [48, 49]. Moreover, this protein was also being studied by Brown et al. in 2014, which discovered the actual pose of their selected inhibitors against the EBOV VP35 in their perspective binding site and also deposited their work in RCSB Protein Databank (PDB) through several PDB IDs [50]. Thus, their proteins can be used as the template for pharmacophore mapping model for our docking simulation approach. Moreover, we also deployed the Indonesian natural product compounds for virtual screening purpose to find the suitable lead compounds for combating Ebola. The reason for choosing the Indonesian natural product compounds because of Indonesia, as one of the largest megadiversity countries, has no less than 38,000 flowering plants that grow around the nation, with 55% of them are endemic plants [51, 52].
First, we prepared the Indonesian natural product compounds by searching the molecular structures through several journals and databases [53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69], after which we were drawing them using ChemBioDraw 14.0 software. From this step, we obtained about 3429 compounds in the process. All of these ligands were then protonated, washed, and minimized by using MOE 2014.09 software [70]. These ligands were saved for the docking simulation purpose. For the EBOV VP35 protein, we selected the PDB ID: 4IBC as our protein, and we determined the pharmacophore site through standard protein-ligand interaction fingerprints (PLIF) protocol of MOE 2014.09 software. This step generated the pharmacophore model around the binding site of EBOV VP35 after we performed the protonating process of EBOV VP35 through “LigX” feature of MOE 2014.09 software. Later on, we conducted molecular docking simulation using the modification of our current approach [71, 72]. Instead of using “Triangle Matcher” and “London dG,” we used “Pharmacophore” and “Affinity dG” for “Placement” and “Rescoring 1” parameters to accommodate the pharmacophore model that created in an earlier phase, while the rest of parameters were set according to the default setup. First, the STD1 ligand (IUPAC name: 2-(4-(4-(2-chlorobenzoyl)-5-(2-chlorophenyl)-2,3-dioxo-2,3-dihydro-1H-pyrrol-1-yl)phenyl)acetic acid) and 100 decoy ligands were docked into the binding site to validate the pharmacophore model. “Rigid Receptor” and “Induced-Fit” protocols were performed against the Indonesian natural product compounds and STD1 ligand later on.
In an attempt of searching the proper pharmacophore site in the binding site of EBOV VP35, we utilized the PLIF protocol from MOE 2014.09 software by using STD1 ligand as the template. From this approach, we figured out that the binding site of EBOV VP35 protein consists of three pharmacophore sites, as it displayed in Figure 1. One hydrophobic spot is affiliated with Lys248 residues through arene-hydrogen interaction, while two H-bond acceptors, lone-pair sites, are connected with Gln241 and Lys251. These sites were responsible for the binding attachment of the STD01 ligand when bound to EBOV VP35 protein. Thus, it can be predicted that any ligands that bind to these residues may exhibit the same antiviral activities like STD01 ligand.
The pharmacophore model of the STD01 ligand in the binding site of EBOV VP35 protein. According to the PLIF feature of MOE 2014.09 software, the STD01 ligand comprises three pharmacophore sites: one hydrophobic point and two acceptor/lone-pair points (left). In the docking simulations, we deployed the “exclude points” to indicate the residues that exist in the VP35 binding site and prevent the larger ligands to interact with the binding site.
The pharmacophore sites were later validated by having the STD01 ligand and 100 decoys to be screened through molecular docking simulation. In this phase, we deployed “virtual screening” approach as our docking protocol, with pharmacophore model that was included in the simulation. After the screening was conducted, we discovered that all of the decoys did not pass the test, indicating this method was validated and did not create the “false-positive” ligand that may result during docking simulation. Furthermore, the STD01 ligand passed this test with a ∆Gbinding score of −5.2778 kcal/mol and RMSD value of 1.5487 Å. This result was shown that the parameters that were set earlier were decent enough to be reproduced in the next simulation. The comparison of the initial and screened poses of STD01 ligand is shown in Figure 2.
The binding interaction of the STD01 ligand and EBOV VP35 binding site. The 2D interaction after docking simulation is displayed in the left figure, while the right figure presents the difference between the initial pose (shown in yellow) and after the docking simulation was conducted (shown in pink).
The pharmacophore-based docking simulation of EBOV VP35 protein was later performed against the 3429 Indonesian natural product ligands that were already prepared. From the simulations, we acquired 20 ligands that matched with the pharmacophore model of EBOV VP35, which means that other 3409 ligands did not possess the properties that needed to pass the initial pharmacophore screening. In the first docking simulation (Rigid Docking protocol), we found four Indonesian natural product ligands, namely, multifloroside, myricetin 3-robinobioside, kaempferol 3-(6G-malonylneohesperidoside), and theasaponin, which have the ∆Gbinding score lower than the STD01 ligand. The molecular structures of these ligands can be seen in Figure 3.
The molecular structure of multifloroside (top left), myricetin 3-robinobioside (top middle), kaempferol 3-(6G-malonylneohesperidoside) (top right), theasaponin (bottom left), and 2-(4-(4-(2-chlorobenzoyl)-5-(2-chlorophenyl)-2,3-dioxo-2,3-dihydro-1H-pyrrol-1-yl)phenyl)acetic acid (bottom right).
After the first docking simulation had been performed, the second docking simulation (Induced-Fit protocol) was utilized against these four proteins to revalidate the docking pose that was produced in the previous simulations. If the RMSD difference was lower than 2.0 Å, it means that the docking pose is good enough and may be reproduced in the actual simulation [73]. In this simulation, we found that multifloroside ligand has the lowest ∆Gbinding score of −10.8405 kcal/mol, followed by myricetin 3-robinobioside (−10.0897 kcal/mol), kaempferol 3-(6G-malonylneohesperidoside) (−9.8721 kcal/mol), and theasaponin (−9.0175 kcal/mol). These results were significantly lower than the STD01 ligand, which sits in −9.0175 kcal/mol. However, we must take into account that the RMSD value of multifloroside ligand was 3.2691 Å, higher than 2.0 Å; it means that the docking pose that was generated during the docking simulation was not acceptable. Meanwhile, the other three ligands possessed the tolerable RMSD value (1.2275, 1.0311, and 0.4352 Å for myricetin 3-robinobioside, kaempferol 3-(6G-malonylneohesperidoside), and theasaponin, respectively). Furthermore, we also observed the interactions between the ligands and the binding site of EBOV VP35. From the docking simulation, we figured out that all three remaining ligands made interactions with Gln241 and Lys251, which are important in suppressing the EBOV VP35 activity. The full results of molecular docking simulations can be seen in Table 1 and Figure 4.
Molecule name | ∆Gbinding (RMSD) | H-bond interaction residues |
---|---|---|
Multifloroside | −10.8405 kcal/mol (3.2691) | Arg225, Tyr229, Lys 248, and Lys251 |
Myricetin 3-robinobioside | −10.0897 kcal/mol (1.2275) | Lys222, Arg225, Gln241, and Lys251 |
Kaempferol 3-(6G-malonylneohesperidoside) | −9.8721 kcal/mol (1.0311) | Gln241, Gln244, Lys251, and His296 |
Theasaponin | −9.0175 kcal/mol (0.4352) | Arg225, Gln241, and Lys251 |
STD01 ligand (standard) | −8.4579 kcal/mol (0.7747) | Gln241, Lys248, and Lys251 |
The results of molecular docking simulation.
The interacting residues of EBOV VP35 protein with myricetin 3-robinobioside (left), kaempferol 3-(6G-malonylneohesperidoside) (middle), and theasaponin (right).
Without no doubt, the drug developments of Ebola are desperately needed due to high pathogenicity and mortality rate that emitted by this disease. Through this chapter, we present that bioinformatics and CADDD, especially the pharmacophore-based drug design, may be the solution to significantly increase the viability of the newly discovered lead compounds that can be introduced as the drug candidate of Ebola virus, which can be supported later through in vitro study to validate the results that we found in previous research. The dry lab experiments should play a significant role in the development of drugs, not only Ebola but also for all diseases due to low cost and not a time-consuming process. Therefore, the improvements and developments of bioinformatics and CADDD should also speed up the time that we needed to obtain the drug candidates for our health problems.
This book chapter is financially supported by Penelitian Unggulan Perguruan Tinggi (PUPT) 2017, granted by Ministry of Research, Technology, and Higher Education, the Republic of Indonesia through Directorate of Research and Community Engagements, Universitas Indonesia, with no: 2716/UN2.R3.1/HKP.05.00/2017.
None are declared.
The universal aging of the population is a global concern because of its association with degenerative diseases, which can cause disabilities in humans, limit their productivity in society, and negatively affect their quality of life [1, 2, 3, 4, 5].
In all societies, blindness has profound human and socioeconomic consequences. The costs of loss of productivity, rehabilitation, and education for the blind constitute a significant economic burden for the individual, the family, and society [6].
Thus, it is interesting to know that total or partial opacification of the lens is the main cause of bilateral blindness and severe visual impairment represents about 48% of cases of visual impairment in the world and is known to have a multifactorial cause. In addition, it incapacitates the individual and increases their dependence and early retirement from life [7].
According to the WHO, visual function is subdivided into four levels: normal vision, moderate visual impairment, severe visual impairment, and blindness. Visual disability includes moderate and severe visual impairment and blindness [8, 9], see Table 1.
Category | Visual acuity |
---|---|
Normal vision | 20/20–20/60 |
Moderate visual impairment | 20/60–20/200 |
Severe visual disability | 20/200–20/400 |
Blindness | ≥20/400 |
Count the fingers at 1, 2, 3 m | |
HM | |
PL | |
DNPL |
Classification of visual function according to the WHO.
Symbology: Hand movement (HM), perceive light (PL), do not perceive light (DNPL), meter (m).
The International Classification of Diseases (WHO ICD-10) contains the following definitions:
Blindness: visual acuity (AV) less than 20/400 in the best eye with the available correction (AVCD), with the best possible correction AVMC or with pinhole hole (AVAE)
Severe visual impairment (DVG): AV 20/200–20/400 in the best eye with the AVCD, AVMC, or AVAE
Moderate visual impairment (MVD): AV 20/60–20/200 in the best eye with AVCD, AVMC, or AVAE [7, 10, 11]
Low vision: alteration of visual function, even after treatment and/or standard correction of refraction and an AV less than 20/60 to perception of light but useful for planning or executing a task [7, 8, 10, 11]
According to the WHO data, it is estimated that, worldwide, approximately 1300 million people live with some form of visual impairment. More than 314 million have a severe visual impairment. Of these, 37 million are blind and 124 million suffer from low vision. Eighty percent of all these cases are considered avoidable [12, 13].
According to WHO estimates, of the more than 26 million people with visual disorders in the Region of the Americas in 2010, more than 3 million were blind, and most of them were 50 years of age or older [12].
Most of the national and local surveys were published and published in Latin America, and refractive errors were not corrected in the main cause of visual impairment, both severe (19.7%) and moderate (58.6%) [14, 15, 16].
Between 1990 and 2010, the prevalences normalized according to the age of blindness, and moderate and severe visual impairment decreased in Latin America and the Caribbean [17].
The WHO estimated the prevalence of blindness in 2002 in people over 50 years by subregions [18], see Table 2. In Latin America, the prevalence of blindness in people over 50 responds between 1% in urban areas with good socioeconomic development and more than 4% in rural and marginal areas [19]. In Central America, the prevalence of blindness is 2.1% (95% CI: 1.7–2.7) [17], and in countries such as Panama, it is 3.0% (95% CI: 2.3–3.6) [20], Costa Rica 1.7% (2.1%, IC95%: 1.7–2.7) [21], and Honduras 1.9% (95% CI: 1.4–2.4%) [22].
WHO subregion | Country | Prevalence of blindness in people aged 50+ (%) |
---|---|---|
Amr-A | Canada, Cuba, USA | 0.4 |
Amr-B | Argentina, Bahamas, Belize, Brazil, Chile, Colombia, Costa Rica, Dominica, Dominican Republic, El Salvador, Grenada, Guyana, Honduras, Jamaica, Mexico, Panama, Paraguay, Suriname, Uruguay, Venezuela | 1.3 |
Amr-C | Bolivia, Ecuador, Guatemala, Haiti, Nicaragua, Peru | 2.6 |
Estimates of the prevalence of blindness in 2002 in people over 50 years of age by subregion of the WHO.
Source: Silva [18].
In Latin America, cataract without correction represents by far the main cause of blindness in adults over 50 years, followed by glaucoma, diabetic retinopathy (DR), age-related macular degeneration, and uncorrected refractive errors [23], see Table 3.
Country | Uncorrected refractive error (%) | Uncorrected cataract (%) | Non-trachomatous corneal opacity (%) | Glaucoma (%) | Diabetic retinopathy (%) | Age-related macular degeneration (%) |
---|---|---|---|---|---|---|
Argentina | 8.0 | 44.0 | 0.0 | 8.0 | 16.0 | 4.0 |
El Salvador | 4.0 | 68.7 | 7.1 | 5.1 | 5.1 | 4.0 |
Honduras | 3.0 | 59.2 | 2.6 | 21.1 | 0.0 | 3.9 |
Panamá | 0.1 | 66.4 | 2.2 | 10.2 | 1.5 | 5.1 |
Paraguay | 3.1 | 43.8 | 9.4 | 15.6 | 6.3 | 9.4 |
Peru | 1.5 | 58.0 | 5.3 | 13.7 | 0.8 | 11.5 |
Uruguay | 2.9 | 48.6 | 0.0 | 14.3 | 5.7 | 8.6 |
Main reported causes of blindness adults over 50 years, Latin America, 2011–2013.
Source: Silva [23].
The causes from one country to another. The visual impairment attributable to cataract is greater in low- and middle-income countries than in high-income countries. In high-income countries, diseases such as diabetic retinopathy, glaucoma, and macular degeneration are related to the most frequent age [24].
Johns Hopkins University has found that the main cause of blindness in white people is macular degeneration associated with age, while in the black population, it is due to glaucoma or cataract. In addition, in the elderly, blindness is three times more frequent in blacks than in whites [25].
The main causes of blindness in order of frequency are cataract (39%), uncorrected refractive errors (18%), glaucoma (10%), macular degeneration related to age (7%), corneal opacities (4%), diabetic retinopathy (4%), trachoma (3%), childhood eye diseases (3%), and onchocerciasis (0.7%). Cataract is the leading cause of easily curable blindness [7, 26].
For this reason, a description of the main causes is made, see Table 4.
Causes | Definition |
---|---|
Cataract | It is the opacity of the lens, which is understood as the passage of light to the retina, causes a slow and progressive loss of vision, and can appear at any stage of life, from birth to older age than being human [27, 28, 29, 30] |
Glaucoma | It is an optic neuropathy that presents with a characteristic structural damage, associated with the progressive death of retinal ganglion cells, loss of nerve fibers, and loss of pathognomonic visual field [31, 32, 33, 34] |
Uncorrected refraction | In myopia, the point of focus is in front of the retina, because the cornea has too much curvature or the axial length of the eye is excessive In hyperopia, the focus point is behind the retina because the cornea has too flat a curvature or the axial length is too short Astigmatism, a non-spherical (variable) curvature of the cornea or lens, causes light rays of different orientations (e.g., vertical, oblique, horizontal) to focus on different points [35] Presbyopia is a clinical loss of the amplitude of accommodation or, in other words, the loss of the ability to change the shape of the lens to focus on nearby objects [35, 36] |
The most common causes of visual disability and blindness.
The different etiologies are known to have multifactorial causes; in cataract modifiable risk factors are identified as exposure to ultraviolet rays, mainly UV-B, deficiency in the diet of antioxidants and proteins, smoking, diabetes mellitus, the use of corticosteroids, and severe dehydration. And non-modifiable risk factors are genetic, with a probability three times higher in relatives of people with the disease [37, 38, 39, 40, 41].
In glaucoma it is said that age increases the probability of suffering ocular hypertension. A glaucoma can evolve of various etiologies. The prevalence increases from 4 to 10 times in people older than 60 years [42]. Other risk factors are myopia, inheritance, African-American race, exfoliation, and pigmentary dispersion [43].
Refractive errors are associated with racial factors, the myopia and astigmatism are more prevalent in the Chinese population and hyperopia is the most common in the Hispanic population [44].
Regarding diabetic retinopathy (DR), it corresponds to one of the microvascular complications of diabetes mellitus.
The risk factors are the time of evolution of DM and poor glycemic control, glycosylated hemoglobin (HbA1c) level greater than 6.9% [45], associated arterial hypertension [46, 47], juvenile type 2 DM of early onset [48], and genetic susceptibility (the haptoglobin genotype 1-1) [49].
In Figure 1, the relationship between glycemic control and the duration of diabetes with diabetic retinopathy is shown as a function of the time of follow-up, with different curves for the different HbA1C values [50].
The relationship between glycemic control and duration of diabetes with diabetic retinopathy. Source: Longo et al. [50].
Between 80 and 95% corresponds to simple or nonproliferative DR and the remaining 5–10% to proliferative DR [51].
Basic knowledge of ocular symptoms is required to perform an adequate ophthalmological evaluation. It is always necessary to completely define the characteristics of the symptoms and discomforts.
The ocular symptoms can be classified in the fundamental categories: abnormalities of the eyes, anomalies of the ocular aspect and abnormalities of the sensations, pains, and ocular discomforts.
Therefore, it can be useful to make one order and ask the following questions:
Has the disorder started gradually, quickly, or asymptomatically? For example, was blurred vision in one eye discovered until the other eye was inadvertently covered?
Was the duration of the problem brief, or did the symptom persist until the current consultation? If the symptom has been intermittent, how has been its frequency?
Is the location of the disorder focal or diffuse, and is it a unilateral or bilateral condition? Finally, does the patient rate the degree of the disorder as mild, moderate, or severe?
In Table 5, some of the main characteristics of the most common pathologies associated with preventable blindness are observed.
Of all the organs of the body, the eye is the most accessible to direct examination. The visual function can be evaluated by means of simple subjective tests. The same can be taken care of from an adequate primary care service.
The clinic plays a decisive role in the initial evaluation of any patient, so the correct approach orderly and systematic is essential in the sequence of subsequent processes for the consolidation of a presumptive diagnosis and complementary tests and to achieve an accurate diagnosis and therapeutic approach suitable.
Therefore, an adequate anamnesis that includes general, sociodemographic data, personal and family pathological history, and ocular and non-ocular as well as traumatic surgical history is imperative and invariably its symptomatology.
The external anatomy of the eye is visible and can be examined with the naked eye or with simple instruments.
The eye is the only part of the body where you have direct vision to blood vessels and tissues of the central nervous system (retina and optic nerve). Thanks to this it is possible to identify, by ocular examination, important systemic effects of infectious, autoimmune, neoplastic, and vascular diseases.
And so, a basic physical examination aimed at the search of suspected abnormalities that merit its timely reference to a higher level of specialty is essential in the primary care physician, see Figure 2.
Basic ophthalmologic exploration.
And it is in this sense that it can describe certain characteristic findings of these pathologies, the same ones that can guide our mental scheme to achieve a presumptive diagnosis; some of them are described in Table 6.
Clinic of the main causes of visual disability and blindness.
Physical examination | |
---|---|
Cataract [56] | Opacification of the lens Pupillary reflexes may be slowed down, but they do not disappear |
Uncorrected refraction [52] | Improvement of the AV with the pinhole hole test |
Glaucoma [54, 55] | Closed-angle glaucoma
|
Diabetic retinopathy [57] | Vascular microaneurysms, hemorrhage, cotton-wool exudates, vein caliber alterations, neovascularizations |
Findings of the physical examination in the main causes of visual disability and blindness.
The Latin America and the Caribbean region are considered one of the most inequitable in the world in terms of the distribution of goods and services, social determinants, and health.
Using a standard methodology for international use [58], it has been possible to determine the prevalence of blindness and visual impairment, coverage, and the quality of cataract services and barriers to access them in several countries [56].
The Vision 2020 program in Latin America, with the participation of PAHO/WHO, the Christian Blind Mission, and the International Agency for the Prevention of Blindness, has proposed to document the problem of blindness and visual impairment in people over 50 years of age and designed a statistical instrument called “rapid assessment of avoidable blindness” (ERCE). To date, ERCE activities have been conducted to determine the prevalence of blindness [16, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63].
And it is through this instrument that in nine countries of Latin America, the following barriers have been determined for cataract surgery: lack of knowledge about the existence of a treatment, it is thought to be the destination, there is no availability of surgery services or very distant, fear of the operation or loss of vision, cannot pay for the operation, indication of waiting until it “matures” (possible waiting list), no one can accompany to the ophthalmological care, and other diseases and contraindications for surgery [64, 65, 66].
All are surmountable through information and education campaigns.
To control blindness and visual impairment, it is essential to implement plans to (a) detect cases of low vision and operate cataract cases, (b) detect and give optical correction to cases with refractive errors and presbyopia, and (c) integrate eye care in primary health care. These three interventions could solve around 67% of cases of blindness and could help detect people with glaucoma, in order to treat them in early stages.
Eighty percent of all these cases are considered avoidable. Therefore, the exhaustive evaluation in the patient with determining risks plays a key role, together with the fact that the visual function can be evaluated by means of simple subjective tests and be attended to by an adequate primary care service.
The difficulties in the supply of surgeries vary according to the country, being very available for most of the population in developed countries and becoming the most performed surgery in the elderly. In developing countries, the situation varies according to the regions or countries.
Visual disability and blindness correspond to one of the microvascular complications of diabetes mellitus, where the relationship that keeps the glycemic control in function of the time of presenting the disease is widely demonstrated. Between 80 and 95% corresponds to nonproliferative DR and the remaining 5–10% to proliferative DR. Here is the need for a holistic approach to the patient aimed at prevention and proper medical management.
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
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\n\nA Retraction of a Chapter will be issued by the Academic Editor, either following an Author’s request to do so or when there is a 3rd party report of scientific misconduct. Upon receipt of a report by a 3rd party, the Academic Editor will investigate any allegations of scientific misconduct, working in cooperation with the Author(s) and their institution(s).
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\n\n1.2. REMOVALS AND CANCELLATIONS
\n\n2. STATEMENTS OF CONCERN
\n\nA Statement of Concern detailing alleged misconduct will be issued by the Academic Editor or publisher following a 3rd party report of scientific misconduct when:
\n\nIntechOpen believes that the number of occasions on which a Statement of Concern is issued will be very few in number. In all cases when such a decision has been taken by the Academic Editor the decision will be reviewed by another editor to whom the author can make representations.
\n\n3. CORRECTIONS
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\n\n3.1. ERRATUM
\n\nAn Erratum will be issued by the Academic Editor when it is determined that a mistake in a Chapter originates from the production process handled by the publisher.
\n\nA published Erratum will adhere to the Retraction Notice publishing guidelines outlined above.
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\n'}]},successStories:{items:[]},authorsAndEditors:{filterParams:{sort:"featured,name"},profiles:[{id:"105746",title:"Dr.",name:"A.W.M.M.",middleName:null,surname:"Koopman-van Gemert",slug:"a.w.m.m.-koopman-van-gemert",fullName:"A.W.M.M. Koopman-van Gemert",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/105746/images/5803_n.jpg",biography:"Dr. Anna Wilhelmina Margaretha Maria Koopman-van Gemert MD, PhD, became anaesthesiologist-intensivist from the Radboud University Nijmegen (the Netherlands) in 1987. She worked for a couple of years also as a blood bank director in Nijmegen and introduced in the Netherlands the Cell Saver and blood transfusion alternatives. She performed research in perioperative autotransfusion and obtained the degree of PhD in 1993 publishing Peri-operative autotransfusion by means of a blood cell separator.\nBlood transfusion had her special interest being the president of the Haemovigilance Chamber TRIP and performing several tasks in local and national blood bank and anticoagulant-blood transfusion guidelines committees. Currently, she is working as an associate professor and up till recently was the dean at the Albert Schweitzer Hospital Dordrecht. She performed (inter)national tasks as vice-president of the Concilium Anaesthesia and related committees. \nShe performed research in several fields, with over 100 publications in (inter)national journals and numerous papers on scientific conferences. \nShe received several awards and is a member of Honour of the Dutch Society of Anaesthesia.",institutionString:null,institution:{name:"Albert Schweitzer Hospital",country:{name:"Gabon"}}},{id:"83089",title:"Prof.",name:"Aaron",middleName:null,surname:"Ojule",slug:"aaron-ojule",fullName:"Aaron Ojule",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Port Harcourt",country:{name:"Nigeria"}}},{id:"295748",title:"Mr.",name:"Abayomi",middleName:null,surname:"Modupe",slug:"abayomi-modupe",fullName:"Abayomi Modupe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/no_image.jpg",biography:null,institutionString:null,institution:{name:"Landmark University",country:{name:"Nigeria"}}},{id:"94191",title:"Prof.",name:"Abbas",middleName:null,surname:"Moustafa",slug:"abbas-moustafa",fullName:"Abbas Moustafa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94191/images/96_n.jpg",biography:"Prof. Moustafa got his doctoral degree in earthquake engineering and structural safety from Indian Institute of Science in 2002. He is currently an associate professor at Department of Civil Engineering, Minia University, Egypt and the chairman of Department of Civil Engineering, High Institute of Engineering and Technology, Giza, Egypt. He is also a consultant engineer and head of structural group at Hamza Associates, Giza, Egypt. Dr. Moustafa was a senior research associate at Vanderbilt University and a JSPS fellow at Kyoto and Nagasaki Universities. He has more than 40 research papers published in international journals and conferences. He acts as an editorial board member and a reviewer for several regional and international journals. His research interest includes earthquake engineering, seismic design, nonlinear dynamics, random vibration, structural reliability, structural health monitoring and uncertainty modeling.",institutionString:null,institution:{name:"Minia University",country:{name:"Egypt"}}},{id:"84562",title:"Dr.",name:"Abbyssinia",middleName:null,surname:"Mushunje",slug:"abbyssinia-mushunje",fullName:"Abbyssinia Mushunje",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Fort Hare",country:{name:"South Africa"}}},{id:"202206",title:"Associate Prof.",name:"Abd Elmoniem",middleName:"Ahmed",surname:"Elzain",slug:"abd-elmoniem-elzain",fullName:"Abd Elmoniem Elzain",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Kassala University",country:{name:"Sudan"}}},{id:"98127",title:"Dr.",name:"Abdallah",middleName:null,surname:"Handoura",slug:"abdallah-handoura",fullName:"Abdallah Handoura",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Supérieure des Télécommunications",country:{name:"Morocco"}}},{id:"91404",title:"Prof.",name:"Abdecharif",middleName:null,surname:"Boumaza",slug:"abdecharif-boumaza",fullName:"Abdecharif Boumaza",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Abbès Laghrour University of Khenchela",country:{name:"Algeria"}}},{id:"105795",title:"Prof.",name:"Abdel Ghani",middleName:null,surname:"Aissaoui",slug:"abdel-ghani-aissaoui",fullName:"Abdel Ghani Aissaoui",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/105795/images/system/105795.jpeg",biography:"Abdel Ghani AISSAOUI is a Full Professor of electrical engineering at University of Bechar (ALGERIA). He was born in 1969 in Naama, Algeria. He received his BS degree in 1993, the MS degree in 1997, the PhD degree in 2007 from the Electrical Engineering Institute of Djilali Liabes University of Sidi Bel Abbes (ALGERIA). He is an active member of IRECOM (Interaction Réseaux Electriques - COnvertisseurs Machines) Laboratory and IEEE senior member. He is an editor member for many international journals (IJET, RSE, MER, IJECE, etc.), he serves as a reviewer in international journals (IJAC, ECPS, COMPEL, etc.). He serves as member in technical committee (TPC) and reviewer in international conferences (CHUSER 2011, SHUSER 2012, PECON 2012, SAI 2013, SCSE2013, SDM2014, SEB2014, PEMC2014, PEAM2014, SEB (2014, 2015), ICRERA (2015, 2016, 2017, 2018,-2019), etc.). His current research interest includes power electronics, control of electrical machines, artificial intelligence and Renewable energies.",institutionString:"University of Béchar",institution:{name:"University of Béchar",country:{name:"Algeria"}}},{id:"99749",title:"Dr.",name:"Abdel Hafid",middleName:null,surname:"Essadki",slug:"abdel-hafid-essadki",fullName:"Abdel Hafid Essadki",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Nationale Supérieure de Technologie",country:{name:"Algeria"}}},{id:"101208",title:"Prof.",name:"Abdel Karim",middleName:"Mohamad",surname:"El Hemaly",slug:"abdel-karim-el-hemaly",fullName:"Abdel Karim El Hemaly",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/101208/images/733_n.jpg",biography:"OBGYN.net Editorial Advisor Urogynecology.\nAbdel Karim M. A. El-Hemaly, MRCOG, FRCS � Egypt.\n \nAbdel Karim M. A. El-Hemaly\nProfessor OB/GYN & Urogynecology\nFaculty of medicine, Al-Azhar University \nPersonal Information: \nMarried with two children\nWife: Professor Laila A. Moussa MD.\nSons: Mohamad A. M. El-Hemaly Jr. MD. Died March 25-2007\nMostafa A. M. El-Hemaly, Computer Scientist working at Microsoft Seatle, USA. \nQualifications: \n1.\tM.B.-Bch Cairo Univ. June 1963. \n2.\tDiploma Ob./Gyn. Cairo Univ. April 1966. \n3.\tDiploma Surgery Cairo Univ. Oct. 1966. \n4.\tMRCOG London Feb. 1975. \n5.\tF.R.C.S. Glasgow June 1976. \n6.\tPopulation Study Johns Hopkins 1981. \n7.\tGyn. Oncology Johns Hopkins 1983. \n8.\tAdvanced Laparoscopic Surgery, with Prof. Paulson, Alexandria, Virginia USA 1993. \nSocieties & Associations: \n1.\t Member of the Royal College of Ob./Gyn. London. \n2.\tFellow of the Royal College of Surgeons Glasgow UK. \n3.\tMember of the advisory board on urogyn. FIGO. \n4.\tMember of the New York Academy of Sciences. \n5.\tMember of the American Association for the Advancement of Science. \n6.\tFeatured in �Who is Who in the World� from the 16th edition to the 20th edition. \n7.\tFeatured in �Who is Who in Science and Engineering� in the 7th edition. \n8.\tMember of the Egyptian Fertility & Sterility Society. \n9.\tMember of the Egyptian Society of Ob./Gyn. \n10.\tMember of the Egyptian Society of Urogyn. \n\nScientific Publications & Communications:\n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Asim Kurjak, Ahmad G. Serour, Laila A. S. Mousa, Amr M. Zaied, Khalid Z. El Sheikha. \nImaging the Internal Urethral Sphincter and the Vagina in Normal Women and Women Suffering from Stress Urinary Incontinence and Vaginal Prolapse. Gynaecologia Et Perinatologia, Vol18, No 4; 169-286 October-December 2009.\n2- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nFecal Incontinence, A Novel Concept: The Role of the internal Anal sphincter (IAS) in defecation and fecal incontinence. Gynaecologia Et Perinatologia, Vol19, No 2; 79-85 April -June 2010.\n3- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nSurgical Treatment of Stress Urinary Incontinence, Fecal Incontinence and Vaginal Prolapse By A Novel Operation \n"Urethro-Ano-Vaginoplasty"\n Gynaecologia Et Perinatologia, Vol19, No 3; 129-188 July-September 2010.\n4- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n5- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n6- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n7-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n8-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n9-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n10-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n11-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n12- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n13-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n14- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n15-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n\n16-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n17- Abdel Karim M. El Hemaly. Nocturnal Enureses: An Update on the pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecology/?page=/ENHLIDH/PUBD/FEATURES/\nPresentations/ Nocturnal_Enuresis/nocturnal_enuresis\n\n18-Maternal Mortality in Egypt, a cry for help and attention. The Second International Conference of the African Society of Organization & Gestosis, 1998, 3rd Annual International Conference of Ob/Gyn Department � Sohag Faculty of Medicine University. Feb. 11-13. Luxor, Egypt. \n19-Postmenopausal Osteprosis. The 2nd annual conference of Health Insurance Organization on Family Planning and its role in primary health care. Zagaziz, Egypt, February 26-27, 1997, Center of Complementary Services for Maternity and childhood care. \n20-Laparoscopic Assisted vaginal hysterectomy. 10th International Annual Congress Modern Trends in Reproductive Techniques 23-24 March 1995. Alexandria, Egypt. \n21-Immunological Studies in Pre-eclamptic Toxaemia. Proceedings of 10th Annual Ain Shams Medical Congress. Cairo, Egypt, March 6-10, 1987. \n22-Socio-demographic factorse affecting acceptability of the long-acting contraceptive injections in a rural Egyptian community. Journal of Biosocial Science 29:305, 1987. \n23-Plasma fibronectin levels hypertension during pregnancy. The Journal of the Egypt. Soc. of Ob./Gyn. 13:1, 17-21, Jan. 1987. \n24-Effect of smoking on pregnancy. Journal of Egypt. Soc. of Ob./Gyn. 12:3, 111-121, Sept 1986. \n25-Socio-demographic aspects of nausea and vomiting in early pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 35-42, Sept. 1986. \n26-Effect of intrapartum oxygen inhalation on maternofetal blood gases and pH. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 57-64, Sept. 1986. \n27-The effect of severe pre-eclampsia on serum transaminases. The Egypt. J. Med. Sci. 7(2): 479-485, 1986. \n28-A study of placental immunoreceptors in pre-eclampsia. The Egypt. J. Med. Sci. 7(2): 211-216, 1986. \n29-Serum human placental lactogen (hpl) in normal, toxaemic and diabetic pregnant women, during pregnancy and its relation to the outcome of pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:2, 11-23, May 1986. \n30-Pregnancy specific B1 Glycoprotein and free estriol in the serum of normal, toxaemic and diabetic pregnant women during pregnancy and after delivery. Journal of the Egypt. Soc. of Ob./Gyn. 12:1, 63-70, Jan. 1986. Also was accepted and presented at Xith World Congress of Gynecology and Obstetrics, Berlin (West), September 15-20, 1985. \n31-Pregnancy and labor in women over the age of forty years. Accepted and presented at Al-Azhar International Medical Conference, Cairo 28-31 Dec. 1985. \n32-Effect of Copper T intra-uterine device on cervico-vaginal flora. Int. J. Gynaecol. Obstet. 23:2, 153-156, April 1985. \n33-Factors affecting the occurrence of post-Caesarean section febrile morbidity. Population Sciences, 6, 139-149, 1985. \n34-Pre-eclamptic toxaemia and its relation to H.L.A. system. Population Sciences, 6, 131-139, 1985. \n35-The menstrual pattern and occurrence of pregnancy one year after discontinuation of Depo-medroxy progesterone acetate as a postpartum contraceptive. Population Sciences, 6, 105-111, 1985. \n36-The menstrual pattern and side effects of Depo-medroxy progesterone acetate as postpartum contraceptive. Population Sciences, 6, 97-105, 1985. \n37-Actinomyces in the vaginas of women with and without intrauterine contraceptive devices. Population Sciences, 6, 77-85, 1985. \n38-Comparative efficacy of ibuprofen and etamsylate in the treatment of I.U.D. menorrhagia. Population Sciences, 6, 63-77, 1985. \n39-Changes in cervical mucus copper and zinc in women using I.U.D.�s. Population Sciences, 6, 35-41, 1985. \n40-Histochemical study of the endometrium of infertile women. Egypt. J. Histol. 8(1) 63-66, 1985. \n41-Genital flora in pre- and post-menopausal women. Egypt. J. Med. Sci. 4(2), 165-172, 1983. \n42-Evaluation of the vaginal rugae and thickness in 8 different groups. Journal of the Egypt. Soc. of Ob./Gyn. 9:2, 101-114, May 1983. \n43-The effect of menopausal status and conjugated oestrogen therapy on serum cholesterol, triglycerides and electrophoretic lipoprotein patterns. Al-Azhar Medical Journal, 12:2, 113-119, April 1983. \n44-Laparoscopic ventrosuspension: A New Technique. Int. J. Gynaecol. Obstet., 20, 129-31, 1982. \n45-The laparoscope: A useful diagnostic tool in general surgery. Al-Azhar Medical Journal, 11:4, 397-401, Oct. 1982. \n46-The value of the laparoscope in the diagnosis of polycystic ovary. Al-Azhar Medical Journal, 11:2, 153-159, April 1982. \n47-An anaesthetic approach to the management of eclampsia. Ain Shams Medical Journal, accepted for publication 1981. \n48-Laparoscopy on patients with previous lower abdominal surgery. Fertility management edited by E. Osman and M. Wahba 1981. \n49-Heart diseases with pregnancy. Population Sciences, 11, 121-130, 1981. \n50-A study of the biosocial factors affecting perinatal mortality in an Egyptian maternity hospital. Population Sciences, 6, 71-90, 1981. \n51-Pregnancy Wastage. Journal of the Egypt. Soc. of Ob./Gyn. 11:3, 57-67, Sept. 1980. \n52-Analysis of maternal deaths in Egyptian maternity hospitals. Population Sciences, 1, 59-65, 1979. \nArticles published on OBGYN.net: \n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n2- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n3- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n4-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n5-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n6-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n7-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n8-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n9- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n10-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n11- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n12-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n13-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n14- Abdel Karim M. El Hemaly. 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