Objective: To evaluate the effectiveness of the National Health Screening Program for Infants and Children (NHSPIC) in the early diagnosis of neurodevelopmental disorders (NDDs) utilizing data from the National Health Insurance Database of South Korea. Methods: We enrolled children born between 2011 and 2018 who completed the first to fourth stages of the NHSPIC. A positive finding was defined as a recommendation for further evaluation during one or more stages. Participants were categorized into the positive and negative finding groups. Following 1:1 propensity score matching, 82,138 participants were assigned to each group. Results: Comparative analysis revealed that participants with positive findings exhibited a higher risk of developing all seven NDDs, particularly for autism spectrum disorder (hazard ratio [HR], 19.70; 95% confidence interval [CI], 17.48–22.20), intellectual disability (HR, 17.11; 95% CI, 14.69–19.93), developmental language disorder (HR, 11.74; 95% CI, 10.73– 12.84), and cerebral palsy (HR, 11.34; 95% CI, 8.67–14.84). The HR for learning disability was 4.31 (95% CI, 2.94–6.34), whereas attention-deficit hyperactivity disorder had an HR of 3.57 (95% CI, 3.37–3.78). Tic disorder had the lowest HR (HR, 1.64; 95% CI, 1.48–1.82). Additionally, HRs were calculated for each NHSPIC stage, demonstrating the utility of specific stages in the early detection of each NDD. Conclusion Developmental screening tests in the NHSPIC contributed to the early diagnosis of NDDs. This study underscores the significance of the NHSPIC and provides foundational evidence to inform and enhance policies related to child health screenings.

Objective: Cognitive impairment is common in patients with Parkinson’s disease (PD), and few pharmacological options are available for treating this condition. We evaluated the effects of a digital cognitive training program (SUPERBRAIN), which was previously shown to be effective in populations at risk of Alzheimer’s disease, on cognitive function in individuals with PD. Methods: Twenty-three individuals with PD and mild cognitive impairment (PD-MCI) from four clinics were randomized to the intervention (n=16) or control (n=7) groups. The intervention group completed a 12-week, home-based, tablet-based cognitive training program (25–30 min/day, 7 days/week). Cognitive outcomes were assessed using the Seoul Neuropsychological Screening Battery pre- and post-intervention. Results: The adherence rate was 79.36%. The intervention group showed significant improvements in the Seoul Verbal Learning Test (SVLT) delayed recall and the Controlled Oral Word Association Test, while no changes were observed in the control group. Analysis of covariance confirmed greater SVLT improvement in the intervention group (F statistic=7.15, p=0.015, partial η2=0.28). Conclusion SUPERBRAIN is feasible and can improve cognitive function in individuals with PD-MCI.

Purpose: To evaluate the short-term outcomes of intravitreal injection therapy using the ranibizumab biosimilar CKD-701 in macular edema due to retinal vein occlusion. Methods: We conducted a retrospective analysis of medical records from patients diagnosed with macular edema secondary to retinal vein occlusion who received intravitreal injections of CKD-701. The best-corrected visual acuity (BCVA) and central retinal thickness (CRT) before and after a single injection were compared. Additionally, differences in these indicators were assessed between central and branch retinal vein occlusion (CRVO/BRVO). Results: The study included 22 subjects, with 17 cases of BRVO and 5 cases of CRVO. The efficacy was evaluated at 6.0 ± 2.2 weeks after injection. CRT decreased significantly from 534.8 ± 224.9 µm before injection to 367.8 ± 162.7 µm after injection (p < 0.001). The logarithm of the minimum angle of resolution BCVA improved significantly from 0.58 ± 0.41 to 0.48 ± 0.37 after injection (p = 0.002). The CRVO group showed a greater reduction in CRT compared to the BRVO group (p = 0.006). Conclusions A single injection of CKD-701 significantly improved both functional and anatomical outcomes in patients with macular edema secondary to retinal vein occlusion. Additional long-term studies are needed.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Purpose: To report five cases of macular hole (MH) coexisting with uveal melanoma (UM) and review the literature. Methods: Seventeen patients (5 new and 12 from previous reports) with coexisting MH and UM were reviewed. The patients were divided into two groups based on whether the MH was diagnosed before or after tumor treatment. The clinical features, pathogenesis, management options, and clinical outcomes were reviewed. Results: Of 505 patients with UM in our institution, 5 (1.0%) had a concurrent MH in the ipsilateral eye. The 17 patients reviewed had a mean age of 63.9 years at the time of MH diagnosis. Of 16 patients with available data on sex, 11 (64.7%) were female. There were no major differences in the demographic or clinical data of the groups. Of the 15 known tumor locations, 6 (35.3%) were juxtapapillary or macular. In patients who developed MH after UM treatment, the durations from tumor treatment (radiotherapy or transpupillary thermotherapy) to MH diagnosis were 3 to 56 months (median, 8.5 months). MH surgery was performed in nine eyes, and hole closure was achieved in seven eyes with postoperative data. The mean visual acuity showed a tendency of improvement after surgery. No intraocular or extraocular tumor dissemination associated with surgery was observed. Conclusions MH is observed in approximately 1% of patients with UM, either before or after tumor treatment. Of patients with coexisting MH and UM, MH surgery appears to be safe and effective in those with stable tumors and visual potential.

Purpose: To report five cases of macular hole (MH) coexisting with uveal melanoma (UM) and review the literature. Methods: Seventeen patients (5 new and 12 from previous reports) with coexisting MH and UM were reviewed. The patients were divided into two groups based on whether the MH was diagnosed before or after tumor treatment. The clinical features, pathogenesis, management options, and clinical outcomes were reviewed. Results: Of 505 patients with UM in our institution, 5 (1.0%) had a concurrent MH in the ipsilateral eye. The 17 patients reviewed had a mean age of 63.9 years at the time of MH diagnosis. Of 16 patients with available data on sex, 11 (64.7%) were female. There were no major differences in the demographic or clinical data of the groups. Of the 15 known tumor locations, 6 (35.3%) were juxtapapillary or macular. In patients who developed MH after UM treatment, the durations from tumor treatment (radiotherapy or transpupillary thermotherapy) to MH diagnosis were 3 to 56 months (median, 8.5 months). MH surgery was performed in nine eyes, and hole closure was achieved in seven eyes with postoperative data. The mean visual acuity showed a tendency of improvement after surgery. No intraocular or extraocular tumor dissemination associated with surgery was observed. Conclusions MH is observed in approximately 1% of patients with UM, either before or after tumor treatment. Of patients with coexisting MH and UM, MH surgery appears to be safe and effective in those with stable tumors and visual potential.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Purpose: To evaluate the short-term outcomes of intravitreal injection therapy using the ranibizumab biosimilar CKD-701 in macular edema due to retinal vein occlusion. Methods: We conducted a retrospective analysis of medical records from patients diagnosed with macular edema secondary to retinal vein occlusion who received intravitreal injections of CKD-701. The best-corrected visual acuity (BCVA) and central retinal thickness (CRT) before and after a single injection were compared. Additionally, differences in these indicators were assessed between central and branch retinal vein occlusion (CRVO/BRVO). Results: The study included 22 subjects, with 17 cases of BRVO and 5 cases of CRVO. The efficacy was evaluated at 6.0 ± 2.2 weeks after injection. CRT decreased significantly from 534.8 ± 224.9 µm before injection to 367.8 ± 162.7 µm after injection (p < 0.001). The logarithm of the minimum angle of resolution BCVA improved significantly from 0.58 ± 0.41 to 0.48 ± 0.37 after injection (p = 0.002). The CRVO group showed a greater reduction in CRT compared to the BRVO group (p = 0.006). Conclusions A single injection of CKD-701 significantly improved both functional and anatomical outcomes in patients with macular edema secondary to retinal vein occlusion. Additional long-term studies are needed.

Purpose: To evaluate the short-term outcomes of intravitreal injection therapy using the ranibizumab biosimilar CKD-701 in macular edema due to retinal vein occlusion. Methods: We conducted a retrospective analysis of medical records from patients diagnosed with macular edema secondary to retinal vein occlusion who received intravitreal injections of CKD-701. The best-corrected visual acuity (BCVA) and central retinal thickness (CRT) before and after a single injection were compared. Additionally, differences in these indicators were assessed between central and branch retinal vein occlusion (CRVO/BRVO). Results: The study included 22 subjects, with 17 cases of BRVO and 5 cases of CRVO. The efficacy was evaluated at 6.0 ± 2.2 weeks after injection. CRT decreased significantly from 534.8 ± 224.9 µm before injection to 367.8 ± 162.7 µm after injection (p < 0.001). The logarithm of the minimum angle of resolution BCVA improved significantly from 0.58 ± 0.41 to 0.48 ± 0.37 after injection (p = 0.002). The CRVO group showed a greater reduction in CRT compared to the BRVO group (p = 0.006). Conclusions A single injection of CKD-701 significantly improved both functional and anatomical outcomes in patients with macular edema secondary to retinal vein occlusion. Additional long-term studies are needed.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.