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Using an expert consensus-based approach, a netball video analysis consensus (NVAC) group of researchers and practitioners was formed to develop a video analysis framework of descriptors and definitions of physical, technical and contextual aspects for netball research. The framework aims to improve the consistency of language used within netball investigations. It also aims to guide injury mechanism reporting and identification of injury risk factors. The development of the framework involved a systematic review of the literature and a Delphi process. In conjunction with commercially used descriptors and definitions, 19 studies were used to create the initial framework of key descriptors and definitions in netball. In a two round Delphi method consensus, each expert rated their level of agreement with each of the descriptors and associated definition on a 5-point Likert scale (1—strongly disagree; 2—somewhat disagree; 3—neither agree nor disagree; 4—somewhat agree; 5—strongly agree). The median (IQR) rating of agreement was 5.0 (0.0), 5.0 (0.0) and 5.0 (0.0) for physical, technical and contextual aspects, respectively. The NVAC group recommends usage of the framework when conducting video analysis research in netball. The use of descriptors and definitions will be determined by the nature of the work and can be combined to incorporate further movements and actions used in netball. The framework can be linked with additional data, such as injury surveillance and microtechnology data.

Background:In many cell types, basolateral K+channels are important in maintaining transepithelial Na+absorption and regulatory volume decrease (RVD) after hyposmolar stress. However, in the esophagus the effect of K+transport in maintaining baseline short-circuit current (SCC) (Na+absorption) and RVD is unknown. Methods:Ussing chambers were used to evaluate changes in SCC of rabbit esophageal mucosa in response to serosal Ba2+(4 mmol/L), quinine (1 mmol/L), and increasing serosal [K+]. To determine whether K+channel(s) are activated in RVD, changes in SCC in response to serosal hyposmolarity (156 mOsm) were assessed in the presence or absence of serosal quinine. Results:Serosal Ba2+, quinine, or increased serosal [K+] caused a decline in baseline SCC. Serosal hyposmolarity caused an increase in SCC that was not blocked by mucosal application of amiloride (10−4mmol/L). In contrast, serosal quinine completely blocked the hyposmolar-induced increase in SCC. Conclusions:These studies suggest that rabbit esophageal cells possess Ba2+- and quinine-sensitive basolateral K+channel(s) that are active under baseline conditions. Potassium conductance(s) also appear to be activated by external serosal hyposmolarity and may be involved in the process of RVD.

Background:Regulatory volume decrease (RVD) after osmotic cellular swelling has been shown in several gastrointestinal epithelia but not in esophageal cells. In acid reflux disease, esophageal injury may be related in part to loss of RVD. Methods:Isolated basal esophageal cells were exposed to an external hyposmolar solution, and changes in relative cell size were assessed using a Coulter counter (Hialeah, FL) in the presence of K+and Cl−transport inhibitors and at varying extracellular pH (pH0). Results:At pH07.4, a 30% hyposmotic dilution of the external solution caused an initial peak cell swelling (1.15 ± 0.05-fold) followed by a return to starting cell size by 5 minutes (RVD). RVD was inhibited by Ba2+(4 mmol/L), quinine (1 mmol/L), or increasing the [K+]0≥ 10 mmol/L. RVD was also inhibited by depleting [Cl−]1or in the presence of 0.5 mmol/L 4,4′-diisothiocyanastostilbene-2,2′-disulfonic acid disodium salt (DIDS) or 50 μmol/L diphenylamine-2-carboxylate, a Cl−conductance inhibitor. To test the effect of pH on RVD, cells in solutions at pH07.4, 7.0, or 6.8 were subjected to hyposmotic stress; RVD was significantly inhibited at pH06.8. This pH-dependent inhibition of RVD was reversed in the presence of valinomycin, a K+ionophore. Conclusions:These studies show that isolated esophageal cells possess RVD mechanisms that are mediated by Cl−- and pH-dependent K+effluxes. RVD appears to be inhibited by a decrease in pH0, suggesting the possibility that acid-induced esophageal injury results from inhibition of normal volume regulatory mechanisms.