Cardiopulmonary resuscitation (CPR) must be interrupted for reliable rhythm analysis in current automatic external defibrillators because of artifacts produced by chest compressions. However, interruptions in CPR adversely affect the restoration of spontaneous circulation and survival. Suppressing CPR artifacts by digital signal processing techniques is a promising method to enable rhythm analysis during chest compressions, which would eliminate CPR interruptions for rhythm analysis. Although numerous methods have been developed to suppress CPR artifacts, the accuracy of rhythm analysis is still inadequate due to the residual artifact components in the filtered signal. This study proposes an enhanced adaptive filtering method to suppress CPR artifacts. A total of 183 shockable and 453 nonshockable segments of ECG signal, together with CPR-related reference signal, were extracted from 233 out of hospital cardiac arrest patients. The method was optimized on a training set with 85 shockable and 211 nonshockable segments, and evaluated on a testing set with 98 shockable and 242 nonshockable segments. Compared with artifact corrupted ECG signals, the signal-to-noise ratio (SNR) increased from -9.8 ± 12.5 to 11.2 ± 11.8 dB, and the accuracy was improved from 74.1% to 92.0% after filtering with the proposed method. Compared with the traditional adaptive filter, the SNR was improved by 1.7 dB and the accuracy was improved by 5.6 points. These results indicated that the proposed method could effectively suppress the chest compression related artifacts and improve the accuracy of rhythm analysis during uninterrupted CPR.

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Background: Amplitude spectrum area (AMSA) calculated from ventricular fibrillation (VF) can be used to monitor the effectiveness of chest compression (CC) and optimize the timing of defibrillation.However, reliable AMSA can only be obtained during CC pause because of artifacts. In this study, we sought to develop a method for estimating AMSA during cardiopulmonary resuscitation (CPR) using only the electrocardiogram (ECG) waveform.Methods: Intervals of 8 seconds ECG and CC-related references, including 4 seconds during CC and an adjacent 4 seconds without CC, were collected before 1,008 defibrillation shocks from 512 out-of-hospital cardiac arrest patients. Signal quality was analyzed based on the irregularity of autocorrelation of VF. If signal quality index (SQI) was high, AMSA would be calculated from the original signal. Otherwise, CC-related artifacts would be constructed and suppressed using the least mean square filter from VF before calculation of AMSA. The algorithm was optimized using 480 training shocks and evaluated using 528 independent testing shocks.Results: Overall, CC resulted in lower SQI [0.15 (0.04-0.61) with CC vs. 0.75 (0.61-0.83) without CC, P<0.01] and higher .2) with CC vs. 7.2 (4.9-10.6) mVHz without CC, P<0.01] values.The predictive accuracy (49.2% vs. 66.5%, P<0.01) and area under the receiver operating characteristic curve (AUC) (0.647 vs. 0.734, P<0.01) were significantly decreased during CC. Using the proposed method, the estimated AMSA was 7.1 (5.0-15.2) mVHz, the predictive accuracy was 67.0% and the AUC was 0.713, which were all comparable with those calculated without CC.Conclusions: Using the signal quality-based artifact suppression method, AMSA can be reliably estimated and continuously monitored during CPR.

Background: Chronic kidney disease (CKD), characterized by sustained inflammation and immune dysfunction, is highly prevalent and can eventually progress to end-stage kidney disease. However, there is still a lack of effective and reliable diagnostic markers and therapeutic targets for CKD.Methods: First, we merged data from GEO microarrays (GSE104948 and GSE116626) to identify differentially expressed genes (DEGs) in CKD and healthy patient samples. Then, we conducted GO, KEGG, HPO, and WGCNA analyses to explore potential functions of DEGs and select clinically significant modules. Moreover, STRING was used to analyse protein-protein interactions. CytoHubba and MCODE algorithms in the cytoscape plug-in were performed to screen hub genes in the network. We then determined the diagnostic significance of the obtained hub genes by ROC and two validation datasets. Meanwhile, the expression level of the biomarkers was verified by IHC. Furthermore, we examined immunological cells’ relationships with hub genes. Finally, GSEA was conducted to determine the biological functions that biomarkers are significantly enriched. STITCH and AutoDock Vina were used to predict and validate drug–gene interactions.Results: A total of 657 DEGs were screened and functional analysis emphasizes their important role in inflammatory responses and immunomodulation in CKD. Through WGCNA, the interaction network, ROC curves, and validation set, four hub genes (IL10RA, CD45, CTSS, and C1QA) were identified. Furthermore, IHC of CKD patients confirmed the results above. Immune infiltration analysis indicated that CKD had a significant increase in monocytes, M0 macrophages, and M1 macrophages but a decrease in regulatory T cells, activated dendritic cells, and so on. Moreover, four hub genes were statistically correlated with them. Further analysis exhibited that IL10RA, which obtained the highest expression level in hub genes, was involved in abnormalities in various immune cells and regulated a large number of immune system responses and inflammation-related pathways. In addition, the drug–gene interaction network contained four potential therapeutic drugs targeting IL10RA, and molecular docking might make this relationship viable.Conclusion: IL10RA and its related hub molecules might play a key role in the development of CKD and could be potential biomarkers in CKD.

Introduction: Amplitude spectrum area (AMSA) is a well-established measure than can predict defibrillation outcome and guiding individualized resuscitation of ventricular fibrillation (VF) patients. However, accurate AMSA can only be calculated during cardiopulmonary resuscitation (CPR) pause due to artifacts produced by chest compression (CC). In this study, we developed a real-time AMSA estimation algorithm using a convolutional neural network (CNN).Methods: Data were collected from 698 patients, and the AMSA calculated from the uncorrupted signals served as the true value for both uncorrupted and the adjacent corrupted signals. An architecture consisting of a 6-layer 1D CNN and 3 fully connected layers was developed for AMSA estimation. A 5-fold cross-validation procedure was used to train, validate and optimize the algorithm. An independent testing set comprised of simulated data, real-life CC corrupted data, and preshock data was used to evaluate the performance.Results: The mean absolute error, root mean square error, percentage root mean square difference and correlation coefficient were 2.182/1.951 mVHz, 2.957/2.574 mVHz, 22.887/28.649% and 0.804/0.888 for simulated and real-life testing data, respectively. The area under the receiver operating characteristic curve regarding predicting defibrillation success was 0.835, which was comparable to that of 0.849 using the true value of the AMSA.Conclusions: AMSA can be accurately estimated during uninterrupted CPR using the proposed method.

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