Search Results (23,582)

Background/Objectives: The Nutrition Care Process (NCP) is a standardized model designed to improve the quality and consistency of nutrition care. However, its implementation remains variable across settings, influenced by factors such as time constraints, training, peer support, and technological infrastructure. This systematic review aims to synthesize the available evidence on barriers and facilitators influencing the implementation of the NCP/NCPT and to explore how different documentation formats may influence its adoption. Methods: This systematic review was conducted in accordance with PRISMA 2020 guidelines and included peer-reviewed studies published between 2009 and 2024 in English or Greek. Searches were conducted in MEDLINE, EMBASE, Scopus, CINAHL, and the Cochrane Library. Study quality was assessed using the National Heart, Lung, and Blood Institute (NIH) tool. A total of 11 reports representing eight studies were included, comprising cross-sectional, cohort, qualitative, and pilot designs. Results: The most commonly reported barriers to NCP implementation were lack of training, time constraints, and limited technological infrastructure. Key facilitators included support from national dietetic associations, peer collaboration, and access to electronic health records (EHRs). Electronic formats were more frequently described as supporting improved documentation practices, practitioner confidence, and workflow efficiency, whereas manual approaches were commonly reported as time-consuming and less structured. Conclusions: Digital integration of the NCP may support more consistent documentation practices and improved workflow processes; however, the current evidence is largely observational and heterogeneous. Evidence regarding patient-level outcomes remains limited, and definitive conclusions regarding the comparative effectiveness of implementation formats cannot be drawn. Further high-quality research is needed to evaluate the long-term clinical impact of NCP implementation. Full article

Background/Objectives: Effective cardiovascular prevention requires improved risk perception and appropriate communication strategies that support cost-effective interventions. This study evaluated one-year changes in cardiovascular risk estimation accuracy and examined associations between communication strategies, accuracy, and health outcomes. Methods: We analyzed 200 participants (mean age: 56.06 ± 6.26; 32.2% male) in a population-based study conducted in Hungary. Cardiovascular risk was calculated using the Framingham Risk Score based on laboratory and anthropometric measures, and subjective risk perception was assessed and categorized as realistic, optimistic, or pessimistic relative to objective risk. All participants received written risk feedback, while subgroups additionally participated in individual or group-based risk communication. Results: After 12 months, the proportion of participants with accurate risk perception increased from 39.0% to 50.5% (p = 0.012), accompanied by a significant reduction in pessimistic estimations (p = 0.013). We could not observe significant differences in estimation accuracy between communication strategies. The written-only communication group showed a significant decrease in cardiovascular risk factors (weight (p = 0.014), BMI (p = 0.042), blood pressure (p = 0.035), and LDL levels (p = 0.001)). No significant differences were found in health outcomes between risk communication groups. Conclusions: These results demonstrate that even written-only communication may be an effective way to improve cardiovascular health outcomes, possibly by correcting risk perception gaps, suggesting that cost-effective, low-intensity communication strategies may be sufficient to support primary prevention efforts. Full article

Objective: This study aimed to assess quality of life (QoL) and its determinants among Saudi adults diagnosed with type 2 diabetes mellitus (T2DM). Methods: A cross-sectional study was conducted among 200 (45% male and 55% female) Saudi adults with T2DM aged 30–65 years. Data were collected using the Audit of Diabetes–Dependent Quality of Life (ADDQoL) and the Personal Diabetes Questionnaire (PDQ). Anthropometric and clinical measures included weight, height, body mass index (BMI), blood pressure, and glycated hemoglobin (HbA1c). Results: Most participants (73.5%) were ≤50 years of age, and the majority were obese (56.0%) or overweight (28.0%). Nearly half (54.5%) had HbA1c levels ≥ 8.0%, while (50.5%) were hypertensive. Overall, 96% of participants reported a poor to extremely poor QoL. Female sex (p = 0.003), higher BMI (p = 0.034), diet type (p = 0.039), and satisfaction with glucose control (p < 0.001) were significantly associated with the QoL. Conclusions: T2DM substantially impairs the QoL of affected Saudi adults. Psychosocial and lifestyle-related factors, particularly obesity, gender, dietary practices, and perceived glucose control, are more influential than traditional clinical markers. Culturally tailored interventions targeting these determinants may improve patient outcomes. Full article

Glucagon-like peptide (GLP)-1 receptor (GLP1R) agonists exert a multitude of beneficial cardiovascular effects beyond control of blood glucose levels and obesity reduction. GLP-1R is a G protein-coupled receptor (GPCR), coupling to adenylyl cyclase (AC)-stimulatory Gs proteins to raise cyclic 3′-5′-adenosine monophosphate (cAMP) levels in cells. cAMP exerts various effects mainly via protein kinase A (PKA) and Exchange protein directly activated by cAMP (Epac). Cardiac GLP-1R has been reported to induce atrial natriuretic peptide (ANP) secretion via Epac2, while ANP is known to inhibit aldosterone secretion from adrenocortical zona glomerulosa (AZG) cells. Herein, we tested the effects of the GLP-1R agonist liraglutide on ANP secretion in H9c2 cardiomyocytes and on angiotensin II (AngII)-induced aldosterone secretion. We also examined whether phosphodiesterase (PDE)-4 inhibition with roflumilast could potentiate liraglutide’s effects. We found that liraglutide stimulated ANP secretion from H9c2 cardiomyocytes, an effect potentiated by roflumilast but blocked by AC inhibition. Epac inhibition with ESI-09 also significantly reduced liraglutide-dependent ANP secretion in H9c2 cardiomyocytes. Moreover, application of medium from liraglutide-treated H9c2 cardiomyocytes, but not from control cardiomyocytes, led to suppression of AngII-dependent aldosterone secretion from H295R cells. This effect was blocked by cyclic guanosine monophosphate (cGMP)-dependent protein kinase inhibition (an effector of ANP) in H295R cells, while direct application of liraglutide to these cells failed to suppress AngII-induced aldosterone secretion. Again, aldosterone suppression was more potent when medium from liraglutide plus roflumilast-treated cardiomyocytes was applied to H295R cells. Taken together, these results suggest that roflumilast enhances the adrenocortical aldosterone suppression induced by GLP-1R agonists via cardiac GLP-1R/cAMP/Epac-dependent ANP secretion. Given the cardio-toxic effects of elevated aldosterone levels in the context of various heart diseases, such as post-myocardial infarction heart failure, combination of a GLP-1R agonist drug with a PDE4 inhibitor drug may be more advantageous than either agent alone in treatment of certain cardiovascular diseases. Full article

Background: Red ginseng (RG) exhibits enhanced bioactivity compared to white ginseng. Although the beneficial effects of RG have been well investigated in disease models, its impacts on the metabolome, gut microbiota, and immune response under normal physiological conditions remain poorly understood. Methods: Rats were randomized into three groups: control (normal diet), RL (low-dose RGE at 100 mg/kg body weight), and RH (high-dose RGE at 200 mg/kg body weight). After five weeks, metabolite profiles of the blood, liver, kidney, and large intestinal contents were analyzed and the gut microbiota was assessed. Splenocytes were isolated and treated with or without ethanol-precipitated carbohydrate fractions isolated from RGE or from intestinal contents, and IL-12 secretion was measured. Additionally, the correlations among biochemical characteristics, metabolites, gut microbiota, and immune markers were analyzed. Results: RGE intake decreased plasma triglycerides, liver function biomarkers, and epididymal adipose tissue weight. It also altered metabolite profiles for plasma, liver, kidney, and intestinal contents and increased the hepatic NAD⁺/NADH ratio. RGE intake reduced the populations of harmful bacteria, whereas it increased Lachnospiraceae. RGE intake enhanced IL-12 production in splenocytes. Furthermore, splenocytes treated with carbohydrates isolated from the small and large intestinal contents of RGE-fed rats secreted higher IL-12 levels than those of the control group. Conclusions: RGE modulated the gut microbiota, metabolism, and immune responses in healthy rats under normal physiological conditions, warranting further investigation into the underlying mechanisms. Full article

Background: Lymph node metastasis (LNM) is a determinant of prognosis and in guiding chemotherapy decisions in breast cancer. Herein, we aimed to discover the protease content of the circulating large extracellular vesicles (L-EVs) as potential markers for LNM. Methods: L-EVs were isolated from the plasma of chemotherapy-naïve breast cancer patients with negative LNM (nLNM, n = 40) and positive LNM (pLNM, n = 32) patients using differential centrifugation. The isolated L-EVs were characterized by Transmission Electron Microscopy, dynamic light scattering and EV marker profiling, and their protease content was profiled using unbiased proteome profiler human protease array. Results: Protease profiling uncovered that L-EVs contained significantly elevated levels of MMP-8 (p < 0.001) and MMP-9 (p < 0.05) in pLNM versus nLNM patients. Further validation by Western blotting confirmed that latent MMP-8 was significantly increased (p < 0.01) in L-EVs from pLNM patients. Interestingly, zymography revealed that L-EVs isolated from pLNM patients contained higher levels of latent MMP-9 compared with those from nLNM patients, whereas gelatinolytically active MMP-2 was only detected in L-EVs from pLNM patients and not in those from nLNM. Online datasets revealed that higher MMP-8 and MMP-9 mRNA levels were associated with poorer overall, relapse-free, and distant metastasis-free survival. Receiver operating characteristic (ROC) plotter analyses indicated that MMP-2 and MMP-8 may serve as predictive biomarkers for response to specific chemotherapeutic regimens. Conclusions: These findings highlight the potential clinical utility of L-EV-derived MMP-2, MMP-8, and MMP-9 expressions and/or activities, as non-invasive blood-based markers associated with nodal progression and therapeutic response. Full article

Background: The global healthcare system faces a significant challenge due to the escalating prevalence of type 2 diabetes, affecting over 10% of the world’s population. Suppression of postprandial hyperglycemia through inhibition of carbohydrate-hydrolyzing enzymes is an effective therapeutic strategy. Although curcumin effectively inhibits α-amylase and α-glucosidase activities, its lower solubility and bioavailability restrict its clinical application. In this study, five mono-carbonyl curcumin analogues (CA1–CA5) were synthesized and evaluated for their antidiabetic potential following selective experimental methods both in vitro, and in vivo. Enhanced delivery for the most potent analogue was achieved through PEGylated graphene oxide (PEG-GO) to overcome the shortcomings of curcumin compounds. Methods: In silico ADME profiling was conducted using SwissADME, and molecular docking studies were performed with AutoDock Vina (v1.5.7) to assess enzyme binding interaction. The synthesized compounds were further evaluated using in vitro α-amylase and α-glucosidase inhibition assays, followed by in vivo blood profile analysis. The most active analogue CA3 (chloro derivative) was loaded onto PEG-GO and characterized using UV–visible spectroscopy, Fourier-transform infrared spectroscopy, and scanning electron microscopy. Results: Among all of the compounds, CA3 exhibits the strongest binding affinity and highest enzyme inhibitory activity, followed by CA2 and CA4. PEG-GO-CA3 demonstrated significantly enhanced biological activity compared to its free form. In vivo studies showed marked improvements in body weight and lipid profile, along with significant reductions in blood glucose, glycated hemoglobin, urea, creatinine, alanine aminotransferase, and aspartate aminotransferase levels over a 28-day treatment period as compared to a diabetic control. Spectroscopic and morphological analyses confirmed successful loading of CA3 onto PEG-GO (27.7–31.5%) with a release profile of 38–57% after 12 and 36 h in a controlled environment at pH 7. Conclusions: These findings suggest that PEG-GO-loaded mono-carbonyl curcumin analogues represent promising therapeutic candidates for the management of T2DM. Full article

Interleukin-5 (IL-5) has long been positioned as a lineage-restricted cytokine primarily responsible for eosinophil differentiation and survival. However, emerging mechanistic and clinical evidence supports a broader conceptual shift: IL-5 should no longer be viewed solely as an eosinophil growth factor, but as a context-dependent regulator embedded within dynamic airway immune networks. Drawing on advances in eosinophil subset biology, receptor signaling, and tissue-level immune crosstalk, this review reframes IL-5 biology through the lens of systems-level inflammatory regulation across airway and systemic eosinophilic diseases. Recent data reveal functional heterogeneity between resident and inflammatory eosinophil subsets, challenging the assumption that blood eosinophilia uniformly reflects pathogenic activity. In parallel, functional IL-5 receptor expression has been identified on multiple structural and immune cell populations—including epithelial cells, mast cells, plasma cells, basophils, neutrophils, and fibroblasts—supporting a broader tissue-signaling paradigm. Experimental and translational studies further link IL-5 to epithelial integrity, airway remodeling, and mucus pathology, suggesting structural and network-level effects beyond simple eosinophil depletion. Comparative analyses across asthma, chronic rhinosinusitis with nasal polyps, and COPD demonstrate that eosinophilic inflammation is biologically heterogeneous and context-dependent. While IL-5-targeted therapies yield consistent benefit in severe asthma, therapeutic responses in other airway diseases appear to be shaped by local tissue architecture and mixed inflammatory programs. Together, these observations illustrate a paradigm shift from pathway-specific inhibition toward network-informed disease control and highlight key areas for future mechanistic investigation. Full article

Background: Alpha-thalassemia is one of the most common hereditary hemoglobin disorders worldwide and is caused mainly by deletions in the α-globin gene cluster. Understanding the regional mutation spectrum is important for screening programs and genetic counseling. Methods: This retrospective study included 115 patients evaluated for suspected alpha-thalassemia in Antalya, Türkiye. Molecular analysis was performed using multiplex ligation-dependent probe amplification (MLPA) to detect deletions and duplications in the α-globin gene cluster. Hematological parameters and hemoglobin (Hb) fractions were analyzed and compared among mutation groups. Results: The most frequent mutation detected was the −α^3.7 deletion followed by the (−α)^20.5 deletion. Patients with compound heterozygous deletions demonstrated lower Hb, mean corpuscular volume (MCV), and mean corpuscular hemoglobin)_(MCH) values compared with other groups. Significant correlations were observed between Hb levels and red blood cell (RBC), MCV, and MCH, while red cell distribution width (RDW) showed an inverse relationship. Conclusions: The results demonstrate that −α^3.7 and (−α)^20.5 are the predominant α-globin gene variants in the Antalya region. These findings contribute to the characterization of the α-thalassemia mutation spectrum in a clinical cohort and may help improve carrier screening strategies, prenatal diagnosis programs, and genetic counseling services. Full article

Background: Routine fundus photography is widely accessible; however, its utility in stratifying systemic vascular risk in asymptomatic, general populations remains understudied. We utilized a large-scale health screening cohort in South Korea to evaluate the clinical validity of the retinal arteriosclerosis index (RAI) in a generally healthy population. Methods: We conducted a cross-sectional study of 74,608 adults who underwent routine health screening (2003–2010) at a tertiary center. Retinal arteriosclerosis was graded (0–4) by masked readers with a modified Scheie classification; a higher eye grade was defined as a person-level grade. High-grade RAI was prespecified as ≥2. Associations with systemic conditions (hypertension, type 2 diabetes, hyperlipidemia, metabolic syndrome, cardiovascular disease, and stroke) were examined by using multivariable logistic regression adjusted for demographic, lifestyle, and laboratory covariates; moreover, analyses were stratified by age and sex. Results: High-grade RAI was present in 4.5% of the participants and increased with age. After adjustment, high-grade RAI was associated with hypertension (OR, 2.97; 95% CI, 2.73–3.23), diabetes mellitus (OR, 1.35; 95% CI, 1.22–1.50), cardiovascular disease (OR, 1.46; 95% CI, 1.25–1.71), metabolic syndrome (OR, 1.63; 95% CI, 1.49–1.78), and stroke (OR, 1.98; 95% CI, 1.41–2.79) but not with hyperlipidemia. Sex-stratified analyses revealed broadly similar patterns, although high-grade RAI was associated with stroke in women and cardiovascular disease in men. Age-stratified analyses demonstrated consistent associations with hypertension, metabolic syndrome, and stroke across all age groups, with stronger effect sizes being observed in younger individuals. With respect to lifestyle factors, frequent alcohol consumption was associated with higher odds of high-grade RAI. Laboratory correlates included higher uric acid levels and lower red blood cell, albumin, and bilirubin levels (all p < 0.001). Conclusions: Fundus-defined arteriosclerotic changes were independently associated with multiple systemic vascular and metabolic conditions. An association with stroke in adults younger than 40 years of age was also observed, although this finding should be interpreted with caution given the cross-sectional design and limited number of events. These findings support the potential role of retinal vascular changes as cross-sectional correlates of systemic vascular health. Longitudinal studies are needed to clarify temporal relationships and causality. Full article

Observing fluctuations in blood sugar during competitive events yields significant data regarding the metabolic demands placed upon athletes. This investigation sought to delineate the glycemic characteristics of top-level female soccer players throughout official matches. A total of ten elite women’s soccer players (age: 27.2 ± 3.8 years; BMI: 21.7 ± 1.5 kg/m²) from the same team had their interstitial glucose (iG) levels recorded via continuous glucose monitoring (CGM) throughout two distinct match cycles. External physical workloads were captured using global positioning systems. The athletes were categorized by their playing role, as starters or bench players, and the observation window was partitioned into four segments: night-time, pre-match, match, and post-match. Data indicated a between-subject coefficient of variation (CV) of 13% and a within-subject CV of 17%. Starting players showed elevated variability (16% between; 20% within) relative to bench players (9% and 13%). While temporal factors remained stable, playing status influenced iG significantly (F = 5.44, p = 0.006, ηp² = 0.44). Specifically, starters experienced higher iG during competition versus night (+26.5 mg/dL, p = 0.001), pre-match (+22.2 mg/dL, p = 0.002), and post-match (+25.9 mg/dL, p = 0.004). These findings suggest that CGM may assist staff in developing tailored nutritional interventions, given the wide range of individual responses found in this unexplored field. Full article

To date, we and others have demonstrated that GBA1-associated Parkinson’s disease (GBA1-PD) exhibits hyperactivation of mTOR and impairment of mTOR-regulated autophagy. Our previous study showed that the degree of autophagy impairment depends on the type of GBA1 mutation in peripheral blood mononuclear cell (PBMC)-derived macrophages. Moreover, the type of GBA1 mutation (“mild”—e.g., p.N370S or “severe”—e.g., p.L444P) correlates with PD severity and may influence therapeutic response. Here, we investigated the dose-dependent effects of GCase inhibition by conduritol β-epoxide (CBE) in SH-SY5Y cells on mTOR signaling, as well as the effects of mTOR inhibition by Torin 1 on mTOR-dependent autophagy-related proteins, lysosomal morphology, and lysosomal hydrolase activities in PBMC-derived macrophages from PD patients carrying GBA1-L444P or GBA1-N370S mutations. CBE induced dose-dependent activation of mTOR signaling in SH-SY5Y, as evidenced by dose-dependent accumulation of p-RPS6 (Ser235/236). mTOR inhibition decreased Beclin-1 protein levels while increasing the LC3B-II/LC3B-I ratio, LC3B–lysosome colocalization, and lysosome number regardless of mutation type in PBMC-derived macrophages. However, Torin1 reduced p62 levels in GBA1-N370S-PD, whereas lysosomal size decreased in GBA1-L444P-PD. Interestingly, Torin 1 increased GCase activity in both patient groups. These findings suggest that mTOR inhibition restores GCase function and autophagy and may represent a potential therapeutic strategy for GBA1-PD. Full article

Background: Point-of-care (POC) glucometers are essential for rapid blood glucose monitoring but are subject to interference and hematocrit variations. This study evaluated the analytical performance of the new Cobas Pulse glucometer against the Accu-Chek Inform II meter in the presence of N-acetylcysteine (NAC, 0.32–2.5 mmol/L), ascorbic acid (0.28–2.84 mmol/L), D-galactose (5.5–27 mmol/L), hemolysis (0.5–5 g/L hemoglobin), icterus (200–1600 μmol/L bilirubin), lipemia (2.5–15 g/L Intralipid), and hematocrit variations (20–60%). Methods: Interference testing followed CLSI EP07 guidelines using three whole blood pools with low (2.0–2.7 mmol/L), medium (4.5–7.4 mmol/L), and high (16.3–23 mmol/L) glucose levels. Interferents were spiked into these whole blood pools. Duplicate glucose levels were measured by 2 Pulse meters and 2 Inform II meters. The results were then assessed using the international standards, e.g., ISO 15197:2017 criteria (±15% or ±0.83 mmol/L). Results: Accu-Chek Inform II showed severe positive interference from galactose (up to 446.3%, p < 0.001), ascorbic acid (up to 98.8%, p = 0.002), and NAC (up to 61.4%, p = 0.001), exceeding ISO limits. Cobas Pulse demonstrated minimal interference (maximum biases: −3.7% for galactose, −4.4% for ascorbic acid, 7.7% for NAC, all p > 0.05). Both meters showed similar hematocrit-dependent bias (positive at 20–30%, negative at 50–60%) and acceptable performance for hemolysis, icterus (≤800 μmol/L), and lipemia. Conclusions: Compared to the Accu-Chek Inform II, the Cobas Pulse demonstrated greater resilience to interferences. Cobas Pulse meets strict accuracy standards (±10% for hospital use) with low interference, which makes it suitable for care of critically ill patients. The Cobas Pulse is more dependable for POCT across various clinical situations, supporting its role in critical care. Full article

Background/Objectives: There is growing interest among researchers in improved biological risk factor indices or combinations of indices, which have emerged as a major focus in evaluating the risk of cardiovascular disease (CVD). This study aimed to identify latent profiles based on the clustering of biological factors and to explore associations between lifestyle factors and CVD outcomes across the identified latent profiles. Methods: This epidemiological health survey was performed during 2023–2024. A random sample of Kaunas inhabitants aged 25–69 years, stratified by sex and age, was randomly selected from the Lithuanian population register. The 3426 individuals were screened. Latent profile analysis was performed using Latent Gold 6.1 and IBM SPSS Statistics 30. Multinomial logistic regression and multivariable binary logistic regression were used to evaluate the associations between biological risk factor profiles, lifestyle factors, and CVD outcome. Results: Three biological risk factor profiles were identified: low-risk profile (42.6%) was considered the healthiest, having the lowest levels of body mass index (BMI), fasting glucose, systolic blood pressure (SBP), and the highest level of high-density lipoprotein (HDL) cholesterol. Medium-risk profile (50.4%), having intermediate indicators of those factors. The high-risk profile (7.0%) was characterized by the lowest HDL cholesterol and the highest values of triglycerides, fasting glucose, SBP, and BMI. Conclusions: Compared to the low-risk profile, medium- and high-risk biological profiles were independently associated with higher odds of CVD, according to sociodemographic and lifestyle factors. The study suggests that integrating multiple biological risk factors rather than a single risk factor in clinical practice may enhance diagnostic accuracy. Full article

Background/Objectives: Radon exposure has recently been associated with asthma morbidity, including increased airway inflammation and school absenteeism in children, though limited data on underlying biological mechanisms exist. Interleukin-6 (IL-6), a pleiotropic cytokine implicated in both Type 2-low airway inflammation and radon-related lung carcinogenesis, may represent a key mechanistic link between radon exposure and asthma morbidity. We aimed to evaluate the association between indoor radon exposure and plasma IL-6 levels in children with asthma and whether this relationship differs by allergic sensitization status. Methods: We analyzed baseline data from the School Inner-City Asthma Study, a prospective cohort of children aged 4–13 years with persistent asthma. Monthly indoor radon concentrations at each participant’s residential ZIP Code Tabulation Area were estimated using a validated spatiotemporal prediction model. Plasma IL-6 was measured from baseline blood samples. Multivariable linear mixed-effects models with random intercepts for school were used to assess the association between radon exposure and IL-6, adjusting for demographic, clinical, and socioeconomic covariates. Effect modification by allergic sensitization was evaluated using an interaction term. Results: Among 144 participants, 62.5% were allergen-sensitized. The median home radon concentration was 46.6 Bq/m³ (range 30.7–99.9), and the mean plasma IL-6 was 0.22 pg/mL (SD 0.41). A significant interaction was observed between radon exposure and allergic sensitization status (β-interaction = –0.012; p = 0.014), indicating differential effects by phenotype. Among non-sensitized children, higher radon exposure was associated with increased IL-6 levels (β = 0.0088; p = 0.044), corresponding to a 0.32 pg/mL rise in IL-6 per 37 Bq/m³ increase in radon. No significant association was observed among sensitized children. Conclusions: Indoor radon exposure is associated with higher plasma IL-6 levels in non-sensitized children with asthma, suggesting a potential IL-6–mediated pathway linking radon exposure to asthma morbidity in the Type 2-low phenotype. These findings highlight heterogeneity in environmental asthma responses and support further investigation into radon mitigation as a modifiable factor to improve asthma outcomes. IL-6 may serve as a biomarker to identify children most susceptible to radon-related airway inflammation, guiding personalized mitigation strategies and targeted interventions to improve asthma outcomes. Future studies should incorporate direct home radon measurements, comprehensive endotyping panels, and longitudinal biomarker sampling to validate these findings and elucidate whether IL-6 trans-signaling pathways mediate radon-induced airway injury in non-allergic asthma. Full article