Epilepsy is one of the few neurologic disorders that requires a constant treatment during pregnancy. Epilepsy affects 0.3–0.8% of pregnant women. Prescription of antiepileptic drugs (AEDs) to pregnant women with epilepsy requires monitoring and maintaining a balance between limiting seizures and decreasing fetal exposure to the potential teratogenic effects. AEDs are also commonly used for psychiatric disorders, pain disorders, and migraines. The types of malformations that can result in fetuses exposed to AEDs include minor anomalies, major congenital malformations, intrauterine growth retardation, cognitive dysfunction, low IQ, microcephaly, and infant mortality. In the present review, we analyzed and summarized the current understanding of neurological development in fetuses that are exposed to various AEDs administered to pregnant epileptic women.
The catalytic subunit of human telomerase reverse transcriptase (hTERT), is the necessary and rate-limiting component to telomerase activation in cancer cells. To develop monoclonal antibodies (MAbs) against hTERT, a peptide-hTERT(9)-derived from specific motif T of hTERT was synthesized. Through fusion of splenocytes of BALB/c mice immunized with hTERT(9) with mouse myeloma cells, hybridomas were generated and clones secreting anti-hTERT(9) antibody were screened. After three rounds of limited dilution of candidate clones, three of which present stable and constant antibody production. The MAbs were hTERT(9)-specific and reactive with native hTERT of human cancer cells or tissues in Western blot and immunohistochemistry. The heavy chain variable regions from three hybridomas were cloned and sequenced confirming their mouse Ig derivation. The described investigation suggested that the generated MAbs to hTERT(9) could recognize native hTERT and be useful to cancer research.
The aim of the present study was to examine the effect of lamotrigine and the expression of myeloid-related protein 8 (MRP8) and interleukin-7 (IL-7) in the treatment of focal cortical dysplasia with secondary intractable epilepsy. In this study, rats with focal cortical dysplasia with secondary intractable epilepsy (constructed by our laboratory) were selected and used for experimentation, 21-day Sprague-Dawley rats were randomly divided into the control group (38 rats), the observation group I (39 rats), and the observation group II (38 rats). Rats in the observation group I received daily intraperitoneal injection of 0.02 mg/kg lamotrigine, and those in the observation group II and the control group received daily intraperitoneal injection of 0.02 mg/kg normal saline. Expression quantities of MRP8 and IL-7 in the hippocampus sample tissues of mice in the control group, observation group I, and observation group II were measured via fluorescence quantitative polymerase chain reaction assay, western blot analysis, enzyme-linked immunosorbent assay, and immunohistochemistry 48 h later. MRP8 and IL-7 gene mRNA levels of the control group, the observation group I and the observation group II had no significant differences (P>0.05). The expression quantity on the protein level of MRP8 and IL-7 showed no significant differences (P>0.05) between the observation group I (7.91±1.3, 3.86±0.38) and the control group (7.52±1.03, 3.62±0.29). The expression quantity of MRP8 and IL-7 showed significant differences (P<0.05) between observation group II (27.47±1.13, 19.45±0.48) and observation group I (7.91±1.3, 3.86±0.38). It was found that MRP8 and IL-7 were focused on the nerve cell membrane of hippocampus of rats in the observation group by immunohistochemistry experiments. In conclusion, the results from the present study show that lamotrigine can be used to treat rats with focal cortical dysplasia with secondary intractable epilepsy by reducing the expression levels of MRP8 and IL-7 in the body, providing a new therapeutic target to the follow-up treatment of focal cortical dysplasia with secondary intractable disease.
Background. Cancer stem cells (CSCs) are responsible for tumorigenesis, chemoresistance, and metastasis. Chemoresistance is a major challenge in the management of lung cancer. Glutathione-sulphur-transferase-π (GST-π) plays an important role in the origin and development of various types of cancer by regulating the cellular redox balance. Recent investigations have demonstrated that GST-π is associated with the chemoresistance of lung CSCs (LCSCs). However, the mechanism of GST-π in lung cancer, particularly in LCSCs, remains unclear. The present study is aimed at exploring the potential role of GST-π in stemness and cisplatin (DDP) resistance of LCSCs. Materials and methods. In the present study, lung cancer cell spheres were established using the A549 cell line, which according to our previous research, was confirmed to exhibit characteristics of stem cells. Next, GST-π protein expression, apoptosis percentage, and intracellular reactive oxygen species (ROS) concentration in A549 adherent cells and A549 cell spheres were analyzed by western blotting and flow cytometry, respectively. Finally, DDP resistance, ROS concentration, and GST-π expression in LCSCs were analyzed following the interference with GST-π using DL-buthionine-(S,R)-sulphoximine and N-acetylcysteine. Results. The results revealed that GST-π was highly expressed in A549 cell spheres compared with A549 adherent cells and was associated with a decreased intracellular ROS concentration (both P < 0.05 ). Regulating GST-π protein expression could alter DDP resistance of LCSCs by influencing ROS. Conclusion. These results suggested that GST-π may be important for LCSC drug resistance by downregulating ROS levels. These findings may contribute to the development of new adjuvant therapeutic strategies for lung cancer.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.