Purpose: Asthma is characterized by chronic type 2/eosinophilic inflammation in the airway mucosa. This study aimed to explore the clinical value of 2 cutoffs of blood eosinophil counts (≥ 300/μL and ≥ 150/μL) in eosinophilic asthma, with relation to eosinophilderived neurotoxin (EDN), a surrogate marker of eosinophilic activity. Methods: To compare clinical features and eosinophil-related mediators according to 2 cutoffs of peripheral blood eosinophil counts (≥ 300/μL and ≥ 150/μL), 137 adult asthmatics who had maintained antiasthmatic medications, including inhaled corticosteroid and long-acting beta 2 agonist, without biologics, were enrolled. EDN levels in serum, urine and sputum were measured by enzymelinked immunosorbent assay. Results: Patients with asthma and higher blood eosinophil counts ( ≥ 300/μL) had a higher prevalence of severe asthma, chronic rhinosinusitis, partly controlled/uncontrolled status, and higher levels of sputum eosinophils and EDN in serum/sputum than those with lower blood eosinophil counts (< 300/μL). When compared between patients with asthma having higher blood eosinophils ( ≥ 150/μL) and those with lower eosinophils ( < 150/μL), there were no differences in symptom severity, control status or lung function parameters. Conclusion These findings suggest that blood eosinophil count ≥ 300/μL may identify asthma patients at higher risk for severity and heightened eosinophil activity, supporting its utility as a biomarker in a real clinical setting.

Background: Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli is among the most important multidrug-resistant pathogens causing bloodstream infections (BSIs).Cefotaximase (CTX-M) enzymes are the most common and highly diverse ESBL family in E.coli. CTX-M-15 in group CTX-M-1 and CTX-M-14 in group CTX-M-9 are the most extensively disseminated enzymes. Multidrug-resistant E. coli strains complicate empirical therapy and increase healthcare burden globally and in Korea. We investigated the molecular epidemiology, sequence types (STs), and ESBL genotypes of E. coli bloodstream isolates in Korea and identified clinical risk factors for cefotaxime resistance. Methods: We collected all non-duplicated isolates of E. coli and related clinical information from patients with BSIs at eight sentinel hospitals in the Korean Global Antimicrobial Resistance Surveillance System (Kor-GLASS) collection network during 2017–2021. Duplicate isolates were removed to ensure representativeness of the data. Antimicrobial susceptibility was tested using disk diffusion tests, and multilocus sequence typing and betalactamase genotyping were performed. Results: Among 9,232 E. coli blood isolates, resistance rates to cefotaxime and ceftazidime were 36.4% and 11.4%, respectively. Among the clinical factors, age > 65 yrs (adjusted odds ratio [aOR], 1.36), hospital-origin infection (aOR, 2.55), and admission type (intensive care unit [ICU] vs. general ward; aOR, 1.34) were significant cefotaxime resistance risk factors. ST131 was the most prevalent among cefotaxime-resistant E. coli (64.8%, 2,180/3,363), followed by ST1193 (5.3%, N = 177), and ST69 (5.1%, N = 170).ST131, ST648, ST405, and ST410 cefotaxime-resistant E. coli isolates frequently harbored blaCTX-M-15, whereas ST1193 and ST68 showed a high proportion of blaCTX-M-27 carriers, and most ST457 and ST5150 isolates carried blaCTX-M-55. Conclusions Continuous monitoring of ESBL-producing E. coli is required to prevent further dissemination, guide empirical therapy, inform infection control policies, and ensure early detection of multidrug-resistant clones with the potential for widespread transmission.

Background: Precision oncology is advancing, increasing the demand for comprehensive, non-invasive genomic profiling tools. Liquid biopsy using circulating tumor DNA (ctDNA) enables real-time molecular profiling, treatment monitoring, and early detection of resistance variants. We developed the PAN100 panel (Dxome), a hybridization capture panel targeting 101 genes, as a pan-cancer genotyping assay to detect clinically actionable variants across various cancer types. This study presents the first comprehensive validation of the PAN100 panel including both analytical and clinical performance across eight cancer types using reference materials and matched tissue samples. Methods: For analytical validation, we assessed accuracy, limit of detection (LoD), and precision using Seraseq ctDNA v2 Reference Materials (SeraCare, Milford, MA, USA). Clinical validation was performed using plasma samples from 27 patients with eight types of cancer and 17 matched tumor samples. Positive percent agreement (PPA) between ctDNA and tissue next-generation sequencing (NGS) results was assessed using TruSight Oncology 500 and TruSight Tumor 170 assays. The limit of blank (LoB) was evaluated in 34 healthy individuals. Results: The PAN100 panel demonstrated high precision and linearity (LoD, 0.3%; 95.0% confidence interval, 0.29–0.35) variant allele frequency. The PPA between ctDNA and tissue NGS was 73.1% for single-nucleotide variants, 80.0% for insertions/deletions, and 74.2% overall. The LoB was 0.00001%. Conclusions The PAN100 panel is a robust tool for detecting clinically significant variants with high concordance with tissue NGS. Its sensitivity for low-frequency variants enables real-time treatment adaptation, supporting precision oncology. Its comprehensive design is particularly valuable for challenging diagnoses and clonal evolution monitoring.

Background/Aims: Spinal cord injury (SCI) frequently impairs defecation, severely affecting the quality of life. This study examines compensatory neural remodeling after SCI, focusing on basal colonic contractility, neural responses to electrical field stimulation, and alterations in excitatory cholinergic and inhibitory nitrergic pathways. Methods: Female Sprague–Dawley rats underwent either sham surgery or T10 spinal cord transection and were categorized into 3 groups: sham, 1-week post-SCI (acute), and 4-week post-SCI (chronic). Colonic contractility was assessed in an organ bath using electrical field stimulation in the presence of a nitric oxide synthase inhibitor. Neural protein expression was analyzed by immunofluorescence and Western blotting. Results: SCI produced region- and time-dependent impairments in colonic contractility, with distinct alterations in the proximal circular and longitudinal muscles across acute and chronic phases. Neural excitability shifted dynamically, showing enhanced excitatory activity in the proximal longitudinal muscle at 1-week and the distal circular muscle at 4-week post-SCI. Protein analysis revealed increased neuronal nitric oxide synthase in the proximal colon, decreasedsoluble guanylyl cyclase in the distal colon, upregulated muscarinic M3 receptor in the proximal colon, and reduced vaso-active intestinal peptide receptor 1 in both proximal and distal regions. Conclusion SCI induces spatiotemporal remodeling of excitatory and inhibitory neural pathways, contributing to colonic dysmotility and revealing potential targets for therapeutic intervention.

Purpose: This study evaluates the Korean Cancer Study Group Geriatric Score-7 (KG-7) frailty screening tool’s effectiveness in elderly multiple myeloma (MM) patients to prevent under and overtreatment. Materials and Methods: This prospective pilot cohort study included 100 elderly patients aged 70 and older with newly diagnosed MM who had not undergone transplantation from August 2020 to January 2022. Results: The median age was 77 years, and 73.0% of patients were classified at International Staging System stages 2 or 3. Using a 5-point cutoff on the KG-7 index (non-frail, score ≥ 5; frail, score < 5), 31% were categorized as frail. After a median follow-up of 26.8 months, the 3-year overall survival rate was 73.0%. There was no statistically significant association between any frailty index and the risk of death. However, frail patients defined by the simplified frailty index (hazard ratio [HR], 2.49; 95% confidence interval [CI], 1.09 to 5.95; p=0.030) and by KG-7 (HR, 2.43; 95% CI, 1.03 to 5.86; p=0.043) had a significantly higher risk of grade 3-4 non-hematologic toxicity, whereas the International Myeloma Working Group definition did not. Over a 24-month tracking period, vulnerability as measured by KG-7 either improved or deteriorated. Conclusion The pilot study, which had a limited number of participants, did not demonstrate KG-7’s effectiveness in predicting survival; however, it successfully predicted severe non-hematologic toxicities. We plan to conduct larger studies in elderly MM patients to determine whether KG-7 can help tailor their treatment regimens.

Microglial activation during aging is associated with neuroinflammation and cognitive impairment. Galectin-3 plays a crucial role in microglial activation and phagocytosis. However, the role of galectin-3 in the aged brain is not completely understood. In the present study, we investigated aging-related mechanisms and microglial galectin-3 expression in the mouse hippocampus using female 6-, 12-, and 24-month-old C57BL/6 mice. Western blot analysis revealed neurodegeneration, blood-brain barrier leakage, and increased levels of neuroinflammation-related proteins in 24-month-old mice compared to 6- and 12-month-old mice. Immunohistochemistry revealed an increase in activated microglia in the hippocampus of 24-month-old mice compared to 6- and 12-month-old mice. Furthermore, we found more galectin-3 and triggering receptor expressed on myeloid cells-2-positive microglia in 24-month-old mice compared to 6- and 12-month-old mice. Using primary mouse microglial cells, galectin -3 was also increased by lipopolysaccharide treatment. These findings suggest that galectin-3 may play an important role in microglial activation and neuroinflammation during brain aging.

Progesterone hypersensitivity is mediated by type I, III, and IV hypersensitivity reactions to endogenous or exogenous progesterone, involving autoimmune mechanisms in females of reproductive age. It presents with a range of dermatologic manifestations, most commonly urticaria, angioedema, eczema, and maculopapular rashes. Systemic and severe symptoms, such as generalized erythema multiforme or lesions resembling severe cutaneous adverse reactions, have rarely been reported. We describe a case of a 42-year-old woman who developed drug reaction with eosinophilia and systemic symptoms (DRESS) following exogenous progesterone therapy administered for assisted reproduction. She received high-dose subcutaneous progesterone and vaginal tablets. Despite this being her first procedure, she achieved pregnancy. However, at 8 weeks of gestation and during the third month of progesterone treatment, she developed generalized erythema multiforme, pruritus, and high-grade fever. Her laboratory findings showed increased blood eosinophil counts and inflammatory markers. After oral corticosteroid (OCS) treatment for several weeks, her skin lesions were partially improved. However, after tapering of OCS, her skin lesions were aggravated with increased blood eosinophil counts. Despite daily OCS (prednisolone, 12.5–60 mg/day) treatment after childbirth, her skin symptoms and eosinophilia persisted. Reslizumab treatment was also attempted, but only the eosinophilia resolved. These clinical findings were much improved after Janus kinase (JAK) inhibitor (upadacitinib 15 mg/day) treatment; consequently, OCS was stopped. Here, we report a case of relapsing DRESS triggered by exogenous progesterone, which has been controlled by JAK inhibitor treatment.

Cat-pork syndrome is an uncommon food allergy induced by red meat (pork/beef) that cross-reacts with cat/dog allergens, which is mediated by immunoglobulin E (IgE) response to the cat/dog albumin component. We report 2 cases of cat-pork syndrome occurred in adult pet breeders. They had suffered from allergic rhinitis/atopic dermatitis sensitive to cat/dog dander as well as house dust mites for several years, during which an immediate type of food allergy due to red meats developed whenever taking pork or beef. ImmunoCAP results showed the increased levels of serum-specific IgE to pork and beef allergens (f26, f27) as well as cat and dog dander (e1, e5); moreover, increased level of serum-specific IgE to the cat albumin component (e224) was noted. In conclusion, cat-food allergy can be found in allergic patients among whom are sensitive to cats and dogs and develop food allergy due to red meat.

Progesterone hypersensitivity is mediated by type I, III, and IV hypersensitivity reactions to endogenous or exogenous progesterone, involving autoimmune mechanisms in females of reproductive age. It presents with a range of dermatologic manifestations, most commonly urticaria, angioedema, eczema, and maculopapular rashes. Systemic and severe symptoms, such as generalized erythema multiforme or lesions resembling severe cutaneous adverse reactions, have rarely been reported. We describe a case of a 42-year-old woman who developed drug reaction with eosinophilia and systemic symptoms (DRESS) following exogenous progesterone therapy administered for assisted reproduction. She received high-dose subcutaneous progesterone and vaginal tablets. Despite this being her first procedure, she achieved pregnancy. However, at 8 weeks of gestation and during the third month of progesterone treatment, she developed generalized erythema multiforme, pruritus, and high-grade fever. Her laboratory findings showed increased blood eosinophil counts and inflammatory markers. After oral corticosteroid (OCS) treatment for several weeks, her skin lesions were partially improved. However, after tapering of OCS, her skin lesions were aggravated with increased blood eosinophil counts. Despite daily OCS (prednisolone, 12.5–60 mg/day) treatment after childbirth, her skin symptoms and eosinophilia persisted. Reslizumab treatment was also attempted, but only the eosinophilia resolved. These clinical findings were much improved after Janus kinase (JAK) inhibitor (upadacitinib 15 mg/day) treatment; consequently, OCS was stopped. Here, we report a case of relapsing DRESS triggered by exogenous progesterone, which has been controlled by JAK inhibitor treatment.

Cat-pork syndrome is an uncommon food allergy induced by red meat (pork/beef) that cross-reacts with cat/dog allergens, which is mediated by immunoglobulin E (IgE) response to the cat/dog albumin component. We report 2 cases of cat-pork syndrome occurred in adult pet breeders. They had suffered from allergic rhinitis/atopic dermatitis sensitive to cat/dog dander as well as house dust mites for several years, during which an immediate type of food allergy due to red meats developed whenever taking pork or beef. ImmunoCAP results showed the increased levels of serum-specific IgE to pork and beef allergens (f26, f27) as well as cat and dog dander (e1, e5); moreover, increased level of serum-specific IgE to the cat albumin component (e224) was noted. In conclusion, cat-food allergy can be found in allergic patients among whom are sensitive to cats and dogs and develop food allergy due to red meat.