Injury Incidence Rates and Profiles in Elite Taekwondo during Competition and Training.

This study aimed to investigate exposure adjusted injury incidence rates and profiles associated with training and competition in an elite taekwondo athlete population. 82 athletes were investigated for injuries over a period of 5 years. Individual fight time exposure for training and competition was recorded. The type and location of the injuries were classified and exposure-adjusted injury incidence rates (IIR) were calculated per 1000 h for training and competition. 66 athletes with a mean age of 19.3±4.2 years and 172 injuries were included in the final data assessment. The exposure adjusted IIR was significantly higher during competition (p<0.001) with a rate ratio of 6.33 (95% CI 4.58-8.69). Ankle and foot region as well as hand and wrist were most affected with significant higher IIR in competition (p<0.001). Joint injuries, fractures, and bruising occurred the most. Fractures occurred mainly to the hand and wrist region. Future investigations should focus on exposure adjusted injury data including analyses of the detailed mechanism leading to especially severe injuries to improve specific injury prevention in competition and promote evolution of protective gear.

[How dangerous is American football in a German amateur league? An injury analysis according to playing position over a period of four seasons]. / Wie gefährlich ist American Football im deutschen Amateurbereich? Eine positionsbezogene Verletzungsanalyse über vier Spielzeiten.

BACKGROUND: American football is known for its high risk of injury, especially in the professional field. Although the number of players in the German football league (GFL) has risen in recent years, data concerning the injury rates of German amateur players in American football are scarce. OBJECTIVE: Analysis of the injury rates in league games and training sessions in amateur football according to playing positions and body region. MATERIAL AND METHODS: Injuries of 123 American football players in a club playing in the second GFL (first and second team) were prospectively recorded over a period of 4 seasons (2014-2018). A complete history of injuries was obtained from 72 players. The injuries were classified using the Orchard sports injury classification system 10.1 (OSICS 10.1). The injury rates were calculated per 1000 athlete exposures (AE) for training as well as for league games with respect to the playing position and for each body region. RESULTS: Overall 142 injuries were recorded. On average there were 35.5 injuries per season and 1.9 injuries per player. Of the injuries 54.7% occurred during training and 46.1% during games. The risk of injury was significantly increased during league games (15.6 ± 16.3) compared to training (3.1 ± 2.7, p < 0.0001). While wide receivers and cornerbacks had the highest overall injury rates, running backs had the highest injury risk during games (p = 0.046). Injuries to knees (27.3%) and shoulders (20.1%) were the most frequent. The shoulder was the body region injured most frequently during games (p = 0.002). Regarding the injury pattern, distorsions (30.9%) and contusions (22.5%) occurred more often compared to fractures (12.6%) and dislocations (16.1%). Concussion only contributed to 2.9% of the injuries. CONCLUSION: American football is a contact sport with high injury rates even in the German amateur field, especially during league games. Regarding body regions, shoulders and knees were predominantly affected while regarding the playing position, wide receivers and cornerbacks were particularly jeopardized. Therefore, a continuous close medical supervision during games and an intensive position-specific training seem to be necessary even in the amateur field in order to reduce the injury rate.

Hepatic topographical changes of endoplasmic reticulum stress and unfolded protein response signaling after hemorrhagic shock and reperfusion.

BACKGROUND: Endoplasmic reticulum (ER) stress plays a crucial role in cell death decisions in context of various diseases. Although it is known that ER stress occurs in livers subjected to hemorrhagic shock and reperfusion (HS/R), there is no understanding about the influence of the liver architecture on ER stress and the activation of the unfolded protein response (UPR). MATERIALS AND METHODS: Mice were subjected to a pressure-controlled HS (30 ± 5 mmHg) for 90 min. Mice were sacrificed 2, 4, 6, 8, 10, 14, 18, and 24 h after shock induction. Plasma levels of inflammatory cytokines (IL-6, CXCL1, CXCL9, CXCL10, CCL2, CCL3) and transaminases were measured. Hematoxylin and eosin stains of paraffin-embedded liver tissue sections were evaluated for liver damage. Immunohistochemistry was used to analyze the hepatic topography of ER stress marker binding immunoglobulin protein and the activation of the three major pathways of the UPR. RESULTS: Compared with sham-operated mice, HS/R led to profound liver damage and an elevation of inflammatory cytokines. We found time-dependent topographical changes of ER stress in the livers. Furthermore, the three major pathways of the UPR represented by protein kinase RNA-like ER kinase, activating transcription factor 6, and inositol-requiring enzyme 1 were activated in differing ways dependent on the zonation within the liver acinus. CONCLUSIONS: These findings show that the liver architecture must be taken into account when investigating the role of ER stress and the UPR in ischemia-reperfusion injury after HS/R.

ER stress preconditioning ameliorates liver damage after hemorrhagic shock and reperfusion.

The mismatch of oxygen supply and demand during hemorrhagic shock disturbs endoplasmic reticulum (ER) homeostasis. The resulting accumulation of unfolded proteins in the ER lumen, which is a condition that is defined as ER stress, triggers the unfolded protein response (UPR). Since the UPR influences the extent of organ damage following hemorrhagic shock/reperfusion (HS/R) and mediates the protective effects of stress preconditioning before ischemia-reperfusion injury, the current study investigated the mechanisms of ER stress preconditioning and its impact on post-hemorrhagic liver damage. Male C56BL/6-mice were injected intraperitoneally with the ER stress inductor tunicamycin (TM) or its drug vehicle 48 h prior to being subjected to a 90 min pressure-controlled hemorrhagic shock (30±5 mmHg). A period of 14 h after hemorrhagic shock induction, mice were sacrificed. Hepatocellular damage was quantified by analyzing hepatic transaminases and hematoxylin-eosin stained liver tissue sections. Additionally, the topographic expression patterns of the ER stress marker binding immunoglobulin protein (BiP), UPR signaling pathways, and the autophagy marker Beclin1 were evaluated. TM injection significantly increased BiP expression and modified the topographic expression patterns of the UPR signaling proteins. In addition, immunohistochemical analysis of Beclin1 revealed an increased pericentral staining intensity following TM pretreatment. The histologic analysis of hepatocellular damage demonstrated a significant reduction in cell death areas in HS/R+TM (P=0.024). ER stress preconditioning influences the UPR and alleviates post-hemorrhagic liver damage. The beneficial effects were, at least partially, mediated by the upregulation of BiP and autophagy induction. These results underscore the importance of the UPR in the context of HS/R and may help identify novel therapeutic targets.

Modulation of Endoplasmic Reticulum Stress Influences Ischemia-Reperfusion Injury After Hemorrhagic Shock.

BACKGROUND: Impaired function of the endoplasmic reticulum (ER) results in ER stress, an accumulation of proteins in the ER lumen. ER stress is a major contributor to inflammatory diseases and is part of the pathomechanism of ischemia-reperfusion injury (IRI). Since severe traumatic injury is often accompanied by remote organ damage and immune cell dysfunction, we investigated the influence of ER stress modulation on the systemic inflammatory response and liver damage after hemorrhagic shock and reperfusion (HS/R). MATERIAL AND METHODS: Male C56BL/6-mice were subjected to hemorrhagic shock with a mean arterial pressure of 30 ±â€Š5 mm Hg. After 90 min mice were resuscitated with Ringer solution. Either the ER stress inductor tunicamycin (TM), its drug vehicle (DV), or the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) were added to reperfusion solution. Animals were sacrificed 14 h after shock induction and plasma concentrations of liver transaminases as well as inflammatory cytokines were measured. In addition, liver tissue sections were embedded in paraffin. For the quantification of hepatocellular damage hematoxylin and eosin stained tissue sections were analyzed. Furthermore, the topographic patterns of ER stress marker proteins were evaluated using immunohistochemistry. RESULTS: ER stress modulation influenced the topographic pattern of ER stress marker proteins. The alterations were particularly seen in the transition zone between vital liver parenchyma and cell death areas. Furthermore, the application of tunicamycin during reperfusion inhibited the secretion of pro-inflammatory cytokines and increased the hepatocellular damage significantly. However, the injection of TUDCA resulted in a significantly reduced liver damage, as seen by lower transaminases and smaller cell death areas. CONCLUSION: ER stress modulation influences post-hemorrhagic IRI. Moreover, the ER stress inhibitor TUDCA diminished the hepatocellular damage following HS/R significantly. This may help to provide a therapeutic target to ameliorate the clinical outcome after trauma-hemorrhage.