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glucocorticoid receptor</title> <meta name="description" content="Search results for: glucocorticoid receptor"> <meta name="keywords" content="glucocorticoid receptor"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button 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action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="glucocorticoid receptor"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 508</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: glucocorticoid receptor</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">508</span> Targeting Glucocorticoid Receptor Eliminate Dormant Chemoresistant Cancer Stem Cells in Glioblastoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aoxue%20Yang">Aoxue Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Weili%20Tian"> Weili Tian</a>, <a href="https://publications.waset.org/abstracts/search?q=Yonghe%20Wu"> Yonghe Wu</a>, <a href="https://publications.waset.org/abstracts/search?q=Haikun%20Liu"> Haikun Liu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain tumor stem cells (BTSCs) are resistant to therapy and give rise to recurrent tumors. These rare and elusive cells are likely to disseminate during cancer progression, and some may enter dormancy, remaining viable but not increasing. The identification of dormant BTSCs is thus necessary to design effective therapies for glioblastoma (GBM) patients. Little progress has been made in therapeutic treatment of glioblastoma in the last decade despite rapid progress in molecular understanding of brain tumors1. Here we show that the stress hormone glucocorticoid is essential for the maintenance of brain tumor stem cells (BTSCs), which are resistant to conventional therapy. The glucocorticoid receptor (GR) regulates metabolic plasticity and chemoresistance of the dormant BTSC via controlling expression of GPD1 (glycerol-3-phosphate dehydrogenase 1), which is an essential regulator of lipid metabolism in BTSCs. Genomic, lipidomic and cellular analysis confirm that GR/GPD1 regulation is essential for BTSCs metabolic plasticity and survival. We further demonstrate that the GR agonist dexamethasone (DEXA), which is commonly used to control edema in glioblastoma, abolishes the effect of chemotherapy drug temozolomide (TMZ) by upregulating GPD1 and thus promoting tumor cell dormancy in vivo, this provides a mechanistic explanation and thus settle the long-standing debate of usage of steroid in brain tumor patient edema control. Pharmacological inhibition of GR/GPD1 pathway disrupts metabolic plasticity of BTSCs and prolong animal survival, which is superior to standard chemotherapy. Patient case study shows that GR antagonist mifepristone blocks tumor progression and leads to symptomatic improvement. This study identifies an important mechanism regulating cancer stem cell dormancy and provides a new opportunity for glioblastoma treatment. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cancer%20stem%20cell" title="cancer stem cell">cancer stem cell</a>, <a href="https://publications.waset.org/abstracts/search?q=dormancy" title=" dormancy"> dormancy</a>, <a href="https://publications.waset.org/abstracts/search?q=glioblastoma" title=" glioblastoma"> glioblastoma</a>, <a href="https://publications.waset.org/abstracts/search?q=glycerol-3-phosphate%20dehydrogenase%201" title=" glycerol-3-phosphate dehydrogenase 1"> glycerol-3-phosphate dehydrogenase 1</a>, <a href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor" title=" glucocorticoid receptor"> glucocorticoid receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=dexamethasone" title=" dexamethasone"> dexamethasone</a>, <a href="https://publications.waset.org/abstracts/search?q=RNA-sequencing" title=" RNA-sequencing"> RNA-sequencing</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphoglycerides." title=" phosphoglycerides."> phosphoglycerides.</a> </p> <a href="https://publications.waset.org/abstracts/150825/targeting-glucocorticoid-receptor-eliminate-dormant-chemoresistant-cancer-stem-cells-in-glioblastoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/150825.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">84</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">507</span> Toward Understanding the Glucocorticoid Receptor Network in Cancer </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Swati%20Srivastava">Swati Srivastava</a>, <a href="https://publications.waset.org/abstracts/search?q=Mattia%20Lauriola"> Mattia Lauriola</a>, <a href="https://publications.waset.org/abstracts/search?q=Yuval%20Gilad"> Yuval Gilad</a>, <a href="https://publications.waset.org/abstracts/search?q=Adi%20Kimchi"> Adi Kimchi</a>, <a href="https://publications.waset.org/abstracts/search?q=Yosef%20Yarden"> Yosef Yarden</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The glucocorticoid receptor (GR) has been proposed to play important, but incompletely understood roles in cancer. Glucocorticoids (GCs) are widely used as co-medication of various carcinomas, due to their ability to reduce the toxicity of chemotherapy. Furthermore, GR antagonism has proven to be a strategy to treat triple negative breast cancer and castration-resistant prostate cancer. These observations suggest differential GR involvement in cancer subtypes. The goal of our study has been to elaborate the current understanding of GR signaling in tumor progression and metastasis. Our study involves two cellular models, non-tumorigenic breast epithelial cells (MCF10A) and Ewing sarcoma cells (CHLA9). In our breast cell model, the results indicated that the GR agonist dexamethasone inhibits EGF-induced mammary cell migration, and this effect was blocked when cells were stimulated with a GR antagonist, namely RU486. Microarray analysis for gene expression revealed that the mechanism underlying inhibition involves dexamenthasone-mediated repression of well-known activators of EGFR signaling, alongside with enhancement of several EGFR’s negative feedback loops. Because GR mainly acts primarily through composite response elements (GREs), or via a tethering mechanism, our next aim has been to find the transcription factors (TFs) which can interact with GR in MCF10A cells.The TF-binding motif overrepresented at the promoter of dexamethasone-regulated genes was predicted by using bioinformatics. To validate the prediction, we performed high-throughput Protein Complementation Assays (PCA). For this, we utilized the Gaussia Luciferase PCA strategy, which enabled analysis of protein-protein interactions between GR and predicted TFs of mammary cells. A library comprising both nuclear receptors (estrogen receptor, mineralocorticoid receptor, GR) and TFs was fused to fragments of GLuc, namely GLuc(1)-X, X-GLuc(1), and X-GLuc(2), where GLuc(1) and GLuc(2) correspond to the N-terminal and C-terminal fragments of the luciferase gene.The resulting library was screened, in human embryonic kidney 293T (HEK293T) cells, for all possible interactions between nuclear receptors and TFs. By screening all of the combinations between TFs and nuclear receptors, we identified several positive interactions, which were strengthened in response to dexamethasone and abolished in response to RU486. Furthermore, the interactions between GR and the candidate TFs were validated by co-immunoprecipitation in MCF10A and in CHLA9 cells. Currently, the roles played by the uncovered interactions are being evaluated in various cellular processes, such as cellular proliferation, migration, and invasion. In conclusion, our assay provides an unbiased network analysis between nuclear receptors and other TFs, which can lead to important insights into transcriptional regulation by nuclear receptors in various diseases, in this case of cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=epidermal%20growth%20factor" title="epidermal growth factor">epidermal growth factor</a>, <a href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor" title=" glucocorticoid receptor"> glucocorticoid receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=protein%20complementation%20assay" title=" protein complementation assay"> protein complementation assay</a>, <a href="https://publications.waset.org/abstracts/search?q=transcription%20factor" title=" transcription factor"> transcription factor</a> </p> <a href="https://publications.waset.org/abstracts/56709/toward-understanding-the-glucocorticoid-receptor-network-in-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/56709.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">227</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">506</span> Targeting Glucocorticoid Receptor Eliminate Dormant Chemoresistant Cancer Stem Cells in Glioblastoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aoxue%20Yang">Aoxue Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Weili%20Tian"> Weili Tian</a>, <a href="https://publications.waset.org/abstracts/search?q=Haikun%20Liu"> Haikun Liu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain tumor stem cells (BTSCs) are resistant to therapy and give rise to recurrent tumors. These rare and elusive cells are likely to disseminate during cancer progression, and some may enter dormancy, remaining viable but not increasing. The identification of dormant BTSCs is thus necessary to design effective therapies for glioblastoma (GBM) patients. Glucocorticoids (GCs) are used to treat GBM-associated edema. However, glucocorticoids participate in the physiological response to psychosocial stress, linked to poor cancer prognosis. This raises concern that glucocorticoids affect the tumor and BTSCs. Identifying markers specifically expressed by brain tumor stem cells (BTSCs) may enable specific therapies that spare their regular tissue-resident counterparts. By ribosome profiling analysis, we have identified that glycerol-3-phosphate dehydrogenase 1 (GPD1) is expressed by dormant BTSCs but not by NSCs. Through different stress-induced experiments in vitro, we found that only dexamethasone (DEXA) can significantly increase the expression of GPD1 in NSCs. Adversely, mifepristone (MIFE) which is classified as glucocorticoid receptors antagonists, could decrease GPD1 protein level and weaken the proliferation and stemness in BTSCs. Furthermore, DEXA can induce GPD1 expression in tumor-bearing mice brains and shorten animal survival, whereas MIFE has a distinct adverse effect that prolonged mice lifespan. Knocking out GR in NSC can block the upregulation of GPD1 inducing by DEXA, and we find the specific sequences on GPD1 promotor combined with GR, thus improving the efficiency of GPD1 transcription from CHIP-Seq. Moreover, GR and GPD1 are highly co-stained on GBM sections obtained from patients and mice. All these findings confirmed that GR could regulate GPD1 and loss of GPD1 Impairs Multiple Pathways Important for BTSCs Maintenance GPD1 is also a critical enzyme regulating glycolysis and lipid synthesis. We observed that DEXA and MIFE could change the metabolic profiles of BTSCs by regulating GPD1 to shift the transition of cell dormancy. Our transcriptome and lipidomics analysis demonstrated that cell cycle signaling and phosphoglycerides synthesis pathways contributed a lot to the inhibition of GPD1 caused by MIFE. In conclusion, our findings raise concern that treatment of GBM with GCs may compromise the efficacy of chemotherapy and contribute to BTSC dormancy. Inhibition of GR can dramatically reduce GPD1 and extend the survival duration of GBM-bearing mice. The molecular link between GPD1 and GR may give us an attractive therapeutic target for glioblastoma. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cancer%20stem%20cell" title="cancer stem cell">cancer stem cell</a>, <a href="https://publications.waset.org/abstracts/search?q=dormancy" title=" dormancy"> dormancy</a>, <a href="https://publications.waset.org/abstracts/search?q=glioblastoma" title=" glioblastoma"> glioblastoma</a>, <a href="https://publications.waset.org/abstracts/search?q=glycerol-3-phosphate%20dehydrogenase%201" title=" glycerol-3-phosphate dehydrogenase 1"> glycerol-3-phosphate dehydrogenase 1</a>, <a href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor" title=" glucocorticoid receptor"> glucocorticoid receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=dexamethasone" title=" dexamethasone"> dexamethasone</a>, <a href="https://publications.waset.org/abstracts/search?q=RNA-sequencing" title=" RNA-sequencing"> RNA-sequencing</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphoglycerides" title=" phosphoglycerides"> phosphoglycerides</a> </p> <a href="https://publications.waset.org/abstracts/146108/targeting-glucocorticoid-receptor-eliminate-dormant-chemoresistant-cancer-stem-cells-in-glioblastoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/146108.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">132</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">505</span> The 10-year Risk of Major Osteoporotic and Hip Fractures Among Indonesian People Living with HIV</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Iqbal%20Pramukti">Iqbal Pramukti</a>, <a href="https://publications.waset.org/abstracts/search?q=Mamat%20Lukman"> Mamat Lukman</a>, <a href="https://publications.waset.org/abstracts/search?q=Hasniatisari%20Harun"> Hasniatisari Harun</a>, <a href="https://publications.waset.org/abstracts/search?q=Kusman%20Ibrahim"> Kusman Ibrahim</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: People living with HIV had a higher risk of osteoporotic fracture than the general population. The purpose of this study was to predict the 10-year risk of fracture among people living with HIV (PLWH) using FRAX™ and to identify characteristics related to the fracture risk. Methodology: This study consisted of 75 subjects. The ten-year probability of major osteoporotic fractures (MOF) and hip fractures was assessed using the FRAX™ algorithm. A cross-tabulation was used to identify the participant’s characteristics related to fracture risk. Results: The overall mean 10-year probability of fracture was 2.4% (1.7) for MOF and 0.4% (0.3) for hip fractures. For MOF score, participants with parents’ hip fracture history, smoking behavior and glucocorticoid use showed a higher MOF score than those who were not (3.1 vs. 2.5; 4.6 vs 2.5; and 3.4 vs 2.5, respectively). For HF score, participants with parents’ hip fracture history, smoking behavior and glucocorticoid use also showed a higher HF score than those who were not (0.5 vs. 0.3; 0.8 vs. 0.3; and 0.5 vs. 0.3, respectively). Conclusions: The 10-year risk of fracture was higher among PLWH with several factors, including the parent’s hip. Fracture history, smoking behavior and glucocorticoid used. Further analysis on determining factors using multivariate regression analysis with a larger sample size is required to confirm the factors associated with the high fracture risk. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=HIV" title="HIV">HIV</a>, <a href="https://publications.waset.org/abstracts/search?q=PLWH" title=" PLWH"> PLWH</a>, <a href="https://publications.waset.org/abstracts/search?q=osteoporotic%20fractures" title=" osteoporotic fractures"> osteoporotic fractures</a>, <a href="https://publications.waset.org/abstracts/search?q=hip%20fractures" title=" hip fractures"> hip fractures</a>, <a href="https://publications.waset.org/abstracts/search?q=10-year%20risk%20of%20fracture" title=" 10-year risk of fracture"> 10-year risk of fracture</a>, <a href="https://publications.waset.org/abstracts/search?q=FRAX" title=" FRAX"> FRAX</a> </p> <a href="https://publications.waset.org/abstracts/184625/the-10-year-risk-of-major-osteoporotic-and-hip-fractures-among-indonesian-people-living-with-hiv" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/184625.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">49</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">504</span> Signaling of Leucine-Rich-Repeat Receptor-Like Kinases in Higher Plants</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Man-Ho%20Oh">Man-Ho Oh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Membrane localized Leucine-Rich-Repeat Receptor-Like Kinases (LRR-RLKs) play crucial roles in plant growth and abiotic/biotic stress responses in higher plants including Arabidopsis and Brassica species. Among several Receptor-Like Kinases (RLKs), Leucine-Rich-Repeat Receptor-Like-Kinases (LRR-RLKs) are the major group of genes that play crucial roles related to growth, development and stress conditions in plant system. Since it is involved in several functional roles, it seems to be very important to investigate their roles in higher plants. We are particularly interested in brassinosteroid (BR) signaling, which is mediated by the BRASSINOSTEROID INSENSITIVE 1 (BRI1) receptor kinase and its co-receptor, BRI1-ASSOCIATED KINASE 1 (BAK1). Autophosphorylation of receptor kinases is recognized to be an important process in activation of signaling in higher plants. Although the plant receptors are generally classified as Ser/Thr protein kinases, many other receptor kinases including BRI1 and BAK1 are shown to autophosphorylate on Tyr residues in addition to Ser/Thr. As an interesting result, we determined that several 14-3-3 regulatory proteins bind to BRI1-CD and are phosphorylated by several receptor kinases in vitro, suggesting that BRI1 is critical for diverse signaling. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=autophosphorylation" title="autophosphorylation">autophosphorylation</a>, <a href="https://publications.waset.org/abstracts/search?q=brassinosteroid" title=" brassinosteroid"> brassinosteroid</a>, <a href="https://publications.waset.org/abstracts/search?q=BRASSINOSTEROID%20INSENSITIVE%201" title=" BRASSINOSTEROID INSENSITIVE 1"> BRASSINOSTEROID INSENSITIVE 1</a>, <a href="https://publications.waset.org/abstracts/search?q=BRI1-ASSOCIATED%20KINASE%201" title=" BRI1-ASSOCIATED KINASE 1"> BRI1-ASSOCIATED KINASE 1</a>, <a href="https://publications.waset.org/abstracts/search?q=Leucine-Rich-Repeat%20Receptor-Like%20Kinases%20%28LRR-RLKs%29" title=" Leucine-Rich-Repeat Receptor-Like Kinases (LRR-RLKs)"> Leucine-Rich-Repeat Receptor-Like Kinases (LRR-RLKs)</a> </p> <a href="https://publications.waset.org/abstracts/76545/signaling-of-leucine-rich-repeat-receptor-like-kinases-in-higher-plants" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/76545.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">224</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">503</span> Conformational Switch of hRAGE upon Self-Association</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ikhlas%20Ahmed">Ikhlas Ahmed</a>, <a href="https://publications.waset.org/abstracts/search?q=Jamillah%20Zamoon"> Jamillah Zamoon</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The human receptor for advanced glycation end product is a plasma membrane receptor with an intrinsically disordered region. The protein consists of three extracellular domains, a single membrane spanning transmembrane domain, and a cytosolic domain which is intrinsically disordered and responsible for signaling. The disordered nature of the cytosolic domain allows it to be dynamic in solution. This receptor self-associates to higher forms. The association is triggered by ligand, metal or by the extracellular domain. Fluorescence spectroscopy technique is used to test the self-association of the different concentrations of the cytosolic domain. This work has concluded that the cytosolic domain of this receptor also self-associates. Moreover, the self-association does not require ligand or metal. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=fluorescence%20spectroscopy" title="fluorescence spectroscopy">fluorescence spectroscopy</a>, <a href="https://publications.waset.org/abstracts/search?q=hRAGE" title=" hRAGE"> hRAGE</a>, <a href="https://publications.waset.org/abstracts/search?q=IDP" title=" IDP"> IDP</a>, <a href="https://publications.waset.org/abstracts/search?q=Self-association" title=" Self-association"> Self-association</a> </p> <a href="https://publications.waset.org/abstracts/44509/conformational-switch-of-hrage-upon-self-association" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/44509.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">361</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">502</span> Using of Bimolecular Fluorescence Complementation (BiFC) Assays to Study Homo and/ or Heterodimerization of Laminin Receptor 37 LRP/ 67 LR with Galectin-3</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Fulwah%20Alqahtani">Fulwah Alqahtani</a>, <a href="https://publications.waset.org/abstracts/search?q=Jafar%20Mahdavi"> Jafar Mahdavi</a>, <a href="https://publications.waset.org/abstracts/search?q=Lee%20Weldon"> Lee Weldon</a>, <a href="https://publications.waset.org/abstracts/search?q=Nick%20Holliday"> Nick Holliday</a>, <a href="https://publications.waset.org/abstracts/search?q=Dlawer%20Ala%27Aldeen"> Dlawer Ala'Aldeen</a> </p> <p class="card-text"><strong>Abstract:</strong></p> There are two isoforms of laminin receptor; monomeric 37 kDa laminin receptor precursor (37 LRP) and mature 67 kDa laminin receptor (67 LR). The relationship between the 67 LR and its precursor 37 LRP is not completely understood, but previous observations have suggested that 37 LRP can undergo homo- and/or hetero- dimerization with Galectin-3 (Gal-3) to form mature 67 LR. Gal-3 is the only member of the chimera-type group of galectins, and has one C-terminal carbohydrate recognition domain (CRD) that is responsible for binding the ß-galactoside moieties of mono- or oligosaccharides on several host and microbial molecules. The aim of this work was to investigate homo- and hetero-dimerization among the 37 LRP and Gal-3 to form mature 67 LR in mammalian cells using bimolecular fluorescence complementation (BiFC). <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=37%20LRP" title="37 LRP">37 LRP</a>, <a href="https://publications.waset.org/abstracts/search?q=67%20LR" title=" 67 LR"> 67 LR</a>, <a href="https://publications.waset.org/abstracts/search?q=Gal-3" title=" Gal-3"> Gal-3</a>, <a href="https://publications.waset.org/abstracts/search?q=BiFC" title=" BiFC"> BiFC</a> </p> <a href="https://publications.waset.org/abstracts/15423/using-of-bimolecular-fluorescence-complementation-bifc-assays-to-study-homo-and-or-heterodimerization-of-laminin-receptor-37-lrp-67-lr-with-galectin-3" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/15423.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">504</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">501</span> Role of Imaging in Predicting the Receptor Positivity Status in Lung Adenocarcinoma: A Chapter in Radiogenomics</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sonal%20Sethi">Sonal Sethi</a>, <a href="https://publications.waset.org/abstracts/search?q=Mukesh%20Yadav"> Mukesh Yadav</a>, <a href="https://publications.waset.org/abstracts/search?q=Abhimanyu%20Gupta"> Abhimanyu Gupta</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The upcoming field of radiogenomics has the potential to upgrade the role of imaging in lung cancer management by noninvasive characterization of tumor histology and genetic microenvironment. Receptor positivity like epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) genotyping are critical in lung adenocarcinoma for treatment. As conventional identification of receptor positivity is an invasive procedure, we analyzed the features on non-invasive computed tomography (CT), which predicts the receptor positivity in lung adenocarcinoma. Retrospectively, we did a comprehensive study from 77 proven lung adenocarcinoma patients with CT images, EGFR and ALK receptor genotyping, and clinical information. Total 22/77 patients were receptor-positive (15 had only EGFR mutation, 6 had ALK mutation, and 1 had both EGFR and ALK mutation). Various morphological characteristics and metastatic distribution on CT were analyzed along with the clinical information. Univariate and multivariable logistic regression analyses were used. On multivariable logistic regression analysis, we found spiculated margin, lymphangitic spread, air bronchogram, pleural effusion, and distant metastasis had a significant predictive value for receptor mutation status. On univariate analysis, air bronchogram and pleural effusion had significant individual predictive value. Conclusions: Receptor positive lung cancer has characteristic imaging features compared with nonreceptor positive lung adenocarcinoma. Since CT is routinely used in lung cancer diagnosis, we can predict the receptor positivity by a noninvasive technique and would follow a more aggressive algorithm for evaluation of distant metastases as well as for the treatment. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=lung%20cancer" title="lung cancer">lung cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=multidisciplinary%20cancer%20care" title=" multidisciplinary cancer care"> multidisciplinary cancer care</a>, <a href="https://publications.waset.org/abstracts/search?q=oncologic%20imaging" title=" oncologic imaging"> oncologic imaging</a>, <a href="https://publications.waset.org/abstracts/search?q=radiobiology" title=" radiobiology"> radiobiology</a> </p> <a href="https://publications.waset.org/abstracts/129528/role-of-imaging-in-predicting-the-receptor-positivity-status-in-lung-adenocarcinoma-a-chapter-in-radiogenomics" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/129528.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">136</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">500</span> Produced Gas Conversion of Microwave Carbon Receptor Reforming</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Young%20Nam%20Chun">Young Nam Chun</a>, <a href="https://publications.waset.org/abstracts/search?q=Mun%20Sup%20Lim"> Mun Sup Lim</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Carbon dioxide and methane, the major components of biomass pyrolysis/gasification gas and biogas, top the list of substances that cause climate change, but they are also among the most important renewable energy sources in modern society. The purpose of this study is to convert carbon dioxide and methane into high-quality energy using char and commercial activated carbon obtained from biomass pyrolysis as a microwave receptor. The methane reforming process produces hydrogen and carbon. This carbon is deposited in the pores of the microwave receptor and lowers catalytic activity, thereby reducing the methane conversion rate. The deposited carbon was removed by carbon gasification due to the supply of carbon dioxide, which solved the problem of microwave receptor inactivity. In particular, the conversion rate remained stable at over 90% when the ratio of carbon dioxide to methane was 1:1. When the reforming results of carbon dioxide and methane were compared after fabricating nickel and iron catalysts using commercial activated carbon as a carrier, the conversion rate was higher in the iron catalyst than in the nickel catalyst and when no catalyst was used.  <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=microwave" title="microwave">microwave</a>, <a href="https://publications.waset.org/abstracts/search?q=gas%20reforming" title=" gas reforming"> gas reforming</a>, <a href="https://publications.waset.org/abstracts/search?q=greenhouse%20gas" title=" greenhouse gas"> greenhouse gas</a>, <a href="https://publications.waset.org/abstracts/search?q=microwave%20receptor" title=" microwave receptor"> microwave receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=catalyst" title=" catalyst"> catalyst</a> </p> <a href="https://publications.waset.org/abstracts/77831/produced-gas-conversion-of-microwave-carbon-receptor-reforming" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/77831.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">379</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">499</span> On the Thermodynamics of Biological Cell Adhesion</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ben%20Nadler">Ben Nadler</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cell adhesion plays a vital role in many cell activities. The motivation to model cell adhesion is to study important biological processes, such as cell spreading, cell aggregation, tissue formation, and cell adhesion, which are very challenging to study by experimental methods alone. This study provides important insight into cell adhesion, which can lead to improve regenerative medicine and tissue formation techniques. In this presentation the biological cells adhesion is mediated by receptors–ligands binding and the diffusivity of the receptor on the cell membrane surface. The ability of receptors to diffuse on the cell membrane surface yields a very unique and complicated adhesion mechanism, which is exclusive to cells. The phospholipid bilayer, which is the main component in the cell membrane, shows fluid-like behavior associated with the molecules’ diffusivity. The biological cell is modeled as a fluid-like membrane with negligible bending stiffness enclosing the cytoplasm fluid. The in-plane mechanical behavior of the cell membrane is assumed to depend only on the area change, which is motivated by the fluidity of the phospholipid bilayer. In addition, the presence of receptors influences on the local mechanical properties of the cell membrane is accounted for by including stress-free area change, which depends on the receptor density. Based on the physical properties of the receptors and ligands the attraction between the receptors and ligands is modeled as a charged-nonpolar which is a noncovalent interaction. Such interaction is a short-range type, which decays fast with distance. The mobility of the receptor on the cell membrane is modeled using the diffusion equation and Fick’s law is used to model the receptor–receptor interactions. The resultant interaction force, which includes receptor–ligand and receptor–receptor interaction, is decomposed into tangential part, which governs the receptor diffusion, and normal part, which governs the cell deformation and adhesion. The formulation of the governing equations and numerical simulations will be presented. Analysis of the adhesion characteristic and properties are discussed. The roles of various thermomechanical properties of the cell, receptors and ligands on the cell adhesion are investigated. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cell%20adhesion" title="cell adhesion">cell adhesion</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20membrane" title=" cell membrane"> cell membrane</a>, <a href="https://publications.waset.org/abstracts/search?q=receptor-ligand%20interaction" title=" receptor-ligand interaction"> receptor-ligand interaction</a>, <a href="https://publications.waset.org/abstracts/search?q=receptor%20diffusion" title=" receptor diffusion"> receptor diffusion</a> </p> <a href="https://publications.waset.org/abstracts/37546/on-the-thermodynamics-of-biological-cell-adhesion" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/37546.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">342</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">498</span> Study of Functional Relevant Conformational Mobility of β-2 Adrenoreceptor by Means of Molecular Dynamics Simulation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=G.%20V.%20Novikov">G. V. Novikov</a>, <a href="https://publications.waset.org/abstracts/search?q=V.%20S.%20Sivozhelezov"> V. S. Sivozhelezov</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20S.%20Kolesnikov"> S. S. Kolesnikov</a>, <a href="https://publications.waset.org/abstracts/search?q=K.%20V.%20Shaitan"> K. V. Shaitan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The study reports about the influence of binding of orthosteric ligands as well as point mutations on the conformational dynamics of β-2-adrenoreceptor. Using molecular dynamics simulation we found that there was a little fraction of active states of the receptor in its apo (ligand free) ensemble corresponded to its constitutive activity. Analysis of MD trajectories indicated that such spontaneous activation of the receptor is accompanied by the motion in intracellular part of its alpha-helices. Thus receptor’s constitutive activity directly results from its conformational dynamics. On the other hand the binding of a full agonist resulted in a significant shift of the initial equilibrium towards its active state. Finally, the binding of the inverse agonist stabilized the receptor in its inactive state. It is likely that the binding of inverse agonists might be a universal way of constitutive activity inhibition in vivo. Our results indicate that ligand binding redistribute pre-existing conformational degrees of freedom (in accordance to the Monod-Wyman-Changeux-Model) of the receptor rather than cause induced fit in it. Therefore, the ensemble of biologically relevant receptor conformations is encoded in its spatial structure, and individual conformations from that ensemble might be used by the cell in conformity with the physiological behaviour. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=seven-transmembrane%20receptors" title="seven-transmembrane receptors">seven-transmembrane receptors</a>, <a href="https://publications.waset.org/abstracts/search?q=constitutive%20activity" title=" constitutive activity"> constitutive activity</a>, <a href="https://publications.waset.org/abstracts/search?q=activation" title=" activation"> activation</a>, <a href="https://publications.waset.org/abstracts/search?q=x-ray%20crystallography" title=" x-ray crystallography"> x-ray crystallography</a>, <a href="https://publications.waset.org/abstracts/search?q=principal%20component%20analysis" title=" principal component analysis"> principal component analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=molecular%20dynamics%20simulation" title=" molecular dynamics simulation"> molecular dynamics simulation</a> </p> <a href="https://publications.waset.org/abstracts/5618/study-of-functional-relevant-conformational-mobility-of-v-2-adrenoreceptor-by-means-of-molecular-dynamics-simulation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/5618.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">257</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">497</span> Targeting Trypanosoma brucei Using Antibody Drug Conjugates against the Transferrin Receptor</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Camilla%20Trevor">Camilla Trevor</a>, <a href="https://publications.waset.org/abstracts/search?q=Matthew%20K.%20Higgins"> Matthew K. Higgins</a>, <a href="https://publications.waset.org/abstracts/search?q=Andrea%20Gonzalez-Munoz"> Andrea Gonzalez-Munoz</a>, <a href="https://publications.waset.org/abstracts/search?q=Mark%20Carrington"> Mark Carrington</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Trypanosomiasis is a devastating disease affecting both humans and livestock in sub-Saharan Africa. The diseases are caused by infection with African trypanosomes, protozoa transmitted by tsetse flies. Treatment currently relies on the use of chemotherapeutics with ghastly side effects. Here, we describe the development of effective antibody-drug conjugates that target the T. brucei transferrin receptor. The receptor is essential for trypanosome growth in a mammalian host but there are approximately 12 variants of the transferrin receptor in the genome. Two of the most divergent variants were used to generate recombinant monoclonal immunoglobulin G using phage display and we identified cross-reactive antibodies that bind both variants using phage ELISA, fluorescence resonance energy transfer assays and surface plasmon resonance. Fluorescent antibodies were used to demonstrate uptake into trypanosomes in culture. Toxin-conjugated antibodies were effective at killing trypanosomes at sub-nanomolar concentrations. The approach of using antibody-drug conjugates has proven highly effective. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antibody-drug%20conjugates" title="antibody-drug conjugates">antibody-drug conjugates</a>, <a href="https://publications.waset.org/abstracts/search?q=phage%20display" title=" phage display"> phage display</a>, <a href="https://publications.waset.org/abstracts/search?q=transferrin%20receptor" title=" transferrin receptor"> transferrin receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=trypanosomes" title=" trypanosomes"> trypanosomes</a> </p> <a href="https://publications.waset.org/abstracts/99250/targeting-trypanosoma-brucei-using-antibody-drug-conjugates-against-the-transferrin-receptor" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/99250.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">155</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">496</span> An Unbiased Profiling of Immune Repertoire via Sequencing and Analyzing T-Cell Receptor Genes</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yi-Lin%20Chen">Yi-Lin Chen</a>, <a href="https://publications.waset.org/abstracts/search?q=Sheng-Jou%20Hung"> Sheng-Jou Hung</a>, <a href="https://publications.waset.org/abstracts/search?q=Tsunglin%20Liu"> Tsunglin Liu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Adaptive immune system recognizes a wide range of antigens via expressing a large number of structurally distinct T cell and B cell receptor genes. The distinct receptor genes arise from complex rearrangements called V(D)J recombination, and constitute the immune repertoire. A common method of profiling immune repertoire is via amplifying recombined receptor genes using multiple primers and high-throughput sequencing. This multiplex-PCR approach is efficient; however, the resulting repertoire can be distorted because of primer bias. To eliminate primer bias, 5’ RACE is an alternative amplification approach. However, the application of RACE approach is limited by its low efficiency (i.e., the majority of data are non-regular receptor sequences, e.g., containing intronic segments) and lack of the convenient tool for analysis. We propose a computational tool that can correctly identify non-regular receptor sequences in RACE data via aligning receptor sequences against the whole gene instead of only the exon regions as done in all other tools. Using our tool, the remaining regular data allow for an accurate profiling of immune repertoire. In addition, a RACE approach is improved to yield a higher fraction of regular T-cell receptor sequences. Finally, we quantify the degree of primer bias of a multiplex-PCR approach via comparing it to the RACE approach. The results reveal significant differences in frequency of VJ combination by the two approaches. Together, we provide a new experimental and computation pipeline for an unbiased profiling of immune repertoire. As immune repertoire profiling has many applications, e.g., tracing bacterial and viral infection, detection of T cell lymphoma and minimal residual disease, monitoring cancer immunotherapy, etc., our work should benefit scientists who are interested in the applications. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=immune%20repertoire" title="immune repertoire">immune repertoire</a>, <a href="https://publications.waset.org/abstracts/search?q=T-cell%20receptor" title=" T-cell receptor"> T-cell receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=5%27%20RACE" title=" 5' RACE"> 5' RACE</a>, <a href="https://publications.waset.org/abstracts/search?q=high-throughput%20sequencing" title=" high-throughput sequencing"> high-throughput sequencing</a>, <a href="https://publications.waset.org/abstracts/search?q=sequence%20alignment" title=" sequence alignment"> sequence alignment</a> </p> <a href="https://publications.waset.org/abstracts/88972/an-unbiased-profiling-of-immune-repertoire-via-sequencing-and-analyzing-t-cell-receptor-genes" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/88972.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">194</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">495</span> Correlation of Leptin with Clinico-Pathological Features of Breast Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Saad%20Al-Shibli">Saad Al-Shibli</a>, <a href="https://publications.waset.org/abstracts/search?q=Nasser%20Amjad"> Nasser Amjad</a>, <a href="https://publications.waset.org/abstracts/search?q=Muna%20Al%20Kubaisi"> Muna Al Kubaisi</a>, <a href="https://publications.waset.org/abstracts/search?q=Norra%20Harun"> Norra Harun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shaikh%20Mizan"> Shaikh Mizan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Leptin is a multifunctional hormone produced mainly by adipocyte. Leptin and its receptor have long been found associated with breast cancer. The main aim of this study is to investigate the correlation between Leptin/Leptin receptor and the clinicopathological features of breast cancer. Blood samples for ELISA, tissue samples from tumors and adjacent breast tissue were taken from 51 women with breast cancer with a control group of 40 women with a negative mammogram. Leptin and Leptin receptor in the tissues were estimated by immunohistochemistry (IHC). They were localized at the subcellular level by immunocytochemistry using transmission electron microscopy (TEM). Our results showed significant difference in serum leptin level between control and the patient group, but no difference between pre and post-operative serum leptin levels in the patient group. By IHC, we found that the majority of the breast cancer cells studied, stained positively for leptin and leptin receptors with co-expression of leptin and its receptors. No significant correlation was found between leptin/leptin receptors expression with the race, menopausal status, lymph node metastasis, estrogen receptor expression, progesterone receptor expression, HER2 expression and tumor size. Majority of the patients with distant metastasis were associated with high leptin and leptin receptor expression. TEM views both Leptin and Leptin receptor were found highly concentrated within and around the nucleus of the cancer breast cells, indicating nucleus is their principal seat of actions while the adjacent breast epithelial cells showed that leptin gold particles are scattered all over the cell with much less than that of the cancerous cells. However, presence of high concentration of leptin does not necessarily prove its over-expression, because it could be internalized from outside by leptin receptor in the cells. In contrast, leptin receptor is definitely over-expressed in the ductal breast cancer cells. We conclude that reducing leptin levels, blocking its downstream tissue specific signal transduction, and/or blocking the upstream leptin receptor pathway might help in prevention and therapy of breast cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=breast%20cancer" title="breast cancer">breast cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=expression" title=" expression"> expression</a>, <a href="https://publications.waset.org/abstracts/search?q=leptin" title=" leptin"> leptin</a>, <a href="https://publications.waset.org/abstracts/search?q=leptin%20receptors" title=" leptin receptors"> leptin receptors</a> </p> <a href="https://publications.waset.org/abstracts/99477/correlation-of-leptin-with-clinico-pathological-features-of-breast-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/99477.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">140</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">494</span> Ageing Gingiva: A New Hope for Autologous Stem Cell Therapy</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ankush%20M.%20Dewle">Ankush M. Dewle</a>, <a href="https://publications.waset.org/abstracts/search?q=Suditi%20Bhattacharya"> Suditi Bhattacharya</a>, <a href="https://publications.waset.org/abstracts/search?q=Prachi%20R.%20Abhang"> Prachi R. Abhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Savita%20Datar"> Savita Datar</a>, <a href="https://publications.waset.org/abstracts/search?q=Ajay%20J.%20Jog"> Ajay J. Jog</a>, <a href="https://publications.waset.org/abstracts/search?q=Rupesh%20K.%20Srivastava"> Rupesh K. Srivastava</a>, <a href="https://publications.waset.org/abstracts/search?q=Geetanjali%20Tomar"> Geetanjali Tomar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objectives: The aim of this study was to investigate the quality of mesenchymal stem cells (MSCs) obtained from ageing gingival tissues, in order to suggest their potential role in autologous stem cell therapy for old individuals. Methods: MSCs were isolated from gingival tissues of young (18-45 years) and old (above 45 years) donors by enzymatic digestion. MSCs were analysed for cfu-f, surface marker expression by flow-cytometry and multilineage differentiation potential. The angiogenic potential was compared in a chick embryo yolk sac membrane model. The aging and differentiation markers including SA-β-galactosidase and p21 respectively were analysed by staining and flow-cytometry analysis. Additionally, osteogenic markers such as glucocorticoid receptor (GR), vitamin D receptor (VDR) were measured by flow-cytometry and RT-qPCR was performed for quantification of osteogenic gene expression. Alizarin Red S and alkaline phosphatase (ALP) activity were also quantitated. Results: Gingival MSCs (GMSCs) from both the age groups were similar in their morphology and displayed cfu-f. They had similar expression of MSC surface markers and p21, comparable rate of proliferation and differentiated to all the four lineages. GMSCs from young donors had a higher adipogenic differentiation potential as compared to the old GMSCs. Moreover, these cells did not display a significant difference in ALP activity probably due to comparable expression of GR, VDR, and osteogenic genes. Conclusions: Ageing of GMSCs occurs at a much slower rate than stem cells from other sources. Thus we suggest GMSCs as an excellent candidate for autologous stem cell therapy in degenerative diseases of elderly individuals. Clinical Significance: GMSCs could help overcome the setbacks in clinical implementation of autologous stem cell therapy for regenerative medicine in all age group of patient. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bone%20regeneration" title="bone regeneration">bone regeneration</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20therapy" title=" cell therapy"> cell therapy</a>, <a href="https://publications.waset.org/abstracts/search?q=senescence" title=" senescence"> senescence</a>, <a href="https://publications.waset.org/abstracts/search?q=stem%20cell" title=" stem cell"> stem cell</a> </p> <a href="https://publications.waset.org/abstracts/81618/ageing-gingiva-a-new-hope-for-autologous-stem-cell-therapy" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/81618.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">184</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">493</span> The Role of Estradiol-17β and Type IV Collagen on the Regulation and Expression Level Of C-Erbb2 RNA and Protein in SKOV-3 Ovarian Cancer Cell Line </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Merry%20Meryam%20Martgrita">Merry Meryam Martgrita</a>, <a href="https://publications.waset.org/abstracts/search?q=Marselina%20Irasonia%20Tan"> Marselina Irasonia Tan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> One of several aggresive cancer is cancer that overexpress c-erbB2 receptor along with the expression of estrogen receptor. Components of extracellular matrix play an important role to increase cancer cells proliferation, migration and invasion. Both components can affect cancer development by regulating the signal transduction pathways in cancer cells. In recent research, SKOV-3 ovarian cancer cell line, that overexpress c-erbB2 receptor was cultured on type IV collagen and treated with estradiol-17β, to reveal the role of both components on RNA and protein level of c-erbB2 receptor. In this research we found a modulation phenomena of increasing and decreasing of c-erbB2 RNA level and a stabilisation phenomena of c-erbB2 protein expression due to estradiol-17β and type IV collagen. It seemed that estradiol-17β has an important role to increase c-erbB2 transcription and the stability of c-erbB2 protein expression. Type IV collagen has an opposite role. It blocked c-erbB2 transcription when it bound to integrin receptor in SKOV-3 cells. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=c-erbB2" title="c-erbB2">c-erbB2</a>, <a href="https://publications.waset.org/abstracts/search?q=estradiol-17%CE%B2" title=" estradiol-17β"> estradiol-17β</a>, <a href="https://publications.waset.org/abstracts/search?q=SKOV-3" title=" SKOV-3"> SKOV-3</a>, <a href="https://publications.waset.org/abstracts/search?q=type%20IV%20collagen" title=" type IV collagen"> type IV collagen</a> </p> <a href="https://publications.waset.org/abstracts/27964/the-role-of-estradiol-17v-and-type-iv-collagen-on-the-regulation-and-expression-level-of-c-erbb2-rna-and-protein-in-skov-3-ovarian-cancer-cell-line" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/27964.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">284</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">492</span> Berberine Ameliorates Glucocorticoid-Induced Hyperglycemia: An In-Vitro and In-Vivo Study</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mrinal%20Gupta">Mrinal Gupta</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohammad%20Rumman"> Mohammad Rumman</a>, <a href="https://publications.waset.org/abstracts/search?q=Babita%20Singh%20Abbas%20Ali%20Mahdi"> Babita Singh Abbas Ali Mahdi</a>, <a href="https://publications.waset.org/abstracts/search?q=Shivani%20Pandey"> Shivani Pandey</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Berberine (BBR), a bioactive compound isolated from Coptidis Rhizoma, possesses diverse pharmacological activities, including anti-bacterial, anti-inflammatory, antitumor, hypolipidemic, and anti-diabetic. However, its role as an anti-diabetic agent in animal models of dexamethasone (Dex)-induced diabetes remains unknown. Studies have shown that natural compounds, including aloe, caper, cinnamon, cocoa, green and black tea, and turmeric, can be used for treating Type 2 diabetes mellitus (DM). Compared to conventional drugs, natural compounds have fewer side effects and are easily available. Herein, we studied the anti-diabetic effects of BBR in a mice model of Dex-induced diabetes. Methods: HepG2 cell line was used for glucose release and glycogen synthesis studies. Cell proliferation was measured by methylthiotetrazole (MTT) assay. For animal studies, mice were treated with Dex (2 mg/kg, i.m.) for 30 days and the effect of BBR at the doses 100, 200, and 500 mg/kg (p.o.) was analyzed. Glucose, insulin, and pyruvate tests were performed to evaluate the development of the diabetic model. An echo MRI was performed to assess the fat mass. Further, to elucidate the mechanism of action of BBR, mRNA expression of genes regulating gluconeogenesis, glucose uptake, and glycolysis were analyzed. Results: In vitro BBR had no impact on cell viability up to a concentration of 50μM. Moreover, BBR suppressed the hepatic glucose release and improved glucose tolerance in HepG2 cells. In vivo, BBR improved glucose homeostasis in diabetic mice, as evidenced by enhanced glucose clearance, increased glycolysis, elevated glucose uptake, and decreased gluconeogenesis. Further, Dex treatment increased the total fat mass in mice, which was ameliorated by BBR treatment. Conclusion: BBR improves glucose tolerance by increasing glucose clearance, inhibiting hepatic glucose release, and decreasing obesity. Thus, BBR may become a potential therapeutic agent for treating glucocorticoid-induced diabetes and obesity in the future. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=glucocorticoid" title="glucocorticoid">glucocorticoid</a>, <a href="https://publications.waset.org/abstracts/search?q=hyperglycemia" title=" hyperglycemia"> hyperglycemia</a>, <a href="https://publications.waset.org/abstracts/search?q=berberine" title=" berberine"> berberine</a>, <a href="https://publications.waset.org/abstracts/search?q=HepG2%20cells" title=" HepG2 cells"> HepG2 cells</a>, <a href="https://publications.waset.org/abstracts/search?q=insulin%20resistance" title=" insulin resistance"> insulin resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=glucose" title=" glucose"> glucose</a> </p> <a href="https://publications.waset.org/abstracts/172767/berberine-ameliorates-glucocorticoid-induced-hyperglycemia-an-in-vitro-and-in-vivo-study" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/172767.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">64</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">491</span> Optimization and Evaluation of 177lu-Dotatoc as a Potential Agent for Peptide Receptor Radionuclide Therapy</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=H.%20Yousefnia">H. Yousefnia</a>, <a href="https://publications.waset.org/abstracts/search?q=MS.%20Mousavi-Daramoroudi"> MS. Mousavi-Daramoroudi</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Zolghadri"> S. Zolghadri</a>, <a href="https://publications.waset.org/abstracts/search?q=F.%20Abbasi-Davani"> F. Abbasi-Davani</a> </p> <p class="card-text"><strong>Abstract:</strong></p> High expression of somatostatin receptors on a wide range of human tumours makes them as potential targets for peptide receptor radionuclide tomography. A series of octreotide analogues were synthesized while [DOTA-DPhe1, Tyr3]octreotide (DOTATOC) indicated advantageous properties in tumour models. In this study, 177Lu-DOTATOC was prepared with the radiochemical purity of higher than 99% in 30 min at the optimized condition. Biological behavior of the complex was studied after intravenous injection into the Syrian rats. Major difference uptake was observed compared to 177LuCl3 solution especially in somatostatin receptor-positive tissues such as pancreas and adrenal. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Biodistribution" title="Biodistribution">Biodistribution</a>, <a href="https://publications.waset.org/abstracts/search?q=177Lu" title=" 177Lu"> 177Lu</a>, <a href="https://publications.waset.org/abstracts/search?q=Octreotide" title=" Octreotide"> Octreotide</a>, <a href="https://publications.waset.org/abstracts/search?q=Syrian%20rats" title=" Syrian rats"> Syrian rats</a> </p> <a href="https://publications.waset.org/abstracts/34294/optimization-and-evaluation-of-177lu-dotatoc-as-a-potential-agent-for-peptide-receptor-radionuclide-therapy" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/34294.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">448</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">490</span> The Transcription Factor HNF4a: A Key Player in Haematological Disorders</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Tareg%20Belali">Tareg Belali</a>, <a href="https://publications.waset.org/abstracts/search?q=Mosleh%20Abomughaid"> Mosleh Abomughaid</a>, <a href="https://publications.waset.org/abstracts/search?q=Muhanad%20Alhujaily"> Muhanad Alhujaily</a> </p> <p class="card-text"><strong>Abstract:</strong></p> HNF4a is one of the steroid hormone receptor family of transcription factors with roles in the development of the liver and the regulation of several critical metabolic pathways, such as glycolysis, drug metabolism, and apolipoproteins and blood coagulation. The transcriptional potency of HNF4a is well known due to its involvement in diabetes and other metabolic diseases. However, recently HNF4a has been discovered to be closely associated with several haematological disorders, mainly because of genetic mutations, drugs, and hepatic disorders. We review HNF4a structure and function and its role in haematological disorders. We discuss possible good therapies that are based on targeting HNF4a. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hepatocyte%20nuclear%20factor%204%20alpha" title="hepatocyte nuclear factor 4 alpha">hepatocyte nuclear factor 4 alpha</a>, <a href="https://publications.waset.org/abstracts/search?q=HNF4a%20nuclear%20receptor" title=" HNF4a nuclear receptor"> HNF4a nuclear receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=steroid%20hormone%20receptor%20family%20of%20transcription%20factors" title=" steroid hormone receptor family of transcription factors"> steroid hormone receptor family of transcription factors</a>, <a href="https://publications.waset.org/abstracts/search?q=hematological%20disorders" title=" hematological disorders"> hematological disorders</a> </p> <a href="https://publications.waset.org/abstracts/149357/the-transcription-factor-hnf4a-a-key-player-in-haematological-disorders" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/149357.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">96</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">489</span> Development and Pre-clinical Evaluation of New ⁶⁴Cu-NOTA-Folate Conjugates for PET Imaging of Folate Receptor-Positive Tumors</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Norah%20Al%20Hokbany">Norah Al Hokbany</a>, <a href="https://publications.waset.org/abstracts/search?q=Ibrahim%20Al%20Jammaz"> Ibrahim Al Jammaz</a>, <a href="https://publications.waset.org/abstracts/search?q=Basem%20Al%20Otaibi"> Basem Al Otaibi</a>, <a href="https://publications.waset.org/abstracts/search?q=Yousif%20Al%20Malki"> Yousif Al Malki</a>, <a href="https://publications.waset.org/abstracts/search?q=Subhani%20M.%20Okarvi"> Subhani M. Okarvi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: The folate receptor is over-expressed in a wide variety of human tumors. Conjugates of folate have been shown to be selectively taken up by tumor cells via the folate receptor. In an attempt to develop new folate radiotracers with favorable biochemical properties for detecting folate receptor-positive cancers. Methods: we synthesized ⁶⁴Cu-NOTA- and ⁶⁴Cu-NOTAM-folate conjugates using a straightforward and simple one-step reaction. Radiochemical yields were greater than 95% (decay-corrected) with a total synthesis time of less than 20 min. Results: Radiochemical purities were always greater than 98% without high-performance liquid chromatography (HPLC) purification. These synthetic approaches hold considerable promise as a rapid and simple method for ⁶⁴Cu-folate conjugate preparation with high radiochemical yield in a short synthesis time. In vitro tests on the KB cell line showed that significant amounts of the radio conjugates were associated with cell fractions. Bio-distribution studies in nude mice bearing human KB xenografts demonstrated a significant tumor uptake and favorable bio-distribution profile for ⁶⁴Cu-NOTA- and ⁶⁴Cu-NOTAM-folate conjugate. The uptake in the tumors was blocked by the excess injection of folic acid, suggesting a receptor-mediated process. Conclusion: These results demonstrate that the ⁶⁴Cu-NOTAM-folate conjugate may be useful as a molecular probe for the detection and staging of folate receptor-positive cancers, such as ovarian cancer and their metastasis, as well as monitoring tumor response to treatment. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=folate" title="folate">folate</a>, <a href="https://publications.waset.org/abstracts/search?q=receptor" title=" receptor"> receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=tumor%20imaging" title=" tumor imaging"> tumor imaging</a>, <a href="https://publications.waset.org/abstracts/search?q=%E2%81%B6%E2%81%B4Cu-NOTA-folate" title=" ⁶⁴Cu-NOTA-folate"> ⁶⁴Cu-NOTA-folate</a>, <a href="https://publications.waset.org/abstracts/search?q=PET" title=" PET"> PET</a> </p> <a href="https://publications.waset.org/abstracts/156848/development-and-pre-clinical-evaluation-of-new-64cu-nota-folate-conjugates-for-pet-imaging-of-folate-receptor-positive-tumors" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/156848.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">108</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">488</span> Identification of Target Receptor Compound 10,11-Dihidroerisodin as an Anti-Cancer Candidate</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Srie%20Rezeki%20Nur%20Endah">Srie Rezeki Nur Endah</a>, <a href="https://publications.waset.org/abstracts/search?q=Richa%20Mardianingrum"> Richa Mardianingrum</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cancer is one of the most feared diseases and is considered the leading cause of death worldwide. Generally, cancer drugs are synthetic drugs with relatively more expensive prices and have harmful side effects, so many people turn to traditional medicine, for example by utilizing herbal medicine. Erythrina poeppigiana is one of the plants that can be used as a medicinal plant containing 10,11-dihidroerisodin compounds that are useful anticancer etnofarmakologi. The purpose of this study was to identify the target of 10,11 dihydroerisodin receptor compound as in silico anticancer candidate. The pure isolate was tested physicochemically by MS (Mass Spectrometry), UV-Vis (Ultraviolet – Visible), IR (Infra Red), 13C-NMR (Carbon-13 Nuclear Magnetic Resonance), 1H-NMR (Hydrogen-1 Nuclear Magnetic Resonance), to obtain the structure of 10,11-dihydroerisodin alkaloid compound then identified to target receptors in silico. From the results of the study, it was found that 10,11-dihydroerisodin compound can work on the Serine / threonine-protein kinase Chk1 receptor that serves as an anti-cancer candidate. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-cancer" title="anti-cancer">anti-cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=Erythrina%20poeppigiana" title=" Erythrina poeppigiana"> Erythrina poeppigiana</a>, <a href="https://publications.waset.org/abstracts/search?q=target%20receptor" title=" target receptor"> target receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=10" title=" 10"> 10</a>, <a href="https://publications.waset.org/abstracts/search?q=11-%20dihidroerisodin" title="11- dihidroerisodin">11- dihidroerisodin</a> </p> <a href="https://publications.waset.org/abstracts/92293/identification-of-target-receptor-compound-1011-dihidroerisodin-as-an-anti-cancer-candidate" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/92293.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">246</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">487</span> Insights Into Serotonin-Receptor Binding and Stability via Molecular Dynamics Simulations: Key Residues for Electrostatic Interactions and Signal Transduction</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Arunima%20Verma">Arunima Verma</a>, <a href="https://publications.waset.org/abstracts/search?q=Padmabati%20Mondal"> Padmabati Mondal</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Serotonin-receptor binding plays a key role in several neurological and biological processes, including mood, sleep, hunger, cognition, learning, and memory. In this article, we performed molecular dynamics simulation to examine the key residues that play an essential role in the binding of serotonin to the G-protein-coupled 5-HT₁ᴮ receptor (5-HT₁ᴮ R) via electrostatic interactions. An end-point free energy calculation method (MM-PBSA) determines the stability of the 5-HT1B R due to serotonin binding. The single-point mutation of the polar or charged amino acid residues (Asp129, Thr134) on the binding sites and the calculation of binding free energy validate the importance of these residues in the stability of the serotonin-receptor complex. Principal component analysis indicates the serotonin-bound 5-HT1BR is more stabilized than the apo-receptor in terms of dynamical changes. The difference dynamic cross-correlations map shows the correlation between the transmembrane and mini-Go, which indicates signal transduction happening between mini-Go and the receptor. Allosteric communication reveals the key nodes for signal transduction in 5-HT1BR. These results provide useful insights into the signal transduction pathways and mutagenesis study to regulate the functionality of the complex. The developed protocols can be applied to study local non-covalent interactions and long-range allosteric communications in any protein-ligand system for computer-aided drug design. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=allostery" title="allostery">allostery</a>, <a href="https://publications.waset.org/abstracts/search?q=CADD" title=" CADD"> CADD</a>, <a href="https://publications.waset.org/abstracts/search?q=MD%20simulations" title=" MD simulations"> MD simulations</a>, <a href="https://publications.waset.org/abstracts/search?q=MM-PBSA" title=" MM-PBSA"> MM-PBSA</a> </p> <a href="https://publications.waset.org/abstracts/177882/insights-into-serotonin-receptor-binding-and-stability-via-molecular-dynamics-simulations-key-residues-for-electrostatic-interactions-and-signal-transduction" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/177882.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">87</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">486</span> Microglia Activity and Induction of Mechanical Allodynia after Mincle Receptor Ligand Injection in Rat Spinal Cord</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jihoon%20Yang">Jihoon Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Jeong%20II%20Choi"> Jeong II Choi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Mincle is expressed in macrophages and is members of immunoreceptors induced after exposure to various stimuli and stresses. Mincle receptor activation promotes the production of these substances by increasing the transcription of inflammatory cytokines and chemokines. Cytokines, which play an important role in the initiation and maintenance of such inflammatory pain diseases, have a significant effect on sensory neurons in addition to their enhancement and inhibitory effects on immune and inflammatory cells as mediators of cell interaction. Glial cells in the central nervous system play a critical role in development and maintenance of chronic pain states. Microglia are tissue-resident macrophages in the central nervous system, and belong to a group of mononuclear phagocytes. In the central nervous system, mincle receptor is present in neurons and glial cells of the brain.This study was performed to identify the Mincle receptor in the spinal cord and to investigate the effect of Mincle receptor activation on nociception and the changes of microglia. Materials and Methods: C-type lectins(Mincle) was identified in spinal cord of Male Sprague–Dawley rats. Then, mincle receptor ligand (TDB), via an intrathecal catheter. Mechanical allodynia was measured using von Frey test to evaluate the effect of intrathecal injection of TDB. Result: The present investigation shows that the intrathecal administration of TDB in the rat produces a reliable and quantifiable mechanical hyperalgesia. In addition, The mechanical hyperalgesia after TDB injection gradually developed over time and remained until 10 days. Mincle receptor is identified in the spinal cord, mainly expressed in neuronal cells, but not in microglia or astrocyte. These results suggest that activation of mincle receptor pathway in neurons plays an important role in inducing activation of microglia and inducing mechanical allodynia. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=mincle" title="mincle">mincle</a>, <a href="https://publications.waset.org/abstracts/search?q=spinal%20cord" title=" spinal cord"> spinal cord</a>, <a href="https://publications.waset.org/abstracts/search?q=pain" title=" pain"> pain</a>, <a href="https://publications.waset.org/abstracts/search?q=microglia" title=" microglia"> microglia</a> </p> <a href="https://publications.waset.org/abstracts/79571/microglia-activity-and-induction-of-mechanical-allodynia-after-mincle-receptor-ligand-injection-in-rat-spinal-cord" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/79571.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">159</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">485</span> Non-Signaling Chemokine Receptor CCRL1 and Its Active Counterpart CCR7 in Prostate Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yiding%20Qu">Yiding Qu</a>, <a href="https://publications.waset.org/abstracts/search?q=Svetlana%20V.%20Komarova"> Svetlana V. Komarova</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Chemokines acting through their cognate chemokine receptors guide the directional migration of the cell along the chemokine gradient. Several chemokine receptors were recently identified as non-signaling (decoy), based on their ability to bind the chemokine but produce no measurable signal in the cell. The function of these decoy receptors is not well understood. We examined the expression of a decoy receptor CCRL1 and a signaling receptor that binds to the same ligands, CCR7, in prostate cancer using publically available microarray data (www.oncomine.org). The expression of both CCRL1 and CCR7 increased in an approximately half of prostate carcinoma samples and the majority of metastatic cancer samples compared to normal prostate. Moreover, the expression of CCRL1 positively correlated with the expression of CCR7. These data suggest that CCR7 and CCRL1 can be used as clinical markers for the early detection of transformation from carcinoma to metastatic cancer. In addition, these data support our hypothesis that the non-signaling chemokine receptors actively stimulate cell migration. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bioinformatics" title="bioinformatics">bioinformatics</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20migration" title=" cell migration"> cell migration</a>, <a href="https://publications.waset.org/abstracts/search?q=decoy%20receptor" title=" decoy receptor"> decoy receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=meta-analysis" title=" meta-analysis"> meta-analysis</a>, <a href="https://publications.waset.org/abstracts/search?q=prostate%20cancer" title=" prostate cancer"> prostate cancer</a> </p> <a href="https://publications.waset.org/abstracts/23226/non-signaling-chemokine-receptor-ccrl1-and-its-active-counterpart-ccr7-in-prostate-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/23226.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">470</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">484</span> A Platform to Screen Targeting Molecules of Ligand-EGFR Interactions</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Wei-Ting%20Kuo">Wei-Ting Kuo</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng-Huei%20Lin"> Feng-Huei Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Epidermal growth factor receptor (EGFR) is often constitutively stimulated in cancer owing to the binding of ligands such as epidermal growth factor (EGF), so it is necessary to investigate the interaction between EGFR and its targeting biomolecules which were over ligands binding. This study would focus on the binding affinity and adhesion force of two targeting products anti-EGFR monoclonal antibody (mAb) and peptide A to EGFR comparing with EGF. Surface plasmon resonance (SPR) was used to obtain the equilibrium dissociation constant to evaluate the binding affinity. Atomic force microscopy (AFM) was performed to detect adhesion force. The result showed that binding affinity of mAb to EGFR was higher than that of EGF to EGFR, and peptide A to EGFR was lowest. The adhesion force between EGFR and mAb that was higher than EGF and peptide A to EGFR was lowest. From the studies, we could conclude that mAb had better adhesion force and binding affinity to EGFR than that of EGF and peptide A. SPR and AFM could confirm the interaction between receptor and targeting ligand easily and carefully. It provide a platform to screen ligands for receptor targeting and drug delivery. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=adhesion%20force" title="adhesion force">adhesion force</a>, <a href="https://publications.waset.org/abstracts/search?q=binding%20affinity" title=" binding affinity"> binding affinity</a>, <a href="https://publications.waset.org/abstracts/search?q=epidermal%20growth%20factor%20receptor" title=" epidermal growth factor receptor"> epidermal growth factor receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=target%20molecule" title=" target molecule"> target molecule</a> </p> <a href="https://publications.waset.org/abstracts/27370/a-platform-to-screen-targeting-molecules-of-ligand-egfr-interactions" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/27370.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">433</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">483</span> Analysis of NMDA Receptor 2B Subunit Gene (GRIN2B) mRNA Expression in the Peripheral Blood Mononuclear Cells of Alzheimer's Disease Patients</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ali%CC%87%20Bayram">Ali̇ Bayram</a>, <a href="https://publications.waset.org/abstracts/search?q=Semih%20Dalkilic"> Semih Dalkilic</a>, <a href="https://publications.waset.org/abstracts/search?q=Remzi%20Yigiter"> Remzi Yigiter</a> </p> <p class="card-text"><strong>Abstract:</strong></p> N-methyl-D-aspartate (NMDA) receptor is a subtype of glutamate receptor and plays a pivotal role in learning, memory, neuronal plasticity, neurotoxicity and synaptic mechanisms. Animal experiments were suggested that glutamate-induced excitotoxic injuriy and NMDA receptor blockage lead to amnesia and other neurodegenerative diseases including Alzheimer’s disease (AD), Huntington’s disease, amyotrophic lateral sclerosis. Aim of this study is to investigate association between NMDA receptor coding gene GRIN2B expression level and Alzheimer disease. The study was approved by the local ethics committees, and it was conducted according to the principles of the Declaration of Helsinki and guidelines for the Good Clinical Practice. Peripheral blood was collected 50 patients who diagnosed AD and 49 healthy control individuals. Total RNA was isolated with RNeasy midi kit (Qiagen) according to manufacturer’s instructions. After checked RNA quality and quantity with spectrophotometer, GRIN2B expression levels were detected by quantitative real time PCR (QRT-PCR). Statistical analyses were performed, variance between two groups were compared with Mann Whitney U test in GraphpadInstat algorithm with 95 % confidence interval and p < 0.05. After statistical analyses, we have determined that GRIN2B expression levels were down regulated in AD patients group with respect to control group. But expression level of this gene in each group was showed high variability. İn this study, we have determined that NMDA receptor coding gene GRIN2B expression level was down regulated in AD patients when compared with healthy control individuals. According to our results, we have speculated that GRIN2B expression level was associated with AD. But it is necessary to validate these results with bigger sample size. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Alzheimer%E2%80%99s%20disease" title="Alzheimer’s disease">Alzheimer’s disease</a>, <a href="https://publications.waset.org/abstracts/search?q=N-methyl-d-aspartate%20receptor" title=" N-methyl-d-aspartate receptor"> N-methyl-d-aspartate receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=NR2B" title=" NR2B"> NR2B</a>, <a href="https://publications.waset.org/abstracts/search?q=GRIN2B" title=" GRIN2B"> GRIN2B</a>, <a href="https://publications.waset.org/abstracts/search?q=mRNA%20expression" title=" mRNA expression"> mRNA expression</a>, <a href="https://publications.waset.org/abstracts/search?q=RT-PCR" title=" RT-PCR"> RT-PCR</a> </p> <a href="https://publications.waset.org/abstracts/35375/analysis-of-nmda-receptor-2b-subunit-gene-grin2b-mrna-expression-in-the-peripheral-blood-mononuclear-cells-of-alzheimers-disease-patients" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/35375.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">394</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">482</span> Expression of Interferon-Lambda Receptor-(IFN-λRα) in Mononuclear Phagocyte Cells (MPCs) Is Influenced by the Levels of Newly Discovered Type III IFN-λ4 in Vitro</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hashaam%20Akhtar">Hashaam Akhtar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> IFNλR1 and IL10R2 collectively construct a heterodimer, which is an acknowledged functional receptor for all type III interferons (IFNs). Expression of IFNλR1 is highly tissue specific, which can help in making type III IFNs a drug of choice as comparable to its analogue, type I IFNs, for treating hepatitis C in the near future. Although, expression of IFNλR1 also varies with the concentration of type I IFNs, but in this study it was shown that the expression of IFNλR1 varies with the protein titers of IFN-α, IFN-λ3 and the newly discovered IFN-λ4. High dosage of IFN-α reduces the expression of IFNλR1 in HepG2 cells, which can affect the antiviral activity of type III IFNs in vivo. We premeditated an experimental strategy to differentiate monocytes into dendritic cells (DCs), type I and type II macrophages in vitro and quantified the expression of the IFNλR1 by qPCR. The exposure of newly discovered IFN-λ4 to macrophages and DCs also raised the expression of its own receptor, which shows that expression of IFN-λ4 protein in hepatitis C patient may augment type I treatment and help ease off viral titers. The results of this study may contribute in some understanding towards the mechanisms involved in the selective expression of IFNLR1 and exceptionalities associated with the receptor. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=IFNLR1" title="IFNLR1">IFNLR1</a>, <a href="https://publications.waset.org/abstracts/search?q=Interferon%20Lambda%204%20%28IFN-%CE%BB4%29" title=" Interferon Lambda 4 (IFN-λ4)"> Interferon Lambda 4 (IFN-λ4)</a>, <a href="https://publications.waset.org/abstracts/search?q=Mononuclear%20Phagocyte%20Cells%20%28MPCs%29" title=" Mononuclear Phagocyte Cells (MPCs)"> Mononuclear Phagocyte Cells (MPCs)</a>, <a href="https://publications.waset.org/abstracts/search?q=expression" title=" expression"> expression</a> </p> <a href="https://publications.waset.org/abstracts/17385/expression-of-interferon-lambda-receptor-ifn-lra-in-mononuclear-phagocyte-cells-mpcs-is-influenced-by-the-levels-of-newly-discovered-type-iii-ifn-l4-in-vitro" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17385.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">385</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">481</span> A Theoretical to Conceptual Paper: The Use of Phosphodiesterase Inhibitors, Endothelin Receptor Antagonists and/or Prostacyclin Analogs in Acute Pulmonary Embolism</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ryan%20M.%20Monti">Ryan M. Monti</a>, <a href="https://publications.waset.org/abstracts/search?q=Bijal%20Mehta"> Bijal Mehta</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In cases of massive pulmonary embolism, defined as acute pulmonary embolism presenting with systemic hypotension or right ventricular dysfunction and impending failure, there is indication that unconventional therapies, such as phosphodiesterase inhibitors, endothelin receptor antagonists, and/or prostacyclin analogs may decrease the morbidity and mortality. Based on the premise that dilating the pulmonary artery will decrease the pulmonary vascular pressure, while simultaneously decreasing the aggregation of platelets, it can be hypothesized that increased blood flow through the pulmonary artery will decrease right heart strain and subsequent morbidity and mortality. While this theory has yet to be formally studied, the recommendations for treating massive pulmonary embolism with phosphodiesterase inhibitors, endothelin receptor antagonists, and/or prostacyclin analogs in conjunction with the current standards of care in massive pulmonary embolism should be formally studied. In particular, patients with massive PE who are unable to undergo thrombolysis/surgical intervention may be the ideal population to study the use of these treatments to determine any decrease in mortality and morbidity (short term and long term). <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20pulmonary%20thromboembolism" title="acute pulmonary thromboembolism">acute pulmonary thromboembolism</a>, <a href="https://publications.waset.org/abstracts/search?q=treatment%20of%20pulmonary%20embolism" title=" treatment of pulmonary embolism"> treatment of pulmonary embolism</a>, <a href="https://publications.waset.org/abstracts/search?q=use%20of%20phosphodiesterase%20inhibitors" title=" use of phosphodiesterase inhibitors"> use of phosphodiesterase inhibitors</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelin%20receptor%20antagonists" title=" endothelin receptor antagonists"> endothelin receptor antagonists</a>, <a href="https://publications.waset.org/abstracts/search?q=prostacyclin%20analogs%20in%20PE" title=" prostacyclin analogs in PE"> prostacyclin analogs in PE</a> </p> <a href="https://publications.waset.org/abstracts/49295/a-theoretical-to-conceptual-paper-the-use-of-phosphodiesterase-inhibitors-endothelin-receptor-antagonists-andor-prostacyclin-analogs-in-acute-pulmonary-embolism" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/49295.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">225</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">480</span> Sub-Chronic Exposure to Dexamethasone Impairs Cognitive Function and Insulin in Prefrontal Cortex of Male Wistar Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=A.%20Alli-Oluwafuyi">A. Alli-Oluwafuyi</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20Amin"> A. Amin</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20M.%20Fii"> S. M. Fii</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20O.%20Amusa"> S. O. Amusa</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20Imam"> A. Imam</a>, <a href="https://publications.waset.org/abstracts/search?q=N.%20T.%20Asogwa"> N. T. Asogwa</a>, <a href="https://publications.waset.org/abstracts/search?q=W.%20I.%20Abdulmajeed"> W. I. Abdulmajeed</a>, <a href="https://publications.waset.org/abstracts/search?q=F.%20Olaseinde"> F. Olaseinde</a>, <a href="https://publications.waset.org/abstracts/search?q=B.%20V.%20Owoyele"> B. V. Owoyele </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Chronic stress or prolonged glucocorticoid administration impairs higher cognitive functions in rodents and humans. However, the mechanisms are not fully clear. Insulin and receptors are expressed in the brain and are involved in cognition. Insulin resistance accompanies Alzheimer’s disease and associated cognitive decline. The goal of this study was to evaluate the effects of sub-chronic administration of a glucocorticoid, dexamethasone (DEX) on behavior and biochemical changes in prefrontal cortex (PFC). Male Wistar rats were administered DEX (2, 4 & 8 mg/kg, IP) or saline for seven consecutive days and behavior was assessed in the following paradigms: “Y” maze, elevated plus maze, Morris’ water maze and novel object recognition (NOR) tests. Insulin, lactate dehydrogenase (LDH) and Superoxide Dismutase (SOD) activity were evaluated in homogenates of the prefrontal cortex. DEX-treated rats exhibited impaired prefrontal cortex function manifesting as reduced locomotion, impaired novel object exploration and impaired short- and long-term spatial memory compared to normal controls (p < 0.05). These effects were not consistently dose-dependent. These behavioral alterations were accompanied by a decrease in insulin concentration observed in PFC of 4 mg/kg DEX-treated rats compared to control (10μIU/mg vs. 50μIU/mg; p < 0.05) but not 2mg/kg. Furthermore, we report a modification of brain stress markers LDH and SOD (p > 0.05). These results indicate that prolonged activation of GCs disrupt prefrontal cortex function which may be related to insulin impairment. These effects may not be attributable to a non-specific elevation of oxidative stress in the brain. Future studies would evaluate mechanisms of GR-induced insulin loss. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=dexamethasone" title="dexamethasone">dexamethasone</a>, <a href="https://publications.waset.org/abstracts/search?q=insulin" title=" insulin"> insulin</a>, <a href="https://publications.waset.org/abstracts/search?q=memory" title=" memory"> memory</a>, <a href="https://publications.waset.org/abstracts/search?q=prefrontal%20cortex" title=" prefrontal cortex"> prefrontal cortex</a> </p> <a href="https://publications.waset.org/abstracts/71933/sub-chronic-exposure-to-dexamethasone-impairs-cognitive-function-and-insulin-in-prefrontal-cortex-of-male-wistar-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/71933.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">284</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">479</span> Inhibitory Effects of PPARγ Ligand, KR-62980, on Collagen-Stimulated Platelet Activation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Su%20Bin%20Wang">Su Bin Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Jin%20Hee%20Ahn"> Jin Hee Ahn</a>, <a href="https://publications.waset.org/abstracts/search?q=Tong-Shin%20Chang"> Tong-Shin Chang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The peroxisome proliferator-activated receptors (PPARs) are member of nuclear receptor superfamily that act as a ligand-activated transcription factors. Although platelets lack a nucleus, previous studies have shown that PPARγ agonists, rosiglitazone, inhibited platelet activation induced by collagen. In this study, we investigated the inhibitory effects of KR-62980, a newly synthesized PPARγ agonist, on collagen receptor-stimulated platelet activation. The specific tyrosine phosphorylations of key components (Syk, Vav1, Btk and PLCγ2) for collagen receptor signaling pathways were suppressed by KR-62980. KR-62980 also attenuated downstream responses including cytosolic calcium elevation, P-selectin surface exposure, and integrin αIIbβ3 activation. PPARγ was found to associate with multiple proteins within the LAT signaling complex in collagen-stimulated platelets. This association was prevented by KR-62980, indicating a potential mechanism for PPARγ function in collagen-stimulated platelet activation. Furthermore, KR-62980 inhibited platelet aggregation and adhesion in response to collagen in vitro and prolonged in vivo thrombotic response in carotid arteries of mice. Collectively, these data suggest that KR-62980 inhibits collagen-stimulated platelet activation and thrombus formation through modulating the collagen receptor signaling pathways. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=KR-62980" title="KR-62980">KR-62980</a>, <a href="https://publications.waset.org/abstracts/search?q=PPAR%CE%B3" title=" PPARγ"> PPARγ</a>, <a href="https://publications.waset.org/abstracts/search?q=antiplatelet" title=" antiplatelet"> antiplatelet</a>, <a href="https://publications.waset.org/abstracts/search?q=thrombosis" title=" thrombosis"> thrombosis</a> </p> <a href="https://publications.waset.org/abstracts/47842/inhibitory-effects-of-ppargh-ligand-kr-62980-on-collagen-stimulated-platelet-activation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/47842.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">334</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=glucocorticoid%20receptor&page=6">6</a></li> <li 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