Cochlear Implantation in a Patient with Intractable Tinnitus: A Case Report of an Endoscope-Assisted Approach.

Preservation of residual hearing and vestibular function is a crucial factor in cochlear implantation (CI), especially in patients with residual low-frequency hearing thresholds. We report a case of a patient who underwent unilateral endoscope-assisted CI with a challenging surgical view following rigorous posterior tympanotomy. A 53-year-old male presented with left-sided intractable tinnitus due to sudden sensorineural hearing loss that had occurred 10 years prior. Due to the abnormal location of the round window (RW), which was far more posterior and inferior than usual and impeded insertion of the electrode using the conventional RW approach, endoscope-assisted CI was performed. Pure-tone audiometry at 3 months after CI revealed satisfactory hearing thresholds. Furthermore, there was alleviation of the left-sided tinnitus, which was indicated by a marked decrease in both the subjective visual analog scale loudness and Tinnitus Handicap Inventory scores. With proper indications, we strongly recommend applying the RW approach with endoscopic assistance over conventional bony cochleostomy for the preservation of low-frequency hearing thresholds in cases where RW visualization is insufficient following posterior tympanotomy.

Quantification of glutathione and its associated spontaneous neuronal activity in major depressive disorder and obsessive-compulsive disorder.

BACKGROUND: Glutathione (GSH) is a crucial antioxidant in the human brain. Although proton magnetic resonance spectroscopy (MRS) using the MEscher-GArwood Point RESolved Spectroscopy (MEGA-PRESS) sequence is highly recommended, limited literature has measured cortical GSH using this method in major psychiatric disorders. METHODS: By combining MRS using the MEGA-PRESS and resting-state functional magnetic resonance imaging, we quantified brain GSH and glutamate in the medial prefrontal cortex (mPFC) and precuneus and explore relationships between the GSH levels and intrinsic neuronal activity as well as clinical symptoms among the three groups of healthy controls (HCs, N=30), major depressive disorder (MDD, N=28), and obsessive-compulsive disorder (OCD, N=28). RESULTS: GSH concentrations were lower in both the mPFC and precuneus in both the MDD and OCD groups compared to HCs. In HCs, positive correlations were noted between the GSH and glutamate levels, and between GSH and fractional amplitude of low-frequency fluctuations (fALFF) in both regions. However, while these correlations were absent in both patient groups, they showed a weak positive correlation between glutamate and fALFF values. Moreover, GSH levels negatively correlated with depressive and compulsive symptoms in MDD and OCD, respectively. CONCLUSIONS: These findings suggest that reduced GSH levels and an imbalance between GSH and glutamate could increase oxidative stress and alter neurotransmitter signaling, leading to disruptions in GSH-related neurochemical-neuronal coupling and psychopathologies across MDD and OCD. Understanding these mechanisms could provide valuable insights into the underlying processes of these disorders, potentially becoming a springboard for future directions and advancing our knowledge of their neurobiological foundations.

Disrupted cognitive network revealed by task-induced brain entropy in schizophrenia.

Brain entropy (BEN), which measures the amount of information in brain activity, provides a novel perspective for evaluating brain function. Recent studies using resting-state functional magnetic resonance imaging (fMRI) have shown that BEN during rest can help characterize brain function alterations in schizophrenia (SCZ). However, there is a lack of research on BEN using task-evoked fMRI to explore task-dependent cognitive deficits in SCZ. In this study, we evaluate whether the reduced working memory (WM) capacity in SCZ is possibly associated with dynamic changes in task BEN during tasks with high cognitive demands. We analyzed data from 15 patients with SCZ and 15 healthy controls (HC), calculating task BEN from their N-back task fMRI scans. We then examined correlations between task BEN values, clinical symptoms, 2-back task performance, and neuropsychological test scores. Patients with SCZ exhibited significantly reduced task BEN in the cerebellum, hippocampus, parahippocampal gyrus, thalamus, and the middle and superior frontal gyrus (MFG and SFG) compared to HC. In HC, significant positive correlations were observed between task BEN and 2-back accuracy in several brain regions, including the MFG and SFG; such correlations were absent in patients with SCZ. Additionally, task BEN was negatively associated with scores for both positive and negative symptoms in areas including the parahippocampal gyrus among patients with SCZ. In conclusion, our findings indicate that a reduction in BEN within prefrontal and hippocampal regions during cognitively demanding tasks may serve as a neuroimaging marker for SCZ.

Amyloid-ß-activated microglia can induce compound proteinopathies.

Neuropathological features of Alzheimer's disease include amyloid plaques, neurofibrillary tangles and Lewy bodies, with the former preceding the latter two. However, it is not fully understood how these compound proteinopathies are interconnected. Here, we show that transplantation of amyloid-ß oligomer-activated microglia into the striatum of naïve mice was sufficient to generate all the features of Alzheimer's disease, including widespread tauopathy and synucleinopathy, gliosis, neuroinflammation, synapse loss, neuronal death, and cognitive and motor deficits. These pathological features were eliminated by microglia depletion and anti-inflammatory drug administration. Our results suggest the crucial roles of microglia-driven inflammation in development of mixed pathology. This study provides not only mechanistic insights into amyloid-ß oligomer-triggered proteinopathies but also a novel animal model recapitulating the salient features of Alzheimer's disease.

Pre-drought effects on northern temperate trees and vine invasion in forest gaps hindering regeneration.

Northern temperate coniferous forests serve as crucial connectors between boreal and temperate forests, yet they are vulnerable to various stressors such as climate change and human activities. Severe drought poses a significant threat to plant species within these forests, prompting recent research into its impacts. However, many studies lack explicit definitions of post-disturbance vegetation processes and fail to identify potential interactions with disturbance factors, necessitating comprehensive discussions. This study examines the effects of drought on tree growth patterns of the main dominant species in northern temperate regions: Abies nephrolepis and Picea jezoensis, along with two commonly associated Betula ermanii, and Quercus mongolica. Additionally, new disturbance factors in forests inhabited by these species (A. nephrolepis and P. jezoensis) were evaluated based on community classification. The study sites were located in the Mt. Baekdu (Changbai) and South Korea regions, which are positioned at the southern limit of the phytogeographical patterns of target species. Results indicate that A. nephrolepis and P. jezoensis exhibit high levels of recovery and resilience, while B. ermanii and Q. mongolica demonstrate high resistance. Species-specific responses align with drought intensity, with resistance, recovery, and resilience decreasing notably with increasing pre-drought radial growth. South Korean forests, the invasion of the vine species Tripterygium regelii after the death of A. nephrolepis in the overstory vegetation threatens the regeneration of new trees. However, certain environmental factors, such as high rock exposure and dense overstory canopy, limit vine invasion. Based on the results, pre-drought radial growth emerges as a key determinant in how trees respond to drought. Additionally, the results suggest the potential for new disturbances to emerge in forest gaps due to overstory vegetation mortality induced by global warming. These findings contribute to a deeper understanding of increasing drought stress, aid in identifying climate refugia, and inform conservation priorities based on habitat characteristics.

Ethanol-related transcriptomic changes in mouse testes.

BACKGROUND: Alcohol consumption is widely known to have detrimental effects on various organs and tissues. The effects of ethanol on male reproduction have been studied at the physiological and cellular levels, but no systematic study has examined the effects of ethanol on male reproduction-related gene expression. RESULTS: We employed a model of chronic ethanol administration using the Lieber-DeCarli diet. Ethanol-fed mice showed normal testicular and epididymal integrity, and sperm morphology, but decreased sperm count. Total RNA sequencing analysis of testes from ethanol-fed mice showed that a small fraction (∼ 2%) of testicular genes were differentially expressed in ethanol-fed mice and that, of these genes, 28% were cell-type specific in the testis. Various in silico analyses were performed, and gene set enrichment analysis revealed that sperm tail structure-related genes, including forkhead box J1 (Foxj1), were down-regulated in testes of ethanol-fed mice. Consistent with this result, ethanol-fed mice exhibited decreased sperm motility. CONCLUSION: This study provides the first comprehensive transcriptomic profiling of ethanol-induced changes in the mouse testis, and suggests gene expression profile changes as a potential mechanism underlying ethanol-mediated reproductive dysfunction, such as impaired sperm motility.

Brief guide to senescence assays using cultured mammalian cells.

Cellular senescence is a crucial biological process associated with organismal aging and many chronic diseases. Here, we present a brief guide to mammalian senescence assays, including the measurement of cell cycle arrest, change in cellular morphology, senescence-associated ß-galactosidase (SA-ß-gal) staining, and the expression of senescence-associated secretory phenotype (SASP). This work will be useful for biologists with minimum expertise in cellular senescence assays.

Longitudinal Analysis of Diabetes Mellitus Risk: Smoking Status and Smoking Cessation.

Background/Objectives: Smoking cessation is acknowledged for its health benefits. However, it paradoxically increases diabetes mellitus (DM) risk shortly after quitting due to weight gain. This research aimed to investigate how smoking status could affect the development of DM, focusing on how the risk of acquiring diabetes changed over time after quitting smoking, independent of variables such as weight gain. Methods: The data of 386,558 participants of the Kangbuk Samsung Health Study, excluding those with pre-existing DM, were examined. Smoking status and its long-term effects on DM risk were assessed using multivariate Cox proportional hazards models. Lifestyle factors, including weight change, physical activity levels, and alcohol intake, were adjusted as time-varying covariates throughout the follow-up period. Results: Modified hazard ratios (HRs) indicated no notable disparity in DM risk between individuals who previously smoked and those who had never smoked (HR: 1.04, 95% CI: 0.999-1.08, p-value < 0.001). In contrast, current smokers exhibited a significantly increased DM risk (HR: 1.29, 95% CI: 1.24-1.35, p-value < 0.001). Within the first six years post-cessation, former smokers initially faced a higher DM risk than never smokers (0-2 years, HR: 1.22, 95% CI: 1.15-1.31, p-value < 0.001; 3-5 years, HR: 1.11, 95% CI: 1.04-1.20, p-value < 0.001). After 12 years, they realigned with never smokers (12-46 years, HR: 0.92, 95% CI: 0.86-0.98, p-value = 0.002). Current smokers consistently showed a higher DM risk (0-9 years, HR: 1.29, 95% CI: 1.14-1.46, p-value < 0.001). Adjusting for covariates such as weight change and physical activity did not alter these findings. Conclusions: Our results indicated that former smokers initially experienced an elevated risk of DM relative to never smokers. This increased risk aligned with the risk of never smokers after six years, and the risk continued to improve after 12 years compared to never smokers. This contrasted with current smokers, who maintained a heightened risk of DM, even when adjustments were made for weight change, physical activity, and alcohol intake as time-varying covariates.

Impact of Childhood Maltreatment on Cognitive Function and Its Relationship With Emotion Regulation in Young Adults.

Objectives: Childhood maltreatment can negatively impact cognitive development, including executive function, working memory, and processing speed. This study investigated the impact of childhood maltreatment on cognitive function in young adults using various measurements, including computerized tests, and their relationship with emotional dysregulation. Methods: We recruited 149 healthy individuals with and without maltreatment experiences and used the Wechsler Adult Intelligence Scale IV (WAIS-IV) and a computerized battery to analyze cognitive function. Results: Both the WAIS-IV and computerized tests revealed that individuals with a history of childhood maltreatment had decreased cognitive function, especially in terms of working memory and processing speed. These individuals tended to employ maladaptive emotion regulation strategies. Among cognitive functions, working memory is negatively related to maladaptive emotion regulation strategies such as catastrophizing. Conclusion: This study highlights the effects of childhood maltreatment on cognitive function in young adulthood. Moreover, the study suggests clinical implications of cognitive interventions for improving emotion regulation and cognitive function in individuals with a history of childhood maltreatment.

HLH-30/TFEB mediates sexual dimorphism in immunity in Caenorhabditis elegans.

Sexual dimorphism affects various biological functions, including immune responses. However, the mechanisms by which sex alters immunity remain largely unknown. Using Caenorhabditis elegans as a model species, we showed that males exhibit enhanced immunity against various pathogenic bacteria through the upregulation of HLH-30 (Helix Loop Helix 30/TFEB (transcription factor EB)), a transcription factor crucial for macroautophagy/autophagy. Compared with hermaphroditic C. elegans, males displayed increased activity of HLH-30/TFEB, which contributed to enhanced antibacterial immunity. atg-2 (AuTophaGy (yeast Atg homolog) 2) upregulated by HLH-30/TFEB mediated increased immunity in male C. elegans. Thus, the males appear to be equipped with enhanced HLH-30/TFEB-mediated autophagy, which increases pathogen resistance, and this may functionally prolong mate-searching ability with reduced risk of infection.Abbreviations: atg-2: AuTophaGy (yeast Atg homolog) 2; FUDR: 5-fluoro-2'-deoxyuridine; GSEA: gene set enrichment analysis; HLH-30: Helix Loop Helix 30; LC3: microtubule associated protein 1 light chain 3; NGM: nematode growth media; RNA-seq: RNA sequencing; SEM: standard error of the mean; TFEB: transcription factor EB; WT: wild-type.

Improved resilience and proteostasis mediate longevity upon DAF-2 degradation in old age.

Little is known about the possibility of reversing age-related biological changes when they have already occurred. To explore this, we have characterized the effects of reducing insulin/IGF-1 signaling (IIS) during old age. Reduction of IIS throughout life slows age-related decline in diverse species, most strikingly in the nematode Caenorhabditis elegans. Here we show that even at advanced ages, auxin-induced degradation of DAF-2 in single tissues, including neurons and the intestine, is still able to markedly increase C. elegans lifespan. We describe how reversibility varies among senescent changes. While senescent pathologies that develop in mid-life were not reversed, there was a rejuvenation of the proteostasis network, manifesting as a restoration of the capacity to eliminate otherwise intractable protein aggregates that accumulate with age. Moreover, resistance to several stressors was restored. These results support several new conclusions. (1) Loss of resilience is not solely a consequence of pathologies that develop in earlier life. (2) Restoration of proteostasis and resilience by inhibiting IIS is a plausible cause of the increase in lifespan. And (3), most interestingly, some aspects of the age-related transition from resilience to frailty can be reversed to a certain extent. This raises the possibility that the effect of IIS and related pathways on resilience and frailty during aging in higher animals might possess some degree of reversibility.

Increased risk of epilepsy after transient global amnesia: A population-based study in South Korea.

PURPOSE: This study aimed to investigate the risk of epilepsy after transient global amnesia (TGA). METHODS: Study population was recruited using the International Classification of Diseases codes from the Korean National Health Insurance Service database between 2002 and 2020. The incidence of epilepsy was compared between the TGA (n=12,390) and non-TGA (n=33,868) groups, determined using 1:3 propensity score matching. Using Cox proportional hazard regression model, we obtained adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) for incident epilepsy in the TGA compared with non-TGA group. Logistic regression was performed to examine the independent variables determining incident epilepsy in the TGA group, and adjusted odds ratios (aORs) and 95% CIs were calculated. RESULTS: The TGA group had a significantly higher cumulative incidence of epilepsy than controls (p <0.001, log-rank test). TGA was significantly associated with incident epilepsy in the Cox model (adjusted HR 1.46, 95% CI 1.36-1.56). The adjusted logistic regression showed that age (per 1 year, aOR 1.02, 95% CI 1.01-1.02), female sex (aOR 0.68, 95% CI 0.60-0.77), hypertension (aOR 1.14, 95% CI 1.00-1.30), diabetes (aOR 1.26, 95% CI 1.10-1.44), stroke (aOR 1.22, 95% CI 1.06-1.40), depression (aOR 1.44, 95% CI 1.22-1.69), anxiety (aOR 1.31, 95% CI 1.14-1.51), alcohol-related disease (aOR 1.96, 95% CI 1.38-2.78), low income (aOR 1.18, 95% CI 1.02-1.36) and rural residence (aOR 1.20, 95% CI 1.02-1.42) were associated with incident epilepsy. CONCLUSIONS: Our results suggest a longitudinal association of TGA with incident epilepsy.

7-MEGA™ inhibits adipogenesis in 3T3-L1 adipocytes and suppresses obesity in high-fat-diet-induced obese C57BL/6 mice.

BACKGROUND: Overweight, often known as obesity, is the abnormal and excessive accumulation of fat that exposes the health of a person at risk by increasing the likelihood that they may experience many chronic conditions. Consequently, obesity has become a global health threat, presenting serious health issues, and attracting a lot of attention in the healthcare profession and the scientific community. METHOD: This study aims to explore the anti-adipogenic properties of 7-MEGA™ in an attempt to address obesity, using both in vitro and in vivo research. The effects of 7MEGA™ at three distinct concentrations were investigated in obese mice who were given a high-fat diet (HFD) and 3T3-L1 adipocytes. RESULTS: 7MEGA™ decreased the total fat mass, overall body weight, and the perirenal and subcutaneous white adipose tissue (PWAT and SWAT) contents in HFD mice. Additionally, 7MEGA™ showed promise in improving the metabolic health of individuals with obesity and regulate the levels of insulin hormone, pro-inflammatory cytokines and adipokines. Furthermore, Peroxisome proliferator-activated receptors (PPAR) α and γ, Uncoupling Protein 1 (UCP-1), Sterol Regulatory Element-Binding Protein 1 (SREBP-1), Fatty Acid-Binding Protein 4 (FABP4), Fatty Acid Synthase (FAS), Acetyl-CoA Carboxylase (ACC), Stearoyl-CoA Desaturase-1 (SCD-1) and CCAAT/Enhancer-Binding Protein (C/EBPα) were among the adipogenic regulators that 7MEGA™ could regulate. CONCLUSION: In summary, this study uncovered that 7MEGA™ demonstrates anti-adipogenic and anti-obesity effects, suggesting its potential in combating obesity.

Intravascular Imaging and Angiography Guidance in Complex Percutaneous Coronary Intervention Among Patients With Diabetes: A Secondary Analysis of a Randomized Clinical Trial.

Importance: Data are limited regarding the effects of intravascular imaging guidance during complex percutaneous coronary intervention (PCI) in patients with diabetes. Objective: To compare the clinical outcomes of intravascular imaging-guided vs angiography-guided complex PCI in patients with or without diabetes. Design, Setting, and Participants: This prespecified secondary analysis of a subgroup of patients in RENOVATE-COMPLEX-PCI (Randomized Controlled Trial of Intravascular Imaging Guidance Versus Angiography-Guidance on Clinical Outcomes After Complex Percutaneous Coronary Intervention), an investigator-initiated, open-label multicenter trial, analyzed enrolled patients who underwent complex PCI at 20 sites in Korea from May 2018 through May 2021. Eligible patients were randomly assigned in a 2:1 ratio to undergo either the intravascular imaging-guided PCI or angiography-guided PCI. Data analyses were performed from June 2023 to April 2024. Interventions: Percutaneous coronary intervention was performed either under the guidance of intravascular imaging or angiography alone. Main Outcomes and Measures: The primary end point was target vessel failure (TVF), defined as a composite of cardiac death, target vessel-related myocardial infarction, or target vessel revascularization. Results: Among the 1639 patients included in the analysis (mean [SD] age, 65.6 [10.2] years; 1300 males [79.3%]), 617 (37.6%) had diabetes. The incidence of TVF was significantly higher in patients with diabetes than patients without diabetes (hazard ratio [HR], 1.86; 95% CI, 1.33-2.60; P < .001). Among patients without diabetes, the intravascular imaging-guided PCI group had a significantly lower incidence of TVF compared with the angiography-guided PCI group (4.7% vs 12.2%; HR, 0.41 [95% CI, 0.25-0.67]; P < .001). Conversely, in patients with diabetes, the risk of TVF was not significantly different between the 2 groups (12.9% vs 12.3%; HR, 0.97 [95% CI, 0.60-1.57]; P = .90). There was a significant interaction between the use of intravascular imaging and diabetes for the risk of TVF (P for interaction = .02). Among patients with diabetes, only those with good glycemic control (hemoglobin A1c level ≤7.5%) and who achieved stent optimization by intravascular imaging showed a lower risk of future ischemic events (HR, 0.31; 95% CI, 0.12-0.82; P = .02). Conclusions and Relevance: In this secondary analysis of a subgroup of patients in the RENOVATE-COMPLEX-PCI trial, intravascular imaging guidance reduced the risk of TVF compared with angiography guidance in patients without diabetes (but not in patients with diabetes) during complex PCI. In patients with diabetes undergoing complex PCI, attention should be paid to stent optimization using intravascular imaging and glycemic control to improve outcomes. Trial Registration: ClinicalTrials.gov Identifier: NCT03381872.

Potassium Iodide Doping for Vacancy Substitution and Dangling Bond Repair in InP Core-Shell Quantum Dots.

This work highlights the novel approach of incorporating potassium iodide (KI) doping during the synthesis of In0.53P0.47 core quantum dots (QDs) to significantly reduce the concentration of vacancies (i.e., In vacancies; VIn-) within the bulk of the core QD and inhibit the formation of InPOx at the core QD-Zn0.6Se0.4 shell interfaces. The photoluminescence quantum yield (PLQY) of ~97% and full width at half maximum (FWHM) of ~40 nm were achieved for In0.53P0.47/Zn0.6Se0.4/Zn0.6Se0.1S0.3/Zn0.5S0.5 core/multi-shell QDs emitting red light, which is essential for a quantum-dot organic light-emitting diode (QD-OLED) without red, green, and blue crosstalk. KI doping eliminated VIn- in the core QD bulk by forming K+-VIn- substitutes and effectively inhibited the formation of InPO4(H2O)2 at the core QD-Zn0.6Se0.4 shell interface through the passivation of phosphorus (P)-dangling bonds by P-I bonds. The elimination of vacancies in the core QD bulk was evidenced by the decreased relative intensity of non-radiative unpaired electrons, measured by electron spin resonance (ESR). Additionally, the inhibition of InPO4(H2O)2 formation at the core QD and shell interface was confirmed by the absence of the {210} X-ray diffraction (XRD) peak intensity for the core/multi-shell QDs. By finely tuning the doping concentration, the optimal level was achieved, ensuring maximum K-VIn- substitution, minimal K+ and I- interstitials, and maximum P-dangling bond passivation. This resulted in the smallest core QD diameter distribution and maximized optical properties. Consequently, the maximum PLQY (~97%) and minimum FWHM (~40 nm) were observed at 3% KI doping. Furthermore, the color gamut of a QD-OLED display using R-, G-, and B-QD functional color filters (i.e., ~131.1%@NTSC and ~98.2@Rec.2020) provided a nearly perfect color representation, where red-light-emitting KI-doped QDs were applied.

Impact of Intravascular Imaging-Guided Stent Optimization According to Clinical Presentation in Patients Undergoing Complex PCI.

BACKGROUND: It is unclear whether the beneficial effects of intravascular imaging-guided stent optimization vary by clinical presentation during complex percutaneous coronary intervention (PCI). OBJECTIVES: In this prespecified, stratified subgroup analysis from RENOVATE-COMPLEX-PCI (Randomized Controlled Trial of Intravascular Imaging Guidance versus Angiography-Guidance on Clinical Outcomes After Complex PCI), we sought to compare the outcomes between intravascular imaging vs angiography guidance according to clinical presentation. METHODS: Patients with complex coronary artery lesions were randomly assigned to undergo either intravascular imaging-guided PCI or angiography-guided PCI in a 2:1 ratio. The primary endpoint was target vessel failure (TVF), which is a composite of cardiac death, target vessel-related myocardial infarction, or clinically driven target vessel revascularization. RESULTS: Of 1,639 patients, 832 (50.8%) presented with acute coronary syndrome (ACS) and 807 (49.2%) with chronic coronary syndrome. During a median follow-up of 2.1 years (Q1-Q3: 1.4-3.0 years), there was no significant interaction between the treatment effect of intravascular imaging and clinical presentation (P for interaction = 0.19). Among patients with ACS, the incidences of TVF were 10.4% in the intravascular imaging group and 14.6% in the angiography group (HR: 0.74; 95% CI: 0.48-1.15; P = 0.18). Among patients with CCS, the incidences of TVF were 5.0% in the intravascular imaging group and 10.4% in the angiography group (HR: 0.46; 95% CI: 0.27-0.80; P = 0.006). Achieving stent optimization by intravascular imaging resulted in a reduced risk of TVF among patients with ACS who were randomly assigned to intravascular imaging-guided PCI for complex coronary lesions (optimized vs unoptimized, 6.5% vs 14.1%; HR: 0.49; 95% CI: 0.27-0.87; P = 0.02) but not those with CCS (5.4% vs 4.7%, HR: 1.18; 95% CI: 0.53-2.59; P = 0.69). CONCLUSIONS: No significant interaction was observed between the benefits of intravascular imaging and clinical presentation in the risk of TVF. Stent optimization by intravascular imaging was particularly important for ACS patients. (Intravascular Imaging- Versus Angiography-Guided Percutaneous Coronary Intervention For Complex Coronary Artery Disease [RENOVATE]; NCT03381872).

Predictors of Choledocholithiasis in Cholecystectomy Patients and Their Cutoff Values and Prediction Model in Korea in Comparison with the 2019 ASGE Guidelines.

Background/Aims: : In 2019, the American Society for Gastrointestinal Endoscopy (ASGE) established clinical predictors for choledocholithiasis. Our study was designed to evaluate these predictors within the Korean clinical context, establish cutoff values, and develop a predictive model. Methods: : This retrospective study analyzed patients who underwent laparoscopic cholecystectomy. The relationships between choledocholithiasis and predictors including age, blood tests, and imaging findings were assessed through univariate and multivariate logistic regression analyses. We established Korean cutoff values for these predictors and developed a scoring system for choledocholithiasis using a multivariate logistic regression. The performance of this scoring system was then compared with that of the 2019 ASGE guidelines through a receiver operating characteristic curve. Results: : We established Korean cutoff values for age (>70 years), alanine aminotransferase (>26.5 U/L), aspartate aminotransferase (>28.5 U/L), gamma-glutamyl transferase (GGT; >82.5 U/L), alkaline phosphatase (ALP; >77.5 U/L), and total bilirubin (>0.95 mg/dL). In the multivariate analysis, only age >70 years, GGT >77.5 U/L, ALP >77.5 U/L, and common bile duct dilatation remained significant. We then developed a new Korean risk stratification model from the multivariate analysis, with an area under the curve of 0.777 (95% confidence interval, 0.75 to 0.81). Our model was stratified into the low-risk, intermediate-risk, and high-risk groups with the scores being <1.0, 1.0-5.5, and >5.5, respectively. Conclusions: : Predictors of choledocholithiasis in cholecystectomy patients and their cutoff values in Korean should be adjusted and further studies are needed to develop appropriate guidelines.