The effect of supervised rehabilitation on strength, postural sway, position sense and re-injury risk after acute ankle ligament sprain Holme E, Magnusson SP. Becher K. Bieler T. Aagaard P, Kjm M. The effect of supervised rehabilitation on strength. postural sway. position sense and re-iiijury risk after acute ankle ligament sprain. Scand J Med Sci Sports 1999: 9: 104109. 0 Munksgaard. 1999 The effect of an early rehabilitation program. including postural training, on ankle joint function after an ankle ligament sprain was investigated prospectively. Ninety-two subjects. matched for age. sex. and level of sports activity. were randomized to a control or training group. All subject received the same standard information regarding early ankle mobilization. In addition. the training group participated in supervised physical therapy rehabilitation ( 1 h. twice weekly) with emphasis on balance training. Postural sway. position sense and isometric ankle strength were measured 6 weeks and 4 months after the injury. and at 12 months re-injury data were obtained. In the training group. there was a significant difference between the injured and uninjured side for plantar flexion (P0.05) at 6 weeks, and there were no side-to-side differences at 4 months in either group. In the control group, 11/38 (29%) suffered a re-injury. while this number was only 2/29 (7%)) in the training group (P<0.05). These data showed that an ankle injury resulted in reduced ankle strength and postural control at 6 weeks, but that these variables had normalized at 4 months, independent of the supervised rehabilitation. However. the findings also demonstrated that supervised rehabilitation may reduce the number of re-injuries, and therefore may play a role in injury prevention.

Optimization of cocontraction of antagonistic muscles around the ankle joint has been shown to involve plastic changes in spinal and cortical neural circuitries. Such changes may explain the ability of elite ballet dancers to maintain a steady balance during various ballet postures. Here we investigated whether short-term cocontraction training in ballet dancers and nondancers leads to changes in the coupling between antagonistic ankle motor units. Eleven ballet dancers and 10 nondancers were recruited for the study. Prior to training, ballet dancers and nondancers showed an equal amount of coherence in the 15- to 35-Hz frequency band and short-term synchronization between antagonistic tibialis anterior and soleus motor units. The ballet dancers tended to be better at maintaining a stable cocontraction of the antagonistic muscles, but this difference was not significant (P = 0.09). Following 27 min of cocontraction training, the nondancers improved their performance significantly, whereas no significant improvement was observed for the ballet dancers. The nondancers showed a significant increase in 15- to 35-Hz coherence following the training, whereas the ballet dancers did not show a significant change. A group of control subjects (n = 4), who performed cocontraction of the antagonistic muscles for an equal amount of time, but without any requirement to improve their performance, showed no change in coherence. We suggest that improved ability to maintain a stable cocontraction around the ankle joint is accompanied by short-term plastic changes in the neural drive to the involved muscles, but that such changes are not necessary for maintained high-level performance.

ZBP1 is an interferon-induced cytosolic nucleic acid sensor that facilitates antiviral responses via RIPK3. Although ZBP1-mediated programmed cell death is widely described, whether and how it promotes inflammatory signaling is unclear. Here, we report a ZBP1-induced inflammatory signaling pathway mediated by K63and M1-linked ubiquitin chains, which depends on RIPK1 and RIPK3 as scaffolds independently of cell death. In human HT29 cells, ZBP1 associated with RIPK1 and RIPK3 as well as ubiquitin ligases cIAP1 and LUBAC. ZBP1-induced K63-and M1-linked ubiquitination of RIPK1 and ZBP1 to promote TAK1-and IKK-mediated inflammatory signaling and cytokine production. Inhibition of caspase activity suppressed ZBP1-induced cell death but enhanced cytokine production in a RIPK1-and RIPK3 kinase activitydependent manner. Lastly, we provide evidence that ZBP1 signaling contributes to SARS-CoV-2-induced cytokine production. Taken together, we describe a ZBP1-RIPK3-RIPK1-mediated inflammatory signaling pathway relayed by the scaffolding role of RIPKs and regulated by caspases, which may induce inflammation when ZBP1 is activated below the threshold needed to trigger a cell death response.

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