Background: The design of intensive care units (ICUs) is increasingly acknowledged as a crucial factor affecting patient outcomes. Transitioning from multi-bed patient rooms (MPRs) to single-bed patient rooms (SPRs) aims to improve infection control, patient privacy, and quality of care. However, concerns remain regarding potential patient isolation and reduced staff situational awareness. This study aims to evaluate clinical outcomes in SPR-structured ICUs compared to mixed SPR and MPR ICUs. Methods: This multicenter retrospective cohort study was conducted across three university-affiliated tertiary hospitals between April 2022 and August 2023. The study population included ICU patients aged ≥18 years, excluding those admitted to cardiac and neonatal ICUs. Outcomes assessed included ICU mortality and severity scores based on Simplified Acute Physiology Score 3 and Acute Physiology and Chronic Health Evaluation II scores. Results: This study included 3,179 ICU patients across three sites: site A consisted exclusively of SPRs, while sites B and C had mixed SPR and MPR arrangements. ICU mortality rates were 8.3%, 15.2%, and 9.7% for sites A, B, and C, respectively (P<0.001). Propensity score matching and logistic regression analysis demonstrated that SPRs were associated with significantly reduced ICU mortality (adjusted odds ratio, 0.54; 95% CI, 0.40–0.73). Conclusions SPRs were associated with a protective effect, reducing ICU mortality. Clinical outcomes in ICUs appear to be influenced by structural design improvements alongside other clinical factors.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particular risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of environmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves (EMWs), tobacco and other noxious substances, heavy metals, and microplastics, is linked to damage to the nervous and immune systems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately exposed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins present in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair thetional development in children’s environmental health was the Declaration of the Environment Leaders of the Eight on Children’s Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children’s environmental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Metabolic abnormalities in the liver are closely associated with diverse metabolic diseases such as non-alcoholic fatty liver disease, type 2 diabetes, and obesity. The aim of this study was to evaluate the ameliorating effect of robinetin (RBN) on the significant pathogenic features of metabolic failure in the liver and to identify the underlying molecular mechanism. RBN significantly decreased triglyceride (TG) accumulation by downregulating lipogenesis-related transcription factors in AML-12 murine hepatocyte cell line. In addition, mice fed with Western diet (WD) containing 0.025% or 0.05% RBN showed reduced liver mass and lipid droplet size, as well as improved plasma insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) values.CD38 was identified as a target of RBN using the BioAssay database, and its expression was increased in OPA-treated AML-12 cells and liver tissues of WD-fed mice. Furthermore, RBN elicited these effects through its anti-histone acetyltransferase (HAT) activity. Computational simulation revealed that RBN can dock into the HAT domain pocket of p300, a histone acetyltransferase, which leads to the abrogation of its catalytic activity. Additionally, knock-down of p300 using siRNA reduced CD38 expression.The chromatin immunoprecipitation (ChIP) assay showed that p300 occupancy on the promoter region of CD38 was significantly decreased, and H3K9 acetylation levels were diminished in lipid-accumulated AML-12 cells treated with RBN. RBN improves the pathogenic features of metabolic failure by suppressing the p300–CD38 axis through its anti-HAT activity, which suggests that RBN can be used as a new phytoceutical candidate for preventing or improving this condition.

Purpose: BVAC-B is an autologous B cell– and monocyte-based immunotherapeutic vaccine that contains cells transfected with a recombinant human epidermal growth factor receptor 2 (HER2) gene and loaded with the natural killer T cell ligand alpha-galactosylceramide. Here, we report the first BVAC-B study in patients with HER2-positive advanced gastric cancer. Materials and Methods: Patients with advanced gastric cancer refractory to standard treatment with HER2+ immunohistochemistry ≥ 1 were eligible for treatment. Patients were administered low (2.5×107 cells/dose), medium (5.0×107 cells/dose), or high dose (1.0×108 cells/dose) of BVAC-B intravenously four times every 4 weeks. Primary endpoints included safety and maximum tolerated BVAC-B dose. Secondary endpoints included preliminary clinical efficacy and BVAC-B-induced immune responses. Results: Eight patients were treated with BVAC-B at low (n=1), medium (n=1), and high doses (n=6). No dose-limiting toxicity was observed, while treatment-related adverse events (TRAEs) were observed in patients treated with medium and high doses. The most common TRAEs were grade 1 (n=2) and grade 2 (n=2) fever. Out of the six patients treated with high-dose BVAC-B, three had stable disease with no response. Interferon gamma, tumor necrosis factor-α, and interleukin-6 increased after BVAC-B treatment in all patients with medium and high dose, and HER2-specific antibody was detected in some patients. Conclusion BVAC-B monotherapy had a safe toxicity profile with limited clinical activity; however, it activated immune cells in heavily pretreated patients with HER2-positive gastric cancer. Earlier treatment with BVAC-B and combination therapy is warranted for evaluation of clinical efficacy.

Purpose: Varlitinib is a pan-human epidermal growth factor receptor (HER) inhibitor targeting epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), and HER4. We present a phase Ib/II study of a combination of varlitinib and weekly paclitaxel as a second-line treatment for patients with EGFR/HER2 co-expressing advanced gastric cancer (AGC). Materials and Methods: Patients whose tumors with EGFR and HER2 overexpression by immunohistochemistry (≥ 1+) were enrolled. Varlitinib and paclitaxel were investigated every 4 weeks. After determining the recommended phase II dose (RP2D) in phase Ib, a phase II study was conducted to evaluate the antitumor activity. Results: RP2D was treated with a combination of varlitinib (300 mg twice daily) and paclitaxel. Among 27 patients treated with RP2D, the median progression-free survival and overall survival (OS) were 3.3 months (95% confidence interval [CI], 1.7 to 4.9) and 7.9 months (95% CI, 5.0 to 10.8), respectively, with a median follow-up of 15.7 months. Among 16 patients with measurable disease, the objective response rate (ORR) and disease control rate were 31% and 88%, respectively. Patients with strong HER2 expression (n=8) had a higher ORR and longer OS, whereas those with strong EGFR expression (n=3) had poorer outcomes. The most common adverse events (AEs) of any grade were neutropenia (52%), diarrhea (27%), aspartate aminotransferase/alanine transaminase elevation (22%), and nausea (19%). No treatment-related deaths or unexpected AEs resulting from treatment cessation were observed in patients with RP2D. Conclusion A combination of varlitinib and paclitaxel displayed manageable toxicity and modest antitumor activity in patients with EGFR/HER2 co-expressing AGC who progressed after first-line chemotherapy.

Background: The Korean Endocrine Hormone Reference Standard Data Center (KEHRS DC) has created reference standards (RSs) for endocrine hormones since 2020. This study is the first of its kind, wherein the KEHRS DC established RSs for serum Cpeptide levels in a healthy Korean population. Methods: Healthy Korean adults were recruited from May 2021 to September 2023. After excluding participants according to our criteria, serum samples were collected; each participant could then choose between fasting glucose only or fasting glucose plus an oral glucose tolerance test (OGTT). If their sample showed high glucose (≥100 mg/dL) or hemoglobin A1c (HbA1c) (≥5.70%), their C-peptide levels were excluded from analyzing the RSs. Results: A total of 1,532 participants were recruited; however, only the data of 1,050 participants were analyzed after excluding those whose samples showed hyperglycemia or high HbA1c. Post-30-minute OGTT data from 342 subjects and post-120-minute OGTT data from 351 subjects were used. The means±2 standard deviations and expanded uncertainties of fasting, post-30-minute and 120-minute OGTT C-peptide levels were 1.26±0.82 and 0.34–3.18, 4.74±3.57 and 1.14–8.33, and 4.85±3.58 and 1.25–8.34 ng/mL, respectively. Serum C-peptide levels correlated with obesity, serum glucose levels, and HbA1c levels. Conclusion The RSs for serum C-peptide levels established in this study are expected to be useful in both clinical and related fields.

Background/Aims: This study aimed to assess whether hepatocellular carcinoma (HCC) patients with portal vein tumor thrombosis (PVTT) could have favorable prognoses with proper treatment under selective conditions. Methods: This retrospective, single-center study involved 1,168 patients diagnosed with HCC between January 2005 and December 2006, before the introduction of sorafenib. Overall survival (OS) was estimated using the Kaplan-Meier method, and the Cox proportional hazards model was used to identify and adjust the variables associated with OS. Results: In nodular-type HCC, the OS differed significantly according to the presence of PVTT (log-rank p<0.001), and the level of PVTT, not only its presence, was a major independent factor affecting OS. PVTT at the Vp1-3 branch was associated with significantly longer OS than was PVTT at the Vp4 level (hazard ratio [HR], 1.82; 95% confidence interval [CI], 1.04 to 3.21). In multivariate analysis, the OS was further stratified according to the PVTT level and tumor type, representing that nodular HCC without PVTT exhibited the best OS, whereas nodular HCC with Vp4 PVTT (adjusted HR, 2.59; 95% CI, 1.57 to 4.28) showed a poor prognosis similar to that of infiltrative HCC. The PVTT level was consistently correlated with OS in patients treated with transarterial chemoembolization. Nodular HCC without PVTT showed the best prognosis, while nodular HCC with Vp1-3 PVTT also exhibited a favorable OS, although inferior to that without PVTT (adjusted HR, 1.47, 95% CI, 0.92 to 2.36). Conclusions Active treatment such as transarterial chemoembolization can be considered for selected PVTT cases. The level of PVTT and type of HCC were independent prognostic factors.