Basic characteristics of the considered lead acid battery element.
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
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\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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\r\n\tCrowdfunding can be defined as the collective effort of many individuals who create a network and pool their resources to support projects initiated by other people or organizations, usually through or with the help of the Internet. Individual projects or companies are financed with small contributions by a large number of individuals, allowing innovators, entrepreneurs, and business owners to use their social networks to raise capital.
\r\n\r\n\tCrowdfunding is therefore a sort of business model thanks to which a company or a public administration (including health) entrusts the creation phases of a product or service, from its design to its realization, to a set of individuals (the crowd), through an open call, to which anyone can respond by adding value of their technical and commercial skills. Compared to the traditional form of outsourcing of business activities, crowdfunding not only allows high cost savings but generates a significant benefit in terms of social and innovative capital to which the company can draw for the development of its projects.
\r\n\r\n\tThis book will offer, through its authors, in a clear and easy-to-read style, comprehensive coverage of the various aspects of crowdfunding. The text will focus on real core issues, which are the tools for appraising the performance of an organization that adopts crowdfunding.
\r\n\r\n\tIn this context, the book intends to provide the reader with a comprehensive overview of the current state of the art in crowdfunding.
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He has a degree in Law (1994) and Economics (1996) at the University of Messina (Italy) and earned his PhD degree in Public Administration at the University of Calabria (Italy), in 2005. Currently, he is a professor of Health Management, Budget and Business Organization at the University of Calabria. Furthermore, he is a professor of Business Administration at the University 'Giustino Fortunato” (Italy). He has authored several book chapters and over 60 peer-reviewed journals/proceeding papers. He served as an International Program Committee member for several conferences. 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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"}}]},chapter:{item:{type:"chapter",id:"43666",title:"Nitric Oxide in Pathophysiology and Treatment of Pulmonary Hypertension",doi:"10.5772/55680",slug:"nitric-oxide-in-pathophysiology-and-treatment-of-pulmonary-hypertension",body:'All conditions causing pulmonary hypertension (PH) are characterized by three major changes in the pulmonary vasculature: vasoconstriction, vascular remodeling, and thrombosis [1,2,3]. Vascular remodeling includes muscularization of normally non-muscular peripheral pulmonary arteries, increase in medial wall thickness of muscular arteries, and increase in vascular connective tissue such as collagen and elastin [1,2,3]. Imbalance of vasoconstrictive and vasodilatory mediators might explain the increased vascular tone [1,2,3]. Endothelial cells synthesize and release prostacylin and nitric oxide for vasodilation as well as endothelin and thromboxane for vasoconstriction. Approved treatments for pulmonary arterial hypertension (PAH) include prostacyclins, endothelin receptor blockers, and phosphodiesterase-5 inhibitors as well as inhaled NO for persistent pulmonary hypertension of the neonate (PPHN) [2].
Studies have demonstrated that short- and long-term NO inhalation improves arterial oxygenation and reduces pulmonary artery (PA) pressure in animal models of PH [4,5,6,7,8,9,10] and clinical disease such as post-operative congenital heart disease [11,12], chronic obstructive pulmonary disease (COPD) [13], pulmonary fibrosis [14], and acute respiratory distress syndrome (ARDS) [15]. In chronic hypoxia-induced PH in rats, we showed that low-dose NO (less than 5ppm) induces a submaximal reduction in pulmonary artery pressure, which does not correlate with the severity of pulmonary vascular changes [4]. Clinically, the effect of inhaled NO is based on pulmonary vasorelaxation. In experimental settings, NO inhibits vascular smooth muscle cell proliferation directly through regulating protein kinases modulating gene expression for cell growth and/or indirectly through reducing pressure on the vascular cells by cyclic guanosine-3’,5’-monophosphate (cGMP) dependent vascular relaxation. In this chapter we will discuss NO and its regulation and function with special references to the development of PH as well as pulmonary vascular reactivity in PH.
NO activates soluble guanylyl cyclase (sGC) stimulating cGMP production and subsequent activation of cGMP-dependent protein kinase (PKG). This sGC-cGMP-PKG pathway plays a major role in NO-mediated regulation. In addition to this pathway, NO directly binds to proteins and induces conformational changes with subsequent functional alterations, like phosphorylation. Thus, S-nitration is also called S-nitrosylation, the term which emphasizes a biological effect of the chemical reaction of S-nitration [16]. S-nitrosylation modifies the activity of some kinases and phosphatases, thus raising the possibility that NO modifies phosphorylation and dephosphorylation through S-nitrosylation.
NO reacts with oxygen, transitional metal ions, thiols, and superoxides, exerting its effects via cGMP-dependent and/or -independent pathways. cGMP effector molecules include cGMP-dependent protein kinases type-I and –II, cGMP-activated phosphodiesterases, and cGMP-gated ion channels. Similar to phosphorylation, S-nitrosylation regulates protein function allosterically or by direct modification of cysteine.
In the vascular system, NO reacts with sGC forming cGMP, which activates cGMP-dependent protein kinase decreasing vascular smooth muscle cell cytoplasmic Ca2+ concentration by 1) activation of proteins such as Ca2+-sensitive potassium channels which decrease membrane potential thereby causing hyperpolarization and closing voltage dependent Ca2+ channels; 2) phosphorylation of voltage- and receptor-operated sarcolemmal Ca2+ channels, causing them to close; 3) inhibition of the inositol 1,3,5-trisphospate-sensitive Ca2+ release channel of the sarcoplasmic reticulum [17].
NO mediates vasorelaxation, anticoagulation, and anti-proliferation, as well as neurotransmission. Several earlier studies demonstrated that NO inhibits smooth muscle cell growth by a cGMP-dependent mechanism [18] in addition to inhibiting growth regulating enzymes such as ribonucleotide reductase and thymidine kinase [19,20]. NO also suppresses the hypoxia-induced increase in ET-1 and platelet-derived growth factor-B, both of which have vasoconstriction and growth effects [21]. These effects of NO led investigators to determine whether administration of NO prevents the development of PH. Chronic NO inhalation ameliorates the development of hypertensive pulmonary vascular changes of chronic hypoxia-induced PH in rats [22], but not in monocrotaline (MCT)-induced PH [23]. In contrast, supplementation with the NO precursor, L-arginine, but not D-arginine prevented the development of PH in both models [24]. The reason for the different effects of NO inhalation is unclear, but may be a result of differing pathogenic mechanisms in the two models of PH: the increase in pulmonary pressures precedes the vascular structural changes in chronic hypoxia-induced PH, whereas the reverse sequence of events occurs in MCT-induced PH. Endogenous NO from L-arginine could prevent the development of new muscularization of peripheral pulmonary arteries in both models, whereas exogenous inhaled NO would be effective only in hypoxia-induced PH because of the reduction in pulmonary vascular pressures caused by NO mediated vasodilation.
Inhaled NO likely attenuates the hypertensive vascular structural changes through pulmonary vasodilation by a cGMP-mediated mechanism. Endogenous NO from L-arginine might also prevent the development of structural changes through a cGMP-mediated mechanism. This hypothesis is supported by another study that showed that pulmonary gene transfection of atrial natriuretic peptide (ANP), another inducer of cGMP, attenuates the development of chronic hypoxia-induced pulmonary vascular changes [25]. Treatment to increase NO production in the pulmonary vascular bed by eNOS gene transfection ameliorates the development of PH. Studies have demonstrated that eNOS transfected smooth muscle cell administration prevented the development of MCT-induced PH [26] and that eNOS transfected bone marrow-derived endothelial-like progenitor cell venous administration reversed established MCT-induced PH [27].
NO is produced from L-arginine by nitric oxide synthase (NOS) in the presence of oxygen, tetrahydrobiopterin (BH4), and reduced NADPH[3]. Recent studies have indicated that inorganic anions, nitrate (NO3-) and nitrite (NO2-), can be recycled to NO in vivo as alternative sources of NO in addition to the classical NOS-NO pathway. The source of nitrate includes the endogenous NOS-NO synthase pathway and the diet. Green vegetables such as lettuce and spinach provide nitrate and preservatives in cured meat and bacon include nitrite. Basically reduction of nitrate and nitrite produce NO, thus nitrate and nitrite are considered an ‘endocrine reservoir’ of NO [28].
Nitrate in the plasma is excreted into the saliva, whereas nitrate is reduced by the oral anerobic bacteria producing nitrite. These bacteria use nitrate as an electron acceptor instead of oxygen during respiration. During its subsequent movement into the stomach, nitrite undergoes further reduction to NO, thus leading to gastric NO formation, which may play a role in gastric mucosa maintenance. This is a entro-salivary circulation of nitrate. In the systemic circulation intravascular nitrite is reduced to NO by deoxyHb, respiratory chain enzymes, xanthine oxidoreductase, deoxygenated myoglobin, and protons ( 29 ). They facilitate the transfer of protons to NO2-, causing NO production which is intensified under acidic and hypoxic states. Artery-to-vein gradients in nitrite are observed.
Recycling of NO from NO2- Endogenous NO includes NO produced from L-arginine by NOS and recycled NO from NO2-. NO is converted to NO3- by the reaction with the Hb and /or to NO2- by the oxidation in the plasma with the aid of multicopper oxidase and NO oxidase ceruloplasmin. NO3- is excreted into urine by kidney and/or into oral cavity by salivary gland. In the oral cavity anaerobic bacteria reduces NO3- converting to NO2-, which goes down into stomach and is protonated under the gastric acidic state forming nitrous acid (HNO2) with further decomposition to NO and/or other nitrogen oxides. NO2- in the plasma is reduced and converted to NO by the reductase activity of deoxygenated hemoglobin, xanthine oxidoreductase, respiratory chain enzymes, and hydrogen ion. Hb(FeII), deoxygenated hemoglobin;Hb(FeII)O2, oxygenated hemoglobin; NO, nitric oxide; NOHb(FeII), nitrosylhemoglobin; NOS, nitric oxide synthase; NO2-, nitrite, NO3-, nitrate; XOR, xanthine oxidoreductase; Hb(FeIII), methemoglobin; REC, respiratory chain enzymes
Nitrite has a vasodilatory effect. Inhaled nebulized sodium nitrite reduces pulmonary artery pressure (PAP) without changes in systemic artery pressure in hypoxia- or thromboxane-induced PH [30]. Intravenous administration of sodium nitrite reverses PH induced by hypoxia or thromboxane analogs [31]. Furthermore, intermittent nebulization of sodium nitrite ameliorated the muscularization and hyperplasia of small pulmonary arteries, the development of right ventricular hypertrophy, and the rise in right ventricular pressure in chronic hypoxia- or MCT-induced PH in rats [32], which is similar to L-arginine administration[33].
The effects of inhaled NO are not restricted to the lung. Recent studies have shown that inhaled NO improves neurological and left ventricular dysfunction after successful cardiopulmonary resuscitation [34] as well as liver function after liver transplantation [35]. Inhaled NO is converted to nitrate and nitrite when it enters the blood [36, 37]. NO can be recycled from nitrite and be used to protect organs from ischemia reperfusion injury.
Coupled eNOS (eNOS homodimer) produces NO. (a) eNOS homodimer produces NO, whereas eNOS monomer produces superoxide. eNOS uncoupling occurs during the conversion of eNOS homodimer to eNOS monomer. Two eNOS monomers are connected with the aid of Zn2+, making eNOS homodimer. BH4 strengthen the Zn2+ connection, maintaining the dimer form. In coupled NOS, an electron is transferred to L-arginine, producing NO and L-citrulline. (b) electron(+) from NADPH is transferred to O2 in the uncoupled eNOS in absence of BH4(b-1) and/or L-arginine(b-2), thereby producing superoxide. BH4, tetrahydrobiopterin; eNOS, endothelial nitric oxide synthase; F, flavin; NADPH, nicotinamide adenine dinucleotide phosphate
In the process of NO formation from oxygen and L-arginine, oxygen molecules are incorporated in both NO and L-citrulline, showing that NOS is a dioxygenase [38]. NOS containes both a reductase domain and an oxygenase domain, where electron transfer occurs from the reductase domain to the oxygenase domain. NADPH and flavin bind to the reductase domain, while oxygen, BH4 and L-arginine bind to the oxgenase domain. Electrons are transferred from NADPH through the flavin containing reductase domain to the oxygenase domain [39]. Then two cascades of further electron transfer occur depending on the presence or absence of BH4 and L-arginine. When both BH4 and L-arginine are present, NO is synthesized by oxidative deamination of arginine by NOS, where the electron is transferred to L-arginine. The initial step of L-arginine oxidation is donation of electrons to the ferrous–dioxygen complex from BH4, where trihydrobiopterin is produced and the electron is supplied through flavin regaining BH4 [40]. In contrast, in the absence of L-arginine or BH4, NOS synthesizes the superoxide, where the electron is transferred to ferrous oxygen. Intracellular deficiency of BH4 induces superoxide generation from eNOS [40]. The term “eNOS uncoupling” means functionally that electron transfer to L-arginine is uncoupled, when the electron is transferred to ferrous-dioxygen instead of L-arginine, producing superoxide. NOS homodimer produces NO from L-arginine and oxygen, whereas NOS monomer produces superoxide [41]. Thus, the molecular basis of eNOS uncoupling is conversion of the NOS dimer to the NOS monomer. To maintain the NOS dimer, BH4 is essential and dihydrobiopterin (BH2) is the oxidized form of BH4. Peroxinitrite oxidizes BH4 to BH2, reducing the BH4 amount and/or the BH2/BH4 ratio, both of which induce eNOS uncoupling [42]. The effects of BH4 are mediated through the regulation of NO compared with superoxide synthesis by endothelial NOS. Since BH4 might both augment NO synthesis and decrease superoxide production, BH4 deficiency may play a role in the pathogenesis of PH.
eNOS uncoupling is evaluated by the eNOS dimer/monomer ratio in cold SDS-PAGE Western blot analysis. While oxidative stress reduces the eNOS dimer/monomer ratio in a cardiac hypertrophic model suggesting eNOS uncoupling, exogenous BH4 restored the eNOS dimer/monomer ratio [43]. Administration of exogenous BH4 might be used for eNOS uncoupling diseases. BH4 deficiency might cause PH in mice and BH4 augmentation might ameliorate the development of PH. Mice with low BH4 tissue levels develop PH which is reversed by increasing BH4 with targeted transgenic overexpression of the rate-limiting enzyme in BH4 synthesis, guanosine triphosphate(GTP) cyclohydrolase [44]. Lung BH4 availability is controlled by pulmonary vascular tone, right ventricular hypertrophy, and vascular structural remodeling. BH4 is a cofactor of NOS in the production of NO. BH4 deficiency causes decreased NO production with concomitant production of superoxide by NOS. Chronic administration of BH4 analogues improves NO-mediated pulmonary artery dilatation in rats with chronic hypoxic pulmonary hypertension [45]. Copresence of increased levels of NOS and reduced NO bioactivity might be explained by the deficiency of BH4 and/or L-arginine.
Long-term increases in NO might increase eNOS expression and eNOS uncoupling, thereby producing superoxide. Long-term administration of nitroglycerin (TNG) increased eNOS mRNA and protein expression and vascular superoxide (O2•- ) in intact vessels monitored using ESR spectroscopy [46]. An earlier study showed that endothelial denudation improves vascular relaxation induced by TNG in isolated vessels from nitrate-tolerant animals [47].
Caveolae are flask-shaped invaginations on the cell surface, which contain structural proteins called caveolin and other signaling proteins. In endothelial cells, eNOS is inactivated when it is conjugated to caveolin-1, a structural protein of endothelial caveolae; eNOS is activated when it dissociates from caveolae. Stimulation of β2 adrenergic receptors cause this dissociation through phosphorylation of Tyr in caveolin-1. The mouse pulmonary endothelial β2 adrenergic receptor coupled to Gi/o proteins causes phosphorylation of caveolon-1 by Src kinase and eNOS phosphorylation at ser1177 by the Src kinase - phosphatidylinositol 3 kinase (PI3kinase) - Akt kinase pathway [48]. Thus, stimulation of the β2 adrenergic receptor causes endothelial NO synthase-dependent relaxation.
Loss of caveolin-1 induces chronic activation of eNOS and subsequent tyrosine nitration of PKG in lungs from patients with idiopathic pulmonary hypertension, where activated eNOS is uncoupled eNOS, producing superoxide [49]. Genetic deletion of caveolin in mice causes PH and treatment with a superoxide scavenger and/or a NOS inhibitor prevents PH associated vascular remodeling [49]. Although caveolin expression in total lung determined by Western blotting is not altered in severe PH, its immunohistological expression in plexiform lesions is absent or decreased [50].
A 90-kDa heat shock protein (HSP90) is a molecular chaperone of proteins that modulates protein functions. Along with many other proteins, eNOS and sGC are targets for HSP90. HSP90 interacts with eNOS and HSP90 facilitates the displacement of eNOS from caveolin 1, activating eNOS. HSP90 activity is dependent on adenosine triphosphate (ATP). Asymmetric dimethylarginine (ADMA) inhibits HSP90 activity in pulmonary endothelial cells through mitochondrial dysfunction, caused by ADMA induced eNOS uncoupling with subsequent superoxide production and nitration of mitochondrial protein, which reduce ATP production [51].
To examine whether the change in eNOS expression and its activity is associated with vascular endothelial dysfunction in PH, many studies have been performed in several species of animals and humans, using isolated lung, isolated pulmonary artery, and in vivo. eNOS is expressed in not only vascular endothelial cells, but lung epithelial cells. In addition, eNOS expression and/or activity might be different between conduit PAs and resistance PAs.
Animal models
mRNA and protein expression of eNOS in rat lung and eNOS expression localized in pulmonary vascular endothelial cells and epithelial cells is upregulated in acute hypoxia [52]. In that study, nitrate/nitrite in rat lung homogenate also increased, suggesting augmented eNOS activity. The enhancement of eNOS activity in hypoxic pulmonary vasoconstriction (HPV) in normal rat lung also has been shown in other studies using NOS inhibitors [53, 54] (see sect.3.1). eNOS protein expression was time-dependently increased in rats in chronic hypoxia-induced PH [55,56], while phosphorylated eNOS (peNOS), active form, was impaired [55]. MCT-induced PH rats showed decreased expression of both eNOS [57,58,59] and peNOS [59].
Inactive form of eNOS associated with caveola. eNOS is associated with caveola, which is the inactive form of eNOS. The active form of eNOS is dissociated from caveola. Stimulation of BMPIIR induces dissociation of eNOS from caveola as well as phosphorylation of eNOS through PKA and/or Akt activation. eNOS, endothelial nitric oxide synthase; B2-AR, beta 2-adrenergic receptor; SrcK, src kinase; peNOS, phosphorylated eNOS; BMPIIR, bone morphogenetic ptotein II receptor; PKA, cyclic AMP-dependent protein kinase
Human
Many studies of eNOS expression and its activity have been performed in adult human PAH. However, the results are not consistent: eNOS expression is reduced in pulmonary vessels from adults with primary and secondary PH, but is increased in plexiform lesions [60]. Western blot analysis showed that eNOS expression is not changed in the lung tissue of idiopathic PAH (IPAH) patients [61]. However, several studies reported lower exhaled nitrate/nitrite (NOx) in PAH patients [62,63]. Overall, these results suggest that eNOS activity might be depressed in adult human PAH.
L-NMMA (N omega-monomethyl–L-arginine), L-NNA (N omega-nitro-L-arginine), L-NAME (N omega-nitro-L-arginine methyl ester), L-NA(N omega-nitro-L-arginine) and other NOS inhibitors have been used to examine the physiological role of NO in pulmonary vascular tone. The increase in vascular tone in the presence of NOS inhibitors may indirectly represent NO production and/or release in the pulmonary circulation.
Animals
L-NMMA [53] and L-NNA [64,65] did not change pulmonary basal tone in normal rat PA rings. Normal isolated perfused lungs were not affected by NOS inhibitors such as L-NMMA [53], L-NNA [64], and L-NA [66] except for a few studies showing a moderate increase with L-NAME [67]. In chronic hypoxia, many studies showed markedly enhanced vascular tone by L-NNA [64] or L-NAME [67]. Although these NOS inhibitors caused different results, the findings suggested that 1) NO might not be involved in vascular basal tone in normal pulmonary circulation, and 2) basal NO production might be increased in hypoxia-induced chronic PH. On exposure to acute hypoxia, NOS inhibitors augmented vascular contraction in normal [53,67,68] and hypoxia-induced PH rat models [67]. This finding suggests that NO production in HPV is increased in both normal and hypoxic PH rats.
Humans
Inhibition of NO production by L-NMMA caused the reduction of pulmonary flow in conscious healthy adults [69,70], suggesting the possible role of continuous production of NO in maintaining basal vascular tone. In PAH patients, several studies reported decreased expression of NOS. Although several studies reported decreased exhaled nitrogen oxide (NOx) levels in PAH patients, others have reported higher levels. The results therefore remain inconclusive.
Many studies have been performed using acetylcholine (Ach) and sodium nitroprusside (SNP), endothelium-dependent and -independent NO-related vasorelaxants, to examine functional changes in vascular endothelial and smooth muscle cells in PH. As Ach-induced relaxation was abolished by NOS inhibitors [64] and restored with L-arginine [71,72], reactivity may partly reflect changes in NOS expression and/or activity.
Rats with hypoxic PH
The relaxation response to Ach is impaired in rat isolated conduit pulmonary arteries (PAs) [65,73,74,75,76]. Many of these studies also described an impaired relaxation response to SNP in conduit PAs [65,74,76]. These results suggested 1) decreased production and release of NO in endothelial cells or 2) decreased responsiveness to NO in smooth muscle cells, or both. Impaired relaxation in Ach and SNP was partially restored after exposure to chronic hypoxia. As the recovery process was different between the responses of Ach and SNP [65], it was speculated that NO-related functional abnormalities in endothelial and smooth muscle cells occurred independently.
In contrast, in hypoxic vasoconstriction resistant rat PA rings, the relaxation response to Ach was not changed [74,75] or augmented [77] in chronic hypoxia. It is likely that Ach-reactive NO production and/or release varies in a vascular site-specific manner. Conduit arteries produce and release more eNOS than peripheral arteries. The vascular functional change in response to stimuli such as abnormal shear stress, circumferential wall stretch and hypoxia itself may occur in conduit PAs more than in peripheral resistant arteries. Although conduit arteries do not directly relate to pulmonary vascular resistance, the pathophysiological change in conduit arteries may play a key role in pulmonary vascular remodeling [78].
Impaired response to Ach was partly restored in the presence of a non-selective inhibitor of cyclooxygenase (COX) [65] or prostaglandin (PG) H2 / thromboxane (TX) A2 receptor antagonist [79], suggesting the possibility of 1) imbalance between the production of vasocontracting and vasorelaxing prostanoid in vascular endothelial cells, and 2) simultaneously release of vasocontracting prostanoids such as PGH2 and/or TXA2. Pidgeon et al. showed that the basal expression of COX2, otherwise known as PGH synthase, was increased in rat lungs in chronic hypoxia, and a PGH2/TXA2 receptor antagonist attenuated the rise in PAP induced by chronic hypoxia [80].
MCT-induced PH in rats
PA vascular functional changes in rats with MCT-induced PH have been compared with PAs from animals with chronic hypoxia-induced PH. Many vasodilation studies have reported a depressed relaxation response to Ach in MCT-induced rat conduit PA rings [76,81,82,83,84]. Many of these studies described impaired SNP relaxation, [76,82] with the exception of one study [84]. While Ach-induced relaxation was impaired in the pulmonary circulation in MCT-induced PH, the SNP relaxation response has been reported to be impaired [85] or not impaired [86]. Taken together, in MCT-induced PH, vascular endothelial dysfunction is observed from proximal to distal PAs; however, smooth muscle functional alteration is not apparent in peripheral PAs.
In pulmonary hypertension, endothelial NOS expression is increased, which may not necessarily indicate an increase in NO production [87]. NOS might produce superoxide, which is due to uncoupling of NOS [88]. Increased levels of NOS and reduced NO bioactivity might be explained by the deficiency of BH4 and/or L-arginine. Oxidative stress induces the changes of BH4 to BH2. Oxidative stress also induces S-glutathionylation and subsequent eNOS uncoupling [39], in which S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O2•- generation primarily from the reductase and endothelium-dependent relaxation is impaired. Oxidative stress upregulates nuclear factor (NF)-kappaB, a key transcription factor that is involved in vascular tissue remodeling. NF-kappaB nuclear localization and vascular cell adhesion molecule 1(VCAM-1) expression is temporally and spatially associated with the development of MCT-induced PH in rats, which is ameliorated by administering a NF-kappaB inhibitor, pyrrolidine dithiocarbamate(PDTC)[89].
Peroxynitrite production from NO and superoxide. Superoxide (O2.-) is produced by uncoupled eNOS, NADPH oxidase, and xanthine oxidase. NO reacts with O2.- producing peroxynitrite(ONOO-) with subsequent nitrosylation of protein kinases, thereby activating or suppressing their activities. PKG phosphorylates Rho kinase, Akt, and ion channels. Phosphorylation of ion channels makes Ca2+ ion channels closed and potassium channel open. Peroxynitrite further oxidize BH4 to BH2, inducing eNOS uncoupling with subsequent superoxide production. BH4, tetrahydrobiopterin; BH2, dihydrobiopterin; eNOS, endothelial nitric oxide synthase; ERK, extracellular signal-regulated kinase; IP3, inositol triphosphate receptor; MAPK, mitogen-activated protein kinase; OX, oxidase; ONOO-, peroxynitrite; PKC, protein kinase C; PKG, cyclic-GMP dependent protein kinase( protein kinase G); XOX, xanthine oxidase;
NAD(P)H oxidase enzyme complex catalyzes one electron reduction of oxygen using NADPH or NADH as an electron donor, which produces superoxide : NAD(P)H + 2O2 → NAD(P) + + H+ +2O2-‘ NADPH oxidase expression is increased in pulmonary arteries from a lamb model of persistent pulmonary hypertension of the newborn (PPHN) [90]. The expression was determined by the Western blotting of the levels of p67phox a subunit of the NADPH oxidase complex and immunostaining of the pulmonary vessels in lung sections. Another study demonstrated that expression and activity of the NADPH oxidase complex are upregulated in PH with increased pulmonary blood flow [91].
Deficiency of superoxide dismutase (SOD) may play a role in the development of PH. Expression and activity of mitochondrial SOD2 in patients and animal models of PH is decreased [92,93] in pulmonary arteries and plexiform lesions. SOD produces H2O2 from mitochondrial superoxide. H2O2 is less potent than superoxide and acts as a signaling molecule to inhibit transcriptional factors such as hypoxia-inducible factor-1α. Epigenetic suppression of SOD with selective hypermethylation of CpG islands in SOD2 gene induces excessive proliferation and decreases apoptosis in pulmonary artery smooth muscle cells [92], suggesting a causative role of SOD deficiency in PH.
NO reacts with superoxide more rapidly than SOD producing peroxinitrite. Peroxynitrite is a more potent and versatile oxidant than NO or superoxide, in which HO+ and NO2 produced from peroxynitrous acid (HOONO) and/or its reactive activated isomer (HOONO*) attacks biological targets [94] including cyclic GMP-dependent protein kinase (PKG). In the setting of eNOS uncoupling, eNOS synthesizes superoxide which reacts with NO to create peroxynitrite. Nitrosylation of PKG by ONOO- depresses the function of PKG ( 42 ).
Arginase, an enzyme in the urea cycle, converts arginine to ornithine and urea. NOx concentrations in exhaled gas and serum are decreased in PH patients compared with normal persons [95], suggesting decreased NO availability in PH. The deficiency of the NO precursor L-arginine, the substrate depletion of NOS, might partly explain the decrease in NO availability. Lower levels of arginine in the cell might be due to the increased activity of arginase. In PH patients, lower levels of arginine correlate with higher pulmonary artery pressures. Serum arginase activity is higher and the serum arginine-ornithine ratio is lower in PH patients than in healthy controls, indirectly suggesting increased intracellular arginase activity [33]. Animal studies showed that prolonged administration of L-arginine ameliorated the development of monocrotaine-induced PH [24,96] and chronic hypoxia-induced PH [96]. In patients with PH L-arginine treatment reduces PAP [97]. In addition to functioning as the substrate for NO formation, L-arginine prevents eNOS uncoupling, serves as a direct radical scavenger, and competes with the endogenous eNOS inhibitor ADMA, which decreases superoxide and increases NO formation [41].
The level of asymmetrical dimethylarginine (ADMA) is increased in patients with PAH and MCT-induced PH in rats [98]. Since ADMA is an endogenous competitive inhibitor of NOS and suppresses NOS activity, increases in ADMA inhibit NO production. In atherosclerotic arteries from patients with high serum ADMA, endothelium-dependent relaxation by acetylcholine was impaired and O2•- production was increased [99]. Dysregulation of ADMA might cause PH through the decrease in NO in the lung as well. Dimethylarginine dimethyaminohydrolase (DDAH) is a metabolizing enzyme of ADMA. Thus the increase in DDAH activity reduces ADMA and induces subsequent increases in NOS activity. DDAH has two isoforms: DDAH 1 and DDAH 2. DDHA 1 and DDAH 2 are expressed predominantly in tissues containing neuronal NOS (nNOS) and eNOS, respectively [100]. Phosphodiesterase (PDE) 3/4 inhibitors reduce ADMA and raise NO/cGMP levels [2]; PDE3/4 inhibitors activate the cAMP/protein kinase A (PKA) pathway and induce subsequent activation of the promoter region of DDAH2. Western blot analysis of lung from PH rats 28 days after the injection of MCT showed decreases in eNOS, pNOS, AKT, and DDAH2 and increases in lung and serum ADMA levels [101]. In this PH model, 1) decreased Akt reduces eNOS phosphorylation and thereby decreases eNOS activity 2) decreased DDAH2 reduces ADMA breakdown and thereby the increase in ADMA inhibits eNOS activity. This study showed that rosuvastatin ameliorates MCT-induced PH through the normalization of Akt, eNOS and DDAH2 expression and ADMA levels [101].
Endothelial cells express retinoid receptors and all-trans-retinoic acid (ATRA) increased DDHA2 mRNA levels in endothelial cells. Although eNOS mRNA expression is not increased with ATRA treatment, ATRA increases NO production, suggesting that ATRA increases activity of expressed eNOS indirectly through the decrease in ADMA due to increased DDHA2 [102]. ATRA also upregulates NO production in vascular endothelial cells through the PI3 kinase/Akt pathway [103]. ATRA induces eNOS phosphorylation at ser1177 and Akt phosphorylation at ser473 without changes in protein expression such as occur during DDAH2 upregulation. In terms of inducible NOS(iNOS), interleukin(IL)-1β increases iNOS mRNA levels and ATRA reduces this increase in vascular smooth muscle cell culture [104]. Because iNOS inhibition by the iNOS inhibitor N6-(1-iminoethyl-L-lysine, dihydrochloride(L-NIL) prevented the development of PH [105], the inhibitory effect of ATRA on iNOS expression might reduce the development of PH. Peroxisome proliferator-activated receptors (PPARγs) are a nuclear hormone receptor superfamily of ligand-activated transcription factors of retinoid hormone receptors other than steroid and thyroid hormones. PPARγ or retinoid X receptor (RXR) agonists inhibit smooth muscle proliferation. The PPARγ agonist rosiglitazone attenuates the development of chronic hypoxia-induced vascular structural remodeling [106], although it has little effect on the vasoconstriction component of PH. Since PPARγ mediates effects through the RXR, retinoids might also ameliorate PH vascular changes. PPARγ ligands increase the release of NO from endothelial cells through a transcriptional mechanism probably through the increase in DDAH mRNA expression without changes in eNOS expression [107]. These results suggest that ATRA might prevent the development of experimental PH in rats. ATRA ameliorated the development of MCT-induced PH [108], but not chronic hypoxia-induced PH [109]. These differences in the effect of ATRA on the development of PH may be due to a more pronounced inflammatory response in MCT-induced PH and a more subtle inflammatory reaction in chronic hypoxia-induced PH; endothelial damage precedes the rise in PAP in MCT model whereas the rise in PAP precedes endothelial changes in the chronic hypoxic model [110,111].
Possible pathway to enhance NO production by ATRA, DDAH, PDE3/4 inhibition, and BMPIIR. ADMA supresses NOS activity. DDAH is the enzyme that metabolizes ADMA. The cAMP/PKA pathway activates the promoter region of DDAH2, thereby increasing DDAH2 expression. ATRA increases DDAH2 mRNA, stimulates RAR with a subsequent increase in PI3K activity as well as PI3K protein and mRNA expression, and thereby enhances Akt and eNOS phosphorylation without increasing eNOS expression. Phosphorylated Akt(pAkt) phosphorylates eNOS making peNOS, the activated form of NOS. B2-AR stimulation activates SrcK via Gi/o protein. Activated SrcK phosphorylates PI3K and induces subsequent its downstream eNOS phosphorylation as well as phosphorylation of caveolin -1 to dissociate eNOS from caveola (Figure 3]. ADMA, asymmetric dimethylarginine; ATRA, all trans retinoic acid; B2-AR, beta 2-adrenergic receptor; BMPIIR, bone morphogenetic ptotein II receptor; CREB, cAMP responsive element binding protein; cAMP, cyclic adenosine monophosphate; DDAH, dimethylarginine dimethylaminohydrolase; eNOS, endothelial nitric oxide synthase; peNOS, phosphorylated eNOS; ERK, extracellular signal-regulated kinase; pERK, phosphorylated ERK; Gi/o, GTP binding protein subunit Gi/o; PDE, phosphodiesteras; PI3K, phosphoinositide 3-kinase; PKA, cAMP dependent protein kinase; PKG, cyclic GMP-dependent protein kinase ; PPARγ, peroxisome proliferator-activated receptor; Srck, src kinase; RAR, retinoic acid receptor;
Mutation of the bone morphogenetic protein receptor type II (BMPIIR) gene is one of the causes of familial PAH. The link between BMPIIR and eNOS partly explains the mechanism for the development of PH caused by BMPIIR mutations. Stimulation of BMPIIR induces eNOS phosphorylation, primarily through the cyclic-AMP dependent protein kinase and partially through serine-threonine kinase Akt [112]. Stimulation of BMPIIR also causes dissociation of eNOS from caveolin-1 and increases the eNOS-HSP90 interaction, which facilitates electron transfer through eNOS[112]. Thus, impaired BMPIIR or loss of BMPIIR stimulation might disturb the pulmonary vascular homeostasis, thereby causing PH.
Vascular endothelial growth factor (VEGF) stimulates NO production initially by increasing intracellular Ca++ levels and subsequent Ca++-calmodulin dependent activation of eNOS, and later by increasing intracellular eNOS message and protein levels [113]. VEGF stimulates vasodilation, microvascular hyperpermeability, and angiogenesis. Plexiform lesions show striking expression of VEGF associated with endothelial proliferation. NOS inhibition prevents VEGF-induced proliferation in cultured microvascular endothelial cells, associated with the decrease in cGMP levels [114], suggesting that VEGF-induced proliferation is in part mediated by the NOS-NO-cGMP pathway. VEGF induces translocation of eNOS and caveolin-1 from caveola to the nucleus, where NO production activates transcriptional factors thereby inducing the early growth response gene, c-fos [115] and possibly inducing angiogenesis, and endothelial cell growth. VEGF receptor 2 (VEGF2R) blockade combined with chronic hypoxic exposure causes PH with plexiform like lesions, where decreased expression of VEGF2R, Src, Akt, phosphorylated Akt protein in lung have been demonstrated [116]. Studies have demonstrated that reduced Src and Akt attenuate eNOS phosphorylation [101].
Earlier studies have shown that vascular elastase activity is increased in MCT-induced PH and chronic hypoxia-induced PH in rats [3,117], and that elastase inhibition prevents the development of pulmonary hypertension, right ventricular hypertrophy, muscularization of peripheral pulmonary arteries and medial hypertrophy of muscular arteries [3,117,118]. NO might reduce the elastase activity through its scavenging effect of superoxide. Reactive oxygen species inactivates endogenous elastase inhibitor, α1-protease inhibitor, and might increase elastase activity [119]. Furthermore NO might reduce elastase expression by inhibiting its transcriptional factor, acute myeloid leukemia factor 1 (AML-1), through extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) inhibition which is mediated by cGMP dependent protein kinase activation [120].
Rho/Rho kinase pathway inhibits eNOS/NO/cGMP pathway Rho kinase is activated by the guanosine triphosphate (GTP)-bound, active form of RhoA (GTP RhoA). Activated Rho kinase phosphorylates and subsequently inactivates myosin phosphatase, causing smooth muscle contraction, which is the RhoA/Rho kinase pathway. PKG phosphorylates Rho A at Ser188 and inhibits Rho A function, thereby inactivating the RhoA/Rho kinase pathway. Activated RhoA/Rho kinase decreases eNOS mRNA and protein expression, inactivates Akt, and inhibits PKG activity, thereby supressing the eNOS/ NO/cGMP pathway. VEGF upregulates eNOS mRNA and protein expression. AML-1, acute myeloid leukemia factor 1(transcriptional factor); EVE, endogenous vascular elastase; PKG, cyclic GMP-dependent protein kinase(G kinase); PKB, protein kinase B(=Akt), AML-1, acute myeloid leukemia factor 1; ML, myosin light chain; pML, phosphorylated myosin light chain; MLCK, myosin light chain kinase; ERK MAPK, extracellular signal-regulated kinase mitogen activated protein kinase; VEGF, vascular endothelial growth factor.
Myosin light chain (MLC) phosphorylation by myosin light chain kinase (MLCK) causes vascular smooth muscle contraction. In contrast, myosin light chain dephosphorylation by myosin light chain phosphatase causes relaxation. The phosphorylation status of MLC phosphatase determines the contractility of smooth muscle at the same Ca++ concentration, thereby regulating the Ca++ sensitivity for contraction; the stronger the phosphatase activity, the weaker the vascular tone at the same Ca++ concentration. RhoA/Rho-kinase activation augments the phosphorylation of MLC phosphatase, which results in inhibition of MLC phosphatase. Studies have shown that Rho-kinase in circulating neutrophils is increased in patients with PH and that Rho-kinase expression is upregulated in isolated lung tissue on transplantation [121]. Rho-kinase activity in pulmonary arteries is enhanced in experimental PH [122,123]. NO-cGMP-cGMP dependent protein kinase pathway suppresses Rho/Rho kinase activity [124]. On the other hand Rho/Rho-kinase activation downregulates eNOS expression and eNOS phosphorylation through the inhibition of the protein kinase B/Akt pathway [125].
Renewable energy productions are characterized by the unpredictability and the intermittence of the environmental data such as solar irradiation and wind speed in photovoltaic and wind system productions. Therefore, the main criteria when supplying remote areas from renewable source (wind energy/solar irradiation) are the continuity and reliability of electricity supply. The satisfaction of these two criteria can be reached by inserting storage devices (electrochemical devices, hydraulic devices, etc.), but the high owning cost of such solution denotes a major inconvenient for this alternative [1, 2, 3, 4, 5]. Hence, an optimal sizing design of the renewable production system coupled with the storage device appears as a guarantee to assure reliability and cheap electricity to supply consumers in isolated sites. The optimal design is achieved by performing global optimization process using a several simulations [6, 7, 8, 9, 10, 11, 12]. Nevertheless, these simulations are performed in large time duration, since the environmental data (wind speed, solar irradiation) are characterized by unpredictability which needs great amounts of such data.
In this context, this chapter scrutinizes the optimal design of an electrochemical storage device (a battery bank) associated to a renewable energy system (a wind turbine (WT)) in order to supply continuously a typical farm in a remote site, considering environmental data potentials and load demand variations are a crucial step in the design of these systems. In the case study, the battery bank is exposed to a “time phasing” (Tph) between the generating WT energy/power (consequences of the wind data) and the consumption profile with a time cycle of 24 h, which is a specific problem when sizing the battery bank: indeed, the difference between power production and power consumption profiles is not sufficient to characterize the battery sizing. The time phasing of this power difference is also of prime importance as it sets the battery energy which is also essential in the battery sizing process.
Four generic battery sizing methodologies are investigated. Two methodologies are based on statistical approaches, and two other methodologies are based on compacting environmental data duration. These methodologies are applied, as a case study, on a renewable energy system consisting of 8 kW standalone wind turbine (Figure 1).
Case study: a WT system with battery for standalone application.
Statistical methodologies determine the power and energy constraints associated with the battery bank from temporal Monte-Carlo-based simulations including environmental data and consumption profile variations. Environmental data evolution is considered as stochastic, while the consumption demand is deterministically day to day regenerated (Figure 2). Only slow dynamics of the wind potential is taken into account. This means that fast dynamics of wind speed related to turbulence is neglected. Therefore, a Weibull distribution represents wind speed features. To find the most critical constraints on the battery, we require including all correlations between renewable power production and load profile (e.g., time windows with high wind powers and small load powers and inversely). So, the process computation cost is rather expensive especially when a global integrated design process is performed, where all components have to be simultaneously optimized. Thus, the computation cost of these statistical approaches presents an actual problematic. In order to face this problem, two other methodologies are investigated for reducing environmental data profile durations while keeping their feature trace in terms of variability, intensity, and statistics. These approaches are based on the original approach proposed in [13]. This latter approach is adapted for compacting wind speed profiles. The idea consists of aggregating elementary-parameterized segments to generate a compact environmental data profiles. This is performed by satisfying target indicators representing the environmental data features of a reference profile of larger duration. This inverse problem involving the determination of the segment parameters is solved using a genetic algorithm.
Daily load demand profile.
The considered system is a 8-kW-full WT battery charger without active control and with minimum number of sensors (Figure 1). This WT is sizing in manner that the wind power extraction of this configuration matches very closely the behavior of active WT systems operating at optimal wind powers by using an MPPT control device. The deterministic load profile is set on 24 h and day by day repeated as indicated in Figure 2.
A lead acid Yuasa NP 38-12I is considered as a battery element. The basic characteristics are summarized in Table 1.
Basic characteristics of the considered lead acid battery element.
The battery sizing algorithm is based on an upper saturated integration of powers in the battery bank. The idea of a saturated integration of the battery power is related to considering charge powers are no more integrated if the state of charge (SOC) of the storage device reaches its maximal level. Thus, we consider that charge power is wasted in order to avoid the storage device oversizing occasioned with a simple integration especially during huge wind speeds with reduced consumption.
At a particular location characterized by a specific wind-energy potential, wind speed can be predicted by several statistical distribution models from the wind-energy potential. In this approach, the sizing process is based on the generation of a wind cycle from its statistical distribution [14, 15].
The consumption profile and the power and energy levels which depend on the wind potential magnitude and phase decide the storage device sizing. Hence, determining the pertinent storage device sizing must be under the “worst” case conditions (maximum power and energy). In order to realize these conditions, several wind speed profiles with increasing duration have to be produced until battery sizing stabilization (Figure 6), i.e., battery cells become quasi-constant.
The synoptic of the random process of wind speed generation of the is shown in Figure 3. The continuous temporal wind speed profiles are generated from statistical distribution by interpolating some number of samples generated with a random number generator according to the recognized statistical distribution.
Wind speed generation process.
Figure 4 shows the synoptic battery bank sizing process. The idea consists of generating 11 wind cycles with a progressive duration from 1 to 200 days. These cycles are synthesized from a Weibull distribution of the wind speed during Nd days (Nd = {1, 2, 3, 10, 20, 30, 50, 70, 100, 150, 200 days}). After simulation of the WT system, 11 extracted wind powers (Pwind) are produced. The consumption power (Pload) is daily repeated during the Nd days.
Battery bank sizing process based on wind profile generation form its distribution.
Note that the battery power used by the sizing algorithm is given by:
Table 2 shows the battery element number and the computational time (TCPU) under different wind speed profiles. The computational time is the time needed by the processor to simulate the system model and to perform the storage device sizing process.
Statistical approach results.
In order to reduce TCPU, a critical factor in an integrated optimal design (IOD) context, this approach is based on the direct generation of the extracted power (PWT) histogram instead of the wind speed histogram as proposed in the first methodology. The extracted power for each wind speed interval is estimated by simulating the WT system. PWT is synthesized on the same time scales as with the first methodology.
The PWT histogram is built from wind statistics. Thus, we obtain directly the WT power profile from its distribution by means of random number generation and interpolation techniques exactly as described in the first methodology. Therefore, the PWT can be directly generated before to obtain the battery power PBAT used for the storage bank sizing process (Figure 5). Similarly to the first methodology, 11 PWT cycles are produced with a progressive duration from 1 to 200 days and waiting until stabilization of the number of battery cells.
Storage device sizing process based on extracted power generation profile form its distribution.
To face the stochastic nature of wind speed, several simulations of the 11 wind speed cycles (with an increasing number of days from 1 to 200) have been performed. Table 2 gives the average number of battery cells <Nbt> obtained after 10 simulations for both methodologies. <Nbt> obtained from the 11 generated wind speed cycles are shown in Figure 6.
Plot of battery cell number versus cycle duration.
In this approach an actual wind speed profile of 200 days duration is considered as reference data. In order to generate a compact wind speed profile with a reduced duration Δtcompact, the “compact synthesis process” is applied on this profile. Two methodologies are scrutinized, differenced by the target indicators used for generating the fictitious compact wind speed profile in order to establish its correspondence with reference actual profile.
The principle of compact environmental data synthesis process consists of the generation of a fictitious profile of temperature, solar irradiation, wind speed, etc. by satisfying some constraints related essentially to variable characteristics, i.e., minimum, maximum, and average values, probability distribution function, etc. These constraints are expressed in terms of “target indicators” that can be evaluated from a set of reference profiles usually of large duration: here we have considered a 200-day wind profile. The fictitious profile is obtained by aggregating elementary segments as shown in Figure 7. Each segment is characterized by its amplitude ΔSn (ΔSminref ≤ ΔSn ≤ ΔSmaxref) and its duration Δtn (0 ≤ Δtn ≤ Δtcompact).
Plot of battery cell number versus cycle duration. (a) Variable profile generated by segments, (b) Pattern parameters: ΔSn et Δtn.
In order to fulfill the constraint related to the time duration, i.e., ∑Δtn = Δtcompact, a time scaling step is executed after the variable profile generation. The compact fictitious profile generation synthesis consists of finding all segment parameters fulfilling all target indicators given by the reference data (actual profile) on the reduced duration Δtcompact. This is performed by solving an inverse problem, using evolutionary algorithms, with 2 N parameters where N denotes the compact profile segment number [16]. As evolutionary algorithm we have chosen the clearing method [17] well suited to treat this kind of problem with high dimensionality and high multimodality. Target indicators are also related to the design context itself (in this case study, the WT system has to charge a battery bank for which maximum powers and energy range are pertinent).
The first approach uses, as target indicators, the storage system features. The storage system global sizing is related to the maximum storage power PBATMAX, the minimum storage power PBATMIN, and the maximum energy quantity imposed to this storage ES. These variables target indicators of the inverse problem, and they are extracted from simulation of the WT system over the reference profile of days.
The reference value of the storage useful energy ESref is given by the following equation:
with
To avoid oversizing during wide charge period (reduced consumption versus huge winds), the storage is only sized in discharge mode. Thus, E(t) is computed as a saturated integral, with 0 as upper limit. To take into account the reference wind cycle statistic features, an additional target indicator is considered: the cumulative distribution function CDF(Vref) calculated from the corresponding probability density function PDFref which is evaluated on 20 equally spaced intervals between 0 and the maximum wind speed value Vrefmax and related to the reference wind speed behavior.
Therefore, the inverse problem is set to minimize the global error ε in the synthesis profile process by
where the statistic error εstat denotes the mean squared error between both CDFs relative to reference and generated wind speed profiles:
All “ref” indexed variables are based on the reference wind profile of Figure 8. The inverse problem is solved with the clearing algorithm [17] using a population size of 100 individuals and a number of generations of 500,000.
Actual “reference” wind speed profile, storage power, and energy.
Multiple optimization runs are performed with different compaction times Δtcompact. In order to guarantee a global error ε less than 10−, the minimum compaction time was determined using dichotomous search. The values of ε versus compaction time are shown in Table 3. The minimum value for Δtcompact assuring the completion of the target indicators with adequate accuracy is about 10 days. The generated wind profile is obtained from the aggregation of 109 elementary segments fulfilling all target indicators. The characteristics of this compact wind cycle and its CDF are displayed in Figure 9. It can be seen from this figure that the CDF of this wind profile closely coincides with that of the reference wind profile.
Influence of ΔTcompact on the global error ε.
Generated wind speed with corresponding CDF.
In Table 4 a comparison between the target indicator values related to the storage sizing of the reference profile and the compact profile is generated with the clearing algorithm. A good agreement between those values indicates that the compact wind profile will lead to the same storage device sizing as with the reference wind profile on larger duration.
Target indicators of the generated wind speed profile.
The selected target indicators are only related to the wind features: this approach can then be considered as generic in the case of any WT system whatever its sizing.
We first consider three indicators Vmax, Vmin, and <V3> representing the maximum and minimum speed values and the average cubic wind speed value. Note that <V3> is used instead of the average wind speed value <V> because the WT power is directly proportional to the cubic wind speed value. Similarly to the previous approach, we also add the CDF as target indicator associated with the wind profile in order to take account of the wind statistic. Finally, we consider as last indicator related to “wind energy” with the variable EV which is defined as
with
where EV represents an “intermittent wind pseudo energy”. In fact, EV plays a similar role with ES in the previous approach for the storage system.
Note that the wind power being proportional to V3, Ev is not actually an energy (in Joules or kWh) but can be seen as a “pseudo energy” which is qualitatively related to wind energy.
The global error ε to be minimized with this second approach can be expressed as
where εstat is computed according to (3) and where the reference intermittent wind energy EVref is scaled according to the compact profile duration:
The inverse problem is solved with the clearing algorithm with the same control parameters as in the previous subsection. Multiple optimization runs were performed with different compaction times Δtcompact. The minimum value for this variable ensuring a global error less than 10−2 was identical to that found with the previous approach (i.e., 10 days). Figure 10 shows the characteristics of the generated wind profile obtained for Δtcompact = 10 days, from the aggregation of 130 elementary segments fulfilling all target indicators. The good agreement between the compact generated profile and the reference profile can also be observed in this figure in terms of CDF. Finally, Table 5 shows that the values of the target indicators are very close in both cases.
Generated wind speed with corresponding CDF.
Target indicators of the reference versus generated wind speed profile with Δtcompact = 10 days.
Here, εstat is computed according to (3), and the reference intermittent wind energy EVref is scaled according to the compact profile duration:
The inverse problem is solved with the clearing algorithm with the same control parameters as in the previous subsection. Multiple optimization runs were performed with different compaction times Δtcompact. The minimum value for this variable ensuring a global error less than 10−2 was identical to that found with the previous approach (i.e., 10 days). Figure 10 shows the characteristics of the generated wind profile obtained for Δtcompact = 10 days, from the aggregation of 130 elementary segments fulfilling all target indicators. The good agreement between the compact generated profile and the reference profile can also be observed in this figure in terms of CDF. Finally, Table 5 shows that the values of the target indicators are very close in both cases.
For comparison with the previous approach, we also give the sizing of the battery obtained from the simulation of the compact profile. It should be noted that contrarily to the first approach, the second one does not include phase correlations between wind and load profiles because it only considers wind speed variations to generate the compact wind speed profile. Consequently, the second approach does not ensure finding the most critical constraints on the storage device in terms of production—load phase shift. This can be a posteriori done by sequentially shifting the obtained wind profile on its 10-day time window in compliance with the deterministic load profile day to day repeated. The maximum storage energy quantity ES is computed for each phase shift and the highest (most critical) value is returned (see Figure 11). By this way, a value of 34.4 kWh is obtained for ES which is very close to that resulting from the reference profile simulation (i.e., 32.3 kWh).
Illustration of the phase shift of the wind profile (generated with the second method) on the battery sizing.
In this chapter, new methodologies for sizing electrochemical devices into renewable energy systems are presented. As case of study, a battery bank devoted to a standalone WT system has been developed and compared. A passive WT structure, minimizing the number of sensors and the electronic part, has been chosen because of its reliability and its low cost. The two first sizing methodologies take account of stochastic features of wind energy potential in a particular location with a given deterministic power demand. These approaches are based on the exploitation of wind speed distribution from a Weibull law or directly the extracted power histogram at the WT output. It has been shown that a robust sizing of the storage device can be obtained from the stochastic generation of either the wind speed profile or the extracted WT output power using a specific algorithm. In this algorithm, the battery required active energy is calculated by upper saturated integration of the battery power. Two supplementary approaches have been developed for compacting wind speed profiles. These approaches consist in generating compact wind profiles by aggregating elementary-parameterized segments in order to fulfill target indicators representing the features of a reference wind profile of larger duration. The inverse problem involving the determination of the segment parameters is solved with an evolutionary algorithm. It is shown that both latter approaches are able to represent the main features of the reference profile in terms of wind farm potential and are also relevant for evaluating the critical conditions imposed to the battery storage (i.e., power and energy needs) in a hybrid WT system. All sizing methods have yielded roughly to same battery size but with different wind profiles durations. Statistical methods have provided a gain of 2.5 in time window reduction, while compact synthesis methods have led to a gain of 20. From these compacts profiles, subsequent reduction of the computation time should be obtained in the context of the optimization process of such systems. Note that this synthesis approach is very generic and could be extrapolated beyond the particular field of WT design and may be applied in the whole range of electrical engineering applications, by processing any types of environmental variables (wind speed but also temperature, sun irradiation, etc.).
This work was supported by the Tunisian Ministry of Higher Education, Research and Technology.
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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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