Patients were directed to continuously adjust head orientation an

Patients were directed to continuously adjust head orientation and to maintain the stimulus pattern at the center of the array. Postural tasks that present progressive difficulties were given during the use of the device. Pre- and post-treatment distribution of the sensory organization test (SOT) composite score showed an average value of 38.3 +/- 8.7 and 59.9 +/- 11.3, respectively, indicating a statistically significant improvement (p = 0.01). Electrotactile tongue biofeedback significantly improved the postural control of the study group, even if they had not improved with conventional VR. The electrotactile tongue biofeedback system was able to supply additional information about head position with respect to gravitational

vertical orientation in the absence of vestibular input, improving postural control. Patients with BVL can integrate electrotactile information in their postural Rabusertib order control in order click here to improve stability after conventional VR. These results were obtained and verified not only by the subjective questionnaire but also by the

SOT composite score. The limitations of the study are the small sample size and short duration of the follow-up. The current findings show that the sensory substitution mediated by electrotactile tongue biofeedback may contribute to the improved balance experienced by these patients compared to VR. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Emerging evidence suggests that the neuroprotective effects of valproic acid (VPA) occur via inhibition of histone deacetylases (HDACs) and activation of gene expression. This study assessed the ability of four VPA derivatives to cause histone hyperacetylation and protect against glutamate-induced excitotoxicity in cultured neurons. We found that PF299804 manufacturer (S)-2-pentyl-4-pentynoic acid (compound III) and (+/-)-2-hexyl-4-pentynoic acid (compound V) were far more potent and robust than VPA in inducing histone hyperacetylation and protecting against glutamate excitotoxicity. Thus, the increase in histone acetylation elicited by compounds III and V was significant at 5 mu M and reached a maximal increase of 600-700% at 50-100 mu M, compared with only a 200% increase by VPA

at 100 mu M. The neuroprotective effects of compounds III and V were evident at 10-25 mu M and reached a complete protection at 50-100 mu M, while a significant partial protection by VPA was observed at 100 mu M. These two compounds were also more effective than VPA in increasing HSP70-1a and HSP70-1b mRNA levels. At 50 mu M, compound V was most robust in increasing HSP-1a mRNA levels, followed by compound III, and then by VPA. HSP-1b mRNA was only significantly upregulated by compounds V and III, but not by VPA or other VPA derivatives under these treatment conditions. Our results suggest that these two VPA derivatives may ultimately be developed into potent neuroprotective drugs in preclinical and clinical studies. Published by Elsevier Ireland Ltd.

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