Search Results (1,558)

Background/Objectives: Cerebral amyloid angiopathy (CAA) is one of the most prevalent small vessel diseases (SVDs). Its diagnostic criteria rely mainly on neuroimaging markers, in particular using Magnetic Resonance Imaging (MRI), as pathology-based diagnoses are only occasionally available. Amyloid PET is frequently used to assess parenchymal amyloid deposition in Alzheimer’s disease (AD), but amyloid tracers are not specific to vascular and parenchymal amyloids. The aim of this scoping review is to assess the usefulness of amyloid PET imaging in CAA. Methods: A systematic literature search was performed, aiming to assess amyloid PET performance in the following situations: (I) CAA-related intracerebral hemorrhage (ICH) and convexal subarachnoid hemorrhage; (II) pathology-proven CAA; (III) CAA-related inflammation; (IV) hereditary CAA. Results: A total of 52 studies were retrieved, including three systematic reviews, and from these, a specific selection was taken according to each objective, confirming the diagnostic value of amyloid PET added to MRI and clinical information in all the selected situations, although with some limitations. Conclusions: Amyloid PET reliably detects increased global and region-specific amyloid deposition in CAA patients, with a characteristic occipital-predominant pattern. Continued advancements in tracer development and imaging methodologies are needed to increase specificity. Full article

Coronary artery spasm (CAS) is a reversible vasoconstriction of normal or atherosclerotic epicardial coronary arteries with a subsequent reduction in myocardial blood flow, leading to myocardial ischemia, myocardial infarction, severe arrhythmias, or even sudden death. It is an entity that should be recognized based on a particular clinical presentation. Numerous differences exist between CAS and obstructive coronary disease in terms of mechanisms, risk factors, and therapeutic solutions. The gold standard for CAS diagnosis is represented by transitory and reversible occlusion of the coronary arteries at spasm provocation test, which consists of an intracoronary administration of Ach, ergonovine, or methylergonovine during angiography. The pathophysiology of CAS is not fully understood. However, the core of CAS is represented by vascular smooth muscle cell contraction, with a circadian pattern. The initiating event of this contraction may be represented by endothelial dysfunction, inflammation, or autonomic nervous system unbalance. Our study explores the intricate balance of these factors and their clinical relevance in the management of CAS. Full article

This study describes a novel technique to analyze the extracellular vesicle (EV)-derived microRNA (miRNA) crosstalk between equine chondrocytes and synoviocytes. Donor cells (chondrocytes, n = 8; synoviocytes, n = 9) were labelled with 5-ethynyl uridine (5-EU); EVs were isolated from culture media and incubated with recipient cells (chondrocytes [n = 5] were incubated with synoviocyte-derived EVs, and synoviocytes [n = 4] were incubated with chondrocyte-derived EVs). Total RNA was extracted from recipient cells; the 5-EU-labelled RNA was recovered and sequenced. Differential expression analysis, pathway analysis, and miRNA target prediction were performed. Overall, 198 and 213 miRNAs were identified in recipient synoviocytes and chondrocytes, respectively. The top five most abundant miRNAs were similar for synoviocytes and chondrocytes (eca-miR-21, eca-miR-221, eca-miR-222, eca-miR-100, eca-miR-26a), and appeared to be linked to joint homeostasis. There were nine differentially expressed (p < 0.05) miRNAs (eca-miR-27b, eca-miR-23b, eca-miR-31, eca-miR-191a, eca-miR-199a-5p, eca-miR-143, eca-miR-21, eca-miR-181a, and eca-miR-181b) between chondrocytes and synoviocytes, which appeared to be linked to migration of cells, apoptosis, cell viability of connective tissue cell, and inflammation. In conclusion, the reported technique was effective in recovering and characterizing the EV-derived miRNA crosstalk between equine chondrocytes and synoviocytes and allowed for the identification of EV-communicated miRNA patterns potentially related to cell viability, inflammation, and joint homeostasis. Full article

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a public health concern, linked with immune-metabolic dysfunction. While lifestyle and dietary modifications remain the cornerstone of MASLD management, the optimal dietary approach remains uncertain. Objectives: This systematic review aims to investigate the impact of model dietary patterns on metabolic outcomes in patients with MASLD and evaluate their effects in individuals with coexisting metabolic conditions, such as obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM). Methods: To conduct the review, PubMed, Scopus, Google Scholar, Cochrane CENTRAL, and ClinicalTrials.gov databases were searched for Randomized Controlled Trials (RCTs) on the adult population, published between January 2019 and September 2024, following PRISMA principles. The quality of the included RCTs was assessed qualitatively based on study characteristics. Results: The main findings of this review demonstrated that the use of interventions with dietary model based on Mediterranean diet (MED) and intermittent fasting (IF) approaches, such as alternative-day fasting (ADF) and time-restricted feeding regimens (TRF) may have potential in reducing body weight, BMI, and waist circumference, with additional benefits of improving glycemic control and reducing inflammation. The effects on hepatic functions, although limited, may be linked with reduced enzyme activity and liver stiffness. Additionally, the use of lacto-ovo-vegetarian diet (LOV-D) and the Dietary Approaches to Stop Hypertension (DASH) diet may offer additional health benefits, including blood pressure management. Conclusions: This review suggests that MED and IF-based strategies may reduce BW, improve glycemic control, and lower inflammation, with potential benefits for hepatic function. Further long-term studies are needed to confirm these effects and underlying mechanisms, which will allow for the optimization of protocols and ensure their safety in MASLD. Full article

Insulin resistance (IR) is a metabolic disorder characterized by an impaired response to insulin. This condition is associated with excess adiposity and metabolic inflammation, contributing to an increased risk for related chronic diseases. Single-nucleotide polymorphisms (SNPs) can affect genes related to metabolic pathways which are related to IR and the individual response to nutrients and dietary patterns, affecting metabolic inflammation and insulin sensitivity. This narrative review explores the current evidence on interactions between genetic variants and dietary factors, specifically their effects in modulating IR and metabolic inflammation. A comprehensive search of the literature was conducted in PubMed, Google Scholar, and Web of Science, and a total of 95 articles were reviewed. The key findings reveal that SNPs in the TCF7L2, ADIPOQ, and TNF genes significantly influence metabolic responses and modulate the effects of the Mediterranean diet on biomarkers of inflammation and IR. Genotype-dependent variations in IR and inflammation biomarkers were observed in the response to different diets for SNPs in the TCF7L2, ADIPOQ, and TNF genes. Additionally, polygenic risk scores (PRSs) can also predict the response to the intake of nutrients and specific diets, and offer a promising tool for assessing genetic predisposition to IR. This review underscores the pivotal role of an individual’s genetic background in the effects of their nutrient intake and in the responses to dietetic interventions, thereby laying the foundation for personalized and effective nutritional strategies tailored to each individual’s necessity in mitigating IR and its associated risk factors for chronic diseases. Full article

Background: Fibroblast activation protein (FAP) is a cell surface glycoprotein expressed by myofibroblastic cells in areas of active tissue remodeling, such as wound healing, fibrosis, and certain chronic inflammatory lesions. As FAP is uniquely present in chronic inflammatory lesions and has an important role in extracellular matrix (ECM) turnover, it appears to have all the characteristics necessary for involvement in atherosclerosis and atherosclerotic plaque rupture and has become a potential target in the treatment of myocardial infarction. Methods: To further understand the role of FAP, its expression in atherosclerotic plaques was examined in a genetically modified mouse model of accelerated atherosclerosis (Apobec1 −/− Ldlr −/− double-knockout mice). The immunohistochemical Fap staining of atherosclerotic plaques in a mouse model of atherosclerosis was correlated with quantification of Fap mRNA obtained from the atherosclerotic plaques of the aortic arch. Fap distribution was characterized in mouse atherosclerotic plaques relative to other markers of activated smooth muscle cells, such as alpha smooth muscle actin and myosin heavy chain (Acta2 and Myh2), ECM turnover (Ki-67, procollagen III and Mmp-9), and inflammation in atherosclerosis (Cd-44, Il-12 and Tgf beta) using immunohistochemistry (IH) and RT-PCR analysis. Results: The mouse model of accelerated atherosclerosis showed an increasing presence of Fap with the progression of atherosclerosis and a high expression level in advanced atherosclerotic lesions compared with other markers of ECM turnover and inflammation in atherosclerosis. Conclusions: FAP exhibits a distinct pattern of expression in a mouse model of atherosclerosis as compared to other markers of activated vascular smooth muscle cells, ECM degeneration, and inflammatory cytokines. Full article

Introduction: Immunosenescence alters TNF receptor expression (TNFR1 and TNFR2), contributing to chronic inflammation (inflamm-aging) and age-related diseases. Polymorphisms in TNFRSF1A and TNFRSF1B may influence receptor expression; however, their role in age-dependent modulation remains unclear. This study examines TNFR1/TNFR2 expression dynamics on T cells, B cells, and monocytes across different ages and evaluates the impact of genetic polymorphisms. Methods: PBMCs from 150 donors (18–60 years) were isolated via density-gradient centrifugation and cultured under spontaneous and LPS-stimulated conditions. TNFR1 and TNFR2 expression on immune cell subsets was quantified using flow cytometry with BD QuantiBRITE PE beads. SNP genotyping in TNFRSF1A and TNFRSF1B was performed via PCR with restriction analysis. Nonlinear age-related trends were assessed using polynomial approximation and inflection point analysis (Tukey’s method). Results: Among the 23 analyzed TNF system parameters, the proportion of TNFR2⁺CD3⁺ T cells increased with age, whereas TNFR1⁺ and TNFR2⁺ monocyte populations showed significant negative correlations (p < 0.05). Inflection points (~27, 34–36, and 44–45 years) indicated nonlinear dynamics in TNFRs expression during aging. TNFR2 expression on T cells gradually increased and stabilized at later ages, whereas TNFR1 and TNFR2 expression on monocytes followed distinct declining trajectories. Genetic polymorphisms influenced correlation strength, but did not alter direction, demonstrating a conserved pattern of age-related receptor expression shifts. Conclusions: TNFR expression exhibits nonlinear, age-dependent alterations across immune cells, shaped by immunosenescence and genetic variability. The identified critical age intervals represent key phases of immune remodeling, where assessing TNFR expression may provide insights into inflamm-aging mechanisms and potential targets for immune modulation. Full article

Respiratory viruses such as respiratory syncytial virus (RSV) annually cause respiratory illness, which may result in substantial disease and mortality in susceptible individuals. Viruses exploit host cell machinery for replication, which engages the mitogen-activated protein kinases (MAPK) pathway. The MAPK signaling pathways are triggered by pattern recognition receptors that recognize the pathogen, infection, or external stimuli, leading to the induction and regulation of immunity and inflammation. Probenecid, used to improve renal function by inhibiting the tubular reabsorption of uric acid, has been shown to have therapeutic efficacy in reducing inflammation and blocking viral replication by inhibiting components of the MAPK pathway that preclude virus replication. This review summarizes key molecular cascades in the host response to virus recognition, infection, and replication and how this can be altered by probenecid treatment. Full article

The etiology of acute myeloid leukemia (AML) is complex, including genetic and environmental abnormalities. The immune system anomalies play an essential role in the process of leukemogenesis. However, the immunopathological factors, including abnormal T helper (Th) subsets, contributing to the initiation and progression of this neoplasm, require further investigation. Considering the previously mentioned data, we decided to study the expression pattern of transcription factors T-bet, Foxp3, and RORγt that regulate Th1, Treg, and Th17, respectively, in acute myeloid leukemia with correlation to clinical and other investigation data and treatment outcomes. This study was conducted on 80 newly diagnosed patients with AML recruited from the National Cancer Institute, Cairo University, and 25 healthy control subjects. The AML patient cohort consisted of 30 females (37.5%) and 50 males (62.5%), ranging from 18 to 74 years old. The control group was 8 females (32%) and 17 males (68%), with ages ranging from 23 to 40 years old. Samples were provided from the bone marrow of donor cases for allogeneic bone marrow transplantation. The diagnosis of acute myeloid leukemia was based on morphologic and cytochemical evaluation, immunophenotyping, and complementary cytogenetics according to WHO criteria. Upshift from the normal T-bet intensity of power (MFI), RORγt⁺ CD4⁺ T lymphocyte frequency (%) with downshift from the normal FOXP3 intensity of power (MFI), may suggest a state of inflammation. In contrast, an upshift from the normal FOXP3⁺ CD4⁺ T lymphocyte frequency (%) may reflect a state of immunosuppression in the bone marrow microenvironment of AML. Combined, they constitute a sophisticated scenario of immunological disorder in AML. Co-expression of T-bet and RORγt transcription factors in CD4⁺ T lymphocytes in both normal and AML groups may suggest CD4⁺ T lymphocyte plasticity. Full article

Background: The diet of young people in Spain has changed significantly, with a departure from a balanced dietary pattern and a greater intake of processed foods. Such food generates an acidic environment in the mouth, which promotes the multiplication of bacteria capable of causing inflammation and damage to the gums. Aim: This study aimed to determine the association between the frequency of consuming processed foods and periodontal disease, as well as sex differences, in an adolescent population. Methods: A study was conducted on 233 students aged 15 to examine the frequency of food consumption and its correlation with periodontal disease. Differences were determined via a Student’s t-test to compare the means. A chi-square test was used to compare categorical variables. The 95% confidence interval estimate was used in all cases (p < 0.05). Results: It was observed that girls have a higher mean number of healthy sextants than boys (3.26 $\pm$ 0.20 vs. 2.70 ± 0.21; p = 0.029). A statistically significant difference was noted between healthy and affected subjects in the frequency of consumption of packaged milkshakes (p = 0.003), industrial juices (p = 0.009), industrial pastries (p = 0.018), and fruits in syrup (p = 0.022). When segmented by sex, a statistically significant difference was noted in boys between healthy and affected subjects in the frequency of consumption of packaged milkshakes (p = 0.044), salty snacks (p = 0.032), and cold cuts (p = 0.033); in girls, the difference was detected in industrial juices (0.024). Conclusions: The results of this study suggest that adolescent boys are more affected periodontally than girls. In both sexes, the level of consumption of processed foods affects the presence of periodontal disease. Full article

Background: Alcohol use and hypertriglyceridemia are the second and third common causes of acute pancreatitis after choledocholithiasis. Still, few studies directly compare the severity and outcomes of these two groups, which share pathophysiology pathways. Methods: In our study, we compared the biologic profile, severity according to the Atlanta classification and Balthazar index, intensive care unit admissions, and mortality between patients with hypertriglyceridemia-induced pancreatitis (HTGP) and alcohol-induced acute pancreatitis (AAP). A total of 78 patients were included in this study, 37.17% of which had HTGP, and 62.82% had AAP. Results: HTGP was more severe in terms of the Atlanta revised classification severity assessment (82.76% vs. 46%, p = 0.014), led to more extended hospitalizations (p = 0.024), and resulted in similar serum CRP levels among patients, with a significant difference regarding median serum fibrinogen values (739 vs. 563 mg/dL, p = 0.030) and necrotizing forms (24.13% vs. 10.20%). Hyponatremia was more significant in HTGP patients compared with AAP patients (130 vs. 137 mmol/L, p < 0.000). No differences were found in other inflammation indexes such as NLR (neutrophil count/lymphocyte count), PLR (platelet count/lymphocyte count), MLR (monocyte/lymphocyte count), SII (systemic immune-inflammation index), or SIRI (systemic inflammation response index). Conclusions: The pattern of acute pancreatitis is related to its etiology and may have different grades of severity. In our study, we found that hypertriglyceridemia-induced pancreatitis required twice as many admissions to the intensive care unit and was associated with lower serum sodium levels, and almost twice as many patients with HTGP had moderate or severe forms of acute pancreatitis compared to alcohol-induced pancreatitis cases. Full article

Cardiovascular diseases (CVDs) represent a leading cause of premature mortality and disability worldwide, with their incidence expected to rise, potentially reaching 24 million deaths per year by 2030. These multifactorial diseases, including hypertension, coronary artery disease, arrhythmia, and heart failure, are often linked to metabolic disturbances such as diabetes, oxidative stress, endothelial dysfunction, and inflammation. Natural compounds, such as caffeine, have been explored for their potential therapeutic effects on CVDs. Caffeine, found in coffee, tea, cocoa, and various energy drinks, is a widely consumed psychoactive compound with noted analgesic and anti-inflammatory properties. Despite its long history of use, caffeine’s impact on cardiovascular health remains controversial, with both beneficial and harmful effects reported. This review examines the current literature on the effects of caffeine on cardiovascular diseases (CVDs), with an emphasis on preclinical and clinical studies, its pharmacokinetic properties, and the molecular mechanisms it modulates. There is evidence that moderate caffeine intake can be beneficial for some CVDs, such as hypertension, while for other CVDs, such as dyslipidemia, the evidence collected so far suggests that caffeine intake could be detrimental since it increases total cholesterol levels. But variability in dosage, intake patterns, and individual factors (such as genetics and diet) complicates the reliability of results. Additionally, challenges related to dose standardization and the absence of consistent clinical trial designs hinder the full utilization of caffeine in CVD treatment. Nonetheless, caffeine appears to be safe for individuals without significant cardiovascular conditions. Future research should aim for well-designed studies with precise patient cohorts and standardized methodologies to better assess caffeine’s role in CVD management. Full article

Although periodontal disease (PD) is reported to be associated with changes in various genes and proteins in both invading bacteria and the host, its molecular mechanism of pathogenesis remains unclear. Changes in immune and inflammatory genes play a significant role in PD pathogenesis. Some reports relate alterations in cellular epigenetic patterns to PD characteristics, while several high-throughput analyses indicate thousands of differentially methylated genes in both PD patients and controls. Furthermore, changes in DNA methylation patterns in inflammation-related genes have been linked to the efficacy of periodontal therapy, as demonstrated by findings related to the cytochrome C oxidase II gene. Distinct DNA methylation patterns in mesenchymal stem cells from PD patients and controls persisted despite the reversal of phenotypic PD. Methyl groups for DNA methylation are supplied by S-adenosylmethionine, which is synthesized with the involvement of folate, an essential nutrient known to play a role in maintaining mitochondrial homeostasis, reported to be compromised in PD. Folate may benefit PD through its antioxidant action against reactive oxygen and nitrogen species that are overproduced by dysfunctional mitochondria. As such, DNA methylation, dietary folate, and mitochondrial quality control may interact in PD pathogenesis. In this narrative/hypothesis review, we demonstrate how PD is associated with changes in mitochondrial homeostasis, which may, in turn, be improved by folate, potentially altering the epigenetic patterns of immune and inflammatory genes in both the nucleus and mitochondria. Therefore, a folate-based dietary intervention is recommended for PD prevention and as an adjunct therapy. At the same time, further research is needed on the involvement of epigenetic mechanisms in the beneficial effects of folate on PD studies. Full article

Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of fatty liver disease, presents a significant global health challenge. Despite extensive research, fully elucidating its complex pathogenesis and developing accurate non-invasive diagnostic tools remain key goals. Multi-omics approaches, integrating data from transcriptomics, proteomics, metabolomics, and lipidomics, offer a powerful strategy to achieve these aims. This review summarizes key findings from multi-omics studies in MASH, highlighting their contributions to our understanding of disease mechanisms and the development of improved diagnostic models. Transcriptomic studies have revealed widespread gene dysregulation affecting lipid metabolism, inflammation, and fibrosis, while proteomics has identified altered protein expression patterns and potential biomarkers. Metabolomic and lipidomic analyses have further uncovered significant changes in various metabolites and lipid species, including ceramides, sphingomyelins, phospholipids, and bile acids, underscoring the central role of lipid dysregulation in MASH. These multi-omics findings have been leveraged to develop novel diagnostic models, some incorporating machine learning algorithms, with improved accuracy compared to traditional methods. Further research is needed to validate these findings, explore the complex interplay between different omics layers, and translate these discoveries into clinically useful tools for improved MASH diagnosis and prognosis. Full article

Background: Asthma, a chronic respiratory disease characterized by airway inflammation and hyperresponsiveness, exhibits significant heterogeneity in its presentation. This study aimed to investigate age-related comorbidity patterns, seasonal variations, and demographic trends among a cohort of asthma patients within a defined geographical region. Methods: A retrospective analysis of 13,695 asthma patients admitted to a Romanian hospital from 2013 to 2023 was conducted. Comorbidity patterns were analyzed using network analysis across age groups, and seasonal trends were investigated through spectral analysis. Results: Asthma admissions exhibited non-linear trends with female predominance (57.72%). The pandemic significantly impacted admission rates, with males experiencing greater COVID-19-related effects. Female admissions showed distinct seasonal patterns potentially linked to domestic responsibilities. Comorbidity patterns evolved with age, shifting from lifestyle factors in younger patients to complex cardiovascular and neurological disorders in older groups. The 60–69 age group showed the highest integration of comorbidity communities. Conclusions: The study revealed that asthma management focus should shift with patient age from the disease itself to addressing underlying comorbidities. Understanding these complex patterns may help personalize treatment strategies and improve long-term prognosis for asthma patients. Full article