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3 results on '"Maria Lena Skalkam"'

1. Contributors

Author

Amir Hossein Abdolghaffari, Mohammad Abdollahi, Hamid Ahanchian, Farah N. Ahmad, Fariborz Akbarzadeh, Giovanni Alighieri, Amir Amini, Arturo Anadón, Caterina Anania, Bruno Annibale, Mattia Pia Arena, Angela Arena, Irma Arés, Anthoula A. Argyri, Belma Aslim, Selcen Babaoğlu Aydaş, Amirreza Azimi, Antonio O. Ballesteros, Joana Barbosa, Parvin Bastani, Raquel Bedani, Pasqua Betta, Mohammad-Hossein Biglu, Sandra Borges, C. Bucci, Flávia C.A. Buriti, R.M. Camacho-Ruiz, Vittorio Capozzi, Piero Catenazzi, Camilla Celani, Saikiran Chaluvadi, Claude P. Champagne, Claudio Chiesa, Eva H. Clark, Robert J. Collier, Jacopo Colombo, Alejandra de Moreno de LeBlanc, Elisa Carvalho de Morais, M. Dekker, D. Di Venere, Lorenzo Drago, Edward R. Farnworth, Wojciech Feleszko, Lucia Fernandez-Arrojo, J. Fernández-López, Alberto Finamore, Daniela Fiocco, F.J. Gatesoupe, Farnaz Ghasemi-Niri, Valentina Giacchi, Babak Golkhalkhali, A. Gomez-Zavaglia, Maziar Gooshe, Zuhal Gundogdu, Irene Hanning, Seyed Mohammad Bagher Hashemi, Rajkumar Hemalatha, Aziz Homayouni, Arland T. Hotchkiss, P. Iovino, Susana Marta Isay Saad, Mohammad Asghari Jafarabadi, Seyed Ali Jafari, Rosita Jamaluddin, Ji-Kang Jeong, Felicita Jirillo, Emilio Jirillo, Rheinallt M. Jones, Baljinder Kaur, Gaganjot Kaur, Ata K. Keshtiban, Mohammad Khalili, Leyla Khalili, Leila Khalili, Nina Kirmiz, Manoj Kumar, Edith Lahner, P. Lavermicocca, Jean Guy LeBlanc, Eleni Likotrafiti, Ying-Jye Lim, Jody Lingbeck, Paloma López, Mª Luz Mohedano, Thea Magrone, Reza Mahdavi, Davood Maleki, Fatemeh Mallah, Shreesh J. Marathe, Francesco Marotta, María Aránzazu Martínez, O. Martinez-Augustin, María Rosa Martínez-Larrañaga, Elnaz Vaghef Mehrabany, David A. Mills, Mitchel Graham Stover, P. Mobili, Diya Mohammad, Sakineh Mohammad-Alizadeh-Charandabi, S. Mohd Redzwan, Vicente Monedero, Jose M. Moreno Villares, L. Moreno-Vilet, Lee E. Morrow, Masaaki Motoori, Jayasimha N. Murthy, Montserrat Nácher-Vázquez, Ravinder Nagpal, Dennis Sandris Nielsen, Hossein Nikniaz, Leila Nikniaz, Zeinab Nikniaz, Sara Notararigo, Vânia dos Santos Nunes, Rok Orel, Ali Osman, Arthur C. Ouwehand, Lucia Pacifico, Efstathios Z. Panagou, Kun-Young Park, Laleh Payahoo, Ilaria Peluso, J.A. Pérez-Alvarez, Adrian Pérez-Ramos, Francisco J. Plou, Seyedeh Leila Poorbaghi, D.P. Portales-Pérez, Eamonn M.M. Quigley, Fatemeh Ranjbar, Lea Vodušek Reberšak, Jonathan Rhoades, Steven C. Ricke, Barbara Rodriguez-Colinas, Jesús Rodríguez-Díaz, N. Romano, Pasquale Russo, F. Russo, Marek Ruszczyński, Susana M.I. Saad, F. Sánchez de Medina, A. Santonicola, M.E. Sayas-Barberá, Pietro Sciacca, Antonio Scorrano, E. Sendra, Masood Sepehrimanesh, Mauro Serafini, Lynette Pei-Chi Shek, Behjat Shokrvash, A. Sisto, Katia Sivieri, Maria Lena Skalkam, Shu-E Soh, Giuseppe Spano, Keijiro Sugimura, Koji Tanaka, Chrysoula C. Tassou, Paula Teixeira, Julia Tennilä, Marco Toscano, Alok S. Tripathi, E. Tymczyszyn, F. Valerio, Gabriella van Zanten, Paulo José Fortes Villas Boas, Patrick Alexander Wachholz, Ronald Ross Watson, Maria Wiese, Hariom Yadav, Kit L. Yam, Masahiko Yano, Hongliang Zeng, Yi Zhang, Baodong Zheng, Somayeh Ziyadi, and Antonio Alberto Zuppa

Published
2016
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2. In Vitro Screening and Evaluation of Synbiotics

Author

Gabriella Christina van Zanten, Maria Lena Skalkam, Maria Wiese, and Dennis Sandris Nielsen

Subjects
Intestinal cell, biology, Synbiotics, Immunology, Gut flora, biology.organism_classification, Bioinformatics, Beneficial effects, Intervention studies, In vitro
Abstract

Synbiotics, the combination of probiotics and prebiotics, have many proposed beneficial effects. While human intervention studies are the “gold standard,” in vitro models are more simple, cheap, and noninvasive for assessment of synbiotic effects in the gastrointestinal tract (GIT). Numerous in vitro models simulating upper and lower parts of the GIT exist. They have been used for assessment of synbiotics with regard to survival of probiotics and effects on gut microbiota, while intestinal cell lines have been applied to investigate effects of synbiotics on adhesion, barrier function, and genotoxicity resistance. However, the models and methods used are highly variable with regard to a number of parameters, hampering comparability. Future models, simulating the entire GIT, will facilitate a more complete in vitro evaluation of synbiotics, and standardized guidelines should help increase comparability across different studies.

Published
2016
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3. Many putative endocrine disruptors inhibit prostaglandin synthesis

Author

Niels E. Skakkebæk, Jacob B. Hansen, Bernard Jégou, Søren Brunak, David Møbjerg Kristensen, Henrik Leffers, Hanne Frederiksen, Karine Audouze, Maria Lena Skalkam, Laurianne Lesné, Steffen Junker, Christèle Desdoits-Lethimonier, Brébion, Alice, Department of Growth and Reproduction [Rigshospitalet], Rigshospitalet [Copenhagen], Copenhagen University Hospital-Copenhagen University Hospital, Center for Biological Sequence Analysis [Lyngby], Danmarks Tekniske Universitet = Technical University of Denmark (DTU), Groupe d'Etude de la Reproduction Chez l'Homme et les Mammiferes (GERHM), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Biomedical Sciences [Copenhagen], Faculty of Health and Medical Sciences, University of Copenhagen = Københavns Universitet (UCPH)-University of Copenhagen = Københavns Universitet (UCPH), Department of Human Genetics, the European Commission (EU-F7 grants 212844 and 212502), the Villum Kann Rasmussen Foundation, the Novo Nordisk Foundation, INSERM, the Ministère de l'Enseignement Supérieur et de la Recherche, Technical University of Denmark [Lyngby] (DTU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), and University of Copenhagen = Københavns Universitet (KU)-University of Copenhagen = Københavns Universitet (KU)

Subjects
Male, antiandrogens, Health, Toxicology and Mutagenesis, Cell, Endocrine Disruptors, MESH: Dose-Response Relationship, Drug, parabens, benzophenones, prostaglandins, chemistry.chemical_compound, Mice, 0302 clinical medicine, Testis, MESH: Animals, Fatty Acid Synthesis Inhibitors, Mast Cells, Receptor, 0303 health sciences, phthalates, 030219 obstetrics & reproductive medicine, MESH: Testis, Chemistry, MESH: Mast Cells, Transfection, MESH: Endocrine Disruptors, 3. Good health, cyclooxygenase, medicine.anatomical_structure, Endocrine disruptor, Biochemistry, MESH: Cyclooxygenase 2, medicine.symptom, MESH: Rats, PPARs, Prostaglandin, 03 medical and health sciences, medicine, [SDV.EE.SANT] Life Sciences [q-bio]/Ecology, environment/Health, Animals, Humans, Mode of action, MESH: Mice, 030304 developmental biology, [SDV.EE.SANT]Life Sciences [q-bio]/Ecology, environment/Health, MESH: Humans, Dose-Response Relationship, Drug, Research, Public Health, Environmental and Occupational Health, MESH: Male, Rats, Mechanism of action, MESH: Prostaglandins, Cyclooxygenase 2, Prostaglandins, MESH: Fatty Acid Synthesis Inhibitors
Abstract

International audience; BACKGROUND: Prostaglandins (PGs) play key roles in development and maintenance of homeostasis of the adult body. Despite these important roles, it remains unclear whether the PG pathway is a target for endocrine disruption. However, several known endocrine-disrupting compounds (EDCs) share a high degree of structural similarity with mild analgesics. OBJECTIVES AND METHODS: Using cell-based transfection and transduction experiments, mass spectrometry, and organotypic assays together with molecular modeling, we investigated whether inhibition of the PG pathway by known EDCs could be a novel point of endocrine disruption. RESULTS: We found that many known EDCs inhibit the PG pathway in a mouse Sertoli cell line and in human primary mast cells. The EDCs also reduced PG synthesis in ex vivo rat testis, and this reduction was correlated with a reduced testosterone production. The inhibition of PG synthesis occurred without involvement of canonical PG receptors or the peroxisome proliferator-activated receptors (PPARs), which have previously been described as targets of EDCs. Instead, our results suggest that the compounds may bind directly into the active site of the cyclooxygenase (COX) enzymes, thereby obstructing the conversion of arachidonic acid to PG precursors without interfering with the expression of the COX enzymes. A common feature of the PG inhibitory EDCs is the presence of aromatic groups that may stabilize binding in the hydrophobic active site of the COX enzymes. CONCLUSION: Our findings suggest a hitherto unknown mode of action by EDCs through inhibition of the PG pathway and suggest new avenues to investigate effects of EDCs on reproductive and immunological disorders that have become increasingly common in recent decades.

Published
2010
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