Search Results (246)

Schizopygopsis younghusbandi is an endemic and ecologically important fish species on the Tibetan Plateau. However, its dietary carbohydrate requirement remains unexplored, limiting the development of cost-effective and physiological-friendly artificial feed. This study investigated the effects of different dietary carbohydrate levels on the growth performance, antioxidant capacity, and hepatointestinal morphology of S.younghusbandi. Six experimental diets were formulated with graded carbohydrate levels of 9% (C9), 12% (C12), 15% (C15), 18% (C18), 21% (C21), and 24% (C24). A total of 720 fish (initial weight 37.49 ± 0.25 g) were randomly allocated to six groups in quadruplicate (30 fish per replicate) and reared in tanks (0.6 m × 0.5 m × 0.4 m) for 8 weeks. Results demonstrated that the diet in the C12 group significantly improved weight gain rate (WGR), specific growth rate (SGR), and feed conversion ratio (FCR) (p < 0.05). Regression fitting analysis on growth performance indicated that the optimal carbohydrate level ranged from 10.42% to 10.49%. Additionally, the C12 group exhibited enhanced total superoxide dismutase (T-SOD) activities and reduced malondialdehyde (MDA) content in the liver, along with reduced interleukin-1β (IL-1β) levels in the serum (p < 0.05). Histological analysis revealed superior hepatointestinal integrity in the C12 group, characterized by lower hepatic lipid droplet accumulation, reduced vacuolation, decreased hepatosomatic index (HSI) (p < 0.05), as well as higher intestinal villus height and muscle thickness (p < 0.05). In conclusion, the C12 group optimally enhanced the growth, antioxidant response, and hepatointestinal health of S. younghusbandi, indicating that the suitable dietary carbohydrate level for this species is 12%. Full article

Background/Objectives: Eosinophilic myocarditis (EM) is a rare, life-threatening inflammatory cardiomyopathy driven by eosinophil cytotoxicity and extracellular trap formation. Interleukin-5 (IL-5) inhibition may disrupt this pathogenic cascade. We reviewed contemporary evidence on IL-5 blockade in EM and contextualized it with an illustrative case. Methods: We searched PubMed through May 2025 for reports of EM treated with mepolizumab or benralizumab. Inclusion criteria were consistent with prior cohorts: acute cardiac symptoms with biomarker elevation plus abnormalities on transthoracic echocardiography and/or cardiac magnetic resonance imaging (CMR), along with documented IL-5-targeted therapy. We extracted clinical, imaging, biopsy, treatment-timing, and outcome data and included one institutional case. Results: Twenty-one episodes were analyzed (median age, 45 years; 10 men). Underlying conditions included eosinophilic granulomatosis with polyangiitis (10 cases; 48%), hypereosinophilic syndrome (5 cases; 24%), drug reaction with eosinophilia and systemic symptoms (DRESS, 3 cases; 14%), and eosinophilic asthma (3 cases; 14%). Treatments involved mepolizumab in 17 cases (81%) and benralizumab in 4 (19%); 4 patients received “early-start” therapy within 14 days of EM diagnosis. Among the 11 episodes with reported left ventricular ejection fraction (LVEF) at baseline and follow-up, the median baseline LVEF was 40% (range, 30–62), with 10 of 11 (91%) <50%. On follow-up, all 11 patients improved: 4 normalized (≥50%) and 7 improved to 40–49%. CMR (n = 18) demonstrated late gadolinium enhancement in 14 cases (78%), edema in 9 (50%), and intracardiac thrombus in 4 (22%). Endomyocardial biopsy confirmed eosinophilic infiltration in 13 of 15 cases (87%). Outcomes included one death (fulminant DRESS), one recovery following veno-arterial extracorporeal membrane oxygenation, and one successful heart transplantation. Illustrative case: A 24-year-old man on a steroid taper received mepolizumab 300 mg on Day 4. His LVEF improved from 47% to 59% by Day 15, accompanied by biomarker decline and successful steroid tapering. Conclusions: Across published cases and our institutional experience, IL-5–targeted therapy appears safe, steroid-sparing, and associated with rapid ventricular recovery, particularly when initiated early. Although limited, these findings support the need for prospective trials to define the optimal agent, dosing, timing, and integration with standard immunosuppression and anticoagulation. Full article

Gynostemma pentaphyllum (GP) is a medicinal plant that has long been used as drug for the treatment of rheumatism, liver disease, and diabetes. In this study, GP was extracted with 50% ethanol extract, and then the extract was heat-processed under high pressure to analyze the anti-inflammatory potential of these extract (named actiponin (AP)) and its derived components, damulin A and damulin B, in RAW264.7 cells and carrageenan-induced rat models. Ap had no effect on RAW264.7 cells up to 180 μg/mL, but DA and DB showed cytotoxicity from 18 μM. Pretreatment with AP significantly suppressed the LPS-induced increase in nitric oxide (NO) and inducible nitric oxide synthase (iNOS) protein expression via griess reagent and Western blot analysis, and these effects were similar to those of DA and DB. AP, DA, and DB also significantly suppressed the expression of prostaglandin E2 (PGE2) and cyclooxygenase-2 (COX-2) protein, which were increased by LPS, in a concentration-dependent manner. In addition, AP, DA, and DB inhibited the LPS-induced increase in pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in RAW264.7 cells. The anti-inflammatory activities of AP, DA, and DB are mediated by the suppression of the nuclear factor (NF)-κB and phosphorylation of mitogen-activated protein kinases (MAPKs) signaling pathways. Oral administration of 30, 50, 100, or 200 mg/kg (AP) suppressed carrageenan-induced edema in a concentration-dependent manner. Collectively, these results suggest that AP exerts potential anti-inflammatory activity by suppressing the inflammatory-mediators and pro-inflammatory cytokines via the NF-κB and MAPK pathways in vitro and by reducing the thickness of carrageenan-induced paw edema in vivo. Full article

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) encompasses a spectrum of liver conditions and involves gut–liver axis crosstalk. We aimed to evaluate whether oral vancomycin modifies liver injury and the cecal microbiota in a methionine–choline-deficient (MCD) diet model of NASH. Male C57BL/6J mice (n = 28) were block-randomized to four groups (n = 7 each) for 10 weeks: standard diet (STD); MCD diet; STD + vancomycin (VANC); and MCD + VANC (2 mg/mouse ≈ 50 mg/kg, every 72 h). After 10 weeks, liver tissues were analyzed for histological changes, cytokine levels [interleukin-6 (IL-6), interleukin-8 (IL-8), transforming growth factor beta 1 (TGF-β1)], and immunohistochemical markers [ubiquitin and cytokeratin 18 (CK18)]. Cecal microbiota composition was evaluated with 16S ribosomal RNA (rRNA) sequencing. The MCD reproduced key NASH features (macrovesicular steatosis, lobular inflammation). Vancomycin shifted steatosis toward a microvesicular pattern and reduced hepatocyte injury: CK18 and ubiquitin immunoreactivity were decreased in MCD + VANC vs. MCD, and hepatic IL-8 and TGF-β1 levels were lower in MCD + VANC vs. STD. Taxonomically, STD mice had Lactobacillus-rich microbiota. The MCD diet alone reduced alpha diversity (α-diversity), modestly lowered Firmicutes and increased Desulfobacterota/Fusobacteriota. Vancomycin alone caused a much larger collapse in richness, depleting Gram-positive commensals and promoting blooms of Escherichia–Shigella, Klebsiella, Parabacteroides, and Akkermansia. In the MCD + VANC group, vancomycin profoundly remodeled the microbiota, eliminating key commensals (e.g., Lactobacillus) and enriching Desulfobacterota, Fusobacteriota, and Campylobacterota. Oral vancomycin in the MCD model of NASH improved liver injury markers and altered steatosis morphology, but concurrently reprogrammed the gut into a low-diversity, pathobiont-enriched ecosystem with near-loss of Lactobacillus. These findings highlight a therapeutic trade-off—hepatic benefit accompanied by microbiome cost—that should guide microbiota-targeted strategies for NAFLD/NASH. Full article

The spleen is essential for immunity, mediating host defense against pathogens and regulating immunological homeostasis. Western-style diets commonly cause the aggregation of body fat and the emergence of obesity. This state might lead to damage to the spleen’s functions. However, the effects of Western-style diets on gene expression and metabolic regulation in the spleen have not yet been fully explored. In this study, C57BL/6 mice were fed either a high-fat diet (HFD) or standard chow (CHFD) for 10 weeks starting at 8 weeks old. Weekly weights were recorded, and spleens were weighed at 18 weeks. The results showed that HFD mice had significantly higher body weights from 12 weeks (p < 0.05) and a higher splenic index at 18 weeks (p < 0.01). HE staining revealed disrupted spleen structures and infarcted areas in the HFD group. Transcriptome sequencing highlighted immune-related pathways, including inflammatory response and interleukin-6 production. Among the differentially expressed genes (DEGs), PCK1, ALDH9A1, and ALDH7A1 were significantly upregulated in the HFD group, whereas PLA2G2F and PLA2G4F exhibited significant downregulation. APOB emerged as a key hub gene in PPI analysis. Metabolomics analysis identified significantly different metabolites (SDMs), including Rifamycins, 7-Ketodeoxycholic Acid, Folinic Acid, and Lotaustralin, as key biomarkers for an HFD, while 1-Methylnicotinamide and Prostaglandin E1 were significant for CHFD. KEGG enrichment linked glycerophospholipid and arachidonic acid metabolism to both transcriptome and metabolome results. The joint analysis of transcriptome and metabolome data revealed that SLC22A8 was negatively correlated with Biliverdin and 1-methylnicotinamide, and MCPT1 was inversely correlated with 7-Ketodeoxycholic Acid. These findings offer insights into the molecular mechanisms and metabolites that influence spleen immunity and systemic immune homeostasis. Full article

Background and Objectives: Romania has experienced the highest measles incidence rate in the European Union since late 2023, driven by suboptimal measles–mumps–rubella (MMR) uptake. Contemporary data on bedside predictors of clinical deterioration are scarce. The objective was to characterise demographic, clinical and laboratory differences between severe and non-severe measles and derive a multivariable model for intensive-care-unit (ICU) admission. Methods: We undertook a retrospective cohort study at the “Victor Babeș” University Hospital for Infectious Diseases, Timișoara. All admissions from 1 November 2023 to 15 May 2025 with serological or RT-PCR confirmation and a complete baseline laboratory panel were included. Descriptive statistics compared ward-managed versus ICU-managed patients; independent predictors of ICU transfer were identified through logistic regression that incorporated age, vaccination status, leukocyte count, C-reactive protein (CRP) and interleukin-6 (IL-6). Results: Among 455 patients (median age 3.0 y, interquartile range [IQR] 1.0–7.0), 17 (3.7%) required ICU care. Vaccine coverage was 18.0% overall and 0% among ICU cases. Compared with ward peers, ICU patients exhibited higher leukocyte counts (8.1 × 10⁹ L vs. 6.0 × 10⁹ L; p = 0.003) and a near-five-fold elevation in IL-6 (18 pg mL vs. 4 pg mL; p < 0.001), while CRP, procalcitonin and fibrinogen were similar. ICU admission prolonged median length of stay from 5 days (IQR 4–7) to 8 days (5–12; p = 0.004). In multivariable modelling, IL-6 remained the sole independent predictor (odds ratio [OR] 1.07 per pg mL; 95% confidence interval [CI] 1.03–1.12; p = 0.001); the model’s AUC was 0.83, indicating good discrimination. Complete separation precluded reliable estimation of the protective effect of vaccination, but no vaccinated child required ICU care. Conclusions: A simple admission panel centred on IL-6 accurately identified Romanian measles patients at risk of critical deterioration, whereas traditional markers such as CRP and leukocyte count added little incremental value. Even a single documented MMR dose was associated with the complete absence of ICU transfers, underscoring the urgent need for catch-up immunisation campaigns. Integrating IL-6-guided triage with intensified vaccination outreach could substantially reduce measles-related morbidity and health-system strain in low-coverage EU settings. Full article

Background/Objectives: Increased blood pressure variability (BPV) was found in adults with primary (essential) hypertension (PH) and is associated with increased cardiovascular risk. Our study aimed to analyze the relation between BPV and low-grade inflammation in children with primary hypertension. Methods: In 56 treatment-naive pediatric patients with PH (15.1 ± 2.1 years) and 30 healthy children (14.9 ± 1.4 years), we evaluated BPV: BP dipping, standard deviation (SD) of ambulatory blood pressure measurements (ABPMs), pulse pressure (PP)/systolic blood pressure ratio (24 h PP/SBP), rate–pressure index (24 h RPI), 24-h weighted BPV (24 h WSBPV, 24 h WDBV, 24 h WMAPV), coefficient of variation (24 h CoVSBP, 24 h CoVDBP, 24 h CoVMAP), ambulatory arterial stiffness index (AASI), and morning BP surge. We also analyzed indices of subclinical inflammation (markers derived from complete blood count, high-sensitivity C-reactive protein (CRP), interleukin 18), and office and ambulatory BP. Results: Patients with PH had significantly higher hsCRP, neutrophils, monocytes, and platelets, neutrophil-to-lymphocyte (NLR), platelet-to-mean platelet volume (PMPVR), and lower monocyte-to-neutrophil (MNR) ratios, and higher BPV: 24 h ABPM SBP SD, 24 h ABPM MAP SD, 24 h RPI, 24 h WSBPV, 24 h WDBV, 24 h WMAPV, and 24 h CoVSBP. Low-grade inflammation markers correlated with BPV indices in both groups. In multivariate analysis, MNR predicted 24 h ABPM MAP SD (beta = 0.290, 95CI: 0.029–0.551), 24 h RPI (beta = −0.348, 95CI: −0.587–−0.108), and 24 h WDBPV (beta = 0.286, 95CI: 0.032–0.540); monocyte count—24 h RPI (beta = 0.281, 95CI: 0.041–0.521), and hsCRP—24 h WDBV (beta = 0.310, 95CI: 0.055–0.564). ROC analysis revealed a good diagnostic profile for lymphocyte count as a positive determinant of non-dipping status in PH children (cut-off point 2.59 [×10³/µL]). Conclusions: BPV is higher in children with PH compared to healthy peers and is associated with low-grade inflammation. MNR may be the most helpful indicator of BPV, whereas high lymphocyte count predicts the best non-dipping status in these patients. Full article

Objectives: Evaluation of the predictive potential of pre-CAR-T [¹⁸F]FDG PET/CT in Diffuse Large B-Cell Lymphoma (DLBCL) patients concerning Cytokine Release Syndrome (CRS) and Immune Effector Cell-associated Neurotoxicity Syndrome (ICANS). Methods: Eighteen DLBCL patients (mean age: 60 ± 12 years) who underwent pre-therapeutic [¹⁸F]FDG-PET/CT and CAR-T cell therapy were retrospectively included. Median follow-up time was ten months (IQR6-16) after CAR-T cell infusion. Age, sex, serum lactate dehydrogenase (LDH), interleukin-6 (IL-6), C-reactive protein (CRP), and modified Endothelial Activation and Stress Index (mEASIX) were obtained. Potential occurrence of CRS/ICANS and the SUV_max were evaluated. Pearson and Spearman correlations, group comparisons (Mann–Whitney U-test) and the odds ratio (OR) were calculated. P values below 0.05 were defined as statistically significant and 95%-confidence intervals (CI) were calculated. Results: Pre-therapeutic SUV_max correlated positively with LDH (r = 0.5; p = 0.02), with the grade of CRS (r = 0.5; p = 0.03) and with the grade of ICANS (r = 0.6; p = 0.01). Appearance of ICANS was significantly correlated with pre-therapeutic SUV_max (p = 0.03; U = 7.0; Z = −2.2). Using ROC analysis and Youden’s index, an SUV_max threshold of 17 (AUC: 0.865; p < 0.01) was defined. Patients exceeding a pre-therapeutic SUV_max of 17 had a significantly higher risk of CRS grade > 1 (OR = 22; CI 2, 314; p = 0.03) and ICANS grade > 1 (OR = 18; CI 1, 271; p = 0.04). Conclusions: Pre-therapeutic SUV_max may be a useful marker for identifying DLBCL patients at risk for CRS and ICANS. Full article

Post-traumatic stress disorder (PTSD) is a chronic mental health condition resulting from exposure to traumatic events. It is associated with long-term neurobiological changes and disturbances in emotional regulation. Understanding the sociodemographic profiles, biomarkers, and emotional control in patients with PTSD helps to better comprehend the impact of the disorder on the body and its clinical course. An analysis of biomarkers such as Interleukin-18 (IL-18), Inositol-Requiring Enzyme 1 (IRE1), Phosphorylated Extracellular Signal-Regulated Kinase (pERK), and Activating Transcription Factor–6 (ATF-6) in PTSD patients with varying durations of illness (≤5 years and >5 years) and a control group without PTSD revealed significant differences. Patients with recently diagnosed PTSD (≤5 years) showed markedly elevated levels of inflammatory and cellular stress markers, indicating an intense neuroinflammatory response during the acute phase of the disorder. In the chronic PTSD group (>5 years), the levels of these biomarkers were lower than in the recently diagnosed group, but still significantly higher than in the control group. An opposite trend was observed regarding the suppression of negative emotions, as measured by the Courtauld Emotional Control Scale (CECS): individuals with chronic PTSD exhibited a significantly greater suppression of anger, depression, and anxiety than those with recent PTSD or healthy controls. Correlations between biomarkers were strongest in individuals with chronic PTSD, suggesting a persistent neuroinflammatory dysfunction. However, the relationships between biomarkers and emotional suppression varied depending on the stage of PTSD. These findings highlight the critical role of PTSD duration in shaping the neurobiological and emotional mechanisms of the disorder, which may have important implications for therapeutic strategies and patient monitoring. Full article

Objectives: This study sought to assess the impact of diabetes and hypertension on wound healing and recovery in orthopedic patients, with an emphasis on laboratory correlations. Materials and Methods: This study included 67 orthopedic patients, divided into a geriatric group (n = 49, ≥65 years) and a control group (n = 18). Clinical and laboratory assessments were performed at admission and discharge. Data were analyzed statistically. Results: Geriatric patients showed a higher triglyceride glucose-body mass index (TyG-BMI), glucose, cholesterol, C-reactive protein (CRP), interleukin-6 (IL-6), and leukocytes and lower hemoglobin and platelets (PLTs), with poorer healing and well-being. Elevated CRP, IL-6, and urea and decreased protein and hemoglobin persisted in this group. Diabetes improved outcomes in older adults, while hypertension worsened them in younger patients. Favorable outcomes correlated with higher triglycerides, fibrinogen, hemoglobin, and red blood cells (RBCs), while they did not correlate with elevated CRP, IL-6, leptin, urea, creatinine, and white blood cells (WBCs). Conclusions: Key predictors of healing and well-being included CRP, hemoglobin, RBC, and hematocrit in older patients and hypertension, CRP, hemoglobin, and leptin in younger individuals. Age-specific metabolic and inflammatory profiles influence recovery trajectories and may be used to predict problems in both recovery and patients’ well-being. Further research is required to better understand the correlations between these factors. Full article

Background: Interleukin (IL)-23 exerts its effects by activating Th17 cells, resulting in high neutrophilic infiltration in the colonic mucosal epithelium. We have developed a scoring method for refining the Geboes score Grade 3 to identify active ulcerative colitis (UC) patients with high epithelial neutrophilic infiltration (Geboes Grade 3.2 or 3.3). Methods: Colonoscopy and histology findings were assessed using the Mayo endoscopic subscore (MES) and the Geboes score Grade 3. The percentage of crypts with neutrophilic infiltration, which was calculated as the number of crypts with neutrophilic infiltration/total crypts in a glass slide, was used to subclassify the Geboes score Grade 3 into Grades 3.0, 3.1, 3.2, and 3.3. Results: This scoring method was then applied to 30 enrolled patients (20 men; median age: 46 years), yielding the following distribution: Geboes Grade 3.0 in six (20%) patients, Grade 3.1 in seven (23%) patients, Grade 3.2 in sixteen (53%) patients, and Grade 3.3 in one (3%) patient. Of the 18 UC patients with MES 2, 5 (28%) were classified as Grade 3.1 and 12 (67%) were classified as Grade 3.2. One of the IL-23 antagonists, mirikizumab treatment, resulted in clinical and endoscopic improvements in 10 active UC patients who were classified as Geboes score ≥ 3.2. Conclusions: We developed a novel Geboes score Grade 3 scoring method and applied it to 30 patients; approximately 60% were classified as Grade 3.2 or higher. This method may help to identify UC patients who are likely to respond effectively to IL-23 antagonists. Full article

Background/Objectives: The clinically validated multiplex Oncuria bladder cancer (BC) assay quickly and noninvasively identifies disease risk and tracks treatment success by simultaneously profiling 10 protein biomarkers in voided urine samples. Oncuria uses paramagnetic bead-based fluorescence multiplex technology (xMAP^®; Luminex, Austin, TX, USA) to simultaneously measure 10 protein analytes in urine [angiogenin, apolipoprotein E, carbonic anhydrase IX (CA9), interleukin-8, matrix metalloproteinase-9 and -10, alpha-1 anti-trypsin, plasminogen activator inhibitor-1, syndecan-1, and vascular endothelial growth factor]. Methods: In a pilot study (N = 36 subjects; 18 with BC), Oncuria performed essentially identically across three different common analyzers (the laser/flow-based FlexMap 3D and 200 systems, and the LED/image-based MagPix system; Luminex). The current study compared Oncuria performance across instrumentation platforms using a larger study population (N = 181 subjects; 51 with BC). Results: All three analyzers assessed all 10 analytes in identical samples with excellent concordance. The percent coefficient of variation (%CV) in protein concentrations across systems was ≤2.3% for 9/10 analytes, with only CA9 having %CVs > 2.3%. In pairwise correlation plot comparisons between instruments for all 10 biomarkers, R² values were 0.999 for 15/30 comparisons and R² ≥ 0.995 for 27/30 comparisons; CA9 showed the greatest variability (R² = 0.948–0.970). Standard curve slopes were statistically indistinguishable for all 10 biomarkers across analyzers. Conclusions: The Oncuria BC assay generates comprehensive urinary protein signatures useful for assisting BC diagnosis, predicting treatment response, and tracking disease progression and recurrence. The equivalent performance of the multiplex BC assay using three popular analyzers rationalizes test adoption by CLIA (Clinical Laboratory Improvement Amendments) clinical and research laboratories. Full article

Cardiac arrhythmias, including atrial fibrillation and ventricular arrhythmias, remain leading causes of morbidity and mortality worldwide. While structural, electrical, and metabolic remodeling have long been recognized as drivers of arrhythmogenesis, emerging evidence identifies inflammation—particularly inflammasome signaling—as a central orchestrator of this pathological triad. Among the various inflammasome complexes, the NLRP3 inflammasome has garnered particular attention due to its activation in cardiomyocytes, fibroblasts, and immune cells in diverse clinical contexts. NLRP3 activation precipitates a cascade of downstream events, including interleukin-1β and -18 maturation, oxidative stress amplification, calcium mishandling, and extracellular matrix remodeling, thereby fostering a proarrhythmic substrate. This review synthesizes mechanistic and translational data implicating inflammasome signaling in both atrial and ventricular arrhythmias, with a focus on cellular specificity and electrophysiological sequelae. We explore upstream triggers, such as metabolic stress, gut dysbiosis, and epicardial adipose inflammation, and delineate the downstream impact on cardiac conduction and structural integrity. Emerging therapeutic strategies—including NLRP3 inhibitors, IL-1 antagonists, colchicine, and SGLT2 inhibitors—are critically appraised for their anti-inflammatory and antifibrotic potential. By bridging molecular insights with clinical application, this review underscores the inflammasome as a unifying mechanistic hub in arrhythmia pathogenesis and a promising target for precision-guided therapy. Full article

Background: There are different types of obesity, and the metabolic conditions associated with these phenotypes are also heterogeneous. Overweight and obesity are not only associated with pain but are also identified as risk factors for the development of pain. Objective: This study aimed to compare the levels of inflammatory biomarkers, counting of immune cells, and chronic pain between android and gynoid female patients with obesity. Method: Thirty (n = 30) women took part in this study (18 androids, age: 50.61 ± 9.41 and 12 gynoids, age: 50.67 ± 9.45). The participants underwent anamnesis, Visual Numeric Scale (VNS), dual-energy X-ray absorptiometry, and blood sampling for the analysis of leukocytes, C-reactive protein (CRP), and interleukin (IL)-6. Results: The number of total leukocytes in the blood was not different when comparing the android group (6045 µL) with the gynoid group (5230 µL). No differences were observed for neutrophils (3440 µL in android and 3017 µL in gynoid), lymphocytes (2208 µL in android and 2115 µL in gynoid), for monocytes (429.7 µL in android and 392.8 µL in gynoid), and basophils (17.27 µL in android and 15.41 µL in gynoid). However, there was a significant difference between the number of eosinophils when comparing the android group (137.6 µL) with the gynoid group (204.9 µL), p = 0.04. Although both groups presented CRP values above 0.3 mg/dL—indicative of low-grade inflammation—no statistically significant difference was observed. Similarly, no difference was found in pain intensity between groups, as measured by the Visual Numeric Scale (VNS). Conclusions: Although most inflammatory and pain markers did not differ between groups, the higher eosinophil count in the gynoid phenotype suggests immunological distinctions between obesity types. These findings underline the importance of considering body fat distribution in clinical assessments of inflammation and chronic pain in women with obesity. Full article

Arterial stiffness indicates early atherosclerotic changes prevalent in children and adolescents with type 1 diabetes (T1D), even in those with a well–controlled disease and without additional cardiovascular risk factors. This study aimed to determine whether low–density lipoprotein (LDL) cholesterol and cytokine levels can indicate vascular stiffness in pediatric patients without conventional microangiopathic complications who are not undergoing lipid–lowering therapy. The total study group consisted of 59 pediatric patients divided into two subgroups based on their LDL cholesterol levels and matched for age, age at onset, and duration of diabetes. The investigation involved the precise measurement of several biomarkers including tumor necrosis factor (TNF–α), interleukin 35 (IL-35), interleukin 4 (IL-4), interleukin 10 (IL-10), interleukin 12 (IL-12), interleukin 18 (IL-18), vascular endothelial growth factor (VEGF), Soluble Vascular Cell Adhesion Molecule–1 (sVCAM–1), Intercellular Adhesion Molecule–1 (ICAM-1), Soluble Platelet Selectin (sP–Selectin), Advanced Glycation End Products (AGEs), and Receptors for Advanced Glycation End Products (sRAGE). Arterial stiffness was assessed by calculating pulsatility indices in the common carotid artery and the peripheral arteries in the upper and lower limbs. The comparative analysis indicated that, in the subgroup with LDL cholesterol levels below 100 mg/dL, in comparison to the subgroup with LDL above 100 mg/dL, there was a significant increase in pulsatility indices in elastic and large muscle arteries and notably higher levels of IL-35, IL-10, sVCAM–1, and ICAM-1. This study is the first to recommend the pulsatility index of elastic and large muscular arteries as an effective diagnostic tool for evaluating early atherosclerotic lesions in children and adolescents diagnosed with type 1 diabetes. Elevated LDL cholesterol levels may contribute to vascular stiffness through mechanisms related to a weakened inflammatory response, highlighting the complex interaction between lipid levels, inflammation, and vascular health in patients with type 1 diabetes. Full article