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1. Extreme desert dust storms and COPD morbidity on the island of Crete

Author

Lorentzou C, Kouvarakis G, Kozyrakis GV, Kampanis NA, Trahanatzi I, Fraidakis O, Tzanakis N, Kanakidou M, Agouridakis P, and Notas G

Subjects
Desert dust storms, Emergency Department overcrowding, Particulate matter, COPD, Diseases of the respiratory system, RC705-779
Abstract

Christina Lorentzou,1 Giorgos Kouvarakis,2 Georgios V Kozyrakis,3 Nikolaos A Kampanis,3 Irene Trahanatzi,4 Othon Fraidakis,4 Nikolaos Tzanakis,5 Maria Kanakidou,2 Panagiotis Agouridakis,1 George Notas1,31University of Crete, School of Medicine, University Hospital, Department of Emergency Medicine, Heraklion, Greece; 2Department of Chemistry, Environmental Chemical Processes Laboratory, University of Crete, Heraklion, Greece; 3Foundation for Research and Technology - Hellas (FORTH), Institute of Applied and Computational Mathematics, Coastal and Marine Research Lab, Heraklion, Greece; 4Venizeleion Hospital of Heraklion, Department of Emergency Medicine, Heraklion, Greece; 5University of Crete, School of Medicine, University Hospital, Department of Pulmonary Medicine, Heraklion, GreeceIntroduction and objectives: Short-term extreme increases in desert-derived particulate-matter with aerodynamic diameter below 10 μm (PM10) may affect emergency department (ED) visits due to COPD exacerbations.Research question: Our aim was to identify the effect of extreme increases in desert-derived PM10 on ED visits for dyspnea and COPD exacerbations and on the related hospital admissions.Methods: We performed a retrospective analysis of dyspnea-related ED visits and hospital admissions in Heraklion, Crete, during four consecutive storms of desert-derived PM10 that happened during March 2018. We collected data from over 17,000 ED visits and recorded patients with atopic symptoms, COPD exacerbations, and dyspnea, as well as admissions to the departments of pulmonary medicine, internal medicine, and cardiology. PM10 data were collected from a monitoring station in the same geographic area.Results: Four desert dust storms were recorded during the study period with 238, 203, 1138, and 310 μg/m3 average-daily PM10 and 652, 308, 4262, and 778 μg/m3 hourly mean day-peak PM10, respectively. There was no clinically important increase in total ED visits, total admissions or admissions to the departments of cardiology, pulmonary medicine, or internal medicine, during PM10 peaks. However, during the desert dust storm with daily-average PM10 above 500 μg/m,3 there was a striking increase in dyspnea-related ED visits (including COPD exacerbations, 3.6-fold increase), while there was no clinically important increase in non-asthma allergy-related ED visits.Conclusion: Extreme desert dust storm episodes may cause meaningful increases in ED visits for dyspnea and COPD exacerbations/admissions.Keywords: desert dust storms, emergency department overcrowding, particulate-matter, COPD

Published
2019

2. A Technological Platform to Support Education in Regional Anaesthesia with Patient-Specific Virtual Physiological Human (VPH)-Based Models

Author

Christodoulakis, Georgios, Marias, K., Notas, G., Kampanis, N., Sfakianakis, S., Magjarevic, Ratko, Editor-in-chief, Ładyżyński, Piotr, Series editor, Ibrahim, Fatimah, Series editor, Lacković, Igor, Series editor, Rock, Emilio Sacristan, Series editor, Kyriacou, Efthyvoulos, editor, Christofides, Stelios, editor, and Pattichis, Constantinos S., editor

Published
2016
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3. Polyphenols and cancer cell growth

Author

Kampa, M., Nifli, A.-P., Notas, G., Castanas, E., Amara, S.G., editor, Bamberg, E., editor, Fleischmann, B., editor, Gudermann, T., editor, Hebert, S.C., editor, Jahn, R., editor, Lederer, W.J., editor, Lill, R., editor, Miyajima, A., editor, Offermanns, S., editor, and Zechner, R., editor

Published
2007
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9. Understanding the interplay between COX-2 and hTERT in colorectal cancer using a multi-omics analysis

Author

Ayiomamitis, G.D. Notas, G. Vasilakaki, T. Tsavari, A. Vederaki, S. Theodosopoulos, T. Kouroumalis, E. Zaravinos, A.

Abstract

Background: Cyclooxygenase 2 (COX-2) is involved in the initial steps of colorectal cancer (CRC) formation, playing a key role in the catalysis of arachidonic acid to prostaglandin E2 (PGE2). The human telomerase reverse transcriptase (hTERT or TERT) also plays an important role in colorectal cancer growth, conferring sustained cell proliferation and survival. Although hTERT induces COX-2 expression in gastric and cervical cancer, their interaction has not been investigated in the context of CRC. Methods: COX-2, PGE2 levels, and telomerase activity were evaluated by immunohistochemistry, ELISA, and TRAP assay in 49 colorectal cancer samples. PTGS1, PTGS2, PTGES3, TERT mRNA, and protein levels were investigated using RNA-seq and antibody-based protein profiling data from the TCGA and HPA projects. A multi-omics comparison was performed between PTGS2 and TERT, using RNAseq, DNA methylation, copy number variations (CNVs), single nucleotide polymorphisms (SNPs), and insertions/deletions (Indels) data. Results: COX-2 expression was positive in 40/49 CRCs, bearing cytoplasmic and heterogeneous staining, from moderate to high intensity. COX-2 staining was mainly detected in the stroma of the tumor cells and the adjacent normal tissues. PGE2 expression was lower in CRC compared to the adjacent normal tissue, and inversely correlated to telomerase activity in right colon cancers. COX-1 and COX-2 were anticorrelated with TERT. Isoform structural analysis revealed the most prevalent transcripts driving the differential expression of PTGS1, PTGS2, PTGES3, and TERT in CRC. COX-2 expression was significantly higher among B-Raf proto-oncogene, serine/threonine kinase, mutant (BRAFmut) tumors. Kirsten ras oncogene (KRAS) mutations did not affect COX-2 or TERT expression. The promoter regions of COX-2 and TERT were reversely methylated. Conclusions: Our data support that COX-2 is involved in the early stages of colorectal cancer development, initially affecting the tumor’s stromal microenvironment, and, subsequently, the epithelial cells. They also highlight an inverse correlation between COX-2 expression and telomerase activity in CRC, as well as differentially methylated patterns within the promoter regions of COX-2 and TERT. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.

Published
2019

18. Estrogen anti-inflammatory activity on human monocytes is mediated through cross-talk between estrogen receptor ERα36 and GPR30/GPER1

Author

Pelekanou, V. Kampa, M. Kiagiadaki, F. Deli, A. Theodoropoulos, P. Agrogiannis, G. Patsouris, E. Tsapis, A. Castanas, E. Notas, G.

Subjects
hormones, hormone substitutes, and hormone antagonists
Abstract

Estrogens are known modulators of monocyte/macrophage functions; however, the underlying mechanism has not been clearly defined. Recently, a number of estrogen receptor molecules and splice variants were identified that exert different and sometimes opposing actions. We assessed the expression of estrogen receptors and explored their role in mediating estrogenic anti-inflammatory effects on human primary monocytes. We report that the only estrogen receptors expressed are estrogen receptor-α 36-kDa splice variant and G-protein coupled receptor 30/G-protein estrogen receptor 1, in a sex-independent manner. 17-β-Estradiol inhibits the LPS-induced IL-6 inflammatory response, resulting in inhibition of NF-κB transcriptional activity. This is achieved via a direct physical interaction of ligand-activated estrogen receptor-α 36-kDa splice variant with the p65 component of NF-κB in the nucleus. G-protein coupled receptor 30/G-protein estrogen receptor 1, which also physically interacts with estrogen receptor-α 36-kDa splice variant, acts a coregulator in this process, because its inhibition blocks the effect of estrogens on IL-6 expression. However, its activation does not mimic the effect of estrogens, on neither IL-6 nor NF-κB activity. Finally, we show that the estrogen receptor profile observed in monocytes is not modified during their differentiation to macrophages or dendritic cells in vitro and is shared in vivo by macrophages present in atherosclerotic plaques. These results position estrogen receptor-α 36-kDa splice variant and G-protein coupled receptor 30 as important players and potential therapeutic targets in monocyte/macrophage-dependent inflammatory processes. © Society for Leukocyte Biology.

Published
2016

20. 2009: ERa17p, a peptide corresponding to the regulatory platform P295-T311 of ER-alpha: role in apotosis

Author

Pelekanou, V., Kampa, Marilena, Notas, G., Jacquot, Y., Castanas, E., Leclercq, G., Perron, Nicolas, Laboratory of Experimental Endocrinology, University of Crete [Heraklion] (UOC), Université Pierre et Marie Curie - Paris 6 (UPMC), Synthèse, Structure et Fonction de Molécules Bioactives (SSFMB), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Laboratoire J.-C. Heuson de Recherche Translationnelle en Cancérologie Mammaire [Brussels] (BCTL), Institut Jules Bordet [Bruxelles], Faculté de Médecine [Bruxelles] (ULB), Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB)-Faculté de Médecine [Bruxelles] (ULB), and Université libre de Bruxelles (ULB)-Université libre de Bruxelles (ULB)

Subjects
[CHIM.ORGA]Chemical Sciences/Organic chemistry, [CHIM.ORGA] Chemical Sciences/Organic chemistry
Published
2009

42. Polyphenols and cancer cell growth.

Author

Kampa, M., Nifli, A.-P., Notas, G., and Castanas, E.

Abstract

Polyphenols constitute an important group of phytochemicals that gained increased research attention since it was found that they could affect cancer cell growth. Initial evidence came from epidemiologic studies suggesting that a diet that includes regular consumption of fruits and vegetables (rich in polyphenols) significantly reduces the risk of many cancers. In the present work we briefly review the effects of polyphenols on cancer cell fate, leading towards growth, differentiation and apoptosis. Their action can be attributed not only to their ability to act as antioxidants but also to their ability to interact with basic cellular mechanisms. Such interactions include interference with membrane and intracellular receptors, modulation of signaling cascades, interaction with the basic enzymes involved in tumor promotion and metastasis, interaction with oncogenes and oncoproteins, and, finally, direct or indirect interactions with nucleic acids and nucleoproteins. These actions involve almost the whole spectrum of basic cellular machinery—from the cell membrane to signaling cytoplasmic molecules and to the major nuclear components—and provide insights into their beneficial health effects. In addition, the actions justify the scientific interest in this class of compounds, and provide clues about their possible pharmaceutical exploitation in the field of oncology. [ABSTRACT FROM AUTHOR]

Published
2008
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46. κ-opioids induce a reversible inhibition of CFU-GM from CD133 + cord blood cells.

Author

Dimitriou, H, Bakogeorgou, E, Kampa, M, Notas, G, Stiakaki, E, Kouroumalis, E, Kalmanti, M, and Castanas, E

Subjects
CANCER cells, HEMATOPOIETIC system, OPIOIDS, IMMUNOPHENOTYPING, SOMATOSTATIN
Abstract

Background Opioid agonists have been shown to exert an inhibitory action on a number of malignant and non-malignant cell types. However, there are no reports dealing with their effect on hemopoietic progenitors. Based upon our previous experience of opioid agonists we examined whether opioids could interfere with the growth of CFU-GM from CD133 + cord blood cells. Methods Cord blood samples were subjected to CD133 + column selection, with subsequent exposure to opioid agonists and antagonists or both, in semi-solid cultures for CFU-GM growth. Colonies of day 7 of culture were replated in fresh medium in the absence of opioids. The colonies were evaluated at 7 and 14 days of culture. RT-PCR was performed for the detection of opioid and somatostatin receptors. Apoptosis tests and immunophenotypic evaluations were employed in liquid cultures in conditions identical to those of the semi-solid ones. Results and discussion Our results suggest that opioids can induce a significant inhibition of CFU-GM growth, which is reversible and not mediated through opioid or somatostatin receptors, while apoptosis is not implicated. Whether this finding could be used for clinical intervention remains to be examined. [ABSTRACT FROM AUTHOR]

Published
2006
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50. Membrane initiated estrogen actions on the cytoskeleton.

Author

Kampa, M., Pelekanou, V., Notas, G., and Castanas, E.

Subjects
ESTROGEN, KINASES, ESTRADIOL
Abstract

During the last decade our knowledge on estrogen action has been highly enriched by new data on their ability to exert rapid effects that are initiated at the membrane and activate a number of membrane related kinases and subsequently modify intracellular signaling cascades. One of the major targets of membrane initiated action of estradiol in a variety of cell types is actin cytoskeleton. Cytoskeletal modifications are of great importance since they can lead to changes in a wide range of cellular functions. More specifically estradiol has been shown to induce endothelial remodeling (Simoncini et al, 2006), axonal growth (Sanchez et al, 2009) and modulate cell migration of both normal (e.g. endometrial stromal cells) (Flamini et al, 2011) and cancerous (e.g. breast cancer cells) (Kampa et al, 2008, Sanchez et al, 2010) cells. Indeed in breast cancer, estrogens have been reported to induce actin cytoskeleton redistribution that favors cell migration which is required for cancer cell invasion and metastasis. Their action occurs through membrane estrogen receptors that trigger specific signaling events, involving G proteins, small GTPases, src, FAK, cdc42 and N-WASP. Even though the nature of membrane estrogen receptor has not been fully elucidated, it has been shown both biochemically (Sanchez et al, 2010) and verified by our group by a transcriptome analysis that the membrane receptor involved in this cytoskeletal action is ERα (Kampa et al, 2012). Interestingly, this is not the only role for ERα, which has in its sequence an interesting motif (P295-T311) that is located between the D- (hinge) and E- (Ligand Binding Domain) regions, in the autonomous activation function AF-2a, and is considered as an important platform for various post-translational modifications and calmodulin binding. In fact a peptide corresponding to this motif (ERα17p) that could be liberated after the proteosomal degradation of ERα, we have equally found to induce rapid actin cytoskeleton re-arrangements and affect cell migration independently of the presence of ERα (Kampa et al, 2011) . This finding is very interesting since ERα bearing cells can affect the migration of ER negative cells and modulate one of the major problems of breast cancer, metastasis. [ABSTRACT FROM AUTHOR]

Published
2013

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