Human mesenchymal stem cell-based tumor therapeutic gene delivery is regarded as a promising strategy for the treatment of glioblastoma (GBM). However, the efficiency of these stem cells to home to the target sites limits their potential curative effect and clinical application. In this work, we provide a novel pretreatment approach for enhancing the homing capacity of human adipose-derived mesenchymal stem cells (hAMSCs) for stem cell-based tumor gene delivery for GBM therapy. Pre-exposure of these stem cells to TGF-β resulted in enhanced homing ability to GBM through increasing CXC chemokine receptor 4 (CXCR4) expression, as evidenced by a diminishing homing capacity when inhibition of the TGF-β receptor II and CXCR4 was applied. In addition, by pretreating hAMSCs expression of tumor necrosis factor-related apoptosis-inducing ligand with TGF-β, we achieved significant enhancements in the therapeutic efficacy as demonstrated by an increased number of migrated hAMSCs to target sites, decreased tumor volume, and prolonged survival time in a murine model of GBM. These findings highlight a straightforward method in which cell preconditioning methodology is utilized to promote therapeutic efficacy of a biological treatment for GBM.

Introduction: Acute pain is a common complication following cesarean section under general anesthesia. Post–cesarean section pain management is important for both the mother and the newborn. This study compared the effects of patient-controlled intravenous analgesia (PCIA) using sufentanil or tramadol on postoperative pain control and initiation time of lactation in patients who underwent cesarean section under general anesthesia. Methods: Primiparas (n=146) scheduled for cesarean section under general anesthesia were randomized to receive PCIA with sufentanil or tramadol. Movement-evoked and rest-pain intensity were assessed by the Numerical Rating Scale (NRS) postoperatively. The number of PCIA attempts, amount of drug consumed, initiation time of lactation, and Quality of Recovery Score 40 (QoR-40) were recorded at 4, 8, 12, and 24 h postoperatively. Pre- and postoperative serum prolactin levels were recorded. Results: No between-group difference existed in the NRS at rest at any time point postoperatively. Patients on sufentanil had more movement-evoked pain and a higher sedation score at 4, 8, and 12 h postoperatively, as compared with the tramadol group. At 24 h, the QoR-40 was higher in the tramadol group compared with the sufentanil group. No significant between-group differences were present in patient satisfaction and nausea/vomiting scores. Postpartum prolactin levels were significantly higher in the tramadol group versus the sufentanil group, corresponding with a significant delay in initiation of lactation in the latter. Conclusion: PCIA with tramadol may be preferred due to lower movement-evoked pain, higher quality of recovery, and earlier lactation in patients following cesarean section under general anesthesia.

The aim of the present study is to investigate the role of RNA interference in the inhibition of MUC1 gene expression in occurrence and metastasis of oral squamous cell carcinoma (OSCC) and its in-depth mechanisms. The OSCC and normal oral mucosa tissues, as well as normal oral epithelial cell line HOK and OSCC cell line SCC-4, Cal-27, TSCCA, Tca8113 were obtained to detect the expression of MUC1. Slug expression in OSCC and normal oral mucosa tissues was also determined. The OSCC cells were grouped to investigate the role of MUC1 gene silencing on proliferation, DNA replication, cell cycle distribution, apoptosis, colony formation ability, epithelial-mesenchymal transition (EMT), invasion, and migration of OSCC cells. We first found higher positive rate of MUC1 and Slug expression in OSCC tissues. Next, it was determined that higher expression of MUC1 was found in OSCC tissues and cells. Furthermore, silencing of MUC1 declined Slug expression, inhibited the proliferation, DNA replication, cell cycle progression, and EMT while inducing apoptosis of OSCC cells. Our study suggests that overexpression of MUC1 is found in OSCC, and MUC1 gene silencing could inhibit the proliferation, invasion, and migration while inducing apoptosis of OSCC cells.