BackgroundThere is an established risk of injury to young athletes exposed to high training loads. Identifying and monitoring injury risk is essential to aid prevention. The aim of this study was to use the consensus statement to determine the incidence and pattern of injury in 1 English Premier League soccer academy during 1 season.MethodsA prospective cohort study included 181 elite academy soccer players during the 2012–2013 season. Players were divided into 5 age groups between 9 and 18 years. The number, type and incidence of injuries were recorded during matches and training. Incidence was calculated per 1000 hours of exposure.Results127 injuries occurred during 29 346 hours of soccer exposure. 72% of injuries were non-contact related. Under (U)18 players sustained the highest number of match injuries. U12–14 players sustained the highest number of training injuries and injuries overall. U16 players sustained the highest number of severe injuries, and U18 players sustained the highest number of moderate injuries. U18 players sustained the highest number of injuries/1000 hours of training and overall. U15 players sustained the highest number of injuries/1000 hours of matches, the highest number of recurrent injuries and the highest incidence of recurrence. The most common injuries were muscle injuries in U15 and U18 players. The most common injury location was the anterior thigh, with the majority of these occurring in training.ConclusionsUsing the consensus statement, this study used a repeatable method to identify the injury profile of elite academy-level soccer players.

A range of water-soluble fluorescent dyes and dye conjugates have been injected into cells in Elodea canadensis Michx. leaves. All compounds are unable to cross the plasmalemma between living cells and the external solution, are not degraded to other fluorescent compounds by tissue homogenates, and do not affect cytoplasmic streaming. Despite being unable to cross the plasmalemma, molecules up to 874 dalton pass from cell to cell, smaller molecules showing greater mobility. The conjugate of fluorescein isothiocyanate and leucyl-diglutamylleucine (874 dalton) appears to be close to the limit for movement: in only three out of 17 injections was any movement visible; this movement was only to adjacent cells and was close to the limit of detection. Dye molecules of 1678 dalton and larger did not pass from cell to cell. From the relationship between the size of the dye molecules, measured using molecular models, and their intercellular mobility, the equivalent pore diameter of the Elodea leaf plasmodesmata has been estimated to lie within the range 3.0-5.0 nm.

A set of hydrophilic fluorescent dyes of known molecular weight has been used to determine the molecular exclusion limit and the extent of apical, epidermal and cortical symplasts in the root, stem and leaf of Egeria densa. These dyes are unable to pass the plasmalemma, so that any cell-to-cell movement of injected dye must occur via the symplast. The shoot-apex symplast has a high molecular exclusion limit, excluding dyes with a molecular weight of 749 dalton (fluorescein hexaglycine) and greater but allowing dyes of up to 665 dalton (fluorescein diglutamic acid) to pass. The leaf epidermal symplast is similar to that in the apex: fluorescein pentaglycine (674 dalton) moves to a limited extent, but fluorescein hexaglycine is immobile. Stem and root epidermal cells have a lower molecular exclusion limit, only the dye 6-carboxyfluorescein (376 dalton) is able to move from cell-to-cell. Cortical and epidermal tissues in both the stem and the root have similar symplast permeabilities. However, a barrier to dye (6-carboxyfluorescein) movement is found between the epidermis and the cortex in both organs. Barriers are also found at the nodes between expanded internodes. The stem barriers are not found in the unexpanded nodes near the shoot tip; apparently they are formed early during internode expansion. In the root tip, a barrier to the movement of dye is found between the root cap and the remainder of the root. Plasmodesmata are found linking all cell types studied, even cells where barriers to dye movement occur. Thus, the plant, far from being one uniform symplast, consists of a large number of symplast domains, which may or may not differ in molecular exclusion limit.

Background Sensitivity‐related trait characteristics involving physical and emotional sensitivities and high trait anxiety personality types have been observed in individuals with nonspecific chronic low back pain (NSCLBP). High trait sensitivity to sensory stimulation combined with interpretation biases based on personality type may contribute to the development of central sensitization (CS) symptoms. To date, there is limited research that has considered both sensitivity levels and personality type in NSCLBP with CS. The purpose of this study was to investigate (1) relationships between trait sensory profiles, trait anxiety, and CS symptoms, and (2) the predictive capacity of sensory profiles, trait anxiety, and personality types on CS symptoms in people with NSCLBP. Methods This was a cross‐sectional observational study using 4 self‐report measures on adults (N = 165, mean age = 45 ± 12 [standard deviation] years) from physiotherapy clinics in England, Ireland, and New Zealand. Inclusion: NSCLBP > 6 months, age 18 to 64 years, predominant CS pain presentation, no other pathology. Parametric and nonparametric correlation statistics and regression analyses were used. Results Positive correlations were found between central sensitization inventory (CSI) scores and sensory hypersensitivity profiles and trait anxiety. CSI score increases could be predicted by sensory‐sensitive, low‐registration profiles; trait anxiety scores; and extreme defensive high anxious personality type. Conclusions Trait sensory hyper‐ and/or hyposensitivity and high trait anxiety–related personality type characteristics predict the extent of CS symptoms in people with NSCLBP. Further investigation is required to establish causality between these characteristics and CS symptoms.