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Background: We compared the effects of thoracic epidural analgesia (TEA) to conventional patient‐controlled analgesia (PCA) on several postoperative parameters of recovery after elective video‐assisted thoracoscopic (VATS) lobectomy. Methods: Ninety‐eight patients undergoing elective VATS lobectomy were enrolled. The primary endpoint was pain score. Recovery of bowel function, length of stay in the postanesthesia care unit (PACU), duration of postoperative hospital stay, and complications were assessed. Continuous variables were expressed and compared between groups using either a two‐tailed Student's t or Mann‐Whitney U test. Recovery of bowel function was compared using the log‐rank test. Results: Baseline characteristics between the groups were similar. Dynamic pain scores on postoperative days (PODs) 0–2 were significantly lower in the TEA group, as were resting pain scores on PODs 1 and 2 (P < 0.05). The mean duration to first flatus (16 ± 0.7 vs. 26 ± 0.7 hours; P < 0.001) and the mean length of stay in the PACU (34 vs. 67 minutes; P = 0.027) were shorter in the TEA compared to the PCA group, respectively. The only difference in postoperative complications was regarding confusion (5 TEA vs. 18 PCA patients; P = 0.002). No difference in overall length of stay was noted. Conclusions: Compared to PCA, TEA provided better postoperative pain control after VATS lobectomy and facilitated postoperative recovery of bowel function without increasing the length of hospital stay. This beneficial effect of TEA might be attributed to the attenuation of sympathetic hyperactivation, improved analgesia, and reduced opioid use. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a progressive and degenerative disorder of the central nervous system, characterized by the loss of dopaminergic neurons and muscular rigidity. Treatment with propofol (2,6-diisopropylphenol) has been observed to attenuate oxidative stress injury via inhibition of programmed cell death. Results from the present study indicate that propofol treatment attenuates 1-methyl-4-phenylpyridinium (MPP+)-induced oxidative stress, which was demonstrated by increased levels of reactive oxygen species, 4-hydroxy-2-nonenal and protein carbonyls. Furthermore, it was demonstrated that propofol may ameliorate MPP+-induced mitochondrial dysfunction by increasing the level of ATP and the mitochondrial membrane potential. MTT and lactate dehydrogenase assays indicated that propofol treatment reduces cell vulnerability to MPP+-induced insult. Propofol was also observed to prevent apoptotic signals by reducing the ratio of Bcl-2-associated X protein to B-cell lymphoma 2, reducing the expression level of cleaved caspase-3 and attenuating cytochrome c release. Thus, propofol may present as a novel therapeutic strategy for the treatment of PD. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that the Wnt/β-catenin signaling pathway is critical to the induction and maintenance of chronic neuropathic pain caused by peripheral inflammation and nerve damage. Emerging evidence from recent studies suggests that epigenetic mechanisms may also be critical to the pathogenesis of chronic pain. The present study aimed to elucidate the epigenetic mechanisms underlying altered Wnt signaling and their involvement in CCI-induced neuropathic pain in rat sciatic nerves. The results of the present study demonstrated a significant increase in the expression levels of Wnt3a in the dorsal horn of the rats with CCI. In addition, a significant increase in histone H3 acetylation, and a significant decrease in cytosine methylation in the promoter region of Wnt3a was observed in the dorsal horn of the rats with CCI. Intrathecal application of XAV939, which acts as an inhibitor of Wnt signaling, significantly decreased the expression levels of active β-catenin, and attenuated the rat behavioral responses to thermal and mechanical pain stimuli. These results suggest that the epigenetic upregulation of Wnt3a in the dorsal horn contributes to the maintenance of pain-induced behavior in rats with CCI. [ABSTRACT FROM AUTHOR]