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260 results on '"Sblattero D"'

6. Defining theHelicobacter pyloriDisease-Specific Antigenic Repertoire

Author

Soluri, M. F., Puccio, S., Caredda, G., Edomi, P., D'Elios, M. M., Cianchi, F., Troilo, A., Santoro, C., Sblattero, D., and Peano, C.

Subjects
next generation sequencing, gastric cancer, autoimmune gastritis, interactome, pyloriinfection, MALT lymphoma, phage display
Published
2020

7. Mass screening for coeliac disease using antihuman transglutaminase antibody assay

Author

Tommasini, A., Not, T., Kiren, V., Baldas, V., Santon, D., Trevisiol, C., Berti, I., Neri, E., Gerarduzzi, T., Bruno, I., Lenhardt, A., Zamuner, E., Spano, A., Crovella, S., Martellossi, S., Torre, G., Sblattero, D., Marzari, R., Bradbury, A., Tamburlini, G., and Ventura, A.

Subjects
Children -- Health aspects, Celiac disease -- Diagnosis, Transglutaminases, Medical screening, Epidemiology
Published
2004

8. Anti-tissue transglutaminase antibodies from coeliac patients inhibit transglutaminase activity both in vitro and in situ. (Coeliac Disease)

Author

Esposito, C., Paparo, F., Caputo, I., Rossi, M., Maglio, M., Sblattero, D., Not, T., Porta, R., Auricchio, S., Marzari, R., and Troncone, R.

Subjects
Transglutaminases -- Physiological aspects, Celiac disease -- Physiological aspects, Viral antibodies -- Physiological aspects, Immunoglobulin A -- Physiological aspects, Immunoglobulin G -- Physiological aspects, Antibodies -- Physiological aspects, Health
Abstract

Background and aims: Coeliac disease (CD) is a multifactorial disarder which has an autoimmune camponent characterised by the occurrence of disease specific autoreactive antibodies against the enzyme tissue transglutaminase (tTG). [...]

Published
2002

9. A novel quantitative ELISA as accurate and reproducible tool to detect epidermal transglutaminase antibodies in patients with Dermatitis Herpetiformis

Author

Ziberna, F., primary, Sblattero, D., additional, Lega, S., additional, Stefani, C., additional, Dal Ferro, M., additional, Marano, F., additional, Gaita, B., additional, De Leo, L., additional, Vatta, S., additional, Berti, I., additional, Caproni, M., additional, Bonciani, D., additional, Lindfors, K., additional, Salmi, T., additional, Reunala, T., additional, Kaukinen, K., additional, Kalliokoski, S., additional, Kurppa, K., additional, Ura, B., additional, Barbi, E., additional, Bramuzzo, M., additional, and Not, T., additional

Published
2020
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10. Diagnostic delays in children with coeliac disease in the central european region

Author

Riznik P, De Leo L, Dolinsek J, Gyimesi J, Klemenak M, Koletzko B, Koletzko S, Korponay- Szabó IR, Krencnik T, Not T, Palcevski G, Sblattero D, Vogrincic M, Werkstetter KJ, Dolinsek J

Subjects
Central Europe, children, coeliac disease, diagnostic delays
Abstract

Objectives: Coeliac disease (CD) is a systemic autoimmune disorder affecting about 1% of the population. Many patients remain undiagnosed or are diagnosed with substantial delay. We assessed diagnostic delays in symptomatic CD children in Central Europe (CE). Methods: Paediatric gastroenterologists in 5 CE countries retrospectively reported data of their patients diagnosed in 2016. Age at first CD-related symptom(s), first visit to paediatric gastroenterologist and confirmed diagnosis were used to determine diagnostic delays. Results: Data from 393 children (65% girls, median age 7 years, range 7 months to 18.5 years) from Croatia, Hungary, Germany, Italy, and Slovenia were analysed. Median duration from first symptom(s) to visit to paediatric gastroenterologist was 5 months (range 0-10 years ; preschool 4 months, school- aged 5 months), and further duration until final diagnosis was 1 month (range 0-5 years) with significant regional differences (P < 0.001). Median diagnostic delay was 6 months (range 0-10 years ; preschool 5 months, school- aged 7 months). Type of clinical presentation had little, however, significant effect on delays. Reduced body mass in delays longer than 3 years compared with delays shorter than 1 year was found (z score -0.93 vs -0.39, P < 0.05). Conclusions: Time from first symptoms to CD diagnosis in children in 5 CE countries is slightly shorter compared with few other small paediatric studies, and significantly shorter than reported for adults. Nevertheless, delays of more than 3 years in 6.6% of children are worrisome. Raising awareness about the variable symptoms and implementation of reliable diagnostic tools will further reduce diagnostic delays.

Published
2019

14. Identification of novel proteins binding the AU-rich element of ?-prothymosin mRNA through the selection of open reading frames (RIDome)

Author

Patrucco L, Peano C, Chiesa A, Guida F, Luisi I, Boria I, Mignone F, De Bellis G, Zucchelli S, Gustincich S, Santoro C, Sblattero D, and Cotella D.

Subjects
AU-rich element, ELAVL1, R3HDM2, RALY, RBM38, RBPome, RNA-binding protein, next-generation DNA sequencing, open reading frame, phage display
Abstract

We describe here a platform for high-throughput protein expression and interaction analysis aimed at identifying the RNA-interacting domainome. This approach combines the selection of a phage library displaying "filtered" open reading frames with next-generation DNA sequencing. The method was validated using an RNA bait corresponding to the AU-rich element of ?-prothymosin, an RNA motif that promotes mRNA stability and translation through its interaction with the RNA-binding protein ELAVL1. With this strategy, we not only confirmed known RNA-binding proteins that specifically interact with the target RNA (such as ELAVL1/HuR and RBM38) but also identified proteins not previously known to be ARE-binding (R3HDM2 and RALY). We propose this technology as a novel approach for studying the RNA-binding proteome

Published
2015

15. DEVELOPMENT OF CHLORAMBUCIL/HYDROXYCHLOROQUINE-LOADED ANTI-CD20 NANOPARTICLES FOR THE TREATMENT OF CHRONIC LYMPHOCYTIC LEUKEMIA : IN VITRO MODEL

Author

MEZZAROBA, NELLY, MACOR, PAOLO, Mansilla E, 1, ZORZET, SONIA, Calvaruso M, 1, Tripodo C, 3, Núñez L, 3, Tedesco F, 4, Nabergoj M, 1, Sblattero D, 6, Granzotto M, 5, Pozzato G, 7, Mezzaroba, Nelly, Mansilla E, 1, Zorzet, Sonia, Calvaruso M, 1, Tripodo C, 3, Núñez L, 3, Tedesco F, 4, Nabergoj M, 1, Sblattero D, 6, Granzotto M, 5, Pozzato G, 7, and Macor, Paolo

Subjects
Chronic lymphocytic leukemia, anti-CD20, nanoparticles, Chronic lymphocytic leukemia, nanoparticles, anti-CD20
Abstract

DEVELOPMENT OF CHLORAMBUCIL/HYDROXYCHLOROQUINE-LOADED ANTI-CD20 NANOPARTICLES FOR THE TREATMENT OF CHRONIC LYMPHOCYTIC LEUKEMIA : IN VITRO MODEL Mezzaroba N,1 Mansilla E,2 Zorzet S,1 Calvaruso M,3 Tripodo C,3 Núñez L,4 Tedesco F,1 Nabergoj M,6 Sblattero D,5 Granzotto M,7 Pozzato G,6 Macor P1 1 Department of Life Science, University of Trieste, Italy; 2 CUCAIBA, Ministry of Health, La Plata, Buenos Aires, Argentina; 3 Department of Human Pathology, University of Palermo, Italy; 4 University of Chicago, Chicago, USA and BioTarget, Chicago, USA; 5 Department of Medical Sciences, University of Eastern Piedmont, Novara, Italy; 6 Department of Medical and Surgical Sciences, University of Trieste; 7 Department of Molecular and Laboratory Medicine, IRCCSS Burlo Garofolo, Trieste, Italy Introduction. The actual challenge of tumor therapy is to design new therapeutic agents able to maximize the efficacy minimizing the adverse effects. Nanoparticles (NP) have emerged as important tools to modify the release profile for a large number of drugs. The aim of this study was to determine whether anti-CD20-coated biocompatible FDA-approved NP loaded with Chlorambucil (CLB) and Hydroxychloroquine (HCQ) could induce apoptosis of the B-Chronic Lymphocytic Leukemia (CLL) cell line MEC-1, as well as of circulating neoplastic B-cells isolated from patients with B-CLL. Methods. Nanoparticles were prepared by the copolymerization of polylactic acid and polycaprolactone and had an diameter of 250 nm. The NP with HCQ and CLB were prepared by encapsulation of the two drugs at concentrations of 165 µg per mg of polymer inside their core, and then modified by anti-CD20 adsorption. The NP were resuspended in PBS with 10% Bovine Serum Albumin (BSA) and maintained at 4°C before use. To investigate the ability of NP to affect cell viability and induce cellular apoptosis, MEC-1 cells (2 x 105) were incubated with anti-CD20 coated and CLB-HCQ loaded NP for 48 hours and the residual viable cells was determined with MTT assay. Cell death program activation was also evaluated by analyzing PARP-1 cleavage and Annexin V detection. Monoclonal B-cells were obtained from 44 patients affected by CLL. In each case the IGHV gene mutational status was assessed using standard methods and CD38 and ZAP-70 expressions were determined by flow cytometry. Interphase FISH was performed on nuclei preparations of PBMC and each case was investigated for 13q deletion, 11q deletion, 17p deletion or presence of trisomy 12. Results. Anti-CD20 NP with HCQ and CLB were able to induce a strong reduction (95%) in cell viability of MEC-1 cells. The cytotoxicity was present in a dose-dependent manner and was apoptosis-dependent as confirmed by the PARP- 1 activation and by the binding of Annexin V on cell surface. The same high cytotoxicity rate (>90%) was found also in patient-derived B-cells. The killing rate was independent from IGVH mutational status or from ZAP70 and CD38 expression or from the presence of 17p deletion. An efficient cytotoxicity was present even in CLL B-lymphocytes expressing low CD20 antigen levels on cell surface. The effects of NP were also tested on CD20-negative human and animal cells (CHO, HUVEC, MEL- 28, LoVo cell lines) and no specific cytotoxicity was obtained. On the contrary, incubation of CD20-negative cells with free HCQ + CLB induced cell killing between 58 and 71%. Conclusions. These results indicate that anti-CD20 coated and CLB-HCQ loaded NP show a high toxicity rate in CLL cell line as well as in B-cell obtained from CLL patients. The toxic effect is present also in 17p deleted cases, usually resistant to chemo-immuno-therapy. These results should be confirmed in animal models in order to introduce this promising technology into human clinical trials

Published
2012

16. Serum immunoglobulins A and G, and Monoclonal antibodies anti tissue transglutaminase from coeliac patients inhibit the catalytic activity both in vitro and in situ

Author

ESPOSITO C., PAPARO F., CAPUTO I., ROSSI M., MAGLIO M., SBLATTERO D., NOT T., PORTA R., MARZARI R., TRONCONE, RICCARDO, AURICCHIO, SALVATORE, MAKI M, TOSSAVAINEN M., Esposito, C, Paparo, F, Caputo, I, Rossi, M, Maglio, M, Sblattero, D, Not, T, Porta, Raffaele, Auricchio, S, Marzari, R, Troncone, Riccardo, Esposito, C., Paparo, F., Caputo, I., Rossi, M., Maglio, M., Sblattero, D., Not, T., Porta, R., Auricchio, Salvatore, and Marzari, R.

Published
2001

18. A novel quantitative ELISA as accurate and reproducible tool to detect epidermal transglutaminase antibodies in patients with Dermatitis Herpetiformis.

Author

Ziberna, F., Sblattero, D., Lega, S., Stefani, C., Dal Ferro, M., Marano, F., Gaita, B., De Leo, L., Vatta, S., Berti, I., Caproni, M., Bonciani, D., Lindfors, K., Salmi, T., Reunala, T., Kaukinen, K., Kalliokoski, S., Kurppa, K., Ura, B., and Barbi, E.

Subjects
*GLUTEN allergenicity, *SKIN inflammation, *IMMUNOGLOBULINS, *CELIAC disease, *ANTIBODY formation, *GLUTEN-free diet
Abstract

I Editor i Serology for anti-epidermal transglutaminase antibodies (Anti-TG3 Abs) has attracted interest, being inexpensive and non-invasive and could ideally replace skin biopsy for the diagnosis of Dermatitis Herpetiformis (DH).1 The current commercially available ELISA (Elisa kit) for serum Anti-TG3 Abs overall has a good specificity (84-100%)2-4; however, its clinical use is limited due to variable sensitivity (45-100%) and low specificity in Coeliac Disease (CD) patients (47-85%) in whom Anti-TG3 Abs may be present in the absence of DH.2,3,5-7 Here, we developed and evaluated the diagnostic performance of a novel ELISA to quantitatively measure Anti-TG3 Abs. Interestingly, the specificity of the novel ELISA varied when considering CD patients by age and was higher in patients <=25 years (specificity 97%) versus patients >25 years (specificity 55%). [Extracted from the article]

Published
2021
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23. Anti-transglutaminase and age, Clinical Chemestry

Author

BALDAS V, TOMMASINI A, ANSALDI F, DEMARINI S, SBLATTERO D, BURLINA A, NOT, TARCISIO, MARZARI, ROBERTO, TORELLI, LUCIO, TIRIBELLI, CLAUDIO, VENTURA, ALESSANDRO, Baldas, V, Not, Tarcisio, Tommasini, A, Ansaldi, F, Demarini, S, Sblattero, D, Marzari, Roberto, Torelli, Lucio, Burlina, A, Tiribelli, Claudio, and Ventura, Alessandro

Subjects
Anti-Transglutaminase Antibodies, Celiac disease, Anti-Transglutaminase Antibodie
Abstract

The tendency within the general population to produce both organ and non-organ-specific autoantibodies is well recognized. It is not clear whether these autoantibodies represent the subclinical spectrum of certain autoimmune diseases or whether they are one effect of aging on the autoimmune system.

Published
2004

24. Celiac anti-type 2 transglutaminase antibodies induce phosphoproteome modification in intestinal epithelial caco-2 cells

Author

Paolella G, Caputo I, Marabotti A, Lepretti M, Salzano AM, Scaloni A, Vitale M, Zambrano N, Sblattero D, and Esposito C.

Abstract

Background Celiac disease is an inflammatory condition of the small intestine that affects genetically predisposed individuals after dietary wheat gliadin ingestion. Type 2-transglutaminase (TG2) activity seems to be responsible for a strong autoimmune response in celiac disease, TG2 being the main autoantigen. Several studies support the concept that celiac anti-TG2 antibodies may contribute to disease pathogenesis. Our recent findings on the ability of anti-TG2 antibodies to induce a rapid intracellular mobilization of calcium ions, as well as extracellular signal-regulated kinase phosphorylation, suggest that they potentially act as signaling molecules. In line with this concept, we have investigated whether anti-TG2 antibodies can induce phosphoproteome modification in an intestinal epithelial cell line. Methods and Principal Findings We studied phosphoproteome modification in Caco-2 cells treated with recombinant celiac anti-TG2 antibodies. We performed a two-dimensional electrophoresis followed by specific staining of phosphoproteins and mass spectrometry analysis of differentially phosphorylated proteins. Of 14 identified proteins (excluding two uncharacterized proteins), three were hypophosphorylated and nine were hyperphosphorylated. Bioinformatics analyses confirmed the presence of phosphorylation sites in all the identified proteins and highlighted their involvement in several fundamental biological processes, such as cell cycle progression, cell stress response, cytoskeletal organization and apoptosis. Conclusions Identification of differentially phosphorylated proteins downstream of TG2-antibody stimulation suggests that in Caco-2 cells these antibodies perturb cell homeostasis by behaving as signaling molecules. We hypothesize that anti-TG2 autoantibodies may destabilize the integrity of the intestinal mucosa in celiac individuals, thus contributing to celiac disease establishment and progression. Since several proteins here identified in this study were already known as TG2 substrates, we can also suppose that transamidating activity and differential phosphorylation of the same targets may represent a novel regulatory mechanism whose relevance in celiac disease pathogenesis is still unexplored.

Published
2013
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25. B7H triggering inhibits migration of tumor cell lines

Author

Dianzani, Chiara, Minelli, Rosalba, Gigliotti, Cl, Occhipinti, Sergio, Giovarelli, Mirella, Conti, L, Boggio, E, Shivakumar, Y, Baldanzi, G, Fantozzi, Roberto, Sblattero, D, Chiocchetti, A, and Dianzani, U.

Published
2013

26. Serum immunoglobulin A and G, and monoclonal antibodies anti-tissue transglutaminase from coeliac patients inhibit the catalytic activity both in vitro and in situ

Author

ESPOSITO C, PAPARO F, CAPUTO I, ROSSI M, MAGLIO D, SBLATTERO D, NOT, TARCISIO, PORTA S, TRONCONE R., MARZARI, ROBERTO, Esposito, C, Paparo, F, Caputo, I, Rossi, M, Maglio, D, Sblattero, D, Not, Tarcisio, Porta, S, Marzari, Roberto, and Troncone, R.

Subjects
Celiac disease Transglutaminase Cloned antibodies Phage display
Published
2002

28. A method for rapid and high-yield production of the tick-borne encephalitis virus E and DIII recombinant proteins in E. coliwith preservation of the antigenic properties

Author

Rizzo, S., Mora-Cárdenas, E., Faoro, V., D’Agaro, P., Edomi, P., Marcello, A., and Sblattero, D.

Abstract

Tick-borne encephalitis virus (TBEV) is a member of the Flavivirus genus and is the main pathogenic arbovirus circulating in Europe, Russia and China. The envelope (E) protein is exposed on the viral surface and is the main antigen that is employed in diagnostic tests based on the detection of protein-specific antibodies from serum samples of infected individuals. The high degree of similarity among the E proteins of flaviviruses can, in some cases, lead to cross-reactivity and false-positive results in serological tests. Increased specificity in the detection of positive sera for different Flavivirus infections is often obtained by using a portion of the E protein, namely, the DIII domain. Different strategies and expression systems have been described for E and DIII protein production. Here, we present the optimization of an easy and fast method for TBEV E and DIII antigen production and partial purification from E. coliinclusion bodies. The antigenic properties of the produced antigens are retained, as validated by ELISAs with anti-TBEV murine sera as well as sera from infected human patients. The potential applications of both proteins as diagnostic reagents were confirmed.

Published
2019
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29. Molecular dissection of the tissue transglutaminase antoantibody response in celiac disease

Author

Marzari R, Sblattero D, Florian F, Tongiorgi E, Not T, Tommasini A, Ventura A, Bradbury A, Marzari, R, Sblattero, D, Florian, F, Tongiorgi, E, Not, T, Tommasini, A, Ventura, A, and Bradbury, A

Subjects
Celiac disease, Phage display, antibodies, autoimmunity, autoimmunity, Celiac disease, antibodies, Phage display
Abstract

Celiac disease (CD) is an intestinal malabsorption characterized by intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and tissue transglutaminase, an autoantigen located in the endomysium. Tissue transglutaminase belongs to the family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis, The role of gliadins in eliciting the immune response in CB and holy transglutaminase is linked to the primary reaction are still unclear, In this work, we report the production and analysis of six phage Ab libraries from the peripheral and intestinal lymphocytes of three CD patients, We were able to isolate Abs to transglutaminase from all intestinal lymphocytes libraries but not from those obtained from peripheral lymphocytes, This is in contrast to Abs against gliadin, which could be obtained from all libraries, indicating that the humoral response against transglutaminase occurs at the local level, whereas that against gliadin occurs both peripherally and centrally, Abs from all three patients recognized the same transglutaminase epitopes with a bias toward the use of the V(H)5 Ab variable region family, The possible role of these anti-transglutaminase Abs in the onset of CD and associated autoimmune pathologies is discussed.

Published
2001

30. Antibodies in proteomics

Author

Bradbury, A. R., Velappan, N., Verzillo, V., Ovecka, M., Marzari, R., Sblattero, D., Chasteen, L., Robert Siegel, Pavlik, P., Bradbury, Ar, Velappan, N, Verzillo, V, Ovecka, M, Marzari, Roberto, Sblattero, D, Chasteen, L, Siegel, R, and Pavlik, P.

Subjects
proteomics, Phage display
Published
2001

40. Bispecific antibodies targeting tumor-associated antigens and neutralizing complement regulators increase the efficacy of antibody-based immunotherapy in mice

Author

Macor, P, primary, Secco, E, additional, Mezzaroba, N, additional, Zorzet, S, additional, Durigutto, P, additional, Gaiotto, T, additional, De Maso, L, additional, Biffi, S, additional, Garrovo, C, additional, Capolla, S, additional, Tripodo, C, additional, Gattei, V, additional, Marzari, R, additional, Tedesco, F, additional, and Sblattero, D, additional

Published
2014
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47. Cryptic genetic gluten intolerance revealed by intestinal antitransglutaminase antibodies and response to gluten-free diet

Author

Not, T., primary, Ziberna, F., additional, Vatta, S., additional, Quaglia, S., additional, Martelossi, S., additional, Villanacci, V., additional, Marzari, R., additional, Florian, F., additional, Vecchiet, M., additional, Sulic, A.-M., additional, Ferrara, F., additional, Bradbury, A., additional, Sblattero, D., additional, and Ventura, A., additional

Published
2011
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49. Sunday, 18 July 2010

Author

Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., additional, Piccini, I., additional, Fortmueller, L., additional, Kuhlmann, M., additional, Schaefers, M., additional, Carmeliet, P., additional, Kirchhof, P., additional, Fabritz, L., additional, Sanchez, J., additional, Rodriguez-Sinovas, A., additional, Agullo, E., additional, Garcia-Dorado, D., additional, Lymperopoulos, A., additional, Rengo, G., additional, Gao, E., additional, Zincarelli, C., additional, Koch, W., additional, Morgan, P., additional, Diez, A., additional, Perez, N., additional, Cingolani, H., additional, Zahradnikova, A., additional, Polakova, E., additional, Zahradnik, I., additional, Fluschnik, N., additional, Sossalla, S., additional, Ort, K., additional, Neef, S., additional, Hasenfuss, G., additional, Maier, L., additional, Weinert, S., additional, Poitz, D., additional, Herold, J., additional, Schmeisser, A., additional, Strasser, J., additional, Braun-Dullaeus, R., additional, Nazari-Jahantigh, M., additional, Weber, C., additional, Schober, A., additional, Leuner, A., additional, Eichhorn, B., additional, Ravens, U., additional, Morawietz, H., additional, Babes, E., additional, Babes, V., additional, Popescu, M., additional, Ardelean, A., additional, Rus, M., additional, Bustea, C., additional, Gwozdz, P., additional, Csanyi, G., additional, Luzak, B., additional, Gajda, M., additional, Mateuszuk, L., additional, Chmura-Skirlinska, A., additional, Watala, C., additional, Chlopicki, S., additional, Kierzkowska, I., additional, Sulicka, J., additional, Kwater, A., additional, Strach, M., additional, Surdacki, A., additional, Siedlar, M., additional, Grodzicki, T., additional, Olieslagers, S., additional, Pardali, L., additional, Tchaikovski, V., additional, Ten Dijke, P., additional, Waltenberger, J., additional, Renner, M., additional, Redwan, B., additional, Winter, M., additional, Panzenboeck, A., additional, Jakowitsch, J., additional, Sadushi-Kolici, R., additional, Bonderman, D., additional, Lang, I., additional, Toso, A., additional, Tanini, L., additional, Pizzetti, T., additional, Leoncini, M., additional, Maioli, M., additional, Tedeschi, D., additional, Oliviero, C., additional, Bellandi, F., additional, Casprini, P., additional, Amato, M., additional, Molins, B., additional, Pena, E., additional, Badimon, L., additional, Ferreiro Gutierrez, J., additional, Ueno, M., additional, Alissa, R., additional, Dharmashankar, K., additional, Capodanno, D., additional, Desai, B., additional, Bass, T., additional, Angiolillo, D., additional, Chabielska, E., additional, Gromotowicz, A., additional, Szemraj, J., additional, Stankiewicz, A., additional, Zakrzeska, A., additional, Mohammed, S., additional, Molla, F., additional, Soldo, A., additional, Russo, I., additional, Germano, G., additional, Balconi, G., additional, Staszewsky, L., additional, Latini, R., additional, Lynch, F., additional, Austin, C., additional, Prendergast, B., additional, Keenan, D., additional, Malik, R., additional, Izzard, A., additional, Heagerty, A., additional, Czikora, A., additional, Lizanecz, E., additional, Rutkai, I., additional, Boczan, J., additional, Porszasz, R., additional, Papp, Z., additional, Edes, I., additional, Toth, A., additional, Colantuoni, A., additional, Vagnani, S., additional, Lapi, D., additional, Maroz-Vadalazhskaya, N., additional, Koslov, I., additional, Shumavetz, V., additional, Glibovskaya, T., additional, Ostrovskiy, Y., additional, Koutsiaris, A., additional, Tachmitzi, S., additional, Kotoula, M., additional, Giannoukas, A., additional, Tsironi, E., additional, Darago, A., additional, Orosz, P., additional, Megyesi, Z., additional, Schudeja, S., additional, Matschke, K., additional, Deussen, A., additional, Castro, M., additional, Cena, J., additional, Walsh, M., additional, Schulz, R., additional, Poddar, K., additional, Rha, S., additional, Ramasamy, S., additional, Park, J., additional, Choi, C., additional, Seo, H., additional, Park, C., additional, Oh, D., additional, Almeida, J., additional, Pimenta, S., additional, Bernardes, J., additional, Machado, J., additional, Sabatasso, S., additional, Laissue, J., additional, Hlushchuk, R., additional, Brauer-Krisch, E., additional, Bravin, A., additional, Blattmann, H., additional, Michaud, K., additional, Djonov, V., additional, Hirschberg, K., additional, Tarcea, V., additional, Pali, S., additional, Korkmaz, S., additional, Loganathan, S., additional, Merkely, B., additional, Karck, M., additional, Szabo, G., additional, Pagliani, L., additional, Faggin, E., additional, Rattazzi, M., additional, Puato, M., additional, Presta, M., additional, Grego, F., additional, Deriu, G., additional, Pauletto, P., additional, Kaiser, R., additional, Albrecht, K., additional, Schgoer, W., additional, Theurl, M., additional, Beer, A., additional, Wiedemann, D., additional, Steger, C., additional, Bonaros, N., additional, Kirchmair, R., additional, Kharlamov, A., additional, Cabaravdic, M., additional, 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2010
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