Objective: Cardiac arrest and cardiopulmonary resuscitation (CA/R) lead to whole-body ischemia and reperfusion (IR) injury, causing multiple organ dysfunction, including ischemic spinal cord injury. The thoracic spinal cord levels are crucial for maintaining the sympathetic functions vital for life. This study examined blood-spinal cord barrier (BSCB) leakage and astrocyte endfeet (AEF) disruption and their effects on survival, physiological variables, and neuronal damage/death in the intermediate zone (IMZ) at the seventh thoracic spinal cord level after asphyxial CA/R in rats. Methods: The rats underwent whole-body IR injury by asphyxial CA/R. Kaplan-Meier analysis was conducted to assess the cumulative survival post-CA/R. The histological changes post-CA/R were evaluated using immunohistochemistry, histofluorescence, and double histofluorescence. Results: No significant differences in body weight, mean arterial pressure, and heart rate were found between the sham and CA/R groups post-CA/R. The survival rates in the CA/R group at 12, 24, and 48 hours were 62.58%, 36.37%, and 7.8%, respectively. Neuronal loss and BSCB leakage began 12 hours post-CA/R, increasing with time. Reactive astrogliosis appeared at 12 hours and increased, while AEF disruption around blood vessels was evident at 48 hours. Conclusion The survival rate declined significantly by 48 hours post-CA/R. Neuronal loss and BSCB leakage in the thoracic spinal cord IMZ was evident at 12 hours and significant by 48 hours, aligning with AEF disruption. Neuronal loss in the thoracic spinal cord IMZ post-CA/R may be related to BSCB leakage and AEF disruption.

Human rhinovirus (HRV) causes the common cold and exacerbates chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease. Despite its significant impact on public health, there are currently no approved vaccines or antiviral treatments for HRV infection. Apoptosis is the process through which cells eliminate themselves through the systematic activation of intrinsic death pathways in response to various stimuli. It plays an important role in viral infections and serves as a key immune defense mechanism in the interactions between viruses and the host. In the present study, we investigated the antiviral effects of quercetin-3-methyl ether, a flavonoid isolated from Serratula coronata, on human rhinovirus 1B (HRV1B). Quercetin-3-methyl ether significantly inhibited HRV1B replication in HeLa cells in a concentration-dependent manner, thereby reducing cytopathic effects and viral RNA levels. Time-course and time-of-addition analyses confirmed that quercetin-3-methyl ether exhibited antiviral activity during the early stages of viral infection, potentially targeting the replication and translation phases. Gene expression analysis using microarrays revealed that pro-apoptotic genes were upregulated in quercetin-3-methyl ether-treated cells, suggesting that quercetin-3-methyl ether enhances early apoptosis to counteract HRV1B-induced immune evasion. In vivo administration of quercetin-3-methyl ether to HRV1B-infected mice significantly reduced viral RNA levels and inflammatory cytokine production in the lung tissues. Our findings demonstrated the potential of quercetin-3-methyl ether as a novel antiviral agent against HRV1B, thereby providing a promising therapeutic strategy for the management of HRV1B infections and related complications.

Objective: Cardiac arrest and cardiopulmonary resuscitation (CA/R) lead to whole-body ischemia and reperfusion (IR) injury, causing multiple organ dysfunction, including ischemic spinal cord injury. The thoracic spinal cord levels are crucial for maintaining the sympathetic functions vital for life. This study examined blood-spinal cord barrier (BSCB) leakage and astrocyte endfeet (AEF) disruption and their effects on survival, physiological variables, and neuronal damage/death in the intermediate zone (IMZ) at the seventh thoracic spinal cord level after asphyxial CA/R in rats. Methods: The rats underwent whole-body IR injury by asphyxial CA/R. Kaplan-Meier analysis was conducted to assess the cumulative survival post-CA/R. The histological changes post-CA/R were evaluated using immunohistochemistry, histofluorescence, and double histofluorescence. Results: No significant differences in body weight, mean arterial pressure, and heart rate were found between the sham and CA/R groups post-CA/R. The survival rates in the CA/R group at 12, 24, and 48 hours were 62.58%, 36.37%, and 7.8%, respectively. Neuronal loss and BSCB leakage began 12 hours post-CA/R, increasing with time. Reactive astrogliosis appeared at 12 hours and increased, while AEF disruption around blood vessels was evident at 48 hours. Conclusion The survival rate declined significantly by 48 hours post-CA/R. Neuronal loss and BSCB leakage in the thoracic spinal cord IMZ was evident at 12 hours and significant by 48 hours, aligning with AEF disruption. Neuronal loss in the thoracic spinal cord IMZ post-CA/R may be related to BSCB leakage and AEF disruption.

Human rhinovirus (HRV) causes the common cold and exacerbates chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease. Despite its significant impact on public health, there are currently no approved vaccines or antiviral treatments for HRV infection. Apoptosis is the process through which cells eliminate themselves through the systematic activation of intrinsic death pathways in response to various stimuli. It plays an important role in viral infections and serves as a key immune defense mechanism in the interactions between viruses and the host. In the present study, we investigated the antiviral effects of quercetin-3-methyl ether, a flavonoid isolated from Serratula coronata, on human rhinovirus 1B (HRV1B). Quercetin-3-methyl ether significantly inhibited HRV1B replication in HeLa cells in a concentration-dependent manner, thereby reducing cytopathic effects and viral RNA levels. Time-course and time-of-addition analyses confirmed that quercetin-3-methyl ether exhibited antiviral activity during the early stages of viral infection, potentially targeting the replication and translation phases. Gene expression analysis using microarrays revealed that pro-apoptotic genes were upregulated in quercetin-3-methyl ether-treated cells, suggesting that quercetin-3-methyl ether enhances early apoptosis to counteract HRV1B-induced immune evasion. In vivo administration of quercetin-3-methyl ether to HRV1B-infected mice significantly reduced viral RNA levels and inflammatory cytokine production in the lung tissues. Our findings demonstrated the potential of quercetin-3-methyl ether as a novel antiviral agent against HRV1B, thereby providing a promising therapeutic strategy for the management of HRV1B infections and related complications.

Human rhinovirus (HRV) causes the common cold and exacerbates chronic respiratory diseases, such as asthma and chronic obstructive pulmonary disease. Despite its significant impact on public health, there are currently no approved vaccines or antiviral treatments for HRV infection. Apoptosis is the process through which cells eliminate themselves through the systematic activation of intrinsic death pathways in response to various stimuli. It plays an important role in viral infections and serves as a key immune defense mechanism in the interactions between viruses and the host. In the present study, we investigated the antiviral effects of quercetin-3-methyl ether, a flavonoid isolated from Serratula coronata, on human rhinovirus 1B (HRV1B). Quercetin-3-methyl ether significantly inhibited HRV1B replication in HeLa cells in a concentration-dependent manner, thereby reducing cytopathic effects and viral RNA levels. Time-course and time-of-addition analyses confirmed that quercetin-3-methyl ether exhibited antiviral activity during the early stages of viral infection, potentially targeting the replication and translation phases. Gene expression analysis using microarrays revealed that pro-apoptotic genes were upregulated in quercetin-3-methyl ether-treated cells, suggesting that quercetin-3-methyl ether enhances early apoptosis to counteract HRV1B-induced immune evasion. In vivo administration of quercetin-3-methyl ether to HRV1B-infected mice significantly reduced viral RNA levels and inflammatory cytokine production in the lung tissues. Our findings demonstrated the potential of quercetin-3-methyl ether as a novel antiviral agent against HRV1B, thereby providing a promising therapeutic strategy for the management of HRV1B infections and related complications.

Objective: Cardiac arrest and cardiopulmonary resuscitation (CA/R) lead to whole-body ischemia and reperfusion (IR) injury, causing multiple organ dysfunction, including ischemic spinal cord injury. The thoracic spinal cord levels are crucial for maintaining the sympathetic functions vital for life. This study examined blood-spinal cord barrier (BSCB) leakage and astrocyte endfeet (AEF) disruption and their effects on survival, physiological variables, and neuronal damage/death in the intermediate zone (IMZ) at the seventh thoracic spinal cord level after asphyxial CA/R in rats. Methods: The rats underwent whole-body IR injury by asphyxial CA/R. Kaplan-Meier analysis was conducted to assess the cumulative survival post-CA/R. The histological changes post-CA/R were evaluated using immunohistochemistry, histofluorescence, and double histofluorescence. Results: No significant differences in body weight, mean arterial pressure, and heart rate were found between the sham and CA/R groups post-CA/R. The survival rates in the CA/R group at 12, 24, and 48 hours were 62.58%, 36.37%, and 7.8%, respectively. Neuronal loss and BSCB leakage began 12 hours post-CA/R, increasing with time. Reactive astrogliosis appeared at 12 hours and increased, while AEF disruption around blood vessels was evident at 48 hours. Conclusion The survival rate declined significantly by 48 hours post-CA/R. Neuronal loss and BSCB leakage in the thoracic spinal cord IMZ was evident at 12 hours and significant by 48 hours, aligning with AEF disruption. Neuronal loss in the thoracic spinal cord IMZ post-CA/R may be related to BSCB leakage and AEF disruption.

Objective: The 2020 Cardiopulmonary Resuscitation (CPR) guidelines recommend the use of feedback devices during CPR training and do not limit their use in actual CPR. Although there have been various studies on metronome-assisted CPR that use a metronome as a feedback device, there are no research results to determine a specific metronome setting rate. We analyzed the quality of CPR and the effectiveness of the metronome feedback according to the metronome setting rate within the recommended chest compression rate range. Methods: Fifty healthcare providers who had received CPR training or had performed CPR in the previous 2 years participated, and all of them performed CPR at three rates (100/min, 110/min, and 120/min). The CPR was performed for 2 minutes with only chest compressions. The smartphone metronome (Metronome version 13.0 Android, KHTSXR, Seoul, Korea) application was used for the rate setting, and Resusci Anne QCPR Mk II (Laerdal Medical, Stavanger, Norway) was used to measure the CPR quality. The difference in the CPR quality according to the setting rate was analyzed. Results: There was no significant difference in the “average compression depth (mm),” “adequate compression depth ratio (%),” and “adequate release ratio (%)” at the three set rates. The “adequate compression rate ratio (%)” was 98.48±5.27% at 110/min, which was higher than that at 120/min or 100/min, and this was a statistically significant difference (P=0.000). There was no significant difference in the “adequate compression site ratio (%).” Conclusion When performing metronome-assisted CPR, setting the rate to 110/min can more appropriately maintain the recommended chest compression rate range and can result in high-quality CPR.