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.

Purpose: To evaluate the relationship between distal fusion level in correction and fusion surgery for adolescent idiopathic scoliosis (AIS) and radiologic changes in the sacroiliac (SI) joint. Materials and Methods: This retrospective cohort study evaluated patients who underwent correction and fusion for AIS between 2005 and 2017 with at least 5 years of follow-up. We categorized patients into two groups: Group 1 (distal fusion above L2, 74 patients) and Group 2 (distal fusion at L3 and below, 52 patients). Radiologic parameters and SI joint changes were evaluated on plain radiographs obtained from preoperative to 5 years postoperatively. We also investigated other risk factors for SI joint change. Results: Analysis of demographic factors revealed no significant difference between the two groups. There was a significant difference in the incidence of SI joint change between Group 1 (5 patients, 6.75%) and Group 2 (18 patients, 34.61%), with Group 2 showing a faster increase in incidence according to the Kaplan-Meier method (p<0.0001). Preoperative lumbar lordosis (LL) and ΔLL had a significant relationship with SI joint changes [preoperative LL, hazard ratio (HR)=0.77, 95% confidence interval (CI)=0.64– 0.93, p=0.008; ΔLL, HR=0.79, 95% CI=0.67–0.95, p=0.01). Conclusion After AIS surgery, patients who had fusion to the lower lumbar vertebrae (L3 or L4) experienced a higher incidence and faster progression of degenerative changes in the SI joint. Low preoperative LL and inadequate correction of LL during the operation were also risk factors for SI joint degeneration.

Purpose: To evaluate the relationship between distal fusion level in correction and fusion surgery for adolescent idiopathic scoliosis (AIS) and radiologic changes in the sacroiliac (SI) joint. Materials and Methods: This retrospective cohort study evaluated patients who underwent correction and fusion for AIS between 2005 and 2017 with at least 5 years of follow-up. We categorized patients into two groups: Group 1 (distal fusion above L2, 74 patients) and Group 2 (distal fusion at L3 and below, 52 patients). Radiologic parameters and SI joint changes were evaluated on plain radiographs obtained from preoperative to 5 years postoperatively. We also investigated other risk factors for SI joint change. Results: Analysis of demographic factors revealed no significant difference between the two groups. There was a significant difference in the incidence of SI joint change between Group 1 (5 patients, 6.75%) and Group 2 (18 patients, 34.61%), with Group 2 showing a faster increase in incidence according to the Kaplan-Meier method (p<0.0001). Preoperative lumbar lordosis (LL) and ΔLL had a significant relationship with SI joint changes [preoperative LL, hazard ratio (HR)=0.77, 95% confidence interval (CI)=0.64– 0.93, p=0.008; ΔLL, HR=0.79, 95% CI=0.67–0.95, p=0.01). Conclusion After AIS surgery, patients who had fusion to the lower lumbar vertebrae (L3 or L4) experienced a higher incidence and faster progression of degenerative changes in the SI joint. Low preoperative LL and inadequate correction of LL during the operation were also risk factors for SI joint degeneration.

Purpose: We assessed human papillomavirus (HPV) genotype-based risk stratification and the efficacy of cytology testing for cervical cancer screening in patients with atypical squamous cells of undetermined significance (ASCUS)/low-grade squamous intraepithelial lesion (LSIL). Materials and Methods: Between 2010 and 2021, we monitored 1,273 HPV-positive women with ASCUS/LSIL every 6 months for up to 60 months. HPV infections were categorized as persistent (HPV positivity consistently observed post-enrollment), negative (HPV negativity consistently observed post-enrollment), or non-persistent (neither consistently positive nor negative). HPV genotypes were grouped into high-risk (Hr) groups 1 (types 16, 18, 31, 33, 45, 52, and 58) and 2 (types 35, 39, 51, 56, 59, 66, and 68) and a low-risk group. Hr1 was subdivided into types (a) 16 and 18; (b) 31, 33, and 45; and (c) 52 and 58. Cox regression and machine learning (ML) algorithms were used to analyze progression rates. Results: Among 1,273 participants, 17.6% with persistent HPV infections experienced disease progression versus no progression in the HPV-negative group (p < 0.001). Cox analysis revealed the highest hazard ratios (HRs) for Hr1-a (11.6, p < 0.001), followed by Hr1-b (9.26, p < 0.001) and Hr1-c (7.21, p < 0.001). HRs peaked at 12-24 months, with Hr1-a maintaining significance at 24-36 months (10.7, p=0.034). ML analysis identified the final cytology change pattern as the most significant factor, with 14-15 months the optimal time for detecting progression from the first examination. Conclusion In ASCUS/LSIL cases, follow-up strategies should be based on HPV risk types. Annual follow-up was the most effective monitoring for detecting progression/regression.

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.

Purpose: To evaluate the relationship between distal fusion level in correction and fusion surgery for adolescent idiopathic scoliosis (AIS) and radiologic changes in the sacroiliac (SI) joint. Materials and Methods: This retrospective cohort study evaluated patients who underwent correction and fusion for AIS between 2005 and 2017 with at least 5 years of follow-up. We categorized patients into two groups: Group 1 (distal fusion above L2, 74 patients) and Group 2 (distal fusion at L3 and below, 52 patients). Radiologic parameters and SI joint changes were evaluated on plain radiographs obtained from preoperative to 5 years postoperatively. We also investigated other risk factors for SI joint change. Results: Analysis of demographic factors revealed no significant difference between the two groups. There was a significant difference in the incidence of SI joint change between Group 1 (5 patients, 6.75%) and Group 2 (18 patients, 34.61%), with Group 2 showing a faster increase in incidence according to the Kaplan-Meier method (p<0.0001). Preoperative lumbar lordosis (LL) and ΔLL had a significant relationship with SI joint changes [preoperative LL, hazard ratio (HR)=0.77, 95% confidence interval (CI)=0.64– 0.93, p=0.008; ΔLL, HR=0.79, 95% CI=0.67–0.95, p=0.01). Conclusion After AIS surgery, patients who had fusion to the lower lumbar vertebrae (L3 or L4) experienced a higher incidence and faster progression of degenerative changes in the SI joint. Low preoperative LL and inadequate correction of LL during the operation were also risk factors for SI joint degeneration.

Background: and Purpose This study evaluated the diagnostic utility of an anti-signal-recognition particle 54 (anti-SRP54) antibody-based enzyme-linked immunosorbent assay (ELISA) as well as the clinical, serological, and pathological characteristics of patients with SRP immune-mediated necrotizing myopathy (IMNM). Methods: We evaluated 87 patients with idiopathic inflammatory myopathy and 107 healthy participants between January 2002 and December 2023. The sensitivity and specificity of the ELISA for anti-SRP54 antibodies were assessed, and the clinical profiles of patients with antiSRP54 antibodies were determined. Results: The ELISA for anti-SRP54 antibodies had a sensitivity and specificity of 88% and 99%, respectively, along with a test–retest reliability of 0.92 (p<0.001). The 32 patients diagnosed with anti-SRP IMNM using a line-blot immunoassay included 28 (88%) who tested positive for anti-SRP54 antibodies using the ELISA, comprising 12 (43%) males and 16 (57%) females whose median ages at symptom onset and diagnosis were 43.0 years and 43.5 years, respectively. Symptoms included proximal muscle weakness in all 28 (100%) patients, neck weakness in 9 (32%), myalgia in 15 (54%), dysphagia in 5 (18%), dyspnea in 4 (14%), dysarthria in 2 (7%), interstitial lung disease in 2 (7%), and myocarditis in 2 (7%). The median serum creatine kinase (CK) level was 7,261 U/L (interquartile range: 5,086–10,007 U/L), and the median anti-SRP54 antibody level was 2.0 U/mL (interquartile range: 1.0–5.6 U/mL). The serum CK level was significantly higher in patients with coexisting anti-Ro-52 antibodies. Conclusions This study has confirmed the reliability of the ELISA for anti-SRP54 antibodies and provided insights into the clinical, serological, and pathological characteristics of South Korean patients with anti-SRP IMNM.