Background: Handgrip strength (HGS) is an indicator of late-life health, associated with disability, cardiovascular and all-cause mortality. While exercise helps maintain HGS, diabetes may reduce its benefits. This study investigated the association between exercise and low HGS (LHGS) stratified by diabetes status and sex. Methods: Data from 16,443 participants in the 2017–2019 Korea National Health and Nutrition Examination Survey were analyzed. HGS was measured using a digital dynamometer. Exercise type and frequency were assessed by questionnaire. Three-way and twoway interaction terms were analyzed for exercise, sex and diabetes. Results: Aerobic exercise, resistance exercise, and diabetes were significantly associated with LHGS (P<0.05). A significant interaction between diabetes and aerobic exercise was observed in females (odds ratio [OR] of LHGS=1.704, 95% confidence interval= 1.073–2.707). Among males, both exercise types were associated with lower odds of LHGS regardless of diabetes status, except for aerobic exercise in non-diabetic males. Among males, the ORs of LHGS for aerobic and resistance exercise were 0.479 (0.278– 0.827) and 0.317 (0.165–0.611) with diabetes, 0.757 (0.554–1.035) and 0.536 (0.360–0.798) without diabetes. Among females, the ORs of LHGS for aerobic exercise and resistance exercise were 1.109 (0.716–1.719) and 0.529 (0.224–1.249) with diabetes, 0.676 (0.539–0.848) and 0.795 (0.564–1.121) without diabetes. Conclusions The modifying effect of diabetes on the relationship between exercise and grip strength was observed in females but not in males. Females with diabetes may require tailored exercise guideline to prevent LHGS.

Purpose: This study aimed to identify the incidence and related factors of delirium among cancer patients admitted to the general wards of a tertiary hospital. Methods: A retrospective analysis was performed on 9,749 adult cancer patients. Patients who screened positive for delirium were assessed using the Korean version of the Nursing Delirium Screening Scale (NuDESC). Data were analyzed using χ² tests, t-tests, and multiple logistic regression. Results: The incidence of delirium was 2.5% (n=243) based on screening results. Significant predictors included older age, longer hospital stays, emergency room admission, 90-day readmission, completion of life-sustaining treatment decisions, surgical department admission, altered consciousness (the strongest predictor), elevated white blood cell and blood urea nitrogen levels, and low albumin levels (p<.050).These 10 factors showed high discriminatory power for delirium (AUC=.91, 95% CI: 0.90~0.93). Conclusion The Nu-DESC should be actively utilized in clinical practice for early delirium detection. Nursing interventions must prioritize managing modifiable factors such as nutritional status, infection, and dehydration. Furthermore, case-sharing systems and regular education are essential to enhance nursing expertise and ensure patient safety.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a global health issue due to its increasing prevalence associated with lifestyle changes and its strong correlation with metabolic syndrome. Farnesoid X receptor (FXR) is a nuclear receptor that plays a pivotal role in regulating bile acid, lipid, and glucose metabolism, making it an attractive therapeutic target for liver and metabolic diseases. In this study, we investigated the effects of MHY5456, a synthetic agonist of FXR, on hepatic metabolism and fibrosis. MHY5456 enhanced the transcriptional activity of FXR in a concentration-dependent manner.Treatment of AC2F rat liver-derived cells with MHY5456 resulted in the downregulation of genes involved in lipid accumulation and an upregulation of mitochondrial-related gene expression. Additionally, MHY5456 significantly reduced oleic acid (OA)-induced lipid accumulation. To assess its anti-fibrotic potential, we tested its effects on transforming growth factor-beta (TGF-β)-induced fibrosis in LX2 human hepatic stellate cells (HSCs). MHY5456 significantly suppressed the expression of fibrosis-related genes and proteins. In vivo, administration of MHY5456 to mice fed a methionine-choline-deficient (MCD) diet alleviated hepatic fibrosis, inflammation, and lipid accumulation. These results show that FXR activation by MHY5456 modulates lipid metabolism and fibrotic pathways, suggesting its potential as a pharmacological candidate for liver and metabolic disorders, including MASLD. Further pharmacological and toxicological studies are needed to confirm its therapeutic relevance.

Objective: Perinatal depression often remains undertreated due to concerns about antidepressant exposure during fertility treatment, pregnancy, or breastfeeding. Non-pharmacological, home-based interventions such as transcranial direct current stimulation (tDCS) present a promising alternative; however, real-world evidence in perinatal populations remains limited. Methods: This prospective observational study included 38 women who received infertility, pregnancy, or postpartum treatment at four hospitals in South Korea. Participants self-administered anodal tDCS targeting the left dorsolateral prefrontal cortex for 20–28 sessions over 4 weeks. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale (CES-D) at baseline and weeks 2, 4, and 8. Subjective health perception was measured at baseline using a 5-point Likert scale. Results: Time had a significant effect on depressive symptoms (Wald χ2=90.75, p<0.001), with the largest reduction observed during the first 2 weeks. The CES-D scores remained significantly lower than baseline at week 8, 4 weeks after treatment ended. Subjective health perception was significantly associated with baseline depression severity (Wald χ2=26.41, p<0.001), and its interaction with time was also significant (Wald χ2=320.18, p<0.001). Participants with poorer perceived health (scores 4–5) experienced greater depressive symptom reductions than those with more favorable perceptions (scores 1–2). Conclusion Home-based tDCS was feasible and associated with clinically meaningful improvement in depressive symptoms among perinatal women. Those who initially perceived their health more negatively showed greater response, suggesting subjective health perception may serve as a useful moderator and potential marker to inform personalized treatment strategies.

Objectives: This study aimed to investigate the impact of coronavirus disease 2019 (COVID-19) on admission rates and in-hospital mortality among patients with ischemic and hemorrhagic stroke. Methods: We constructed a dataset detailing the monthly hospitalizations and mortality rates of inpatients with stroke from January 2017 to December 2021. Employing an interrupted time series analysis, we explored the impact of COVID-19 on hospitalizations and 30-day in-hospital mortality among stroke patients. Results: The number of ischemic stroke admissions decreased by 18.5%, from 5335 to 4348, immediately following the COVID-19 outbreak (p<0.001). The in-hospital mortality rate for ischemic stroke increased slightly from 3.3% to 3.4% immediately after the outbreak, although it showed a decreasing trend over time. The number of hemorrhagic stroke admissions fell by 7.5%, from 2014 to 1864, immediately following the COVID-19 outbreak. The 30-day in-hospital mortality rate for hemorrhagic stroke initially decreased from 12.9% to 12.7%, but subsequently showed an increasing trend. Conclusions We confirmed that COVID-19 impacted both the admission and death rates of stroke patients. The admission rate for both ischemic and hemorrhagic strokes decreased, while in-hospital mortality increased. Specifically, in-hospital mortality from ischemic stroke rose initially after the outbreak before stabilizing. Additionally, our findings indicate variable effects based on sex, age, and socioeconomic status, suggesting that certain groups may be more susceptible. This underscores the need to identify and support vulnerable populations to mitigate adverse health outcomes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.

Background: The accuracy of Logical Observation Identifiers Names and Codes (LOINC) mappings is reportedly low, and the LOINC codes used for research purposes in Korea have not been validated for accuracy or usability. Our study aimed to evaluate the discrepancies and similarities in interoperability using existing LOINC mappings in actual patient care settings. Methods: We collected data on local test codes and their corresponding LOINC mappings from seven university hospitals. Our analysis focused on laboratory tests that are frequently requested, excluding clinical microbiology and molecular tests. Codes from nationwide proficiency tests served as intermediary benchmarks for comparison. A research team, comprising clinical pathologists and terminology experts, utilized the LOINC manual to reach a consensus on determining the most suitable LOINC codes. Results: A total of 235 LOINC codes were designated as optimal codes for 162 frequent tests.Among these, 51 test items, including 34 urine tests, required multiple optimal LOINC codes, primarily due to unnoted properties such as whether the test was quantitative or qualitative, or differences in measurement units. We analyzed 962 LOINC codes linked to 162 tests across seven institutions, discovering that 792 (82.3%) of these codes were consistent. Inconsistencies were most common in the analyte component (38 inconsistencies, 33.3%), followed by the method (33 inconsistencies, 28.9%), and properties (13 inconsistencies, 11.4%). Conclusion This study reveals a significant inconsistency rate of over 15% in LOINC mappings utilized for research purposes in university hospitals, underlining the necessity for expert verification to enhance interoperability in real patient care.

Objectives: This study aimed to investigate the impact of coronavirus disease 2019 (COVID-19) on admission rates and in-hospital mortality among patients with ischemic and hemorrhagic stroke. Methods: We constructed a dataset detailing the monthly hospitalizations and mortality rates of inpatients with stroke from January 2017 to December 2021. Employing an interrupted time series analysis, we explored the impact of COVID-19 on hospitalizations and 30-day in-hospital mortality among stroke patients. Results: The number of ischemic stroke admissions decreased by 18.5%, from 5335 to 4348, immediately following the COVID-19 outbreak (p<0.001). The in-hospital mortality rate for ischemic stroke increased slightly from 3.3% to 3.4% immediately after the outbreak, although it showed a decreasing trend over time. The number of hemorrhagic stroke admissions fell by 7.5%, from 2014 to 1864, immediately following the COVID-19 outbreak. The 30-day in-hospital mortality rate for hemorrhagic stroke initially decreased from 12.9% to 12.7%, but subsequently showed an increasing trend. Conclusions We confirmed that COVID-19 impacted both the admission and death rates of stroke patients. The admission rate for both ischemic and hemorrhagic strokes decreased, while in-hospital mortality increased. Specifically, in-hospital mortality from ischemic stroke rose initially after the outbreak before stabilizing. Additionally, our findings indicate variable effects based on sex, age, and socioeconomic status, suggesting that certain groups may be more susceptible. This underscores the need to identify and support vulnerable populations to mitigate adverse health outcomes.

Recent studies have shown an increased abundance of Sphingomonas paucimobilis, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that S. paucimobilis is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of S. paucimobilis-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that Spa-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by SpaEV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, Spa-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of Spa-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that Spa-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.