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IntechOpen Book Series will also publish a program of research-driven Thematic Edited Volumes that focus on specific areas and allow for a more in-depth overview of a particular subject.
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\\n\\nLaunching 2021
\\n\\nArtificial Intelligence, ISSN 2633-1403
\\n\\nVeterinary Medicine and Science, ISSN 2632-0517
\\n\\nBiochemistry, ISSN 2632-0983
\\n\\nBiomedical Engineering, ISSN 2631-5343
\\n\\nInfectious Diseases, ISSN 2631-6188
\\n\\nPhysiology (Coming Soon)
\\n\\nDentistry (Coming Soon)
\\n\\nWe invite you to explore our IntechOpen Book Series, find the right publishing program for you and reach your desired audience in record time.
\\n\\nNote: Edited in October 2021
\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/132"}},components:[{type:"htmlEditorComponent",content:'With the desire to make book publishing more relevant for the digital age and offer innovative Open Access publishing options, we are thrilled to announce the launch of our new publishing format: IntechOpen Book Series.
\n\nDesigned to cover fast-moving research fields in rapidly expanding areas, our Book Series feature a Topic structure allowing us to present the most relevant sub-disciplines. Book Series are headed by Series Editors, and a team of Topic Editors supported by international Editorial Board members. Topics are always open for submissions, with an Annual Volume published each calendar year.
\n\nAfter a robust peer-review process, accepted works are published quickly, thanks to Online First, ensuring research is made available to the scientific community without delay.
\n\nOur innovative Book Series format brings you:
\n\nIntechOpen Book Series will also publish a program of research-driven Thematic Edited Volumes that focus on specific areas and allow for a more in-depth overview of a particular subject.
\n\nIntechOpen Book Series will be launching regularly to offer our authors and editors exciting opportunities to publish their research Open Access. We will begin by relaunching some of our existing Book Series in this innovative book format, and will expand in 2022 into rapidly growing research fields that are driving and advancing society.
\n\nLaunching 2021
\n\nArtificial Intelligence, ISSN 2633-1403
\n\nVeterinary Medicine and Science, ISSN 2632-0517
\n\nBiochemistry, ISSN 2632-0983
\n\nBiomedical Engineering, ISSN 2631-5343
\n\nInfectious Diseases, ISSN 2631-6188
\n\nPhysiology (Coming Soon)
\n\nDentistry (Coming Soon)
\n\nWe invite you to explore our IntechOpen Book Series, find the right publishing program for you and reach your desired audience in record time.
\n\nNote: Edited in October 2021
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A Multidimensional Approach",slug:"child-abuse-and-neglect-a-multidimensional-approach",publishedDate:"July 11th 2012",bookSignature:"Alexander Muela",coverURL:"https://cdn.intechopen.com/books/images_new/2663.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"138437",title:"Dr.",name:"Alexander",middleName:null,surname:"Muela Aparicio",slug:"alexander-muela-aparicio",fullName:"Alexander Muela Aparicio"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},ofsBook:{item:{type:"book",id:"11493",leadTitle:null,title:"Solar Radiation - Enabling Technologies, Recent Innovations, and Advancements for Energy Transition",subtitle:null,reviewType:"peer-reviewed",abstract:"\r\n\tSolar radiation is the radiant energy that originates from the sun in the form of electromagnetic radiation at various wavelengths. Almost all renewable energy comes from the sun, either directly or indirectly. A very vast amount of solar energy (173,000 terawatts) reaches the atmosphere and surface of the earth, which is more than 10,000 times greater than the total energy use in the world. To harness and convert a tiny part of such amount of energy into various forms (e.g., electricity and heat), we need much more innovation and progress in the current technologies as well as cost-efficient and smarter approaches for energy system integration in the built environment. The energy transition is a pathway toward the transformation of the global energy sector from fossil-based to zero-carbon. To achieve this, the world needs to reduce energy-related CO2 emissions to limit climate change. The decarbonization of the energy sector requires urgent action on a global scale to reduce carbon emissions and mitigate the effects of climate change. Renewable energy and energy efficiency can potentially play a major role (up to 90%) in the required carbon reductions. The energy transition will be powered by enabling technologies such as Artificial Intelligence (AI), Internet of Things (IoT), Digital Twin (DT), 3D Printing, Autonomous technology, Robotics, Unmanned Aerial Vehicle (UAV), Big Data Analytics, Blockchain, etc. This will aim to develop promising solutions and lead the world to meet the sustainable development goals (SDGs) as well as make energy cleaner, accessible, and more efficient.
\r\n\r\n\tThis book will aim to provide detailed information about recent innovations and advancements in the relevant enabling technologies for an energy transition which will be beneficial for a broad range of readership, including undergraduate and postgraduate students, young or experienced researchers, and engineers.
\r\n\tThis book will address the various modern, technical, and practical aspects of smart technology for capturing solar radiation and converting it into different forms of energy, as well as enabling it for renewables integration in energy generation and transformation, built environment, transportation, buildings, and agriculture.
\r\n\tThe book will cover the most recent developments, innovations and applications concerning the following topics:
\r\n\t• Solar radiation – Smart and enabling technologies for measurement, modelling, and forecasting
\r\n\tHigh-resolution measurement sensor and instrument technology (Pyranometers, Albedometers, Pyrheliometers, UV Radiometers, Sun Trackers, Spectroradiometer, Pyrgeometers, etc.), Artificial intelligence techniques for modelling and forecasting of solar radiation, Solar Irradiance forecast with satellite data, Solar potential analysis, Short-term forecasting of photovoltaic power and solar irradiance prediction with sky imagers.
\r\n\t• Renewable energy integration – Smart solutions for integration of RE in distributed generation, energy storage, and demand-side management.
\r\n\tIntegrated Photovoltaics: Smart technology for vehicle-integrated PV, Building Integrated PV, Agrivoltaics, Road-Integrated PV, Floating PV, Product-integrated PV.
\r\n\tRenewable Energy Applications in Built Environment and mobility: Solar cars, solar-powered electric charging stations, passive solar systems, solar heating, and cooling systems, building-integrated vegetation, multifunctional solar systems, solar pumps, solar lighting, solar shading, Natural lighting, Solar dryer, Greenhouse.
There is increasing focus on platelet functions in people living with HIV/AIDS. This is because of the high incidence of cardiovascular events in these individuals that is 10 times higher than general population [1] independent of traditional risk factors such as age, hyperlipidemia, and ethnic/racial differences. Acquired platelet dysfunctions are often observed in association with HIV/AIDS. Of the available tests for platelet functions [2, 3], none fully captures the complexity involved in this population group.
The results of the functional assays are modified by the viral count, CD4/CD8 ratio, and immunological response and whether or not on antiretroviral treatment. The effects of combined antiretroviral therapy (cART) on platelet functions are complex. Despite achieving viral suppression, these drugs have been demonstrated to have independent effects on platelet functions.
Complete blood count and microscopic examination of formed elements are often the first investigations in suspected hemostatic disorders in clinical situations. Platelet count and morphological changes have impact on bleeding or thrombosis.
Globally, the prevalence of HIV-associated thrombocytopenia is 4–40% [4] though there are geographical, racial as well as ethnic differences from the same locality [5] and stage of disease. Indeed, thrombocytopenia has been considered as a marker of disease progression and improvement [6]. Whereas platelet counts improve with initiation of combined antiretroviral therapy (cART) viral suppression [7], beneficial effect does not apply to zidovudin (AZT) [8].
Despite thrombocytopenia, very low rates of clinical hemorrhage have been reported, estimated at only 3.2% among HIV thrombocytopenic patients [9] even with platelet count as low as 50 × 109/L [10] casting doubt on the clinical relevance of the laboratory results. As a result of lack of clear correlation between HIV-associated thrombocytopenia and clinical significance, some authors have questioned benefit of treatments purely directed toward improvement of platelet count [11].
The prevalence of HIV-associated thrombocytosis, defined as platelet count of more than 400× 109/L [12], is low but depends on the population studied and concurrent medications. Reported prevalence of thrombocytosis in pediatric group who were also HIV-positive cART naive was found at 6% [13], though could be higher at 14% (more than thrombocytopenia at 7% in same cohort) for children on co-trimoxazole prophylaxis [14]. Whether these findings were independent or dependent on co-administered drugs remains undetermined.
Thrombocytosis is an emerging toxic complication accounting for 9% on stable cART depending on the regimen [7] up from 5.8% in treatment-naïve individuals [7]. It remains undetermined the relationship between HIV-associated thrombocytosis and accelerated thrombosis.
Despite the thrombocytopenia being associated with HIV, peripheral blood film smears of platelets are either unremarkable or hypogranular, which are of different sizes appearing as fragments [15].
Ultrastructure of platelets from HIV individuals, apart from showing normal features of hyperactivated aggregates having membrane pseudopodia/filopodia formation, in addition have shriveled aggregates with irregular and torn membrane surfaces, membrane blebbing and shedding of vesicles [16, 17]. The most distinctive features are alteration of granular structure though data are limited.
Most studies on platelet aggregation in HIV have used single or fewer than the recommended panel of agonists with conflicting results [18]. Application of escalating agonist concentrations has uncovered dose-response patterns [19]. In this study, while epinephrine demonstrated greater potency indicating hyperresponsiveness, responses with collagen, TRAP, and ADP showed lesser maximum aggregation indicating lesser efficacy and hyporesponsiveness. The agonist dose-response curve is, however, modified by cART viral suppression, especially abacavir-containing regimens [20] depending on agonist [21]. It must be remembered that although cART is a commonly mentioned modifier, the effects of fever associated with HIV are neither reported nor analyzed in these studies. Hyperthermic conditions such as fever are associated with reduced platelet aggregation [22].
A study comparing whole blood platelet aggregation using MEA found hyporeactivity in both HIV-treated and untreated individuals [23], similar to findings by impedance aggregometry [24]. It is worth noting that co-infection with HBV (6 vs. 4%) and HCV (0 vs. 2%) and low CRP levels [23] could have obscured the overall response. Co-infection with other viruses modulates platelet responses in HIV [25].
Few studies have been performed using thromboelastography (TEG) in HIV individuals. Of the few studies done, MA amplitude was low despite higher normal fibrinogen levels in both cART-treated [21] and untreated HIV subjects [23]. These study results of hypocoagulability are not in keeping with other tests, probably reflecting lack of sensitivity of TEG as a platelet function assay.
Activated platelets are characterized by surface expression of activation-specific molecules such as P-selectin or CD62P, active GPIIbIIIa (PAC-1), phosphatidyleserine (PS) externalization; platelet-leukocyte aggregates (PLA); platelet microparticle formation (PMP), in addition to granule secretion such as platelet factor 4(PF4), β-thromboglobulin, and intracellular calcium flux [26].
A number of studies have documented platelet hyperactivity in HIV characterized by increased plasma membrane surface expression of CD62P, PAC-1, PS, CD63, [27], but paradoxically decreased GPIbα [28]. The levels positively correlate with viral loads but not CD4 count [29].
Although activation markers are higher in HIV sero-positive individuals who are cART naïve compared to healthy controls [30], with cART treatment levels decrease but do not normalize to pre-treatment levels [20, 31]. The persistent levels are related to inflammatory markers in virally suppressed individuals [32].
There is evidence of altered signal transduction affecting protein synthesis, degranulation, and activation functioning in HIV platelets. Experimental data show that HIV platelets had upregulation of ABCC4 (ATP-binding cassette subfamily 4), increase in cAMP, decrease in vasodilator-stimulated phosphoprotein (VASP), which correlated with increased membrane expression of CD62P and integrin αIIbβ3 (GPIIbIIIa) [33]. It must be noted that VASP is only sensitive to PY12 inhibitors, and not much data are available from HIV patients.
People living with HIV have increased secretion of alpha granule contents such as RANTES, sP-selectin, and sCD40L [34], despite viral suppression [33]. The persistence of these chemokines, especially anomalous secretion of RANTES, despite cART treatment [28] remains unexplained to date.
HIV platelets have low basal dense granule content and diminished secretion response as evidenced by low mepacrine uptake and release [33]. Although platelet mepacrine uptake and release have been considered among dense granule assays, it is not as specific as serotonin and lummiaggregometry for ATP [35, 36]. Despite this knowledge, the measurements of platelet serotonin and ATP remain largely undescribed in people living with HIV.
Although HIV-associated platelets display increased baseline expression of surface activation markers compared to healthy controls [32], there is evidence of refractoriness to further agonist stimulation. This behavior has been referred to as “platelet exhaustion” in many publications [25, 28, 32, 37, 38].
Platelet “exhaustion” as a concept was postulated in references to previous observations, before HIV era, where activated platelets continued to circulate [39, 40] and were shown to be activated [41] but with decreased aggregation [42, 43]. They were considered refractory to further agonist stimulation [44] owing to acquired storage pool granule depletion [45, 46].
In HIV, stimulation with increased agonist concentration leads to lesser response at each corresponding dose [21]. Specifically, decreased thrombin dose-response curve for granule content and secretions for P-selectin, PFA/CXCL4,TXA and RANTES in HIV platelets less than healthy controls [32]. The decreased P-selectin and PAC-1 secretory responses correspond to impaired c-AMP, ABCC4 and VASP signal transduction mechanisms [33]. Furthermore, HIV platelets display decreased mepacrine uptake and release [33], and wheat germ agglutinin staining (WGA) [32] indicating reduction of dense and alpha granule contents respectively.
Despite many studies mentioning “platelet exhaustion” in HIV, however the results in support are neither consistent for all agonists nor confirmed by other tests. In patients who are cART naïve, stimulation with AA, ADP or collagen, the dose-response curves for CD62P are higher than the uninfected controls [30]. None of the LTA aggregation tests have been accompanied by corresponding Lummiaggregometry test which could have better characterized platelet ATP dense granule secretion [47, 48]. Platelet lumiaggregometry testing remains largely un-described in HIV. Furthermore, the studies are on people who are already infected by HIV, but platelet responses prior to HIV infection remains unknown.
From the foregoing, evidence in support for “platelet exhaustion” in HIV is suggestive but inconclusive. Although decreased dose-response to thrombin has been described, however response to epinephrine was enhanced in some studies. The maintained response to epinephrine casts doubt on granule exhaustion, since true storage pool disorder do not respond to epinephrine [49] or variable [50]. Indeed HIV platelets maintain both alpha and dense granule secretions to collagen and ADP agonists stimulation [51]. Perhaps a better term to use could be “anergy,” refractory or “tired” platelets.
HIV platelets have enhanced adherence to fibrinogen-coated surfaces [32, 33]. However, testing by this method is technically difficult and not available in clinical situations.
Although platelet PFA-100/200 testing is always recorded as aggregation in most studies, in actual fact it is marker of adhesion [2, 52]. The few tests of PFA-100 in HIV compared those on cART treatment with untreated [31], or in addition to [53] all of which showed shorter closure time in treatment-naïve individuals. The short closure times were neither normalized with aspirin nor with cART. The results are strongly indicative of influence of vWF as a third dimension in platelet function testing [54, 55].
People living with HIV (PLWHIV) despite having very low platelet counts do not have issues of bleeding [56, 57, 58]. Instead, HIV-associated thrombotic complications [59] are an emerging issue of concern [60]. Although congenital thrombotic thrombocytopenic purpura (TTP) is very rare, acquired TTP is on the increase and associated with HIV estimated to be 15–40 times than the HIV negative in the general population [61]. It has been reported that HIV is responsible for 80% of TTP cases [62].
TTP is characterized by reduced or absent ADAMTS-13 and elevated vWF antigen as well as activity [63] especially the Unusually Ultralarge vWF multimers [64]. Elevated vWF Ag and high-molecular-weight vWF multimers [65] with reduced ADAMTS-13 have been detected in acute and chronic HIV [66, 67] and those with confirmed thrombosis [68]. Unusually, ultralarge vWF multimers that have increased adhesion to platelet GPIbα-V-IX receptors [69] compensates for hemostasis in the presence of the low platelet count in HIV.
It has been demonstrated that blood from HIV individuals have abundant circulating platelet microparticles [70], and this is despite viral suppression [71, 72]. The levels were associated with increased cellular ROS, caspases, eNOS [72], and mitochondrial membrane depolarization [73] indicative of apoptosis [74] . Further, co-existence of platelet microparticles with increased LPS and platelet P-selectin and TF [29] are strong indicators that they are products of platelet activation.
Recently, in mice, HIV particles were shown to be endocytosed by platelets by binding to TLR-7&9 leading to increased secretion of alpha (PFA-4) and dense granules (serotonin), and membrane expression of P-selectin [75]. Additionally, HIV interacts directly with platelets CLEC-2 and DC-SIGN receptors [76]
HIV preferentially infects CD4-T lymphocytes present in the gut leading to reduction in number and function [79]. The consequence is loss of gut epithelial immune protection and disruption of gut epithelial barrier allowing luminal indigenous intestinal bacteria to translocate out of the mucosa and into circulation [80]. Once in circulation, bacterial products such as lipopolysaccharides (LPS) interact with platelet toll-like receptors 4 (TLR4) [81]. The microbial products induce signal transduction mechanisms that eventually lead to facilitating platelet membrane receptor expression [82, 83]. The phenomenon of gut microbial translocation has been used to explain enhanced platelet reactivity despite therapy with antiplatelets such as ticagrelor in myocardial infarction [84]. However, some studies have disputed the role of LPS in platelet activation instead of reporting attenuation of receptor expression and aggregation in the presence of agonists [85] contradicting earlier findings. The paradoxical result may be due to the absence or presence of other factors such as soluble CD14 that prime TLR4 sensing of LPS [86], extent of TLR expression [87] or the different LPS isoforms [88], and experimental conditions [89] as well as clinical condition [89].
HIV infection is associated with elaboration of cytokines from inflammatory cells, and these have been shown to induce platelet activation [90, 91] The platelet activation is not limited to interleukins only, since tumor necrosis factor in blood leads to dose- and time-dependent increase in platelet expression of GPIIbIIIa, PS, and mitochondrial dysfunction [92]. The role of TNF-α in platelet activation and apoptosis are well supported by empirical evidence [93].
Platelets express FcRIIA (CD32a) or simply FcR receptor that recognizes the constant region of IgG in immune complexes [94]. The consequence of platelet-immune complex binding leads to platelet activation [95], aggregation and release of contents from alpha and dense granules [94], and microparticle formation [96]. The platelet activation from immune complexes is dependent on membrane GP IIbIIIa [97]. However, the immune complex-induced platelet aggregation is dependent on dose and charge [98].
Cross-reactive antibodies between HIV epitopes and platelet receptors have been described [99, 100].
When neutrophils encounter viruses such as HIV, they respond by releasing reactive oxygen species and net-like structures called neutrophil extracellular traps [101, 102]. The NETs, composed of DNA, histones, myeloperoxidase, citrinulated histones, and elastases, are the potent inducers of platelet aggregation and activation [103, 104, 105].
There is often cross-talk between platelets and leukocytes associated with bidirectional priming and activation of each other [106, 107]. These two cells interact through platelets such as P-selecti-PSGL-1, GPIb-vWF-CD18, integrin IIaIIIb-fibrinogen-MAC-1 neutrophil linkages that lead to the formation of platelet-leukocyte aggregates (PLA) [108] linked by P-selectin-PSGL. These PLA conjugates have been found in HIV patients involving T-cells associated with CD42b and CD62P [109]. Elevated PLA together with other immune markers is positively correlated with increased platelet CD36, CD62P, and platelet aggregation but inversely with CD4 count [110].
There is evidence of endothelial damage [111] and increased vWF levels in HIV patients [66, 67, 68, 112, 113]. Apart from the high vWF Ag levels, of significant is the persistently high functionally active Ultralarge vWF multimers (ULvWFM) in HIV individuals [65] that causes adhesion even at low platelet counts [114]. Correspondingly, as HIV disease progresses, platelet expression of the integrin GPIbα decreases paradoxically unlike the other surface receptors indicating consumption [28].
There are similarities in markers of platelet activation and apoptosis [115]. In both processes, there is phosphatidyleserine (PS) exposure on the membrane [116] and microparticles [117]. However, specific features of platelet apoptosis include mitochondrial membrane leakage characterized by changes in membrane depolarization (Δψm) and increase in cytosolic caspases 3&8, [118, 119]. Indeed, features of platelet apoptosis and activation have been demonstrated in HIV patients [25, 32, 38]. It should be noted that the few studies demonstrating occurrence of full spectra of apoptosis in HIV individuals were confounded by cART viral suppression [32] and dengue co-infection [25] and therefore, whether results were specific to HIV in itself largely remains undetermined.
Some of the consequences of platelet apoptosis include thrombocytopenia [120, 121]. This is because, apart from the fact that apoptotic platelet eventually disintegrates [74], the surface exposure of PS acts as “eat me” signal for engulfment by the macrophages thus removing the altered cells from circulation shortening survival [122, 123, 124].
Despite the success attained by cART in viral suppression and recovery of platelet counts [125, 126], their effects on platelet function remain variable. In general, platelet surface markers such as CD62P, PAC-1 and CD40L, soluble sCD62P, sCD40L as well as platelet-secreted chemokines such as RANTES persist despite cART viral suppression [27] with some variations between the individual drugs and study designs.
Platelet signal transduction and secretory effects are enhanced by HIV, but these effects are accentuated by cART. This was demonstrated by Pastori et al.’s [78] study in which levels of sCD40L, platelet sNOX-dp, and 8-iso-PGF2-α were elevated, the effects of PIs greater than NNRTI. The mechanism appears to be induction of oxidative stress, ROS, and arachidonic pathways that synergistically augment AA platelet activation. cART causes mitochondrial toxicities [127]
Abacavir is unique among cART [51] since it is a guanosine analogue and induces platelet activation
Despite other studies reporting levels of platelets MP remaining unchanged [29] or increased [71] after initiating antiretrovirals, one study found MP TF levels decreased with cART treatment [133]. The difference could be attributed to monocyte phenotypes [134] and level of activation and attendant TF expression with cART [135]. This is because platelets undergo decryption [136] and transfer TF to monocytes using microparticles as vehicles [137, 138].
The effects of cART on platelets are complicated by other factors such as TNF-α, a known platelet activator and apoptosis inducer. Although TNF levels are often elevated in HIV infection, levels persist despite cART [139] even if used over 24-month period [34]. Whereas cART treatment decreases circulating bacterial LPS levels in HIV patients, platelet reactivity is increased instead [23] suggesting intrinsic effects of the drugs independent of bacterial translocation.
People living with HIV/AIDS are at increased risk of cardiovascular events [140, 141], especially coronary heart disease [142, 143] and ischemic stroke [144, 145], than the general population. The increased risk is due to HIV infection alone and accentuated by cART [146, 147].
Although there is evidence of enhanced platelet activation in association with HIV [27], studies of antiplatelet therapy in these patients have yielded inconsistent results, perhaps owing to drug interactions [148]. It should be noted that the studies so far done were on patients concurrently taking cART.
In a study of HIV-1 infected patients who had been on 6-month cART, it was found that 325 mg of oral aspirin-attenuated platelet aggregation to agonists, activation markers [37]. In the same study, although levels of urinary thromboxane were decreased in both HIV-positive cART untreated and treated, it was least responsive to aspirin. Furthermore, despite aspirin administration, suppression of platelet hyperactivity did not decline to baseline levels indicating the contributory effects of cART. Apart from the small sample size and short duration of therapy, other limitations of this pilot study are that it evaluated only one antiplatelet drug, and it did not perform subgroup analysis among the different cART drugs (NNRTI, PI, Raltegravir, and abacavir) as well as the racial and ethnic differences.
Although aspirin and R406 (thromboxane analogue) but not ticagrelor inhibits platelet engulfment, they do not inhibit CD62P expression or PMA complex formation [149]. Other studies have confirmed the suboptimal effects of aspirin on platelets agonist (collagen and epinephrine)-induced aggregation, surface expression of CD62P, CD40L, and PAC-1 from individuals with HIV taking ABC [53]. This study identified subjects taking abacavir-containing cART as poor responders. While cART is currently standard of care in the treatment of HIV, there are no data on effects of antiplatelets in PLWH before adoption of practice.
Clopidogrel reduces thrombogenicity and platelet hyperreactivity better than aspirin in PLWH on cART [21]. The question whether dual antiplatelet therapy compared to single agent may have a better reduction in platelet hyperreactivity in HIV concurrently taking cART was evaluated in the EVERE2ST-HIV [18]. This study evaluated the extent of platelet inhibition patients with acute coronary patients on dual antiplatelet therapy undergoing PCI utilizing various platelet function assays [18]. The findings were that P2Y12 inhibitors (clopidogrel, prasugrel, and ticagralor) and aspirin were all associated with residual platelet reactivity on light transmission aggregometry (LTA), VerifyNow, and VASP assays. Furthermore, HIV infection was an independent risk factor for the high on antiplatelet reactivity that was increased by combined antiretroviral therapy (cART). Of the cART, protease inhibitors had greater effects than the NNRTIs. The residual platelet reactivity in PLWHIV despite viral suppression and dual antiplatelet therapy can probably be accounted by the active immune mechanisms and drug interactions [148].
Overall, few studies have evaluated the effects of antiplatelets in persons living with HIV. The available studies suffer from small sample sizes and have not been performed in populations not taking cART. Furthermore, the different classes of antiplatelets have not been evaluated. Of the studies done so far, the results do demonstrate neither efficacy nor improved outcomes with either aspirin or clopidogrel.
Infection with HIV is associated with reduced platelet count; extent of thrombocytopenia inversely correlates with viral load and disease progression. Despite thrombocytopenia, cardiovascular events are on the increase. There is associated platelet hyperactivity, as evidenced by increased surface expression of CD62P, CD40L, platelet microparticles, and platelet leukocyte aggregates. There is enhanced secretion of chemokines such as RANTES. Combined antiretroviral drugs independently and synergistically with HIV enhance platelet hyperactivity that persists despite viral suppression. Data on the effects of antiplatelets in this population can at best be described as clinical equipoise.
Autor’s ORCID identifier: 0000-0001-6466-172X.
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The CC BY 3.0 and CC BY 4.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
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The CC BY 3.0 and CC BY 4.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
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Hypertension-induced structural remodeling is associated with an increased risk of life-threatening arrhythmias and heart failure in both humans and experimental animals. Recent studies suggest that abnormal distribution and/or downregulation of Cx43 accompanied with altered protein kinase C (PKC)ε signaling in spontaneously hypertensive rats were linked with increased propensity to ventricular fibrillation compared to normotensive rats. By contrast, the long-term treatment of hypertensive rats with cardioprotective compounds such as melatonin, omega-3 fatty acids, or red palm oil resulted in protection from lethal arrhythmia. Their antiarrhythmic effect was attributed to the attenuation of abnormal Cx43 topology and modulation of Cx43 mRNA as well as protein expression and its functional phosphorylated forms. The latter might be attributed to upregulation of PKCε. It appears that maladaptive consequences of hypertension resulting in abnormal myocardial distribution of Cx43 and its downregulation can contribute to arrhythmogenesis and occurrence of malignant arrhythmias. On the other hand, the attenuation of myocardial Cx43 abnormalities by treatment with melatonin, omega-3 fatty acids, or red palm oil confers arrhythmia protection in rodent model of essential hypertension. Findings uncover novel mechanisms of cardioprotective effects of melatonin, omega-3 fatty acids, and red palm oil. Well-designed clinical trials are needed to explore antiarrhythmic potential of these compounds in human essential hypertension.",book:{id:"5216",slug:"update-on-essential-hypertension",title:"Update on Essential Hypertension",fullTitle:"Update on Essential Hypertension"},signatures:"Tamara Egan Benova, Barbara Szeiffova Bacova, Csilla Viczenczova,\nMiroslav Barancik and Narcis Tribulova",authors:[{id:"181938",title:"D.Sc.",name:"Narcisa",middleName:null,surname:"Tribulova",slug:"narcisa-tribulova",fullName:"Narcisa Tribulova"},{id:"185905",title:"Dr.",name:"Tamara",middleName:null,surname:"Egan Benova",slug:"tamara-egan-benova",fullName:"Tamara Egan Benova"},{id:"185907",title:"Dr.",name:"Barbara",middleName:null,surname:"Szeiffova Bacova",slug:"barbara-szeiffova-bacova",fullName:"Barbara Szeiffova Bacova"},{id:"185908",title:"Dr.",name:"Csilla",middleName:null,surname:"Viczenczova",slug:"csilla-viczenczova",fullName:"Csilla Viczenczova"}]},{id:"48384",doi:"10.5772/60418",title:"A Review on Amiodarone as an Antiarrhythmic Drug",slug:"a-review-on-amiodarone-as-an-antiarrhythmic-drug",totalDownloads:2769,totalCrossrefCites:4,totalDimensionsCites:5,abstract:"Antiarrhythmic drugs are used to suppress abnormal heart rhythms by different mechanisms. Amiodarone as an iodinated benzofuran derivative is a potent antiarrhythmic drug that is being used for the treatment of a wide variety of cardiac arrhythmias. Amiodarone has been reported to cause frequent and potentially serious toxicity. It was estimated that the prevalence of side effects was 15 % in the first year and increased to 50% with long-term therapy. Thyroid, lung, liver, ophthalmologic and neurologic systems can be affected by Amiodarone. Most of the adverse effects of the drug are related to its dosage and duration of administration. Therefore the effectiveness of Amiodarone in long-term treatment of patients with heart arrhythmia is limited because of the development of its adverse side effects.",book:{id:"4584",slug:"abnormal-heart-rhythms",title:"Abnormal Heart Rhythms",fullTitle:"Abnormal Heart Rhythms"},signatures:"Fereshteh Mehraein",authors:[{id:"173324",title:"Associate Prof.",name:"Fereshteh",middleName:null,surname:"Mehraein",slug:"fereshteh-mehraein",fullName:"Fereshteh Mehraein"}]},{id:"41776",doi:"10.5772/52512",title:"Principles of External Defibrillators",slug:"principles-of-external-defibrillators",totalDownloads:3710,totalCrossrefCites:2,totalDimensionsCites:5,abstract:null,book:{id:"3289",slug:"cardiac-defibrillation",title:"Cardiac Defibrillation",fullTitle:"Cardiac Defibrillation"},signatures:"Hugo Delgado, Jorge Toquero, Cristina Mitroi, Victor Castro and Ignacio Fernández Lozano",authors:[{id:"38793",title:"Dr.",name:"Jorge",middleName:null,surname:"Toquero",slug:"jorge-toquero",fullName:"Jorge Toquero"}]}],mostDownloadedChaptersLast30Days:[{id:"41776",title:"Principles of External Defibrillators",slug:"principles-of-external-defibrillators",totalDownloads:3705,totalCrossrefCites:2,totalDimensionsCites:4,abstract:null,book:{id:"3289",slug:"cardiac-defibrillation",title:"Cardiac Defibrillation",fullTitle:"Cardiac Defibrillation"},signatures:"Hugo Delgado, Jorge Toquero, Cristina Mitroi, Victor Castro and Ignacio Fernández Lozano",authors:[{id:"38793",title:"Dr.",name:"Jorge",middleName:null,surname:"Toquero",slug:"jorge-toquero",fullName:"Jorge Toquero"}]},{id:"46160",title:"Basic Mechanisms of Cardiac Arrhythmias",slug:"basic-mechanisms-of-cardiac-arrhythmias",totalDownloads:4459,totalCrossrefCites:1,totalDimensionsCites:1,abstract:null,book:{id:"3815",slug:"cardiac-arrhythmias-mechanisms-pathophysiology-and-treatment",title:"Cardiac Arrhythmias",fullTitle:"Cardiac Arrhythmias - Mechanisms, Pathophysiology, and Treatment"},signatures:"Andrey Moskalenko",authors:[{id:"63235",title:"Dr.",name:"Andrey",middleName:"V.",surname:"Moskalenko",slug:"andrey-moskalenko",fullName:"Andrey Moskalenko"}]},{id:"48384",title:"A Review on Amiodarone as an Antiarrhythmic Drug",slug:"a-review-on-amiodarone-as-an-antiarrhythmic-drug",totalDownloads:2764,totalCrossrefCites:4,totalDimensionsCites:5,abstract:"Antiarrhythmic drugs are used to suppress abnormal heart rhythms by different mechanisms. Amiodarone as an iodinated benzofuran derivative is a potent antiarrhythmic drug that is being used for the treatment of a wide variety of cardiac arrhythmias. Amiodarone has been reported to cause frequent and potentially serious toxicity. It was estimated that the prevalence of side effects was 15 % in the first year and increased to 50% with long-term therapy. Thyroid, lung, liver, ophthalmologic and neurologic systems can be affected by Amiodarone. Most of the adverse effects of the drug are related to its dosage and duration of administration. Therefore the effectiveness of Amiodarone in long-term treatment of patients with heart arrhythmia is limited because of the development of its adverse side effects.",book:{id:"4584",slug:"abnormal-heart-rhythms",title:"Abnormal Heart Rhythms",fullTitle:"Abnormal Heart Rhythms"},signatures:"Fereshteh Mehraein",authors:[{id:"173324",title:"Associate Prof.",name:"Fereshteh",middleName:null,surname:"Mehraein",slug:"fereshteh-mehraein",fullName:"Fereshteh Mehraein"}]},{id:"61466",title:"Idiopathic Ventricular Arrhythmias",slug:"idiopathic-ventricular-arrhythmias",totalDownloads:1526,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Idiopathic ventricular arrhythmias (VAs) occur with a mechanism that is unrelated to myocardial scar. Idiopathic VAs most commonly occur in patients without structural heart disease, but can occur in those with structural heart disease. Idiopathic VAs present as a sustained or a non-sustained ventricular tachycardia or premature ventricular contractions. Imaging examinations such as echocardiography, nuclear tests, and cardiac magnetic resonance imaging are helpful for excluding any association of an idiopathic VA occurrence with myocardial scar. For the past two decades, the sites of idiopathic VA origins, commonly endocardial but sometimes epicardial, have been increasingly recognized. Idiopathic VAs usually originate from specific anatomical structures and exhibit characteristic electrocardiograms based on their anatomical background. Idiopathic VAs are basically benign, but they require medical treatment or catheter ablation when idiopathic VAs are symptomatic, frequent, or cause tachycardia-induced cardiomyopathy. This book chapter describes the up-to-date information on the prevalence of idiopathic VA origins relevant to the anatomy, diagnosis, and treatment of idiopathic VAs.",book:{id:"6536",slug:"cardiac-arrhythmias",title:"Cardiac Arrhythmias",fullTitle:"Cardiac Arrhythmias"},signatures:"Takumi Yamada",authors:[{id:"68148",title:"Prof.",name:"Takumi",middleName:null,surname:"Yamada",slug:"takumi-yamada",fullName:"Takumi Yamada"}]},{id:"59994",title:"Atrial Flutter: Diagnosis and Management strategies",slug:"atrial-flutter-diagnosis-and-management-strategies",totalDownloads:1496,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Atrial flutter (AFL) is a regular, macro reentrant arrhythmia traditionally defined as a supraventricular tachycardia with an atrial rate of 240–320 beats per minute (bpm). Pathophysiology of atrial flutter and atrial fibrillation (AF) is closely related to the similar risk of stroke and they coexist clinically. 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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). 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Possible contributions can address (but are not limited to) the following research topics: Bioinspired design and control of exoskeletons, orthoses, and prostheses; Experimental evaluation of the effect of assistive devices (e.g., influence on gait, balance, and neuromuscular system); Bioinspired technologies for rehabilitation, including clinical studies reporting evaluations; Application of neuromuscular and biomechanical models to the development of bioinspired technology.',annualVolume:11404,isOpenForSubmission:!0,coverUrl:"https://cdn.intechopen.com/series_topics/covers/8.jpg",editor:{id:"144937",title:"Prof.",name:"Adriano",middleName:"De Oliveira",surname:"Andrade",fullName:"Adriano Andrade",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRC8QQAW/Profile_Picture_1625219101815",institutionString:null,institution:{name:"Federal University of Uberlândia",institutionURL:null,country:{name:"Brazil"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"49517",title:"Prof.",name:"Hitoshi",middleName:null,surname:"Tsunashima",fullName:"Hitoshi Tsunashima",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYTP4QAO/Profile_Picture_1625819726528",institutionString:null,institution:{name:"Nihon University",institutionURL:null,country:{name:"Japan"}}},{id:"425354",title:"Dr.",name:"Marcus",middleName:"Fraga",surname:"Vieira",fullName:"Marcus Vieira",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003BJSgIQAX/Profile_Picture_1627904687309",institutionString:null,institution:{name:"Universidade Federal de Goiás",institutionURL:null,country:{name:"Brazil"}}},{id:"196746",title:"Dr.",name:"Ramana",middleName:null,surname:"Vinjamuri",fullName:"Ramana Vinjamuri",profilePictureURL:"https://mts.intechopen.com/storage/users/196746/images/system/196746.jpeg",institutionString:"University of Maryland, Baltimore County",institution:{name:"University of Maryland, Baltimore County",institutionURL:null,country:{name:"United States of America"}}}]},{id:"9",title:"Biotechnology - Biosensors, Biomaterials and Tissue Engineering",keywords:"Biotechnology, Biosensors, Biomaterials, Tissue Engineering",scope:"The Biotechnology - Biosensors, Biomaterials and Tissue Engineering topic within the Biomedical Engineering Series aims to rapidly publish contributions on all aspects of biotechnology, biosensors, biomaterial and tissue engineering. We encourage the submission of manuscripts that provide novel and mechanistic insights that report significant advances in the fields. Topics can include but are not limited to: Biotechnology such as biotechnological products and process engineering; Biotechnologically relevant enzymes and proteins; Bioenergy and biofuels; Applied genetics and molecular biotechnology; Genomics, transcriptomics, proteomics; Applied microbial and cell physiology; Environmental biotechnology; Methods and protocols. Moreover, topics in biosensor technology, like sensors that incorporate enzymes, antibodies, nucleic acids, whole cells, tissues and organelles, and other biological or biologically inspired components will be considered, and topics exploring transducers, including those based on electrochemical and optical piezoelectric, thermal, magnetic, and micromechanical elements. Chapters exploring biomaterial approaches such as polymer synthesis and characterization, drug and gene vector design, biocompatibility, immunology and toxicology, and self-assembly at the nanoscale, are welcome. Finally, the tissue engineering subcategory will support topics such as the fundamentals of stem cells and progenitor cells and their proliferation, differentiation, bioreactors for three-dimensional culture and studies of phenotypic changes, stem and progenitor cells, both short and long term, ex vivo and in vivo implantation both in preclinical models and also in clinical trials.",annualVolume:11405,isOpenForSubmission:!0,coverUrl:"https://cdn.intechopen.com/series_topics/covers/9.jpg",editor:{id:"126286",title:"Dr.",name:"Luis",middleName:"Jesús",surname:"Villarreal-Gómez",fullName:"Luis Villarreal-Gómez",profilePictureURL:"https://mts.intechopen.com/storage/users/126286/images/system/126286.jpg",institutionString:null,institution:{name:"Autonomous University of Baja California",institutionURL:null,country:{name:"Mexico"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"35539",title:"Dr.",name:"Cecilia",middleName:null,surname:"Cristea",fullName:"Cecilia Cristea",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYQ65QAG/Profile_Picture_1621007741527",institutionString:null,institution:{name:"Iuliu Hațieganu University of Medicine and Pharmacy",institutionURL:null,country:{name:"Romania"}}},{id:"40735",title:"Dr.",name:"Gil",middleName:"Alberto Batista",surname:"Gonçalves",fullName:"Gil Gonçalves",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYRLGQA4/Profile_Picture_1628492612759",institutionString:null,institution:{name:"University of Aveiro",institutionURL:null,country:{name:"Portugal"}}},{id:"211725",title:"Associate Prof.",name:"Johann F.",middleName:null,surname:"Osma",fullName:"Johann F. 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