"The 11" was successfully implemented in a countrywide campaign and proved effective in reducing soccer injuries in amateur players. An effect of the prevention program was also observed in the population-based insurance data and health-care costs.

Microglia are the resident tissue macrophages of the central nervous system including the retina. Under pathophysiological conditions, microglia can signal to Müller cells, the major glial component of the retina, affecting their morphological, molecular, and functional responses. Microglia–Müller cell interactions appear to be bidirectional shaping the overall injury response in the retina. Hence, microglia and Müller cell responses to disease and injury have been ascribed both positive and negative outcomes. However, Müller cell reactivity and survival in the absence of immune cells after injury have not been investigated in detail in adult zebrafish. Here, we develop a model of focal retinal injury combined with pharmacological treatments for immune cell depletion in zebrafish. The retinal injury was induced by a diode laser to damage photoreceptors. Two pharmacological treatments were used to deplete either macrophage–microglia (PLX3397) or selectively eliminate peripheral macrophages (clodronate liposomes). We show that PLX3397 treatment hinders retinal regeneration in zebrafish, which is reversed by microglial repopulation. On the other hand, selective macrophage elimination did not affect the kinetics of retinal regeneration. The absence of retinal microglia and macrophages leads to dysregulated Müller cell behavior. In the untreated fish, Müller cells react after injury induction showing glial fibrillary acidic protein (GFAP), Phospho‐p44/42 MAPK (Erk1/2), and PCNA upregulation. However, in the immunosuppressed animals, GFAP and phospho‐p44/42 MAPK (Erk1/2) expression was not upregulated overtime and the reentry in the cell cycle was not affected. Thus, microglia and Müller cell signaling is pivotal to unlock the regenerative potential of Müller cells in order to repair the damaged retina.

PurposeThere are several approaches to quantifying physical load in team sports using positional data. Distances in different speed zones are most commonly used. Recent studies have used acceleration data in addition in order to take short intense actions into account. However, the fact that acceleration decreases with increasing initial running speed is ignored and therefore introduces a bias. The aim of our study was to develop a new methodological approach that removes this bias. For this purpose, percentage acceleration was calculated as the ratio of the maximal acceleration of the action (amax,action) and the maximal voluntary acceleration (amax) that can be achieved for a particular initial running speed (percentage acceleration [%] = amax,action / amax * 100).MethodsTo define amax, seventy-two highly trained junior male soccer players (17.1 ± 0.6 years) completed maximal sprints from standing and three different constant initial running speeds (vinit; trotting: ~6.0 km·h–1; jogging: ~10.8 km·h–1; running: ~15.0 km·h–1).ResultsThe amax was 6.01 ± 0.55 from a standing start, 4.33 ± 0.40 from trotting, 3.20 ± 0.49 from jogging and 2.29 ± 0.34 m·s–2 from running. The amax correlated significantly with vinit (r = –0.98) and the linear regression equation of highly-trained junior soccer players was: amax = –0.23 * vinit + 5.99.ConclusionUsing linear regression analysis, we propose to classify high-intensity actions as accelerations >75% of the amax, corresponding to acceleration values for our population of >4.51 initiated from standing, >3.25 from trotting, >2.40 from jogging, and >1.72 m·s–2 from running. The use of percentage acceleration avoids the bias of underestimating actions with high and overestimating actions with low initial running speed. Furthermore, percentage acceleration allows determining individual intensity thresholds that are specific for one population or one single player.