\\n\\n
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.
\\n\\n\\n\\n
\\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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Optical Properties of Dental Composite Resin",slug:"effects-of-filler-content-on-mechanical-and-optical-properties-of-dental-composite-resin",signatures:"Seyed Mostafa Mousavinasab",authors:[{id:"27931",title:"Prof.",name:"Seyed Mostafa",middleName:null,surname:"Mousavinasab",fullName:"Seyed Mostafa Mousavinasab",slug:"seyed-mostafa-mousavinasab"}]},{id:"16718",title:"Tuneable Composites Containing Magnetic Microwires",slug:"tuneable-composites-containing-magnetic-microwires",signatures:"Larissa Panina, Mihail Ipatov, Julian Gonzalez, Valentina Zhukova and Arcady Zhukov",authors:[{id:"43039",title:"Dr.",name:"Arcady",middleName:null,surname:"Zhukov",fullName:"Arcady Zhukov",slug:"arcady-zhukov"},{id:"44060",title:"Prof.",name:"Larissa",middleName:null,surname:"Panina",fullName:"Larissa Panina",slug:"larissa-panina"},{id:"44061",title:"Dr.",name:"Mihail",middleName:null,surname:"Ipatov",fullName:"Mihail Ipatov",slug:"mihail-ipatov"},{id:"44062",title:"Prof.",name:"Julian",middleName:null,surname:"Gonzalez",fullName:"Julian Gonzalez",slug:"julian-gonzalez"},{id:"44063",title:"Dr.",name:"Valentina",middleName:null,surname:"Zhukova",fullName:"Valentina Zhukova",slug:"valentina-zhukova"}]},{id:"16719",title:"3D Network SiC-metals Composites for Heavy Duty Brake Applications",slug:"3d-network-sic-metals-composites-for-heavy-duty-brake-applications",signatures:"Hongqiang Ru, Jingyang Li and Wei Wang",authors:[{id:"40171",title:"Prof.",name:"Hongqiang",middleName:null,surname:"Ru",fullName:"Hongqiang Ru",slug:"hongqiang-ru"},{id:"43627",title:"Dr.",name:"Jingyang",middleName:null,surname:"Li",fullName:"Jingyang Li",slug:"jingyang-li"},{id:"83538",title:"Dr.",name:"Wei",middleName:null,surname:"Wang",fullName:"Wei Wang",slug:"wei-wang"}]},{id:"16720",title:"Smart Magnetic Composites (SMC)",slug:"smart-magnetic-composites-smc-",signatures:"Jerzy Kaleta, Daniel Lewandowski, Rafał Mech and Piotr Zając",authors:[{id:"19069",title:"Prof.",name:"Jerzy",middleName:null,surname:"Kaleta",fullName:"Jerzy Kaleta",slug:"jerzy-kaleta"},{id:"45935",title:"Dr.",name:"Daniel",middleName:null,surname:"Lewandowski",fullName:"Daniel Lewandowski",slug:"daniel-lewandowski"},{id:"45936",title:"Mr.",name:"Rafał",middleName:null,surname:"Mech",fullName:"Rafał Mech",slug:"rafal-mech"},{id:"45938",title:"Mr.",name:"Piotr",middleName:null,surname:"Zając",fullName:"Piotr Zając",slug:"piotr-zajac"}]},{id:"16721",title:"Magnetic and Dynamic Mechanical Properties of Nd-Fe-B Composite Materials with Polymer Matrix",slug:"magnetic-and-dynamic-mechanical-properties-of-nd-fe-b-composite-materials-with-polymer-matrix",signatures:"Jasna Stajic-Trosic, Mirko Stijepovic, Jasmina Stevanovic, Radoslav Aleksic and Aleksandar Grujic",authors:[{id:"31975",title:"Dr.",name:"Aleksandar",middleName:null,surname:"Grujic",fullName:"Aleksandar Grujic",slug:"aleksandar-grujic"},{id:"43859",title:"Dr.",name:"Jasna",middleName:null,surname:"Stajic-Trosic",fullName:"Jasna Stajic-Trosic",slug:"jasna-stajic-trosic"},{id:"43860",title:"Dr.",name:"Mirko",middleName:null,surname:"Stijepovic",fullName:"Mirko Stijepovic",slug:"mirko-stijepovic"},{id:"43861",title:"Dr.",name:"Jasmina",middleName:null,surname:"Stevanovic",fullName:"Jasmina Stevanovic",slug:"jasmina-stevanovic"},{id:"83749",title:"Prof.",name:"Radoslav",middleName:null,surname:"Aleksic",fullName:"Radoslav Aleksic",slug:"radoslav-aleksic"}]},{id:"16722",title:"Composite Materials for Some Radiophysics Applications",slug:"composite-materials-for-some-radiophysics-applications",signatures:"Sergey Bibikov and Mikhail Prokof'Ev",authors:[{id:"30318",title:"Dr.",name:"Sergey",middleName:null,surname:"Bibikov",fullName:"Sergey Bibikov",slug:"sergey-bibikov"},{id:"92431",title:"Dr.",name:"Mikhail",middleName:null,surname:"Prokof'ev",fullName:"Mikhail Prokof'ev",slug:"mikhail-prokof'ev"}]},{id:"16723",title:"The Composite Materials for Localization of Volatile Radioactive Iodine Forms from Steam-Air Phase during Severe Accidents at NPPs",slug:"the-composite-materials-for-localization-of-volatile-radioactive-iodine-forms-from-steam-air-phase-d",signatures:"Sergey Kulyukhin, Lubov Mizina, Igor Rumer and Nikolai Mikheev",authors:[{id:"30586",title:"Prof.",name:"Sergey",middleName:null,surname:"Kulyukhin",fullName:"Sergey Kulyukhin",slug:"sergey-kulyukhin"},{id:"39221",title:"Mrs.",name:"Lubov",middleName:null,surname:"Mizina",fullName:"Lubov Mizina",slug:"lubov-mizina"},{id:"39229",title:"Mr.",name:"Igor",middleName:null,surname:"Rumer",fullName:"Igor Rumer",slug:"igor-rumer"},{id:"39230",title:"Prof.",name:"Nikolai",middleName:null,surname:"Mikheev",fullName:"Nikolai Mikheev",slug:"nikolai-mikheev"}]},{id:"16724",title:"Composite Materials under Extreme Radiation and Temperature Environments of the Next Generation Nuclear Reactors",slug:"composite-materials-under-extreme-radiation-and-temperature-environments-of-the-next-generation-nucl",signatures:"Nikolaos Simos",authors:[{id:"43298",title:"Dr.",name:"Nikolaos",middleName:null,surname:"Simos",fullName:"Nikolaos Simos",slug:"nikolaos-simos"}]},{id:"16725",title:"Graphite-Composites Alternatives for Electrochemical Biosensor",slug:"graphite-composites-alternatives-for-electrochemical-biosensor",signatures:"Eliana Alhadeff and Ninoska Bojorge",authors:[{id:"29947",title:"Prof.",name:"Ninoska",middleName:null,surname:"Bojorge",fullName:"Ninoska Bojorge",slug:"ninoska-bojorge"},{id:"104432",title:"Prof.",name:"Eliana",middleName:null,surname:"Alhadeff",fullName:"Eliana Alhadeff",slug:"eliana-alhadeff"}]},{id:"16726",title:"Composite Cathode Material for Li-Ion Batteries Based on LiFePO4 System.",slug:"composite-cathode-material-for-li-ion-batteries-based-on-lifepo4-system-",signatures:"Janina Molenda and Marcin Molenda",authors:[{id:"44051",title:"Prof.",name:"Janina",middleName:null,surname:"Molenda",fullName:"Janina Molenda",slug:"janina-molenda"},{id:"44072",title:"Dr.",name:"Marcin",middleName:null,surname:"Molenda",fullName:"Marcin Molenda",slug:"marcin-molenda"}]},{id:"16727",title:"Multilayer Fresnel Zone Plate with High-Diffraction Efficiency: Application of Composite Layer to X-Ray Optics",slug:"multilayer-fresnel-zone-plate-with-high-diffraction-efficiency-application-of-composite-layer-to-x-r",signatures:"Shigeharu Tamura",authors:[{id:"33763",title:"Dr",name:"Shigeharu",middleName:null,surname:"Tamura",fullName:"Shigeharu Tamura",slug:"shigeharu-tamura"}]},{id:"16728",title:"New Composite Materials for Decreasing of Radioactive Molecular Iodine in the Water Coolant in Working and New Developed NPPs",slug:"new-composite-materials-for-decreasing-of-radioactive-molecular-iodine-in-the-water-coolant-in-worki",signatures:"Lubov Mizina and Sergey Kulyukhin",authors:[{id:"30586",title:"Prof.",name:"Sergey",middleName:null,surname:"Kulyukhin",fullName:"Sergey Kulyukhin",slug:"sergey-kulyukhin"},{id:"39221",title:"Mrs.",name:"Lubov",middleName:null,surname:"Mizina",fullName:"Lubov Mizina",slug:"lubov-mizina"}]},{id:"16729",title:"The Glass Transition Temperature in Dental Composites",slug:"the-glass-transition-temperature-in-dental-composites",signatures:"J.C.S. Moraes, M.M.D.S. Sostena and Carlos Roberto Grandini",authors:[{id:"42590",title:"Dr.",name:"J.C.S.",middleName:null,surname:"Moraes",fullName:"J.C.S. Moraes",slug:"j.c.s.-moraes"},{id:"42878",title:"Dr.",name:"M.M.D.S.",middleName:null,surname:"Sostena",fullName:"M.M.D.S. Sostena",slug:"m.m.d.s.-sostena"},{id:"42880",title:"Prof.",name:"Carlos Roberto",middleName:null,surname:"Grandini",fullName:"Carlos Roberto Grandini",slug:"carlos-roberto-grandini"}]}]}]},onlineFirst:{chapter:{type:"chapter",id:"66295",title:"Fat Embolism: What We Have Learned from Animal Models",doi:"10.5772/intechopen.85178",slug:"fat-embolism-what-we-have-learned-from-animal-models",body:'\n
Fat embolism was described many years ago. As early as 1862 [1] as cited in a 1971 review by Herndon [2], there was a report of fat droplets in the lungs of a factory worker who died after a crushing injury to his chest and abdomen. The term “fat embolism” itself includes many types of conditions in which some type of fatty substance is embedded in a tissue remote from its source. The most common source is from bone marrow that escapes into the venous system after trauma and surgery, including bone marrow reaming [3], liposuction [4], fat injection [5], or necrosis, as in sickle cell disease resulting in acute chest syndrome [6]. There are also some forms that do not result from trauma or surgery [7]. What distinguishes fat embolism from other strictly physical forms is that in addition to the physical obstruction of the vasculature that can accompany the lodging in capillaries, there are also biochemical consequences in response to the ensuing lipid metabolism and also pathological processes that are triggered intracellularly after engulfing of the fat. The most common target for embolic fat is the lung, but other significant sites include the skin, the eyes, and the brain with subsequent clinical sequelae [8].
\nThe clinical consequences of fat embolism have been reviewed many times over the years, including this year [8]. The symptoms may be so minor that they can be missed [9] or appear after an interval as much as 48–96 h leading to acute respiratory distress syndrome [ARDS] with mortality ranging from 10 to 15% [8, 9]. This has been called fat embolism syndrome [FES], sometimes with accompanying CNS [10], ocular [11] or dermal pathology [12]. Treatment has been supportive: recent reviews indicate that there is no specific treatment available [8, 12]. Although a patent foramen ovale is sometimes a contributing factor in systemic consequences of fat embolism, for instance, in the eye and the brain, this is clearly not the case in most cases of FES.
\nTherefore, there have been many attempts to produce an animal model in hopes of delineating the underlying pathophysiology, so specific treatment could be obtained. Animal models have included rats [13], mice [14], rabbits [15], dogs [16], sheep [17], pigs [18], and even baboons [19]. While a majority of these studies have focused on orthopedic-related problems [20], it would help to examine a wide variety of initiating causes in order to find some common underlying pathophysiological processes. This might lead to more specific methods to treat or prevent this condition before the array of downstream mediators, such as peptides and cytokines, have been activated. The aim of this chapter is to review what has been learned from the diverse animal studies and provide one unifying concept based on the role of the renin-angiotensin system as a key player in fat embolism syndrome.
\nIn order to simulate in animals the surgical procedure used in humans that can lead to fat embolism syndrome, a number of different animals have been subjected to nailing, with or without reaming [3]. It was concluded that more experiments should be carried out in order to determine the optimal method to perform the surgical procedures. It was also made clear that other factors influence the development of systemic and pulmonary complications [3]. A comprehensive review of animal studies of intramedullary nailing concludes that events that may predispose to adverse postsurgical impact are important and that studies should take these into consideration [20].
\nA number of studies have been carried out with infusions of bone marrow extracts or non-marrow fat. An excellent review on animal studies of acute lung injury, which includes oleic acid as a possible model for fat embolism, indicates that this model does not really mimic the clinical syndrome of FES [21]. In addition, a study on rats showed that the intravenous injection of oleic acid, unlike neutral fat, did not result in the deposition of fat droplets [22].
\nA study on liposuction in rats performed on the lateral flank and the abdomen showed that fat was delivered to the lungs and other organs [23]. Some animal studies on fat embolism have utilized subcutaneous fat [22]. This has clinical parallels in which subcutaneous injection in humans has caused fatal fat embolism [24].
\nSince neutral fat seems to be the main culprit in fat embolism and is the major fat in bone marrow and subcutaneous tissues [25] and pulmonary emboli [26], the neutral fat triolein has been the most studied in vivo and in vitro. Although a number species have been studied, the rat has been studied the most, particularly after the groundbreaking work of L.F. Peltier [27, 28, 29]. He studied fat embolism in cats and dogs but mostly in rats. This work included description of the fat content of bone marrow and body fat, distribution of labeled triolein after i.v. injection, changes in blood and lung lipase after embolism, kinetics of the phenomena, and other studies in animals and patients. Some advantages of triolein studies in the rat are described below.
\nTriolein [glyceryl trioleate] is available as a pure liquid that can be injected i.v. directly or after emulsification. We have used conscious animals since there are studies indicating that anesthesia alters pulmonary response to fat embolism [30]. Although oleic acid is a well-known pulmonary toxicant, as mentioned above, it is not a suitable model for fat embolism syndrome. The conversion of triolein to oleic acid by pulmonary tissue [31] provides support for the proposed sequence of events postulated by Szabo [32].
\nInitial histopathological studies on the time course of triolein-induced lung injury revealed changes as early as 12–24 h which included thickening of the arterial and arteriolar media, mostly with myofibroblasts and inflammation in the septa with increased numbers of macrophages. Bronchial alveolar lavage (BAL) at 24 h revealed macrophages, some of which showed inflammatory response and fat droplets. Inflammation was still present at 11 days with damage to the bronchial epithelium [33].
\nLater studies at 3 and 6 weeks showed that after the first peak [48–72 h] and partial resolution, there were persistent and progressive inflammatory and fibrotic changes up to 6 weeks after injection of triolein [34]. This was associated with an increase in angiotensin peptides [34], implicating the renin-angiotensin system (RAS) in the pathophysiology (see below).
\nIn order to determine if the lungs of the animals at this late time would be especially sensitive to another pulmonary insult, the animals were exposed to the known pulmonary toxicant lipopolysaccharide (LPS) at 6 weeks. Forty-eight hours after this “second hit,” there was an enhanced histopathological response in animals previously exposed to triolein [35].
\nThese animals had apparently recovered completely at 6 weeks from the initial triolein treatment as judged by normal weight gain and no observable behavioral changes. It was concluded that the compromised lungs seen at 6 weeks exposed the vulnerability of animals long after they had seemingly recovered. The histopathology was also found at 10 weeks along with the persistence of some small fat droplets extracellularly and also in some macrophages [36] [see below].
\nBecause the renin-angiotensin system (RAS) has been implicated in a wide variety of other pulmonary experimental models [37, 38], we examined whether this might hold true for the fat embolism model, and in fact it has since been proposed that most forms of pulmonary inflammatory disease involve the RAS, but that list did not include fat embolism [39]. We found that three different agents that interfere with the RAS were found to ameliorate the pulmonary damage found at 48 h after triolein: the angiotensin-converting enzyme (ACE) inhibitor captopril [40], the angiotensin II type 1 receptor blocker losartan [40], and the renin inhibitor aliskiren [41]. In addition, it was found that the remaining inflammation that was evident at 6 weeks was also reduced when losartan was given at this late time period and the animals were sacrificed 4 weeks later (10 weeks after the initial exposure to triolein) [36]. These results suggest that angiotensin II, produced by the angiotensin-converting enzyme (ACE) and acting on the type 1 receptor, is a critical pathological actor in the pathophysiology of fat embolism both acutely and after a substantial delay. However, it does not indicate precisely where this peptide comes from or how it is formed. All of the components of the RAS have been found or implicated in the lung [42]. Possible players in its formation prior to ACE activity could be renin or prorenin that is catalytically active when bound to its receptor [43]. Furthermore, other angiotensin peptides with anti-inflammatory and antifibrotic activity could be counterbalancing forces as well. Most of the extrarenal renin is in the form of prorenin which also has angiotensin-independent pro-fibrotic properties [44, 45, 46].
\nThere are many possible cells that could provide components of the RAS to the pulmonary inflammatory process. These include mast cells [47], fibroblasts [48], myofibroblasts [49], vascular smooth muscle [50], and macrophages [51].
\nThere are a number of studies suggesting a critical role of mast cells in RAS mediation of pulmonary pathology [52, 53, 54]. It has been suggested that activated macrophages stimulate pulmonary mast cells to release renin and the subsequent production of angiotensin peptides leads to adverse reactions [54]. Mast cells have also been shown to stimulate fibroblasts in the lung [55]. Triolein increases mast cell accumulation in a chronic model, and their appearance is reduced by losartan [56], and aliskiren reduces the triolein-induced increase of mast cell number found at 48 hours [57]. Another mast cell enzyme that has been implicated in angiotensin formation is chymase [58, 59]. It is known that there is mast cell heterogeneity in rodents and humans [60, 61, 62], and in humans this includes the presence of renin and its localization within the lungs [62].
\nIn support of the importance of renin/prorenin in fat embolism, we have found an increase in renin staining at 48 hours (Figure 1) and 6 weeks after triolein-induced fat embolism [63, 64].
\nTriolein increases lung renin staining: enhanced by captopril and losartan [64].
It has long been speculated that angiotensin II, acting through the type 1 receptor, was a primary inflammatory molecule [65]. In recent years it has become apparent that angiotensin II acting through its type 2 receptor has anti-inflammatory actions [66] and the literature on similar anti-inflammatory actions through the Ang 1-7/Mas receptor have exploded [67]. It appears that the pathophysiological state of the lungs is a balance between the pro-inflammatory, pro-fibrotic arm of the RAS, and the counterbalancing peptide/receptor activity. It is not surprising that Ang 1-7 has been found to have beneficial effects in the lung [68, 69].
\nHow is the renin-angiotensin system activated in fat embolism, and what is the connection to fat (neutral and fatty acids)? One suggestion based on the work of Gonzalez et al. [52, 54, 70] would have a sequence of fat engulfment by macrophages, and subsequently the activated cells would release monocyte chemoattractant-1 (MCP-1) that stimulates mast cells (nearby or remote) to release renin and angiotensin generation. However, activated macrophages themselves might act in an autocrine or paracrine manner to release renin, and there is evidence for intracrine generation of angiotensin as well [71, 72]. There may be intracrine actions of angiotensin as well on mitochondria and nuclei.
\nIf the RAS is involved in many aspects, including initiating a cascade of downstream malevolent molecules, where does the fat enter the picture? As a host of review articles have discussed, there is a strictly mechanical phase during which the fat emboli obstruct capillaries and cause a short-term hypoxia. It is known that hypoxia itself can lead to pulmonary dysfunction and this can be offset experimentally by angiotensin-converting enzyme inhibition (ACEI) [73] and is associated with an increase in circulating angiotensin peptides [74].
\nIt is clear from the vast literature on metabolism of fat after embolism that most of the lipolysis of neutral fat (mostly triolein) takes place near pulmonary endothelial cells that convert triolein to the toxic oleic acid by lipoprotein lipase. It is now known that oleic acid, although not thought to enter cells [21], can activate its own fatty acid receptor (FFAR/GPR120) which can evoke pulmonary edema [75, 76]. Interestingly, the toxic effects of oleic acid (including pulmonary edema) are antagonized by the non-specific angiotensin receptor blocker 1-sarcosine, 8-isoleucine angiotensin II [77]. This implicates angiotensin II in another way as a key mediatory in pulmonary pathology. It has also been reported that oleic acid and angiotensin II are synergistic in promoting a mitogenic effect in vascular smooth muscle [78]. Oleic acid emanating from triolein thus is a co-conspirator in evoking pulmonary (and probably other) pathological conditions, such as cerebral fat embolism [10, 79]. Pathways that oleic acid and angiotensin utilize in producing pathological responses are listed in Figure 2.
\nFat embolism pathways.
To explain how the sudden appearance of fat in the pulmonary circulation can sometimes produce an acute respiratory distress syndrome and why the neutral fat (primarily triolein) has the potential to lead to longer-term pulmonary damage, the following hypothesis is presented (Figure 3). The initial mechanical phase of vascular obstruction which leads to hypoxia is known to be ameliorated by the angiotensin receptor blocker losartan [80].
\nOleic acid-angiotensin cycle: OA ↑ Ang release; Ang ↑ triolein lipolysis.
The delayed metabolic phase is related to breakdown of the most abundant fat in emboli which is hydrolyzed by several triglyceride lipases to yield oleic acid. These include endothelial lipase (EL) and lipoprotein lipase (LIPL) [81, 82] as well as macrophage LIPL [83]. This in turn leads to the evolution of free fatty acids, mainly oleic acid, which is toxic to the endothelium and is released in part in close proximity to endothelial cells. Macrophages become activated after phagocytosing lipid particles which leads to paracrine and endocrine activation of mast cells that induces angiotensin generation [54].
\nIn addition, there is generation of angiotensin and oleic acid intracellularly in macrophages (both of which are toxic to mitochondria [84, 85]). Since oleic acid has been shown to increase angiotensin II release from several cell types [86] and angiotensin increases the expression of various lipases [87], the cycle continues until rescue mechanisms ensue (Figure 4). It should be noted that losartan and perindopril, ACE inhibitors, prevent fatty acid-induced endothelial dysfunction in humans in response to elevated blood lipids [88]. Furthermore, oleic acid also increases serum renin and angiotensin, and its effects on pulmonary edema are blocked by blocked by an ACE inhibitor [89].
\nRepair mechanisms for fat embolism.
Most cases of fat embolism do not lead to fat embolism syndrome because the amount of the fat is not of sufficient volume or due to the countervailing mechanisms. These include actions of angiotensin II on AT2 receptors, metabolism of angiotensin II by angiotensinases, anti-inflammatory actions of its metabolite, angiotensin (1-7), metabolism of oleic acid, clearance of lipids via vascular or lymphatic channels, and ultimately renal excretion (Figure 4).
\nIt is proposed that elements of the renin-angiotensin system are central mediators of tissue injury after fat embolism. Although hypoxia due to capillary blockage is a contributing factor to lung injury, oleic acid liberated from triolein hydrolysis is a crucial step, and it also is associated with angiotensin biology. Angiotensin II through its type 1 receptor is the major offender. Our animal experiments have indicated that three US Food and Drug Administration (FDA)-approved drugs (captopril, losartan, and aliskiren) may have protective value as mentioned above. However, in a clinical setting where trauma or surgery may be involved, stability of blood pressure may be compromised by these agents. Therefore, it is suggested that some of these types of agents (or a combination) could be administered by inhalation.
\nRather than antagonizing the angiotensin II generation with ACE or renin inhibitors or angiotensin type 1 activity with antagonists (ARBS), it may be possible to treat/prevent fat embolism injury by stimulating the angiotensin type 2 receptor (AT2) with peptide or non-peptide agonists such as C21 [90]. Another possible therapeutic approach would be to activate the ACE2/angiotensin [1-7]/MAS axis with a peptide or non-peptide agonist, such as AVE0091 [68]. A more promising avenue for preventing or treating fat embolism will more likely be satisfactory if multiple points of the early stages of the pathophysiology are attacked simultaneously. That would include not only the RAS drugs mentioned above but also possibly mast stabilizers that can be given by the inhalation route and some of the newly described drugs that act on the FFA receptors mentioned above. In addition it is possible that some of the newer triglyceride lipase inhibitors could be of value as preventive treatment.
\nAlthough the emphasis in this review is on pulmonary fat embolism, there is ample evidence from clinical experience and animal experiments that the eyes, particularly the retina, are frequently targets of fat embolism. Both triolein and oleic acid have been implicated in ocular pathology [91, 92], and the RAS is thought to be an important mediating system in many ocular diseases [93].
\nAnother non-pulmonary target of fat embolism in clinical FES is the brain, and cerebral fat embolism can be fatal [94]. Although a patent foramen ovale is sometimes an important factor in cerebral fat embolism, this is clearly not the case in many instances, and animal models have not provided any new insights of cardiac defects being major players. In a rat model, there is some evidence that cerebral fat embolism may involve a serine protease [79] and maybe this could be related to a non-renin generation of angiotensin by a chymase-like enzyme. The RAS is now believed to be important for much CNS pathology [95].
\nThere now is reason to be optimistic that the next comprehensive review of fat embolism syndrome will describe some new available therapeutic options based on animal experiments. This reinforces the goal of animal experiments to delineate the pathophysiological mechanisms underlying human disease, so specific treatment can be implemented.
\nWe acknowledge the support of Dr. Gary Salzman, M.D., and the Mary Catherine Geldmacher Foundation of St. Louis, MO, the graphical help from Dr. Doud Arif, and the inspiration to begin this research from the late Dr. Federico Adler.
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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). 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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:{topicId:"8"},books:[{type:"book",id:"10454",title:"Technology in Agriculture",subtitle:null,isOpenForSubmission:!0,hash:"dcfc52d92f694b0848977a3c11c13d00",slug:null,bookSignature:"Dr. Fiaz Ahmad and Prof. Muhammad Sultan",coverURL:"https://cdn.intechopen.com/books/images_new/10454.jpg",editedByType:null,editors:[{id:"338219",title:"Dr.",name:"Fiaz",surname:"Ahmad",slug:"fiaz-ahmad",fullName:"Fiaz Ahmad"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10502",title:"Aflatoxins",subtitle:null,isOpenForSubmission:!0,hash:"34fe61c309f2405130ede7a267cf8bd5",slug:null,bookSignature:"Dr. Lukman Bola Abdulra'uf",coverURL:"https://cdn.intechopen.com/books/images_new/10502.jpg",editedByType:null,editors:[{id:"149347",title:"Dr.",name:"Lukman",surname:"Abdulra'uf",slug:"lukman-abdulra'uf",fullName:"Lukman Abdulra'uf"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10504",title:"Crystallization",subtitle:null,isOpenForSubmission:!0,hash:"3478d05926950f475f4ad2825d340963",slug:null,bookSignature:"Dr. Youssef Ben Smida and Dr. Riadh Marzouki",coverURL:"https://cdn.intechopen.com/books/images_new/10504.jpg",editedByType:null,editors:[{id:"311698",title:"Dr.",name:"Youssef",surname:"Ben Smida",slug:"youssef-ben-smida",fullName:"Youssef Ben Smida"}],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:"10572",title:"Advancements in Chromophore and Bio-Chromophore Research",subtitle:null,isOpenForSubmission:!0,hash:"4aca0af0356d8d31fa8621859a68db8f",slug:null,bookSignature:"Dr. Rampal Pandey",coverURL:"https://cdn.intechopen.com/books/images_new/10572.jpg",editedByType:null,editors:[{id:"338234",title:"Dr.",name:"Rampal",surname:"Pandey",slug:"rampal-pandey",fullName:"Rampal Pandey"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10581",title:"Alkaline Chemistry and Applications",subtitle:null,isOpenForSubmission:!0,hash:"4ed90bdab4a7211c13cd432aa079cd20",slug:null,bookSignature:"Dr. Riadh Marzouki",coverURL:"https://cdn.intechopen.com/books/images_new/10581.jpg",editedByType:null,editors:[{id:"300527",title:"Dr.",name:"Riadh",surname:"Marzouki",slug:"riadh-marzouki",fullName:"Riadh Marzouki"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"10582",title:"Chemical Vapor Deposition",subtitle:null,isOpenForSubmission:!0,hash:"f9177ff0e61198735fb86a81303259d0",slug:null,bookSignature:"Dr. Sadia Ameen, Dr. M. 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