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: Identifying the risks related to the complications of electrical cardioversion (ECV) can alert the determinaton of rhythm control in patients with atrial fibrillation (AF). Methods: We retrospectively reviewed 1,058 patients who underwent ECV for persistent or long-standing persistent AF/atrial flutter (AFL) from multiple centers. Patients were classified into the no-complication (1,023 patients) and complication (35 patients) groups based on the following major complications: stroke and/or systemic embolism (SSE), myocardial infarction, major bleeding, implantation of cardiac implantable electronic devices, ventricular tachycardia/fibrillation, and death at 1 year follow-up after ECV. Results: Compared with the no-complication group, the complication group exhibited a higher proportion of female patients (37% vs. 22%), as well as a higher proportion of patients with older age (67 ± 11 vs. 61 ± 10 years), diabetes mellitus (DM) (49% vs. 24%), heart failure (HF) (49% vs. 30%), SSE (23% vs. 9%), high CHA 2 DS 2 -VASc (CV) score (3.6 ± 1.8 vs.2.2 ± 1.4), low left ventricular ejection fraction (LVEF) (50 ± 16% vs. 58 ± 21%), and high left atrial volume index (LAVI) (51 ± 26 vs. 40 ± 20 mL/m 2 ). Class I and III antiarrhythmics were less prescribed in the complication group than in the no-complication group (57% vs.76%). Univariate analysis for complications revealed age (≥ 65 years), female sex, DM, HF, SSE, LVEF (< 50%), LAVI (≥ 40 mL/m 2 ), CV score (≥ 3), bradycardia on Holter (< 60/min), and no antiarrhythmics as risk factors. Among these, multivariate analysis revealed clinical significance of female sex and SSE. Conclusion Female sex and a history of SSE were the most important risk factors of complications in patients with persistent or long-standing persistent AF/AFL who underwent ECV.

The prelacrimal recess approach (PLRA) has advanced endoscopic sinonasal surgery by providing improved access to the maxillary sinus and adjacent anatomical regions while preserving critical structures such as the inferior turbinate (IT) and nasolacrimal duct (NLD). First introduced in 2013, the PLRA has become an important technique for addressing various sinonasal pathologies. This review comprehensively evaluates the advancements, applications, and outcomes associated with the PLRA. The PLRA enables superior visualization and access to regions that are traditionally difficult to reach with conventional techniques. Standardized surgical steps emphasize meticulous preservation of the NLD and IT, while technical modifications have broadened its feasibility in patients with narrow prelacrimal recesses. Applications of the PLRA span diverse pathologies, including sinonasal inverted papilloma, fungal infections, odontogenic cysts, and tumors of the lacrimal system, orbit, and skull base. Anatomical studies reveal significant variations in prelacrimal recess dimensions across populations, affecting surgical feasibility. Sex-specific differences, ethnic variations, and age-related factors are important in patient selection. Clinical outcomes from multiple investigations validate the PLRA’s efficacy in maintaining sinonasal function while achieving comprehensive lesion removal. Comparative analyses with traditional approaches underscore the PLRA’s advantages in reducing postoperative morbidity and recurrence rates. Integration of the PLRA with complementary surgical approaches further expands its therapeutic applications while maintaining favorable safety profiles. The PLRA is a safe and effective surgical method that offers favorable outcomes in disease management, symptom resolution, and anatomical preservation. With ongoing innovations and refinements, the PLRA is poised to remain a cornerstone of minimally invasive sinonasal surgery, enabling the precise and safe treatment of complex pathologies.

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.

Serum and epidermal levels of sphingosine 1-phosphate (S1P) are higher in patients with psoriasis than healthy subjects. Although roles of type 1 S1P receptor, S1P 1, in the development of psoriasis has intensively been investigated, roles of S1P2 have not been elucidated. We aim to investigate whether blockage of S1P2 reduce imiquimod-induced psoriasis-like dermatitis using an S1P2 antagonist, JTE-013, in combination with S1pr2 wild-type (WT) and knock-out (KO) BALB/c mice. Imiquimod induced increase of erythematous papules and plaques with silver scaling, whereas administration of JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene reduced the imiquimod-induced symptoms. Imiquimod increased mRNA expression levels of pro-inflammatory Th1/Th17 cytokines, whereas JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene also suppressed the imiquimod-induced pro-inflammatory cytokine expression.Imiquimod induced enlargement of lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. Imiquimod induced increase of pro-inflammatory Th1/Th17 cytokine levels and Th17 cell numbers in lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. In summary, the present results suggest that blockage of S1P2 could suppress the characteristics of psoriasis-form dermatitis and be a therapeutic strategy.

Purpose: To investigate the role of combined periprostatic nerve block (PNB) and intrarectal local anesthesia with heated lidocaine gel (ILAHL) in reducing pain during transrectal ultrasound (TRUS)-guided prostate biopsy, compared with PNB alone. Materials and Methods: We performed a prospective randomized trial with 140 participants who underwent systematic TRUS-guid ed, 12-core prostate biopsy from July 2021 to June 2022. These participants were divided into two groups. Before prostate biopsy, group 1 (n=70) received PNB and group 2 (n=70) received PNB combined intrarectal local anesthesia with 20 mL of heated (40ºC) 2% lidocaine gel. The primary outcome was pain score on a 0–10 visual analogue scale (VAS) at four time points (VAS A: during local anesthesia procedure, VAS B: during probe insertion, VAS C: during biopsy procedure, VAS D: 30 minutes after biopsy). The secondary outcome included adverse events during and after the procedure. Results: Mean pain scores were significantly lower in group 2 than in group 1 at VAS A (2.53 vs. 1.60, p=0.001) and VAS B (2.47 vs.1.49, p<0.001). The mean VAS C pain score in group 2 was significantly less than in group 1 (3.07 vs. 2.20, p=0.001), while there was no significant difference in the mean VAS D pain score between two groups (1.06 vs. 0.89, p=0.318). There were no significant differences in the occurrence of complications in both groups. Conclusions The combination of PNB and ILAHL provides more effective pain control than PNB alone without increase of complication rates in patients undergoing TRUS-guided prostate biopsy.

Serum and epidermal levels of sphingosine 1-phosphate (S1P) are higher in patients with psoriasis than healthy subjects. Although roles of type 1 S1P receptor, S1P 1, in the development of psoriasis has intensively been investigated, roles of S1P2 have not been elucidated. We aim to investigate whether blockage of S1P2 reduce imiquimod-induced psoriasis-like dermatitis using an S1P2 antagonist, JTE-013, in combination with S1pr2 wild-type (WT) and knock-out (KO) BALB/c mice. Imiquimod induced increase of erythematous papules and plaques with silver scaling, whereas administration of JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene reduced the imiquimod-induced symptoms. Imiquimod increased mRNA expression levels of pro-inflammatory Th1/Th17 cytokines, whereas JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene also suppressed the imiquimod-induced pro-inflammatory cytokine expression.Imiquimod induced enlargement of lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. Imiquimod induced increase of pro-inflammatory Th1/Th17 cytokine levels and Th17 cell numbers in lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. In summary, the present results suggest that blockage of S1P2 could suppress the characteristics of psoriasis-form dermatitis and be a therapeutic strategy.

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.

The prelacrimal recess approach (PLRA) has advanced endoscopic sinonasal surgery by providing improved access to the maxillary sinus and adjacent anatomical regions while preserving critical structures such as the inferior turbinate (IT) and nasolacrimal duct (NLD). First introduced in 2013, the PLRA has become an important technique for addressing various sinonasal pathologies. This review comprehensively evaluates the advancements, applications, and outcomes associated with the PLRA. The PLRA enables superior visualization and access to regions that are traditionally difficult to reach with conventional techniques. Standardized surgical steps emphasize meticulous preservation of the NLD and IT, while technical modifications have broadened its feasibility in patients with narrow prelacrimal recesses. Applications of the PLRA span diverse pathologies, including sinonasal inverted papilloma, fungal infections, odontogenic cysts, and tumors of the lacrimal system, orbit, and skull base. Anatomical studies reveal significant variations in prelacrimal recess dimensions across populations, affecting surgical feasibility. Sex-specific differences, ethnic variations, and age-related factors are important in patient selection. Clinical outcomes from multiple investigations validate the PLRA’s efficacy in maintaining sinonasal function while achieving comprehensive lesion removal. Comparative analyses with traditional approaches underscore the PLRA’s advantages in reducing postoperative morbidity and recurrence rates. Integration of the PLRA with complementary surgical approaches further expands its therapeutic applications while maintaining favorable safety profiles. The PLRA is a safe and effective surgical method that offers favorable outcomes in disease management, symptom resolution, and anatomical preservation. With ongoing innovations and refinements, the PLRA is poised to remain a cornerstone of minimally invasive sinonasal surgery, enabling the precise and safe treatment of complex pathologies.

Serum and epidermal levels of sphingosine 1-phosphate (S1P) are higher in patients with psoriasis than healthy subjects. Although roles of type 1 S1P receptor, S1P 1, in the development of psoriasis has intensively been investigated, roles of S1P2 have not been elucidated. We aim to investigate whether blockage of S1P2 reduce imiquimod-induced psoriasis-like dermatitis using an S1P2 antagonist, JTE-013, in combination with S1pr2 wild-type (WT) and knock-out (KO) BALB/c mice. Imiquimod induced increase of erythematous papules and plaques with silver scaling, whereas administration of JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene reduced the imiquimod-induced symptoms. Imiquimod increased mRNA expression levels of pro-inflammatory Th1/Th17 cytokines, whereas JTE-013 significantly suppressed those increases in S1pr2 WT mice. Deficiency of S1pr2 gene also suppressed the imiquimod-induced pro-inflammatory cytokine expression.Imiquimod induced enlargement of lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. Imiquimod induced increase of pro-inflammatory Th1/Th17 cytokine levels and Th17 cell numbers in lymph nodes and spleens, whereas JTE-013 suppressed them in S1pr2 WT mice. In summary, the present results suggest that blockage of S1P2 could suppress the characteristics of psoriasis-form dermatitis and be a therapeutic strategy.