Search Results (6,110)

Background: Inflammation is a common reason for dogs to present to veterinary clinics. Early diagnosis of systemic inflammation is important. Acute phase proteins, like C-reactive protein, are useful but not specific to infection. In human medicine, the intensive care infection score (ICIS) offers a faster, cost-effective alternative using advanced hematological parameters. While ICIS is not available for veterinary use, some components (e.g., neutrophil side fluorescent light) can be measured using analyzers like the Sysmex XN-1000V. Objectives: This study aimed to establish a control group of healthy dogs for the novel parameters neutrophil side fluorescent light (NE-SFL), neutrophil side scattered light (NE-SSC), and neutrophil forward scattered light (NE-FSC) and assess their utility in detecting inflammation in diseases such as sepsis, pyometra, steroid-responsive meningitis-arteritis (SRMA), and idiopathic epilepsy. Methods & Results: Value ranges were calculated based on 21 healthy dogs. Compared to controls, NE-SFL levels were significantly elevated in sepsis, pyometra, and SRMA, while NE-SSC was only elevated in sepsis and pyometra and NE-FSC only in sepsis. No increases were observed in idiopathic epilepsy. Manual gating of the white blood cell differential scattergram was necessary in samples showing high neutrophil toxicity and the presence of bands. Conclusion: NE-SFL and NE-SSC, obtainable from routine complete blood count, may serve as novel, accessible markers for inflammation in dogs. Further research is needed to validate their broader diagnostic use. Full article

Carum carvi, commonly known as caraway, is a medicinal and culinary plant recognized for its anti-inflammatory properties, primarily attributed to its essential oil components. However, the thermogenic potential of caraway—particularly the biological activity of its water-soluble extract—remains largely unexplored. In this study, we investigated the effects and underlying mechanisms of caraway on Ucp-1 mRNA expression in beige adipocytes and on inflammation-mediated suppression of thermogenesis, by treating C3H10T1/2 adipocytes with caraway water extract (CWE) or caraway hexane extract (CHE) during both the induction and maturation phases, followed by isoproterenol stimulation, and measurement of mRNA levels of Ucp-1 and differentiation-related genes. Additionally, RAW264.7 cells were treated with CWE prior to stimulation with lipopolysaccharides followed by evaluation of inflammatory marker expression. CWE increased Ucp-1 mRNA expression directly by enhancing adrenergic sensitivity and promoting beige adipocyte differentiation during the induction phase of differentiation. Further, CWE mediated an indirect effect on Ucp-1 expression by suppressing macrophage inflammation, thus restoring Ucp-1 expression otherwise inhibited under inflammatory conditions. These results suggest that caraway extracts—especially the water-soluble compounds—may serve as therapeutic candidates for obesity-related conditions by enhancing energy expenditure and mitigating chronic inflammation. Full article

This study investigated the pro-inflammatory and pro-oxidative effects of popular electronic cigarette aerosols (ECAs) compared with conventional cigarette smoke (CS) in the cultured human alveolar epithelial cell line (A549). Using cytotoxicity assays and four ECAs, substantial differences in biological impact were observed. CS exposure led to significant declines in cell viability and pronounced morphological changes, consistent with the presence of toxic combustion byproducts. Most ECAs caused negligible cytotoxicity except for the tobacco-flavoured variant, which demonstrated marked toxicity. DNA damage and altered cell cycle profiles were minor. Oxidative stress analysis revealed stable superoxide dismutase activity but notable glutathione depletion, especially with watermelon- and strawberry-flavoured ECAs, and unaltered mitochondrial transmembrane potential, indicating the importance of individual flavour additives in cellular antioxidant defence. Inflammatory markers, such as TNF-α, NF-κB, and IL-6, were differentially elevated across the CS and ECA groups, with IL-6 consistently increased, underscoring its role in regulating epithelial cells. Advanced double fluorescence analysis revealed increased cellular heterogeneity and inflammation, which was distinct for all ECA flavours. Overall, the findings demonstrate considerable heterogeneity in biological effects among ECA flavourings and propose a simple ECA biomonitoring model. The results emphasise the necessity for individualised toxicity assessments, especially regarding subclinical inflammation and potential long-term health outcomes. Full article

Background and Objectives: Despite modern therapy algorithms, ST-elevation myocardial infarction (STEMI) substantially contributes to cardiovascular morbidity and mortality worldwide. Early Risk assessment is crucial to guide therapy allocation, especially in countries with limited healthcare resources. Electrocardiographic parameters such as QRS fragmentation (fQRS) evolved as an important prognostic marker. The underlying mechanisms and specific risk factors for the occurrence of fQRS in patients with STEMI undergoing PCI have not been analyzed yet. Materials and Methods: Between 09/2020 and 06/2021, out of 179 consecutive patients with STEMI undergoing primary percutaneous coronary intervention (pPCI), 122 patients were included in this study. The occurrence of fQRS was analyzed and correlated to clinical as well as biochemical parameters. Results: In this population, the fQRS pattern was present in 33.6% (n = 41) of patients. Besides gender, no statistically significant differences in baseline characteristics or comorbidities were observed between the two groups. In univariable logistic regression analysis, both glomerular filtration rate (GFR) (p = 0.050) and C-reactive protein (CRP) (p = 0.014) were significantly associated with the presence of fQRS. However, in the multivariable logistic regression model, only CRP levels on admission remained independently associated with fQRS (OR = 3.44, 95% CI: 1.95; 6.05), (p = 0.029). Conclusions: In this analysis, a correlation between fQRS and CRP levels in patients with STEMI undergoing pPCI could be demonstrated. Consequently, fQRS might serve as a marker for extensive inflammation in the context of myocardial ischemia. Full article

Background and Objectives: Systemic inflammation plays a critical role in cancer progression and prognosis. The Systemic Inflammation Response Index (SIRI), a novel marker integrating neutrophil, monocyte, and lymphocyte counts, has been suggested as a prognostic indicator in various malignancies. This study aimed to evaluate the prognostic significance of SIRI in patients with metastatic pancreatic cancer receiving first-line chemotherapy. Materials and Methods: This retrospective study included 147 patients with metastatic pancreatic cancer who received first-line chemotherapy or best supportive care between 2010 and 2024. Clinical and laboratory data were collected from medical records. Overall survival (OS) and progression-free survival (PFS) were assessed using the Kaplan–Meier method, and prognostic factors were identified by univariate and multivariate Cox regression analyses. Results: The median OS and PFS were 7 and 4 months, respectively. Multivariate analysis revealed that ECOG ≥ 2 (HR: 2.094, p = 0.019), liver metastasis (HR: 2.039, p = 0.027), and each unit increase in SIRI (HR: 1.156, p < 0.001) were independent predictors of poorer OS. Patients with SIRI > 1.86 had significantly shorter OS compared to those with SIRI ≤ 1.86 (median OS: 4 vs. 9 months, p = 0.019). Conclusions: SIRI is an independent prognostic marker for survival in metastatic pancreatic cancer patients undergoing first-line and subsequent lines of chemotherapy. These inflammation-based markers are simple, cost-effective tools that could be integrated into routine clinical practice to aid in risk assessment and treatment planning. Full article

Pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) are characterized by high morbidity and mortality. We retrospectively analyzed 468 hospital admissions from 80 patients to evaluate the prognostic value of inflammation-based hematologic indices, including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), neutrophil-percentage-to-albumin ratio (NPAR), lymphocyte-to-monocyte ratio (LMR), and systemic immune-inflammation index (SII). All biomarker–outcome associations were specified a priori as exploratory in this hypothesis-generating design. In PAH, both NPAR and SII were associated with in-hospital mortality (odds ratio [OR] 1.129, 95% confidence interval [CI] 1.011–1.261, p = 0.031; OR 1.001, 95% CI 1.000–1.002, p = 0.002), post-discharge mortality (NPAR OR 1.181, 95% CI 1.062–1.313, p = 0.002), and poorer overall survival (log-rank p = 0.002 and p = 0.012, respectively). Higher LMR was associated with reduced in-hospital mortality (OR 0.291, 95% CI 0.108–0.790, p = 0.015), while NLR predicted increased in-hospital mortality. In CTEPH, NLR and LMR were the strongest predictors, correlating with worse survival (log-rank p = 0.007 and p = 0.044) and higher post-discharge mortality (NLR OR 1.289, 95% CI 1.029–1.615, p = 0.027). Receiver operating characteristic (ROC) analysis suggests the potential value of SII in PAH and the promising performance of NPAR in CTEPH. Inflammation-based hematologic indices, particularly NPAR, SII, and NLR, may provide valuable prognostic information and may serve as practical, non-invasive tools for predicting hospitalization duration and mortality in PAH and CTEPH. Full article

Osteoarthritis (OA) involves cartilage breakdown and inflammation. This study compares juvenile and OA chondrocytes in gene expression, metabolism, and kinase activity, and tests mechanical stimulation to better understand cartilage health and degeneration. Juvenile (jCH) and OA (pCH-OA) primary chondrocytes were mechanically stimulated using the Flexcell™ FX5K system. Gene expression, protein phosphorylation, and metabolism were analyzed pre- and post-stimulation. Principal component analysis and effect size analyses identified molecular and signaling differences. Gene expression revealed significant differences between jCH and pCH-OA, with COL1 and RUNX2 upregulated in jCH, and MMP3 and ACAN downregulated. PCA revealed distinct expression patterns and marker correlations. Cyclic tensile strain affected biomarkers such as RUNX2, IL8, TLR4, BMP2, and MMP1 in a cell type-specific manner. Metabolic profiling indicated lower ROS and NAD⁺/NADH, and higher glutamate, lactate, and formate, with changes primarily driven by mechanical stimulation rather than cell type. Protein analysis showed altered AKT, STAT3, and MAPK phosphorylation, reflecting different mechanotransduction in healthy versus OA chondrocytes. Juvenile and OA chondrocytes show distinct molecular, metabolic, and signaling profiles, with mechanical stimulation driving key biomarker and metabolic changes. These differences highlight altered mechanotransduction in OA, providing insights into cartilage degeneration and potential therapeutic targets. Full article

Background and Objectives: Left ventricular diastolic dysfunction (LVDD) is a known precursor of heart failure with preserved ejection fraction (HFpEF), particularly in patients with metabolic comorbidities. Acute coronary syndrome (ACS) and percutaneous coronary interventions (PCI) may exacerbate LVDD via systemic inflammation. This study aimed to explore the association between post-procedural systemic inflammation and the severity of diastolic dysfunction in patients with ACS and metabolic comorbidities. Materials and Methods: A retrospective observational study was conducted in 181 patients with ACS who underwent PCI. Inflammatory markers (leukocytes, neutrophils, and C-reactive protein [CRP]) measured at 24–48 h post-intervention were analyzed in relation to diastolic dysfunction, assessed by echocardiography. Multivariable ordinal logistic regression and correlation analyses were performed. Results: CRP showed a non-significant trend toward association with more advanced diastolic dysfunction (p = 0.081). Hypertension had a positive but nonsignificant coefficient. Other metabolic comorbidities (diabetes, dyslipidemia, and obesity) were not significantly associated. The correlation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin was exploratory. NT-proBNP was the only marker significantly correlated with high-sensitivity troponin (TrHS) at 48 h, indicating a link between myocardial injury and wall stress. Conclusions: CRP may be weakly associated with the severity of diastolic dysfunction post-PCI. However, classical metabolic comorbidities were not independently predictive. Post-PCI inflammation showed only modest, non-significant trends toward diastolic impairment, warranting confirmation in larger prospective studies. Full article

Owing to the great demand for healthy ageing promotion, and the anti-ageing reputation of anthocyanins and amino acids, we aimed to assess the effect of anthocyanin- and anti-ageing amino acids-enriched pigmented rice innovation on age-related cognitive decline, facial wrinkles, and a cardiovascular risk, and explored its mechanisms and safety. A total of 90 male and female volunteers (45–65 years old) participated in a 3-arm randomized, double blinded, placebo-controlled parallel study for 12 weeks. They were randomly allocated to one of the following groups: placebo, “Zuper rice” (Zup) 2 g/day and “Zuper Rice” 4 g/day. Cognition, facial wrinkles, atherogenic index in plasma (AIP), telomere length, telomerase, oxidative stress and inflammatory markers, together with safety parameters, were assessed every 6 weeks until the end of the study and compared to the baseline data. A high dose of “Zup” improved cognition, facial wrinkles, AIP and oxidative stress, while a low dose of “Zup” improved cognition, telomere length, telomerase and inflammation. No toxicity signs were observed. Therefore, “Zup” is a potential healthy ageing promotion innovation which improves telomere length, telomerase activity and inflammation at a low dose, resulting in an improvement in cognitive decline and the suppression of oxidative stress. At a high dose, it gives rise to improvements in cognition, facial wrinkles and cardiovascular risk. Full article

Endurance exercise is widely recognized for its cardiovascular benefits, including improved longevity and metabolic health. However, excessive endurance training may lead to adverse cardiac adaptations, such as myocardial fibrosis, detected via late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR). This review examines the dual role of myocardial fibrosis in athletes—as a potential risk marker for life-threatening arrhythmias or a benign byproduct of physiological remodeling. While moderate exercise promotes beneficial cardiac hypertrophy, ultra-endurance athletes exhibit a 10–20% increase in ventricular size and mass, alongside elevated cardiac biomarkers post-exercise. Myocardial fibrosis, particularly in the left ventricle (LV), is associated with arrhythmias and sudden cardiac death, especially when presenting as a subepicardial/midmyocardial patchy pattern. Studies report that 22% of athletes with this pattern experienced malignant arrhythmias, underscoring its clinical significance. Conversely, fibrosis may also reflect adaptive remodeling in some cases, complicating its interpretation. The mechanisms underlying fibrosis in athletes remain unclear but may involve repeated cardiac stress, inflammation, or distinct atherosclerotic plaque dynamics. CMR is critical for detecting fibrosis, though differentiating pathological from physiological patterns requires careful clinical correlation. Risk stratification must consider LGE patterns, arrhythmia history, and symptoms. Despite concerns, elite athletes generally exhibit increased longevity, highlighting the complex interplay between exercise benefits and risks. Further research is needed to clarify fibrosis mechanisms, refine diagnostic criteria, and guide management strategies to ensure athlete safety while preserving the advantages of endurance training. Full article

Background: Mucins, particularly MUC1, are involved in the pathogenesis of chronic respiratory diseases. In chronic rhinosinusitis with nasal polyposis (CRSwNP), altered mucin expression may contribute to chronic inflammation and tissue remodeling. However, the specific role of MUC1 in CRSwNP and its correlation with clinical severity and inflammatory pathway remains unclear. Objective: We aimed to evaluate the MUC-1 expression in nasal polyps of patients with CRSwNP and to assess the correlation of MUC-1 expression and disease severity, according to Clinical-Cytological Grading (CCG). Methods: Eighteen consecutive patients with CRSwNP who underwent endoscopic sinus surgery (ESS) were enrolled. A double-label immunofluorescence was performed to evaluate the expression of MUC-1, CD15 and Tryptase and their eventual co-localization on histological samples. Double-positive MUC-1+CD15+ and MUC-1+Tryptase+ inflammatory cells were counted by confocal microscopy. Results: MUC1 was expressed in all samples, with a significantly increasing expression in relation to CCG (p < 0.001). A significant co-localization between MUC1 and CD15+ eosinophils was observed, with a progressive increase in the number of double-positive cells from low to high CCG (p < 0.001). On the contrary, the co-localization between MUC1 and Tryptase+ mast cells was not significant, although both markers showed a higher expression in cases with high CCG (p < 0.001). Conclusions: A strong correlation between CRSwNP severity and MUC-1 expression, mainly colocalized with infiltrating eosinophils, was shown. This offers a promising perspective for the use of MUC-1 as a biomarker of CRSwNP. Full article

Aging is associated with changes in body composition that lead to low-grade chronic inflammation, compromising the health of the elderly. This condition can be mitigated by resistance training (RT) and vitamin D supplementation, promoting the health of this population. This study aimed to investigate the effects of 12 weeks of RT combined with vitamin D supplementation on body composition, muscle strength, and inflammatory status in older adults. A total of 26 participants were randomly assigned to an Experimental Group (EG: n = 12; 11 Female; 70.6 ± 4.7 years; RT + 2000 IU/day of vitamin D) and a Control Group (EG: n = 14; 11 Female; 69.6 ± 4.6 years; RT + placebo). Both groups performed the same RT program (8 exercises; 2 sets; 10 RM, twice per week). Before and after the intervention, participants were assessed using DEXA, strength tests (sit-to-stand test and handgrip strength), and serum biomarkers (IL-6, TNF-α, 25(OH)D). Both groups showed significant strength gains, particularly in the lower limbs (p < 0.05 for all tests and groups), with no between-group differences in body composition or inflammatory markers (p > 0.05 for all tests and groups). A time × group interaction was observed for IL-6 (p = 0.03), with a slight reduction in the EG and an increase in the CG, although post-intervention differences were not statistically significant (p = 0.49). No statistically significant between-group difference in 25(OH)D change (p = 0.11). These findings suggest that vitamin D supplementation at the tested dose did not enhance adaptations to resistance training in older adults with normal baseline vitamin D levels. Further studies are warranted to explore potential benefits in deficient populations and with alternative dosing strategies. Full article

Oral squamous cell carcinoma (OSCC) remains one of the most prevalent and aggressive malignancies worldwide, with late diagnosis contributing to poor survival rates. Recent evidence suggests that periodontitis may act as a co-factor in development of OSCC through persistent inflammation, microbial dysbiosis, and subsequent tissue remodeling. Identifying molecular signatures that link periodontitis with early oral cancerization is therefore of paramount importance for risk assessment, prevention, and timely intervention. This narrative review aims to provide an integrative overview of the current knowledge on molecular, genetic, and epigenetic biomarkers associated with oral cancer risk in patients with periodontitis. Specifically, periodontal pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum promote oral cancerization by modulating molecular, genetic, and epigenetic pathways, including p53, Cyclin D1, Ki-67, p16^INK4A, DNA methylation, histone modifications, and microRNA regulation. Therefore, this review provides a discussion about the role of inflammatory mediators, oxidative stress-related molecules, microbial-derived products, genetic markers and epigenetic mechanisms as early molecular signals of malignant transformation. The study of these salivary biomarkers (salivaomics) has emerged as a promising non-invasive diagnostic tool, although variability in sampling, biomarker stability, and confounding factors such as coexisting periodontal disease remain significant limitations. By synthesizing the available evidence, this review summarizes recent evidence linking periodontitis to oral cancerization, highlights potential salivary, proteomic, and inflammatory biomarkers, and considers the role of periodontal therapy in improving inflammatory profiles and modulating tumor-related biomarkers. Finally, it explores future perspectives, including the integration of Artificial Intelligence (AI) to enhance biomarker-based diagnosis and risk stratification in OSCC patients. Full article

Background and Objectives: Chronic inflammation (CIn) is common among peritoneal dialysis (PD) patients and contributes to adverse outcomes. However, the prognostic value of the neutrophil-to-lymphocyte ratio (NLR) and fibrinogen-to-albumin ratio (FAR) in PD remains uncertain. Methodology: In this prospective cohort study, 65 PD patients were followed for 18 months. Baseline demographic, clinical and laboratory data were collected and inflammatory indices were calculated. The composite outcome was all-cause mortality or transfer to hemodialysis (HD). Logistic regression analyses were used to identify independent predictors of outcomes. Results: Over the 18-month follow-up, 23 patients (35.4%) died and 13 (20.0%) transferred to HD. Patients with adverse outcomes had higher baseline FAR, C-reactive protein (CRP) and serum glucose (Glc) levels and lower triglycerides (TG). In multivariate analysis, higher FAR (OR 5.28, 95% CI 1.16–24.12), CRP (OR 1.28, 95% CI 1.02–1.62) and PTH (OR 1.01, 95% CI 1.00–1.01) were independently associated with adverse outcomes, while NLR showed marginal significance. In the mortality-only model, FAR (OR 3.99, 95% CI 1.17–13.61) and PTH remained significant predictors. Conclusions: FAR demonstrated a significant prognostic association with mortality and composite adverse outcomes in PD patients, whereas NLR had limited predictive value. Albumin-based inflammatory indices such as FAR may complement established markers for risk stratification. Larger multicenter studies are warranted to validate these findings. Full article

The dedifferentiation of smooth muscle cells (SMCs) is the main cause of atherosclerosis and vascular calcification. This study integrated the gene expression data of multiple microarrays to identify relevant marker molecules. A total of 72 Gene Expression Omnibus (GEO) samples (GSM) were collected from 10 gene expression data series (GSE) and divided into five groups: non-SMC, SMC, atherosclerotic SMC (SMC-ath), calcified SMC (SMC-calc), and treated SMC (SMC-t). The SMC-t group included synthetic SMCs that had undergone treatment to inhibit proliferation, migration, or inflammation. The gene expression data were merged, normalized, and batch effects were removed before differential gene expression (DGE) analysis was performed via linear models for microarray data (limma) and statistical analysis of metagenomic profiles (STAMPs). The genes with expressions that significantly differed were subsequently subjected to protein-protein interaction (PPI) and functional prediction analyses. In addition, the random forest method was used for classification. Twelve proteins that may be marker molecules for SMC differentiation and dedifferentiation were identified, namely, Proprotein convertase subtilisin/kexin type 1 (PCSK1), Transforming growth factor beta-induced (TGFBI), Complement C1s (C1S), Phosphomannomutase 1 (PMM1), Claudin 7 (CLDN7), Calcium binding and coiled-coil domain 2 (CALCOCO2), SAC3 domain-containing protein 1 (SAC3D1), Natriuretic peptide B (NPPB), Monoamine oxidase A (MAOA), Regulator of the Cell Cycle (RGCC), Alpha-crystallin B Chain (CRYAB), and Alcohol dehydrogenase 1B (ADH1B). Finally, their possible roles in SMCs are discussed. This study highlights the feasibility of bioinformatics analysis for studying SMC dedifferentiation. Full article