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",isbn:"978-1-83969-150-8",printIsbn:"978-1-83969-149-2",pdfIsbn:"978-1-83969-151-5",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"7409b2acd5150a93004300800918b736",bookSignature:"Prof. Karmen Pažek",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10548.jpg",keywords:"Lean Manufacturing, Agriculture, Production and Process, Costs Reduction, Lean Principles, Industry, Tools, Implementation, Sustainability, Modeling, Environment, Planning",numberOfDownloads:7,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 20th 2020",dateEndSecondStepPublish:"November 17th 2020",dateEndThirdStepPublish:"January 16th 2021",dateEndFourthStepPublish:"April 6th 2021",dateEndFifthStepPublish:"June 5th 2021",remainingDaysToSecondStep:"2 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"Dr. Pažek is Head of the undergraduate study program Agricultural economics and rural development and Vice-dean for education. She is the author or co-author of 61 scientific papers, 6 scientific books, and 24 book chapters.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"179642",title:"Prof.",name:"Karmen",middleName:null,surname:"Pažek",slug:"karmen-pazek",fullName:"Karmen Pažek",profilePictureURL:"https://mts.intechopen.com/storage/users/179642/images/system/179642.jpg",biography:"Karmen Pažek achieved her Ph.D. at University of Maribor, Faculty of Agriculture in 2006. She is active as Full Professor for Farm management in the Department for Agriculture Economics and Rural Development on Faculty of Agriculture and Life Sciences, University of Maribor. Her research includes development of decision support tools and systems for farm management (simulation modeling, multi-criteria decision analysis, option models, investment analysis) and economics of agricultural production. She is involved in teaching activities as thesis supervisor at postgraduate study programs and involved in national and international research projects. She is author or coauthor of 61 scientific papers (including 34 papers in journals with impact factor), 6 scientific books and 24 book chapters. Currently she is Head of the undergraduate study program Agricultural economics and rural development and Vice dean for education. \r\n\r\nAcademic activities\r\nResearch:\r\n-\tFarm management\r\n-\tDecision support, simulation, forecasting, multi criteria decision making in the area of agriculture with emphasis on field crops, farm tourism and fruit producon\r\n\r\nCurrent Research work:\r\n- Financial parameters assessment based on perfect and in-perfect information in agrifood \r\n systems \r\n- Option modeling of agrifood projects\r\n-\tEfficiency assessment in farm tourism \r\n-\tEfficiency of sugar beet production systems \r\n\r\nTeaching:\r\nUndergraduate Programmes and Courses\r\n-\tFarm management I and II\r\n-\tIntroduction to decision theory\r\n-\tOrganic fam management\r\n-\tManagement od supplementary activities\r\n-\tEconomics and management of rural tourism\r\n-\tSelected issues in agricultural entrepreneurship\r\n\r\nMaster Programmes and Courses\r\n\r\n-\tResearch methods in farm management\r\n-\tDecision theory\r\n-\tProject planning and quality management\r\n-\tOrganic fam management\r\n\r\n \r\nPhD Programme and Course\r\n\r\n-\tProject management (transferable skills)\r\n-\tSelected issues in farm management",institutionString:"University of Maribor",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"3",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Maribor",institutionURL:null,country:{name:"Slovenia"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"11",title:"Engineering",slug:"engineering"}],chapters:[{id:"74769",title:"Development of Integrated Lean Six Sigma-Baldrige Framework for Manufacturing Waste Minimization: A Case of NAS Foods Plc",slug:"development-of-integrated-lean-six-sigma-baldrige-framework-for-manufacturing-waste-minimization-a-c",totalDownloads:7,totalCrossrefCites:0,authors:[null]}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"247865",firstName:"Jasna",lastName:"Bozic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/247865/images/7225_n.jpg",email:"jasna.b@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"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3621",title:"Silver Nanoparticles",subtitle:null,isOpenForSubmission:!1,hash:null,slug:"silver-nanoparticles",bookSignature:"David Pozo Perez",coverURL:"https://cdn.intechopen.com/books/images_new/3621.jpg",editedByType:"Edited by",editors:[{id:"6667",title:"Dr.",name:"David",surname:"Pozo",slug:"david-pozo",fullName:"David Pozo"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"47006",title:"Dry eye — An Insight into Meibomian Gland Dysfunction",doi:"10.5772/58566",slug:"dry-eye-an-insight-into-meibomian-gland-dysfunction",body:'The term ‘Dry Eyes’ was first coined in 1950 by the Ophthalmologist Andrew De Roeth (1893–1981): a dacryologist who introduced the term dry eye. For decades it was thought dry eyes was limited to a reduction in the aqueous phase of the tear film. It was as recent as 1995 that dry eyes was eventually recognised as a multifaceted ocular pathology which was due to decreased tear production and increased tear evaporation [1]. In this chapter we will focus on the latter, specifically looking at meibomian gland dysfunction.
An estimate of the prevalence of dry eyes is difficult given that many sufferers may be asymptomatic or dismissive of subjective questionnaires of their symptoms if mild. Various studies estimate the prevalence as between 7.4% to 33.7% [2-3]. The epidemiology of dry eye depends on the mode of diagnosis, population surveyed and study cited.
Large American epidemiological studies estimate symptomatic dry eyes to affect 7% of women and 4% of men over the age of 50 years in the United States [4]. Similar data is seen in Australian studies [3]. The far eastern studies report the largest proportion of dry eye sufferers with Taiwan having the highest at 33.7% [5] followed by Japan and Indonesia [6].
The meibomian glands, named after the German physician Meibom in 1966, are specialised sebaceous glands within the eyelids. They number 20-5 on the lower lids and up to 50 on the upper lid. Meibomian glands are responsible for secretion of a lipid rich mixture call meibum onto the tear surface through small openings found on the lid margin. A single gland consists of a central duct linked to multiple acini via ductules. Meibum is loaded into acini and released into the central duct where it moves to the openings on the lid margin and ocular surface. The glands undergo constant renewal and are delicate owing to their holocrine nature.
Diagram courtesy of International Workshop on Meibomian Gland Dysfunction
It is widely thought that reduced meibum quality and quantity in addition to hyperkeratinisation of the ductal epithelium are the main reasons for meibomian gland dysfunction (MGD). Hyperkeratinised ducts and thicker meibum secretions lead to obstruction of the ducts. A progressive increase in pressure from continuous meibum secretion causes widening of the duct, acinar atrophy with cornification of duct epithelia. Ultimately there is reduced meibum secretion and gland drop out causing an unstable tear film. [7]
Lower lid meibomian glands
The tear film lubricates the ocular surface, which is vital to its maintaining its function and well being. It also forms a vital role in light refraction in the air-tear-cornea interface. Tear film is structured into 3 primary layers: The inner layer comprises mucin and a layer of glycocalyx that is synthesised by the conjunctiva and epithelial cells. The lacrimal gland primarily secretes the middle aqueous layer. The outermost lipid layer is secreted by the meibomian gland. This superficial layer stabilises the tear film by preventing its evaporation. Meibomian gland dysfunction is the most common cause of evaporative dry eye. Left untreated dry eye initially causes irritating ocular surface symptoms and signs that can threaten visual impairment, cause corneal perforation and blindness.[8]
Broadly meibomian gland dysfunction can be defined as a chronic, diffuse abnormality of the meibomian glands commonly characterized by terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion. It may result in alteration of the tear film, symptoms of eye irritation, clinically apparent inflammation, and ocular surface disease[9-10].
Meibomian gland dysfunction can affect many different groups.
Age is a major risk factor for the development of MGD. It is more common in the elderly. Studies in humans seem to mirror the effects in animals [9]. Decreased acinar proliferation, atrophy and altered localisation of the lipogenesis factor PPARγ (regulates meibomian differentiation and secretion) are seen in mice. Elderly patients have been noted to have a higher rate of meibomian glad dropout [10-11] with half as many functioning glands between 20 to 80 years of age. Human cadaveric studies show gland orifice metaplasia and narrowing [12-13] with hyperkeratinisation and lipogranulomatous inflammatory changes. Additionally meibum composition changes with age yielding a reduced volume and increased viscosity [10-14].
Androgens are known to be integrally involved in differentiation of sebaceous glands all over the body and have been shown to promote genes essential for meibomian function [13-14] Furthermore, complete androgen insensitivity syndrome has been shown to have altered meibomian glands and composition of lipid secretions that resulted in clinically apparent signs and symptoms of MGD [15-16].
Confusingly, chronic blepharitis has been suggested as a cause for MGD. Whilst MGD itself is a cause of chonic blepharitis, there is considerable overlap with other causes of chronic blepharitis that may accentuate MGD. One study showed 74% (42 of 57) chronic blepharitis sufferers had evidence of meibomian gland loss on meibography whereas 20% (4) of matched normal patients had any dropout. More detailed understanding is needed regarding the overlap of MGD with chronic blepharitis [18-19].
Lower lid meibomian glands and dropout in an elderly patient (courtesy of S Tuft)
Meibum secretions of elderly patient showing increased plugging and viscosity (courtesy of S Tuft)
Demodex mites are the most common ectoparasites found in human skin. Of this species D.brevis is thought to be the most pertinent in MGD [20]. Current thinking is that the mite burrows deep into sebaceous and meibomian glands to feed on sebum and meibum respectively, as this forms as its main food source. Its chitinous exoskeleton causes a granulomatous reaction which ultimately leads to a mechanical blockage of the gland. D.brevis has been found in the centre of granulomatous meibomian glands surrounded by histocytes, epithelioid cells, fibroblasts and plasma cells which may thus offer a potential explanation for refractory and recurrent chalazia in some patients. [21]
Desmodex infested lashes with meibomian gland dysfunction
Contact lens wear can increase the risk of MGD. Studies utilising meibography have shown that contact lenses alter meibomian gland morphology with greater rates of dropout than non-contact lens wearers. The duration and type of contact lens was weakly associated with this. By inserting and removing contact lenses, desquamated epithelial cells have been shown to obstruct the duct orifice leading to stagnation and atrophy [22-23]. While some studies show a statistically significant increase in MGD in contact lens wearers [22-24] others did not show significant differences [25-26]. It is important however to bear in mind these studies defined meibomain gland dysfunction differently. Damage to stem cells at the limbus is likely to be different based on duration on contact lens wear and may help account for the differences.
Environment may play a role in MGD. It is likely that factors such as temperature, humidity and visual undertaking have an accentuating impact rather than develop MGD. For example, concentrated computer use may be associated with reduced blink rate, exacerbating symptoms of MGD. One study of 70 patients found 74% of video display terminal users had MGD [27]. Decreased conjunctival temperature has been suggested to cause obstructive MGD through increased meibum viscosity [28-29].
Various medical conditions have been associated with MGD. Polycystic ovary syndrome (PCOS), where there is often insulin resistance and hyperinsulinaemia can result in increased androgen synthesis. Androgen receptors have been found in meibomian glands with a possible effect on function [30-33]. Twenty two (22)% of PCOS patients had MGD compared to 13% of normals in one study [34].
Dyslipidaemia appears to be associated with MGD. Patients with moderate to severe MGD have a higher incidence of dyslipidemia with respect to elevated total cholesterol than the general population [35-36]. Higher meibomian cholesterol ester levels are associated with MGD in humans [37].
Sjorgen’s syndrome has been shown to have a higher incidence of MGD. One study found a higher incidence of MGD in MGD related dry eye to other causes of dry eye. The actual association, whether causative or a consequence of dry eye is not established and further study is needed [38-39]
Multiple medications have been implicated as possible risk factors for MGD. Studies looking at the acne treatment isotretinoin, 13-cis retinoic acid, have found that this resulted in altered meibum secretion, atrophy of the gland, reduced tear break up time and dry eye symptoms [40-41]. Other studies have looked at medication under the umbrella category of dry eye, not specially MGD. There may however be some overlap with MGD. Included in this category are antihistamines. One study has shown that treatment of allergic conjunctivitis with once daily loratidine resulted in signs of ocular dryness [42-43].
Post-menopausal hormone therapy has been associated with MGD [44-47] although the pathophysiology is not fully understood. Whilst established that sex hormone levels change from pre-to post-menopause, it is presumed that PMH results in changes to meibum gland secretions that can lead to MGD. Higher estrogen levels post-menopausally have been implicated in reduced tear function [45]. The largest of the studies, looking at 3500 patients from the Blue Mountain Study has shown a statistically significant 60% higher prevalence of dry eye in PMH users. A longer duration of use has been associated with longer symptoms [44].
Anitidepressant use has been associated with a higher risk of evaporative dry eye symptoms. Often many such medications simply have visual blurring only as a side effect without any mention of dry eye disease [48-51].
Omega 3 oils have been shown to have a beneficial effect on MGD whilst omega 6 oils have an opposite effect. Both are essential for growth and development. The omega 3 oils are found naturally in Mediterranean diets, flaxseed and cod liver oil [52]. Omega 6 oils are found typically in Northern European diets containing high red meat and less of the above [52]. The most detailed study to date showed a reduction in meibum thickness, dry eye signs and tear break up time in those with a high omega 3 to omega 6 ratio [53], agreeing with previous findings [52, 54. 55]. These oils compete for an enzyme involved in the inflammatory pathwaytherefore it is the ratio of omega 3 and 6 that is crucial. The ideal omega 6:3 ratio is 4:1 but typical Northern European and American diets are in the realm of 14:1 A higher omega 6 to 3 ratio results in overproduction of pro-inflammatory PGE2 from omega 6 and underproduction of anti-inflammatory PGE1 and PGE3 via omega 3 that induces MGD [53].
Meibomian gland dysfunction is the leading cause of evaporative dry eye. As such patients will present with dry eye symptoms.
Most patients with MGD are likely to be asymptomatic. The vast majority will not experience any symptoms unless it is moderate in nature or exacerbated by other causes of evaporative dry eye. Burning, irritation, redness, watering or intermittent visual blur are frequently described. It is important to ask what time of day this occurs to try to distinguish from other causes of dry eye. Blepharitis is typically worse in the morning with redness, crusting, puffiness, itchy lids or a ‘gritty sensation’ within the eyes.
There are different ways to assess meibomian gland dysfunction. Whilst a slit lamp is certainly beneficial and the commonest form of assessment, one can simply use a direct ophthalmoscope for those in primary care settings. Though it does not give as detailed a view the principles are the same as for slit lamp examination. The key is to observe the meibomian glands and ocular surface. With the ophthalmoscope one needs to place on high magnification to view the state of the meibomian glands which are located posterior to the greyline Often orifices can be seen to be plugged, or pouting. Surrounding tissue can be erythematous with telangiectatic vessels. Misdirected eyelashes can also be a sign of eyelid inflammatory changes. A good clinical examination will also include eversion of the eyelids which will often show white, hard deposits called concretions on the tarsal conjunctiva, follicles or granulomatous changes from previous chalazia. The ocular surface should also be assessed. Important to evaporative dry eyes is assessment of the tear film break up (TFBUT). This is done by instilling fluorescein sodium 2% (although 0.25% is an acceptable alternative) and asking the patient to blink a few times. The patient should then be asked to keep their eyes open and careful note of the time taken for vacuoles to appear in the tear film. A normal time frame is 10-15 seconds. The ocular surface should also be noted for punctate epithelial erosions which can be wide-spread or mainly inferior. In severe cases mucous filaments have been noted on the cornea. Abrasions can also be seen in those with associated in-turned eyelashes. The conjunctiva can be injected to varying degrees. As MGD is almost always bilateral, a unilateral presentation must alert the clinician of the possibility of basal cell carcinoma or meibomian cell carcinoma.
Thickened meibomian secretions i
Concretions on the lower lid (courtesy of S Tuft)
Follicles and sebaceous material (courtesy of S Tuft)
Chalazion on lower lid (courtesy of S Tuft)
Rosacea above is associated with meibomian gland dysfunction (courtesy of S Tuft)
Trichiatic lashes resulting in corneal damage (courtesy of S Tuft)
There is no universal classification system of MGD. Different approaches have been used. The International Workshop Meibomian Gland subcommittee have recommended categorisation into 4 subtypes, although this is not universally applied.
MGD alone Asymptomatic Symptomatic (noncicatricial, cicatricial)
MGD with associated with ocular surface damage
MGD-related evaporative dry eye
MGD associated with other ocular disorders.
Alternatively, clinical measurement has been described. This is based on lid signs and meibum quality. Meibum can be graded on the Oxford score scale 0-3 (0=clear, 1=cloudy, 2=cloudy/particulate and 3=toothpaste like) [107].
cloudy and particulate meibum: Oxford scale 2
Toothpaste like meibum: Oxford score 3
A common misnomer is that MGD and posterior blepharitis are interchangeable terms [56-58]. Some previous literature has used the terms as such. MGD though, is one cause of posterior blepharitis (inflammation of the lid margins) and must be distinguished from other causes based on the anatomical structures of the posterior lid. Other causes include conjunctivitis (allergic or infective) and dermatological (acne rosacea or sebhorreic dermatitis).
Anterior blepharitis is another differential. This refers to inflammation anterior to the gray line, particularly around the lashes. The gray line anatomically subdivides the anterior and posterior lamellae of the lid. Anterior blepharitis can result in scurf on lashes, collarettes at the lash base and vascular changes of the eyelids.
Typically treatment is predominantly based on the general term ‘lid hygeine’, ocular lubricants and antibiotics. There are more recent advances in the field and these are described further below.
Lid hygeine as a method varies across different centres [59]. Currently there is no standardised method. Commonly patients are told to either to place a warm compress over the lids at least twice daily or massage the lids for 10 minutes during each session. Compresses alone have been shown to cause transient visual blurring [60-61]. Active massage is encouraged. MGD secretions have been shown to have higher melting (35 C) points relative to normal (32C) [62-63]. The warmness melts the pathological meibum within the glands and active massage helps to unblock the glands. The authors feel that cotton wool whilst more gentle on the eye is often not firm enough to dislodge meibum that a flannel or towel is able to do. Lid hygeine is made more efficient by encouraging active massage just under the lashes themselves so the patient can directly affect the glands themselves. This needs to be demonstrated to patients directly. By pressing the lateral canthus firmly, traction can be provided and using a flannel the pulp of the finger swept gently over the inner aspect of the upper and lower lids. This needs to be balanced against any possible damage to the ocular and careful explanation and assessment of patient technique needs to be balanced against this [64-65]. The use of mild baby shampoo over the lids has also been advocated as part of lid hygeine. Ultimately patients need to be educated that lid hygiene is the basis upon which MGD will be controlled and that compliance is crucial in not only reducing symptoms but preventing recurrence.
Physical expression of the meibomian glands has been described [66-67]. Methods vary from gentle lid palpation to forceful squeezing of the lids. Use of a finger on the outer lid and a rigid object on the inner aspect like a metal paddle have been reported [68]. Often considerable force is needed to express pathological meibum and transient visual blurring owing to corneal distortion has been reported [60-61]. We believe that the risks involved and potential discomfort from this outweigh any benefit and do not recommend this.
Ocular lubricants are helpful to provide symptomatic relief. They help to alleviate symptoms experienced secondary to evaporative dry eye and do not treat the MGD itself. It is important for patients to realise that they are not a cure but give temporary respite. Ocular lubricants are helpful in bolstering the tear film volume, spreading of tears [69] and providing a layer over the cornea that reduced the possibility of corneal erosion from friction of the lid moving over the cornea by blinking [70-71]. The ocular lubricants may also help wash away pro-inflammatory molecules and dilute the concentration of inflammatory cytokines in tears. This has not been tested and remains a speculative theory presently.
Much research has been based around the contents of ocular lubricants. Preservatives can cause discomfort and toxicity to the corneal epithelium. Frequently used preservatives like benzylalkonium chloride and polyquaternium have been shown to decrease goblet cell density and thus affect tear film stability [72-77]. There is no evidence nor consensus on frequency of usage. It should be based on an individual level. Preservative free drops are recommended in severe dry eye where high frequency drops are required. More recently so called vanishing preservatives such as sodium perborate or sodium chlorite have been incorporated into artificial tears. There is a lack of data to date to suggest whether these have the intended less preservative toxicity than the traditional preservatives mentioned.
Lipid supplemented tears have been shown of benefit in MGD [79-84]. Patients have reported reduced symptoms with an increased tear break up time and thicker lipid layer of the tear film. Castor oil drops have been shown to reduce tear break up time in a randomised control trial [84]. Temporary visual blurring has been reported in older studies that used ointments but more recent formulations have not been shown to have this problem [84]
Leading from this is the viscosity of the ocular lubricant. The greater the viscosities the more benefit in bulking tear film thickness and volume in dry eyes [85-87] as well as increased transit time on the eye. This needs to be counterbalanced against visual blurring and inconvenience.
Antibiotics are often used in MGD. The exact pathogenesis of bacteria remains not entirely understood. However the presence of bacterial flora on the lid surface, notably staphylococcus epidermidis, staph aureus, propion acnes amongst others is known. It may be the case that the keratinisation of the meibum and abnormal lipids provide prime conditions for normal bacterial flora to produce enzymes such as lipases and exotoxins resulting in proinflammatory changes. Thus an antibiotic would need to be effective against common flora.
Macrolides are commonly used. Studies have shown that they exert many anti-inflammatory effects. Neutrophil activity is affected by downregulating adhesion protein expression [88]. Phagocytosis and chemotaxis are affected through this. A reduction in proinflammatory cytokines has been demonstrated [89-90].
Tetracyclines have multiple helpful anti-inflammatory properties, including influencing neutrophil chemotaxis and proliferation of lymphocytes [91-92]. Matrix metalloproteinases and inflammatory cytokines like IL1 are suppressed as are anti-angiogenesis properties [93-94]. Collagenase 2 (matrix metalloproteinase P8) is directly suppressed by doxycycline specifically. They have been established for treatment of acne rosacea. Lipase production of the typical bacterial flora such as S epidermidis is suppressed. The lipases are responsible for production of pro-inflammatory free fatty acids that can detstabilise the tear film and directly alter meibum composition. The tetracyclines as a group have varying lipophillicity that alters individual drug pharmacokinetics. The international workshop on meibomian gland dysfunction recommend the use of doxycycline and minocycline [96]. These have been shown to be clinically effective at lower doses relative to tetracycline, which is poorly lipophilic and has been found at lower relative concentrations in tears after 5 days [97-100]. Typically doxycycline or monocycline are given at 100mg dosage for 2 months.
Dietary modification have been popular treatments amongst patients. Omega 3 rich foods as can be found in flax seed or cod-liver oil have been shown to have improved meibum scores, tear break up time and surface signs [100-102]. Omega 6 rich foods such as red meat have a counter effect and should be discouraged [101].
Surgical management is reserved for complications from MGD. Typically this would occur where the MGD is severe. Chalazia can be treated with incision and curettage where they are inflamed and affecting vision. Eyelid cicatrisation may cause trichiatic lashes that can commonly undergo epilation or electrolysis. Lid laxity, ectropion or entropion may be treated surgically.
Recently, devices have been created to be worn by patients to help with lid hygiene. These include blepharitis goggles, which aim to provide heat and moisture via steam to unclog blocked meibomian glands [103-104].LipiFlow® Thermal Pulsation System is similar but provides heat therapy and physical pressure to express the meibomian glands [105]. These variables can be adjusted accordingly, and seems to offer more favourable outcomes over 12 months than typical lid hygiene and lubricating drops [105]. The evidence base for such devices is currently limited further studies on outcomes and potential side effects are needed.
It is understandably difficult to make an unambiguous diagnosis of meibomian gland dysfunction without a slit lamp in primary care or on the ward.
However through careful history of symptoms and possible risk factors mentioned earlier, along with a direct ophthalmoscope on high magnification, an informed judgment can be made. Use of the direct ophthalmoscope does require practice to look at anterior surface structures in detail. Most hand held ophthalmoscopes have a cobalt blue mode, meaning that with available fluroscein drops an evaluation of the tear break up time and state of the corneal surface can be undertaken.
Where MGD is suspected, we would recommend starting lid hygiene, taking care to assess whether the patient is capable of performing this safely without damage to anterior structures. If there is suspicion of anterior surface structure damage from unsafe hygiene measures or possible other causes we recommend referral without starting lid hygiene. Prescribing suitable preservative free lubricating eye drops is recommended before ophthalmic referral.
Meibomian gland dysfunction is the most common ocular sign encountered in patients and cause of evaporative dry eye. Whilst awareness of the condition improves and research continues to be undertaken, a universal consensus on the definition, pathophysiology, signs and management is still being awaited. This is needed to allow for earlier detection and optimal structured treatment for MGD. Further questions do need to be answered regarding meibomian gland dysfunction too. Owing to a lack in consensus over definition and clinical tests performed in studies there is difficulty comparing results in different studies. The International Workshop for Meibomian Gland Dysfunction have suggested future research aim to prioritise a specific validated questionnaire for symptoms, a standard grading system of signs and validated outcomes for MGD [106]. It is hoped this will provide greater clarity in diagnosing, understanding the extent and severity of disease. Ultimately this would allow the most suitable treatment to be started improving the level of patient care in meibomian gland dysfunction.
Coronavirus (CoV) is a positive-sense single-strand RNA genome, which is the largest known RNA virus, constitutes Riboviria of Coronaviridae family and Orthocoronavirinae subfamily with a genome size of 27–34 kilobases. The name coronavirus is derived from the Latin word corona, meaning crown or halo, which is the feature appearance under electron microscope. Regarding COVID-19, it is similar to the other RNA viruses with additional endoribonuclease and exoribonuclease terminal caps (Figure 1) [1].
Structure of SARS-CoV2.
Formerly different researches were done to identify the cause of obscure respiratory tract infections. The identified novel agents were severe acute respiratory syndrome coronavirus (SARS-CoV) and human coronavirus NL63 (HCoV-NL63) [2] CoV causes human acute respiratory infection in about 5–30% of the total respiratory infection. In the past, between 2002 and 2003, an epidemic had been shown caused by SARS-CoV, which causes severe acute respiratory syndrome in 8000 subjects with 750 deaths. SARS-CoV is a second coronavirus group, while HCoV-NL63 is called group 1 coronavirus [3, 4].
On December 2019, a number of cases with a novel coronavirus (COVID-19) led to infected pneumonia in Wuhan in central China. Four cases with pneumonia of unknown etiology were reported on 29 December 2019, which heralds the similar outbreak of 2003 SARS-CoV [5].
At this time, no vaccines or effective antiviral agents are approved for the treatment or prevention of human COVID-19. Therefore, the emergence of COVID-19 is regarded as a priority by the World Health Organization (WHO), Center for Disease Control and Prevention (CDC), and health agencies for the developing a therapeutic effective drug against COVID-19. In general COVID-19 as other positive-sense RNA virus is characterized by high genetic plasticity and mutations due to short replication time, with a higher rate of recombination. These criteria limit and challenge for discovering novel antiviral agents [6, 7]. However, nucleotide and nucleoside analogue inhibitors (NIs) may be an effective agent by the reduction of genetic mapping of COVID-19 [8]. NIs such as ribavirin, remdesivir, and beta-D-N4-hydroxycytidine could be effective agents despite emergence of rapid resistance [9].
Previously, it has been reported by Li et al. [11] and Kuba et al. [10] that the entry-point receptor for SARS-CoV is angiotensin-converting enzyme 2 (ACE2) at the lung [10, 11]. Besides, Eckerle et al. reported that dipeptidyl peptidase-4 (DPP-4) which cluster of differentiation 26 (CD26) is widely expressed on the surface of human cells which acts as a receptor for Middle East respiratory syndrome coronavirus (MERS-CoV) [12]. Since there is a 80% similarity between MERS-CoV and SARS-CoV with SARS-CoV-2, this study was planned to review the potential link between the incidence and severity of COVID-19 regarding the modulation of DPP-4 and ACE2 by DPP-4 and renin angiotensin system (RAS) inhibitors, respectively.
In general, an endeavor of this study article was to present a mini review concerning DPP-4 and RAS and their inhibitors in relation to the incidence and severity of COVID-19. Evidences and substantiations from experimental, preclinical, and clinical studies are assessed, given the nature and character of the subject area; it remains clear that this literature search cannot be considered as a systemic review. A multiplicity and array of search policy took on and are assumed, which is integrated by electronic database searches of Scopus, Web of Science, Medline, Cochrane Central Register of Controlled Trials (CCTR), and PubMed using MeSH terms, keywords, and title words during the search. The terms used for these searches were as follows: COVID-19 or coronavirus or SARS-CoV-2 and DPP-4 OR renin angiotensin system; COVID-19 or SARS-CoV-2 and DPP-4 inhibitors or sitagliptin, vildagliptin, and insulin resistance; incidence of COVID-19 or coronavirus or SARS-CoV-2; and hypertension or orphan drugs or glucagone-like peptide 1 (GLP-1) or dipeptidyl peptidase-IV inhibitors (DPPIV) or thiazolidinediones (TZDs).
Reference lists of previous and recent notorious articles were reviewed. In addition, only English articles were measured, and case reports were also of concerned in this review. The key features of predictable and suitable search studies were considered, and the conclusions were summarized and summed up in a mini review.
RAS is a signaling pathway for the regulation of blood pressure, blood volume, natriuresis, and other vascular functions [13]. RAS consists of different effector peptides that control the dynamic vascular functions. Angiotensinogen from the liver is converted to angiotensin I (AngI), which is converted to angiotensin II (AngII) by angiotensin-converting enzyme 1(ACE1). AngII activates two types of receptors which are AT1 (vasoconstrictor) 90% and AT2 (vasodilator) 10%. The overall effect of AngII is vasoconstriction with sympathetic activation and aldosterone release. Excess of AngII is metabolized by ACE2 into vasodilator Ang (1–7) which act on specific receptor called MAS receptor (Figure 2). AngII can also be converted to angiotensin A by mononuclear leukocyte-derived aspartate decarboxylase (MLDAD), leading to the formation of alamandine, which has been shown to bind to the mas-related G protein-coupled receptor D [14].
Renin angiotensin system (RAS).
In COVID-19, SARS-CoV-2 binds ACE2 which is highly expressed by the epithelial cells of the blood vessel, intestine, and lung. The expression of ACE2 is augmented by angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) (Figure 3) [15] as well as ibuprofen and thiazolidinediones, and cigarette smoking also increases the expression of ACE2 at epithelial cells of the lung. Therefore, hypertensive patients on ACEIs or ARBs are at higher risk for COVID-19 [16, 17].
Role of angiotensin-converting enzyme 2 (ACE2).
Recently, Zhou et al. [18] found that the COVID-19 genome is 96% identical to the bat CoV, so spike glycoprotein (S protein) and receptor binding domain (RBD) of both SARS-CoV-2 and bat CoV bind ACE2, which might explain the cross-species transmission, which means from bat to human and from human to human [19]. In addition, the affinity of COVID-19-RBD to ACE2 is approximately 10–20 times more than that of SARS-CoV [20]. It has been shown that smoking upregulates ACE2 via activation of pulmonary platelet factor and induction of oxidative stress and inflammatory reactions. Increased ACE activity also contributes to impaired vascular relaxation observed in smokers. Irbesartan, an AT1R antagonist (also known as angiotensin receptor blocker), was found to reduce arterial stiffness in hypertensive patients. When stratified by smoking status, smokers were found to have stiffer arteries before treatment, and irbesartan was able to reduce arterial stiffness to a greater extent in smokers than in nonsmokers, indicating that overactivity of the RAS contributes to increased arterial stiffness in smokers. On the other hand, overexpression and upregulation of ACE2 is regarded as a protective measure via the reduction of pro-inflammatory cytokines mainly tumor necrosis factor (TNF-α) which is augmented in smoker subjects [21]. Therefore, active cigarette smoking subjects are at high risk for COVID-19 regardless of gender difference (Figure 4).
Nicotine smoking and ACE2.
The activity of RAS is high in the lung, which is the main source of circulating AngII due to higher expression of ACE. Lung ACE2 controls the balance of RAS activation through regulating AngII/Ang 1–7 ratio. Local pulmonary AngII provokes vascular permeability, causing pulmonary edema [22]. However, in acute respiratory distress syndrome (ARDS), the activation of RAS is necessary to maintain oxygenation since ACE2 knockout mice illustrated more sever pulmonary damage than the controls. Thereby, pulmonary ACE2 seems to be a protective defense pathway during ARDS [23]. In addition, ACE2 has an important anti-inflammatory action, and so ACE2 therapy is effective in the treatment of hypertension and diabetic nephropathy through attenuation of AngII-induced inflammation and oxidative stress [24]. Even so recombinant ACE2 is effective in the management of animal model ARDS, the inhibition of ACE2 may lead to fatal outcomes due to the reduction of vasodilator Ang1–7. However, chronic intravenous administration of Ang1–7 or MAS agonists leads to vasodilatation independent of circulating AngII levels [25].
Depending on these observations, different studies illustrate that RAS inhibitors might be of value in the reduction of ARDS, respiratory failure, and acute pneumonia that are induced by SARS-CoV-2 [26]. Though Wang [27] confirms that RAS inhibitors increase the risk of COVID-19 due to the upregulation of pulmonary ACE2, this study recommends stopping RAS inhibitors during COVID-19 outbreak. Nonetheless, all recruited patients with COVID-19 developed ARDS without any evidence of AKI [27]. Thus, RAS system mainly ACE2/Ang1–7 grows to be the focus and meeting point of different researches to implicate this pathway in the pathogenesis of COVID-19.
Guo et al. found that the expression of ACE2 is higher renal tubules than in lung tissues; nevertheless COVID-19 leads to ARDS in much at higher than that of acute kidney injury (AKI), suggesting other mechanism other than ACE2 binding in the pathogenesis of COVID-19 [28]. AT2 receptor is activated by ACE2 and Ang1–7 that oppose the activity of AT1 receptor [29]. Similarly, AT2 receptors are highly expressed in lung epithelial cells compared with kidney tissues. Pulmonary AT2 receptors mediate lung injury through the augmentation of pulmonary inflammation and vascular permeability as well as the development of pulmonary fibrosis [30]. Consequently, pulmonary AT2 receptor antagonists are regarded as a novel pathway in COVID-19-induced pneumonia and ARDS. This finding does not rule out the responsibility of ACE2, since the activation of ACE2 by SARS-CoV-2 causes considerable activation of pulmonary AT2 receptors (Figure 5).
Role of AT2 receptors in COVID-19.
Amid myriad literature survey, polymorphism of ACE2 has been associated with different cardio-metabolic disorders; thus, the implication of ACE2 and AT2 receptors in COVID-19-induced pneumonia should be considerably regarded with ACE2 polymorphisms [31]. Furthermore, the expression of ACE2 might not be necessary for COVID-19 infection and viral entry, as the absence of SARS-CoV-2 in some ACE2 expressing cell types as well; this infection was observed in some cell line lacking ACE2, suggesting a vague pathway, and cofactors might be necessary for human infection [32]. Amusingly, Gurwitz [33] animal model study shows that pulmonary COVID-19 infection leads to significant lung injury through the downregulation of ACE2, which is attenuated by the administration of ARB. This study suggests the protective role of RAS inhibitors in COVID-19-induced ARDS [33]. Indeed, most of reported data from various social media during this dangerous outbreak was not legitimate due to overwhelming lay press and sparked concerns. Therefore, the high incidence of COVID-19 in patients receiving ACEIs or ARBs might be not because of these drugs but because those patients were often older, hypertensive, or diabetic which in fact increase the risk of COVID-19 infection. In addition, a recent clinical trial on the effectiveness of recombinant ACE2 (rACE) in the management of COVID-19 infection has been started [34], and we are waiting for these results. Thus, according to the guideline for the management of hypertension, RAS inhibitors should be used irrespective of COVID-19 infection, as sudden withdrawal of these therapeutic regimens may increase the risk of deleterious outcomes in critically ill patients.
Regarding gender differences in the expression of ACE2, ACE2 gene is located on the X chromosome, which gives the possibility of gender differences in the susceptibility for COVID-19 infection. Females have lower levels of ACE2 compared with males, which gives a clue of male vulnerability to COVID-19 infection as compared with females [35]. In addition, Shenoy et al. report that estrogen attenuates AngII-induced pulmonary fibroblast proliferation due to the upregulation of ACE2 [36]. The expression of ACE2 is regulated by different endogenous hormones and peptides; both endothelin-1 and aldosterone downregulate ACE2 expression in a rat model. So, RAS inhibitors may improve ACE2 expression via suppression of endogenous endothelin-1 and aldosterone (Figure 6) [37].
Potential effects of endothelin-1 and aldosterone on the expression of ACE2.
Moreover, ACE2 contains ectodomain and endodomain at cytoplasmic membrane; the shedding part (ectodomain) is essential for the replication of SARS-CoV-2 (Figure 7) [38].
Shedding of ACE2 during SARS-CoV-2 entry.
At the heart of the dilemma, extensive researches are recommended to explore the specific role of ACE2 and RAS inhibitors during precarious COVID-19 worldwide outbreak.
DPP4, also called adenosine deaminase complexing protein 2 (ADCP2) or adenosine deaminase binding protein (ADBP), is widely distributed on the surface of human cells. DPP4 is involved in the regulation of blood glucose, oxidative stress, inflammation, immune system, cell adhesion, and apoptosis [39]. The substrates of DPP4 are glucagone-like peptide 1 (GLP-1), stromal cell-derived factor 1 (SDF-1), brain natriuretic peptide (BNP), substance P, and neuropeptide Y (NPY). Furthermore, DPP4 interacts with different ligands such as caveolin-1, chemokine receptor type 4 (CXCR4), adenosine deaminase (ADA), and fibronectin [40].
DPP4 inhibitors (DPP4i) such as sitagliptin, saxagliptin, and vildagliptin are approved in the management of type 2 diabetes mellitus (T2DM). Additionally, DPP4i have a potential therapeutic effect regarding hypertension, endothelial dysfunction, cardioprotection, and connective tissue diseases (Figure 8) [41].
Metabolic effects of DDP-4 inhibitors.
Regarding the role of DPP4 in viral entry and replication, Widagdo et al. [42] found that DPP4 is an important receptor for MERS-CoV transmission. DPP4 receptors are found in the human upper respiratory tract epithelium. Lacking of these receptors may restrict the transmission of MERS-CoV.
S protein of MERS-CoV binds specifically to DPP4 receptors. These interactions provoke proteolytic activation for viral entry and fusion of viral membrane with the cell membrane [43].
It has been observed that polymorphism in DPP4 gene is concerned with different cardio-metabolic disorders and transmission of MERS-CoV [44]. The polymorphism in DPP4 reduces the interactions between S proteins of MERS-CoV with cellular membranes. The difference in the incidence between Arabian and African MERS-CoV is mainly related to the genotype polymorphism of DPP4 [45].
Since there is a higher genomic similarity between SARS-CoV-2 and SARS-CoV, the implication of DPP4 as a receptor or a pathogenetic pathway in COVID-19-induced ARDS is reasonable. In COVID-19 infection, ARDS is developed due to massive cytokine release (cytokine storm), due to uncontrolled systemic inflammatory response, and due to the release of pro-inflammatory cytokine, including INF-α-, IL-6, IL-12, IL-33, etc., which cause multiple organ failure [46].
It has been reported that DPP4 is highly expressed on alveolar cells (type I and type II), alveolar macrophage, pleural mesothelium, and vascular endothelium. Besides, pulmonary vascular endothelial cells (PVECs) are the main source of pro-inflammatory cytokines in ARDS. DPP4 is upregulated in pneumonia, asthma, and ARDS; therefore, DPP4 inhibitors may reduce the inflammatory reaction and cytokine release in acute lung injury and ARDS through immune-modulation effect [47].
Different studies illustrated that DPP4 inhibitors inhibit the release of IL-6 and TNF-α in ARDS without effect on the blood glucose when used in a small dose [48]. Therefore, DPP4 inhibitors might be a therapeutic option in the management of COVID-19-induced ARDS.
DPP4 is involved in the activation of T-cell, so the activated T-cell can synthesize and secret AngII by local RAS. So, AngII-dependent T-cell activation is inhibited by DPP4i, leading to a significant reduction of endothelial inflammation and vasoconstriction [49]. Similarly, Bengsch et al. [50] disclosed that DPP4 receptors are highly expressed on Th17 which induced AngII release during ARDS. High circulating AngII level leads to the activation of inflammatory reactions via activation of the release of IL-18, 1 L-17, IL-6, and TNF-α. These mediators are essential for the induction of epithelial and endothelial cell injury during ARDS. DPP4i plays an integral role in the attenuation of IL-6 and TNF-α and associated inflammation and endothelial damage [51].
Therefore, DPP4i interferes with RAS at different levels; as teneligliptin attenuates AngII action, liraglutide downregulates AT1 and upregulates AT2 receptors during intravenous AngII infusion. Besides, exenatide inhibits the secretion of renin, AngII, and angiotensinogen [52].
What is more, DPP4i has a nephroprotective effect through the regulation of sodium and water reabsorption. Both DPP4i and GLP-1 increase sodium excretion through direct effect on proximal renal tubules or indirect effect via the activation of brain natriuretic peptide (BNP) (Figure 9) [53].
Metabolic effects of DDP-4 inhibitors regarding obesity and insulin resistance.
Consequently, DPP4i exerts protective effects on the lung and kidney which are the main tropism of COVID-19 through direct modulation of inflammatory reactions or indirectly through the attenuation of AngII. The interaction between DPP4i and RAS inhibitors seems to augment the expression of AT2 receptor which is under extensive researches to find the pathophysiological pathway of COVID-19 infection. Indeed, this interaction sheds light for possible attenuation of COVID-19-induced ARDS and AKI mainly in critically ill patients with systemic hypertension.
ACE2 is regarded as a portal entry-point for SARS-CoV-2; however, human cell lines with higher expression of ACE2 are not infected by this virus. The overexpression of AT2 receptors by ACE2 and Ang1–7 is regarded as a novel pathway in COVID-19-induced pneumonia and ARDS. Females have lower levels of ACE2 than males, which give a clue of male vulnerability to COVID-19 infection as compared with females. Even so, ACE2 is regarded as a protective pathway which reduces COVID-19-induced acute inflammatory reactions. RAS inhibitors and DPP4i increase the expression of pulmonary ACE2, so the implication of RAS inhibitors and DPP4i as augmenters of COVID-19 is not practical. Therefore, addition of, DPP4i to RAS inhibitors in hypertensive patients with COVID-19 may reduce the risk of ARDS and AKI.
Nil.
Nil.
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\n\nOur platform – IntechOpen is the world’s leading publisher of OA books, built by scientists, for scientists.
\n\nOur reputation – Everything we publish goes through a two-stage peer review process. We’re proud to count Nobel laureates among our esteemed authors. We meet European Commission standards for funding, and the research we’ve published has been funded by the Bill and Melinda Gates Foundation and the Wellcome Trust, among others. IntechOpen is a member of all relevant trade associations (including the STM Association and the Association of Learned and Professional Society Publishers) and has a selection of books indexed in Web of Science's Book Citation Index.
\n\nOur expertise – We’ve published more than 4,500 books by more than 118,000 authors and editors.
\n\nOur reach – Our books have more than 130 million downloads and more than 108,170 Web of Science citations. We increase citations via indexing in all the major databases, including the Book Citation Index at Web of Science and Google Scholar.
\n\nOur services – The support we offer our authors and editors is second to none. Each book in our program receives the following:
\n\nOur end-to-end publishing service frees our authors and editors to focus on what matters: research. We empower them to shape their fields and connect with the global scientific community.
\n\n"In developing countries until now, advancement in science has been very limited, because insufficient economic resources are dedicated to science and education. These limitations are more marked when the scientists are women. In order to develop science in the poorest countries and decrease the gender gap that exists in scientific fields, Open Access networks like IntechOpen are essential. Free access to scientific research could contribute to ameliorating difficult life conditions and breaking down barriers." Marquidia Pacheco, National Institute for Nuclear Research (ININ), Mexico
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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. 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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. Nocturnal Enureses: An Update on the pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecology/?page=/ENHLIDH/PUBD/FEATURES/\nPresentations/ Nocturnal_Enuresis/nocturnal_enuresis",institutionString:null,institution:{name:"Al Azhar University",country:{name:"Egypt"}}},{id:"113313",title:"Dr.",name:"Abdel-Aal",middleName:null,surname:"Mantawy",slug:"abdel-aal-mantawy",fullName:"Abdel-Aal Mantawy",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Ain Shams University",country:{name:"Egypt"}}}],filtersByRegion:[{group:"region",caption:"North America",value:1,count:5681},{group:"region",caption:"Middle and South America",value:2,count:5161},{group:"region",caption:"Africa",value:3,count:1683},{group:"region",caption:"Asia",value:4,count:10200},{group:"region",caption:"Australia and Oceania",value:5,count:886},{group:"region",caption:"Europe",value:6,count:15610}],offset:12,limit:12,total:1683},chapterEmbeded:{data:{}},editorApplication:{success:null,errors:{}},ofsBooks:{filterParams:{hasNoEditors:"0",sort:"dateEndThirdStepPublish"},books:[{type:"book",id:"10542",title:"Molecular Epidemiology Study of Mycobacterium Tuberculosis Complex",subtitle:null,isOpenForSubmission:!0,hash:"29279e34f971687dc28de62534335ac4",slug:null,bookSignature:"Ph.D. Yogendra Shah",coverURL:"https://cdn.intechopen.com/books/images_new/10542.jpg",editedByType:null,editors:[{id:"278914",title:"Ph.D.",name:"Yogendra",surname:"Shah",slug:"yogendra-shah",fullName:"Yogendra Shah"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10552",title:"Montmorillonite",subtitle:null,isOpenForSubmission:!0,hash:"c4a279761f0bb046af95ecd32ab09e51",slug:null,bookSignature:"Prof. Faheem Uddin",coverURL:"https://cdn.intechopen.com/books/images_new/10552.jpg",editedByType:null,editors:[{id:"228107",title:"Prof.",name:"Faheem",surname:"Uddin",slug:"faheem-uddin",fullName:"Faheem Uddin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10281",title:"Nanopores",subtitle:null,isOpenForSubmission:!0,hash:"73c465d2d70f8deca04b05d7ecae26c4",slug:null,bookSignature:"Dr. Sadia Ameen, Dr. M. 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