In this paper, the analysis of intracavitary electrocardiograms is used to guide the mining of abnormal cardiac rhythms in patients with hidden heart disease, and the algorithm is improved to address the data imbalance problem existing in the abnormal electrocardiogram signals, and a weight-based automatic classification algorithm for deep convolutional neural network electrocardiogram signals is proposed. By preprocessing the electrocardiogram data from the MIT-BIH arrhythmia database, the experimental dataset training algorithm model is obtained, and the algorithm model is migrated into the project. In terms of system design and implementation, by comparing the advantages and disadvantages of the electrocardiogram monitoring system platform, the overall design of the system was carried out in terms of functional and performance requirements according to the system realization goal, and a mobile platform system capable of classifying common abnormal electrocardiogram signals was developed. The system is capable of long-term monitoring and can invoke the automatic classification algorithm model of electrocardiogram signals for analysis. In this paper, the functional logic test and performance test were conducted on the main functional modules of the system. The test results show that the system can run stably and monitor electrocardiogram signals for a long time and can correctly call the deep convolutional neural network-based automatic electrocardiogram signal classification algorithm to analyze the electrocardiogram signals and achieve the requirements of displaying the electrocardiogram signal waveform, analyzing the heartbeat type, and calculating the average heart rate, which achieves the goal of real-time continuous monitoring and analysis of the electrocardiogram signals.
Background This is the first study to explore the potential functions and expression patterns of RNA N6-methyladenosine (m6A) and potential related genes in preeclampsia. Methods We identified two m6A modification patterns through unsupervised cluster analysis and validated them by principal component analysis. We quantified the relative abundance of specific infiltrating immunocytes using single-sample gene set enrichment analysis (ssGSEA) and the Wilcoxon test. To screen hub genes related to m6A regulators, we performed weighted gene coexpression network analysis. Functional enrichment analysis was conducted for differential signalling pathways and cellular processes. Preeclampsia patients were grouped by consensus clustering based on differentially expressed hub genes and the relationship between different gene-mediated classifications and clinical features. Results Two m6A clusters in preeclampsia, cluster A and cluster B, were determined based on the expression of 17 m6A modification regulators; ssGSEA revealed seven significantly different immune cell subtypes between the two clusters. A total of 1393 DEGs and nine potential m6A-modified hub genes were screened. We divided the patients into two groups based on the expression of these nine genes. We found that almost all the patients in m6A cluster A were classified into hub gene cluster 1 and that a lower gestational age may be associated with more m6A-associated events. Conclusions This study revealed that hub gene-mediated classification is consistent with m6A modification clusters for predicting the clinical characteristics of patients with preeclampsia. Our results provide new insights into the molecular mechanisms of preeclampsia.
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