Chul-Ho Kim

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder associated with a considerable disease burden. Despite the advent of biologics a substantial unmet need remains for effective treatment. We aimed to evaluate the effects of non-thermal argon plasma (NAP) in patients with mild-to-moderate AD. The Eczema Area Severity Index (EASI), Numeric Rating Scale (NRS), and Dermatology Life Quality Index (DLQI) were evaluated following AD treatment. 16 S rRNA sequencing was used to assess alterations in the skin microbiome. A mouse model of house dust mite (HDM)-induced AD was used to evaluate the effects of NAP on AD-like lesions, immune cell recruitment, and cytokine expression. Oxidative stress parameters and related molecular markers were analyzed after NAP treatment. NAP treatment led to a significant reduction in EASI, NRS, and DLQI scores compared with the sham group, reflecting an alleviation of AD symptoms and an enhancement in the quality of life. Microbiome analysis revealed significant alterations in the microbial diversity after NAP treatment. NAP ameliorated HDM-induced AD in mice, showing a decrease in epidermal thickness, immune cell recruitment, and the expression of key cytokines, particularly interleukin (IL)− 33, in keratinocytes. Furthermore, NAP treatment downregulated oxidative stress markers, corroborating the reduced IL-33 expression and underscoring the role of oxidative stress in AD pathology. Our study suggests the therapeutic potential of nonthermal plasma in the management of mild-to-moderate AD. Further extensive clinical trials are warranted to validate these findings and understand their long-term effects and implications. Trial registration : CRIS, KCT0008949, retrospectively registered on October 10, 2023, at https://cris.nih.go.kr/cris/search/detailSearch.do?seq=25713 .

Objective: Airway emergencies in patients with tracheostomies are life-threatening and may arise from tube obstruction, bleeding, or accidental decannulation owing to improper handling. We describe our institutional experience with measures to prevent accidental decannulation-related emergencies, including the inferior-based tracheal flap technique combined with peri-operative care bundles and its impact on reducing accidental decannulation-related morbidity and mortality. Methods: A retrospective review was conducted on 1485 patients who underwent open tracheostomy at Ajou University Hospital between January 2011 and February 2026. In 2015, a standardized institutional protocol, incorporating the inferior-based tracheal flap as the primary incision technique and a peri-operative care bundle, was introduced following a root-cause analysis. The cohort was divided into pre-protocol (2011–2014; n = 179) and post-protocol (2015–2026; n = 1306) periods, and a long-term-followable analytic subset (Björk flap n = 363; conventional vertical-incision n = 61) was used for per-outcome comparison. These data were integrated with prior comparative studies from the literature in a random-effects meta-analysis; six literature studies plus the institutional cohort were included in the qualitative synthesis, and those with extractable arm-specific event data contributed to the quantitative synthesis. Risk of bias was assessed with ROBINS-I and the Newcastle–Ottawa Scale, and the certainty of evidence was rated using GRADE. Pre-specified sensitivity analyses, including the Hartung–Knapp–Sidik–Jonkman adjustment, were performed. All analyses were performed in R using the metafor package. Results: Pre-protocol, accidental decannulation-related emergencies occurred one to two times per year, including at least one fatal event; post-protocol, only a single event occurred over 12 years, with no associated mortality. In the analytic subset, accidental decannulation occurred in 1/363 Björk patients (0.28%) versus 3/61 conventional patients (4.92%; odds ratio [OR] 0.05, 95% confidence interval [CI] 0.01–0.52). All six pooled meta-analytic domains were directionally favorable to the Björk flap. The primary outcome (accidental decannulation/tube displacement) did not reach statistical significance in the main analysis (pooled OR 0.44, 95% CI 0.03–5.86, p = 0.531, I² = 77%, k = 3). A pre-specified sensitivity analysis excluding İnan 2025 (the heterogeneity-driving outlier) yielded an OR of 0.12 (95% CI 0.02–0.70, p = 0.019, I² = 9%, k = 2); this result is exploratory and hypothesis-generating. Secondary outcomes, including stomal infection (OR 0.26), granulation (OR 0.15), tube blockage (OR 0.21), subcutaneous emphysema (OR 0.38), and bleeding (OR 0.59), all directionally favored the Björk flap. No tracheal stenosis or decannulation failure occurred in either arm of our cohort. Under GRADE, the certainty of evidence was very low for the primary outcome and low for the secondary outcomes. Conclusions: A standardized institutional safety bundle centered on the inferior-based tracheal flap was associated with a low rate of accidental decannulation-related emergencies and no related mortality over a 12-year post-implementation period; because the flap was introduced together with concurrent peri-operative and nursing changes, its independent contribution cannot be isolated. Meta-analytic synthesis showed directionally favorable effects across all complication domains, although the primary outcome reached significance only in an exploratory sensitivity analysis and the overall certainty of evidence was low to very low. These findings are hypothesis-generating and support the inferior-based tracheal flap as a reasonable option within a structured safety bundle for elective surgical tracheostomy, particularly in patients at higher risk for accidental decannulation; prospective comparative studies are warranted.

Background: Previous attempts to classify lymphoma subtypes based on metabolic features extracted from ¹⁸F-FDG PET imaging have been hindered by inconsistencies in imaging protocols, scanner types, and inter-institutional variability. To overcome these limitations, we propose a multimodal deep learning framework that integrates harmonized PET imaging features with structured clinical information. The proposed framework is designed to perform hierarchical classification of clinically meaningful lymphoma subtypes through two sequential binary classification tasks. Methods: We collected multi-center data comprising ¹⁸F-FDG PET images and structured clinical variables of patients with lymphoma. To mitigate domain shifts caused by different scanner manufacturers, we integrated a Scanner-Conditioned Normalization (SCN) module, which adaptively harmonizes feature distributions using manufacturer-specific parameters. Performance was validated using internal and external cohorts, with the statistical significance of performance gains assessed via DeLong’s test and bootstrap-based CI analysis. Results: The proposed model achieved an area under the curve (AUC) of 0.89 (internal) and 0.84 (external) for Hodgkin lymphoma versus non-Hodgkin lymphoma classification and 0.84 (internal) and 0.76 (external) for diffuse large B-cell lymphoma versus follicular lymphoma classification (p > 0.05). These results were obtained using a multimodal model that integrated anterior and lateral maximum intensity projection (MIP) images with clinical data. Conclusions: This study demonstrates the potential of a deep learning-based approach for lymphoma subtype classification using non-invasive ¹⁸F-FDG PET imaging combined with clinical data. While further validation in larger, more diverse cohorts is necessary to address the challenges of rare subtypes and biological heterogeneity, LymphoMAP serves as a meaningful step toward developing assistive tools for early clinical decision-making. These findings underscore the feasibility of using automated pipelines to support, rather than replace, conventional diagnostic workflows in personalized lymphoma management.

Yeou SH, et al. Yonsei Med J. 2026 ;67:e73. https://doi.org/10.3349/ymj.2026.0092

This study investigated the intraoral applicability of plasma-activated water (PAW) by evaluating its antibacterial efficacy, cytotoxicity, and effects on

Anaplastic thyroid cancer (ATC) is an aggressive cancer with a poor prognosis and resistance to multimodal treatments. Various drugs have a short response time and are likely ineffective against ATC. Therefore, new molecular therapies and novel targets are needed. Recently, plasma medicine has been used in biomedical applications on skin, wound healing, and cancer treatment of the liver, colon, and head and neck. However, direct plasma has difficulty treating, sustaining, and permeating the various affected areas. In this study, we prepared Liquid-type plasma (LP) and investigated their effect on ATC cells. The physicochemical properties and ion composition of liquid-type plasma (LP) were analyzed using ion chromatography, after which anaplastic thyroid cancer (ATC) cell lines, primary fibroblasts, and keratinocytes were employed to evaluate its biological effects. Cell viability, apoptosis/pyroptosis, and redox status were assessed by biochemical assays, flow cytometry, and Western blotting, while transcriptomic profiling (RNA-seq) with gene ontology analysis was performed to identify regulated pathways. Finally, an orthotopic ATC xenograft mouse model was used to validate the therapeutic efficacy of LP in vivo. The pH of LP decreased to 1.92 And remained stable for 14 days, while electrical conductivity was measured at 4.76 mS/cm without significant Change. Additionally, the oxidation-reduction potential was maintained at 652.2 mV for 14 days. Cl, NO2, and NO3 Anions were identified as 62 ppb, 12.6 ppm, And 1044 ppm, respectively, And Na, K, And Ca cations were measured as 169 ppb, 27 ppb, And 25 ppb, respectively. Therefore, a significant concentration of nitrogen species is involved in the LP, which is attributed to the secondary reaction of reactive oxygen species (ROS) formed during this treatment. LP reduced ATC cell viability, which exhibited cell swelling and bubble formation morphologically. Gasdermin E (GSDME) was cleaved by LP and induced pyroptosis in ATC cells. Inhibiting caspase activity and knock down of GSDME showed reduced caspase-3 dependent cleavage of GSDME, consequently increasing cell viability and decreasing lactate dehydrogenase release. LP enhanced the production of intracellular RONS and induced phosphorylation of IRE1α that is associated with endoplasmic reticulum (ER) stress. Therefore, GSDME-mediated LP induced pyroptosis downstream of the RONS/ER stress pathway and activated caspase-3. We then confirmed tumor shrinkage through in vivo and histological analysis, with a focus on the increasing GSDME-N terminal. LP induces pyroptosis via GSDME activation and RONS generation in vitro and in vivo in ATC models, suggesting a novel mechanism and indicating a potential chemotherapeutic approach for the treatment of ATC. - Liquid-type plasma (LP) characteristics: LP exhibited stable physicochemical properties, including a pH of 1.92, electrical conductivity of 4.76 mS/cm, and oxidation-reduction potential (ORP) of 652.2 mV, with sustained active ion presence for 14 days. - Ion composition: Ion chromatography identified high concentrations of nitrogen species, suggesting the involvement of reactive oxygen and nitrogen species (RONS) in LP’s effects. - Pyroptosis induction in ATC cells: LP reduced ATC cell viability by cleaving Gasdermin E (GSDME), leading to pyroptosis via caspase-3 activation, which was RONS/ER stress-dependent. - Orthotopic in vivo efficacy: LP treatment resulted in tumor shrinkage and increased GSDME-N expression, highlighting its potential as a novel chemotherapeutic approach for anaplastic thyroid cancer.

Background: Several types of regulated cell deaths are known, including apoptosis, necroptosis, autophagy, ferroptosis, and pyroptosis. Among these types of cell deaths, apoptosis is induced by many cancer therapeutic agents. In the case of resistance, however, induction of other regulated cell death, such as necroptosis, are required. Liquid plasma, which is prepared by treatment of non-thermal plasma to solution, induces various types of regulated cell death via reactive oxygen and nitrogen species. Methods: Liquid plasma was generated by N2/Ar plasma treatment in culture medium (minimum essential medium (MEM), Dulbecco’s modified Eagle medium (DMEM), or Roswell Park Memorial Institute (RPMI)-1640) for 120 s per milliliter of medium (2 cm). Cell viability was determined using Cell Counting Kit-8 (CCK8), and apoptosis was determined by terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assay. Tumor necrosis factor alpha (TNF-α), cycloheximide (CHX), and zVAD-fmk were used to induce necroptosis in head and neck squamous cell carcinoma (HNSCC) cells, and necroptosis inhibitors, such as necrostatin-1 (Nec-1, 50 µM), GSK872 (10 µM), and necrosulfonamide (NSA, 2 µM) were used to inhibit necroptosis. Statistical comparisons between groups were carried out using the Student’s t-test. Results: Here, we determined the type of cell death induced by liquid plasma in head and neck cancer (HNC) cells. Our results show that liquid plasma caused necroptosis in HNC cells, and peroxynitrite in the liquid plasma might be involved in the cell death. The expression of inflammation-related molecules, including nuclear factor kappa B (NF-κB), interleukin (IL)-6, and mitochondrial antiviral signaling proteins, were detected in HNC cells, and treatment of HNC cells with liquid plasma decreased their expression. Conclusions: These results suggest that liquid plasma could be used to treat HNC by inducing necroptosis without inflammatory responses. In this study, we demonstrated that liquid plasma treatment may kill HNC cells without causing necroptosis-induced inflammation and inflammation-mediated diseases.

Supplementary Figure 1 and Legend

Head and neck squamous cell carcinoma (HNSCC) remains a clinically challenging malignancy with limited targeted therapy options and poor patient outcomes. Thus, identifying unique dependencies, including HNSCC-specific metabolic reprogramming, is imperative for improving treatment strategies for this disease. In this study, we show that HNSCC relies on elevated glucose transporter 1 (GLUT1)–mediated glucose uptake to support redox homeostasis and tumor growth. Analyses of GLUT1 expression data in tumors and cancer cell lines reveal significant upregulation of GLUT1 in HNSCC relative to both normal tissue and other cancer subtypes and that high GLUT1 expression correlates with poorer clinical outcomes. Using a basal epithelial layer–specific GLUT1-knockout mouse model, we demonstrate that GLUT1 ablation in HNSCC cells of origin markedly attenuates tumor initiation and progression, implicating the necessity of GLUT1 in HNSCC tumorigenesis. Building on this observation, combining pharmacologic inhibition of GLUT1 with pro-oxidants such as vitamin C and auranofin induces potent cytotoxicity in vitro and in vivo, partly by precipitating oxidative stress. We further observe that insulin signaling is required to sustain glucose uptake and redox homeostasis, as insulin receptor knockdown decreases proliferation and increases reactive oxygen species levels. Together, these results suggest that although GLUT1 overexpression is a key driver of glucose uptake, insulin signaling also contributes to the metabolic and oncogenic pathways underlying HNSCC progression. Consequently, strategies that co-target GLUT1 and insulin signaling to restrict glucose flux may synergize with pro-oxidant therapies, offering a promising therapeutic avenue for HNSCC.Significance:Enhanced GLUT1 expression and oncogenic insulin signaling drive elevated glucose uptake in HNSCC, which contribute to the maintenance of redox homeostasis and tumor growth. Disrupting both glucose uptake and redox balance may offer a promising therapeutic approach.