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101. Changes in antioxidant status, protein concentration, acetylcholinesterase, (Na+,K+)-, and Mg2+-ATPase activities in the brain of hyper- and hypothyroid adult rats

Author

Carageorgiou, H. Pantos, C. Zarros, A. Mourouzis, I. Varonos, D. Cokkinos, D. Tsakiris, S.

Subjects
endocrine system, endocrine system diseases, hormones, hormone substitutes, and hormone antagonists
Abstract

It is a common knowledge that metabolic reactions increase in hyperthyroidism and decrease in hypothyroidism. The aim of this work was to investigate how the metabolic reactions could affect the total antioxidant status (TAS), protein concentration (PC) and the activities of acetylcholinesterase (AChE), (Na+,K+)-ATPase and Mg 2+-ATPase in the brain of hyper- and hypothyroid adult male rats. Hyperthyroidism was induced in rats by subcutaneous administration of thyroxine (25 μg/100 g body weight) once daily for 14 days, while hypothyroidism was induced by oral administration of propylthiouracil (0.05%) for 21 days. TAS, PC, and enzyme activities were evaluated spectrophotometrically in the homogenated brain of each animal. TAS, PC, and Mg2+-ATPase activity were found unaffected in hyperthyroidism, while AChE and Na+,K +-ATPase activities were reduced by 25% (p < 0.01). In contrast, TAS, (Na+,K+)-ATPase and Mg2+-ATPase activities were found to be increased (approx. 23-30%, p < 0.001) in the hypothyroid brain, while AChE activity and PC were shown to be inhibited (approx. 23-30%, p < 0.001). These changes on brain enzyme activities may reflect the different metabolic effects of hyper- and hypothyroidism. Such changes of the enzyme activities may differentially modulate the brain intracellular Mg2+, neural excitability, as well as the uptake and release of biogenic amines. © 2005 Springer Science+Business Media, Inc.

Published
2005

103. This title is unavailable for guests, please login to see more information.

Author

Pantos, C. Mourouzis, I. and Pantos, C. Mourouzis, I.

Abstract

Thyroid hormone (TH) is critical for adapting living organisms to environmental stress. Plasma circulating tri-iodothyronine (T3) levels drop in most disease states and are associated with increased oxidative stress. In this context, T3 levels in plasma appear to be an independent determinant for the recovery of cardiac function after myocardial infarction in patients. Thyroid hormone receptor 1 (TR1) seems to be crucial in this response; TR1 accumulates to cell nucleus upon activation of stress induced growth kinase signaling. Furthermore, overexpression of nuclear TR1 in cardiomyocytes can result in pathological or physiological growth (dual action) in absence or presence of its ligand, respectively. Accordingly, inactivation of TR1 receptor prevents reactive hypertrophy after myocardial infarction and results in heart failure with increased phospholamban (PLB) expression and marked activation of p38MAPK. In line with this evidence, TH is shown to limit ischemia/reperfusion injury and convert pathologic to physiologic growth after myocardial infarction via TR1 receptor. TR1 receptor may prove to be a novel pharmacological target for cardiac repair/regeneration therapies. © 2014 Constantinos Pantos and Iordanis Mourouzis.

Published
2014

104. Mepivacaine Alters Vascular Responsiveness to Vasoconstrictors in Aortic Rings from Normal and Aortic-Banded Rats

Author

Mourouzis, C. Pantos, C. Mourouzis, I. Saranteas, T. Tesseromatis, C. Kostopanagiotou, G. Karageorgiou, C. Varonos, D. Cokkinos, D.

Subjects
cardiovascular system
Abstract

The present study investigated the effects of mepivacaine on the response of rat aorta to vasoconstrictors in normal and aortic-banded animals. Cardiac hypertrophy was induced in Wistar rats by aortic banding, while shamoperated animals served as controls. Isolated aortic rings with or without endothelium were contracted with potassium chloride and phenylephrine in the presence of mepivacaine (10-3 M). Maximal tension was measured at the highest concentration of potassium chloride and phenylephrine. Maximal response to potassium chloride was reduced in the presence of mepivacaine both in normal and aortic-banded rings. As regards the vascular reactivity to phenylephrine, aortic rings with intact endothelium from aortic-banded rats have shown increased response as compared to normal. After mepivacaine administration this difference between normal and aortic-banded rats was abolished. In conclusion, in a model of cardiac hypertrophy such as that of aortic-banding, increased response to α1-adrenergic stimulation is observed, which is blunted by mepivacaine administration.

Published
2003

105. Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection

Author

Pantos, C Malliopoulou, V Mourouzis, I Moraitis, P and Tzeis, S Thempeyioti, A Paizis, I Cokkinos, A and Carageorgiou, H Varonos, DD Cokkinos, DV

Abstract

The present study investigated whether heat stress-induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2-terminal kinase (JNK) activation during ischaemia-reperfusion in a model of isolated perfused rat heart. Wistar rats were subjected to whole-body hyperthermia at 42degreesC for 15 min (HS), while untreated animals served as controls (CON). Twenty four hours later, CON and HS isolated hearts were perfused in a Langendorff mode and subjected to 20 min of zero-flow global ischaemia followed by 45 min of reperfusion. Postischaemic recovery of left ventricular developed pressure at 45 min of reperfusion was expressed as % of the initial value (LVDP%). Activation of p38 MAPK and JNK was assessed by standard Western blotting techniques using a dual phospho-p38 MAPK and phospho-p46 JNK and p54 JNK antibodies. The levels of phospho-p38 MAPK at the end of reperfusion were not different in HS as compared to CON hearts. The levels of phospho-p46. JNK and p54 JNK were 1.4- and 1.6-fold less in HS than in CON hearts respectively, p < 0.05. LVDP% was 60.3 (s.e.m., 6.3) for HS and 42.9 (4.1) for CON, p < 0.05. In summary, beat stress pretreatment improves postischaemic recovery of function in isolated rat hearts and this is associated with sup. pressed JNK activation in response to ischaemia-reperfusion.

Published
2003

106. Thyroid hormone and cardioprotection: Study of p38 MAPK and JNKs during ischaemia and at reperfusion in isolated rat heart

Author

Pantos, C Malliopoulou, V Paizis, I Moraitis, P and Mourouzis, I Tzeis, S Karamanoli, E Cokkinos, DD and Carageorgiou, H Varonos, D Cokkinos, DV

Abstract

It has been recently shown that long-term thyroxine administration increases the tolerance of the heart to ischaemia. The present study investigated whether thyroxine induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2-terminal kinases (JNKs) activation during ischaemia-reperfusion. L-thyroxine (T4) was administered in Wistar rats (25 mug/100 g/day, subcutaneously) for 2 weeks (THYR), while normal animals served as controls (NORM). NORM and THYR isolated rat hearts were perfused in Langendorff mode and subjected to 10 or 20 min of zero-flow global ischaemia only and also to 20 min of ischaemia followed by 10, 20 or 45 min of reperfusion. Postischaemic recovery of left ventricular developed pressure at 45 min of reperfusion was expressed as % of the initial value. Activation of p38 MAPK and JNKs was assessed at the different times of the experimental setting by standard Western blotting techniques using a dual phospho p38MAPK and phospho JNKs (p46/p54) antibodies. Activation of p38 MAPK was significantly attenuated during ischaemia and reperfusion in thyroxine treated hearts compared to normal hearts. JNKs were found to be activated only during the reperfusion period. The levels of phospho JNKs were found to be lower in thyroxine treated hearts as compared to untreated hearts, though not at a statistically significant level. Postischaemic functional recovery was higher in THYR as compared to NORM, p < 0.05. In summary, in hearts pretreated with thyroxine, p38 MAPK was attenuated during ischaemia and at reperfusion and this was associated with improved postischaemic recovery of function.

Published
2003

107. Dobutamine administration exacerbates postischaemic myocardial dysfunction in isolated rat hearts: An effect reversed by thyroxine pretreatment

Author

Pantos, C. Mourouzis, I. Tzeis, S. Moraitis, P. Malliopoulou, V. Cokkinos, D.D. Carageorgiou, H. Varonos, D. Cokkinos, D.

Abstract

The present study has investigated the effects of dobutamine on postischaemic dysfunction in the setting of global ischaemia and reperfusion in a model of isolated heart preparation. Isolated rat hearts were subjected to 20 min of zero-flow global ischaemia followed by 45 min of reperfusion. Dobutamine administration (10 μg/kg/min) during the reperfusion period resulted in deterioration of functional recovery, which was abolished by propranolol administration. Long-term thyroxine pretreatment (12.5 μg 100 g-1 body weight, b.i.d., s.c., for 2 weeks) reversed the detrimental effect of dobutamine and increased postischaemic recovery of function. We conclude that the combination of thyroxine pretreatment and dobutamine administration could potentially be a new therapeutic strategy to improve postischaemic dysfunction particularly in clinical settings such as cardiopulmonary bypass and/or myocardial infarction. © 2003 Elsevier Science B.V. All rights reserved.

Published
2003

108. Thyroxine pretreatment increases basal myocardial heat-shock protein 27 expression and accelerates translocation and phosphorylation of this protein upon ischaemia

Author

Pantos, C. Malliopoulou, V. Mourouzis, I. Karamanoli, E. Moraitis, P. Tzeis, S. Paizis, I. Cokkinos, A.D. Carageorgiou, H. Varonos, D.D. Cokkinos, D.V.

Subjects
endocrine system, animal structures, embryonic structures
Abstract

Thyroxine pretreatment increases the tolerance of the heart to ischaemia, and heat-shock protein 27 (HSP27) is considered to play an important role in cardioprotection. The present study investigated whether long-term thyroxine administration can induce changes in the expression, translocation and phosphorylation of HSP27 at baseline and upon ischaemic stress. L-Thyroxine (T4) was administered to Wistar rats (25 μg/100 g/day s.c.) for 2 weeks, while normal animals served as controls. Hearts from normal and thyroxine-treated rats were perfused in Langendorff mode and subjected to 10 or 20 min of zero-flow global ischaemia only or to 20 min of ischaemia followed by 45 min of reperfusion. Total and phospho-HSP27 expression were assessed at different times in the Triton-soluble (cytosol-membrane), S fraction, and the Triton-insoluble (cytoskeleton-nucleus) fraction, P fraction. Postischaemic recovery of left ventricular developed pressure at 45 min of reperfusion was expressed as % of the initial value. In hearts from thyroxine-treated animals, the levels of basal total HSP27 and phospho-HSP27 in the P fraction were significantly increased as compared to normal. In response to ischaemia, in hearts from thyroxine-treated rats, the levels of total HSP27 and phospho-HSP27 were found to be significantly increased in the P fraction at 10 and 20 min of ischaemia as compared to preischaemic values, whereas in normal hearts, the levels of total HSP27 and phospho-HSP27 were significantly increased at 20 min only. Postischaemic functional recovery was significantly greater in thyroxine-treated than in untreated hearts. In summary, long-term thyroxine pretreatment results in an increased basal expression and phosphorylation of HSP27 and in an earlier and sustained redistribution of HSP27 from the S to the P fraction in response to ischaemia. This effect might be of important therapeutic relevance. © 2003 Elsevier B.V. All rights reserved.

Published
2003

109. Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion

Author

Pantos, C Malliopoulou, V Mourouzis, I Sfakianoudis, K and Tzeis, S Doumba, P Xinaris, C Cokkinos, AD Carageorgiou, H Varonos, DD Cokkinos, DV

Abstract

The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C epsilon (PKCepsilon) and PKCdelta and phosphorylation of p46 and p54 c-jun NH2-terminal kinases (JNKs) in response to I/R, were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCepsilon expression was 1.4-fold more in HYPO than in NORM hearts, P

Published
2003

110. Effects of dronedarone and amiodarone on plasma thyroid hormones and on the basal and postischemic performance of the isolated rat heart

Author

Pantos, C. Mourouzis, I. Delbruyère, M. Malliopoulou, V. Tzeis, S. Cokkinos, D.D. Nikitas, N. Carageorgiou, H. Varonos, D. Cokkinos, D. Nisato, D.

Abstract

The present study investigated the effects of dronedarone and amiodarone on plasma thyroid hormones and the possible consequences on the response of the heart to ischemia. Amiodarone (30 mg/kg/day per os) or dronedarone (30 mg/kg/day per os) were administered for 2 weeks in normal and thyroxine-treated animals (25 μg/100 g body weight od sc, for 2 weeks), while animals without amiodarone and dronedarone served as controls. Isolated rat hearts were perfused in a Langendorff mode and subjected to 20 and 30 min of zero-flow global ischemia followed by 45 min of reperfusion. Functional changes were assessed by measuring left ventricular developed pressure (LVDP) under resting conditions and in response to ischemia-reperfusion, LVDP%, as well as the severity of ischemic contracture. Amiodarone resulted in increased T4, T4/T3 and rT3, whereas dronedarone did not alter the thyroid hormone profile in normal animals. In thyroxine-treated animals, amiodarone increased T4/T3 ratio but T4, T3 and rT3 levels were not altered. Basal functional parameters and ischemic contracture did not change by amiodarone and/or dronedarone neither in normal nor in thyroxine-treated hearts. In normal hearts, postischemic functional recovery, LVDP%, was not altered by amiodarone or dronedarone administration. LVDP% was statistically higher in thyroxine-treated hearts than in normal and this beneficial effect was not abolished by amiodarone or dronedarone treatment. © 2002 Elsevier Science B.V. All rights reserved.

Published
2002

112. Thyroid hormone and tissue repair: New tricks for an old hormone?

Author

Mourouzis, I. Politi, E. Pantos, C. and Mourouzis, I. Politi, E. Pantos, C.

Abstract

Although the role of thyroid hormone during embryonic development has long been recognized, its role later in adult life remains largely unknown. However, several lines of evidence show that thyroid hormone is crucial to the response to stress and to poststress recovery and repair. Along this line, TH administration in almost every tissue resulted in tissue repair after various injuries including ischemia, chemical insults, induction of inflammation, or exposure to radiation. This novel action may be of therapeutic relevance, and thyroid hormone may constitute a paradigm for pharmacologic-induced tissue repair/regeneration. © 2013 Iordanis Mourouzis et al.

Published
2013

114. Hemostasis parameters disturbances in healthy individuals with prehypertension

Author

Papadopoulos, D. Mourouzis, I. Kotrotsou, A. Papazachou, U. Sanidas, E. Tsioufis, K. Makris, T. and Papadopoulos, D. Mourouzis, I. Kotrotsou, A. Papazachou, U. Sanidas, E. Tsioufis, K. Makris, T.

Abstract

Prehypertension (PH) seems to be related to increased cardiovascular risk in healthy normotensive subjects, while essential hypertension is associated with hemostasis balance disturbances. The aim of our study was to examine the impact of PH on hemostasis parameters in healthy individuals with PH and to compare the findings with those of healthy normotensives with normal blood pressure (NBP) levels. This study was performed in 204 (96 M, 108 F) subjects who attended our hypertension clinic. Seventy-eight (36 M, 42 F) subjects with PH, mean age 52 ± 5 years, and body mass index (BMI) 23 ± 1.5 kg/m2 made up group A, and 126 (60 M, 66 F) subjects with NBP, mean age 53 ± 6 years, and BMI 23.2 ± 1.4 kg/m2 without any history of cardiovascular disease or diabetes mellitus made up group B. Systolic blood pressure and diastolic blood pressure were measured in three sequential visits, which were performed by the same trained nurse. Serum lipid levels, fibrinogen (F), thrombomodulin (TM), and plasminogen activator inhibitor-1 antigen, and tissue plasminogen activator antigen were determined in the whole population. Plasminogen activator inhibitor-1 antigen and tissue plasminogen activator antigen levels were significantly higher in the PH group as compared with normotensives, while in PH subjects, significantly higher plasma levels of F and TM were found compared with normotensive group. The two groups were matched for age, sex, BMI, and serum lipid levels. Our findings indicate that PH is associated with hemostasis disturbances predisposing to hypercoagulability and impaired fibrinolysis. This observation may be of prognostic value for future cardiovascular events in this group and needs further investigation. © 2012 Informa Healthcare USA, Inc.

Published
2012

115. Thyroid hormone and cardiac disease: Frombasic concepts to clinical application

Author

Mourouzis, I. Forini, F. Pantos, C. Iervasi, G. and Mourouzis, I. Forini, F. Pantos, C. Iervasi, G.

Abstract

Nature's models of regeneration provide substantial evidence that a natural healing process may exist in the heart. Analogies existing between the damaged myocardium and the developing heart strongly indicate that regulatory factors which drive embryonic heart development may also control aspects of heart regeneration. In this context, thyroid hormone (TH) which is critical in heart maturation during development appears to have a reparative role in adult life. Thus, changes in TH-thyroid hormone receptor (TR) homeostasis are shown to govern the return of the damaged myocardium to the fetal phenotype. Accordingly, thyroid hormone treatment preferentially rebuilds the injured myocardium by reactivating developmental gene programming. Clinical data provide further support to this experimental evidence and changes in TH levels and in particular a reduction of biologically active triiodothyronine (T3) in plasma after myocardial infarction or during evolution of heart failure, are strongly correlated with patients morbidity and mortality. The potential of TH to regenerate a diseased heart has now been testing in patients with acutemyocardial infarction in a phase II, randomized, double blind, placebo-controlled study (the THiRST study). Copyright © 2011 Iordanis Mourouzis et al.

Published
2011

119. Thyroid hormone signalling is altered in response to physical training in patients with end-stage heart failure and mechanical assist devices: potential physiological consequences?

Author

Adamopoulos, S., primary, Gouziouta, A., additional, Mantzouratou, P., additional, Laoutaris, I. D., additional, Dritsas, A., additional, Cokkinos, D. V., additional, Mourouzis, I., additional, Sfyrakis, P., additional, Iervasi, G., additional, and Pantos, C., additional

Published
2013
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120. This title is unavailable for guests, please login to see more information.

Author

Pantos, C. Mourouzis, I. Xinaris, C. Kokkinos, A.D. Markakis, K. Dimopoulos, A. Panagiotou, M. Saranteas, T. Kostopanagiotou, G. Cokkinos, D.V. and Pantos, C. Mourouzis, I. Xinaris, C. Kokkinos, A.D. Markakis, K. Dimopoulos, A. Panagiotou, M. Saranteas, T. Kostopanagiotou, G. Cokkinos, D.V.

Published
2007

124. Prognostic impact of ventricular indices: Systemic hypertension

Author

Zahid, W., primary, Haugaa, K., additional, Bergestuen, D., additional, Skulstad, H., additional, Thiis-Evensen, E., additional, Fosse, E., additional, Edvardsen, T., additional, Magnino, C., additional, Omede', P., additional, Grosso Marra, W., additional, Chiarlo, M., additional, Presutti, D., additional, Bucca, C., additional, Moretti, C., additional, Gaita, F., additional, Veglio, F., additional, Milan, A., additional, Smith, B., additional, Dobson, G., additional, Grapsa, J., additional, Nihoyannopoulos, P., additional, Jaroch, J., additional, Loboz-Grudzien, K., additional, Magda, S., additional, Florescu, M., additional, Bociaga, Z., additional, Ciobanu, A., additional, Kruszynska, E., additional, Dudek, K., additional, Vinereanu, D., additional, Ryabikov, A., additional, Malyutina, S., additional, Shakhmatov, S., additional, Simonova, G., additional, Gafarov, V., additional, Veryovkin, E., additional, Krol, W., additional, Braksator, W., additional, Konopka, M., additional, Kuch, M., additional, Gierlak, W., additional, Krysztofiak, H., additional, Burkhard-Jagodzinska, K., additional, Mamcarz, A., additional, Dluzniewski, M., additional, Ciecierzynska, B., additional, Loboz-Rudnicka, M., additional, Rychard, W., additional, Polanski, J., additional, Granstam, S.-O., additional, Bjorklund, E., additional, Roos, M., additional, Shah, D., additional, Coghlan, G., additional, Papadimitraki, E., additional, Dellaportas, A., additional, Kotrotsou, A., additional, Mourouzis, I., additional, Vlachodimitris, I., additional, Spiropoulos, S., additional, Karagiannakis, D., additional, Anastasiadis, G., additional, and Economou, C., additional

Published
2012
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125. Poster session 3

Author

Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. L., additional, Pinho, M., additional, Pinho, S., additional, Sena, C., additional, Seica, R., additional, Leite-Moreira, A., additional, Dabroi, F., additional, Schiaffino, S., additional, Kiseleva, E., additional, Krukov, N., additional, Nikitin, O., additional, Ardatova, L., additional, Mourouzis, I., additional, Pantos, C., additional, Kokkinos, A. D., additional, Cokkinos, D. V., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M. A., additional, Pellegrino, M., additional, Calabriso, N., additional, Gastaldelli, A., additional, Storelli, C., additional, De Caterina, R., additional, Lindner, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschope, C., additional, Westermann, D., additional, Everaert, B. R., additional, Nijenhuis, V. J., additional, Reith, F. C. M., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, Vrints, C. 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2012
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126. Poster session 2

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Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. Y., additional, Arvanitis, D. A., additional, Mourouzis, I., additional, Pantos, C., additional, Kranias, E. G., additional, Cokkinos, D. V., additional, Sanoudou, D., additional, Vladimirskaya, T. E., additional, Shved, I. A., additional, Kryvorot, S. G., additional, Schirmer, I. M., additional, Appukuttan, A., additional, Pott, L., additional, Jaquet, K., additional, Ladilov, Y., additional, Archer, C. R., additional, Bootman, M. D., additional, Roderick, H. L., additional, Fusco, A., additional, Sorriento, D., additional, Santulli, G., additional, Trimarco, B., additional, Iaccarino, G., additional, Hagenmueller, M., additional, Riffel, J., additional, Bernhold, E., additional, Katus, H. A., additional, Hardt, S. 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F., additional, Villar, A. V., additional, Perez-Moreno, A., additional, Gilabert, R., additional, and Ros, E., additional

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Dimova, I., primary, Hlushchuk, R., additional, Makanya, A., additional, Djonov, V., additional, Theurl, M., additional, Schgoer, W., additional, Albrecht, K., additional, Beer, A., additional, Patsch, J. R., additional, Schratzberger, P., additional, Mahata, S., additional, Kirchmair, R., additional, Didie, M., additional, Christalla, P., additional, Rau, T., additional, Eschenhagen, T., additional, Schumacher, U., additional, Lin, Q., additional, Zenke, M., additional, Zimmmermann, W., additional, Hoch, M., additional, Fischer, P., additional, Stapel, B., additional, Missol-Kolka, E., additional, Erschow, S., additional, Scherr, M., additional, Drexler, H., additional, Hilfiker-Kleiner, D., additional, Diebold, I., additional, Petry, A., additional, Kennel, P., additional, Djordjevic, T., additional, Hess, J., additional, Goerlach, A., additional, Castellano, J., additional, Aledo, R., additional, Sendra, J., additional, Costales, P., additional, Badimon, L., additional, Llorente-Cortes, V., additional, Dworatzek, E., additional, Mahmoodzadeh, S., additional, Regitz-Zagrosek, V., additional, Posa, A., additional, Varga, C., additional, Berko, A., additional, Veszelka, M., additional, Szablics, P., additional, Vari, B., additional, Pavo, I., additional, Laszlo, F., additional, Brandenburger, M., additional, Wenzel, J., additional, Bogdan, R., additional, Richardt, D., additional, Reppel, M., additional, Hescheler, J., additional, Terlau, H., additional, Dendorfer, A., additional, Heijman, J., additional, Rudy, Y., additional, Westra, R., additional, Volders, P., additional, Rasmusson, R., additional, Bondarenko, V., additional, Ertas Gokhan, M. D., additional, Ural Ertan, M. D., additional, Karaoz Erdal, P. H. D., additional, Aksoy Ayca, P. H. D., additional, Kilic Teoman, M. D., additional, Kozdag Guliz, M. D., additional, Vural Ahmet, M. D., additional, Ural Dilek, M. D., additional, Poulet, C., additional, Christ, T., additional, Wettwer, E., additional, Ravens, U., additional, Van Der Pouw Kraan, C., additional, Schirmer, S., additional, Fledderus, J., additional, Moerland, P., additional, Leyen, T., additional, Piek, J., additional, Van Royen, N., additional, Horrevoets, A., additional, Fleissner, F., additional, Jazbutyte, V., additional, Fiedler, J., additional, Galuppo, P., additional, Mayr, M., additional, Ertl, G., additional, Bauersachs, J., additional, Thum, T., additional, Protze, S., additional, Bussek, A., additional, Li, F., additional, Hoo, R., additional, Lam, K., additional, Xu, A., additional, Subramanian, P., additional, Karshovska, E., additional, Megens, R., additional, Akhtar, S., additional, Heyll, K., additional, Jansen, Y., additional, Weber, C., additional, Schober, A., additional, Zafeiriou, M., additional, Noack, C., additional, Renger, A., additional, Dietz, R., additional, Zelarayan, L., additional, Bergmann, M., 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Shih, J., additional, Kass, D., additional, Di Lisa, F., additional, Paolocci, N., additional, Vinet, L., additional, Pezet, M., additional, Briec, F., additional, Previlon, M., additional, Rouet-Benzineb, P., additional, Hivonnait, A., additional, Charpentier, F., additional, Mercadier, J., additional, Cobo, M., additional, Llano, M., additional, Montalvo, C., additional, Exposito, V., additional, Meems, L., additional, Westenbrink, B., additional, Biesmans, L., additional, Bito, V., additional, Driessen, R., additional, Huysmans, C., additional, Mourouzis, I., additional, Pantos, C., additional, Galanopoulos, G., additional, Gavra, M., additional, Perimenis, P., additional, Spanou, D., additional, Cokkinos, D., additional, Panasenko, T., additional, Partsch, S., additional, Harjung, C., additional, Bogdanova, A., additional, Mihov, D., additional, Mocharla, P., additional, Yakushev, S., additional, Vogel, J., additional, Gassmann, M., additional, Tavakoli, R., additional, Johansen, 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Dos Santos, P., additional, Fusco, A., additional, Sorriento, D., additional, Cervero, P., additional, Feliciello, A., additional, Barnucz, E., additional, Kozichova, K., additional, Hlavackova, M., additional, Neckar, J., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Barsanti, C., additional, Abraham, N., additional, Muntean, D., additional, Mirica, S., additional, Duicu, O., additional, Raducan, A., additional, Hancu, M., additional, Fira-Mladinescu, O., additional, Ordodi, V., additional, Voelkl, J., additional, Haubner, B., additional, Neely, G., additional, Moriell, C., additional, Seidl, S., additional, Pachinger, O., additional, Penninger, J., additional, and Metzler, B., additional

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2010
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