Objective:To investigate the effects of ketogenic diet on seizures, electroencephalogram(EEG) changes and neurobehavioral development in children diagnosed with epilepsy.Methods:A total of 122 children diagnosed with spastic epilepsy in Nanyang Central Hospital from March 2016 to March 2019 were enrolled.The patients were divided into the observation group and the control group, by the computerized random number table method with 61 cases in each group.The children in the control group were treated with conventional therapy, and the children in the observation group were combined with the ketogenic diet on the basis of conventional treatment.The Gesell developmental schedules scale scores were compared between the two groups to evaluate seizure control and EEG improvement.Results:The seizure control in the observation group was significantly better than that in the control group [78.69%(48/61 cases) vs.54.10%(33/61 cases)], and the difference was statistically significant ( χ2 = 12.114, P <0.05). The EEG improvement in the observation group was significantly better than that in the control group [81.97%(50/61 cases) vs.55.74%(34/61 cases)], and the difference was statistically significant ( χ2=13.623, P<0.05). After 12 months of treatment, the children in the observation group had significantly higher fitness, gross motor, fine motor, language, and personal social, and total development quotient scores than the control group [(56.64±13.29) scores vs.(46.04±12.86) scores, (54.84±12.18) scores vs.(47.62±11.91) scores, (54.44±10.70) scores vs.(44.31±11.56) scores, (51.48±12.99) scores vs.(42.04±11.18) scores, (57.88±11.04) scores vs.(47.42±13.16) scores, (275.28±54.71) scores vs.(227.42±55.79) scores], the differences were statistically significant ( t=5.997, 5.887, 6.003, 5.889, 6.007, 6.010, all P<0.05). Conclusion:The ketogenic diet can significantly reduce seizures, improve EEG and neurobehavioral development in children with epilepsy.

The membrane protein claudin-3 (CLDN3) is critical for the formation and maintenance of tight junction and its high expression has been implicated in dictating malignant progression in various cancers. However, the post-translational modification of CLDN3 and its biological function remains poorly understood. Here, we report that CLDN3 is positively correlated with ovarian cancer progression both and Of interest, CLDN3 undergoes -palmitoylation on three juxtamembrane cysteine residues, which contribute to the accurate plasma membrane localization and protein stability of CLDN3 Moreover, the deprivation of -palmitoylation in CLDN3 significantly abolishes its tumorigenic promotion effect in ovarian cancer cells. By utilizing the co-immunoprecipitation assay, we further identify ZDHHC12 as a CLDN3-targating palmitoyltransferase from 23 ZDHHC family proteins. Furthermore, the knockdown of ZDHHC12 also significantly inhibits CLDN3 accurate membrane localization, protein stability and ovarian cancer cells tumorigenesis Thus, our work reveals -palmitoylation as a novel regulatory mechanism that modulates CLDN3 function, which implies that targeting ZDHHC12-mediated CLDN3 -palmitoylation might be a potential strategy for ovarian cancer therapy.