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5. BIOACTIVE COMPOUNDS IN HUMAN MILK AND INTESTINAL HEALTH AND MATURITY IN PRETERM NEWBORN: AN OVERVIEW

Author

Garcia C, Rd, Duan, Brévaut-Malaty V, Gire C, Millet V, Simeoni U, Bernard M, Martine ARMAND, Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Gastroenterology and Nutrition Laboratory, Department of Clinical Pathology, Institution of Clinical Sciences, Lund University [Lund]-Lund University [Lund], Service de Néonatologie, Hôpital Nord [CHU - APHM], Hôpital de la Conception [CHU - APHM] (LA CONCEPTION), Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Armand, Martine, Ben Dahan, David, and Hôpital de la Conception [CHU - APHM] (LA CONCEPTION )

Subjects
Macromolecular Substances, [SPI] Engineering Sciences [physics], MUC-1, [SPI]Engineering Sciences [physics], Humans, enteral nutrition, sphingomyelinase, intestine, ComputingMilieux_MISCELLANEOUS, phospholipids, miRNA, milk hormones, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, sphingolipids, necrotizing enterocolitis, Milk, Human, Human milk, Infant, Newborn, lactadherin, cholesterol, sCD14, lactoferrin, Intestines, DHA, [SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, premature newborn, probiotics, Health, Premature Birth, milk growth factors, lipids (amino acids, peptides, and proteins), prebiotics, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, immunological programming, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Premature births are increasing worldwide (about 15 millions per year) due to several reasons (an advanced maternal age, fertility treatments, stress, smoking, nutritional deficiencies) and lead to a high societal overall cost. Among neonatal care procedures, the clinical nutrition practices are essential to promote the development and to minimize the sequelae. Prema-ture newborns are at major risk of death by infections due to the immaturity of their intestine. Human milk provides not only nutrients but also a plethora of biologically active components that are tailored to contribute to the development of the intes-tinal tract early in postnatal life. Among them, some bioactive molecules exhibit trophic effects (LC-PUFA, sphingomyelin, IGF-I and IGF-II, EGF, insulin, leptin, adiponectin, lactoferrin, lactadherin, probiotics, prebiotics, miRNA) or are part of the intestinal cell membranes (PUFA, LC-PUFA, phospholipids, sphingolipids, cholesterol), others educate the intestine for innate microbial recognition (sCD14, sTLR-2, miRNA), many of them display direct fighting against pathogens (some fatty acids and monoglycerides, some phospholipids and sphingolipids, BSSL, insulin, lactoferrin, sIgAs, MUC-1, lactadherin, probiotics, prebiotics), or contribute to establish the gut microbiota (LC-PUFA, lactoferrin, probiotics, prebiotics). A syn-ergetic action exists between several bioactive molecules. All together these precious agents regulate the maturation of the intestinal mucosal barrier, and might program early in postnatal life the future adult intestinal health. This review lists the main bioactive compounds and addresses their plausible roles and mechanisms of action.

Published
2013

6. [Efficacy of early cerebral MR in the detection of brain lesions in high risk preterm infants compared with conventional US]

Author

Vendemmia M, Millet V, Umberto Simeoni, Girard N, Paludetto R, Vendemmia, M, Millet, V, Simeoni, U, Girard, N, and Paludetto, Roberto

Subjects
Male, Brain Diseases, Early Diagnosis, Risk Factors, Infant, Newborn, Humans, Infant, Female, Infant, Premature, Diseases, Magnetic Resonance Imaging, Retrospective Studies, Ultrasonography
Abstract

To identify the efficacy of early cerebral MR, performed in the first month of birth, in the detection of brain lesions in high risk preterm infants, compared with conventional US, we recruited into the study a group of 30 preterm infants born at or below a gestational age of 30 weeks, who had a pathologic scan. The findings on US were compared with those of the early MR scan, performed in the same days, the results of which were considered as the final diagnosis. The value of cranial US as a predictor of MR signal intensity was assessed by calculating sensitivity, specificity, positive and negative predictive values. Agreement between two investigations was evaluated by calculating the K coefficient. US showed 33 haemorrhagic lesions in 25 preterms; MR showed 27 haemorrhagic lesions in 22 infants: in 16 cases MR gave the same results of US. Cranial US was reliable in detecting lesions such as GLH and IVH, but less sensitive in the definition of their size and distribution. Sensitivity of US for haemorrhagic lesions was 96.3%, PPV 78.8%, K coefficient 0.55 (p0.001). About the White Matter, cranial US demonstrated 20 lesions in 20 preterms; MR showed 16 lesions in 16 infants: in 3 cases MR was agree to US. US showed high reliability in the detection of cystic lesions, but significant limitations in the demonstration of non-cystic injury. We founded that normal WM echogenicity on US is not a good predictor of normal WM signal intensity on MR (30%). Sensitivity of US for WM lesions was 81.3%, PPV 65%, K coefficient 0.23 (p = 0.04). Finally US showed 4 lesions in other brain locations, MR confirmed 3 of them and discovered other 10. Sensitivity of US for these lesions was 23.1%, PPV 75%, K coefficient 0.21 (p = 0.11). We founded that cranial US is a good method for detecting GLH, IVH, HPI and severe WM lesions (cystic PVL), but it can miss non-cystic PVL, punctate haemorrhages, WMD and lesions in other brain locations, that, on the other hand, MR detects clearly.

Published
2005

9. Clinical Nephrology - Lab methods and other markers

Author

Kleophas, W., primary, Bieber, B., additional, Robinson, B., additional, Duttlinger, J., additional, Fliser, D., additional, Lonneman, G., additional, Rump, L., additional, Pisoni, R., additional, Port, F., additional, Reichel, H., additional, Daniela, R., additional, Ciocalteu, A., additional, Checherita, I. A., additional, Peride, I., additional, Spataru, D. M., additional, Niculae, A., additional, Laetitia, K., additional, Amna, K., additional, Laurence, D., additional, Aoumeur, H.-A., additional, Flamant, M., additional, Haymann, J.-P., additional, Letavernier, E., additional, Vidal-Petiot, E., additional, Boffa, J.-J., additional, Vrtovsnik, F., additional, Bianco, F., additional, Pessolano, G., additional, Carraro, M., additional, Panzetta, G. O., additional, Ebert, N., additional, Gaedeke, J., additional, Jakob, O., additional, Kuhlmann, M., additional, Martus, P., additional, Van der Giet, M., additional, Scha  ner, E., additional, Khan, I., additional, Law, Y., additional, Turgutalp, K., additional, Ozhan, O., additional, Gok Oguz, E., additional, Kiykim, A., additional, Donadio, C., additional, Hatmi, Z. N., additional, Mahdavi-Mazdeh, M., additional, Morales, E., additional, Gutierrez-Millet, V., additional, Rojas-Rivera, J., additional, Huerta, A., additional, Gutierrez, E., additional, Gutierrez-Solis, E., additional, Polanco, N., additional, Caro, J., additional, Gonza z, E., additional, Praga, M., additional, Marco Mayayo, M., additional, Valdivielso, J., additional, Marti  z, M., additional, Fernaez Giraez, E., additional, Obrador, G., additional, Olvera, N., additional, Ortiz de la Pe, D., additional, Gutie ez, V., additional, Villa, A., additional, Redal-Baigorri, B., additional, Sombolos, K., additional, Tsakiris, D., additional, Boletis, J., additional, Vlahakos, D., additional, Siamopoulos, K., additional, Vargiemezis, V., additional, Nikolaidis, P., additional, Iatrou, C., additional, Dafnis, E., additional, Argyropoulos, C., additional, Xynos, K., additional, Schock-Kusch, D., additional, Shulhevich, Y., additional, Geraci, S., additional, Hesser, J., additional, Stsepankou, D., additional, Neudecker, S., additional, Koenig, S., additional, Hoecklin, F., additional, Pill, J., additional, Gretz, N., additional, Schweda, F., additional, Schreiber, A., additional, Kudo, K., additional, Konta, T., additional, Choi, S. O., additional, Kim, J. S., additional, Kim, M. K., additional, Yang, J. W., additional, Han, B. G., additional, Delanaye, P., additional, Cavalier, E., additional, Masson, I., additional, Mehdi, M., additional, Nicolas, M., additional, Lambermont, B., additional, Dubois, B., additional, Damas, P., additional, Krzesinski, J.-M., additional, Morel, J., additional, Lautrette, A., additional, Christophe, M., additional, Gagneux-Brunon, A., additional, Anne, F., additional, Fre (C)ric, L., additional, Bevc, S., additional, Ekart, R., additional, Hojs, R., additional, Gorenjak, M., additional, Puklavec, L., additional, Hashimoto, N., additional, Suzuki, A., additional, Mitsumoto, K., additional, Shimizu, M., additional, Niihata, K., additional, Kawabata, A., additional, Sakaguchi, Y., additional, Hayashi, T., additional, Shoji, T., additional, Okada, N., additional, Tsubakihara, Y., additional, Hamano, T., additional, Nakano, C., additional, Fujii, N., additional, Obi, Y., additional, Mikami, S., additional, Inoue, K., additional, Matsui, I., additional, Isaka, Y., additional, Rakugi, H., additional, Edvardsson, V., additional, Siguron, B., additional, Thorsteinsdottir, M., additional, Palsson, R., additional, Matsumoto, J., additional, Miyazaki, N., additional, Murata, I., additional, Yoshida, G., additional, Morishita, K., additional, Ushikoshi, H., additional, Nishigaki, K., additional, Ogura, S., additional, Minatoguchi, S., additional, Werneke, U., additional, Ott, M., additional, Salander-Renberg, E., additional, Taylor, D., additional, Stegmayr, B., additional, Surel, S., additional, Wenzlova, M., additional, Silva Junior, G., additional, Vieira, A. P., additional, Couto Bem, A., additional, Alves, M., additional, Torres, A., additional, Meneses, G., additional, Martins, A., additional, Liborio, A., additional, Daher, E., additional, Gluhovschi, G., additional, Modilca, M., additional, Daminescu, L., additional, Gluhovschi, C., additional, Velciov, S., additional, Petrica, L., additional, Gadalean, F., additional, Balgradean, C., additional, Schmeiser, H. H., additional, Kolesnyk, M., additional, Stepanova, N., additional, Surzhko, L., additional, Stashevska, N., additional, Filiopoulos, V., additional, Hadjiyannakos, D., additional, Arvanitis, D., additional, Panagiotopoulos, K., additional, Vlassopoulos, D., additional, Kaesler, N., additional, Schettgen, T., additional, Magdeleyns, E., additional, Brandenburg, V., additional, Vermeer, C., additional, Floege, J., additional, Kr, T., additional, Randone, O., additional, Ferraresi, M., additional, Aroasio, E., additional, Depascale, A., additional, Scognamiglio, S., additional, Consiglio, V., additional, Piccoli, G. B., additional, Jensen, L. V., additional, Lizakowski, S., additional, Rutkowski, P., additional, Tylicki, L., additional, Renke, M., additional, Sulikowska, B., additional, Donderski, R., additional, Bednarski, R., additional, Heleniak, Z., additional, Przybylska, M., additional, Manitius, J., additional, Rutkowski, B., additional, Bobrova, L., additional, Kozlovskaya, N., additional, Kanayama, K., additional, Hasegawa, M., additional, Kitagawa, F., additional, Ishii, J., additional, Yuzawa, Y., additional, Tanaka, K., additional, Sakai, K., additional, Hara, S., additional, Suzuki, Y., additional, Tanaka, Y., additional, Aikawa, A., additional, Hinoshita, F., additional, Hamano, N., additional, Sasaki, E., additional, Kato, A., additional, Katsuki, T., additional, Katsuma, A., additional, Imai, E., additional, Shibata, M., additional, Tada, M., additional, Shimbo, T., additional, Kikuchi, Y., additional, Oka, S., additional, Muramatsu, T., additional, Yanagisawa, N., additional, Fukutake, K., additional, Yamamoto, Y., additional, Ajisawa, A., additional, Tsuchiya, K., additional, Nitta, K., additional, Ando, M., additional, Liang, X., additional, Wang, P., additional, Liu, Z., additional, Zhao, Z., additional, Luyckx, V., additional, Bowker, S., additional, Miekle, A., additional, Toth, E., additional, Heguilen, R., additional, Malvar, A., additional, Hermes, R., additional, Cohen, L., additional, Muguerza, G., additional, Lococo, B., additional, Bernasconi, A., additional, Loboda, O., additional, Dudar, I., additional, Krot, V., additional, Alekseeva, V., additional, Ichinose, M., additional, Sasagawa, N., additional, Toyama, K., additional, Saito, A., additional, Kayamori, Y., additional, Kang, D., additional, Kim, H. W., additional, Yoshioka, K., additional, Hara, M., additional, Ohashi, K., additional, Maksudova, A., additional, Khalfina, T., additional, Cuoghi, A., additional, Bellei, E., additional, Caiazzo, M., additional, Bergamini, S., additional, Palladino, G., additional, Monari, E., additional, Tomasi, A., additional, Loiacono, E., additional, Camilla, R., additional, Dapr, V., additional, Morando, L., additional, Gallo, R., additional, Peruzzi, L., additional, Conrieri, M., additional, Bianciotto, M., additional, Bosetti, F. M., additional, Coppo, R., additional, DI Lullo, L., additional, Floccari, F., additional, Rivera, R., additional, Granata, A., additional, Faiola, R., additional, Feliziani, C., additional, Villani, A., additional, Malaguti, M., additional, Santoboni, A., additional, Kyriaki, K., additional, Droulias, J., additional, Bogdanova, M., additional, Rameev, V. V., additional, Simonyan, A. H., additional, Kozlovskaya, L. V., additional, Altiparmak, M. R., additional, Trabulus, S., additional, Akalin, N., additional, Yalin, A. S., additional, Esenkaya, A., additional, Yalin, S. F., additional, Serdengeae(C), K., additional, Arita, D., additional, Cunha, T., additional, Perez, J., additional, Sakata, M., additional, Arita, L., additional, Nogueira, M., additional, Jara, Z., additional, Souza, N., additional, Casarini, D., additional, Metzger, M., additional, Vallet, M., additional, Karras, A., additional, Froissart, M., additional, Stengel, B., additional, Houillier, P., additional, Paul, K., additional, Kretzschmar, D., additional, Yilmaz, A., additional, Ba hlein, B., additional, Titze, S., additional, Figulla, H.-R., additional, Wolf, G., additional, Busch, M., additional, Korotchaeva, Y., additional, Gordovskaya, N., additional, Kozlovskaya, L., additional, Ng, K. P., additional, Sharma, P., additional, Stringer, S., additional, Jesky, M., additional, Dutton, M., additional, Ferro, C., additional, Cockwell, P., additional, Moon, S. J., additional, Lee, S. C., additional, Yoon, S. Y., additional, Lee, J. E., additional, Han, S. J., additional, Anna, B., additional, Kirsch, T., additional, Svjetlana, L., additional, Joon-Keun, P., additional, Jan, B., additional, Johanna, K., additional, Haller, H., additional, Haubitz, M., additional, Smirnov, A., additional, Kayukov, I., additional, Rafrafi, N., additional, Degtereva, O., additional, Dobronravov, V., additional, Koch, M., additional, Stefan, H., additional, Dika, G., additional, Antoine, M.-H., additional, Husson, C., additional, Kos, J., additional, Milic, M., additional, Fucek, M., additional, Cvoriocec, D., additional, Bourgeade, M.-F., additional, Nortier, J. L., additional, Jelakovic, B., additional, Nawal, E. H., additional, Naoufal, M., additional, Nabila, M., additional, Fadwa, E. M., additional, Salma, E. K., additional, Nisrine, B., additional, Mohamed, Z., additional, Guislaine, M., additional, Mohamed Gharbi, B., additional, Benyounes, R., additional, Sotila, G. G., additional, Sorin, R., additional, Irina Magdalena, D., additional, Roxana, C., additional, Claudia, R., additional, Correa Barcellos, F., additional, Hallal, P. H., additional, Bohlke, M., additional, Boscolo Del Vechio, F., additional, Reges, A., additional, Santos, I., additional, Mielke, G., additional, Fortes, M., additional, Antunez, B., additional, Laganovic, M., additional, Vukovic Lela, I., additional, Karanovic, S., additional, Seric, J., additional, Premuic, V., additional, Fitrek, M., additional, Fodor, L., additional, Meljkovic Vrkic, T., additional, Bansal, V., additional, Hoppensteadt, D., additional, and Fareed, J., additional

Published
2012
Full Text
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10. AKI - Clinical

Author

Gok Oguz, E., primary, Olmaz, R., additional, Turgutalp, K., additional, Muslu, N., additional, Sungur, M. A., additional, Kiykim, A., additional, Van Biesen, W., additional, Vanmassenhove, J., additional, Glorieux, G., additional, Vanholder, R., additional, Chew, S., additional, Forster, K., additional, Kaufeld, T., additional, Kielstein, J., additional, Schilling, T., additional, Haverich, A., additional, Haller, H., additional, Schmidt, B., additional, Hu, P., additional, Liang, X., additional, Chen, Y., additional, LI, R., additional, Jiang, F., additional, LI, Z., additional, Shi, W., additional, Lim, C. C. W., additional, Chia, C. M. L., additional, Tan, A. K., additional, Tan, C. S., additional, Ng, R., additional, Subramani, S., additional, Perez de Jose, A., additional, Bernis Carro, C., additional, Madero Jarabo, R., additional, Bustamante, J., additional, Sanchez Tomero, J. A., additional, Chung, W., additional, Ro, H., additional, Chang, J. H., additional, Lee, H. H., additional, Jung, J. Y., additional, Fazzari, L., additional, Giuliani, A., additional, Scrivano, J., additional, Pettorini, L., additional, Benedetto, U., additional, Luciani, R., additional, Roscitano, A., additional, Napoletano, A., additional, Coclite, D., additional, Cordova, E., additional, Punzo, G., additional, Sinatra, R., additional, Mene, P., additional, Pirozzi, N., additional, Shavit, L., additional, Manilov, R., additional, Algur, N., additional, Wiener-Well, Y., additional, Slotki, I., additional, Pipili, C., additional, Vrettou, C. S., additional, Avrami, K., additional, Economidou, F., additional, Glynos, K., additional, Ioannidou, S., additional, Markaki, V., additional, Douka, E., additional, Nanas, S., additional, De Pascalis, A., additional, Cofano, P., additional, Proia, S., additional, Valletta, A., additional, Vitale, O., additional, Russo, F., additional, Buongiorno, E., additional, Filiopoulos, V., additional, Biblaki, D., additional, Lazarou, D., additional, Chrysis, D., additional, Fatourou, M., additional, Lafoyianni, S., additional, Vlassopoulos, D., additional, Zakiyanov, O., additional, Kriha, V., additional, Vachek, J., additional, Svarcova, J., additional, Zima, T., additional, Tesar, V., additional, Kalousova, M., additional, Kaushik, M., additional, Ronco, C., additional, Cruz, D., additional, Zhang, L., additional, Zhang, W., additional, Chen, N., additional, Ejaz, A. A., additional, Kambhampati, G., additional, Ejaz, N., additional, Dass, B., additional, Lapsia, V., additional, Arif, A. A., additional, Asmar, A., additional, Shimada, M., additional, Alsabbagh, M., additional, Aiyer, R., additional, Johnson, R., additional, Chen, T.-H., additional, Chang, C.-H., additional, Chang, M.-Y., additional, Tian, Y.-C., additional, Hung, C.-C., additional, Fang, J.-T., additional, Yang, C.-W., additional, Chen, Y.-C., additional, Cantaluppi, V., additional, Quercia, A. D., additional, Figliolini, F., additional, Giacalone, S., additional, Pacitti, A., additional, Gai, M., additional, Guarena, C., additional, Leonardi, G., additional, Biancone, L., additional, Camussi, G., additional, Segoloni, G. P., additional, De Cal, M., additional, Lentini, P., additional, Clementi, A., additional, Virzi, G. M., additional, Scalzotto, E., additional, Lacquaniti, A., additional, Donato, V., additional, Fazio, M. R., additional, Lucisano, S., additional, Cernaro, V., additional, Lupica, R., additional, Buemi, M., additional, Helvaci, I., additional, Anik, E., additional, Wani, M., additional, Wani, D. I., additional, Bhat, D. M. A., additional, Banday, D. K., additional, Najar, D. M. S., additional, Reshi, D. A. R., additional, Palla, D. N. A., additional, Iglesias, P., additional, Olea, T., additional, Vega-Cabrera, C., additional, Heras, M., additional, Bajo, M. A., additional, Del Peso, G., additional, Arias, M. J., additional, Selgas, R., additional, Diez, J. J., additional, Daher, E., additional, Costa, P. L., additional, Pereira, E. N. S., additional, Santos, R. D. P., additional, Abreu, K. L., additional, Silva Junior, G., additional, Pereira, E. D. B., additional, Raimundo, M., additional, Crichton, S., additional, Syed, Y., additional, Martin, J., additional, Whiteley, C., additional, Bennett, D., additional, Ostermann, M., additional, Gjyzari, A., additional, Thereska, N., additional, Koroshi, A., additional, Barbullushi, M., additional, Kodra, S., additional, Idrizi, A., additional, Strakosha, A., additional, Petrela, E., additional, Lemmich Smith, J., additional, Klimenko, A., additional, Tuykhmenev, E., additional, Villevalde, S., additional, Kobalava, Z., additional, Avdoshina, S., additional, Tyukhmenev, E., additional, Efremovtseva, M., additional, Hayashi, H., additional, Suzuki, S., additional, Kataoka, K., additional, Kondoh, Y., additional, Taniguchi, H., additional, Sugiyama, D., additional, Nishimura, K., additional, Sato, W., additional, Maruyama, S., additional, Matsuo, S., additional, Yuzawa, Y., additional, Geraldine, D., additional, Muriel, F., additional, Alexandre, H., additional, Eric, R., additional, Fu, P., additional, Pozzato, M., additional, Ferrari, F., additional, Cecere, P., additional, Mesiano, P., additional, Vallero, A., additional, Livigni, S., additional, Quarello, F., additional, Hudier, L., additional, Decaux, O., additional, Haddj-Elmrabet, A., additional, Mandart, L., additional, Lino-Daniel, M., additional, Bridoux, F., additional, Renaudineau, E., additional, Sawadogo, T., additional, Le Pogamp, P., additional, Vigneau, C., additional, Famee, D., additional, Koo, H. M., additional, Oh, H. J., additional, Han, S. H., additional, Choi, K. H., additional, Kang, S.-W., additional, Mehdi, M., additional, Nicolas, M., additional, Mariat, C., additional, Shah, P., additional, Kute, V. B., additional, Vanikar, A., additional, Gumber, M., additional, Patel, H., additional, Trivedi, H., additional, Manetos, C., additional, Poulaki, S., additional, Tripodaki, E.-S., additional, Papastylianou, A., additional, Routsi, C., additional, Uchida, K., additional, Kensuke, U., additional, Yamagata, K., additional, Saitou, C., additional, Okada, M., additional, Chita, G., additional, Davies, M., additional, Veriawa, Y., additional, Naicker, S., additional, Mukhopadhyay, P., additional, Mukherjee, D., additional, Mishra, R., additional, Kar, M., additional, Zickler, D., additional, Wesselmann, H., additional, Schindler, R., additional, Gutierrez*, E., additional, Egido, J., additional, Rubio-Navarro, A., additional, Buendia, I., additional, Blanco-Colio, L. M., additional, Toldos, O., additional, Manzarbeitia, F., additional, De Lorenzo, A., additional, Sanchez, R., additional, Praga^, M., additional, Moreno^, J. A., additional, Kim, M. Y., additional, Kang, N. R., additional, Jang, H. R., additional, Lee, J. E., additional, Huh, W., additional, Kim, Y.-G., additional, Kim, D. J., additional, Hong, S.-C., additional, Kim, J.-S., additional, Oh, H. Y., additional, Okamoto, T., additional, Kamata, K., additional, Naito, S., additional, Tazaki, H., additional, Kan, S., additional, Anne-Kathrin, L.-G., additional, Matthias, K., additional, Speer, T., additional, Andreas, L., additional, Heinrich, G., additional, Thomas, V., additional, Poppleton, A., additional, Danilo, F., additional, Lai, C.-F., additional, Wu, V.-C., additional, Shiao, C.-C., additional, Huang, T.-M., additional, Wu, K.-D., additional, Bedford, M., additional, Farmer, C., additional, Irving, J., additional, Stevens, P., additional, Patera, F., additional, Mattozzi, F., additional, Battistoni, S., additional, Fagugli, R. M., additional, Park, M. Y., additional, Choi, S. J., additional, Kim, J. G., additional, Hwang, S. D., additional, Xie, H., additional, Chen, H., additional, Xu, S., additional, He, Q., additional, Liu, J., additional, Hu, W., additional, Liu, Z., additional, Dalboni, M., additional, Blaya, R., additional, Quinto, B. M., additional, Narciso, R., additional, Oliveira, M., additional, Monte, J., additional, Durao, M., additional, Cendoroglo, M., additional, Batista, M., additional, Hanemann, A. L., additional, Liborio, A., additional, Martins, A., additional, Pinheiro, M. C. C., additional, Meneses, G., additional, De Paula Pessoa, R., additional, Sousa, M., additional, Bezerra, F. S. M., additional, Albuquerque, P. L. M. M., additional, Lima, J. B., additional, Lima, C. B., additional, Veras, M. D. S. B., additional, Nemoto Matsui, T., additional, Totoli, C., additional, Cruz Andreoli, M. C., additional, Vilela Coelho, M. P., additional, Guimaraes de Souza, N. K., additional, Ammirati, A. L., additional, De Carvalho Barreto, F., additional, Ferraz Neto, B.-H., additional, Fortunato Cardoso Dos Santos, B., additional, Abraham, A., additional, Abraham, G., additional, Mathew, M., additional, Duarte, P. M. A., additional, Duarte, F. B., additional, Barros, E. M., additional, Castro, F. Q. S., additional, Palomba, H., additional, Castro, I., additional, Sousa, S. R., additional, Jesus, A. N., additional, Romano, T., additional, Burdmann, E., additional, Yu, L., additional, Kwon, S. H., additional, You, J. Y., additional, Hyun, Y. K., additional, Woo, S. A., additional, Jeon, J. S., additional, Noh, H. J., additional, Han, D. C., additional, Tozija, L., additional, Petronievic, Z., additional, Selim, G., additional, Nikolov, I., additional, Stojceva-Taneva, O., additional, Cakalaroski, K., additional, Lukasz, A., additional, Beneke, J., additional, Menne, J., additional, Schiffer, M., additional, Polanco, N., additional, Hernandez, E., additional, Gutierrez, E., additional, Gutierrez Millet, V., additional, Gonzalez Monte, E., additional, Morales, E., additional, Praga, M., additional, Francisco Javier, L., additional, Nuria, G.-F., additional, Jose Maria, M.-G., additional, Bes Rastrollo, M., additional, Angioi, A., additional, Conti, M., additional, Cao, R., additional, Atzeni, A., additional, Pili, G., additional, Matta, V., additional, Murgia, E., additional, Melis, P., additional, Binda, V., additional, Pani, A., additional, Thome*, F., additional, Leusin, F., additional, Barros, E., additional, Morsch, C., additional, Balbinotto, A., additional, Pilla, C., additional, Premru, V., additional, Buturovic-Ponikvar, J., additional, Ponikvar, R., additional, Marn-Pernat, A., additional, Knap, B., additional, Kovac, J., additional, Gubensek, J., additional, Kersnic, B., additional, Krnjak, L., additional, Prezelj, M., additional, Granatova, J., additional, Havrda, M., additional, Hruskova, Z., additional, Kratka, K., additional, Remes, O., additional, Mokrejsova, M., additional, Bolkova, M., additional, Lanska, V., additional, Rychlik, I., additional, Uniacke, M. D., additional, Lewis, R. J., additional, Harris, S., additional, Roderick, P., additional, Martin, N., additional, Ulrich, K., additional, Jan, B., additional, Jorn, B., additional, Reinhard, B., additional, Jan, K., additional, Hermann, H., additional, Meyer Tobias, F., additional, Leyla, R., additional, Schmidt Bernhard, M. W., additional, Harald, S., additional, Jurgen, S., additional, Tanja, K., additional, Mario, S., additional, Sang Hi, E., additional, Claus, M., additional, Frank, V., additional, Aleksej, S., additional, Sengul, S., additional, Robert, S., additional, Karin, W., additional, Feikah, G., additional, Menne Tobias, F., additional, Meyer Tobias, N., additional, Beutel, G., additional, Fleig, S., additional, Steinhoff, J., additional, Meyer, T., additional, Hafer, C., additional, Bramstedt, J., additional, Busch, V., additional, Vischedyk, M., additional, Kuhlmann, U., additional, Ries, W., additional, Mitzner, S., additional, Mees, S., additional, Stracke, S., additional, Nurnberger, J., additional, Gerke, P., additional, Wiesner, M., additional, Sucke, B., additional, Abu-Tair, M., additional, Kribben, A., additional, Klause, N., additional, Merkel, F., additional, Schnatter, S., additional, Dorresteijn, E., additional, Samuelsson, O., additional, Brunkhorst, R., additional, Stec-Hus Registry, G., additional, Reising, A., additional, Bange, F.-C., additional, Hiss, M., additional, Vetter, F., additional, Bode-Boger, S. M., additional, Martens-Lobenhoffer, J., additional, Schmidt, B. M. W., additional, Kielstein, J. T., additional, Shin, H. S., additional, Jung, Y. S., additional, and Rim, H., additional

Published
2012
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13. iemer niuwe: Wiederholung in Gottfrieds 'Tristan'

Author

Huber, Christoph, Millet, Victor, Huber, C ( Christoph ), Millet, V ( Victor ), Köbele, Susanne, Huber, Christoph, Millet, Victor, Huber, C ( Christoph ), Millet, V ( Victor ), and Köbele, Susanne

Published
2002

25. Vanin-1-/- Mice Exhibit a Glutathione-Mediated Tissue Resistance to Oxidative Stress.

Author

Berruyer, C., Martin, F. M., Castellano, R., Macone, A., Malergue, F., Garrido-Urbani, S., Millet, V., Imbert, J., Duprè, S., Pitari, G., Naquet, P., and Galland, F.

Subjects
OXIDATIVE stress, GLUTATHIONE, PANTOTHENIC acid, THIOLS, APOPTOSIS, CELL death, ANTIOXIDANTS
Abstract

Vanin-1 is an epithelial ectoenzyme with pantetheinase activity and generating the amino-thiol cysteamine through the metabolism of pantothenic acid (vitamin B5). Here we show that Vanin-1-/- mice, which lack cysteamine in tissues, exhibit resistance to oxidative injury induced by whole-body γ-irradiation or paraquat. This protection is correlated with reduced apoptosis and inflammation and is reversed by treating mutant animals with cystamine. The better tolerance of the Vanin-1-/- mice is associated with an enhanced gamma-glutamylcysteine synthetase activity in liver, probably due to the absence of cysteamine and leading to elevated stores of glutathione (GSH), the most potent cellular antioxidant. Consequently, Vanin-1-/- mice maintain a more reducing environment in tissue after exposure to irradiation. In normal mice, we found a stress-induced biphasic expression of Vanin-1 regulated via antioxidant response elements in its promoter region. This process should finely tune the redox environment and thus change an early inflammatory process into a late tissue repair process. We propose Vanin-1 as a key molecule to regulate the GSH-dependent response to oxidative injury in tissue at the epithelial level. Therefore, Vanin/pantetheinase inhibitors could be useful for treatment of damage due to irradiation and pro-oxidant inducers. [ABSTRACT FROM AUTHOR]

Published
2004
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26. Evidence for the involvement of the IgE-basophil system in acute serum sickness.

Author

Benveniste, J., Egido, J., and Gutierrez-Millet, V.

Subjects
BASOPHILS, GRANULOCYTES, MAST cells, SERUM albumin, BLOOD proteins, IMMUNOGLOBULIN G
Abstract

The role of the basophils in acute serum sickness of rabbits was examined by monitoring daily the absolute number of basophils before, during and after the disease period. After antigen (bovine serum albumin, BSA) elimination, levels of serum IgE, and in vitro basophil degranulation in the presence of BSA were determined. The results showed that the onset of glomerular lesions depends upon the simultaneous occurrence of circulating immune complexes greater than 19 S and of an in vivo basophil depletion-probably equivalent to degranulation-reaching 70% of the pre-disease number. Post-disease antigen-dependent in vitro degranulation of the basophils and levels of serum IgE anti BSA did not prove to be good indexes of basophil sensitization. Our data suggest that basophils are instrumental at early stages of the deposition of immune complexes, most probably through their sensitization by membrane-bound IgE antibodies. [ABSTRACT FROM AUTHOR]

Published
1976

27. Immunological studies in a familial IgA nephropathy.

Author

Egido, J., Blasco, R., Sancho, J., Lozano, L., and Gutierrez-Millet, V.

Subjects
IGA glomerulonephritis, LYMPHOCYTES, T cells, SERUM, BLOOD plasma, B cells
Abstract

The hypothesis that abnormalities of immune function might occur in healthy first degree relatives of two patients with a familial IgA nephropathy was tested. After 7 days of culture, pokeweed mitogen stimulated peripheral blood mononuclear cells from the two affected members with IgA nephropathy (father and older son), as well as two other healthy sons, produced significantly more polymeric IgA than the controls. The fact that only the two patients with IgA nephropathy presented high serum levels of polymeric IgA favours the idea that a defect in the clearance of this immunoglobulin might be an important step in the appearance of this nephropathy. All the healthy members of the family had a normal OKT4+/OKT8+ cell ratio and a normal concanavalin A generated IgA suppressor cell function in contrast with the abnormalities observed in the two affected members and the previous results in a large number of patients with IgA nephropathy. These data suggest that the primary cellular abnormality might reside in B cells, being the T cell alterations observed in patients a secondary or subsequent phenomenon. These results further support the existence of genetic bases for the susceptibility to this disease. [ABSTRACT FROM AUTHOR]

Published
1983

28. Double-blind controlled study of central nervous system side effects of amantadine, rimantadine, and chlorpheniramine

Author

Millet, V M, Dreisbach, M, and Bryson, Y J

Abstract

A total of 52 healthy, adult volunteers were randomly assigned to five treatment groups to be treated twice daily for 4 days with 100 mg of amantadine, 100 mg of rimantadine, 4 mg of chlorpheniramine or placebo alone, or 100 mg of amantadine in combination with chlorpheniramine. The results of tests measuring performance on tasks of attention, reasoning, and memory were unaffected by treatment. Subjective side effects in recipients of amantadine, rimantadine, and chlorpheniramine were comparable and minimal. Side effects appeared to be enhanced in subjects receiving both amantadine and chlorpheniramine.

Published
1982
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38. The coenzyme A precursor pantethine enhances antitumor immunity in sarcoma.

Author

Miallot R, Millet V, Roger A, Fenouil R, Tardivel C, Martin JC, Tranchida F, Shintu L, Berchard P, Sousa Lanza J, Malissen B, Henri S, Ugolini S, Dutour A, Finetti P, Bertucci F, Blay JY, Galland F, and Naquet P

Subjects
Humans, Mice, Animals, Coenzyme A pharmacology, Pantothenic Acid pharmacology, Tumor Microenvironment, CD8-Positive T-Lymphocytes, Sarcoma drug therapy
Abstract

The tumor microenvironment is a dynamic network of stromal, cancer, and immune cells that interact and compete for resources. We have previously identified the Vanin1 pathway as a tumor suppressor of sarcoma development via vitamin B5 and coenzyme A regeneration. Using an aggressive sarcoma cell line that lacks Vnn1 expression, we showed that the administration of pantethine, a vitamin B5 precursor, attenuates tumor growth in immunocompetent but not nude mice. Pantethine boosts antitumor immunity, including the polarization of myeloid and dendritic cells towards enhanced IFNγ-driven antigen presentation pathways and improved the development of hypermetabolic effector CD8 + T cells endowed with potential antitumor activity. At later stages of treatment, the effect of pantethine was limited by the development of immune cell exhaustion. Nevertheless, its activity was comparable with that of anti-PD1 treatment in sensitive tumors. In humans, VNN1 expression correlates with improved survival and immune cell infiltration in soft-tissue sarcomas, but not in osteosarcomas. Pantethine could be a potential therapeutic immunoadjuvant for the development of antitumor immunity., (© 2023 Miallot et al.)

Published
2023
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39. An OMA1 redox site controls mitochondrial homeostasis, sarcoma growth, and immunogenicity.

Author

Miallot R, Millet V, Groult Y, Modelska A, Crescence L, Roulland S, Henri S, Malissen B, Brouilly N, Panicot-Dubois L, Vincentelli R, Sulzenbacher G, Finetti P, Dutour A, Blay JY, Bertucci F, Galland F, and Naquet P

Subjects
Mice, Animals, Cysteine metabolism, Mitochondrial Proteins genetics, Mitochondrial Proteins metabolism, Mitochondria metabolism, Mammals metabolism, Metalloproteases genetics, Metalloproteases metabolism, GTP Phosphohydrolases genetics, GTP Phosphohydrolases metabolism, Sarcoma genetics, Sarcoma metabolism
Abstract

Aggressive tumors often display mitochondrial dysfunction. Upon oxidative stress, mitochondria undergo fission through OMA1-mediated cleavage of the fusion effector OPA1. In yeast, a redox-sensing switch participates in OMA1 activation. 3D modeling of OMA1 comforted the notion that cysteine 403 might participate in a similar sensor in mammalian cells. Using prime editing, we developed a mouse sarcoma cell line in which OMA1 cysteine 403 was mutated in alanine. Mutant cells showed impaired mitochondrial responses to stress including ATP production, reduced fission, resistance to apoptosis, and enhanced mitochondrial DNA release. This mutation prevented tumor development in immunocompetent, but not nude or cDC1 dendritic cell-deficient, mice. These cells prime CD8 + lymphocytes that accumulate in mutant tumors, whereas their depletion delays tumor control. Thus, OMA1 inactivation increased the development of anti-tumor immunity. Patients with complex genomic soft tissue sarcoma showed variations in the level of OMA1 and OPA1 transcripts. High expression of OPA1 in primary tumors was associated with shorter metastasis-free survival after surgery, and low expression of OPA1, with anti-tumor immune signatures. Targeting OMA1 activity may enhance sarcoma immunogenicity., (© 2023 Miallot et al.)

Published
2023
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40. Metabolic landscapes in sarcomas.

Author

Miallot R, Galland F, Millet V, Blay JY, and Naquet P

Subjects
Animals, Gene Expression Regulation, Neoplastic, Humans, Metabolomics, Sarcoma genetics, Signal Transduction, Transcriptome, Tumor Microenvironment, Metabolic Networks and Pathways, Metabolome, Sarcoma metabolism
Abstract

Metabolic rewiring offers novel therapeutic opportunities in cancer. Until recently, there was scant information regarding soft tissue sarcomas, due to their heterogeneous tissue origin, histological definition and underlying genetic history. Novel large-scale genomic and metabolomics approaches are now helping stratify their physiopathology. In this review, we show how various genetic alterations skew activation pathways and orient metabolic rewiring in sarcomas. We provide an update on the contribution of newly described mechanisms of metabolic regulation. We underscore mechanisms that are relevant to sarcomagenesis or shared with other cancers. We then discuss how diverse metabolic landscapes condition the tumor microenvironment, anti-sarcoma immune responses and prognosis. Finally, we review current attempts to control sarcoma growth using metabolite-targeting drugs., (© 2021. The Author(s).)

Published
2021
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41. Vnn1 pantetheinase limits the Warburg effect and sarcoma growth by rescuing mitochondrial activity.

Author

Giessner C, Millet V, Mostert KJ, Gensollen T, Vu Manh TP, Garibal M, Dieme B, Attaf-Bouabdallah N, Chasson L, Brouilly N, Laprie C, Lesluyes T, Blay JY, Shintu L, Martin JC, Strauss E, Galland F, and Naquet P

Abstract

Like other tumors, aggressive soft tissue sarcomas (STS) use glycolysis rather than mitochondrial oxidative phosphorylation (OXPHOS) for growth. Given the importance of the cofactor coenzyme A (CoA) in energy metabolism, we investigated the impact of Vnn1 pantetheinase-an enzyme that degrades pantetheine into pantothenate (vitamin B5, the CoA biosynthetic precursor) and cysyteamine-on tumor growth. Using two models, we show that Vnn1 + STS remain differentiated and grow slowly, and that in patients a detectable level of VNN1 expression in STS is associated with an improved prognosis. Increasing pantetheinase activity in aggressive tumors limits their growth. Using combined approaches, we demonstrate that Vnn1 permits restoration of CoA pools, thereby maintaining OXPHOS. The simultaneous production of cysteamine limits glycolysis and release of lactate, resulting in a partial inhibition of STS growth in vitro and in vivo. We propose that the Warburg effect observed in aggressive STS is reversed by induction of Vnn1 pantetheinase and the rewiring of cellular energy metabolism by its products., Competing Interests: The authors declare that they have no conflict of interest.

Published
2018
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42. Serum pantetheinase/vanin levels regulate erythrocyte homeostasis and severity of malaria.

Author

Rommelaere S, Millet V, Rihet P, Atwell S, Helfer E, Chasson L, Beaumont C, Chimini G, Sambo Mdo R, Viallat A, Penha-Gonçalves C, Galland F, and Naquet P

Subjects
Adolescent, Adult, Amidohydrolases metabolism, Anemia, Animals, Child, Child, Preschool, Disease Models, Animal, Disease Susceptibility, Female, GPI-Linked Proteins blood, GPI-Linked Proteins metabolism, Homeostasis, Humans, Infant, Male, Mice, Mice, Inbred C57BL, Oxidative Stress, Young Adult, Amidohydrolases blood, Erythrocytes physiology, Malaria physiopathology
Abstract

Tissue pantetheinase, encoded by the VNN1 gene, regulates response to stress, and previous studies have shown that VNN genes contribute to the susceptibility to malaria. Herein, we evaluated the role of pantetheinase on erythrocyte homeostasis and on the development of malaria in patients and in a new mouse model of pantetheinase insufficiency. Patients with cerebral malaria have significantly reduced levels of serum pantetheinase activity (PA). In mouse, we show that a reduction in serum PA predisposes to severe malaria, including cerebral malaria and severe anemia. Therefore, scoring pantetheinase in serum may serve as a severity marker in malaria infection. This disease triggers an acute stress in erythrocytes, which enhances cytoadherence and hemolysis. We speculated that serum pantetheinase might contribute to erythrocyte resistance to stress under homeostatic conditions. We show that mutant mice with a reduced serum PA are anemic and prone to phenylhydrazine-induced anemia. A cytofluorometric and spectroscopic analysis documented an increased frequency of erythrocytes with an autofluorescent aging phenotype. This is associated with an enhanced oxidative stress and shear stress-induced hemolysis. Red blood cell transfer and bone marrow chimera experiments show that the aging phenotype is not cell intrinsic but conferred by the environment, leading to a shortening of red blood cell half-life. Therefore, serum pantetheinase level regulates erythrocyte life span and modulates the risk of developing complicated malaria., (Copyright © 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

Published
2015
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43. Sox17 regulates liver lipid metabolism and adaptation to fasting.

Author

Rommelaere S, Millet V, Vu Manh TP, Gensollen T, Andreoletti P, Cherkaoui-Malki M, Bourges C, Escalière B, Du X, Xia Y, Imbert J, Beutler B, Kanai Y, Malissen B, Malissen M, Tailleux A, Staels B, Galland F, and Naquet P

Subjects
Amidohydrolases blood, Amidohydrolases metabolism, Animals, Fasting blood, GPI-Linked Proteins blood, GPI-Linked Proteins metabolism, HMGB Proteins genetics, Mice, Mice, Transgenic, PPAR alpha genetics, PPAR alpha metabolism, SOX9 Transcription Factor genetics, SOX9 Transcription Factor metabolism, SOXF Transcription Factors genetics, Transcriptome, Adaptation, Physiological physiology, Fasting metabolism, HMGB Proteins metabolism, Lipid Metabolism genetics, Liver metabolism, SOXF Transcription Factors metabolism
Abstract

Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is depressed. This mouse carries a mutation in the HMG domain of the Sox17 transcription factor. Mutant mice display a metabolic phenotype featuring lipid abnormalities and inefficient adaptation to fasting. Upon fasting, a fraction of the PPARα-driven transcriptional program is no longer induced and associated with impaired fatty acid oxidation. The transcriptional phenotype is partially observed in heterozygous Sox17+/- mice. In mutant mice, the fasting phenotype but not all transcriptomic signature is rescued by the administration of the PPARalpha agonist fenofibrate. These results identify a novel role for Sox17 in adult liver as a modulator of the metabolic adaptation to fasting.

Published
2014
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44. PPARalpha regulates the production of serum Vanin-1 by liver.

Author

Rommelaere S, Millet V, Gensollen T, Bourges C, Eeckhoute J, Hennuyer N, Baugé E, Chasson L, Cacciatore I, Staels B, Pitari G, Galland F, and Naquet P

Subjects
Amidohydrolases genetics, Animals, Caco-2 Cells, Female, GPI-Linked Proteins blood, GPI-Linked Proteins genetics, Gene Expression, Gene Expression Regulation, Hepatocytes enzymology, Hepatocytes metabolism, Humans, Liver cytology, Male, Mice, Mice, Inbred C57BL, Amidohydrolases blood, Liver enzymology, PPAR alpha metabolism
Abstract

The membrane-bound Vanin-1 pantetheinase regulates tissue adaptation to stress. We investigated Vnn1 expression and its regulation in liver. Vnn1 is expressed by centrolobular hepatocytes. Using novel tools, we identify a soluble form of Vnn1 in mouse and human serum and show the contribution of a cysteine to its catalytic activity. We show that liver contributes to Vanin-1 secretion in serum and that PPARalpha is a limiting factor in serum Vnn1 production. Functional PPRE sites are identified in the Vnn1 promoter. These results indicate that serum Vnn1 might be a reliable reporter of PPARalpha activity in liver., (Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.)

Published
2013
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45. Quantitative and qualitative study of gastric lipolysis in premature infants: do MCT-enriched infant formulas improve fat digestion?

Author

Roman C, Carriere F, Villeneuve P, Pina M, Millet V, Simeoni U, and Sarles J

Subjects
Gastric Mucosa metabolism, Humans, Hydrogen-Ion Concentration, Infant, Newborn, Infant Formula metabolism, Infant, Premature, Stomach physiology, Triglycerides metabolism
Abstract

Intragastric fat digestion was investigated by analyzing the products of lipolysis and the gastric lipase (HGL) levels of premature infants fed with a formula enriched with medium chain triglycerides (MCT) and those of infants fed with human milk. Infants were fed using a gastric tube and the gastric contents were aspirated twice a day for 5 d, before and at various times after gavage feeding. HGL levels were measured using the pHstat technique. After extraction, lipids were separated and quantified using thin-layer chromatography coupled to a flame ionization detector. Fatty acid methyl esters were analyzed by gas chromatography. HGL concentration increased during digestion, reaching 77.4 +/- 43.1 microg/mL (around 75% of those recorded in adults). Mean HGL output was 115 +/- 43 microg for 3 h and the overall intragastric lipolysis was 6.1 +/- 2.6%. Although the formula was enriched with octanoic and decanoic acid, the main fatty acids released in the stomach were palmitic (C16:0, 17.03 +/- 0.23% wt/wt) and oleic (C18:1 n-9, 28.23 +/- 1.26% wt/wt) acid. Similar results were obtained with infants fed with human milk. MCT supplementation has no quantitative or qualitative effects on the intragastric lipolysis, which is not higher in premature infant than in adults.

Published
2007
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46. Vanin-1 licenses inflammatory mediator production by gut epithelial cells and controls colitis by antagonizing peroxisome proliferator-activated receptor gamma activity.

Author

Berruyer C, Pouyet L, Millet V, Martin FM, LeGoffic A, Canonici A, Garcia S, Bagnis C, Naquet P, and Galland F

Subjects
Active Transport, Cell Nucleus drug effects, Active Transport, Cell Nucleus physiology, Amidohydrolases, Animals, Benzhydryl Compounds, Body Weight, Cell Adhesion Molecules deficiency, Cell Adhesion Molecules genetics, Cell Line, Cell Nucleus drug effects, Cell Nucleus metabolism, Chemokine CCL2 genetics, Chemokine CCL2 metabolism, Chemokine CXCL2, Chemokines genetics, Chemokines metabolism, Colitis chemically induced, Colitis pathology, Colon drug effects, Colon metabolism, Colon pathology, Cyclooxygenase 2 metabolism, Cystamine pharmacology, Cytokines genetics, Cytokines metabolism, Epithelial Cells drug effects, Epoxy Compounds pharmacology, GPI-Linked Proteins, Gene Expression Regulation drug effects, Interleukin-1beta pharmacology, Mice, Mice, Inbred BALB C, Mice, Knockout, Mice, SCID, PPAR gamma antagonists & inhibitors, PPAR gamma genetics, Prostaglandin D2 analogs & derivatives, Prostaglandin D2 pharmacology, Survival Analysis, Trinitrobenzenesulfonic Acid, Cell Adhesion Molecules physiology, Colitis metabolism, Epithelial Cells metabolism, PPAR gamma metabolism
Abstract

Colitis involves immune cell-mediated tissue injuries, but the contribution of epithelial cells remains largely unclear. Vanin-1 is an epithelial ectoenzyme with a pantetheinase activity that provides cysteamine/cystamine to tissue. Using the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis model we show here that Vanin-1 deficiency protects from colitis. This protection is reversible by administration of cystamine or bisphenol A diglycidyl ether, a peroxisome proliferator-activated receptor (PPAR)gamma antagonist. We further demonstrate that Vanin-1, by antagonizing PPARgamma, licenses the production of inflammatory mediators by intestinal epithelial cells. We propose that Vanin-1 is an epithelial sensor of stress that exerts a dominant control over innate immune responses in tissue. Thus, the Vanin-1/pantetheinase activity might be a new target for therapeutic intervention in inflammatory bowel disease.

Published
2006
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47. Vanin-1-/- mice exhibit a glutathione-mediated tissue resistance to oxidative stress.

Author

Berruyer C, Martin FM, Castellano R, Macone A, Malergue F, Garrido-Urbani S, Millet V, Imbert J, Duprè S, Pitari G, Naquet P, and Galland F

Subjects
Amidohydrolases, Animals, Apoptosis physiology, Cell Adhesion Molecules genetics, Cell Line, Cystamine administration & dosage, Cystamine metabolism, Cysteamine metabolism, Epithelial Cells cytology, Epithelial Cells drug effects, Epithelial Cells metabolism, Epithelial Cells radiation effects, GPI-Linked Proteins, Gamma Rays, Gene Expression Regulation, Enzymologic, Glutamate-Cysteine Ligase metabolism, Herbicides administration & dosage, Inflammation metabolism, Mice, Mice, Inbred BALB C, Mice, Knockout, Paraquat administration & dosage, Promoter Regions, Genetic, Radiation-Protective Agents metabolism, Reactive Oxygen Species metabolism, Thymus Gland cytology, Thymus Gland physiology, Thymus Gland radiation effects, Cell Adhesion Molecules metabolism, Glutathione metabolism, Oxidative Stress
Abstract

Vanin-1 is an epithelial ectoenzyme with pantetheinase activity and generating the amino-thiol cysteamine through the metabolism of pantothenic acid (vitamin B(5)). Here we show that Vanin-1(-/-) mice, which lack cysteamine in tissues, exhibit resistance to oxidative injury induced by whole-body gamma-irradiation or paraquat. This protection is correlated with reduced apoptosis and inflammation and is reversed by treating mutant animals with cystamine. The better tolerance of the Vanin-1(-/-) mice is associated with an enhanced gamma-glutamylcysteine synthetase activity in liver, probably due to the absence of cysteamine and leading to elevated stores of glutathione (GSH), the most potent cellular antioxidant. Consequently, Vanin-1(-/-) mice maintain a more reducing environment in tissue after exposure to irradiation. In normal mice, we found a stress-induced biphasic expression of Vanin-1 regulated via antioxidant response elements in its promoter region. This process should finely tune the redox environment and thus change an early inflammatory process into a late tissue repair process. We propose Vanin-1 as a key molecule to regulate the GSH-dependent response to oxidative injury in tissue at the epithelial level. Therefore, Vanin/pantetheinase inhibitors could be useful for treatment of damage due to irradiation and pro-oxidant inducers.

Published
2004
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48. Short-term BMP-2 expression is sufficient for in vivo osteochondral differentiation of mesenchymal stem cells.

Author

Noël D, Gazit D, Bouquet C, Apparailly F, Bony C, Plence P, Millet V, Turgeman G, Perricaudet M, Sany J, and Jorgensen C

Subjects
Animals, Bone Morphogenetic Protein 2, Bone Morphogenetic Proteins genetics, Bone and Bones cytology, Bone and Bones embryology, Bone and Bones metabolism, Cartilage embryology, Cartilage metabolism, Cell Communication physiology, Cell Differentiation genetics, Cell Lineage genetics, Chondrocytes cytology, Chondrocytes metabolism, Extracellular Fluid metabolism, Gene Expression Regulation, Developmental genetics, Growth Substances metabolism, Joints cytology, Joints growth & development, Joints surgery, Mice, Mice, Inbred C3H, Muscle, Skeletal cytology, Muscle, Skeletal growth & development, Muscle, Skeletal surgery, NIH 3T3 Cells, Osteogenesis genetics, Promoter Regions, Genetic drug effects, Promoter Regions, Genetic genetics, Stem Cell Transplantation, Bone Morphogenetic Proteins biosynthesis, Cartilage cytology, Cell Differentiation physiology, Mesenchymal Stem Cells cytology, Mesenchymal Stem Cells metabolism, Osteogenesis physiology, Transforming Growth Factor beta
Abstract

Currently available murine models to evaluate mesenchymal stem cell (MSC) differentiation are based on cell injection at ectopic sites such as muscle or skin. Due to the importance of environmental factors on the differentiation capacities of stem cells in vivo, we investigated whether the peculiar synovial/cartilaginous environment may influence the lineage specificity of bone morphogenetic protein (BMP)-2-engineered MSCs. To this aim, we used the C3H10T1/2-derived C9 MSCs that express BMP-2 under control of the doxycycline (Dox)-repressible promoter, Tet-Off, and showed in vitro, using the micropellet culture system that C9 MSCs kept their potential to differentiate toward chondrocytes. Implantation of C9 cells, either into the tibialis anterior muscles or into the joints of CB17-severe combined immunodeficient bg mice led to the formation of cartilage and bone filled with bone marrow as soon as day 10. However, no differentiation was observed after injection of naïve MSCs or C9 cells that were repressed to secrete BMP-2 by Dox addition. The BMP-2-induced differentiation of adult MSCs is thus independent of soluble factors present in the local environment of the synovial/cartilaginous tissues. Importantly, we demonstrated that a short-term expression of the BMP-2 growth factor is necessary and sufficient to irreversibly induce bone formation, suggesting that a stable genetic modification of MSCs is not required for stem cell-based bone/cartilage engineering.

Published
2004
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49. Tetracycline transcriptional silencer tightly controls transgene expression after in vivo intramuscular electrotransfer: application to interleukin 10 therapy in experimental arthritis.

Author

Perez N, Plence P, Millet V, Greuet D, Minot C, Noel D, Danos O, Jorgensen C, and Apparailly F

Subjects
Animals, Dose-Response Relationship, Drug, Electroporation, Female, Injections, Intramuscular, Interleukin-10 administration & dosage, Interleukin-10 metabolism, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Plasmids, Transfection, Arthritis, Experimental genetics, Arthritis, Experimental therapy, Gene Expression Regulation, Viral, Genetic Therapy, Genetic Vectors administration & dosage, Interleukin-10 genetics, Tetracycline metabolism
Abstract

The doxycycline (Dox)-inducible reverse tetracycline transactivator (rtTA) is often used to control gene expression. However, the Tet-on system displays a high background activity. To overcome this unregulated expression we used the tetracycline-dependent transcriptional silencer (tTS), which binds the tetO inducible promoter in the absence of Dox. Controlled gene expression was analyzed in vivo by delivering combinations of Dox-regulated luciferase reporter construct, rtTA, and tTS expression plasmids into mouse muscle, using electrotransfer. Elevated luciferase expression levels were observed in the absence of doxycycline, and a 10-fold induction was obtained after drug administration. In contrast, when tTS was added, background expression was dramatically lowered by three to four orders of magnitude, and induction was maintained. The tTS system was then used to control expression of a therapeutic gene in experimental arthritis. DBA/1 mice were coinjected with plasmids encoding the antiinflammatory interleukin-10 cytokine under the control of the tetO promoter, the rtTA, and the tTS. Electrotransfer resulted in a dose-dependent increase in IL-10 expression, maintained over a 3-month period, and significant inhibitory effects on collagen-induced arthritis. We conclude that the use of tTS significantly improves the utility of the rtTA system for somatic gene transfer by reducing background activity.

Published
2002
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50. Tetracycline-inducible interleukin-10 gene transfer mediated by an adeno-associated virus: application to experimental arthritis.

Author

Apparailly F, Millet V, Noël D, Jacquet C, Sany J, and Jorgensen C

Subjects
Animals, Gene Expression, Gene Expression Regulation, Genetic Vectors, Genome, Viral, HeLa Cells, Humans, Male, Mice, Mice, Inbred DBA, Organ Specificity, Arthritis, Experimental therapy, Dependovirus genetics, Gene Transfer Techniques, Genetic Therapy, Interleukin-10 genetics, Tetracycline pharmacology
Abstract

The adeno-associated viruses (AAV) offer new perspectives for cytokine gene transfer in rheumatoid arthritis (RA) because they are nonpathogenic and allow long-term transgene expression in vivo. Moreover, the use of a tetracycline-inducible promoter allows regulation of therapeutic gene expression. This study assessed the potential long-term gene regulation of a recombinant AAV vector expressing viral interleukin-10 (vIL-10) in human rheumatoid synovium and the therapeutic efficiency in a mouse model of RA. We constructed a recombinant AAV vector in which the transcription of vIL-10 cDNA is controlled by the TetON system. Transduction of human primary RA synovial cells with AAV-tetON-vIL10 conferred in vitro controlled vIL-10 expression. After intramuscular injection, both incidence and severity of collagen-induced arthritis were significantly reduced at macroscopic, radiological, and histological levels in the group of DBA1 mice treated with AAV-TetON-vIL10 vector plus doxycycline after immunization and boosting compared to control groups. When coinjecting two separate AAV vectors, one encoding the inducible vIL-10 and the other the transcriptional activator, a 10 times excess of the transactivator vector dose allowed efficient control of vIL-10 secretion by doxycycline administration or withdrawal, over an 8-week period. Our results supported, for the first time, the utility of AAV-tetON-vIL10 as a therapeutic tool for gene therapy in RA.

Published
2002
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