Reliable methods for the isolation of microplastics (MPs) from human feces are essential for advancing exposure and health risk assessment. However, the cellulose-rich fecal matrix is analytically very challenging. This study evaluated two different pre-treatments in protocols for MPs isolation from fecal samples. Protocol A, involved pre-treatment with a urea/thiourea/KOH (UTS) solution, followed by a comprehensive four-step digestion process (acidic, enzymatic, alkaline, and oxidative digestion) and Protocol B, involved Schweizer's reagent (copper(II) hydroxide in ammonium hydroxide, SR) for pre-treatment, followed by the same four digestion steps. The protocol based on SR pre-treatment was further optimized. The developed protocol achieved >99.8% removal of biological matrix and a 98 +/- 3% recovery rate across five polymer standards, without interfering with polymer identification by & micro;-FTIR. The method was successfully applied to children's stool samples, detecting MPs in 7 of 14 cases with concentrations ranging from 1.18 to 7.25 items g(-)& sup1; feces. The size of the detected MPs ranged from 40 to 300 mu m. Polyethylene was the dominant polymer (56%), and fragments represented the main morphology (69%). Compared to conventional digestion workflows, the SR-based approach offers clear advantages in efficiency, reproducibility, and cost, making it well-suited for routine application in clinical and environmental health laboratories. By facilitating standardization in fecal MP analysis, this method may provide a practical tool for large-scale biomonitoring studies. Building on its established use in ASTM D8333 for water and wastewater, this is the first application of SR to cellulose-rich biological matrices.
BACKGROUND/OBJECTIVES:The co-occurrence of asthma and obesity presents a significant clinical challenge, but the underlying mechanisms remain unclear. Reduced adiponectin and vitamin D levels have been associated with both conditions, suggesting that their potential modulatory roles warrant further investigation. This study aimed to evaluate whether vitamin D and adiponectin levels differ among pediatric groups defined by their asthma and obesity status, to better characterize the metabolic and inflammatory profile of the obesityasthma phenotype. METHODS:A total of 120 participants aged 6-18 were enrolled and categorized into four groups: Asthma (n = 30), Obesity (n = 30), Asthma + Obesity (n = 30), and Control group (n = 30). All participants underwent lung function testing, anthropometric assessment and measurement of fraction of exhaled nitric oxide (FeNO). Participants were further categorized according to BMI percentiles. Adiponectin levels were measured using ELISA, while vitamin D levels were detected using HPLC. RESULTS:Vitamin D levels and lung function parameters did not differ across groups, although deficiency was most prevalent in the obesity group. FeNO was elevated in asthmatics relative to obese children (p = 0.038) and in obese asthmatics compared with both controls (p = 0.040) and obese children (p = 0.021). Adiponectin levels were lower in obese asthmatic children compared to the controls (p = 0.024). A similar difference was observed between the controls and obese asthmatics among children with low vitamin D levels (p = 0.014). CONCLUSIONS:The dominant mechanisms underlying the obesity-asthma phenotype remain unclear; however, our findings indicate a link between adiponectin dysregulation and heightened airway inflammation, as evidenced by increased FeNO levels, though the precise pathways involved are still not well-understood. The role of vitamin D appears less consistent. These results highlight the need for further research to clarify the interplay between metabolic and inflammatory pathways and to support more personalized management strategies in children with obesity-related asthma.
Abstract Glycosylation is a key structural modification of immunoglobulin G (IgG) that modulates its effector functions and has multiple roles in balancing inflammation. Altered IgG glycosylation has been reported in many diseases, often years before clinical manifestation, suggesting its causal role and biomarker potential. Here, we analyzed IgG glycome composition in 20,405 individuals from 42 different studies processed at the Genos Glycoscience Research Laboratory between 2008 and 2025. Across nearly all diseases, specific IgG glycome profiles reflected accelerated biological aging. Accelerated glycan aging was strongly associated with increased risk of all-cause mortality, independent of established clinical risk factors and potential confounders. Moreover, interventions known to reduce mortality risk, including hormone replacement therapy, therapeutic plasma exchange and caloric restriction, were associated with reversal of glycan aging. Given their role in modulating low-grade systemic inflammation, IgG glycans may represent a functional link between chronic inflammation, aging, disease susceptibility and all-cause mortality.
BACKGROUND:T2 low asthma in children is an emerging yet underexplored endotype that challenges traditional views of type 2 inflammation. Recent data suggest that it is more prevalent than previously thought and is defined by low type 2 biomarkers, non-allergic clinical profiles, and strong associations with modifiable comorbidities such as obesity, passive smoke exposure, and recurrent respiratory infections. This phenotype often shows a poor response to standard inhaled corticosteroid therapy and T2-targeted biologics, underscoring the urgent need for improved diagnostic and therapeutic approaches. METHODS:This narrative review conducted a literature search from PubMed and WoS databases (2020-2025), focusing on T2-low asthma defined by low blood eosinophils (<150-300/µL), FeNO (<20-25 ppb), and absent atopy in children under 18. RESULTS:This review highlights the heterogeneity of T2-low asthma, including subtypes from neutrophilic/Th 17-high to paucigranulocytic airway remodeling and metabolic driven forms, as well as diagnostic challenges from biomarker supresssion by high-dose therapies. Pragmatic phenotyping algorithms using routine tests enable identification, directing comorbidity management over ineffective biologics. CONCLUSIONS:Systematic T2-low phenotyping in pediatric practice, alongside prospective studies and non-T2 therapy trials, promises precision medicine to enhance outcomes for these children, moving beyond eosinophil-centric care.
