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.

To investigate the relationship between depression and AD, water avoidance stress (WAS) was induced for 10 days in both Tg2576 mice and wild-type (WT) mice. After WAS, memory function and depressive-like behavior were investigated in Tg2576 mice. Tg2576 WAS mice exhibited more depressive-like behaviors than WT WAS and Tg2576 control (CON) mice. Strikingly, Tg2576 CON mice showed more depressive-like behaviors than WT mice. Moreover, corticosterone and phospho-glucocorticoid receptor (p-GR) levels were also higher in Tg2576 WAS mice in comparison to Tg2576 CON mice. Spinster homologue 2 (SPNS2) is a member of non-ATP-dependent transporter. The role of SPNS2 was widely known as a sphingosine-1-phosphate (S1P) transporter, which export intracellular S1P from cells. Using GEO database to analyze SPNS2 gene expression changes in patients with AD and depression, we show that SPNS2 gene expression correlates with AD and depression. Interestingly, Tg2576 WAS mice displayed significantly increased levels of SPNS2 w1hen compared to Tg2576 CON counterparts. SPNS2 levels were also higher in Tg2576 CON mice in comparison with WT CON mice. Remarkably, we found a decrease in S1P brain levels and an increase in S1P serum levels of Tg2576 WAS mice in comparison with Tg2576 CON mice. Accordingly, WAS induced group further decreased S1P levels in the brains. However, the level in the serum further increased in comparison with non-induced group. Therefore, these results suggest that AD and depression could be associated, and that Tg2576 transgenic mice are more susceptible to stress-induced depression through the release of S1P by SPNS2 up-regulation.

Background: This study aimed to evaluate the degree of glenoid concavity restoration and its effect on surgical failure after arthroscopic bony Bankart repair for recurrent anterior shoulder instability with a bony Bankart lesion. Methods: Forty-one patients who underwent arthroscopic bony Bankart repair for recurrent anterior shoulder instability with a bony Bankart lesion were retrospectively evaluated. All patients underwent 3-dimensional computed tomography (3D-CT) preoperatively to evaluate the glenoid concavity using the bony shoulder stability ratio (BSSR). Bony fragments were incorporated to the anterior glenoid during arthroscopic stabilization procedure. All patients were reevaluated by 3D-CT at postoperative 1 year to assess the changes in the BSSR and the final glenoid bone defect size after bony Bankart repair. Clinical outcomes including surgical failure were evaluated at least 2 years after surgery. Results: The BSSR significantly increased after surgery (26.0% ± 14.0% preoperatively and 35.5% ± 13.2% postoperatively, p < 0.001). Preoperative glenoid bone defect size was 16.2% ± 8.1%, and bony Bankart fragment size was 11.3% ± 7.2%. Four patients (9.8%) had recurrent instability requiring revision surgery. In patients with surgical failure, the BSSR was not improved after surgery (18.2% ± 13.3% preoperatively and 23.1% ± 17.3% postoperatively, p = 0.24). In contrast, patients without surgical failure showed significantly improved BSSR after surgery (26.9% ± 14.0% preoperatively and 36.9% ± 12.2% postoperatively, p < 0.001).No significant differences were found in the final glenoid bone defect size (6.6% ± 5.9% in patients with surgical failure vs. 6.2% ± 5.7% in patients without surgical failure, p = 0.92) and bony Bankart fragment nonunion rate (0% in patients with surgical failure vs. 5.4% in patients without surgical failure, p = 0.99) between patients with and without surgical failure. Conclusions Glenoid concavity, as represented by the BSSR, improved after arthroscopic bony Bankart repair, and satisfactory restoration of the glenoid concavity led to successful clinical outcomes without surgical failure. The BSSR could be considered an important factor for predicting clinical outcomes after arthroscopic bony Bankart repair. However, further research including more contributing factors is needed to better analyze the impact of the BSSR on clinical outcomes.

Purpose: Since 1995, the Korean Gastric Cancer Association (KGCA) has been periodically conducting nationwide surveys on patients with surgically treated gastric cancer. This study details the results of the survey conducted in 2023. Materials and Methods: The survey was conducted from March to December 2024 using a standardized case report form. Data were collected on 86 items, including patient demographics, tumor characteristics, surgical procedures, and surgical outcomes. The results of the 2023 survey were compared with those of previous surveys. Results: Data from 12,751 cases were collected from 66 institutions. The mean patient age was 64.6 years, and the proportion of patients aged ≥71 years increased from 9.1% in 1995 to 31.7% in 2023. The proportion of upper-third tumors slightly decreased to 16.8% compared to 20.9% in 2019. Early gastric cancer accounted for 63.1% of cases in 2023.Regarding operative procedures, a totally laparoscopic approach was most frequently applied (63.2%) in 2023, while robotic gastrectomy steadily increased to 9.5% from 2.1% in 2014.The most common anastomotic method was the Billroth II procedure (48.8%) after distal gastrectomy and double-tract reconstruction (51.9%) after proximal gastrectomy in 2023.However, the proportion of esophago-gastrostomy with anti-reflux procedures increased to 30.9%. The rates of post-operative mortality and overall complications were 1.0% and 15.3%, respectively. Conclusions The results of the 2023 nationwide survey demonstrate the current status of gastric cancer treatment in Korea. This information will provide a basis for future gastric cancer research.

Physician–scientists play a pivotal role in bridging clinical practice and biomedical research, advancing medical science, and tackling complex healthcare challenges. In South Korea, the declining number of medical doctors engaging in basic medical sciences has prompted the implementation of various training initiatives since the 2000s. Notable initiatives, such as the Integrated Physician–Scientist Training Program (2019) and the Global Physician–Scientist Training Program (2024), aim to cultivate multidisciplinary physician–scientists capable of addressing unmet medical needs. This study offers a comprehensive overview of the current training systems, funding mechanisms, and strategic approaches for physician–scientists in South Korea, compares them with international best practices, and proposes actionable policy recommendations to enhance their effectiveness and long-term sustainability.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aimed to investigate the prevalence and characteristics of impacted teeth (ITs) in orthodontic patients at university dental hospitals in Korea. Methods: This study included 14,774 patients who visited the Department of Orthodontics at 10 university dental hospitals in Korea between 2020 and 2022 and underwent orthodontic diagnosis. The prevalence and characteristics of ITs were investigated using orthodontic diagnostic records, radiographs, and diagnostic casts. Results: The prevalence of ITs, excluding third molar impaction, in Korean orthodontic patients was 13.6% (n = 2,014).The prevalence of ITs in pediatric orthodontic patients was 24.5% (n = 1,614).Of these patients, 68.2% had one IT, 27.5% had two ITs, 24.3% had bilateral IT, and 75.7% had unilateral IT. The most frequent IT was the maxillary canine (50.1%), followed by the mandibular second molar (11.7%), and maxillary second premolar (9.6%). An abnormal eruption path (46.5%) was the most frequent etiology. Orthodontic traction after surgical exposure (70.6%) was the most frequent treatment option. Among the patients with ITs, 29.8% had other dental anomalies, such as tooth agenesis (8.7%), microdontia (8.0%), and supernumerary teeth (5.1%). Furthermore, 50.8% had complications such as cystic lesions (18.3%), transposition (17.7%), and root resorption (14.8%).Among the patients with maxillary canine impaction, 62.2% had labial maxillary canine impaction and 21.1% had palatal maxillary canine impaction. Conclusions The prevalence of ITs in Korean orthodontic patients at university dental hospitals was high, particularly in pediatric orthodontic patients.