Insufficient sleep is common among high school students and has been associated with an increased risk for motor vehicle crashes (1), sports injuries (2), and occupational injuries (3). To evaluate the association between self-reported sleep duration on an average school night and several injury-related risk behaviors (infrequent bicycle helmet use, infrequent seatbelt use, riding with a driver who had been drinking, drinking and driving, and texting while driving) among U.S. high school students, CDC analyzed data from 50,370 high school students (grades 9-12) who participated in the national Youth Risk Behavior Surveys (YRBSs) in 2007, 2009, 2011, or 2013. The likelihood of each of the five risk behaviors was significantly higher for students who reported sleeping ≤7 hours on an average school night; infrequent seatbelt use, riding with a drinking driver, and drinking and driving were also more likely for students who reported sleeping ≥10 hours compared with 9 hours on an average school night. Although insufficient sleep directly contributes to injury risk, some of the increased risk associated with insufficient sleep might be caused by engaging in injury-related risk behaviors. Intervention efforts aimed at these behaviors might help reduce injuries resulting from sleepiness, as well as provide opportunities for increasing awareness of the importance of sleep.
There is dogma that higher training load causes higher injury rates. However, there is also evidence that training has a protective effect against injury. For example, team sport athletes who performed more than 18 weeks of training before sustaining their initial injuries were at reduced risk of sustaining a subsequent injury, while high chronic workloads have been shown to decrease the risk of injury. Second, across a wide range of sports, well-developed physical qualities are associated with a reduced risk of injury. Clearly, for athletes to develop the physical capacities required to provide a protective effect against injury, they must be prepared to train hard. Finally, there is also evidence that under-training may increase injury risk. Collectively, these results emphasise that reductions in workloads may not always be the best approach to protect against injury.
Inositol kinase and its product accelerate wound healing by modulating calcium levels, Rho GTPases, and F-actin assembly
- Proceedings of the National Academy of Sciences of the United States of America
- Published over 6 years ago
Wound healing is essential for survival. We took advantage of the Xenopus embryo, which exhibits remarkable capacities to repair wounds quickly and efficiently, to investigate the mechanisms responsible for wound healing. Previous work has shown that injury triggers a rapid calcium response, followed by the activation of Ras homolog (Rho) family guanosine triphosphatases (GTPases), which regulate the formation and contraction of an F-actin purse string around the wound margin. How these processes are coordinated following wounding remained unclear. Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzymatic product inositol 1,3,4,5-tetrakisphosphate (InsP4) plays an essential role during wound healing by modulating the activity of Rho family GTPases and F-actin ring assembly. Furthermore, we show that Itpkb and InsP4 modulate the speed of the calcium wave, which propagates from the site of injury into neighboring uninjured cells. Strikingly, both overexpression of itpkb and exogenous application of InsP4 accelerate the speed of wound closure, a finding that has potential implications in our quest to find treatments that improve wound healing in patients with acute or chronic wounds.
The vertebral arteries are rarely injured in penetrating neck trauma due to their deep location in the foramen transversarium. These injuries in isolation are not associated with neurological deficits or ischemic changes on radiology as the collaterals are usually sufficient. We report a case of fatal unilateral vertebral artery stab injury leading to bilateral cerebellar and brainstem infarction. The carotid Doppler ruled out the presence of any carotid artery injury. Life-threatening injuries are possible in the presence of hypoplastic contralateral vertebral artery or inadequate flow from the anterior circulation not making up for the deficit. This emphasizes that thorough evaluation and timely management of suspected injuries to even a single vertebral artery should be undertaken.
Complete brachial plexus avulsion injury is a severe disabling injury due to traction to the brachial plexus. Brachial plexus re-implantation is an emerging surgical technique for the management of complete brachial plexus avulsion injury.
Do coaches' leadership styles affect injury rates and the availability of players in professional football? Certain types of leadership behaviour may cause stress and have a negative impact on players' health and well-being.
To assess the efficacy of a programme of supervised physiotherapy on the recovery of simple grade 1 and 2 ankle sprains.
Why do some hamstring and quadriceps strains take much longer to repair than others? Which injuries are more prone to recurrence? Intramuscular tendon injuries have received little attention as an element in ‘muscle strain’. In thigh muscles, such as rectus femoris and biceps femoris, the attached tendon extends for a significant distance within the muscle belly. While the pathology of most muscle injures occurs at a musculotendinous junction, at first glance the athlete appears to report pain within a muscle belly. In addition to the musculotendinous injury being a site of pathology, the intramuscular tendon itself is occasionally injured. These injuries have a variety of appearances on MRIs. There is some evidence that these injuries require a prolonged rehabilitation time and may have higher recurrence rates. Therefore, it is important to recognise the tendon component of a thigh ‘muscle strain’.
- The Journal of sports medicine and physical fitness
- Published over 5 years ago
Aim: The purpose of this study was to clarify training-related risk factors for overuse injuries. Methods: This was twelve-month retrospective study which was done by self-reported postal questionnaire. The study group consisted of 446 men and women top-level Finnish athletes representing three different endurance sports (cross-country skiing, swimming, long-distance running) between the ages of 15-35. Self-reported anthropometric and training-related variables (such as starting age of training, years of active training, hours trained yearly, competition hours and weekly resting days) and occurrence of overuse injuries. Results: Athletes with less than 2 rest days per week during the training season had 5.2-fold risk (95% confidence intervals [CI] 1.89-14.06, P=0.001) for an overuse injury, and athletes who trained more than 700 hours during a year had 2.1-fold risk (95% CI 1.21-3.61, P=0.008) for an overuse injury compared to the others. Athletes who reported a tendon injury were on average two years older than athletes without such an injury (P<0.001). Conclusion: We found that low number of recovery days and a high amount of training are training-related risk factors for overuse injuries in top-level endurance athletes. The higher number of tendon overuse injuries in older than younger athletes may indicate that age-related degeneration plays an important role in the etiology of tendon injuries. These findings should be taken into account when planning exercise programs for endurance athletes.
In the United States over 1.7 million cases of traumatic brain injury are reported yearly, but predictive correlation of cellular injury to impact tissue strain is still lacking, particularly for neuronal injury resulting from compression. Given the prevalence of compressive deformations in most blunt head trauma, this information is critically important for the development of future mitigation and diagnosis strategies. Using a 3D in vitro neuronal compression model, we investigated the role of impact strain and strain rate on neuronal lifetime, viability, and pathomorphology. We find that strain magnitude and rate have profound, yet distinctively different effects on the injury pathology. While strain magnitude affects the time of neuronal death, strain rate influences the pathomorphology and extent of population injury. Cellular injury is not initiated through localized deformation of the cytoskeleton but rather driven by excess strain on the entire cell. Furthermore we find that, mechanoporation, one of the key pathological trigger mechanisms in stretch and shear neuronal injuries, was not observed under compression.