107 results on '"Sternberg, F."'
Search Results
2. On line continuous monitoring of subcutaneous tissue glucose in men by combining portable glucosensor with microdialysis
- Author
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Meyerhoff, C., Bischof, F., Sternberg, F., Zier, H., and Pfeiffer, E. F.
- Published
- 1992
- Full Text
- View/download PDF
Catalog
3. Prevalence and associated risk factors of latent tuberculosis infection in a Spanish prison
- Author
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López de Goicoechea-Saiz, ME, Sternberg, F, and Portilla-Sogorb, J
- Subjects
tuberculosis latente ,prevalence ,prevalencia ,España ,Mycobacterium tuberculosis ,prisons ,tuberculina ,prisiones ,salud pública ,Spain ,latent tuberculosis ,risk factors ,factores de riesgo ,Public Health ,tuberculin - Abstract
Aim: To determine the prevalence of latent tuberculosis infection (LTI) in a Spanish prison, analyze the main sociodemographic and clinical variables associated with this condition and estimate the percentage of individuals with LTI who have received chemoprophylactic treatment. Materials and methods: Cross-sectional study including inmates hosted in the Madrid VI Prison on 16/07/2016. Exclusion criteria: history of tuberculosis; non-updated tuberculin test according to the Tuberculosis Prevention and Control Program in Prisons protocol. Information of the variables was collected from SANIT and SIP programs, and by checking the clinical records of inmates. Description of the participant population and comparison between the frequency of distribution of the independent variables in LTI present and absent groups were performed, the last calculating the p value with Ji2 and Mann-Whitney U tests. Bivariate and multivariate analysis have been carried out with a logistic regression model. Results: 936 individuals have been included. The prevalence of LTI in prison is 54.6%. This condition has been linked to the sociodemographic variables age, sex and nationality of origin, being age the one that has shown the strongest association. Among the other factors analyzed, only HCV infection behaves as a predictor of LTI. 30.3% of the individuals with LTI have completed or are receiving chemoprophylactic treatment in the moment of the study. Discussion: LTI prevalence is high in the Spanish current prison population. The results of the study emphasize the relevance of the LTI screening in the prison setting, specially among high risk groups, and point out the need of a greater effort in the indication and completion of the chemoprophylactic treatment. Resumen Objetivo: Determinar la prevalencia de infección tuberculosa latente (ITL) en un centro penitenciario tipo español, analizar las principales variables sociodemográficas y clínicas asociadas a este padecimiento, y estimar el porcentaje de individuos con ITL que han realizado tratamiento quimioprofiláctico. Materiales y métodos: Estudio descriptivo transversal incluyendo a los internos registrados en el Centro Penitenciario Madrid VI a fecha de 16/07/2016. Criterios de exclusión: antecedente de enfermedad tuberculosa o no disponer de prueba de tuberculina actualizada conforme al Programa de Prevención y Control de Tuberculosis en el Medio Penitenciario. Recogida de las variables desde los programas SANIT, SIP y mediante revisión de los historiales clínicos de los internos. Descripción de la población participante y comparación de la frecuencia de distribución de las variables predictoras en los grupos de ITL presente y ausente, calculando el valor p mediante las pruebas de Chi cuadrado y U de Mann-Whitney. Análisis bivariante y multivariante mediante regresión logística. Resultados: 936 pacientes incluidos. La prevalencia de ITL es del 54,6%, y se ha relacionado con las variables edad, sexo y nacionalidad de procedencia, siendo la edad la que mayor fuerza de asociación ha demostrado. Entre el resto de los factores analizados, solo la infección por el virus de la hepatitis C se comporta como elemento predictor de ITL. El 30,3% de los individuos con ITL ha completado o se encuentra realizando tratamiento quimioprofiláctico en el momento del estudio. Discusión: La prevalencia de ITL en la población penitenciaria española actual es alta. Los resultados refuerzan la importancia de su cribado en el medio penitenciario, especialmente en aquellos grupos de mayor riesgo, así como la necesidad de un mayor esfuerzo en la indicación y la cumplimentación del tratamiento quimioprofiláctico. more...
- Published
- 2018
4. Comments on subcutaneous glucose monitoring
- Author
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Sternberg, F., Meyerhoff, C., Mennel, F. J., Bischof, F., Mayer, H., and Pfeiffer, E. F.
- Published
- 1994
- Full Text
- View/download PDF
5. Development and Validation of a Clinical Scale for the Evaluation of Forearm Skin Photoaging
- Author
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Guimarães, C.O.Z., primary, Bagatin, E., additional, Guadanhim, L.R.S., additional, Sternberg, F., additional, Picosse, F.R., additional, Nunes, G., additional, Milanez, C., additional, and Miot, H.A., additional more...
- Published
- 2015
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6. Der Rectum-Resektor
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Ungern-Sternberg, F. W. v., primary, Geister, H., additional, and Hancken, G., additional
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- 1974
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7. Kombination von Kunststoff und Gips (Kombigips) in der Frakturbehandlung Combination of plastics and gypsum bandages (Kombigips) in fracture treatment
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Adam, O., v. Ungern-Sternberg, F. W., and v. Hallern, B.
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- 1985
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8. Galanin modulates human and murine neutrophil activation in vitro
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Sternberg, F., primary, Lang, A. A., additional, Koller, A., additional, Lang, R., additional, Bianchini, R., additional, and Kofler, B., additional
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- 2015
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9. Subcutaneous glucose concentration in humans. Real estimation and continuous monitoring.
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Sternberg F, Meyerhoff C, Mennel FJ, Bischof F, Pfeiffer EF, Sternberg, F, Meyerhoff, C, Mennel, F J, Bischof, F, and Pfeiffer, E F
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- 1995
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10. 253. Der Rectum-Resektor
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v. Ungern-Sternberg, F. W., Geister, H., and Hancken, G.
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- 1974
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11. Self-Monitoring of Blood Glucose Compared With Continuous Tissue Glucose Measurement
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Sternberg, F., primary, Hoss, U., additional, Salgado, M., additional, and Pfeiffer, E. F., additional
- Published
- 1997
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12. Current Status of the Glucose Sensor
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Meyerhoff, C., primary, Mennel, F. J., additional, Sternberg, F., additional, Hoss, U., additional, and Pfeiffer, E. F., additional
- Published
- 1996
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13. Combination of Microdialysis and Glucose Sensor for Continuous On Line Measurement of the Subcutaneous Glucose Concentration: Theory and Practical Application
- Author
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Meyerhoff, C., primary, Mennel, F., additional, Bischof, Friederike, additional, Sternberg, F., additional, and Pfeiffer, E., additional
- Published
- 1994
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- View/download PDF
14. Calibration Problems of Subcutaneous Glucosensors when Applied “In-Situ” in Man
- Author
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Sternberg, F., primary, Meyerhoff, C., additional, Mennel, F., additional, Hoß, U., additional, Mayer, H., additional, Bischof, Friederike, additional, and Pfeiffer, E., additional
- Published
- 1994
- Full Text
- View/download PDF
15. Measurement of Subcutaneous Glucose Concentration: Influence of the method on the result
- Author
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Meyerhoff, C., primary, Sternberg, F., additional, Bischof, F., additional, Mennel, F. J., additional, and Pfeiffer, E. F., additional
- Published
- 1993
- Full Text
- View/download PDF
16. Use of the Microdialysis Technique in the Monitoring of Subcutaneous Tissue Glucose Concentration
- Author
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Meyerhoff, C., primary, Bischof, F., additional, Mennel, F.J., additional, Sternberg, F., additional, and Pfeiffer, E.F., additional
- Published
- 1993
- Full Text
- View/download PDF
17. On line continuous monitoring of blood lactate in men by a wearable device based upon an enzymatic amperometric lactate sensor
- Author
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Meyerhoff, C., primary, Bischof, F., additional, Mennel, F.J., additional, Sternberg, F., additional, Bican, J., additional, and Pfeiffer, E.F., additional
- Published
- 1993
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18. 178. Laparoskopie: Technik und chirurgische Indikationen
- Author
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Lindenschmidt, Th.-Otto and Ungern-Sternberg, F. W. v.
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- 1977
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19. 155. Der Rectum-Resektor, Modell Stade
- Author
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Ungern-Sternberg, F. W. v., Geister, H., and Hancken, G.
- Published
- 1976
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- View/download PDF
20. Laparoskopie—Technik und chirurgische Indikationen: Film
- Author
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Lindenschmidt, O. and v. Ungern-Sternberg, F. W.
- Published
- 1966
- Full Text
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21. Prevalence and associated risk factors of latent tuberculosis infection in a Spanish prison
- Author
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Lopez Goicoechea-Saiz, M. E., Sternberg, F., and Joaquín Portilla
- Subjects
España ,prevalence ,lcsh:Medicine ,prisons ,salud pública ,latent tuberculosis ,factores de riesgo ,Humans ,risk factors ,tuberculosis latente ,Tuberculin Test ,lcsh:Public aspects of medicine ,prevalencia ,lcsh:R ,lcsh:RA1-1270 ,Original Articles ,Mycobacterium tuberculosis ,tuberculina ,prisiones ,Spain ,Medicine ,Public Health ,Public aspects of medicine ,RA1-1270 ,tuberculin - Abstract
Aim: To determine the prevalence of latent tuberculosis infection (LTI) in a Spanish prison, analyze the main sociodemographic and clinical variables associated with this condition and estimate the percentage of individuals with LTI who have received chemoprophylactic treatment. Materials and methods: Cross-sectional study including inmates hosted in the Madrid VI Prison on 16/07/2016. Exclusion criteria: history of tuberculosis; non-updated tuberculin test according to the Tuberculosis Prevention and Control Program in Prisons protocol. Information of the variables was collected from SANIT and SIP programs, and by checking the clinical records of inmates. Description of the participant population and comparison between the frequency of distribution of the independent variables in LTI present and absent groups were performed, the last calculating the p value with Ji2 and Mann-Whitney U tests. Bivariate and multivariate analysis have been carried out with a logistic regression model. Results: 936 individuals have been included. The prevalence of LTI in prison is 54.6%. This condition has been linked to the sociodemographic variables age, sex and nationality of origin, being age the one that has shown the strongest association. Among the other factors analyzed, only HCV infection behaves as a predictor of LTI. 30.3% of the individuals with LTI have completed or are receiving chemoprophylactic treatment in the moment of the study. Discussion: LTI prevalence is high in the Spanish current prison population. The results of the study emphasize the relevance of the LTI screening in the prison setting, specially among high risk groups, and point out the need of a greater effort in the indication and completion of the chemoprophylactic treatment. more...
22. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Véricel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P.-O., MŞengül, A., Salman, F., Sargrn, M., Özer, E., Karşidaǧ, K., Salman, S., Gedik, S., Satman, İ., Dinççaǧ, N., Yılmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. R., Hayes, J., Simonson, D. C., van der Ven, N. C. W., Lubach, C. H. C., Snoek, F. J., Mollema, E. D., van der Ploeg, H. M., Danne, T., Hoey, H., McGee, H., Fitzgerald, H., Lernmark, B., Thernlund, G., Fredin, K., Hägglöf, B., Lugari, R., Dell’Anna, C., Ugolotti, D., Dei Cas, A., Barilli, A. L., Sard, L., Marani, B., Iotti, M., Zandomeneghi, R., Gnudi, A., Kjems, L. L., Volund, Aa., Toft-Nielsen, M., Damholt, M. B., Hilsted, L., Hughes, T. E., Krarup, T., Holst, J. J., Young, A., Gottlieb, A., Fineman, M., Kolterman, O., Cancelas, J., García-Martínez, J. A., Villanueva-Peñacarrillo, M. L., Valverde, I., Malaisse, W. J., Filipsson, K., Ahrén, B., Balkan, B., Kwasnik, L., Battle, B., Li, X., Egan, J. M., Clocquet, A. R., Elahi, D., Petrella, E., Pricket, K., Petersen, K. F., Sullivan, J. T., Amatruda, J. M., Livingston, J. N., Shulman, G. I., Freyse, E.-J., Knospe, S., Glund, K., Demuth, H.-U., Walker, D., Malik, R. A., Reljanovic, M., Barada, A., Milicevic, Z., Tack, Cees J., Goldstein, David S., Van Huysen, C., Stevens, M. 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A., López, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., van Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs., Farkas, Gy., Török, T., Légrády, P., Várkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnás, Gy., Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermányi, Zs., Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksöyek, S., Kabakçι, G., Erbaş, T., Galicka-Latała, D., Surdacki, A., Gerritsen, J., TenVoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigová, S., Rušavý, Z., Kárová, R., Perrild, H., Kay, L., Jørgensen, T., Bień, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Doménech, A., Leitão, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O’Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Höffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grüβer, M., Hartmann, P., Hoffstadt, K., van Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, Ş., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemández, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch., Hammes, H.-P., Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G., Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Yılmaz, M., Güvener, N., Güvener, M., Kocagöz, T., Böke, E., Paşaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Rutter, M. K., Kestevan, P., McComb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch., Lario, S., Campistol, J. M., Cases, A., Clària, J., Iñigo, P., Esmatjcs, E., Sármán, B., Tóth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stańczyk, L., Watala, C., Stradina, P., Wiśniewska-Jarosińska, M., Marciniak, D., Więcławska, B., Watała, C., Golański, J., Zinnat, R., Mahmud, I., Büyükasik, Yahya, Demiroğlu, H., Szczepanik, A., Skowroński, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Šimková, R., Jirsa, M., Hadoke, P. W. F., McIntyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., McKnight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tunçdemir, M., Oztürk, M., Sultuybek, G., Akkan, A. G., Özyazgan, S., Unlücerci, Y., Bekpınar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Dell’Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Matthäei, S., Pfohl, M., McInerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvári, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Pótó, L., Wagner, L., Mazák, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D’Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A.-S., Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O’Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M. more...
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23. 35th Annual Meeting of the European Association for the Study of Diabetes : Brussels, Belgium, 28 September-2 October 1999
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Ad Darts Memo, Morris For The Collaboration, Juhl, C., Porksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th, Muller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Bjorn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H-M, Oksanen, L., Tuomainen, T-P, Kontula, K., Salonen, J. T., Dekker, J. M., Boks, P., Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., Macalpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M. Jr, Kozakova, H., Kaas, A., Kofronova, O., Tlaskalova-Hogenova, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sorensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Hasko, G., Szabo, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H-H, Genediab, Study Group, Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabak, A. Gy, Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Canton, A., Burgos, R., Hernandez, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simo, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., Mcdermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y-S, Sternesjo, J., Sandler, S., Chen, M-C, Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Breant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessieres-Lacombe, S., Gedec, Study Group, Tauber, J-P, Home, P. D., Lindholm, A., Riis, A., European Insulin Aspart Study Group, Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Us Dm, Study Group Of Insulin Glargine In Type, Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Hvidore Study group on Childhood Diabetes, Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Ukpds, Group, Steiner, G., Dais, Project Group, Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Verges, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph, Benko, B., Ljubic, S., Turk, Z., Granic, M., Marz, W., Wollschlager, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O Rahilly, S., Hattersley, A. T., Mccarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Siman, C., Wisse, Bert, Gittenberger-De Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ozegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rosc, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Skrha, J., Kvasnicka, J., Kalvodova, B., Hilgertova, J., Schatteman, K., Goossens, F., Scharpe, S., Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Haring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., Mckinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnas, A. M., Andersen, N. Aa, Osterhoff, M., Mohlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Furnsinn, C., Nowotny, P., Waldhausl, W., Roden, M., Neeft, M., Meijer, A. J., Bavenholm, P., Pigon, J., Efendic, S., Kastenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovska, A., Kasalicky, P., Hosova, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefebvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valero, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., Galan, B., Netea, M. G., Hancu, N., Smits, P., Meer, J. W. M., Osterbye, T., Jorgensen, K. H., Tranum-Jensen, J., Fredman, P., Hoy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patane, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., Vos, P., Visser, L., Haan, B. J., Klok, P., Schilfgaarde, R., Poppema, S., Juang, J-H, Kuo, C-H, Hsu, B. R-S, Nacher, V., Perez, M., Biarnes, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Busing, M., Becker, T., Klempnauer, J., Hucking, K., Schmiegel, W. H., Nauck, M. A., Boucek, P., Saudek, F., Adamec, M., Kozitarova, R., Jedinakova, T., Vlasakova, Z., Bartos, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J-C, Gillespie, J. S., Mcmaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Vericel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P-O, Msengul, A., Salman, F., Sargrn, M., Ozer, E., Karsidaǧ, K., Salman, S., Gedik, S., Satman, I., Dinccaǧ, N., Yilmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. 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W., Kowalska, I., Telejko, B., Bachorzewska-Gajewska, A., Prokop, J., Kochman, W., Musial, W., Naskret, D., Oleksa, R., Zozulinska, D., Sowinski, J., Wierusz-Wysocka, B., Klamann, A., Jonas, M., Muller-Lung, U., Heuser, L., Launhardt, V., Valensi, P., Paries, J., Torremocha, F., Brulport, V., Sachs, R. N., Vanzetto, G., Levy, M., Lormeau, B., Halimi, S., Perfornis, A., Boumal, D., Zimmermann, C., Bernard, Y., Sabbah, A., Meneveau, N., Gautier, S., Bassand, J. P., Andel, M., Kraml, P., Potockova, J., Dvorakova, H., Treslova, L., Nuttall, S. L., Martin, U., Kendall, M. J., Schiaffini, R., Pantaleo, A., Battocletti, T., Vaccari, V., Brufani, C., Martuscelli, E., Gargiulo, P., Nieszner, E., Posa, I., Kocsis, E., Preda, I., Pogatsa, G., Koltai, M. Z. 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S., Leonhardt, W., Konstadelou, E., Gurlek, Alper, Soedamah-Muthu, S., Taskinen, M. R., Ehnholm, C., Wagner, A., Bayen, Laia, Rigla, M., Ortega, E., Caixas, A., Mestron, A., Ordonez, J., Perez, A., Sotiropoulou, G., Servais, P. L., Bertolotto, A., Pilo, M., Suchankova, G., Andratschke, S., Tschop, M., Strasburger, C-J, Rizzo, L., Aerts, P., Vinckx, M., Ansquer, J. C., Ryan, M., Buter, H., Navis, G. J., Jong, P. E., Zeeuw, D., Carreras, G., Gimenez, G., Pou, J. M., Howorka, K., Gabriel, M., Pumprla, J., Koves, A., Bhowmik, N. B., Haque, A., Rahman, A., Paleari, F., Gamba, P., Mauri, G., Rovaris, G., Giannattasio, C., Piatti, M. L., Zincone, A., Cavaletti, G., Mancia, G., Lan, S., Arezzo, J., Gerber, R. A., Klioze, S. S., Saponara, C., Tartaglione, T., Cercone, S., Caputo, S., Meloni, T., Brunetti, D., Di Lazzaro, V., Xu, G., Jiang, H. Y., Shy, M. E., Sugimoto, K., Zhang, W-X, Kuchmerovskaya, T., Donchenko, G., Shymansky, I., Kuchmerovsky, N., Pakyrbaeva, L., Cameron, N. E., Keegan, A., Cotter, M. A., Mirrlees, D., Smale, S. E., Biessels, G. J., Duis, S. E. J., Kamal, A., Gispen, W. H., Carrington, A., Carman, S., Smiarowski, H., Lavoie, D., Sawicki, D., Sabetta, A., Litchfield, J., Zandt, M., Sredy, J., Smirnova, V., Strokov, I., Ivanova, L., Ichunina, A., Nakamura, J., Nakayama, M., Hamada, Y., Chaya, S., Kato, K., Kasuya, Y., Mizubayashi, R., Miwa, K., Yasuda, Y., Kamiya, H., Hotta, N., Biro, K., Kukorelli, T., Szilagyi, N., Kurthy, M., Komaromy, A., Mogyorosi, T., Nagy, K., Cakir, M., Baskal, N., Gullu, S., Elhan, A. H., Erdogan, G., Ziegler, D., Piolot, R., Neubauer, J., Senesi, B., Bonetti, R., Napolitano, A., Canepa, F., Ottonello, P., Schabmann, A., Gimenez-Perez, G., Arroyo, J. A., Lopez, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs, Farkas, Gy, Torok, T., Legrady, P., Varkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnas, Gy, Eurodiab Iddm, Study Group, Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermanyi, Zs, Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksoyek, S., Kabakciota, G., Erbas, T., Galicka-Latala, D., Surdacki, A., Gerritsen, J., Tenvoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigova, S., Rusavy, Z., Karova, R., Perrild, H., Kay, L., Jorgensen, T., Bien, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Domenech, A., Leitao, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Hoffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grubetaer, M., Hartmann, P., Hoffstadt, K., Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, S., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemandez, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch, Hammes, H-P, Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G. Rd, Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Darts Memo, Collaboration, Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Guvener, N., Guvener, M., Kocagoz, T., Boke, E., Pasaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Pittsburgh Epidemiology of Diabetes Complications (EDC) Study, Rutter, M. K., Kestevan, P., Mccomb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch, Lario, S., Campistol, J. M., Cases, A., Claria, J., Inigo, P., Esmatjcs, E., Sarman, B., Toth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stanczyk, L., Watala, C., Stradina, P., Wisniewska-Jarosinska, M., Marciniak, D., Wieclawska, B., Golanski, J., Zinnat, R., Mahmud, I., Buyukasik, Yahya, Demiroglu, H., Szczepanik, A., Skowronski, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Simkova, R., Jirsa, M., Hadoke, P. W. F., Mcintyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., Mcknight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tuncdemir, M., Sultuybek, G., Akkan, A. G., Unlucerci, Y., Bekpinar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Pfohl, M., Mcinerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvari, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Poto, L., Wagner, L., Mazak, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A-S, Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M. more...
24. 253. Der Rectum-Resektor
- Author
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Ungern-Sternberg, F. W., primary, Geister, H., additional, and Hancken, G., additional
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- 1974
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25. Thrombolytische Purpura und aplastische Anämie
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Sternberg, F., primary
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- 1923
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26. Zur Frage der Pankreasachylie
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Roth, N., primary and Sternberg, F., additional
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- 1922
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27. 155. Der Rectum-Resektor, Modell Stade.
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Ungern-Sternberg, F., Geister, H., and Hancken, G.
- Abstract
Copyright of Langenbeck's Archives of Surgery is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) more...
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- 1976
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28. 178. Laparoskopie: Technik und chirurgische Indikationen.
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Lindenschmidt, Th.-Otto and Ungern-Sternberg, F.
- Abstract
Copyright of Langenbecks Archiv fuer Chirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) more...
- Published
- 1978
- Full Text
- View/download PDF
29. II Consensus of the Brazilian Society of Dermatology for the treatment of alopecia areata.
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Müller Ramos P, Anzai A, Duque-Estrada B, Melo DF, Sternberg F, Santos LDN, Alves LD, and Mulinari-Brenner F
- Abstract
Background: Alopecia areata is a highly frequent disease with great variability in clinical presentation, severity, and prognosis. It has a significant negative impact on quality of life, especially in the moderate and severe forms., Objective: To disseminate guidelines, prepared by a group of Brazilian experts, for the treatment and follow-up of patients with alopecia areata., Methods: Eight specialists from different university centers with experience in alopecia areata were appointed by the Brazilian Society of Dermatology to reach a consensus on its treatment. Using the adapted DELPHI methodology, relevant elements were considered and then an analysis of the recent literature was carried out and the text produced. Consensus on the guidelines was defined with the approval of at least 70% of the panel of experts., Results/conclusions: Treatments vary according to patient age and disease severity. Intralesional injectable corticosteroid therapy was considered the first option for localized disease in adults. In severe cases, Janus Kinase inhibitors are the treatment with the highest level of evidence. Systemic corticosteroid therapy and immunosuppressants (corticosteroid-sparing agents) are also options in these cases. Contact immunotherapy (diphencyprone) is an alternative for stable extensive cases. The assessment of side effects is as important as the hair regrowth rate., (Copyright © 2024 Sociedade Brasileira de Dermatologia. Published by Elsevier España, S.L.U. All rights reserved.) more...
- Published
- 2024
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30. Differential regulation of mitochondrial uncoupling protein 2 in cancer cells.
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Beikbaghban T, Proietti L, Ebner J, Sango R, Rattei T, Weichhart T, Grebien F, Sternberg F, and Pohl EE
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- Humans, Animals, Mice, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Mitochondria metabolism, Cell Proliferation, Cell Hypoxia, Uncoupling Protein 2 metabolism, Uncoupling Protein 2 genetics, Neoplasms metabolism, Neoplasms pathology
- Abstract
The persistent growth of cancer cells is underscored by complex metabolic reprogramming, with mitochondria playing a key role in the transition to aerobic glycolysis and representing new therapeutic targets. Mitochondrial uncoupling protein 2 (UCP2) has attracted interest because of its abundance in rapidly proliferating cells, including cancer cells, and its involvement in cellular metabolism. However, the specific contributions of UCP2 to cancer biology remain poorly defined. Our investigation of UCP2 expression in various human and mouse cancer cell lines aimed to elucidate its links to metabolic states, proliferation, and adaptation to environmental stresses such as hypoxia and nutrient deprivation. We observed significant variability in UCP2 expression across cancer types, with no direct correlation to their metabolic activity or proliferation rates. UCP2 abundance was also differentially affected by nutrient availability in different cancer cells, but UCP2 was generally downregulated under hypoxia. These findings challenge the notion that UCP2 is a marker of malignant potential and suggest its more complex involvement in the metabolic landscape of cancer., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.) more...
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- 2024
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31. Cell-autonomous IL6ST activation suppresses prostate cancer development via STAT3/ARF/p53-driven senescence and confers an immune-active tumor microenvironment.
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Sternberg C, Raigel M, Limberger T, Trachtová K, Schlederer M, Lindner D, Kodajova P, Yang J, Ziegler R, Kalla J, Stoiber S, Dey S, Zwolanek D, Neubauer HA, Oberhuber M, Redmer T, Hejret V, Tichy B, Tomberger M, Harbusch NS, Pencik J, Tangermann S, Bystry V, Persson JL, Egger G, Pospisilova S, Eferl R, Wolf P, Sternberg F, Högler S, Lagger S, Rose-John S, and Kenner L more...
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- Male, Animals, Mice, Humans, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Cyclin-Dependent Kinase Inhibitor p16 metabolism, Cyclin-Dependent Kinase Inhibitor p16 genetics, Disease Models, Animal, STAT3 Transcription Factor metabolism, Prostatic Neoplasms pathology, Prostatic Neoplasms metabolism, Prostatic Neoplasms genetics, Tumor Microenvironment, Tumor Suppressor Protein p53 metabolism, Tumor Suppressor Protein p53 genetics, Cellular Senescence, Signal Transduction
- Abstract
Background: Prostate cancer ranks as the second most frequently diagnosed cancer in men worldwide. Recent research highlights the crucial roles IL6ST-mediated signaling pathways play in the development and progression of various cancers, particularly through hyperactivated STAT3 signaling. However, the molecular programs mediated by IL6ST/STAT3 in prostate cancer are poorly understood., Methods: To investigate the role of IL6ST signaling, we constitutively activated IL6ST signaling in the prostate epithelium of a Pten-deficient prostate cancer mouse model in vivo and examined IL6ST expression in large cohorts of prostate cancer patients. We complemented these data with in-depth transcriptomic and multiplex histopathological analyses., Results: Genetic cell-autonomous activation of the IL6ST receptor in prostate epithelial cells triggers active STAT3 signaling and significantly reduces tumor growth in vivo. Mechanistically, genetic activation of IL6ST signaling mediates senescence via the STAT3/ARF/p53 axis and recruitment of cytotoxic T-cells, ultimately impeding tumor progression. In prostate cancer patients, high IL6ST mRNA expression levels correlate with better recurrence-free survival, increased senescence signals and a transition from an immune-cold to an immune-hot tumor., Conclusions: Our findings demonstrate a context-dependent role of IL6ST/STAT3 in carcinogenesis and a tumor-suppressive function in prostate cancer development by inducing senescence and immune cell attraction. We challenge the prevailing concept of blocking IL6ST/STAT3 signaling as a functional prostate cancer treatment and instead propose cell-autonomous IL6ST activation as a novel therapeutic strategy., (© 2024. The Author(s).) more...
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- 2024
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32. The 2-oxoglutarate/malate carrier extends the family of mitochondrial carriers capable of fatty acid and 2,4-dinitrophenol-activated proton transport.
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Žuna K, Tyschuk T, Beikbaghban T, Sternberg F, Kreiter J, and Pohl EE
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- Animals, Mice, Humans, Malates metabolism, Mitochondria metabolism, Ion Transport drug effects, Membrane Potential, Mitochondrial drug effects, Protons, Ketoglutaric Acids metabolism, Organic Anion Transporters metabolism, Organic Anion Transporters genetics, Membrane Transport Proteins, 2,4-Dinitrophenol pharmacology, Fatty Acids metabolism
- Abstract
Aims: Metabolic reprogramming in cancer cells has been linked to mitochondrial dysfunction. The mitochondrial 2-oxoglutarate/malate carrier (OGC) has been suggested as a potential target for preventing cancer progression. Although OGC is involved in the malate/aspartate shuttle, its exact role in cancer metabolism remains unclear. We aimed to investigate whether OGC may contribute to the alteration of mitochondrial inner membrane potential by transporting protons., Methods: The expression of OGC in mouse tissues and cancer cells was investigated by PCR and Western blot analysis. The proton transport function of recombinant murine OGC was evaluated by measuring the membrane conductance (G
m ) of planar lipid bilayers. OGC-mediated substrate transport was measured in proteoliposomes using14 C-malate., Results: OGC increases proton Gm only in the presence of natural (long-chain fatty acids, FA) or chemical (2,4-dinitrophenol) protonophores. The increase in OGC activity directly correlates with the increase in the number of unsaturated bonds of the FA. OGC substrates and inhibitors compete with FA for the same protein binding site. Arginine 90 was identified as a critical amino acid for the binding of FA, ATP, 2-oxoglutarate, and malate, which is a first step towards understanding the OGC-mediated proton transport mechanism., Conclusion: OGC extends the family of mitochondrial transporters with dual function: (i) metabolite transport and (ii) proton transport facilitated in the presence of protonophores. Elucidating the contribution of OGC to uncoupling may be essential for the design of targeted drugs for the treatment of cancer and other metabolic diseases., (© 2024 The Authors. Acta Physiologica published by John Wiley & Sons Ltd on behalf of Scandinavian Physiological Society.) more...- Published
- 2024
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33. JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.
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Redmer T, Raigel M, Sternberg C, Ziegler R, Probst C, Lindner D, Aufinger A, Limberger T, Trachtova K, Kodajova P, Högler S, Schlederer M, Stoiber S, Oberhuber M, Bolis M, Neubauer HA, Miranda S, Tomberger M, Harbusch NS, Garces de Los Fayos Alonso I, Sternberg F, Moriggl R, Theurillat JP, Tichy B, Bystry V, Persson JL, Mathas S, Aberger F, Strobl B, Pospisilova S, Merkel O, Egger G, Lagger S, and Kenner L more...
- Subjects
- Male, Animals, Mice, Humans, Senescence-Associated Secretory Phenotype, Proto-Oncogene Proteins c-jun metabolism, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Gene Expression Profiling, Cellular Senescence genetics, Disease Models, Animal, Prostatic Neoplasms pathology, Prostatic Neoplasms genetics, Prostatic Neoplasms metabolism, PTEN Phosphohydrolase genetics, PTEN Phosphohydrolase metabolism, Disease Progression, Tumor Microenvironment immunology
- Abstract
Background: Prostate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated as potential oncogenic drivers, the molecular programs contributing to prostate cancer progression are not fully understood., Methods: We analyzed JUN expression in clinical prostate cancer samples across different stages and investigated its functional role in a Pten-deficient mouse model. We performed histopathological examinations, transcriptomic analyses and explored the senescence-associated secretory phenotype in the tumor microenvironment., Results: Elevated JUN levels characterized early-stage prostate cancer and predicted improved survival in human and murine samples. Immune-phenotyping of Pten-deficient prostates revealed high accumulation of tumor-infiltrating leukocytes, particularly innate immune cells, neutrophils and macrophages as well as high levels of STAT3 activation and IL-1β production. Jun depletion in a Pten-deficient background prevented immune cell attraction which was accompanied by significant reduction of active STAT3 and IL-1β and accelerated prostate tumor growth. Comparative transcriptome profiling of prostate epithelial cells revealed a senescence-associated gene signature, upregulation of pro-inflammatory processes involved in immune cell attraction and of chemokines such as IL-1β, TNF-α, CCL3 and CCL8 in Pten-deficient prostates. Strikingly, JUN depletion reversed both the senescence-associated secretory phenotype and senescence-associated immune cell infiltration but had no impact on cell cycle arrest. As a result, JUN depletion in Pten-deficient prostates interfered with the senescence-associated immune clearance and accelerated tumor growth., Conclusions: Our results suggest that JUN acts as tumor-suppressor and decelerates the progression of prostate cancer by transcriptional regulation of senescence- and inflammation-associated genes. This study opens avenues for novel treatment strategies that could impede disease progression and improve patient outcomes., (© 2024. The Author(s).) more...
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- 2024
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34. Editorial: Ketone bodies: friend or foe?
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Sternberg F, Nomura M, Xie M, and Duszka K
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- Ketone Bodies, Diet, Ketogenic
- Abstract
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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- 2024
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35. Mitochondrial network adaptations of microglia reveal sex-specific stress response after injury and UCP2 knockout.
- Author
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Maes ME, Colombo G, Schoot Uiterkamp FE, Sternberg F, Venturino A, Pohl EE, and Siegert S
- Abstract
Mitochondrial networks remodel their connectivity, content, and subcellular localization to support optimized energy production in conditions of increased environmental or cellular stress. Microglia rely on mitochondria to respond to these stressors, however our knowledge about mitochondrial networks and their adaptations in microglia in vivo is limited. Here, we generate a mouse model that selectively labels mitochondria in microglia. We identify that mitochondrial networks are more fragmented with increased content and perinuclear localization in vitro vs. in vivo . Mitochondrial networks adapt similarly in microglia closest to the injury site after optic nerve crush. Preventing microglial UCP2 increase after injury by selective knockout induces cellular stress. This results in mitochondrial hyperfusion in male microglia, a phenotype absent in females due to circulating estrogens. Our results establish the foundation for mitochondrial network analysis of microglia in vivo , emphasizing the importance of mitochondrial-based sex effects of microglia in other pathologies., Competing Interests: The authors declare no competing interests., (© 2023 The Author(s).) more...
- Published
- 2023
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36. STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway.
- Author
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Pencik J, Philippe C, Schlederer M, Atas E, Pecoraro M, Grund-Gröschke S, Li WJ, Tracz A, Heidegger I, Lagger S, Trachtová K, Oberhuber M, Heitzer E, Aksoy O, Neubauer HA, Wingelhofer B, Orlova A, Witzeneder N, Dillinger T, Redl E, Greiner G, D'Andrea D, Östman JR, Tangermann S, Hermanova I, Schäfer G, Sternberg F, Pohl EE, Sternberg C, Varady A, Horvath J, Stoiber D, Malcolm TI, Turner SD, Parkes EE, Hantusch B, Egger G, Rose-John S, Poli V, Jain S, Armstrong CWD, Hoermann G, Goffin V, Aberger F, Moriggl R, Carracedo A, McKinney C, Kennedy RD, Klocker H, Speicher MR, Tang DG, Moazzami AA, Heery DM, Hacker M, and Kenner L more...
- Subjects
- Animals, Humans, Male, Mice, AMP-Activated Protein Kinases metabolism, Mechanistic Target of Rapamycin Complex 1 metabolism, Neoplasm Recurrence, Local, STAT3 Transcription Factor genetics, STAT3 Transcription Factor metabolism, Diabetes Mellitus, Type 2, Metformin pharmacology, Prostatic Neoplasms genetics, Prostatic Neoplasms pathology
- Abstract
Prostate cancer (PCa) is a common and fatal type of cancer in men. Metastatic PCa (mPCa) is a major factor contributing to its lethality, although the mechanisms remain poorly understood. PTEN is one of the most frequently deleted genes in mPCa. Here we show a frequent genomic co-deletion of PTEN and STAT3 in liquid biopsies of patients with mPCa. Loss of Stat3 in a Pten-null mouse prostate model leads to a reduction of LKB1/pAMPK with simultaneous activation of mTOR/CREB, resulting in metastatic disease. However, constitutive activation of Stat3 led to high LKB1/pAMPK levels and suppressed mTORC1/CREB pathway, preventing mPCa development. Metformin, one of the most widely prescribed therapeutics against type 2 diabetes, inhibits mTORC1 in liver and requires LKB1 to mediate glucose homeostasis. We find that metformin treatment of STAT3/AR-expressing PCa xenografts resulted in significantly reduced tumor growth accompanied by diminished mTORC1/CREB, AR and PSA levels. PCa xenografts with deletion of STAT3/AR nearly completely abrogated mTORC1/CREB inhibition mediated by metformin. Moreover, metformin treatment of PCa patients with high Gleason grade and type 2 diabetes resulted in undetectable mTORC1 levels and upregulated STAT3 expression. Furthermore, PCa patients with high CREB expression have worse clinical outcomes and a significantly increased risk of PCa relapse and metastatic recurrence. In summary, we have shown that STAT3 controls mPCa via LKB1/pAMPK/mTORC1/CREB signaling, which we have identified as a promising novel downstream target for the treatment of lethal mPCa., (© 2023. BioMed Central Ltd., part of Springer Nature.) more...
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- 2023
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37. Ketogenic diets composed of long-chain and medium-chain fatty acids induce cardiac fibrosis in mice.
- Author
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Sternberg F, Sternberg C, Dunkel A, Beikbaghban T, Gregor A, Szarzynski A, Somoza V, Walter I, Duszka K, Kofler B, and Pohl EE
- Subjects
- Male, Mice, Animals, Triglycerides metabolism, Fatty Acids, Fibrosis, Diet, Ketogenic adverse effects, Diet, Ketogenic methods, Heart Diseases
- Abstract
Purpose: Heart diseases are the leading cause of death worldwide. Metabolic interventions via ketogenic diets (KDs) have been used for decades to treat epilepsy, and more recently, also diabetes and obesity, as common comorbidities of heart diseases. However, recent reports linked KDs, based on long-chain triglycerides (LCTs), to cardiac fibrosis and a reduction of heart function in rodents. As intervention using medium-chain triglycerides (MCTs) was recently shown to be beneficial in murine cardiac reperfusion injury, the question arises as to what extent the fatty acid (FA)-composition in a KD alters molecular markers of FA-oxidation (FAO) and modulates cardiac fibrotic outcome., Methods: The effects of LCT-KD as well as an LCT/MCT mix (8:1 ketogenic ratio) on cardiac tissue integrity and the plasma metabolome were assessed in adult male C57/BL6NRJ mice after eight weeks on the respective diet., Results: Both KDs resulted in increased amount of collagen fibers and cardiac tissue was immunologically indistinguishable between groups. MCT supplementation resulted in i) profound changes in plasma metabolome, ii) reduced hydroxymethylglutaryl-CoA synthase upregulation, and mitofusin 2 downregulation, iii) abrogation of LCT-induced mitochondrial enlargement, and iv) enhanced FAO profile. Contrary to literature, mitochondrial biogenesis was unaffected by KDs. We propose that the observed tissue remodeling is caused by the accumulation of 4-hydroxy-2-nonenal protein adducts, despite an inconspicuous nuclear factor (erythroid-derived 2)-like 2 pathway., Conclusion: We conclude that regardless of the generally favorable effects of MCTs, they cannot inhibit 4-hydroxy-2-nonenal adduct formation and fibrotic tissue formation in this setting. Furthermore, we support the burgeoning concern about the effect of KDs on the cardiac safety profile., (Copyright © 2023 The Authors. Published by Elsevier GmbH.. All rights reserved.) more...
- Published
- 2023
- Full Text
- View/download PDF
38. Adaptive mechanisms in no flow vs. low flow ischemia in equine jejunum epithelium: Different paths to the same destination.
- Author
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Dengler F, Sternberg F, Grages M, Kästner SB, and Verhaar N
- Abstract
Intestinal ischemia reperfusion injury (IRI) is a frequent complication of equine colic. Several mechanisms may be involved in adaptation of the intestinal epithelium to IRI and might infer therapeutic potential, including hypoxia-inducible factor (HIF) 1α, AMP-activated protein kinase (AMPK), nuclear factor-erythroid 2-related factor 2 (NRF2), and induction of autophagy. However, the mechanisms supporting adaptation and thus cellular survival are not completely understood yet. We investigated the activation of specific adaptation mechanisms in both no and low flow ischemia and reperfusion simulated in equine jejunum epithelium in vivo . We found an activation of HIF1α in no and low flow ischemia as indicated by increased levels of HIF1α target genes and phosphorylation of AMPKα tended to increase during ischemia. Furthermore, the protein expression of the autophagy marker LC3B in combination with decreased expression of nuclear-encoded mitochondrial genes indicates an increased rate of mitophagy in equine intestinal IRI, possibly preventing damage by mitochondria-derived reactive oxygen species (ROS). Interestingly, ROS levels were increased only shortly after the onset of low flow ischemia, which may be explained by an increased antioxidative defense, although NFR2 was not activated in this setup. In conclusion, we could demonstrate that a variety of adaptation mechanisms manipulating different aspects of cellular homeostasis are activated in IRI irrespective of the ischemia model, and that mitophagy might be an important factor for epithelial survival following small intestinal ischemia in horses that should be investigated further., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Dengler, Sternberg, Grages, Kästner and Verhaar.) more...
- Published
- 2022
- Full Text
- View/download PDF
39. A Comparison of the Impact of Restrictive Diets on the Gastrointestinal Tract of Mice.
- Author
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Gregor A, Huber L, Auernigg-Haselmaier S, Sternberg F, Billerhart M, Dunkel A, Somoza V, Ogris M, Kofler B, Longo VD, König J, and Duszka K
- Subjects
- Animals, Diet, Fasting, Gastrointestinal Tract metabolism, Mice, Diet, Ketogenic, Gastrointestinal Microbiome
- Abstract
The rate of gut inflammatory diseases is growing in modern society. Previously, we showed that caloric restriction (CR) shapes gut microbiota composition and diminishes the expression of inflammatory factors along the gastrointestinal (GI) tract. The current project aimed to assess whether prominent dietary restrictive approaches, including intermittent fasting (IF), fasting-mimicking diet (FMD), and ketogenic diet (KD) have a similar effect as CR. We sought to verify which of the restrictive dietary approaches is the most potent and if the molecular pathways responsible for the impact of the diets overlap. We characterized the impact of the diets in the context of several dietary restriction-related parameters, including immune status in the GI tract; microbiota and its metabolites; bile acids (BAs); gut morphology; as well as autophagy-, mitochondria-, and energy restriction-related parameters. The effects of the various diets are very similar, particularly between CR, IF, and FMD. The occurrence of a 50 kDa truncated form of occludin, the composition of the microbiota, and BAs distinguished KD from the other diets. Based on the results, we were able to provide a comprehensive picture of the impact of restrictive diets on the gut, indicating that restrictive protocols aimed at improving gut health may be interchangeable. more...
- Published
- 2022
- Full Text
- View/download PDF
40. Consensus on the treatment of alopecia areata - Brazilian Society of Dermatology.
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Ramos PM, Anzai A, Duque-Estrada B, Melo DF, Sternberg F, Santos LDN, Alves LD, and Mulinari-Brenner F
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- Adult, Brazil, Consensus, Humans, Quality of Life, Alopecia Areata drug therapy, Dermatology
- Abstract
Background: Alopecia areata is a highly frequent disease with an impact on quality of life and several treatment options with little clinical confirmatory evidence., Objective: To disseminate the recommendations of Brazilian dermatologists with expertise in the treatment of alopecia areata., Methods: Eight specialists with expertise in alopecia areata from different university centers were appointed by the Brazilian Society of Dermatology to reach a consensus on its treatment. Based on the adapted DELPHI methodology, the relevant elements were considered; then, an analysis of recent literature was carried out and the consensus was written down. Consensus on the management of alopecia areata was defined with the approval of at least 70% of the panel., Results/conclusions: Intralesional injectable corticotherapy was considered the first option for localized disease in adults. In extensive cases with signs of activity, systemic corticosteroid therapy should be considered and can be used together with immunosuppressants (corticosteroid-sparing agents). The use of an immunosensitizer (diphencyprone) is an option for stable long-term cases. Evaluation of side effects is as important as the rate of hair regrowth., (Copyright © 2020 Sociedade Brasileira de Dermatologia. Published by Elsevier España, S.L.U. All rights reserved.) more...
- Published
- 2020
- Full Text
- View/download PDF
41. The Influence of Ketogenic Diets on Psoriasiform-Like Skin Inflammation.
- Author
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Sternberg F, Leitner J, Aminzadeh-Gohari S, Weber DD, Sanio P, Koller A, Feichtinger RG, Weiss R, Kofler B, and Lang R
- Subjects
- 3-Hydroxybutyric Acid blood, Animals, Biopsy, Blood Glucose analysis, Diet, Ketogenic adverse effects, Disease Models, Animal, Humans, Imiquimod immunology, Male, Mice, Psoriasis blood, Psoriasis diagnosis, Psoriasis immunology, Severity of Illness Index, Skin immunology, Skin pathology, Triglycerides administration & dosage, Weight Gain, Diet, Ketogenic methods, Fatty Acids, Omega-3 administration & dosage, Psoriasis diet therapy, Triglycerides adverse effects
- Published
- 2020
- Full Text
- View/download PDF
42. Validation of antibody-based tools for galanin research.
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Brunner SM, Koller A, Stockinger J, Sternberg F, Leis S, Ernst F, Strasser P, Brodowicz B, Ebner S, Holub BS, Rauch I, Graf K, Lang R, and Kofler B
- Subjects
- Antibodies, Monoclonal, Murine-Derived immunology, Enzyme-Linked Immunosorbent Assay, Galanin immunology, Humans, Peptides immunology, Radioimmunoassay, Antibodies, Monoclonal, Murine-Derived chemistry, Galanin chemistry, Peptides chemistry
- Abstract
Antibodies are an integral biomedical tool, not only for research but also as therapeutic agents. However, progress can only be made with sensitive and specific antibodies. The regulatory (neuro)peptide galanin and its three endogenous receptors (GAL
1-3 -R) are widely distributed in the central and peripheral nervous systems, and in peripheral non-neuronal tissues. The galanin system has multiple biological functions, including feeding behavior, pain processing, nerve regeneration and inflammation, to name only a few. Galanin could serve as biomarker in these processes, and therefore its receptors are potential drug targets for various diseases. For that reason, it is of paramount interest to precisely measure galanin peptide levels in tissues and to determine the cellular and subcellular localization of galanin receptors. A plethora of antibodies and antibody-based tools, including radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA) kits, are commercially available to detect galanin and its receptors. However, many of them lack rigorous validation which casts doubt on their specificity. A goal of the present study was to raise awareness of the importance of validation of antibodies and antibody-based tools, with a specific focus on the galanin system. To that end, we tested and report here about commercially available antibodies against galanin and galanin receptors that appear specific to us. Furthermore, we investigated the validity of commercially available galanin ELISA kits. As the tested ELISAs failed to meet the validation requirements, we developed and validated a specific sandwich ELISA which can be used to detect full-length galanin in human plasma., (Copyright © 2018 Elsevier Inc. All rights reserved.) more...- Published
- 2019
- Full Text
- View/download PDF
43. Acute Hair Loss 3 Years after Bone Marrow Transplant.
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Silva L, De Fraia Souza MN, Teixeira S, Sternberg F, and Dumet Fernandes J
- Abstract
Competing Interests: The authors have no conflicts of interest to declare.
- Published
- 2019
- Full Text
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44. Galanin is a potent modulator of cytokine and chemokine expression in human macrophages.
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Koller A, Brunner SM, Bianchini R, Ramspacher A, Emberger M, Sternberg F, Schlager S, and Kofler B
- Subjects
- Cell Differentiation physiology, Cell Polarity physiology, Cells, Cultured, Humans, Macrophage Activation physiology, RNA, Messenger metabolism, Chemokines metabolism, Cytokines metabolism, Galanin metabolism, Macrophages metabolism
- Abstract
The regulatory peptide galanin is broadly distributed in the central- and peripheral nervous systems as well as in non-neuronal tissues, where it exerts its diverse physiological functions via three G-protein-coupled receptors (GAL
1-3 -R). Regulatory peptides are important mediators of the cross-communication between the nervous- and immune systems and have emerged as a focus of new therapeutics for a variety of inflammatory diseases. Studies on inflammatory animal models and immune cells revealed both pro- and anti-inflammatory functions of galanin. Here, we probed specific immune-related functions of the galanin system and found galanin and GAL1 -R and GAL2 -R mRNA to be expressed in a range of human immune cells. In particular, macrophages displayed differentiation- and polarization-dependent expression of galanin and its receptors. Exposure to exogenous galanin affected the cytokine/chemokine expression profile of macrophages differently, depending on their differentiation and polarization, and mainly modulated the expression of chemokines (CCL2, CCL3, CCL5 and CXCL8) and anti-inflammatory cytokines (TGF-β, IL-10 and IL-1Ra), especially in type-1 macrophages. Cytokine/chemokine expression levels in interferon-gamma- and lipopolysaccharide-polarized macrophages were upregulated whereas in unpolarized macrophages they were downregulated upon galanin treatment for 20 hours. This study illuminates the regulation of important cytokines/chemokines in macrophages by galanin, depending on specific cell activation. more...- Published
- 2019
- Full Text
- View/download PDF
45. Effects of galanin receptor 2 and receptor 3 knockout in mouse models of acute seizures.
- Author
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Drexel M, Sternberg’ F, Kofler B, and Sperk G
- Subjects
- Animals, Disease Models, Animal, Electroencephalography, Hippocampus drug effects, Kainic Acid toxicity, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Pentylenetetrazole toxicity, Reaction Time drug effects, Reaction Time genetics, Receptor, Galanin, Type 2 genetics, Receptor, Galanin, Type 3 genetics, Seizures chemically induced, Receptor, Galanin, Type 2 deficiency, Receptor, Galanin, Type 3 deficiency, Seizures genetics
- Abstract
There exists solid evidence that endogenous galanin and galanin agonists exert anticonvulsive actions mediated both by galanin 1 receptor (GAL1-R) and galanin 2 receptor (GAL2-R). We have now investigated whether depletion of the recently identified third galanin receptor, GAL3-R, and that of GAL2-R, alters the threshold to the systemically applied γ-aminobutyric acid (GABA) antagonist pentylenetetrazole (PTZ) or to intrahippocampally administered kainic acid (KA). In neither model, GAL3-KO mice differed in their latency to the first seizure, mean seizure duration, total number of seizures, or time spent in seizures compared to wild-type controls. In addition, consistent with previous data, the response to PTZ was not altered in GAL2-KO mice. In contrast, intrahippocampal KA resulted in a significantly increased number of seizures and time spent in seizures in GAL2-KO mice, although the latency to the first seizure and the duration of individual seizures was not altered. These results are consistent with the previous data showing that GAL2-R knockdown does not affect the number of perforant path stimulations required for initiating status epilepticus but significantly increases the seizure severity during the ongoing status. In conclusion, our data support a specific role of GAL2-R but not of GAL3-R in mediating the anticonvulsive actions of endogenous galanin., (© The Authors. Epilepsia published by Wiley Periodicals, Inc. on behalf of International League Against Epilepsy.) more...
- Published
- 2018
- Full Text
- View/download PDF
46. Lack of Galanin Receptor 3 Alleviates Psoriasis by Altering Vascularization, Immune Cell Infiltration, and Cytokine Expression.
- Author
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Sternberg F, Vidali S, Holub BS, Stockinger J, Brunner SM, Ebner S, Koller A, Trost A, Reitsamer HA, Schwarzenbacher D, Lang R, and Kofler B
- Subjects
- Adult, Animals, Disease Models, Animal, Female, Humans, Imiquimod immunology, Keratinocytes, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Neovascularization, Pathologic genetics, Nestin metabolism, Neutrophils immunology, Psoriasis diagnosis, Psoriasis genetics, Psoriasis immunology, Receptor, Galanin, Type 2 genetics, Receptor, Galanin, Type 2 metabolism, Receptor, Galanin, Type 3 genetics, Severity of Illness Index, Skin blood supply, Skin drug effects, Skin immunology, Skin pathology, Cytokines metabolism, Neovascularization, Pathologic pathology, Neutrophil Infiltration, Psoriasis pathology, Receptor, Galanin, Type 3 metabolism
- Abstract
The neuropeptide galanin is distributed in the central and peripheral nervous systems and in non-neuronal peripheral organs, including the skin. Galanin acts via three G protein-coupled receptors which, except galanin receptor 1, are expressed in various skin structures. The galanin system has been associated with inflammatory processes of the skin and of several other organs. Psoriasis is an inflammatory skin disease with increased neovascularization, keratinocyte hyperproliferation, a proinflammatory cytokine milieu, and immune cell infiltration. In this study, we showed that galanin receptor 3 is present in endothelial cells in human and murine dermal vessels and is co-expressed with nestin in neo-vessels of psoriatic patients. Moreover, in a murine psoriasis model, we showed that C57/BL6 mice lacking galanin receptor 3 display a milder course of psoriasis upon imiquimod treatment, leading to decreased disease severity, delayed neo-vascularization, reduced infiltration of neutrophils, and significantly lower levels of proinflammatory cytokines compared with wild-type mice. In contrast, galanin receptor 2-knockout animals did not differ significantly from wild type mice at both the macroscopic and molecular levels in their inflammatory response to imiquimod treatment. Our data indicate that galanin receptor 3, but not galanin receptor 2, plays an important role in psoriasis-like skin inflammation., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.) more...
- Published
- 2018
- Full Text
- View/download PDF
47. Prevalence and associated risk factors of latent tuberculosis infection in a Spanish prison.
- Author
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López de Goicoechea-Saiz ME, Sternberg F, and Portilla-Sogorb J
- Subjects
- Adult, Aged, Antitubercular Agents therapeutic use, Cross-Sectional Studies, Female, Humans, Latent Tuberculosis drug therapy, Latent Tuberculosis etiology, Logistic Models, Male, Middle Aged, Prevalence, Prisons, Risk Factors, Spain epidemiology, Latent Tuberculosis epidemiology, Prisoners statistics & numerical data
- Abstract
Aim: To determine the prevalence of latent tuberculosis infection (LTI) in a Spanish prison, analyze the main sociodemographic and clinical variables associated with this condition and estimate the percentage of individuals with LTI who have received chemoprophylactic treatment., Materials and Methods: Cross-sectional study including inmates hosted in the Madrid VI Prison on 16/07/2016. Exclusion criteria: history of tuberculosis; non-updated tuberculin test according to the Tuberculosis Prevention and Control Program in Prisons protocol. Information of the variables was collected from SANIT and SIP programs, and by checking the clinical records of inmates. Description of the participant population and comparison between the frequency of distribution of the independent variables in LTI present and absent groups were performed, the last calculating the p value with Ji2 and Mann-Whitney U tests. Bivariate and multivariate analysis have been carried out with a logistic regression model., Results: 936 individuals have been included. The prevalence of LTI in prison is 54.6%. This condition has been linked to the sociodemographic variables age, sex and nationality of origin, being age the one that has shown the strongest association. Among the other factors analyzed, only HCV infection behaves as a predictor of LTI. 30.3% of the individuals with LTI have completed or are receiving chemoprophylactic treatment in the moment of the study., Discussion: LTI prevalence is high in the Spanish current prison population. The results of the study emphasize the relevance of the LTI screening in the prison setting, specially among high risk groups, and point out the need of a greater effort in the indication and completion of the chemoprophylactic treatment. more...
- Published
- 2018
48. Trichotillomania: a good response to treatment with N-acetylcysteine.
- Author
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Barroso LAL, Sternberg F, Souza MNIFE, and Nunes GJB
- Subjects
- Alopecia diagnosis, Alopecia etiology, Child, Diagnosis, Differential, Humans, Male, Trichotillomania diagnosis, Acetylcysteine therapeutic use, Antioxidants therapeutic use, Trichotillomania drug therapy
- Abstract
Trichotillomania is considered a behavioral disorder and is characterized by the recurring habit of pulling one's hair, resulting in secondary alopecia. It affects 1% of the adult population, and 2 to 4.4% of psychiatric patients meet the diagnostic criteria. It can occur at any age and is more prevalent in adolescents and females. Its occurrence in childhood is not uncommon and tends to have a more favorable clinical course. The scalp, eyebrows and eyelashes are the most commonly affected sites. Glutamate modulating agents, such as N-acetylcysteine, have been shown to be a promising treatment. N-acetylcysteine acts by reducing oxidative stress and normalizing glutaminergic transmission. In this paper, we report a case of trichotillomania with an excellent response to N-acetylcysteine. more...
- Published
- 2017
- Full Text
- View/download PDF
49. Lack of Galanin 3 Receptor Aggravates Murine Autoimmune Arthritis.
- Author
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Botz B, Kemény Á, Brunner SM, Sternberg F, Csepregi J, Mócsai A, Pintér E, McDougall JJ, Kofler B, and Helyes Z
- Subjects
- Animals, Arthritis genetics, Arthritis pathology, Autoimmune Diseases genetics, Autoimmune Diseases pathology, Capillary Permeability, Edema metabolism, Endothelium, Vascular metabolism, Hindlimb pathology, Male, Mice, Neutrophils metabolism, Receptor, Galanin, Type 3 deficiency, Arthritis metabolism, Autoimmune Diseases metabolism, Receptor, Galanin, Type 3 genetics
- Abstract
Neurogenic inflammation mediated by peptidergic sensory nerves has a crucial impact on the pathogenesis of various joint diseases. Galanin is a regulatory sensory neuropeptide, which has been shown to attenuate neurogenic inflammation, modulate neutrophil activation, and be involved in the development of adjuvant arthritis, but our current understanding about its targets and physiological importance is incomplete. Among the receptors of galanin (GAL1-3), GAL3 has been found to be the most abundantly expressed in the vasculature and on the surface of some immune cells. However, since there are minimal in vivo data on the role of GAL3 in joint diseases, we analyzed its involvement in different inflammatory mechanisms of the K/BxN serum transfer-model of autoimmune arthritis employing GAL 3 gene-deficient mice. After arthritis induction, GAL3 knockouts demonstrated increased clinical disease severity and earlier hindlimb edema than wild types. Vascular hyperpermeability determined by in vivo fluorescence imaging was also elevated compared to the wild-type controls. However, neutrophil accumulation detected by in vivo luminescence imaging or arthritic mechanical hyperalgesia was not altered by the lack of the GAL3 receptor. Our findings suggest that GAL3 has anti-inflammatory properties in joints by inhibiting vascular hyperpermeability and consequent edema formation. more...
- Published
- 2016
- Full Text
- View/download PDF
50. In vitro toxicity of the galanin receptor 3 antagonist SNAP 37889.
- Author
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Koller A, Rid R, Beyreis M, Bianchini R, Holub BS, Lang A, Sternberg F, Brodowicz B, Velickovic O, Jakab M, Kerschbaum H, Önder K, and Kofler B
- Subjects
- Animals, Cell Line, Cell Line, Tumor, Cell Survival drug effects, Epithelial Cells drug effects, Humans, In Vitro Techniques, Leukocytes, Mononuclear drug effects, Mice, Microglia drug effects, Neurons drug effects, Apoptosis drug effects, Indoles toxicity, Receptor, Galanin, Type 3 antagonists & inhibitors
- Abstract
Galanin and its receptors (GAL1, GAL2, GAL3) modulate a range of neuronal, immune and vascular activities. In vivo administration of SNAP 37889 (1-phenyl-3-[[3-(trifluoromethyl)phenyl]imino]-1H-indol-2-one), a potent small non-peptidergic antagonist of GAL3, was reported to reduce anxiety- and depression-related behavior, ethanol consumption, and antagonizes the effect of galanin on plasma extravasation in rodent models. Accordingly, SNAP 37889 has been proposed as a potential therapeutic agent to treat anxiety and depression disorders. Therefore, we evaluated the toxicity of SNAP 37889 to different cell types. Our experiments revealed that SNAP 37889 (≥10μM) induced apoptosis in epithelial (HMCB) and microglial (BV-2) cell lines expressing endogenous GAL3, in peripheral blood mononuclear cells and promyelocytic leukemia cells (HL-60) expressing GAL2, and in a neuronal cell line (SH-SY5Y) lacking galanin receptor expression altogether. In conclusion, SNAP 37889 is toxic to a variety of cell types independent of GAL3 expression. We caution that the clinical use of SNAP 37889 at doses that might be used to treat anxiety- or depression- related diseases could have unexpected non-galanin receptor-mediated toxicity, especially on immune cells., (Copyright © 2015 Elsevier Ltd. All rights reserved.) more...
- Published
- 2016
- Full Text
- View/download PDF
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