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Abstract

By now, there is no doubt that regular physical exercise has an overall beneficial effect on each organ of the body. However, the effects of highly competitive sports (HCS) are more complex, as they exert greater demands on the cardiovascular and metabolic systems, among others. Strength, athletic, and aesthetic sport types each has a different exercise intensity and nutritional loading, as well as a different prevalence of cardiometabolic diseases at a later age. HCS athletes experience hypertension and mental stress during competitions and high nutritional loads between them. The post-career effects of this behaviour on the heart, arteries, cellular metabolism, and risk of obesity, are not well known and are not often the focus of research. In this review, we aimed to summarize the post-career effects of HCS. Based on data in the literature, we propose that athletes involved in highly competitive strength sports progressively develop metabolic syndrome and sustained elevated blood pressure.

Open access
Authors: E. Lukács, B. Magyari, L. Tóth, Zs. Petrási, I. Repa, A. Koller and Iván Horváth

There are several experimental models for the in vivo investigation of myocardial infarction (MI) in small (mouse, rat) and large animals (dog, pig, sheep and baboons). The application of large animal models raises ethical concerns, the design of experiments needs longer follow-up times, requiring proper breeding and housing conditions, therefore resulting in higher cost, than in vitro or small animal studies. On the other hand, the relevance of large animal models is very important, since they mostly resemble to human physiological and pathophysiological processes. The first main difference among MI models is the method of induction (open or closed chest, e.g. surgical or catheter based); the second main difference is the presence or absence of reperfusion. The former (i.e. reperfused MI) allows the investigation of reperfusion injury and new catheter based techniques during percutaneous coronary interventions, while the latter (i.e. nonreperfused MI) serves as a traditional coronary occlusion model, to test the effects of new pharmacological agents and biological therapies, as cell therapy. The reperfused and nonreperfused myocardial infarction has different outcomes, regarding left ventricular function, remodelling, subsequent heart failure, aneurysm formation and mortality. Our aim was to review the literature and report our findings regarding experimental MI models, regarding the differences among species, methods, reproducibility and interpretation.

Restricted access
Authors: B Raposa, R Pónusz, G Gerencsér, F Budán, Z Gyöngyi, A Tibold, D Hegyi, I Kiss, Á Koller and T Varjas

It has been reported that some of the food additives may cause sensitization, inflammation of tissues, and potentially risk factors in the development of several chronic diseases. Thus, we hypothesized that expressions of common inflammatory molecules – known to be involved in the development of various inflammatory conditions and cancers – are affected by these food additives. We investigated the effects of commonly used food preservatives and artificial food colorants based on the expressions of NFκB, GADD45α, and MAPK8 (JNK1) from the tissues of liver. RNA was isolated based on Trizol protocol and the activation levels were compared between the treated and the control groups. Tartrazine alone could elicit effects on the expressions of NFκB (p = 0.013) and MAPK8 (p = 0.022). Azorubine also resulted in apoptosis according to MAPK8 expression (p = 0.009). Preservatives were anti-apoptotic in high dose. Sodium benzoate (from low to high doses) dose-dependently silenced MAPK8 expression (p = 0.004 to p = 0.002). Addition of the two preservatives together elicited significantly greater expression of MAPK8 at half-fold dose (p = 0.002) and at fivefold dose (p = 0.008). This study suggests that some of the food preservatives and colorants can contribute to the activation of inflammatory pathways.

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