Purpose: To report a case of primary orbital apocrine adenocarcinoma in a patient diagnosed with gastric adenocarcinoma.Case summary: A 43-year-old male patient diagnosed with gastric adenocarcinoma 3 months prior presented with a gradually enlarging mass in the lower medial aspect of the left eye for 1 year. At initial examination, his best-corrected visual acuity was 1.0 in both eyes and slit-lamp examination revealed no abnormalities. The left eye exhibited proptosis with restricted adduction, abduction, and depression. Orbital magnetic resonance imaging revealed an irregularly shaped mass measuring 56 × 46 × 38 mm in the left inferomedial orbit, invading the medial and inferior rectus muscles. Histopathological analysis of the orbital tumor revealed abundant eosinophilic cytoplasm. Immunohistochemical staining was positive for androgen receptor, and gross cystic disease fluid protein-15, both of which were negative in the gastric adenocarcinoma tissue. Additionally, the mucin phenotypes observed differed from those in the gastric cancer tissue. Based on these findings, the patient was diagnosed with primary orbital apocrine adenocarcinoma. Conclusions Primary orbital apocrine adenocarcinoma is an extremely rare malignant tumor. In patients with gastric cancer, malignant tumors in the orbit can arise as either primary neoplasms or metastatic lesions. Therefore, accurate diagnosis through immunohistochemical staining is essential to determine the appropriate treatment approach.

Objectives: In alignment with the World Health Organization’s goal of eliminating hepatitis C, this study assessed the current treatment status and reasons for non-treatment among patients with hepatitis C in Jeonbuk State, Republic of Korea, to inform strategies for improving care engagement. Methods: Among 311 individuals diagnosed with hepatitis C and reported through the NationalNotifiable Infectious Disease Surveillance system between January 2023 and June 2024, 208 patients were surveyed after excluding those who had died or could not be contacted.Statistical analyses included the chi-square test, the Cochran-Armitage test for trend, and logistic regression. Results: Overall, 116 participants (55.8%) reported having received antiviral therapy. Among the 92 untreated individuals, the most common reason for non-treatment was the absence of symptoms (n = 23; 25.0%), followed by the burden of drug costs (n = 21; 22.8%). Conclusion These findings highlight suboptimal treatment uptake and key barriers that may hinder progress toward hepatitis C elimination. Expanding screening and strengthening linkage-to-care strategies, while addressing financial barriers, will be essential to achievingnational elimination targets.

Background: Laser procedures are integral to dermatologic practice, yet safety measures- particularly regarding ocular protection and plume control- are poorly studied in real-world settings. Objective: To evaluate current practices in eye protection, infection control, and occupational risk awareness among Korean dermatologists performing laser treatments. Methods: A cross-sectional survey was conducted among board-certified dermatologists at the 2024 Korean Society for Dermatologic Laser Surgery meeting. The questionnaire covered demographics, laser frequency, use of goggles and masks, infection control strategies, ophthalmologic monitoring, and history of warts or cancer. Results: Seventy-nine respondents completed the survey. All reported using protective goggles, but only 26.6% and 22.8% did so for CO 2 and erbium-doped yttrium aluminium garnet lasers, respectively. Only 24.1% underwent regular eye exams, and 13.9% reported eye conditions after starting laser practice. While 89.9% used masks, 40.8% used dental masks, which are inadequate for plume protection. Suction devices were used by 94.9%, though performance specifications were unclear. Warts were reported by 46.8% of respondents; two reported cancer diagnoses after initiating laser work. Conclusion Despite high overall adherence to basic safety practices, critical gaps remain. Our findings highlight the need for standardized guidelines and long-term occupational health monitoring to ensure safe laser practice.

Background: Rosacea is a chronic inflammatory skin disorder characterized by erythema, papules, ocular symptoms, and heightened sensitivity. Patients with neurogenic symptoms such as burning or stinging remain particularly difficult to manage. Current guidelines often underrepresent energy-based devices (EBDs), pigmentary sequelae, psychosocial burden, and ocular comorbidities. Objective: To examine Korean dermatologists’ expert perspectives on rosacea management, focusing on skin sensitivity, neurogenic symptoms, pigmentary changes, psychosocial impact, ocular involvement, and EBD use. Methods: A web-based, 29-item survey was administered to 25 board-certified Korean dermatologists (May–June 2025). Quantitative and qualitative responses were analyzed. Results: Erythematotelangiectatic and papulopustular phenotypes with sensitivity skin predominated. EBDs (pulsed dye laser, intense pulsed light) were frequently used but limited by cost and sensitivity issues. Neurogenic symptoms were recognized but rarely treated with neuromodulators. Post-inflammatory hyperpigmentation was infrequent, yet monitoring was inconsistent.Psychosocial and ocular aspects were acknowledged but seldomly systematically addressed.Respondents expressed interest in emerging adjunctive treatments such as cold plasma, skin boosters, and holistic care approaches. Conclusion Korean dermatologists adopt individualized strategies for rosacea, yet practice gaps remain regarding neurogenic symptoms, pigmentary complications, and psychosocial and ocular comorbidities. Findings support the need for updated multidisciplinary, phenotype-driven guidelines aligned with real-world practice.

Background: The significance of risk modification in patients with acute coronary syndrome (ACS) is well recognized; however, the optimal timing for adminstering PCSK9 inhibitors remains unclear. Additionally, the lipid-lowering efficacy of evolocumab and alirocumab has not been fully established. This study evaluated the lipid-lowering effects of these two PCSK9 inhibitors. Methods: Patients diagnosed with ACS, including unstable angina, ST-segment elevation myocardial infarction, and non-ST-segment elevation myocardial infarction, who were treated with a PCSK9 inhibitor (evolocumab or alirocumab) during hospitalization for ACS between 2021 and 2023 were retrospectively analyzed. Baseline low-density lipoprotein cholesterol (LDL-C) levels were assessed, and changes in LDL-C levels during the acute and subacute phases after PCSK9 inhibitor administration were compared between the evolocumab and alirocumab groups. Results: Among 80 patients diagnosed with ACS, 36 received evolocumab, while 44 were treated with alirocumab. The mean baseline LDL-C level was 123 mg/dL in the evolocumab group and 128 mg/dL in the alirocumab group (p=0.456). In the subacute phase, the mean follow-up LDL-C levels were 47.05 mg/dL in the evolocumab group and 49.5 mg/dL in the alirocumab group (p=0.585). The mean percentage reduction in LDL-C levels during the subacute phase was 60.41% in the evolocumab group and 58.51% in the alirocumab group (p=0.431). These differences were not statistically significant. Conclusions No significant differences were observed between evolocumab and alirocumab. LDL-C levels exhibited a similar trend, characterized by a rapid decline in the acute phase, followed by a slight rebound in the subacute phase.

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.

Hypoglossal nerve palsy is a rare complication related to airway management during general anesthesia. Its diagnosis can be delayed when postoperative tongue swelling mimics a neoplasm. This paper reports a case of isolated hypoglossal nerve palsy after endotracheal intubation. A 65-year-old woman developed dysphagia and impaired tongue protrusion after orbital floor fracture surgery. Fiberoptic endoscopic evaluation revealed a 3-mm mass-like lesion at the tongue base, and magnetic resonance imaging showed asymmetric swelling of the left tongue and oropharyngeal wall. The tongue strength measured using the Iowa Oral Performance Instrument (IOPI) at six days post-onset was 10 kPa, which was markedly lower than the age norms. Electromyography revealed the fibrillation potentials and positive sharp waves in the left tongue muscle, confirming isolated hypoglossal nerve palsy. Oral methylprednisolone was administered for five days, followed by a five-day taper, with concurrent tongue-strengthening rehabilitation. One month later, the tongue strength improved, reaching a maximal pressure of 24 kPa. The mass-like lesion had resolved on follow-up and was interpreted as a pseudotumor caused by edema and mechanical compression. Complete recovery was achieved by the six-month follow-up. This case highlights the utility of IOPI for early quantitative assessment of tongue weakness and highlights that early diagnosis and steroid treatment can facilitate recovery.

Background: Psoriasis is a persistent systemic inflammatory condition mediated by the interleukin (IL)-23/IL-17 signaling pathway. Existing murine models, including imiquimod (IMQ)-applied wild-type (WT) mice, may not reflect chronicity and systemic comorbidities of psoriasis, particularly gut-related manifestations linked to the gut–skin axis. Objective: To establish a murine model that more accurately reflects chronic psoriasis, its systemic comorbidities, and associated gut environment alterations. Methods: C57BL/6 IL-10-deficient (IL-10 knockout [KO]) and WT mice received topical IMQ or vehicle for 6 weeks. Subsequently, tissue samples from skin, colon, joints, kidneys, liver, abdominal aortas, lymph nodes, and spleens, as well as fecal and blood samples, were collected for histopathologic, immunologic, gut environment analysis. Results: IMQ-treated IL-10 KO mice developed prolonged psoriatic inflammatory responses with increased epidermal thickness and higher infiltration of CD45+, myeloperoxidase+, and IL-17+ cells. They also exhibited early-onset, severe colitis with marked weight loss, shortened colon length, and elevated colitis severity scores. While IMQ induced systemic inflammation in multiple organs, IL-10 KO mice did not show more severe joint, liver, or kidney involvement than WT mice. Elevated serum tumor necrosis factor alpha and plasminogen activator inhibitor-1 levels, increased heart/body weight ratio, enhanced gut permeability, and distinct gut microbiota profiles were observed in IL-10 KO mice. Conclusion The 6-week IMQ-applied IL-10 KO model may better reflect chronic and severe psoriasis with gut-related comorbidities, offering a valuable platform to investigate the gut–skin axis.

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.