Grip style may be associated with ACL injury occurrence in judo. In addition, direct contact due to the opponent's attack may be a common mechanism for ACL injuries in judo.

To better understand the pathomechanics of the shoulder complex in throwing, we need to take into account the individual contributions of the glenohumeral, scapulothoracic, and thoracic extension movements to the MER.

Previous studies have suggested that resistance training exercise under unstable conditions decreases the isometric force output, yet little is known about its influence on muscular outputs during dynamic movement. The objective of this study was to investigate the effect of an unstable condition on power, force, and velocity outputs during the bench press. Twenty male collegiate athletes (mean age, 21.3 +/- 1.5 years; mean height, 167.7 +/- 7.7 cm; mean weight, 75.9 +/- 17.5 kg) participated in this study. Each subject attempted 3 sets of single bench presses with 50% of 1 repetition maximum (1RM) under a stable condition with a flat bench and an unstable condition with a Swiss ball. Acceleration data were obtained with an accelerometer attached to the center of a barbell shaft, and peak outputs of power, force, and velocity were computed. Although significant loss of the peak outputs was found under the unstable condition (p < 0.017), their reduction rates remained relatively low, approximately 6% for force and 10% for power and velocity outputs, compared with previous findings. Such small reduction rates of muscular outputs may not compromise the training effect. Prospective studies are necessary to confirm whether the resistance training under an unstable condition permits the improvement of dynamic performance and trunk stability.

No abstract

Intrathecal treatment with recombinant high‐mobility group box‐1 (rHMGB1) in naïve mice leads to a persistent and significantly decreased hind paw withdrawal threshold to mechanical stimuli, suggesting that spinal HMGB1 evokes abnormal pain processing. By contrast, repeated intrathecal treatment with anti‐HMGB1 antibody significantly reverses hind paw mechano‐hypersensitivity in mice with a partial sciatic nerve ligation (PSNL). By contrast, the cellular mechanism by which spinal HMGB1 induces neuropathic pain has yet to be fully elaborated. The current study tested the hypothesis that spinal HMGB1 could induce mechanical hypersensitivity through the activation of specific receptor in glial cells. Intrathecal pretreatment with toll‐like receptor (TLR) 4 inhibitors, but not TLR5, receptor for advanced glycation end‐products and C‐X‐C chemokine receptor type 4 inhibitors, prevented rHMGB1‐evoked mechanical hypersensitivity. Activation of spinal astrocytes appears to be crucial for the mechanism of action of rHMGB1 in naïve mice, as intrathecal pretreatment with astrocytic inhibitors prevented the rHMGB1‐induced mechanical hypersensitivity. Interleukin‐1β (IL‐1β) was up‐regulated within activated astrocytes and block of TLR4 prevented the upregulation of IL‐1β. Interleukin‐1β appears to be secreted by activated astrocytes, as IL‐1β neutralizing antibody prevented rHMGB1‐induced mechanical hypersensitivity. Furthermore, intrathecal pretreatment with either MK801 or gabapentin prevented the rHMGB1‐induced mechanical hypersensitivity, suggesting roles for spinal glutamate and the N‐methyl‐d‐aspartate receptor in the mediation of rHMGB1‐induced mechanical hypersensitivity. Thus, the current findings suggest that spinal HMGB1 upregulates IL‐1β in spinal astrocytes through a TLR4‐dependent pathway and increases glutamatergic nociceptive transduction. These spinal mechanisms could be key steps that maintain neuropathic pain.