The co-occurrence of epilepsy and arrhythmia is an increasingly concerned research area, but the underlying biological mechanism is still not fully understood. In recent years, many studies have focused on how mutations in ion channel genes affect the electrophysiological properties of neurons and heart muscle cells, revealing a possible intersection between epilepsy and arrhythmia. Mutations in ion channel genes (such as SCN1A, KCNQ2, and RYR2) may simultaneously affect the electrophysiological properties of neurons and cardiomyocytes, leading to the comorbidity of epilepsy and arrhythmia. During epileptic seizures, activation of the autonomic nervous system may cause abnormal cardiac electrical activity, increasing risks of arrhythmia and sudden death resulting from epilepsy. In addition, the potential effects of antiepileptic drugs on cardiac ion channels can further increase the arrhythmia risk. This article reviews the research progress on the electrophysiological characteristics of ion channels in neurons and cardiomyocytes, the relations of ion channel gene mutations with epilepsy, arrhythmia, and their comorbidity, with the aim of providing new ideas for clinical diagnosis and treatment of epilepsy.

The co-occurrence of epilepsy and arrhythmia is an increasingly concerned research area, but the underlying biological mechanism is still not fully understood. In recent years, many studies have focused on how mutations in ion channel genes affect the electrophysiological properties of neurons and heart muscle cells, revealing a possible intersection between epilepsy and arrhythmia. Mutations in ion channel genes (such as SCN1A, KCNQ2, and RYR2) may simultaneously affect the electrophysiological properties of neurons and cardiomyocytes, leading to the comorbidity of epilepsy and arrhythmia. During epileptic seizures, activation of the autonomic nervous system may cause abnormal cardiac electrical activity, increasing risks of arrhythmia and sudden death resulting from epilepsy. In addition, the potential effects of antiepileptic drugs on cardiac ion channels can further increase the arrhythmia risk. This article reviews the research progress on the electrophysiological characteristics of ion channels in neurons and cardiomyocytes, the relations of ion channel gene mutations with epilepsy, arrhythmia, and their comorbidity, with the aim of providing new ideas for clinical diagnosis and treatment of epilepsy.

Objective:To study the proportion and clinicopathological characteristics of gastric adenocarcinoma with enteroblastic differentiation (GAED) in gastric cancers showing an elevated serum alpha fetoprotein(AFP).Methods:A total of 724 resected gastric adenocarcinomas were collected from 2008 to 2018 at the 904 Hospital of Joint Service Support Force, and cases with pre-operative serum AFP >10 μg/L were screened. From the cases with elevated serum AFP, GAED cases were further evaluated based on morphology. Then the clincopathological features and immunohistochemical phenotypes of GAED were reviewed. In addition, the amplification of HER2 gene was detected with fluorescence in situ hybridization(FISH). When overall survival (OS) and progression-free survival (PFS) of GAED were analyzed, 289 cases ordinary gastric adenocarcinoma with normal serum AFP were employed as a control. Results:The percentage of GAED was 44% (11/25) in gastric cancers with elevated serum AFP. GAED was histologically tubular or papillary with clear cytoplasm, and some GAED cases showed cystadenoid structure similar to embryo sac (5 cases), homogeneous eosinophilic granules (4 cases) and intragland ulareosinophilic material (6 cases). All 11 GAED cases had lymph node metastasis. Liver metastasis and vascular thrombus were observed in 2 cases and 5 cases respectively. GAED was immunohistochemically positive for CDX2 (11/11), CD10 (8/11) and MUC2(3/11), which were intestinal epithelium differentiation markers. Meanwhile, primitive markers SALL4 (8/11), GPC3 (7/11) and AFP (5/11) were also expressed in GAED, and HER2 gene amplification was found in 3 cases (3/11) of GAED. Lastly, the PFS of GAED were significantly shorter than that of the control group ( P=0.02), while OS was not statistically different between these two groups ( P=0.99). Conclusions:Patients with GAED usually have a higher rate of elevated serum AFP in gastric adenocarcinoma, and the cancer exhibites features of both intestinal and primitive differentiation. As GAED is highly invasive, the prognosis of GAED may be poor. For GAED, the diagnosis of well-differentiated or moderately-differentiated adenocarcinoma should be avoided, because this diagnosis leads to underestimated malignant potential.