Authors:Zs. Major, E. Csajági, Zs. Kneffel, T. Kováts, I. Szauder, Z. Sidó and Gábor Pavlik
Characteristics of the athlete’s heart have been investigated mostly in the left ventricle (LV); reports referring to the right ventricle (RV) have only appeared recently. The aim of the present study was to compare the training effects on RV and LV in elite male endurance athletes. To this end, echocardiography was conducted in 52 elite endurance athletes (A) and in 25 non-athletes (NA). Differences between A and NA in the morphology was more marked in the RV (body-size-matched (rel.)) long axis diastolic diameter (RVLADd): 63.4 ± 6.3 vs. 56.4 ± 6.3; rel. short axis diastolic diameter (RVSADd): 27.3 ± 3.6 vs. 23.6 ± 2.7 mm/m, RV diastolic area 28 ± 5.0 vs. 21.3 ± 4.3 cm2 in all cases, p < 0.001) than in the LV (rel. LVLADd: 63.8 mm/m ± 5.6 vs. 60.7 mm/m ± 6.6, p < 0.05, rel.LVSADd 37.8 ± 3.1 vs. 35.3 ± 2.4, no difference). In the athletes ratios of peak early to late diastolic filling velocity (2.07 ± 0.51 vs. 1.75 ± 0.36, p < 0.01), the TDI-determined E’/A’ ratio in the septal (1.89 ± 0.55 vs. 1.62 ± 0.55, p < 0.05) and lateral (2.62 ± 0.72, vs. 2.18 ± 0.87, p < 0.001) walls were significantly higher than in NA only in the LV. Results indicate that in male endurance athletes morphologic adaptation is similar or slightly stronger in the RV than in the LV, functional adaptation seems to be stronger in the LV.
Authors:Gábor Skaliczki, M. Weszl, K. Schandl, T. Major, M. Kovács, J. Skaliczki, H. Redl, M. Szendrői, K. Szigeti, D. Máté, Cs Dobó-Nagy and Zs Lacza
Purpose: The clinical demand for bone grafting materials necessitated the development of animal models. Critical size defect model has been criticized recently, mainly for its inaccuracy. Our objective was to develop a dependable animal model that would provide compromised bone healing, and would allow the investigation of bone substitutes. Methods: In the first group a critical size defect was created in the femur of adult male Wistar rats, and a non-critical defect in the remaining animals (Groups II, III and IV). The defect was left empty in group II, while in groups III and IV a spacer was interposed into the gap. Osteoblast activity was evaluated by NanoSPECT/CT imaging system. New bone formation and assessment of a union or non-union was observed by μCT and histology. Results: The interposition model proved to be highly reproducible and provided a bone defect with compromised bone healing. Significant bone regeneration processes were observed four weeks after removal of the spacer. Conclusion: Our results have shown that when early bone healing is inhibited by the physical interposition of a spacer, the regeneration process is compromised for a further 4 weeks and results in a bone defect during the time-course of the study.