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10. Poster Session 3

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Fabbri, G. M. T., primary, Baldasseroni, S., additional, Panuccio, D., additional, Zoni Berisso, M., additional, Scherillo, M., additional, Lucci, D., additional, Di Pasquale, G., additional, Mathieu, G., additional, Burazor, I., additional, Burazor, M., additional, Perisic, Z., additional, Atanaskovic, V., additional, Erakovic, V., additional, Stojkovic, A., additional, Vogtmann, T., additional, Schoebel, C., additional, Sogorski, S., additional, Sebert, M., additional, Schaarschmidt, J., additional, Fietze, I., additional, Baumann, G., additional, Penzel, T., additional, Mornos, C., additional, Ionac, A., additional, Cozma, D., additional, Dragulescu, D., additional, Mornos, A., additional, Petrescu, L., additional, Pescariu, L., additional, Brembilla-Perrot, B., additional, Khachab, H., additional, Lamberti, F., additional, Bellini, C., additional, Remoli, R., additional, Cogliandro, T., additional, Nardo, R., additional, Bellusci, F., additional, Mazzuca, V., additional, Gaspardone, A., additional, Aguinaga Arrascue, L. 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J., additional, Gibson, D., additional, Pisapia, A., additional, Wazni, O., additional, Natale, A., additional, Arujuna, A., additional, Karim, R., additional, Rinaldi, A., additional, Cooklin, M., additional, Rhode, K., additional, Razavi, R., additional, O'neill, M., additional, Gill, J., additional, Kusa, S., additional, Komatsu, Y., additional, Kakita, K., additional, Takayama, K., additional, Taniguchi, H., additional, Otomo, K., additional, Iesaka, Y., additional, Ammar, S., additional, Reents, T., additional, Fichtner, S., additional, Wu, J., additional, Zhu, P., additional, Kolb, C., additional, Hessling, G., additional, Deisenhofer, I., additional, Gilbert, G., additional, Mohanty, P., additional, Cunningham, J., additional, Metz, T., additional, Horton, R., additional, Tao, S., additional, Yamauchi, Y., additional, Okada, H., additional, Maeda, S., additional, Obayashi, T., additional, Isobe, M., additional, Chan, J., additional, Johar, S., additional, Wong, T., additional, Markides, V., additional, Hussain, W., additional, Konstantinidou, M., additional, Wissner, E., additional, Fuernkranz, A., additional, Yoshiga, Y., additional, Metzner, A., additional, Kuck, K.- H., additional, Ouyang, F., additional, Kettering, K., additional, Gramley, F., additional, Mollnau, H., additional, Weiss, C., additional, Bardeleben, S., additional, Biasco, L., additional, Scaglione, M., additional, Caponi, D., additional, Di Donna, P., additional, Sergi, D., additional, Cerrato, N., additional, Blandino, A., additional, Gaita, F., additional, Fiala, M., additional, Wichterle, D., additional, Sknouril, L., additional, Bulkova, V., additional, Chovancik, J., additional, Nevralova, R., additional, Pindor, J., additional, Januska, J., additional, Choi, J. I., additional, Ban, J. E., additional, Yasutsugu, N., additional, Park, J. S., additional, Jung, J. S., additional, Lim, H. E., additional, Park, S. W., additional, Kim, Y. H., additional, Kuhne, M., additional, Reichlin, T., additional, Ammann, P., additional, Schaer, B., additional, Osswald, S., additional, Sticherling, C., additional, Ohe, M., additional, Goya, M., additional, Hiroshima, K., additional, Hayashi, K., additional, Makihara, Y., additional, Nagashima, M., additional, Fukunaga, M., additional, An, Y., additional, Dorwarth, U., additional, Schmidt, M., additional, Wankerl, M., additional, Krieg, J., additional, Straube, F., additional, Hoffmann, E., additional, Kathan, S., additional, Defaye, P., additional, Mbaye, A., additional, Cassagneau, R., additional, Gagniere, V., additional, Jacon, P., additional, Pokushalov, E., additional, Romanov, A., additional, Artemenko, S., additional, Shabanov, V., additional, Elesin, D., additional, Stenin, I., additional, Turov, A., additional, Losik, D., additional, Kondo, K., additional, Miake, J., additional, Yano, A., additional, Ogura, K., additional, Kato, M., additional, Shigemasa, C., additional, Sekiguchi, Y., additional, Tada, H., additional, Yoshida, K., additional, Naruse, Y., additional, Yamasaki, H., additional, Igarashi, M., additional, Machino, T., additional, Aonuma, K., additional, Chen, S., additional, Liu, S., additional, Chen, G., additional, Meng, W., additional, Zhang, F., additional, Yan, Y., additional, Sciarra, L., additional, Dottori, S., additional, Lanzillo, C., additional, De Ruvo, E., additional, De Luca, L., additional, Minati, M., additional, Lioy, E., additional, Calo', L., additional, Lin, J., additional, Nie, Z., additional, Zhu, M., additional, Wang, X., additional, Zhao, J., additional, Hu, W., additional, Tao, H., additional, Ge, J., additional, Johansson, B., additional, Houltz, B., additional, Edvardsson, N., additional, Schersten, H., additional, Karlsson, T., additional, Wandt, B., additional, Berglin, E., additional, Hoyt, R. 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E., additional, Yaegashi, T., additional, Furusho, H., additional, Kato, T., additional, Chikata, A., additional, Takashima, S., additional, Usui, S., additional, Takamura, M., additional, Kaneko, S., additional, Chudzik, M., additional, Mitkowski, P., additional, Przybylski, A., additional, Lewek, J., additional, Smukowski, T., additional, Maciag, A., additional, Castrejon Castrejon, S., additional, Perez-Silva, A., additional, Estrada, A., additional, Doiny, D., additional, Ortega, M., additional, Lopez-Sendon, J. L., additional, Merino, J. L., additional, O'mahony, C., additional, Coats, C., additional, Cardona, M., additional, Garcia, A., additional, Calcagnino, M., additional, Lachmann, R., additional, Hughes, D., additional, Elliott, P. M., additional, Conti, S., additional, Pruiti, G. P., additional, Puzzangara, E., additional, Romano, S. A., additional, Di Grazia, A., additional, Ussia, G. P., additional, Tamburino, C., additional, Calvi, V., additional, Radinovic, A., additional, Sala, S., additional, Latib, A., additional, Mussardo, M., additional, Sora, S., additional, Paglino, G., additional, Gullace, M., additional, Colombo, A., additional, Ohlow, M.- A. G., additional, Lauer, B., additional, Wagner, A., additional, Schreiber, M., additional, Buchter, B., additional, Farah, A., additional, Fuhrmann, J. T., additional, Geller, J. C., additional, Nascimento Cardoso, R. M., additional, Batista Sa, L. A., additional, Campos Filho, L. F. C., additional, Rodrigues, S. V., additional, Dutra, M. V. F., additional, Borges, T. R. S. A., additional, Portilho, D. R., additional, Deering, T., additional, Bernardes, A., additional, Veiga, A., additional, Gartenlaub, O., additional, Goncalves, A., additional, Jimenez, A., additional, Rousseauplasse, A., additional, Deharo, J. C., additional, Striekwold, H., additional, Gosselin, G., additional, Sitbon, H., additional, Martins, V., additional, Molon, G., additional, Ayala-Paredes, F., additional, Sancho-Tello, M. J., additional, Fazal, I. A., additional, Brady, S., additional, Cronin, J., additional, Mcnally, S., additional, Tynan, M., additional, Plummer, C. J., additional, Mccomb, J. M., additional, Val-Mejias, J. E., additional, Oliveira, R. M., additional, Costa, R., additional, Martinelli Filho, M., additional, Silva, K. R., additional, Menezes, L. M., additional, Tamaki, W. T., additional, Mathias, W., additional, Stolf, N. A. G., additional, Misawa, T., additional, Ohta, I., additional, Shishido, T., additional, Miyasita, T., additional, Miyamoto, T., additional, Nitobe, J., additional, Watanabe, T., additional, Kubota, I., additional, Thibault, B., additional, Ducharme, A., additional, Simpson, C., additional, Stuglin, C., additional, Gagne, C. 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M., additional, Sinha, D., additional, Noelker, G., additional, Brachmann, J., additional, Weidemann, F., additional, Ertl, G., additional, Jones, M., additional, Searle, N., additional, Cocker, M., additional, Ilsley, E., additional, Foley, P., additional, Khiani, R., additional, Nelson, K. E., additional, Turley, A. J., additional, Owens, W. A., additional, James, S. A., additional, Linker, N. J., additional, Velagic, V., additional, Cikes, M., additional, Pezo Nikolic, B., additional, Puljevic, D., additional, Separovic-Hanzevacki, J., additional, Lovric-Bencic, M., additional, Biocina, B., additional, Milicic, D., additional, Kawata, H., additional, Chen, L., additional, Phan, H., additional, Anand, K., additional, Feld, G., additional, Birgesdotter-Green, U., additional, Fernandez Lozano, I., additional, Mitroi, C., additional, Toquero Ramos, J., additional, Castro Urda, V., additional, Monivas Palomero, V., additional, Corona Figueroa, A., additional, Hernandez Reina, L., additional, Alonso Pulpon, L., additional, Gate-Martinet, A., additional, Da Costa, A., additional, Rouffiange, P., additional, Cerisier, A., additional, Bisch, L., additional, Romeyer-Bouchard, C., additional, Isaaz, K., additional, Morales, M.- A., additional, Bianchini, E., additional, Startari, U., additional, Faita, F., additional, Bombardini, T., additional, Gemignani, V., additional, Piacenti, M., additional, Adhya, S., additional, Kamdar, R. H., additional, Millar, L. M., additional, Burchardt, C., additional, Murgatroyd, F. D., additional, Klug, D., additional, Kouakam, C., additional, Guedon-Moreau, L., additional, Marquie, C., additional, Benard, S., additional, Kacet, S., additional, Cortez-Dias, N., additional, Carrilho-Ferreira, P., additional, Silva, D., additional, Goncalves, S., additional, Valente, M., additional, Marques, P., additional, Carpinteiro, L., additional, Sousa, J., additional, Keida, T., additional, Nishikido, T., additional, Fujita, M., additional, Chinen, T., additional, Kikuchi, T., additional, Nakamura, K., additional, Ohira, H., additional, Takami, M., additional, Anjo, D., additional, Meireles, A., additional, Gomes, C., additional, Roque, C., additional, Pinheiro Vieira, A., additional, Lagarto, V., additional, Reis, H., additional, Torres, S., additional, Ortega, D. F., additional, Barja, L. D., additional, Montes, J. 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E., additional, Richmond, M. E., additional, Rusanov, A., additional, Quinn, T. A., additional, Cheng, B., additional, Spotnitz, H. M., additional, Kristiansen, H. M., additional, Vollan, G., additional, Hovstad, T., additional, Keilegavlen, H., additional, Faerestrand, S., additional, Brigesdotter-Green, U., additional, Nawar, A. M. R., additional, Ragab, D. A. L. I. A., additional, Eluhsseiny, R. A. N. I. A., additional, Abdelaziz, A. H. M. E. D., additional, Nof, E., additional, Abu Shama, R., additional, Buber, J., additional, Kuperstein, R., additional, Feinberg, M. S., additional, Barlev, D., additional, Eldar, M., additional, Glikson, M., additional, Badran, H., additional, Samir, R., additional, Tawfik, M., additional, Amin, M., additional, Eldamnhoury, H., additional, Khaled, S., additional, Tolosana, J. M., additional, Martin, A. 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Q., additional, Leclercq, C., additional, Ritter, P., additional, Watanabe, I., additional, Nagashima, K., additional, Okumura, Y., additional, Kofune, M., additional, Ohkubo, K., additional, Nakai, T., additional, Hirayama, A., additional, Mikhaylov, E., additional, Vander, M., additional, Lebedev, D., additional, Zarse, M., additional, Suleimann, H., additional, Bogossian, H., additional, Stegelmeyer, J., additional, Ninios, I., additional, Karosienne, Z., additional, Kloppe, A., additional, Lemke, B., additional, John, S., additional, Gaspar, T., additional, Rolf, S., additional, Sommer, P., additional, Hindricks, G., additional, Piorkowski, C., additional, Fernandez-Armenta, J., additional, Mont, L. L., additional, Zeljko, H., additional, Andreu, D., additional, Herzcku, C., additional, Boussy, T., additional, Brugada, J., additional, Obayahi, T., additional, Hegrenes, J., additional, Lim, E., additional, Mediratta, V., additional, Bautista, R., additional, Teplitsky, L., additional, Van Huls Van Taxis, C. F. B., additional, Wijnmaalen, A. P., additional, Gawrysiak, M., additional, Schuijf, J. D., additional, Bax, J. J., additional, Huo, Y., additional, Richter, S., additional, Arya, A., additional, Bollmann, A., additional, Akca, F., additional, Bauernfeind, T., additional, Schwagten, B., additional, De Groot, N. M. 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H., additional, Hero, M., additional, Mizobuchi, M., additional, Enjoji, Y., additional, Yazaki, Y., additional, Shibata, K., additional, Funatsu, A., additional, Kobayashi, T., additional, Nakamura, S., additional, Amit, G., additional, Pertzov, B., additional, Zahger, D., additional, Medesani, L., additional, Rana, R., additional, Albano, F., additional, Fraguas, H., additional, Pedersen, S. S., additional, Hoogwegt, M. T., additional, Theuns, D. A. M. J., additional, Van Den Broek, K. C., additional, Tekle, F. B., additional, Habibovic, M., additional, Alings, M., additional, Van Der Voort, P., additional, Denollet, J., additional, Vrazic, H., additional, Jilek, C., additional, Lesevic, H., additional, Tzeis, S., additional, Semmler, V., additional, Gold, M. R., additional, Burke, M. C., additional, Bardy, G. H., additional, Varma, N., additional, Pavri, B., additional, Stambler, B., additional, Michalski, J., additional, Investigators, T. R. U. S. T., additional, Safak, E., additional, Schmitz, D., additional, Konorza, T., additional, Wende, C., additional, Schirdewan, A., additional, Neuzner, J., additional, Simmers, T., additional, Erglis, A., additional, Gradaus, R., additional, Goetzke, J., additional, Coutrot, L., additional, Goehl, K., additional, Bazan Gelizo, V., additional, Grau, N., additional, Valles, E., additional, Felez, M., additional, Sanjuas, C., additional, Bruguera, J., additional, Marti-Almor, J., additional, Chu, S. Y., additional, Li, P. W., additional, Ding, W. H., additional, Schukro, C., additional, Leitner, L., additional, Siebermair, J., additional, Stix, G., additional, Pezawas, T., additional, Kastner, J., additional, Wolzt, M., additional, Schmidinger, H., additional, Behar, N. A. T. H. A. L. I. E., additional, Kervio, G., additional, Petit, B., additional, Maison-Balnche, P., additional, Bodi, S., additional, Mabo, P., additional, Foley, P. W. 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A., additional, Iitsuka, K., additional, Kondo, T., additional, Goebbert, K., additional, Karossiene, Z., additional, Goldman, D., additional, Kallen, B., additional, Kerpi, E., additional, Sardo, J., additional, Arsenos, P., additional, Gatzoulis, K., additional, Manis, G., additional, Dilaveris, P., additional, Tsiachris, D., additional, Mytas, D., additional, Asimakopoulos, S., additional, Stefanadis, C., additional, Sideris, S., additional, Kartsagoulis, E., additional, Barbosa, O., additional, Marocolo Junior, M., additional, Silva Cortes, R., additional, Moraes Brandolis, R. A., additional, Oliveira, L. F., additional, Pertili Rodrigues De Resende, L. A., additional, Vieira Da Silva, M. A., additional, Dias Da Silva, V. J., additional, Hegazy, R. A., additional, Sharaf, I. A., additional, Fadel, F., additional, Bazaraa, H., additional, Esam, R., additional, Deshko, M. S., additional, Snezhitsky, V. A., additional, Stempen, T. P., additional, Kuroki, K., additional, Igawa, M., additional, Kuga, K., additional, Ferreira Santos, L., additional, Dionisio, T., additional, Nunes, L., additional, Machado, J., additional, Castedo, S., additional, Henriques, C., additional, Matos, A., additional, Oliveira Santos, J., additional, Kraaier, K., additional, Olimulder, M. A. G. M., additional, Galjee, M. A., additional, Van Dessel, P. F. H. M., additional, Van Der Palen, J., additional, Wilde, A. A. M., additional, Scholten, M. F., additional, Chouchou, F., additional, Poupard, L., additional, Philippe, C., additional, Court-Fortune, I., additional, Barthelemy, J.- C., additional, Roche, F., additional, Dolgoshey, T. S., additional, Madekina, G. A., additional, Sugiura, S., additional, Fujii, E., additional, Senga, M., additional, Dohi, K., additional, Sugiura, E., additional, Nakamura, M., additional, Ito, M., additional, Eitel, C., additional, Mendell, J., additional, Lasseter, K., additional, Shi, M., additional, Urban, L., additional, Hatala, R., additional, Hlivak, P., additional, De Melis, M., additional, Garutti, C., additional, Corbucci, G., additional, Mlcochova, H., additional, Maxian, R., additional, Arbelo, E., additional, Dogac, A., additional, Luepkes, C., additional, Ploessnig, M., additional, Chronaki, C., additional, Hinterbuchner, L., additional, Guillen, A., additional, Bun, S. S., additional, Latcu, D. G., additional, Franceschi, F., additional, Prevot, S., additional, Koutbi, L., additional, Ricard, P., additional, Saoudi, N., additional, Nazari, N., additional, Alizadeh, A., additional, Sayah, S., additional, Hekmat, M., additional, Assadian, M., additional, Ahmadzadeh, A., additional, Wnuk, M., additional, Jedrzejczyk-Spaho, J., additional, Kruszelnicka, O., additional, Piwowarska, W., additional, Fedorowski, A., additional, Burri, P., additional, Juul-Moller, S., additional, Melander, O., additional, Mitro, P., additional, Murin, P., additional, Kirsch, P., additional, Habalova, V., additional, Slaba, E., additional, Matyasova, E., additional, Barlow, M. A., additional, Blake, R. J., additional, Rostoff, P., additional, Wojewodka Zak, E., additional, Froidevaux, L., additional, Sarasin, F. P., additional, Louis-Simonet, M., additional, Hugli, O., additional, Yersin, B., additional, Schlaepfer, J., additional, Mischler, C., additional, Pruvot, E., additional, Occhetta, E., additional, Frascarelli, F., additional, Burali, A., additional, and Dovellini, E., additional

Published
2011
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13. ACE I/D polymorphism in Alzheimer’s disease

Author

Trebunova Marianna, Slaba Eva, Habalova Viera, and Gdovinova Zuzana

Subjects
alzheimer’s disease (ad), angiotensin-converting enzyme (ace), polymorphism, apoe, gene-gene interaction, Biology (General), QH301-705.5
Published
2008
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18. Association Study of BDNF , SLC6A4 , and FTO Genetic Variants with Schizophrenia Spectrum Disorders.

Author

Bednarova A, Habalova V, Krivosova M, Marcatili M, and Tkac I

Abstract

Schizophrenia spectrum disorders (patients with a diagnosis of schizophrenia, schizotypal, and delusional disorders: F20-F29 according to International Classification of Diseases 10th revision (ICD-10)) are considered highly heritable heterogeneous psychiatric conditions. Their pathophysiology is multifactorial with involved dysregulated serotonergic neurotransmission and synaptic plasticity. The present study aimed to evaluate the association of SLC6A4 (5-HTTLPR), FTO (rs9939609), and BDNF (rs6265, rs962369) polymorphisms with schizophrenia spectrum disorders in Slovak patients. We analyzed the genotypes of 150 patients with schizophrenia, schizotypal, and delusional disorders and compared them with genotypes from 178 healthy volunteers. We have found a marginally protective effect of LS + SS genotypes of 5-HTTLPR variant of the serotonin transporter SLC6A4 gene against the development of schizophrenia spectrum disorders, but the result failed to remain significant after Bonferroni correction. Similarly, we have not proven any significant association between other selected genetic variants and schizophrenia and related disorders. Studies including a higher number of subjects are warranted to reliably confirm the presence or absence of the studied associations.

Published
2023
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19. Association of HTTLPR, BDNF, and FTO Genetic Variants with Completed Suicide in Slovakia.

Author

Bednarova A, Habalova V, Iannaccone SF, Tkac I, Jarcuskova D, Krivosova M, Marcatili M, and Hlavacova N

Abstract

Since suicide and suicidal behavior are considered highly heritable phenotypes, the identification of genetic markers that can predict suicide risk is a clinically important topic. Several genes studied for possible associations between genetic polymorphisms and suicidal behaviors had mostly inconsistent and contradictory findings. The aim of this case-control study was to evaluate the associations between completed suicide and polymorphisms in genes BDNF (rs6265, rs962369), SLC6A4 ( 5-HTTLPR ), and FTO (rs9939609) in relation to sex and BMI. We genotyped 119 completed suicide victims and 137 control subjects that were age, sex, and ethnicity matched. A significant association with completed suicide was found for BDNF rs962369. This variant could play a role in completed suicide, as individuals with the CC genotype were more often found among suicides than in control subjects. After sex stratification, the association remained significant only in males. A nominally significant association between the gene variant and BMI was observed for BDNF rs962369 under the overdominant model. Heterozygotes with the TC genotype showed a lower average BMI than homozygotes with TT or CC genotypes. FTO polymorphism (rs9939609) did not affect BMI in the group of Slovak suicide completers, but our findings follow an inverse association between BMI and completed suicide.

Published
2023
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20. Evaluation of 5-HTTLPR (insertion/deletion) and BDNF (rs6265) genetic variations in the Slovakian individuals suffering from affective disorders.

Author

Bednarova A, Cizmarikova M, Habalova V, and Jarcuskova D

Subjects
Genetic Variation, Humans, Male, Mood Disorders genetics, Brain-Derived Neurotrophic Factor genetics, Brain-Derived Neurotrophic Factor metabolism, Serotonin Plasma Membrane Transport Proteins genetics
Abstract

The pathophysiology of affective disorders (AD), including depressive disorders (DD) and anxiety disorders (ANXD), is still unclear. To understand risk factors of the disorders, we evaluated genetic variations of the serotonin reuptake transporter (5-HTTLPR, ins/del) and the brain-derived neurotrophic factor (BDNF, rs6265) in Slovak patients suffering from AD. After genotyping we observed a significantly increased frequency of LS and LL genotypes (5-HTTLPR) in individuals diagnosed with AD compared to controls (OR = 1.99, 95% CI = 1.21-3.27, p = 0.006). There was also a significant relationship between TT (BDNF) genotype and the risk of AD in males (OR = 5.93, 95% CI = 1.42-27.07, p = 0.011). In gene-gene analysis, the LL or LS (5-HTTLPR) and CT or TT (BDNF) genotype combinations had a risk-enhancing effect on AD susceptibility (mainly ANXD in males), while SS (5-HTTLPR) and TT (BDNF) combination had a protective effect on AD risk (mainly ANXD). However, larger prospective studies are needed to confirm our findings.

Published
2021
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21. Answer to Finsterer about "Multisystem presentation of a homozygous POLG2 variant".

Author

Dosekova P, Dubiel A, Karlowicz A, Zietkiewicz S, Rydzanicz M, Habalova V, Pienkowski VM, Skirkova M, Han V, Mosejova A, Gdovinova Z, Kaliszewska M, Tońska K, Szymanski MR, Skorvanek M, and Ploski R

Subjects
Homozygote, Humans, DNA-Directed DNA Polymerase genetics
Abstract

Competing Interests: Declaration of competing interest The authors declare no conflict of interests.

Published
2020
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22. Whole exome sequencing identifies a homozygous POLG2 missense variant in an adult patient presenting with optic atrophy, movement disorders, premature ovarian failure and mitochondrial DNA depletion.

Author

Dosekova P, Dubiel A, Karlowicz A, Zietkiewicz S, Rydzanicz M, Habalova V, Pienkowski VM, Skirkova M, Han V, Mosejova A, Gdovinova Z, Kaliszewska M, Tońska K, Szymanski MR, Skorvanek M, and Ploski R

Subjects
Adult, Female, Humans, Mutation, Missense, DNA, Mitochondrial genetics, DNA-Directed DNA Polymerase genetics, Movement Disorders genetics, Optic Atrophy genetics, Polyneuropathies genetics, Primary Ovarian Insufficiency genetics
Abstract

POLG2 associated disorders belong to the group of mitochondrial DNA (mtDNA) diseases and present with a heterogeneous clinical spectrum, various age of onset, and disease severity. We report a 39-year old female presenting with childhood-onset and progressive neuroophthalmic manifestation with optic atrophy, mixed polyneuropathy, spinal and cerebellar ataxia and generalized chorea associated with mtDNA depletion. Whole-exome sequencing identified an ultra-rare homozygous missense mutation located at Chr17: 062474101-C > A (p.Asp433Tyr) in nuclear POLG2 gene encoding PolγB, an accessory subunits of mitochondrial polymerase γ responsible for mtDNA replication. The healthy parents and 2 sisters of the patient were heterozygous for the variant. To our best knowledge, this is the first case of homozygous variant in the POLG2 gene resulting in mitochondrial depletion syndrome in an adult patient and its clinical manifestations extend the clinical spectrum of POLG2 associated diseases., Competing Interests: Declaration of competing interest The authors declare no conflict of interests., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)

Published
2020
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23. Risk allele of gene variant rs6584389 is associated with increased intima-media thickness in patients with type 2 diabetes.

Author

Kozarova M, Malachovska Z, Zidzik J, Javorsky M, Demkova K, Habalova V, and Tkac I

Subjects
Age Factors, Aged, Asymptomatic Diseases, Biomarkers blood, Carotid Artery Diseases diagnostic imaging, Chi-Square Distribution, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Diabetic Angiopathies diagnostic imaging, Female, Gene Frequency, Genetic Association Studies, Genetic Predisposition to Disease, Glycated Hemoglobin metabolism, Humans, Linear Models, Male, Middle Aged, PAX2 Transcription Factor genetics, Peripheral Arterial Disease diagnostic imaging, Phenotype, Pulse Wave Analysis, Risk Factors, Carotid Artery Diseases genetics, Carotid Intima-Media Thickness, Chromosomes, Human, Pair 10, Diabetes Mellitus, Type 2 genetics, Diabetic Angiopathies genetics, Peripheral Arterial Disease genetics, Polymorphism, Single Nucleotide
Abstract

Background: Genome-wide association studies identified several gene variants associated with peripheral arterial disease (PAD). Among them, rs6584389 A>C was significantly associated with PAD defined by decreased ankle-brachial index (ABI). The aim of this study was to investigate whether the rs6584389 variant is also associated with the earlier stages of atherosclerosis assessed by intima-media thickness (IMT) or pulse-wave velocity (PWV) in clinically asymptomatic subjects with type 2 diabetes (T2DM), a group of patients with a high cardiovascular risk., Patients and Methods: In total, 111 patients with T2DM (56 females, 55 males) with a mean age 63.0 ± 9.1 years were consecutively included in the study. IMT was measured by ultrasound using 7 MHz linear transducer. PWV was measured using a piezoelectric method. Genotyping for rs6584389 was performed by PCR-HRMA method., Results: The carriers of the risk C-allele of rs6584389 variant had significantly higher mean left-side IMT (AA: 0.67 ± 0.12, AC 0.77 ± 0.21, CC 0.78 ± 0.22 mm; p = 0.04). In multiple linear regression analysis, rs6586389 genotype was significantly associated with all measured IMT parameters. The presence of each risk C-allele predicted an increase in left-side IMT by 0.056 mm (p = 0.017), right-side IMT by 0.053 mm (p = 0.039), average IMT by 0.054 mm (p = 0.023), and maximal IMT by 0.058 mm (p = 0.021). Age and HbA1c levels were also significantly associated with increased IMT in all multivariate models., Conclusions: Gene variant rs6584389 A>C near to PAX2 gene was associated with increased carotid IMT in patients with type 2 diabetes independently of the other main risk factors for atherosclerosis.

Published
2018
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24. Type II deiodinase polymorphism: A potential risk factor of type 2 diabetes mellitus.

Author

Sotak S, Felsoci M, Lazurova I, and Habalova V

Subjects
Adult, Aged, Aged, 80 and over, Female, Glycated Hemoglobin, Humans, Male, Middle Aged, Polymorphism, Genetic, Risk Factors, Diabetes Mellitus, Type 2 epidemiology, Diabetes Mellitus, Type 2 genetics, Iodide Peroxidase genetics
Abstract

ype 2 diabetes mellitus (T2DM) remains one of the most challenging global epidemics of the twenty-first century. It is estimated that more than 350 million people worldwide are affected by this metabolic disorder. It has many risk factors. Several studies presume that type II iodothyronine deiodinase polymorphism Thr92Ala (DII-Thr92-Ala, rs225014) is yet another risk factor. The aim of the study was to assess the impact of this polymorphism on parameters of glycid metabolism. Our group consisted of 200 subjects (74 males and 126 females) at average age of 63.85 ± 18.98 without prediabetes, diabetes mellitus or any thyropathy. Blood tests were performed to evaluate glucose metabolism parameters as well as DII-Thr92Ala polymorphism. Our study confirmed the relationship between Ala homozygotes and glycosylated haemoglobin (HbA1c) serum levels (Tab. 2, Ref. 14). Keywords: diabetes mellitus 2, deiodinase II, polymorphism Thr92Ala.

Published
2018
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25. Relationship Between the Apolipoprotein E Genotype and LDL Particle Size in Patients With Obstructive Sleep Apnea.

Author

Vekic J, Joppa P, Habalova V, Tisko R, Zeljkovic A, Pobeha P, Gojkovic T, Spasojevic-Kalimanovska V, Strbova Z, Kuklisova Z, Slaba E, Rizzo M, and Tkacova R

Subjects
Adult, Aged, Apolipoprotein E4 genetics, Cardiovascular Diseases blood, Cardiovascular Diseases genetics, Female, Genetic Predisposition to Disease genetics, Humans, Male, Middle Aged, Particle Size, Polysomnography, Prospective Studies, Sleep Apnea, Obstructive blood, Statistics as Topic, Apolipoproteins E genetics, Genetic Carrier Screening, Genotype, Lipoproteins, LDL blood, Sleep Apnea, Obstructive genetics
Abstract

Obstructive sleep apnea (OSA) is associated with dyslipidemia and increased cardiovascular risk. We assessed the effects of apolipoprotein E ( APOE) genotype on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particle size and lipid subclasses (separated by gradient gel electrophoresis) in patients with OSA. Stable patients (n = 181) prospectively recruited underwent full polysomnography. Both LDL particle size and LDL I proportion were reduced from ∊3∊3 homozygotes to ∊2 carriers and to ∊4 carriers (analysis of variance: P = .024; P = .040, respectively); carriers of the ∊4 allele of the APOE genotype had significantly lower LDL particle size and LDL I proportion compared to ∊3∊3 homozygotes ( P < .05 for both comparisons). Insulin resistance increased from patients with no OSA to those with mild-moderate and to those with severe OSA ( P < .001). In multivariate analysis, LDL size was independently predicted by APOE genotype, male gender, and the presence of metabolic syndrome (MetS; P = .001, P = .020, P = .027, respectively). The HDL particle size was not affected by APOE genotype. Our data demonstrate that both the ∊4 APOE genotype and MetS are independently related to smaller LDL size in patients with OSA.

Published
2016
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26. Gene Polymorphism of the Adenosine A2a Receptor in Patients with Vasovagal Syncope.

Author

Mitro P, Habalova V, Evin L, Muller E, Simurda M, Slaba E, Murin P, and Valocik G

Subjects
Adult, Biomarkers, Female, Genetic Markers genetics, Humans, Male, Middle Aged, Prevalence, Risk Factors, Slovakia epidemiology, Syncope, Vasovagal diagnosis, Genetic Predisposition to Disease epidemiology, Genetic Predisposition to Disease genetics, Polymorphism, Single Nucleotide genetics, Receptor, Adenosine A2A genetics, Syncope, Vasovagal epidemiology, Syncope, Vasovagal genetics
Abstract

Background: Adenosine may play a role in the pathogenesis of vasovagal syncope (VVS). The aim of the study was to evaluate the adenosine A(2A) receptor gene 1083 T > C polymorphism in patients with syncope and its possible association with results of head-up tilt test (HUT)., Methods: Three hundred and forty-seven consecutive patients (mean age 47.3 ± 18.5 years, 132 men, 215 women) with one or more syncopal episodes underwent HUT as part of standardized diagnostic evaluation. HUT was positive in 207 patients (75 males, mean age 44.7 ± 18.6 years) and negative in 140 patients (58 males, mean age 48.17 ± 18.8 years). One thousand and eighty-three T > C single nucleotide polymorphism in the adenosine A(2A) receptor gene (rs5751876) was evaluated in 347 patients with syncope and in 85 subjects without history of syncope (54 men, mean age 41.7 ± 16.3)., Results: Adenosine A(2A) receptor 1083 T > C polymorphism was not associated with the positivity of HUT. Blood pressure and heart rate response to tilting was similar in all genotypes. Low frequency (LF) power was significantly lower in CC genotype compared to CT genotype in early phase of tilt (log LF 2.69 ± 0.61 vs 3.20 ± 0.60; P = 0.01) and at the time of syncope (log LF 2.60 ± 0.63 vs 2.77 ± 0.48; P = 0.04)., Conclusions: Adenosine A(2A) receptor 1083 T > C polymorphism is not associated with the positivity of HUT and its proposed role in predisposition to VVS was not confirmed. CC genotype may be associated with lower sympathetic activity during HUT., (© 2015 Wiley Periodicals, Inc.)

Published
2016
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27. Beta 3 subunit of G-protein and its influence on autonomic nervous system in patients with vasovagal syncope.

Author

Evin L, Mitro P, Habalova V, Simurda M, Muller E, and Murin P

Subjects
Adult, Aged, Autonomic Nervous System physiopathology, Blood Pressure, Female, Heart Rate, Humans, Male, Middle Aged, Polymorphism, Genetic, Prospective Studies, Syncope, Vasovagal physiopathology, Tilt-Table Test, Heterotrimeric GTP-Binding Proteins genetics, Syncope, Vasovagal genetics
Abstract

Objectives: The aim of this prospective study was to investigate the impact of genetic polymorphisms of β3 subunit of G-protein on the occurrence of vasovagal syncope, hemodynamic parameters and heart rate variability during head-up tilt test (HUT)., Background: G-proteins play an important role in the intracellular transmission of impulses in cardiovascular autonomic reflexes., Methods: In 157 patients with suspected vasovagal syncope HUT was performed. Ninety-one patients (38 men, 53 women, mean age 48 ± 17 years) had positive HUT. Control group consisted of 109 subjects (69 men, 40 women, mean age 37 ± 16 years) with no history of syncope. Results of HUT, hemodynamic parameters and LF, HF, LF/HF, SDNN, RMSSD parameters of heart rate variability were compared in patients with different genotypes. C825T polymorphism of β3 subunit of G-protein was determined in the study subjects., Results: There was no significant difference in the distribution of genotypes between patients and control group. Also, there was no significant difference in hemodynamic parameters. A statistically significant difference was found between genotypes in LF/HF in the early HUT (mean rank CC: 48.68 vs CT: 35.51 vs TT: 34.14; p = 0.039) and at RMSSD at the time of syncope (mean rank CC: 32.38 vs CT: 42.74 vs TT: 18.50; p = 0.026)., Conclusions: In this study, the relation of C825T polymorphism of β3 subunit of G-protein to vasovagal syncope was not documented (Tab. 2, Fig. 4, Ref. 37).

Published
2016
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28. MDR1 polymorphisms and idiopathic nephrotic syndrome in Slovak children: preliminary results.

Author

Cizmarikova M, Podracka L, Klimcakova L, Habalova V, Boor A, Mojzis J, and Mirossay L

Subjects
ATP Binding Cassette Transporter, Subfamily B genetics, Alleles, Child, Female, Gene Frequency, Genotype, Glomerulosclerosis, Focal Segmental drug therapy, Glomerulosclerosis, Focal Segmental genetics, Haplotypes, Humans, Male, Pharmacogenetics, Polymerase Chain Reaction, Prednisone therapeutic use, Remission Induction, Retrospective Studies, Slovakia, Steroids therapeutic use, Nephrotic Syndrome drug therapy, Nephrotic Syndrome genetics, Polymorphism, Genetic
Abstract

Background: The role of the multidrug resistance-1 (MDR1 or ABCB1) gene polymorphisms 1236T>C, 2677T>G, and 3435T>C was studied in relation to susceptibility, demographics, and pathological characteristics, as well as their role in the therapeutic response (TR) to prednisone treatment in children with idiopathic nephrotic syndrome (INS)., Material/methods: The polymorphisms were analyzed using the polymerase chain reaction-restriction fragment length polymorphism method in 46 children with INS and in 100 healthy controls. Different genetic models (codominant, dominant, recessive, and overdominant) were used for testing of associations between polymorphisms and phenotypes., Results: Statistical analysis showed a significantly increased chance of TR in children carrying 3435TC genotype (OR=5.13, 95% CI=1.18-22.25; overdominant model). Moreover, INS patients under 6 years of age had significantly decreased frequencies of MDR1 1236CC (7.7% vs. 35%, p=0.029) or 2677GG (3.8% vs. 30.0%, p=0.033) genotypes. We also observed that patients with minimal change in disease and patients under 6 years of age at the onset of INS were initial responders more frequently when compared with children with focal segmental glomerulosclerosis and patients ≥6 years old at the onset (p=0.0001, p=0.027, respectively)., Conclusions: These data suggest that prednisone TR may be influenced by histology, age at the onset of INS, and MDR1 3435T>C polymorphism. The MDR1 1236T>C and 2677T>G polymorphisms were significantly associated with age at onset. Larger multicenter studies and studies across other ethnic groups are needed to elucidate the contradictory implications of MDR1 polymorphisms with INS in children.

Published
2015
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29. Effects of apolipoprotein E genotype on serum lipids in obstructive sleep apnoea.

Author

Tisko R, Sopkova Z, Habalova V, Dorkova Z, Slaba E, Javorsky M, Tkac I, Riha RL, and Tkacova R

Subjects
Adult, Alleles, Dyslipidemias complications, Female, Genetic Predisposition to Disease, Genotype, Heterozygote, Humans, Hypoxia, Male, Middle Aged, Oxygen chemistry, Polymorphism, Genetic, Polysomnography, Prospective Studies, Real-Time Polymerase Chain Reaction, Risk Factors, Sleep, Sleep Apnea, Obstructive complications, Tertiary Care Centers, Triglycerides blood, Apolipoproteins E genetics, Dyslipidemias blood, Dyslipidemias genetics, Lipids blood, Sleep Apnea, Obstructive blood, Sleep Apnea, Obstructive genetics
Abstract

There is increasing evidence that intermittent hypoxia resulting from obstructive sleep apnoea (OSA) is independently associated with dyslipidaemia. Currently, no data exist on potential links between OSA-related dyslipidaemia and susceptibility genes for dyslipidaemia in such patients. Our aim was to study the effects of the apolipoprotein E (APOE) genotype and sleep apnoea severity on atherogenic dyslipidaemia in patients with OSA. 519 clinically stable subjects prospectively recruited at a tertiary referral teaching hospital underwent full polysomnography. APOE gene polymorphisms were assessed using real-time PCR. In all APOE genotype groups, serum triglycerides increased while high-density lipoprotein (HDL) cholesterol was reduced with increasing severity of OSA in each APOE genotype group, whereas the deleterious effects of OSA on serum apolipoprotein (Apo)B levels were observed in ε2 carriers and the ε3/ε3 genotype only. Nevertheless, the ε4 allele carriers had ApoB levels within the risk range, irrespective of nocturnal hypoxia. In addition, among patients with the high-risk ε4 genotype, those with the most severe nocturnal hypoxia had significantly higher triglyceride and lower HDL cholesterol levels compared with nonhypoxic ε4 subjects. APOE genotype and the oxygen desaturation index were both independent predictors of serum triglyceride levels (p=0.009 and p<0.001, respectively; R(2)=0.148) and ApoB levels (p=0.001 and p=0.003, respectively; R(2)=0.104). Our findings suggest that OSA has adverse effects on several lipid parameters over and above the effects carried by APOE genotype. Further st1udies are needed to analyse the effects of high-risk genotypes on metabolic and cardiovascular outcomes in patients with OSA.

Published
2014
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30. Relationship of five type 2 diabetes candidate gene polymorphisms to the age at diagnosis of diabetes in the Slovakian population.

Author

Kozarova M, Javorsky M, Stancakova A, Dobrikova M, Habalova V, Klimcakova L, Zidzik J, Haluskova J, Salagovic J, and Tkac I

Subjects
Age of Onset, Diabetes Mellitus, Type 2 diagnosis, Female, Genotype, Humans, Male, Middle Aged, Slovakia, Diabetes Mellitus, Type 2 genetics, Polymorphism, Genetic
Abstract

Objectives: To examine the relationship between polymorphisms of five candidate genes for type 2 diabetes mellitus (T2DM) and the age at diagnosis of T2DM., Methods: 538 Slovakian patients with T2DM were included and their age at diagnosis of T2DM retrieved from their medical records. Polymorphisms of genes encoding peroxisome proliferator activated receptor gamma (PPARG), PPARG-coactivator-1 (PGC1), insulin-receptor substrate 1 (IRS1), the subunit Kir 6.2 of the ATP-dependent potassium-channel (KCNJ11) and transcription factor 7-like 2 (TCF7L2) were detected by PCR-RFLP methods., Results: No significant relationship between the risk alleles of the examined gene polymorphisms to the lower mean age at diagnosis of T2DM was observed. The carriers of the TT-genotype of TCF7L2 rs7903146 polymorphism had significantly increased odds ratio for diagnosis of diabetes before the age of 40 years [OR 3.02 (1.34, 6.81), p = 0.008], in comparison with the CC/CT genotype carriers., Conclusion: No significant association of PPARG, PGC1, IRS1, KCNJ11 and TCF7L2 gene polymorphisms and the age at diagnosis of T2DM was observed in the present study. Homozygotes for the risk allele of TCF7L2 had more frequently early onset of T2DM, before age of 40 years (Tab. 4, Ref. 15).

Published
2010

31. Gene polymorphisms of renin angiotensin system and serotonin transporter gene in patients with vasovagal syncope.

Author

Mudrakova K, Mitro P, Salagovic J, Habalova V, Kirsch P, and Tkac I

Subjects
Adult, Angiotensinogen genetics, Female, Humans, Male, Middle Aged, Peptidyl-Dipeptidase A genetics, Receptor, Angiotensin, Type 2 genetics, Syncope, Vasovagal diagnosis, Tilt-Table Test, Polymorphism, Genetic, Renin-Angiotensin System genetics, Serotonin Plasma Membrane Transport Proteins genetics, Syncope, Vasovagal genetics
Abstract

Unlabelled: Objective of this study was to compare the distribution frequencies of gene polymorphisms of renin-angiotensin and serotonin system in patients with positive and negative head- up tilt test (HUT)., Methods: DNA from 191 patients (mean age 44+ 18 years, 61 men) was collected. HUT was positive in 117 and negative in 74 patients. Following gene polymorphisms were determined by the PCR method: ACE insertion/deletion (I/D ACE), angiotensinogen (AGT) (M 235), angiotensin II receptor (ATR1) (A 1166C) and serotonin transporter (SERT) polymorphism (5HTTLPR)., Results: No significant differences in the distribution of gene polymorphisms between syncopal patients with positive and negative HUT were dectected. Distribution of polymorphisms included: I/D ACE: II 19 vs 20%, ID 55 vs 52%, DD 26 vs 28%. Angiotensinogen gene polymorphism MM 27% vs 30%, MT 48% vs 46%, TT 25% vs 24%. ATR1 polymorphism AA 44 vs 32%, AC50 vs 60%, CC 6 vs 8%, 5HTTLPR serotonin transporter gene polymorphism LL 42 vs 43%, SL 41 vs 39%, SS 17 vs 18%., Conclusions: An association between polymorphisms of ACE, AGT, ATR1 and SERT gene, and predisposition to VVS was not proven by the present study (Tab. 2, Ref. 22). Full Text (Free, PDF) www.bmj.sk.

Published
2009

32. Beta2-adrenergic receptor haplotype and bronchodilator response to salbutamol in patients with acute exacerbations of COPD.

Author

Mokry M, Joppa P, Slaba E, Zidzik J, Habalova V, Kluchova Z, Micietova L, Rozborilova E, Salagovic J, and Tkacova R

Subjects
Adult, Aged, Codon genetics, Demography, Female, Glutamic Acid genetics, Glycine genetics, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive physiopathology, Respiratory Function Tests, Albuterol therapeutic use, Bronchodilator Agents therapeutic use, Haplotypes, Pulmonary Disease, Chronic Obstructive drug therapy, Pulmonary Disease, Chronic Obstructive genetics, Receptors, Adrenergic, beta-2 genetics
Abstract

Background: The role of the beta2-adrenergic receptor (ADRB2) genotype in patients with chronic obstructive pulmonary disease (COPD) is unclear. In patients with acute exacerbations of COPD (AECOPD), we assessed the role of ADRB2 haplotypes in morning lung function and in the bronchodilator response to salbutamol., Material/methods: In 107 patients with AECOPD, polymorphisms in the amino acid position 16 (Arg16/Gly16) and 27 (Gln27/Glu27) of the ADRB2 gene were assessed by allele-specific polymerase chain reaction, identifying 31 subjects with the Gly16/Glu27-negative and 76 with the Gly16/Glu27-positive ADRB2 haplotype. Pulmonary function and bronchodilator response to salbutamol were assessed using bodyplethysmography., Results: Forced expiratory volume in 1 second (FEV1) and peak expiratory flow (PEF) were significantly higher in the Gly16/Glu27-negative compared to the Gly16/Glu27-positive haplotype group at baseline (49.7+/-2.9% vs 42.4+/-1.8% predicted, P=0.037; 44.0+/-2.2% vs 36.4+/-1.6% predicted, P=0.008, respectively). FEV1, PEF, and forced vital capacity (FVC) increased from baseline to after salbutamol treatment in both the Gly16/Glu27-negative and the Gly16/Glu27-positive ADRB2 haplotype groups (P<0.001 for all comparisons). Values for FEV1 and PEF after administration of the bronchodilator were significantly higher in the Gly16/Glu27-negative haplotype group compared with the Gly16/Glu27-positive haplotype group (P=0.030 and P=0.034, respectively). No differences were observed in DeltaFEV1, DeltaPEF, or DeltaFVC after bronchodilation between the 2 ADRB2 haplotype groups (12.2+/-1.8% vs 14.5+/-1.5% predicted, P=0.393; 12.2+/-3.3% vs 20.8+/-3.2% predicted, P=0.117; 9.1+/-2.3% vs 10.4+/-1.9% predicted, P=0.707, respectively)., Conclusions: The present findings suggest that the ADBR2 gene haplotypes may affect the severity of obstructive ventilatory impairment but not the immediate response to salbutamol during AECOPD.

Published
2008

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