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.

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.

Background: Aortic valve sclerosis (AVS) shares risk factors with atherosclerosis. However, the relationship between AVS progression with cardiovascular (CV) risk has not been researched. This study investigates CV outcomes according to progression of AVS. Methods: This study included 2,901 patients with AVS (irregular leaflet thickening and peak aortic jet veloc‑ ity < 2 m/sec) who underwent serial echocardiograms at least 1 year apart during 2011–2020. The primary outcome was defined as CV death, myocardial infarction, stroke, or revascularization. Results: During a median follow-up period of 3.9 years, 439 of 2,901 AVS patients (15.1%) progressed to mild or greater aortic stenosis. Patients with progression were older and more likely to have atrial fibrillation than those without. In a stepwise regression, age (odds ratio [OR] per 1-year increase, 1.04; 95% confidence interval [CI], 1.01– 1.07), peripheral artery disease (OR, 9.07; 95% CI, 3.12–26.4), and left ventricular mass index (OR per 1-g/m 2 increase, 1.01; 95% CI, 1.00–1.02) were associated with AVS progression. Over a median of 6.3 years, the primary outcome occurred in 858 of 2,901 patients (29.6%). Patients with progression had higher frequency of CV death, myocardial infarction, stroke, or revascularization than those without progression (P < 0.0001). In Cox proportional hazards regres‑ sion, AVS progression (hazard ratio, 1.33; 95% CI, 1.10–1.61) was a significant determinant of CV mortality. Conclusions The progression to aortic stenosis in AVS patients is an independent risk factor for CV mortality. These findings suggest that patients with AVS progression may benefit from stricter CV risk monitoring.

Background: Aortic valve sclerosis (AVS) shares risk factors with atherosclerosis. However, the relationship between AVS progression with cardiovascular (CV) risk has not been researched. This study investigates CV outcomes according to progression of AVS. Methods: This study included 2,901 patients with AVS (irregular leaflet thickening and peak aortic jet veloc‑ ity < 2 m/sec) who underwent serial echocardiograms at least 1 year apart during 2011–2020. The primary outcome was defined as CV death, myocardial infarction, stroke, or revascularization. Results: During a median follow-up period of 3.9 years, 439 of 2,901 AVS patients (15.1%) progressed to mild or greater aortic stenosis. Patients with progression were older and more likely to have atrial fibrillation than those without. In a stepwise regression, age (odds ratio [OR] per 1-year increase, 1.04; 95% confidence interval [CI], 1.01– 1.07), peripheral artery disease (OR, 9.07; 95% CI, 3.12–26.4), and left ventricular mass index (OR per 1-g/m 2 increase, 1.01; 95% CI, 1.00–1.02) were associated with AVS progression. Over a median of 6.3 years, the primary outcome occurred in 858 of 2,901 patients (29.6%). Patients with progression had higher frequency of CV death, myocardial infarction, stroke, or revascularization than those without progression (P < 0.0001). In Cox proportional hazards regres‑ sion, AVS progression (hazard ratio, 1.33; 95% CI, 1.10–1.61) was a significant determinant of CV mortality. Conclusions The progression to aortic stenosis in AVS patients is an independent risk factor for CV mortality. These findings suggest that patients with AVS progression may benefit from stricter CV risk monitoring.

Background: Aortic valve sclerosis (AVS) shares risk factors with atherosclerosis. However, the relationship between AVS progression with cardiovascular (CV) risk has not been researched. This study investigates CV outcomes according to progression of AVS. Methods: This study included 2,901 patients with AVS (irregular leaflet thickening and peak aortic jet veloc‑ ity < 2 m/sec) who underwent serial echocardiograms at least 1 year apart during 2011–2020. The primary outcome was defined as CV death, myocardial infarction, stroke, or revascularization. Results: During a median follow-up period of 3.9 years, 439 of 2,901 AVS patients (15.1%) progressed to mild or greater aortic stenosis. Patients with progression were older and more likely to have atrial fibrillation than those without. In a stepwise regression, age (odds ratio [OR] per 1-year increase, 1.04; 95% confidence interval [CI], 1.01– 1.07), peripheral artery disease (OR, 9.07; 95% CI, 3.12–26.4), and left ventricular mass index (OR per 1-g/m 2 increase, 1.01; 95% CI, 1.00–1.02) were associated with AVS progression. Over a median of 6.3 years, the primary outcome occurred in 858 of 2,901 patients (29.6%). Patients with progression had higher frequency of CV death, myocardial infarction, stroke, or revascularization than those without progression (P < 0.0001). In Cox proportional hazards regres‑ sion, AVS progression (hazard ratio, 1.33; 95% CI, 1.10–1.61) was a significant determinant of CV mortality. Conclusions The progression to aortic stenosis in AVS patients is an independent risk factor for CV mortality. These findings suggest that patients with AVS progression may benefit from stricter CV risk monitoring.

Purpose: This study aims to verify whether the Reflective Practice Questionnaire (RPQ) developed by Priddis and Rogers is valid in the Korean context to identify the level of reflection of medical students in clinical practice. Methods: A total of 202 third- and fourth-year medical students from seven universities participated in the study. After receiving approval for use from the authors, a survey was conducted on the students through an adaptation process. The original scale consists of 10 factors with 40 items. The Self-efficacy in Clinical Performance Scale (SECP), Korean Self-reflection and Insight Scale (K-SRIS), and Reflection-in-Learning Scale (RinLS) were used to validate the scale. Exploratory factor, confirmatory factor, correlation, and reliability analyses were used for data analysis. Results: As a result of exploratory factor analysis, 10 subfactors were extracted (Kaiser-Meyer-Olkin=0.856, Bartlett’s test: χ 2 =5,044.337, degrees of freedom=780, p<0.001). Among the 40 items, one that showed a high overlapping load for other factors was excluded. As a result of confirmatory factor analysis, the 10-factor structure model was found suitable (χ 2 =1.980, comparative fit index=0.859, Tucker-Lewis index=0.841, root mean square error of approximation=0.070). As a result of the criterion validity test, most of the subfactors of the Korean version of the RPQ (K-RPQ) showed a positive correlation with K-SRIS, RinLS, and SECP. The reliability of 10 subfactors was satisfactory, ranging from 0.666 to 0.919. Conclusion The K-RPQ was confirmed to be a reliable and valid tool to evaluate the level of reflection among Korean medical students in clinical clerkship. This scale can be used as a tool to provide feedback on each student’s level of reflection in clinical clerkship.

Background: The gut–brain axis (GBA) in Parkinson’s disease (PD) has only been investigated in limited mice models despite dysbiosis of the gut microbiota being considered one of the major treatment targets for neurodegenerative disease. Therefore, this study examined the compositional changes of fecal microbiota in novel transgenic (Tg) mice overexpressing human α-synuclein (hαSyn) proteins under the neuron-specific enolase (NSE) to analyze the potential as GBA model. Results: The expression level of the αSyn proteins was significantly higher in the substantia nigra and striatum of NSEhαSyn Tg mice than the Non-Tg mice, while those of tyrosine hydroxylase (TH) were decreased in the same group. In addition, a decrease of 72.7% in the fall times and a 3.8-fold increase in the fall number was detected in NSE-hαSyn Tg mice. The villus thickness and crypt length on the histological structure of the gastrointestinal (GI) tract decreased in NSE-hαSyn Tg mice. Furthermore, the NSE-hαSyn Tg mice exhibited a significant increase in 11 genera, including Scatolibacter, Clostridium, Feifania, Lachnoclostridium, and Acetatifactor population, and a decrease in only two genera in Ligilactobacillus and Sangeribacter population during enhancement of microbiota richness and diversity. Conclusions The motor coordination and balance dysfunction of NSE-hαSyn Tg mice may be associated with compositional changes in gut microbiota. In addition, these mice have potential as a GBA model.

Background: To evaluate the chemosensitivity to doxorubicin (DOX) in two primary cells derived from a tumor of FVB/N-Trp53tm1Hw1 knockout (KO) mice with TALEN-mediated Trp53 mutant gene, we evaluated the cell survivability, cell cycle distribution, apoptotic cell numbers and apoptotic protein expression in solid tumor cells and ascetic tumor cells treated with DOX. Results: The primary tumor cells showed a significant (P < 0.05) defect for UV-induced upregulation of the Trp53 pro-tein, and consisted of different ratios of leukocytes, fibroblasts, epithelial cells and mesenchymal cells. The ­ IC50 level to DOX was lower in both primary cells ­(IC50 = 0.12 μM and 0.20 μM) as compared to the CT26 cells ­(IC50 = 0.32  μM), although the solid tumor was more sensitive. Also, the number of cells arrested at the G0/G1 stage was significantly decreased (24.7–23.1% in primary tumor cells treated with DOX, P < 0.05) while arrest at the G2 stage was enhanced to 296.8–254.3% in DOX-treated primary tumor cells compared with DOX-treated CT26 cells. Furthermore, apoptotic cells of early and late stage were greatly increased in the two primary cell-lines treated with DOX when compared to same conditions for CT26 cells. However, the Bax/Bcl-2 expression level was maintained constant in the primary tumor and CT26 cells. Conclusions To the best of our knowledge, these results are the first to successfully detect an alteration in chemosensitivity to DOX in solid tumor cells and ascetic tumor cells derived from tumor of FVB/N-Trp53tm1Hw1 mice TALENmediated Trp53 mutant gene.

Humanity is in the midst of the coronavirus disease 2019 (COVID-19) pandemic, and vaccines—including mRNA vaccines—have been developed at an unprecedented speed. It is necessary to develop guidelines for vaccination for people undergoing treatment with assisted reproductive technology (ART) and for pregnancy-related situations based on the extant laboratory and clinical data. COVID-19 vaccines do not appear to adversely affect gametes, embryos, or implantation; therefore, active vaccination is recommended for women or men who are preparing for ART. The use of intravenous immunoglobulin G (IVIG) for the treatment of immune-related infertility is unlikely to impact the effectiveness of the vaccines, so COVID-19 vaccines can be administered around ART cycles in which IVIG is scheduled. Pregnant women have been proven to be at risk of severe maternal and neonatal complications from COVID-19. It does not appear that COVID-19 vaccines harm pregnant women or fetuses; instead, they have been observed to deliver antibodies against severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) to the fetus. Accordingly, it is recommended that pregnant women receive COVID-19 vaccination. There is no rationale for adverse effects, or clinical cases of adverse reactions, in mothers or neonates after COVID-19 vaccination in lactating women. Instead, antibodies to SARS-CoV-2 can be delivered through breast milk. Therefore, breastfeeding mothers should consider vaccination. In summary, active administration of COVID-19 vaccines will help ensure the safe implementation of ART, pregnancy, and breastfeeding.