METHODS: The hESCs were differentiated into neural stem cells (NSCs), and NSC-DECM was extracted from confluent monolayers of NSCs through treatment with deionized water. DFSCs seeded on NSC-DECM, Geltrex, and tissue culture polystyrene (TCPS) were subjected to neural induction during a period of 21 days. Expression of early/intermediate (Musashi1, PAX6, NSE, and βIII-tubulin) and mature/late (NGN2, NeuN, NFM, and MASH1) neural markers by DFSCs was analyzed at the 7-, 14-, and 21-day time points with quantitative real-time polymerase chain reaction. Immunocytochemistry for detection of βIII-tubulin, PAX6, and NGN2 expression by DFSCs on day 7 of neural induction was also carried out.
RESULTS: Quantitative RT-PCR showed that expression of PAX6, Musashi1, βIII-tubulin, NSE, NGN2, and NFM by DFSCs was enhanced on NSC-DECM versus either the Geltrex or TCPS groups. Immunocytochemistry showed that DFSCs in the NSC-DECM group displayed more intense staining for βIII-tubulin, PAX6, and NGN2 expression, together with more neurite outgrowths and elongated morphology, as compared with either Geltrex or TCPS.
CONCLUSIONS: DECM derived from neurogenesis of hESCs can enhance the neurogenic potential of DFSCs.
METHODS: Between 2019 and 2022, 9 patients with NCs of the subaxial spine underwent an anterior microsurgical approach. Their clinical presentations, radiological features, operative findings, and follow-up data were retrospectively reviewed and analyzed.
RESULTS: All spinal cysts were intradural and extramedullary in origin. Five patients were first-time cases while 4 patients with recurrence underwent revision surgery. The most common clinical manifestation was pain (77.78%). One patient was found to have a concomitant disorder of Klippel-Feil syndrome. Microscopically confirmed gross-total resection was achieved in 8 patients (88.89%) based on clinical comparisons between pre- and postoperative MRI and intraoperative video. One patient had symptom recurrence 1 year after subtotal resection, while there was no evidence of recurrence during follow-up for the other patients. Dense adhesions within the spinal cord were observed in 8 patients (88.89%) intraoperatively. Most importantly, the surgical outcome was significantly improved in all patients, and the mean (± SE) Japanese Orthopaedic Association score increased from 11.33 ± 0.91 preoperatively to 16.22 ± 0.32 postoperatively (p = 0.008).
CONCLUSIONS: An anterior surgical approach was proven to be both safe and effective in treating the ventral or ventrolateral SCNCs. The authors believe that an anterior microsurgical approach should be considered as a useful approach especially in patients with ventral recurrent SCNCs. Its clinical efficacy compared with a posterior approach in ventral spinal cyst may be better as most of the neurenteric cysts are ventrally or ventrolaterally located.
Methods: Triptolide's inhibition of cell viability was detected by sulforhodamine B (SRB) assay. Cell cycle was measured by flow cytometry and cell apoptosis was assessed by flow cytometry and western blot. Expression of β-catenin was analyzed by western blot and immunofluorescence (IF). The anti-tumor effects of triptolide were determined using a subcutaneous in-vivo model. Cell proliferation and apoptosis were evaluated by immunohistochemistry (IHC) and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, respectively. The expression level of p-p70S6K and p-GSK-3α/β was evaluated by western blot and IHC.
Results: Triptolide inhibited cell proliferation, induced S-phase cell cycle arrest and apoptosis in taxol-resistant A549 (A549/TaxR) cells. Moreover, intraperitoneal injection of triptolide resulted in a significant delay of tumor growth without obvious systemic toxicity in mice. Additionally, triptolide reversed epithelial-mesenchymal transition (EMT) through repression of the p70S6K/GSK3/β-catenin signaling pathway.
Conclusions: Our study provides evidence that triptolide can reverse EMT in taxol-resistant lung adenocarcinoma cells and impairs tumor growth by inhibiting the p70S6K/GSK3/β-catenin pathway, indicating that triptolide has potential to be used as a new therapeutic agent for taxol-resistant lung adenocarcinoma.