Purpose: Preterm birth remains a leading cause of long-term neurodevelopmental impairment, yet early evaluations frequently underestimate subsequent deficits. This study examined longitudinal neurodevelopmental trajectories across gestational age groups and identified predictors of developmental delay. Methods: A retrospective cohort of 532 preterm children, stratified by gestational age, was followed from the neonatal period to early preschool age. Neurodevelopment was assessed using the Korean version of the Bayley Scales of Infant and Toddler Development, Third Edition at 8–12 months (n=481), 13–24 months (n=118), and 25–42 months (n=100). Longitudinal trajectories were analyzed using general linear models, and predictors of developmental delay were identified through multivariable logistic regression. Results: During the first year, motor scores differed significantly across gestational age groups, with extremely preterm infants showing the lowest values. By the third to fourth years of life, cognitive and language scores diverged markedly, with extremely preterm children exhibiting the steepest decline and additional deficits in motor and adaptive behavior domains. Lower gestational age remained an independent predictor of both cognitive and language delay at early preschool age, while no independent predictors were identified for motor, social-emotional, or adaptive behavior outcomes. Conclusion Neurodevelopmental outcomes in preterm children follow dynamic, domain-specific trajectories influenced by gestational age and developmental timing. Motor delays are most evident in infancy, whereas cognitive and language impairments emerge by early preschool age. Gestational age remains a consistent predictor of later delay, emphasizing the need for longitudinal, gestational age–stratified monitoring and early, targeted intervention.

The gut microbiome is not just a bystander of colorectal carcinogenesis but is an active driver of colorectal cancer (CRC). CRC-associated microbiome contributes in the tumorigenesis through chronic inflammation, formation of toxic metabolite and genotoxins, oncogenic signal activation, immune evasion, and barrier disruption—all reinforcing a tumor microenvironment. In contrast, beneficial microbiome supports the barrier-immune-metabolic axis by maintaining mucosal integrity and balanced immune tone. Despite extensive studies of microbiome-based CRC biomarkers, microbiome-based CRC biomarkers have not been yet ready for routine clinical use due to variation across populations and lack of standardization of key steps such as sampling, analysis, cutoffs, and interpretation. Microbiome-based therapies aim to change the overall intestinal ecosystem rather than simply adding or removing single strains. At present, dietary modulation and prebiotics are considered supportive measures, while probiotics or synbiotics are in preclinical stage. Fecal microbiota transplantation (FMT) still faces important challenges in effectiveness, standardization and safety. By its role in reshaping the tumor–host immune environment, FMT is viewed as a potential option for cancer therapy after further development through well-controlled clinical trials with careful safety monitoring.

Background: Copy number variations (CNVs) play an important role in human genetic disorders. Detection of exon-level CNVs is crucial for accurate clinical diagnosis. The CytoScan XON Array, a high-resolution microarray, was recently developed to detect exonic CNVs of various genes. Methods: We evaluated the clinical performance of the CytoScan XON Array using 59 patient samples with previously identified CNVs, confirmed via methods including multiple ligation-dependent probe amplification (MLPA), gene-dose PCR, and mRNA assay. Concordance between CytoScan XON and orthogonal methods was evaluated in target regions, and diagnostic utility was compared with that of genome sequencing (GS)-based CNV calling tools through analysis of false-positive CNVs in non-target genomic regions. Results: For target regions, the CytoScan XON Array achieved concordance rates of 89.8% and 92.5% at the exon and gene levels, respectively, for all CNV calls. Concordance was higher for multi-exon CNVs (100%) than that for single-exon CNVs (82.6%, P = 0.03). For non-target regions, false-positive CNV calls were reduced to fewer than 0.01 per gene per person through filtering strategies. The array exhibited false-positive detection rates within dosage-sensitive genes comparable with those of GS-based tools. Conclusions The CytoScan XON Array, a reliable tool for detecting exon-level CNVs in target regions, can serve as a complementary approach to GS-based CNV calling tools for genome-wide CNV screening with high resolution. However, its performance for single-exon CNVs requires further optimization. Cross-validation with GS-based CNV calling tools is recommended to improve diagnostic accuracy.

Purpose: This study aimed to compare perioperative and postoperative outcomes of single-port laparoscopic articulated instrument-assisted versus da Vinci SP-assisted totally extraperitoneal (TEP) inguinal hernia repair using a propensity score-matched multi-institutional cohort. Methods: Between April 2022 and July 2025, 221 patients underwent TEP unilateral inguinal hernia repair at four institutions. Among them, 33 patients underwent da Vinci SP-assisted repair (Intuitive Surgical) and 188 underwent single-port laparoscopy using the articulated instrument, ArtiSential (LivsMed). Propensity score matching was performed in a 1:1 ratio based on demographic and clinical variables, resulting in 30 matched patients in each group. Perioperative outcomes and postoperative complications were analyzed. Results: After matching, baseline characteristics were well balanced between the groups.Operative time was significantly longer in the da Vinci SP group than in the ArtiSential group (median [interquartile range], 82.0 [67.5–105.0] vs. 35.0 [28.5–47.5] minutes; p < 0.001). No open conversions occurred, and conversions to transabdominal preperitoneal repair were rare and comparable. Mesh size selection differed significantly, with smaller meshes more frequently used in the da Vinci SP group (p < 0.001). Postoperative outcomes, including length of hospital stay, overall complication rates, chronic pain, and recurrence, were similar between the groups. No major complications, readmissions, or reoperations were observed. Conclusion Articulated instrument-assisted TEP inguinal hernia repair demonstrated a significantly shorter operative time than da Vinci SP-assisted repair, while perioperative safety and postoperative outcomes were comparable.

This case describes a male with a history of type 1 autoimmune pancreatitis (AIP) who had a concomitant branch-duct intraductal papillary mucinous neoplasm under long-term surveillance. During follow-up, new high-risk radiologic features developed within the pancreatic cyst, raising concern for malignant transformation and ultimately leading to surgical resection. However, final histopathologic examination revealed recurrent type 1 AIP rather than malignant progression of branch-duct intraductal papillary mucinous neoplasm, a finding that represents an uncommon and diagnostically challenging manifestation. This case suggests that when new imaging changes are observed during surveillance of pancreatic cystic lesions, clinicians should consider not only malignant transformation but also the possibility of recurrence or coexistence of underlying diseases such as AIP.

Midline palatal fractures compromise maxillary transverse stability and cause oro-nasal communication. We report a successful minimally invasive reconstruction based on AO CMF principles. A 60-year-old male with Le Fort II and midline palatal fractures following a fall exhibited nasal regurgitation. Associated facial fractures were managed conservatively, while the palatal fracture was addressed with a customized acrylic splint fabricated via model-based virtual surgery to restore pre-traumatic occlusion.Intraoperatively, segments were repositioned through manual reduction, followed by intermolar wire ligation and splint fixation. Nasal regurgitation resolved by postoperative day 4. Evaluation at 10 days confirmed anatomical arch width restoration. Stable occlusion was maintained throughout the 6-week splinting period. Closed reduction using customized splints and interdental ligation is an effective, minimally invasive alternative for managing midline palatal fractures, particularly when open reduction is challenging.

Purpose: Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, necessitating the identification of novel therapeutic targets. The E3 ubiquitin ligase WW domain-containing E3 ubiquitin protein ligase 2 (WWP2) has been implicated in various cancers, yet its specific role and underlying molecular mechanisms in CRC are poorly understood. This study aimed to investigate the functional role of WWP2 in CRC progression and to elucidate its regulatory mechanisms. Methods: WWP2 expression was evaluated in CRC patient tissues and cell lines using immunohistochemistry, quantitative real-time polymerase chain reaction, and western blotting. The biological functions of WWP2 were assessed using in vitro assays for cell proliferation, migration, and invasion following adenovirus-mediated overexpression. The molecular mechanism was investigated by analyzing the protein expression levels of p53 and its downstream target, p21, via western blot. An in vivo xenograft mouse model was used to confirm the oncogenic role of WWP2. Results: WWP2 expression was significantly upregulated in CRC tissues. Overexpression of WWP2 promoted CRC cell proliferation, migration, and invasion. Mechanistically, increased WWP2 expression led to a marked reduction in the protein levels of the tumor suppressor p53. Consequently, the expression of the p53 downstream target, the cell cycle inhibitor p21, was also suppressed. In the xenograft model, WWP2 overexpression significantly enhanced tumor growth. Conclusion Our findings demonstrate that WWP2 functions as an oncogene in CRC. It promotes cancer progression by destabilizing the tumor suppressor p53 and downregulating p21. This study highlights the WWP2-p53-p21 axis as a potential novel therapeutic target for CRC.

Alzheimer’s disease (AD) is characterized by progressive cognitive deterioration and significant depression. However, the mechanisms linking depression to AD pathology remain unclear. Here, we investigated whether Notch2 signaling mediates depressionlike behaviors in presenilin-2 (PS2) N141I mutant mice, an early-onset AD model. PS2 wild-type (WT) and mutant (MT) mice aged 12-15 months were subjected to unpredictable chronic mild stress (UCMS) for 4 weeks, followed by sucrose preference, tail-hanging, and forced swimming tests. Behavioral assessments showed that UCMS exacerbated anhedonia and immobility only in PS2 MT mice. Molecular analysis revealed concomitant increases in plasma corticosterone, hippocampal γ-secretase activity, and Notch2 expression, and elevated total and phosphorylated glucocorticoid receptor levels in PS2 MT-UCMS mice. Gene expression profiling of human hippocampal datasets confirmed upregulation of NOTCH2 in Alzheimer’s disease and depression.Pharmacological inhibition of γ-secretase and Notch signaling with DAPT normalizes depressive behavior, reduces corticosterone release, attenuates GR phosphorylation, and inhibits Notch2 signaling in PS2 MT mice. These findings identify Notch2 as a pivotal mediator linking chronic stress to molecular changes associated with depression and AD, and suggest that targeting Notch2 signaling may provide therapeutic benefits for comorbid mood and neurodegenerative disorders.

Purpose: This study aimed to report the real-world outcomes of intravesical gemcitabine for bacillus Calmette–Guérin (BCG)–unresponsive, high-risk, non–muscle-invasive bladder cancer (HR-NMIBC) in Korean patients who were unable or unwilling to undergo radical cystectomy (RC). Materials and Methods: This retrospective study included 131 patients (median age, 69 years; 88.5% men) treated with intravesical gemcitabine for BCG-unresponsive HR-NMIBC at nine centers between May 2019 and April 2022. The primary endpoint was 1-year recurrence-free survival (RFS). The secondary endpoints included factors influencing RFS, progression-free survival (PFS), cystectomy- free survival, cancer-specific survival (CSS), overall survival (OS), and safety. Survival analysis was performed using the Kaplan-Meier method, and risk factors for recurrence were assessed using Cox regression models. Results: Patients were followed up for a median duration of 25 months, with carcinoma in situ (CIS) in 41.9% of the patients. The 1-year and 2-year RFS rates were 68% and 42%, while the 1-year and 2-year PFS rates were 87% and 77%, respectively. No significant factors influencing RFS were identified. Seventeen patients underwent RC during a median follow-up of 16 months, with the condition in three patients progressing to muscle-invasive disease on final pathological analysis. The 2-year CSS and OS rates were 98% and 97%, respectively. Intravesical gemcitabine was well-tolerated, with only seven patients (5.3%) unable to complete the full induction course. Conclusion Our research highlights the potential of intravesical gemcitabine as a viable bladder-sparing treatment option for BCG-unresponsive HR-NMIBC, providing real-world evidence on its safety, efficacy, and tolerability.