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.

Atopic dermatitis is the most common chronic inflammatory skin disease in children and adolescents. The Korean Academy of Pediatric Allergy and Respiratory Disease published the Atopic Dermatitis Treatment Guideline in 2008, which has been helpful in atopic dermatitis treatment until now. Various reports on the development and effectiveness of new drugs have suggested that there is a need to develop and revise old treatment guidelines. Part 1 aimed to provide evidence-based recommendations for skin care management and topical treatment for atopic dermatitis. Part 2 focuses on systemic treatment, novel therapeutics, and adjuvant therapy. The goal of this guideline is intended to assist front-line doctors treating pediatric and adolescent atopic dermatitis patients make safer, more effective, and more rational decisions regarding systemic treatment, novel therapeutics, and adjuvant therapy by providing evidence-based recommendations with a clear level of evidence and benefit regarding treatment.

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.

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.

Atopic dermatitis is the most common chronic inflammatory skin disease in children and adolescents. The Korean Academy of Pediatric Allergy and Respiratory Disease published the Atopic Dermatitis Treatment Guideline in 2008, which has been helpful in atopic dermatitis treatment until now. Various reports on the development and effectiveness of new drugs have suggested that there is a need to develop and revise old treatment guidelines. Part 1 aimed to provide evidence-based recommendations for skin care management and topical treatment for atopic dermatitis. Part 2 focuses on systemic treatment, novel therapeutics, and adjuvant therapy. The goal of this guideline is intended to assist front-line doctors treating pediatric and adolescent atopic dermatitis patients make safer, more effective, and more rational decisions regarding systemic treatment, novel therapeutics, and adjuvant therapy by providing evidence-based recommendations with a clear level of evidence and benefit regarding treatment.

Atopic dermatitis is the most common chronic inflammatory skin disease in children and adolescents. The Korean Academy of Pediatric Allergy and Respiratory Disease published the Atopic Dermatitis Treatment Guideline in 2008, which has been helpful in atopic dermatitis treatment until now. Various reports on the development and effectiveness of new drugs have suggested that there is a need to develop and revise old treatment guidelines. Part 1 aimed to provide evidence-based recommendations for skin care management and topical treatment for atopic dermatitis. Part 2 focuses on systemic treatment, novel therapeutics, and adjuvant therapy. The goal of this guideline is intended to assist front-line doctors treating pediatric and adolescent atopic dermatitis patients make safer, more effective, and more rational decisions regarding systemic treatment, novel therapeutics, and adjuvant therapy by providing evidence-based recommendations with a clear level of evidence and benefit regarding treatment.

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.