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Search results for: low-dose rosuvastatin
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</div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: low-dose rosuvastatin</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">6</span> Rosuvastatin Improves Endothelial Progenitor Cells in Rheumatoid Arthritis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ashit%20Syngle">Ashit Syngle</a>, <a href="https://publications.waset.org/abstracts/search?q=Nidhi%20Garg"> Nidhi Garg</a>, <a href="https://publications.waset.org/abstracts/search?q=Pawan%20Krishan"> Pawan Krishan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Endothelial Progenitor Cells (EPCs) are depleted and contribute to increased cardiovascular (CV) risk in rheumatoid arthritis (RA). Statins exert a protective effect in CAD partly by promoting EPC mobilization. This vasculoprotective effect of statin has not yet been investigated in RA. We aimed to investigate the effect of rosuvastatin on EPCs in RA. Methods: 50 RA patients were randomized to receive 6 months of treatment with rosuvastatin (10 mg/day, n=25) and placebo (n=25) as an adjunct to existing stable antirheumatic drugs. EPCs (CD34+/CD133+) were quantified by Flow Cytometry. Inflammatory measures included DAS28, CRP and ESR were measured at baseline and after treatment. Lipids and pro-inflammatory cytokines (TNF-α, IL-6, and IL-1) were estimated at baseline and after treatment. Results: At baseline, inflammatory measures and pro-inflammatory cytokines were elevated and EPCs depleted among both groups. At baseline, EPCs inversely correlated with DAS28 and TNF-α in both groups. EPCs increased significantly (p < 0.01) after treatment with rosuvastatin but did not show significant change with placebo. Rosuvastatin exerted positive effect on lipid spectrum: lowering total cholesterol, LDL, non HDL and elevation of HDL as compared with placebo. At 6 months, DAS28, ESR, CRP, TNF-α and IL-6 improved significantly in rosuvastatin group. Significant negative correlation was observed between EPCs and DAS28, CRP, TNF-α, and IL-6 after treatment with rosuvastatin. Conclusion: First study to show that rosuvastatin improves inflammation and EPC biology in RA possibly through its anti-inflammatory and lipid lowering effect. This beneficial effect of rosuvastatin may provide a novel strategy to prevent cardiovascular events in RA. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=RA" title="RA">RA</a>, <a href="https://publications.waset.org/abstracts/search?q=Endothelial%20Progenitor%20Cells" title=" Endothelial Progenitor Cells"> Endothelial Progenitor Cells</a>, <a href="https://publications.waset.org/abstracts/search?q=rosuvastatin" title=" rosuvastatin"> rosuvastatin</a>, <a href="https://publications.waset.org/abstracts/search?q=cytokines" title=" cytokines "> cytokines </a> </p> <a href="https://publications.waset.org/abstracts/17374/rosuvastatin-improves-endothelial-progenitor-cells-in-rheumatoid-arthritis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17374.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">258</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> Stem Cell Augmentation Therapy for Cardiovascular Risk in Ankylosing Spondylitis: STATIN-as Study </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ashit%20Syngle">Ashit Syngle</a>, <a href="https://publications.waset.org/abstracts/search?q=Nidhi%20Garg"> Nidhi Garg</a>, <a href="https://publications.waset.org/abstracts/search?q=Pawan%20Krishan"> Pawan Krishan </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: Bone marrow derived stem cells, endothelial progenitor cells (EPCs), protect against atherosclerotic vascular damage. However, EPCs are depleted in AS and contribute to the enhanced cardiovascular risk. Statins have a protective effect in CAD and diabetes by enhancing the proliferation, migration and survival of EPCs. Therapeutic potential of augmenting EPCs to treat the heightened cardiovascular risk of AS has not yet been exploited. We aimed to investigate the effect of rosuvastatin on EPCs population and inflammation in AS. Methods: 30 AS patients were randomized to receive 6 months of treatment with rosuvastatin (10 mg/day, n=15) and placebo (n=15) as an adjunct to existing stable anti-rheumatic drugs. EPCs (CD34+/CD133+) were quantified by Flow Cytometry. Inflammatory measures (BASDAI, BASFI, CRP and ESR), pro-inflammatory cytokines (TNF-α, IL-6 and IL-1) and lipids were measured at baseline and after treatment. Results: At baseline, inflammatory measures and pro-inflammatory cytokines were elevated and EPCs depleted among both groups. EPCs increased significantly (p < 0.01) after treatment with rosuvastatin. At 6 months, BASDAI, BASFI, ESR, CRP, TNF-α, and IL-6 improved significantly in rosuvastatin group. Significant negative correlation was observed between EPCs and BASDAI, CRP and IL-6 after rosuvastatin treatment. Conclusion: First study to show that rosuvastatin augments EPCs population in AS. This defines a novel mechanism of rosuvastatin treatment in AS: the augmentation of EPCs with improvement in proinflammatory cytokines and inflammatory disease activity. The augmentation of EPCs by rosuvastatin may provide a novel strategy to prevent cardiovascular events in AS. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ankylosing%20spondylitis" title="ankylosing spondylitis">ankylosing spondylitis</a>, <a href="https://publications.waset.org/abstracts/search?q=Endothelial%20Progenitor%20Cells" title=" Endothelial Progenitor Cells"> Endothelial Progenitor Cells</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=pro-inflammatory%20cytokines" title=" pro-inflammatory cytokines"> pro-inflammatory cytokines</a>, <a href="https://publications.waset.org/abstracts/search?q=rosuvastatin" title=" rosuvastatin "> rosuvastatin </a> </p> <a href="https://publications.waset.org/abstracts/17363/stem-cell-augmentation-therapy-for-cardiovascular-risk-in-ankylosing-spondylitis-statin-as-study" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17363.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">353</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> Effects of Hypolipidemic Agents in Aminoglycoside-Induced Experimental Nephrotoxicity in Rats: Biochemical and Histopathological Evidence</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Balakumar%20Pitchai">Balakumar Pitchai</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiang%20Llan%20Ang"> Xiang Llan Ang</a>, <a href="https://publications.waset.org/abstracts/search?q=Sunil%20Prajapati"> Sunil Prajapati</a>, <a href="https://publications.waset.org/abstracts/search?q=Varatharajan%20Rajavel"> Varatharajan Rajavel</a>, <a href="https://publications.waset.org/abstracts/search?q=Sundram%20Karupiah"> Sundram Karupiah</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohd%20Baidi%20Bahari"> Mohd Baidi Bahari</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The study examined the pretreatment and post-treatment effects of low-doses of fenofibrate and rosuvastatin in gentamicin-induced acute nephrotoxicity in rats. Gentamicin (100 mg/kg/day, i.p.) was administered to rats for 8 days. In the pretreatment protocol, low-dose fenofibrate (30 mg/kg/day, p.o.) or low-dose rosuvastatin (2 mg/kg/day, p.o.) treatments were started a day before the administration of gentamicin and continued for 8 days. In the post-treatment protocol, rats administered gentamicin were treated with low-dose fenofibrate (30 mg/kg/day, p.o.) or low-dose rosuvastatin (2 mg/kg/day, p.o.) for 6 days after the completion of 8 days protocol of gentamicin administration. Gentamicin-associated acute nephrotoxicity in rats was assessed in terms of biochemical analysis and renal histopathological studies. Gentamicin-administered rats showed marked renal functional changes as assessed in terms of a significant increase in serum creatinine and urea levels as compared to normal rats. The renal dysfunction noted in gentamicin administered rats was accompanied with elevated serum uric acid level as compared to normal rats while there was no significant change in lipid profile. Low-dose fenofibrate pretreatment in gentamicin-administered rats afforded a significant renal functional improvements and renoprotection while its post-treatment showed no significant renoprotection. On the other hand, pretreatment with low-dose rosuvastatin partially reduced gentamicin-induced increase in serum creatinine level, but its post-treatment did not afford renal functional improvements in gentamicin-administered rats. However, all pre and post-treatments with low-doses of fenofibrate or rosuvastatin significantly reduced the elevated serum uric acid concentration in gentamicin-administered rats. Renal histopathological analysis showed a discernible incidence of acute tubular necrosis in gentamicin-administered rats which were markedly reduced by low-dose fenofibrate or low-dose rosuvastatin pretreatments; but, not by their post-treatments. In conclusion, low-dose fenofibrate pretreatment considerably prevented gentamicin-induced acute tubular necrosis and renal functional abnormalities in rats while its post-treatment resulted in no significant renoprotective action. In spite of effective prevention of gentamicin-induced acute tubular necrosis, the pretreatment with low-dose rosuvastatin had only a partial and fractional protection on renal functional abnormalities. The post-treatment with low-dose rosuvastatin was ineffective in affording a renoprotection in gentamicin-administered rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=gentamicin-nephrotoxicity" title="gentamicin-nephrotoxicity">gentamicin-nephrotoxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=low-dose%20fenofibrate" title=" low-dose fenofibrate"> low-dose fenofibrate</a>, <a href="https://publications.waset.org/abstracts/search?q=low-dose%20rosuvastatin" title=" low-dose rosuvastatin"> low-dose rosuvastatin</a>, <a href="https://publications.waset.org/abstracts/search?q=renoprotection" title=" renoprotection"> renoprotection</a> </p> <a href="https://publications.waset.org/abstracts/55411/effects-of-hypolipidemic-agents-in-aminoglycoside-induced-experimental-nephrotoxicity-in-rats-biochemical-and-histopathological-evidence" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/55411.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">204</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> Systematic Formulation Development and Evaluation of Self-Nanoemulsifying Systems of Rosuvastatin Employing QbD Approach and Chemometric Techniques</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sarwar%20Beg">Sarwar Beg</a>, <a href="https://publications.waset.org/abstracts/search?q=Gajanand%20Sharma"> Gajanand Sharma</a>, <a href="https://publications.waset.org/abstracts/search?q=O.%20P.%20Katare"> O. P. Katare</a>, <a href="https://publications.waset.org/abstracts/search?q=Bhupinder%20Singh"> Bhupinder Singh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The current studies entail development of self-nano emulsifying drug delivery systems (SNEDDS) of rosuvastatin, employing rational QbD-based approach for enhancing its oral bioavailability. SNEDDS were prepared using the blend of lipidic and emulsifying excipients, i.e., Peceol, Tween 80, and Transcutol HP. The prepared formulations evaluated for in vitro drug release, ex vivo permeation, in situ perfusion studies and in vivo pharmacokinetic studies in rats, which demonstrated 3-4 fold improvement in biopharmaceutical performance of the developed formulations. Cytotoxicity studies using MTT assay and histopathological studies in intestinal cells revealed the lack of cytotoxicity and thereby safety and efficacy of the developed formulations. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=SNEDDS" title="SNEDDS">SNEDDS</a>, <a href="https://publications.waset.org/abstracts/search?q=bioavailability" title=" bioavailability"> bioavailability</a>, <a href="https://publications.waset.org/abstracts/search?q=solubility" title=" solubility"> solubility</a>, <a href="https://publications.waset.org/abstracts/search?q=Quality%20by%20Design%20%28QbD%29" title=" Quality by Design (QbD)"> Quality by Design (QbD)</a> </p> <a href="https://publications.waset.org/abstracts/13541/systematic-formulation-development-and-evaluation-of-self-nanoemulsifying-systems-of-rosuvastatin-employing-qbd-approach-and-chemometric-techniques" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13541.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">505</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> Development of Ecofriendly Ionic Liquid Modified Reverse Phase Liquid Chromatography Method for Simultaneous Determination of Anti-Hyperlipidemic Drugs </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hassan%20M.%20Albishri">Hassan M. Albishri</a>, <a href="https://publications.waset.org/abstracts/search?q=Fatimah%20Al-Shehri"> Fatimah Al-Shehri</a>, <a href="https://publications.waset.org/abstracts/search?q=Deia%20Abd%20El-Hady"> Deia Abd El-Hady</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Among the analytical techniques, reverse phase liquid chromatography (RPLC) is currently used in pharmaceutical industry. Ecofriendly analytical chemistry offers the advantages of decreasing the environmental impact with the advantage of increasing operator safety which constituted a topic of industrial interest. Recently, ionic liquids have been successfully used to reduce or eliminate the conventional organic toxic solvents. In the current work, a simple and ecofriendly ionic liquid modified RPLC (IL-RPLC) method has been firstly developed and compared with RPLC under acidic and neutral mobile phase conditions for simultaneous determination of atorvastatin-calcium, rosuvastatin and simvastatin. Several chromatographic effective parameters have been changed in a systematic way. Adequate results have been achieved by mixing ILs with ethanol as a mobile phase under neutral conditions at 1 mL/min flow rate on C18 column. The developed IL-RPLC method has been validated for the quantitative determination of drugs in pharmaceutical formulations. The method showed excellent linearity for analytes in a wide range of concentrations with acceptable precise and accurate data. The current IL-RPLC technique could have vast applications particularly under neutral conditions for simple and greener (bio)analytical applications of pharmaceuticals. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ionic%20liquid" title="ionic liquid">ionic liquid</a>, <a href="https://publications.waset.org/abstracts/search?q=RPLC" title=" RPLC"> RPLC</a>, <a href="https://publications.waset.org/abstracts/search?q=anti-hyperlipidemic%20drugs" title=" anti-hyperlipidemic drugs"> anti-hyperlipidemic drugs</a>, <a href="https://publications.waset.org/abstracts/search?q=ecofriendly" title=" ecofriendly"> ecofriendly</a> </p> <a href="https://publications.waset.org/abstracts/62016/development-of-ecofriendly-ionic-liquid-modified-reverse-phase-liquid-chromatography-method-for-simultaneous-determination-of-anti-hyperlipidemic-drugs" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/62016.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">256</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Role of Lipid-Lowering Treatment in the Monocyte Phenotype and Chemokine Receptor Levels after Acute Myocardial Infarction</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Carolina%20N.%20Fran%C3%A7a">Carolina N. França</a>, <a href="https://publications.waset.org/abstracts/search?q=J%C3%B4natas%20B.%20do%20Amaral"> Jônatas B. do Amaral</a>, <a href="https://publications.waset.org/abstracts/search?q=Maria%20C.O.%20Izar"> Maria C.O. Izar</a>, <a href="https://publications.waset.org/abstracts/search?q=Ighor%20L.%20Teixeira"> Ighor L. Teixeira</a>, <a href="https://publications.waset.org/abstracts/search?q=Francisco%20A.%20Fonseca"> Francisco A. Fonseca</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Atherosclerosis is a progressive disease, characterized by lipid and fibrotic element deposition in large-caliber arteries. Conditions related to the development of atherosclerosis, as dyslipidemia, hypertension, diabetes, and smoking are associated with endothelial dysfunction. There is a frequent recurrence of cardiovascular outcomes after acute myocardial infarction and, at this sense, cycles of mobilization of monocyte subtypes (classical, intermediate and nonclassical) secondary to myocardial infarction may determine the colonization of atherosclerotic plaques in different stages of the development, contributing to early recurrence of ischemic events. The recruitment of different monocyte subsets during inflammatory process requires the expression of chemokine receptors CCR2, CCR5, and CX3CR1, to promote the migration of monocytes to the inflammatory site. The aim of this study was to evaluate the effect of lipid-lowering treatment by six months in the monocyte phenotype and chemokine receptor levels of patients after Acute Myocardial Infarction (AMI). Methods: This is a PROBE (prospective, randomized, open-label trial with blinded endpoints) study (ClinicalTrials.gov Identifier: NCT02428374). Adult patients (n=147) of both genders, ageing 18-75 years, were randomized in a 2x2 factorial design for treatment with rosuvastatin 20 mg/day or simvastatin 40 mg/day plus ezetimibe 10 mg/day as well as ticagrelor 90 mg 2x/day and clopidogrel 75 mg, in addition to conventional AMI therapy. Blood samples were collected at baseline, after one month and six months of treatment. Monocyte subtypes (classical - inflammatory, intermediate - phagocytic and nonclassical – anti-inflammatory) were identified, quantified and characterized by flow cytometry, as well as the expressions of the chemokine receptors (CCR2, CCR5 and CX3CR1) were also evaluated in the mononuclear cells. Results: After six months of treatment, there was an increase in the percentage of classical monocytes and reduction in the nonclassical monocytes (p=0.038 and p < 0.0001 Friedman Test), without differences for intermediate monocytes. Besides, classical monocytes had higher expressions of CCR5 and CX3CR1 after treatment, without differences related to CCR2 (p < 0.0001 for CCR5 and CX3CR1; p=0.175 for CCR2). Intermediate monocytes had higher expressions of CCR5 and CX3CR1 and lower expression of CCR2 (p = 0.003; p < 0.0001 and p = 0.011, respectively). Nonclassical monocytes had lower expressions of CCR2 and CCR5, without differences for CX3CR1 (p < 0.0001; p = 0.009 and p = 0.138, respectively). There were no differences after the comparison between the four treatment arms. Conclusion: The data suggest a time-dependent modulation of classical and nonclassical monocytes and chemokine receptor levels. The higher percentage of classical monocytes (inflammatory cells) suggest a residual inflammatory risk, even under preconized treatments to AMI. Indeed, these changes do not seem to be affected by choice of the lipid-lowering strategy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20myocardial%20infarction" title="acute myocardial infarction">acute myocardial infarction</a>, <a href="https://publications.waset.org/abstracts/search?q=chemokine%20receptors" title=" chemokine receptors"> chemokine receptors</a>, <a href="https://publications.waset.org/abstracts/search?q=lipid-lowering%20treatment" title=" lipid-lowering treatment"> lipid-lowering treatment</a>, <a href="https://publications.waset.org/abstracts/search?q=monocyte%20subtypes" title=" monocyte subtypes"> monocyte subtypes</a> </p> <a href="https://publications.waset.org/abstracts/111555/role-of-lipid-lowering-treatment-in-the-monocyte-phenotype-and-chemokine-receptor-levels-after-acute-myocardial-infarction" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/111555.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">119</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); 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