BackgroundThe conversion of epidural labor analgesia (ELA) to epidural surgical anesthesia (ESA) for intrapartum cesarean section (CS) often fails, resulting in intraoperative pain. Spinal anesthesia (SA) can provide a denser sensory block than ESA. The purpose of this prospective, non-blinded, parallel-arm, randomized trial was to compare the rate of pain-free surgery between ESA and SA following ELA for intrapartum CS.MethodsBoth groups received continuous epidural infusions for labor pain at a rate of 10 ml/h. In the ESA group (n = 163), ESA was performed with 17 ml of 2% lidocaine mixed with 100 µg fentanyl, 1 : 200,000 epinephrine, and 2 mEq bicarbonate. In the SA group (n = 160), SA was induced with 10 mg of 0.5% hyperbaric bupivacaine and 15 µg fentanyl. We investigated the failure rate of achieving pain-free surgery and the incidence of complications between the two groups.ResultsThe failure rate of achieving pain-free surgery was higher in the ESA group than the SA group (15.3% vs. 2.5%, P < 0.001). There was no statistical difference between the two groups in the rate of conversion to general anesthesia; however, the rate of analgesic requirement was higher in the ESA group than in the SA group (12.9% vs. 1.3%, P < 0.001). The incidence of high block, nausea, vomiting, hypotension, and shivering and Apgar scores were comparable between the two groups.ConclusionsSA after ELA can lower the failure rate of pain-free surgery during intrapartum CS compared to ESA after ELA.

Advanced cancer has been shown to be associated with a higher percentage of epigenetic changes than with genetic mutations. Preclinical models have shown that the combination of paclitaxel, sorafenib, and radiation therapy (RT) plays a crucial role in renal cell carcinoma (RCC) and breast cancer. This study aimed to investigate the involvement of mitochondrial cytochrome c–dependent apoptosis in the mechanism of action of a combination of paclitaxel, sorafenib, and RT in RCC and breast cancer. RCC and breast cancer cell lines were exposed to paclitaxel and sorafenib alone or combined in the presence of radiation, and cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The synergistic anticancer effects of the combination therapy on cell cycle and intracellular signaling pathways were estimated using flow cytometry and immunoblot analysis. RCC and breast cancer cell line xenograft models were used to examine the antitumor activity in vivo. Our results suggest that paclitaxel, sorafenib, and RT synergistically decreased the viability of RCC and breast cancer cells and significantly induced their apoptosis, as shown by caspase-3 cleavage. Paclitaxel, sorafenib, and radiation cotreatment reduced antiapoptotic factor levels in these cells and, thereby, significantly reduced the tumor volume of RCC and breast cancer cell xenografts. The current study suggests that paclitaxel, sorafenib, and radiation cotreatment was more effective than cotreatment with paclitaxel or sorafenib and radiation. These findings may offer a new therapeutic approach to RCC and breast cancer.