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Journal articles on the topic 'EBAG9'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Rüder, Constantin, Tatiana Reimer, Ignacio Delgado-Martinez, Ricardo Hermosilla, Arne Engelsberg, Ralf Nehring, Bernd Dörken, and Armin Rehm. "EBAG9 Adds a New Layer of Control on Large Dense-Core Vesicle Exocytosis via Interaction with Snapin." Molecular Biology of the Cell 16, no. 3 (March 2005): 1245–57. http://dx.doi.org/10.1091/mbc.e04-09-0817.

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Regulated exocytosis is subject to several modulatory steps that include phosphorylation events and transient protein–protein interactions. The estrogen receptor-binding fragment-associated gene9 (EBAG9) gene product was recently identified as a modulator of tumor-associated O-linked glycan expression in nonneuronal cells; however, this molecule is expressed physiologically in essentially all mammalian tissues. Particular interest has developed toward this molecule because in some human tumor entities high expression levels correlated with clinical prognosis. To gain insight into the cellular function of EBAG9, we scored for interaction partners by using the yeast two-hybrid system. Here, we demonstrate that EBAG9 interacts with Snapin, which is likely to be a modulator of Synaptotagmin-associated regulated exocytosis. Strengthening of this interaction inhibited regulated secretion of neuropeptide Y from PC12 cells, whereas evoked neurotransmitter release from hippocampal neurons remained unaltered. Mechanistically, EBAG9 decreased phosphorylation of Snapin; subsequently, association of Snapin with synaptosome-associated protein of 25 kDa (SNAP25) and SNAP23 was diminished. We suggest that the occurrence of SNAP23, Snapin, and EBAG9 also in nonneuronal cells might extend the modulatory role of EBAG9 to a broad range of secretory cells. The conjunction between EBAG9 and Snapin adds an additional layer of control on exocytosis processes; in addition, mechanistic evidence is provided that inhibition of phosphorylation has a regulatory function in exocytosis.

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2

Aoki, T., S. Inoue, H. Imamura, J. Fukushima, S. Takahashi, T. Urano, K. Hasegawa, T. Ogushi, Y. Ouchi, and M. Makuuchi. "EBAG9/RCAS1 expression in hepatocellular carcinoma." European Journal of Cancer 39, no. 11 (July 2003): 1552–61. http://dx.doi.org/10.1016/s0959-8049(03)00362-9.

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3

Ikeda, Kazuhiro, Masako Sato, Osamu Tsutsumi, Fujiko Tsuchiya, Michiko Tsuneizumi, Mitsuru Emi, Issei Imoto, Johji Inazawa, Masami Muramatsu, and Satoshi Inoue. "Promoter Analysis and Chromosomal Mapping of Human EBAG9 Gene." Biochemical and Biophysical Research Communications 273, no. 2 (July 2000): 654–60. http://dx.doi.org/10.1006/bbrc.2000.2920.

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4

Takahashi, Satoru, Tomohiko Urano, Fujiko Tsuchiya, Tetsuya Fujimura, Tadaichi Kitamura, Yasuyoshi Ouchi, Masami Muramatsu, and Satoshi Inoue. "EBAG9/RCAS1 expression and its prognostic significance in prostatic cancer." International Journal of Cancer 106, no. 3 (July 1, 2003): 310–15. http://dx.doi.org/10.1002/ijc.11205.

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5

Ogushi, Tetsuo, Takahashi Satoru, Takumi Takeuchi, Tetsuya Fujimura, Tomohiko Urano, Satoshi Inoue, and Tadaichi Kitamura. "655: EBAG9/RCAS1 Expression Enhances Tumor Growth in Renal Cell Carcinoma." Journal of Urology 173, no. 4S (April 2005): 178–79. http://dx.doi.org/10.1016/s0022-5347(18)34895-x.

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6

Kumagai, Jinpei, Tomohiko Urano, Tetsuo Ogushi, Satoru Takahashi, Kuniko Horie-Inoue, Tetsuya Fujimura, Kotaro Azuma, et al. "EBAG9 IS A TUMOR-PROMOTING AND PROGNOSTIC FACTOR FOR BLADDER CANCER." Journal of Urology 181, no. 4S (April 2009): 310. http://dx.doi.org/10.1016/s0022-5347(09)60882-x.

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7

Kumagai, Jinpei, Tomohiko Urano, Tetsuo Ogushi, Satoru Takahashi, Kuniko Horie-Inoue, Tetsuya Fujimura, Kotaro Azuma, et al. "EBAG9 is a tumor-promoting and prognostic factor for bladder cancer." International Journal of Cancer 124, no. 4 (February 15, 2009): 799–805. http://dx.doi.org/10.1002/ijc.23982.

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8

Aoki, T., S. Inoue, H. Imamura, J. Fukushima, T. Urano, K. Hasegawa, and M. Makuuchi. "EBAG9/RCAS1 expression in hepatocellular carcinoma: Correlation with tumor dedifferentiation and proliferation." Journal of Hepatology 38 (April 2003): 74. http://dx.doi.org/10.1016/s0168-8278(03)80308-2.

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9

Suzuki, T., S. Inoue, W. Kawabata, J. Akahira, T. Moriya, F. Tsuchiya, S. Ogawa, M. Muramatsu, and H. Sasano. "EBAG9/RCAS1 in human breast carcinoma: a possible factor in endocrine–immune interactions." British Journal of Cancer 85, no. 11 (November 27, 2001): 1731–37. http://dx.doi.org/10.1054/bjoc.2001.2176.

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10

Akahira, J.-i., M. Aoki, T. Suzuki, T. Moriya, H. Niikura, K. Ito, S. Inoue, K. Okamura, H. Sasano, and N. Yaegashi. "Expression of EBAG9/RCAS1 is associated with advanced disease in human epithelial ovarian cancer." British Journal of Cancer 90, no. 11 (May 26, 2004): 2197–202. http://dx.doi.org/10.1038/sj.bjc.6601832.

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11

Kino, T., and G. P. Chrousos. "Tumor-associated, Estrogen Receptor-related Antigen EBAG9: Linking Intracellular Vesicle Trafficking, Immune Homeostasis, and Malignancy." Molecular Interventions 9, no. 6 (December 1, 2009): 294–98. http://dx.doi.org/10.1124/mi.9.6.4.

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12

Ijichi, Nobuhiro, Takashi Shigekawa, Kazuhiro Ikeda, Toshiaki Miyazaki, Kuniko Horie-Inoue, Chikako Shimizu, Shigehira Saji, et al. "Association of Positive EBAG9 Immunoreactivity With Unfavorable Prognosis in Breast Cancer Patients Treated With Tamoxifen." Clinical Breast Cancer 13, no. 6 (December 2013): 465–70. http://dx.doi.org/10.1016/j.clbc.2013.08.015.

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13

Hong, Xuejun, Yang Liu, Guili Hu, Dekuang Zhao, Jiangen Shen, Fenping Shen, Xuetao Cao, and Qingqing Wang. "EBAG9 inducing hyporesponsiveness of T cells promotes tumor growth and metastasis in 4T1 murine mammary carcinoma." Cancer Science 100, no. 5 (March 24, 2009): 961–69. http://dx.doi.org/10.1111/j.1349-7006.2009.01129.x.

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14

Miyazaki, T., K. Ikeda, K. Horie-Inoue, T. Kondo, S. Takahashi, and S. Inoue. "EBAG9 modulates host immune defense against tumor formation and metastasis by regulating cytotoxic activity of T lymphocytes." Oncogenesis 3, no. 11 (November 2014): e126-e126. http://dx.doi.org/10.1038/oncsis.2014.40.

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15

Wolf, Jana, Tatiana A. Remier, Sebastian Schuck, Constantin Rüder, Kerstin Gerlach, Eva‐Christina Müller, Albrecht Otto, Bernd Dorken, and Armin Rehm. "Role of EBAG9 protein in coat protein complex I‐dependent glycoprotein maturation and secretion processes in tumor cells." FASEB Journal 24, no. 10 (June 22, 2010): 4000–4019. http://dx.doi.org/10.1096/fj.09-153452.

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16

Tsuneizumi, Michiko, Hisaki Nagai, Haruhito Harada, Teruhisa Kazui, and Mitsuu Emi. "A highly polymorphic CA repeat marker at the EBAG9/RCAS1 locus on 8q23 that detected frequent multiplication in breast cancer." Annals of Human Biology 29, no. 4 (January 2002): 457–60. http://dx.doi.org/10.1080/03014460110087762.

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17

Tsuchiya, Fujiko, Kazuhiro Ikeda, Osamu Tsutsumi, Hisahiko Hiroi, Mikio Momoeda, Yuji Taketani, Masami Muramatsu, and Satoshi Inoue. "Molecular Cloning and Characterization of Mouse EBAG9, Homolog of a Human Cancer Associated Surface Antigen: Expression and Regulation by Estrogen." Biochemical and Biophysical Research Communications 284, no. 1 (June 2001): 2–10. http://dx.doi.org/10.1006/bbrc.2001.4892.

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18

Fruhauf, Sebastian, Barbara Novak, Veronika Nagl, Matthias Hackl, Doris Hartinger, Valentina Rainer, Silvia Labudová, et al. "Biotransformation of the Mycotoxin Zearalenone to its Metabolites Hydrolyzed Zearalenone (HZEN) and Decarboxylated Hydrolyzed Zearalenone (DHZEN) Diminishes its Estrogenicity In Vitro and In Vivo." Toxins 11, no. 8 (August 20, 2019): 481. http://dx.doi.org/10.3390/toxins11080481.

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Zearalenone (ZEN)-degrading enzymes are a promising strategy to counteract the negative effects of this mycotoxin in livestock. The reaction products of such enzymes need to be thoroughly characterized before technological application as a feed additive can be envisaged. Here, we evaluated the estrogenic activity of the metabolites hydrolyzed zearalenone (HZEN) and decarboxylated hydrolyzed zearalenone (DHZEN) formed by hydrolysis of ZEN by the zearalenone-lactonase Zhd101p. ZEN, HZEN, and DHZEN were tested in two in vitro models, the MCF-7 cell proliferation assay (0.01–500 nM) and an estrogen-sensitive yeast bioassay (1–10,000 nM). In addition, we compared the impact of dietary ZEN (4.58 mg/kg) and equimolar dietary concentrations of HZEN and DHZEN on reproductive tract morphology as well as uterine mRNA and microRNA expression in female piglets (n = 6, four weeks exposure). While ZEN increased cell proliferation and reporter gene transcription, neither HZEN nor DHZEN elicited an estrogenic response, suggesting that these metabolites are at least 50–10,000 times less estrogenic than ZEN in vitro. In piglets, HZEN and DHZEN did not increase vulva size or uterus weight. Moreover, RNA transcripts altered upon ZEN treatment (EBAG9, miR-135a-5p, miR-187-3p and miR-204-5p) were unaffected by HZEN and DHZEN. Our study shows that both metabolites exhibit markedly reduced estrogenicity in vitro and in vivo, and thus provides an important basis for further evaluation of ZEN-degrading enzymes.

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19

Watanabe, Toru, Satoshi Inoue, Hisahiko Hiroi, Akira Orimo, Hiroyuki Kawashima, and Masami Muramatsu. "Isolation of Estrogen-Responsive Genes with a CpG Island Library." Molecular and Cellular Biology 18, no. 1 (January 1, 1998): 442–49. http://dx.doi.org/10.1128/mcb.18.1.442.

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ABSTRACT In order to isolate novel estrogen-responsive genes, we utilized a CpG island library in which the regulatory regions of genes are enriched. CpG islands were screened for the ability to bind to a recombinant estrogen receptor protein with a genomic binding site (GBS) cloning method. Six CpG islands were selected, and they contained perfect, imperfect, and/or multiple half-palindromic estrogen-responsive elements (EREs). Northern blot analysis of various human cells showed that all these genomic fragments hybridized to specific mRNAs, suggesting that the genes associated with these EREs might be transcribed in human cells. Then cDNAs associated with two of them, EB1 and EB9, were isolated from libraries of human placenta and MCF-7 cells derived from a human breast cancer, respectively. Both transcripts were increased by estrogen in MCF-7 cells. The increase is inhibited by actinomycin D but not by cycloheximide, indicating that no protein synthesis is required for the up-regulation. The cDNA associated with EB1 encodes a 114-amino-acid protein similar to the cytochrome c oxidase subunit VIIa, named COX7RP (cytochromec oxidase subunit VII-related protein). The cDNA associated with EB9 is homologous only to an express sequence tag and was named EBAG9 (estrogen receptor-binding fragment-associated gene 9). The palindromic ERE of EB1 is located in an intron of COX7RP, and that of EB9 is in the 5′ upstream region of the cDNA. Both EREs had significant estrogen-dependent enhancer activities in a chloramphenicol acetyltransferase assay, when they were inserted into the 5′ upstream region of the chicken β-globin promoter. We therefore propose that the CpG-GBS method described here for isolation of the DNA binding site from the CpG island library would be useful for identification of novel target genes of certain transcription factors.

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20

Broussard, Elizabeth Kyungsun, Andrew L. Coveler, Samuel H. Whiting, Rachel Kim, Lauren Rastetter, Ekram Gad, Doreen Higgins, et al. "Characterization of colon cancer–associated antigens that would be key therapeutic targets in the prevention of disease relapse or progression." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 594. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.594.

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594 Background: Colon cancer (CRC) is an immunogenic tumor and adaptive immunity may play a role in inhibiting disease relapse. A vaccine to boost cellular immunity in CRC patients could prevent disease recurrence, but there have been few defined immunogenic proteins identified as vaccine candidates. TVG has shown that overexpressed tumor associated proteins, abundant in the cancer state but expressed at basal levels in normal cells, can be immunogenic. We hypothesized that ideal candidate antigens would be ones already validated as prognostic markers in multivariate analysis. Methods: From a directed literature review we selected antigens based on (1) incidence of expression, (2) independent predictor of poor prognosis or early disease recurrence, and (3) known biologic function in CRC pathogenesis. We identified peptides that were predicted to be high affinity binders across multiple HLA DR alleles. We evaluated immunogenicity of peptides with IFN-g ELISPOT assays in CRC and control patients. We then evaluated the efficacy of vaccination in reducing tumors in the AOM mouse model. We evaluated immunogenicity of peptides with IFN-g ELISPOT assays using vaccinated mice splenocytes. We quantified antigen protein expression in AOM tumors. Results: The eight proteins are: CDC25B, COX-2, EBAG9, EGFR, Fascin-1, IGF-1R, PRL-3 and VCP. For all candidate antigens there was a greater IFN-g response in CRC patients than in controls. Four antigens (COX-2 p<.0001, CDC25B p<.0002, and EGFR p=.01, Fascin-1 p=.05) demonstrated a statistically significant reduction in the development of colon tumors compared to vaccination with adjuvant alone. Conclusions: We conclude that: 1. biologically relevant CRC associated proteins can be identified that are associated with prognosis, 2. epitopes predicted to bind multiple DR alleles, derived from candidate antigens, elicit T cell responses greater in CRC patients than in normal controls, 3. vaccination with peptides derived from four antigens resulted in a statistically significant reduction in the development of colon tumors in a mouse model, and 4. these antigens may represent novel immunologic targets for CRC.

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21

Marquez-Manriquez, Juan Pablo, Pedro Alejandro Lucero-Diaz, Jose Antonio Matute-Briseno, Alejandro Camacho-Hernandez, and Dolores Gallardo-Rincon. "Effect of subcutaneous multipeptide active antigen-specific immunotherapy at lymph nodes and tumor sites on clinical outcomes in progressive tumors." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 2636. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.2636.

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2636 Background: The tumor and lymph nodes (LN) microenvironment clinically speaking are mainly unexplored and there are limited clinical studies of immunotherapeutic approaches manipulating those in progressive cancer patients. The tumor and LN microenvironment offers an opportunity to treat locally with multi-peptide immunotherapy in challenging clinical situations where we can have still a potential safe and effective therapeutic approach using the concept treat locally treat systemically. Methods: N = 11 patients were enrolled after the local IRB ethic committee approved the pilot clinical study number CICS/SS/0035. Previous identified targets such as FAP, b-2-microglobulin, Fascin, RCAS1/EBAG9, Bcl-2, survivin, Sox2, Ape-1, Valosin containing-protein (VCP) and EGFR were analyzed by IHC, Th1 and CD8 long-peptides were predicted, immune assays using PBMCs including tumor microenvironment were performed to detect Granzyme B by ELISPOT, naturally processed epitopes by T-cell expansion and cytokines. Patients were treated subcutaneously (S.C.) eight times in the axillary and inguinal LN area one week apart. Afterwards we treated S.C. as well but now in the areas with tumor activity according with the CT or PET every week 10 times. Initial DTH and at the end of the treatment was performed. Pathological, clinical and immunological correlations were made using multivariate analysis. Results: Despite progressive disease 100% of the patients responded to the treatment. 80% had CR and 20% pseudo-progression and then CR. 100% of the patients increased the levels of Granzyme B against Bcl-2 (p = 0.001), VCP (p = 0.0001), Ape-1 (p = 0.005) and RCAS1 (P = 0.0001) and this correlated with the scans post-treatment. The patients showed more CD8 infiltration in the DTH test at the tumor site (p = 0.002) than in the non-tumor site (p = 0.01). The number of metastatic lesions in lungs (p = 0.004) and hepatic tissue (p = 0.001) disappeared and correlated with increased levels of IL-12 production in vivo. Conclusions: Treating immunologically the LN and the microenvironment of the areas with tumor activity is a feasible and safe approach to limit systemic toxicity and improve the clinical outcomes in patients with progressive cancer including bone sarcoma, epithelial ovarian cancer, PDAC, pediatric sarcomas and TNBC.

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22

Marquez-Manriquez, Juan Pablo, Alejandro Camacho-Hernandez, Pedro Alejandro Lucero-Diaz, Dolores Gallardo-Rincon, Martin Orlando Rosas-Delgado, Karla Ramirez Barron, Alberto Durazo, Jorge Alberto Cisneros Ruiz, Diana Karen Meneses-Velazquez, and Alberto Durazo-Acuna. "Multipeptide vaccine to prevent epithelial ovarian cancer relapse by microenvironment immunomodulation." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e15268-e15268. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e15268.

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e15268 Background: Typically cancer vaccines for relapse prevention in epithelial ovarian cancer (EOC) are administrated in distant anatomical sites away from the primary tumor location. Ideally for EOC relapse prevention vaccines we should explore different anatomical sites related with the original tumor location and nearby lymph nodes, in order to observe if the administration would have better clinical impact due to a potential access to the tumor microenvironment. Moreover most trials for EOC relapse prevention use one or few targets and is mainly unknown if they are relevant to promote EOC relapse. We treated EOC patients with a multi-peptide vaccine administered in lymph nodes (LN) and in the peritoneum area and were able to suppress cancer relapse with not significant adverse effects after eight years. Methods: We enrolled n = 25 EOC patients in our study and identified by systematic review and validated by siRNA six proteins involved in EOC relapse and fourteen peptides were predicted. Twelve peptides were immunogenic by Granzyme B ELISPOT, DTH and ELISA. Patients were immunized with the vaccine in axillary and inguinal LN subcutaneously every week for four weeks, every two-weeks four times and finally every month for a total of thirty-six months. Clinical and laboratory evaluations were performed every 2-months and at the end of the study. Results: 100% of the patients developed both antibodies against all the peptides by ELISA and CD8 specific cells. The peptides of the six proteins were able to induce T cell expansion in both peptides and purified protein (p = 0.0001) and (p = 0.05), respectively for Ape-1. The selected targets were all able to induce DTH and ELISA responses with statistical significance. Peptides predicted from Bcl-2, survivin, Ape-1, Sox2, EGFR and RCAS1/EBAG9 were able to increase and sustain the levels of Granzyme B ELISPOT. Bcl-2 A peptide (p = 0.001), Bcl-2 B (p = 0.005), Bcl-2 C (p.0002), survivin A (p = 0.001), Survivin C (0.05), Ape-1 A (0.0001), Ape-1 D (p = 0.001), Sox2 A (p = 0.003), Sox2 B (p = 0.0001), EGFR B (p = 0.0001) and EGFR D (p = 0.001). Conclusions: Treating EOC patients in remission in zones hardly explored previously in order to potentially improve the activation of antigen-specific Th1 and CD8 cells with specific peptides seems promising as a feasible and safe approach to prevent EOC relapse.

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23

Pumphrey, Graham M., and Eugene L. Madsen. "Field-Based Stable Isotope Probing Reveals the Identities of Benzoic Acid-Metabolizing Microorganisms and Their In Situ Growth in Agricultural Soil." Applied and Environmental Microbiology 74, no. 13 (May 9, 2008): 4111–18. http://dx.doi.org/10.1128/aem.00464-08.

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ABSTRACT We used a combination of stable isotope probing (SIP), gas chromatography-mass spectrometry-based respiration, isolation/cultivation, and quantitative PCR procedures to discover the identity and in situ growth of soil microorganisms that metabolize benzoic acid. We added [13C]benzoic acid or [12C]benzoic acid (100 μg) once, four times, or five times at 2-day intervals to agricultural field plots. After monitoring 13CO2 evolution from the benzoic acid-dosed soil, field soils were harvested and used for nucleic acid extraction and for cultivation of benzoate-degrading bacteria. Exposure of soil to benzoate increased the number of culturable benzoate degraders compared to unamended soil, and exposure to benzoate shifted the dominant culturable benzoate degraders from Pseudomonas species to Burkholderia species. Isopycnic separation of heavy [13C]DNA from the unlabeled fraction allowed terminal restriction fragment length polymorphism (T-RFLP) analyses to confirm that distinct 16S rRNA genes were localized in the heavy fraction. Phylogenetic analysis of sequenced 16S rRNA genes revealed a predominance (15 of 58 clones) of Burkholderia species in the heavy fraction. Burkholderia sp. strain EBA09 shared 99.5% 16S rRNA sequence similarity with a group of clones representing the dominant RFLP pattern, and the T-RFLP fragment for strain EBA09 and a clone from that cluster matched the fragment enriched in the [13C]DNA fraction. Growth of the population represented by EBA09 during the field-dosing experiment was demonstrated by using most-probable-number-PCR and primers targeting EBA09 and the closely related species Burkholderia hospita. Thus, the target population identified by SIP not only actively metabolized benzoic acid but reproduced in the field upon the addition of the substrate.

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24

Mejía Cortázar, Marcela Maria, Luis Alejandro Soto Jácquez, and Radhamés Medina. "Prevalencia de retrinoblastoma en pacientes del Hospital Dr. Elías Santana, Santo Domingo, Rep. Dominicana, marzo 2001-Marzo 2003." Ciencia y Sociedad 30, no. 4 (December 1, 2005): 684–701. http://dx.doi.org/10.22206/cys.2005.v30i4.pp684-701.

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El retinoblastoma es una neoplasia intraocular maligna, primaria, que se origina en los retinoblatos inmaduros. Es el tumor maligno intraocular más común en la infancia, con una incidencia de 1 en 15,000 niños. El gen que debe mutar para que se produzca esta patología es el gen RBI. Se realizó un estudio retrospectivo, para determinar la prevalencia de retinoblastoma en el Hospital Dr. Elías Santana donde se estudió una población total de 376 expedientes de pacientes que en el período marzo 2001-marzo 2003, asistieron a quirófano a recibir Examen Bajo Anetesia General (EBAG). De estos 376 expedientes de pacientes se obtuvo una muestra de 10 expedientes que presentaron Retinoblastoma. Se determinó que 3 de cada 100 niños que acudieron al Hospitl Dr. Elías Santana presentaron dicha patología.

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25

Sharma, Manish, Virendra Patel, Jainendra Tiwari, and U. Rajendra Acharya. "Automated Characterization of Cyclic Alternating Pattern Using Wavelet-Based Features and Ensemble Learning Techniques with EEG Signals." Diagnostics 11, no. 8 (July 30, 2021): 1380. http://dx.doi.org/10.3390/diagnostics11081380.

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Sleep is highly essential for maintaining metabolism of the body and mental balance for increased productivity and concentration. Often, sleep is analyzed using macrostructure sleep stages which alone cannot provide information about the functional structure and stability of sleep. The cyclic alternating pattern (CAP) is a physiological recurring electroencephalogram (EEG) activity occurring in the brain during sleep and captures microstructure of the sleep and can be used to identify sleep instability. The CAP can also be associated with various sleep-related pathologies, and can be useful in identifying various sleep disorders. Conventionally, sleep is analyzed using polysomnogram (PSG) in various sleep laboratories by trained physicians and medical practitioners. However, PSG-based manual sleep analysis by trained medical practitioners is onerous, tedious and unfavourable for patients. Hence, a computerized, simple and patient convenient system is highly desirable for monitoring and analysis of sleep. In this study, we have proposed a system for automated identification of CAP phase-A and phase-B. To accomplish the task, we have utilized the openly accessible CAP sleep database. The study is performed using two single-channel EEG modalities and their combination. The model is developed using EEG signals of healthy subjects as well as patients suffering from six different sleep disorders namely nocturnal frontal lobe epilepsy (NFLE), sleep-disordered breathing (SDB), narcolepsy, periodic leg movement disorder (PLM), insomnia and rapid eye movement behavior disorder (RBD) subjects. An optimal orthogonal wavelet filter bank is used to perform the wavelet decomposition and subsequently, entropy and Hjorth parameters are extracted from the decomposed coefficients. The extracted features have been applied to different machine learning algorithms. The best performance is obtained using ensemble of bagged tress (EBagT) classifier. The proposed method has obtained the average classification accuracy of 84%, 83%, 81%, 78%, 77%, 76% and 72% for NFLE, healthy, SDB, narcolepsy, PLM, insomnia and RBD subjects, respectively in discriminating phases A and B using a balanced database. Our developed model yielded an average accuracy of 78% when all 77 subjects including healthy and sleep disordered patients are considered. Our proposed system can assist the sleep specialists in an automated and efficient analysis of sleep using sleep microstructure.

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26

Ménasché, Gaël, and Geneviève de Saint Basile. "EBAG9 tempers lymphocyte killing activity." Journal of Clinical Investigation, July 20, 2009. http://dx.doi.org/10.1172/jci40270.

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27

Faried, Ahmad, and Leri S. Faried. "EBAG9 (Estrogen receptor-binding fragment-associated antigen 9)." Atlas of Genetics and Cytogenetics in Oncology and Haematology, no. 4 (March 2008). http://dx.doi.org/10.4267/2042/15941.

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28

Rüder, Constantin, Uta E. Höpken, Jana Wolf, Hans-Willi Mittrücker, Boris Engels, Bettina Erdmann, Susanne Wollenzin, Wolfgang Uckert, Bernd Dörken, and Armin Rehm. "The tumor-associated antigen EBAG9 negatively regulates the cytolytic capacity of mouse CD8+ T cells." Journal of Clinical Investigation, July 20, 2009. http://dx.doi.org/10.1172/jci37760.

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29

Miyazaki, Toshiaki, Kazuhiro Ikeda, Wataru Sato, Kuniko Horie-Inoue, and Satoshi Inoue. "Extracellular vesicle-mediated EBAG9 transfer from cancer cells to tumor microenvironment promotes immune escape and tumor progression." Oncogenesis 7, no. 1 (January 2018). http://dx.doi.org/10.1038/s41389-017-0022-6.

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30

Reimer, Tatiana A., Ioannis Anagnostopoulos, Bettina Erdmann, Insa Lehmann, Harald Stein, Peter Daniel, Bernd Dörken, and Armin Rehm. "Reevaluation of the 22-1-1 antibody and its putative antigen, EBAG9/RCAS1, as a tumor marker." BMC Cancer 5, no. 1 (May 17, 2005). http://dx.doi.org/10.1186/1471-2407-5-47.

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31

Japanese Journal of Urology 93, no. 2 (2002): 160. http://dx.doi.org/10.5980/jpnjurol.93.160_1.

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Japanese Journal of Urology 94, no. 2 (2003): 370. http://dx.doi.org/10.5980/jpnjurol.94.370_2.

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Japanese Journal of Urology 92, no. 2 (2001): 372. http://dx.doi.org/10.5980/jpnjurol.92.372_1.

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Japanese Journal of Urology 95, no. 2 (2004): 318. http://dx.doi.org/10.5980/jpnjurol.95.318_2.

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Laseter, Timothy M., Elliot Rabinovich, Johnny Rungtusanatham, Todd Lappi, and Ken Heckel. "eBags: Managing Growth." Darden Business Publishing Cases, January 20, 2017, 1–16. http://dx.doi.org/10.1108/case.darden.2016.000101.

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Laseter, Timothy M., W. P. Carey, Elliot Rabinovich, and M. Johnny Rungtusanatham. "eBags: Managing Growth." Darden Business Publishing Cases, July 1, 2005, 1–16. http://dx.doi.org/10.1108/case.darden.2021.000053.

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Japanese Journal of Urology 101, no. 2 (2010): 527. http://dx.doi.org/10.5980/jpnjurol.101.527_4.

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Japanese Journal of Urology 99, no. 2 (2008): 455. http://dx.doi.org/10.5980/jpnjurol.99.455_2.

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