Search Results (1,419)

Hashimoto’s thyroiditis (HT) is the most common autoimmune thyroid disorder, characterized by progressive lymphocytic infiltration, follicular destruction, tissue fibrosis, and an elevated risk of thyroid carcinoma. While the precise mechanisms underlying HT remain incompletely defined, emerging evidence implicates dysregulated sphingolipid (SPL) metabolism, particularly the sphingosine-1-phosphate (S1P) signaling axis, as a central contributor to disease pathogenesis. S1P, a bioactive lipid mediator, integrates metabolic and immunological cues to regulate immune cell trafficking, cytokine production, apoptosis, and fibroblast activation. Aberrant activation of the sphingosine kinase (SPHK)/sphingosine-1-phosphate (S1P)/S1P receptor (S1PR) pathway has been linked to persistent T helper 1 (Th1) cell recruitment, signal transducer and activator of transcription 3 (STAT3)-mediated immune polarization, epithelial–mesenchymal transition, extracellular matrix remodeling, and the establishment of a chronic inflammatory and fibrotic microenvironment. Moreover, S1P signaling may foster a pro-tumorigenic niche, providing a mechanistic explanation for the strong epidemiological association between HT and papillary thyroid carcinoma. This review summarizes current insights into the role of SPL metabolism in HT, highlighting its potential as a mechanistic link between autoimmunity, fibrosis, and carcinogenesis. Full article

Epidemiological and geochemical evidence suggests that coal-fired fluorosis in Southwest China is mechanistically linked to the presence of fluoride-rich geochemical anomalies. However, the severity of dental fluorosis does not consistently align with the distribution pattern of fluoride geochemistry, suggesting that other factors may interfere with the dose–effect relationship of fluorosis. To investigate the potential biotoxicity impacts of fluoride, this study conducted an analysis of soil fluoride–selenium spatial correlation in the central areas of coal-fired fluorosis in China. The results revealed that 59.1% of soil fluoride contents were more than the average soil fluoride content of China (800 mg·kg⁻¹) and 77.9% of soil selenium contents were above 0.45 mg·kg⁻¹. Soil fluoride (1.11 × 10³ mg·kg⁻¹) and selenium contents (0.78 mg·kg⁻¹) were significantly high states, but agricultural products and drinking water sources showed relatively low levels, not significantly influenced by soil conditions. The severity of fluorosis was evaluated using Dean’s dental fluorosis index (DFI). The spatial association of soil selenium or fluoride with DFI suggested that there was a reverse relationship between soil selenium or selenium/fluoride and the DFI. The generalized additive model (GAM) showed the onset of DFI correlated with soil fluoride content, showcasing a distinctive “W” pattern, while DFI decreased steeply or gradually as soil selenium content or selenium/fluoride ratio increased. In conclusion, our findings suggest that the geochemical anomaly of soil fluoride likely contributes to the occurrence of fluorosis. However, the significantly elevated levels of soil selenium might alleviate the severity of dental fluorosis to some extent. Full article

Purpose: To achieve a better understanding of the environmental factors that contribute to childhood cancers, so as to inform future prevention efforts. Methods: We conducted a comprehensive review of epidemiological studies on environmental risk factors and childhood cancer, which was published between January 2014 and March 2021. Potential exposure sources presented in this review include air pollution, radiation, and parental occupational exposures. We considered exposures during childhood and parental exposures occurring before the child’s conception and during pregnancy in relation to all types of childhood cancer. Results: Aggregated evidence is strong for associations between leukemia and parental/child exposure to traffic pollution, indoor paints, residential pesticides, and parental occupational/nonoccupational exposure to benzene. Evidence is also strong for associations between brain cancer and residential pesticides and parental occupational exposure to agricultural pesticides. Evidence of associations between leukemia and ionizing radiation from radon and nuclear power plants remains mixed, as does evidence of a link between electromagnetic fields (EMFs) and childhood leukemia. Conclusions: Clear associations have been demonstrated between childhood cancer and environmental factors, including parent/child exposure to traffic pollution, occupational/nonoccupational benzene, indoor paints, residential pesticides, and parental occupational exposure to agricultural pesticides. These associations can be used to inform further study of interventions and public health campaigns to reduce risk. Full article

Environmental pollution, driven by industrialization, urbanization, and agricultural practices, has intensified global ecological degradation. Among the most concerning pollutants is PFOS, a synthetic compound known for its chemical stability, environmental persistence, and bioaccumulative potential. Widely utilised in industrial and consumer products, PFOS infiltrates ecosystems and food chains, posing substantial risks to human and animal health. Upon exposure, PFOS disrupts lipid metabolism, damages cellular membranes, and alters signaling pathways through partial metabolism by cytochrome P450 enzymes. Accumulating evidence links PFOS to oxidative stress, mitochondrial dysfunction, endocrine disruption, neurotoxicity, and immunotoxicity. Critically, PFOS contributes to the development and progression of prostate, breast, and ovarian cancers via mechanisms such as hormonal interference, chronic inflammation, and epigenetic modifications. Epidemiological studies further associate elevated PFOS serum levels with increased cancer risk, particularly in occupationally and environmentally exposed populations. This review brings together the latest knowledge on PFOS emissions, mechanistic toxicity, and cancer-causing potential, highlighting the urgent need for focused research and improved regulatory measures to safeguard public health. Full article

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide. Their prevalence is expected to rise with demographic shifts and increasing obesity rates. Excessive sugar consumption, especially from added sugars and sugar-sweetened beverages (SSBs), is a major modifiable risk factor of CVDs. It contributes to obesity, metabolic disorders, type 2 diabetes, and cardiovascular disease. High-sugar diets affect metabolic and cardiovascular health. They also contribute to neurobehavioral dysfunction by influencing the brain’s reward pathways, promoting hedonic eating, and reinforcing dependence on sweet taste. Fruits, a natural source of sweet-tasting compounds, are widely considered healthier than processed sweets. Epidemiological evidence shows a protective link between fruit consumption and lower risk of acute cardiovascular events like stroke and coronary heart disease. This benefit is largely due to bioactive compounds in fruits, such as fiber, polyphenols, and micronutrients. Based on current evidence, fruits can satisfy sweet cravings. In this paper, we will discuss the potential of fruits as an alternative to added sugars, emphasizing their beneficial effects on metabolic and cardiovascular health. Full article

Sports-associated traumatic brain injury is emerging as an under-recognized driver of acute and chronic cardiovascular diseases. Larger population-based studies show that individuals with moderate-to-severe traumatic brain injury experience up to a two-fold excess risk of incident hypertension, coronary artery disease, myocardial infarction, and stroke that persists for at least a decade. Among former professional American-style football players, a higher lifetime concussion burden is uniquely related to a more atherogenic cardiometabolic profile and greater long-term stroke risk. Mechanistically, an acute “sympathetic storm” triggered by cerebral injury provokes catecholamine surges, endothelial dysfunction, and myocardial stunning, manifesting as neurogenic stunned myocardium or Takotsubo-like cardiomyopathy and malignant arrhythmias. Sub-acute to chronic phases are characterized by persistent autonomic imbalance, reflected by reduced heart-rate variability and impaired baroreflex sensitivity weeks to months after concussion, coupled with neuroinflammation, hypothalamic–pituitary–adrenal axis dysregulation, and lifestyle changes that accelerate atherosclerosis. The interplay of these pathways accounts for the elevated burden of cardiovascular disease observed long after neurological function has been restored. Despite robust evidence linking TBI to adverse cardiac outcomes, contemporary sports–cardiology risk stratification prioritizes hemodynamic load, genetics, and performance-enhancing substances, largely overlooking brain injury history. This review integrates epidemiological, clinical, and mechanistic data to (i) delineate acute neurocardiac complications secondary of sports-related traumatic brain injury, (ii) synthesize evidence for chronic cardiovascular risk, (iii) highlight emerging autonomic and inflammatory biomarkers, and (iv) propose surveillance and therapeutic strategies, ranging from heart-rate-variability-guided return-to-play decisions to aggressive cardiometabolic risk modification aiming to mitigate long-term morbidity in this athletic population. By framing sports-related traumatic brain injury as a modifiable cardiovascular risk factor, we aim to foster interdisciplinary collaboration among neurologists, cardiologists, and sports medicine practitioners, ultimately improving both neurological and cardiovascular outcomes across the athlete’s lifespan. Full article

Polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic disorder affecting 6–20% of women of reproductive age, manifesting through hyperandrogenism, ovulatory dysfunction, insulin resistance, and diverse metabolic derangements. Increasing evidence highlights the contribution of environmental factors, particularly endocrine-disrupting chemicals (EDCs), to PCOS susceptibility and severity. Sunscreen ultraviolet (UV) filters such as oxybenzone (benzophenone-3) and octinoxate (ethylhexyl methoxycinnamate) are widely used EDCs with established systemic absorption and biomonitoring evidence in human populations. Their endocrine-disrupting potential encompasses estrogenic and anti-androgenic activity, interference with steroidogenic enzymes, modulation of thyroid hormone, induction of oxidative stress, and epigenetic reprogramming, all of which are mechanistic pathways that overlap with PCOS pathophysiology. This evidence-based study critically appraises the evidence linking oxybenzone and octinoxate exposures to ovarian endocrinology, with a PCOS-specific focus. Human exposure patterns, pharmacokinetics, and regulatory perspectives are summarized alongside preclinical and in vitro data implicating these filters in ovarian dysfunction. Mechanistic intersections with PCOS include hyperandrogenism, disrupted folliculogenesis, oxidative stress-adipokine imbalance, and potential impairment of vitamin D signaling. Although epidemiological studies directly addressing PCOS outcomes remain sparse, the convergence of toxicological evidence with known endocrine vulnerabilities in PCOS underscores a need for targeted investigation. By mapping exposure pathways and mechanistic disruptions, this appraisal emphasizes the translational relevance of UV filter toxicity in the context of PCOS. It advocates for PCOS-specific biomonitoring cohorts, mechanistic studies, and regulatory consideration of reproductive endpoints while balancing the dermatological benefits of photoprotection against reproductive risks. Full article

Background: Acute kidney injury (AKI) remains a serious complication among individuals with type 2 diabetes. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are widely prescribed and often regarded as kidney-protective, yet post-marketing reports have linked them to AKI. Tirzepatide, a newer dual GIP/GLP-1 agonist, shows well-documented metabolic benefits, but its renal safety in real-world use is not well characterized. Methods: We conducted a disproportionality analysis of the U.S. FDA Adverse Event Reporting System (FAERS) from January 2022 to September 2025. Reporting odds ratios (RORs) and proportional reporting ratios (PRRs) were used to compare AKI reporting between tirzepatide and semaglutide. Results: Among 133,872 reports (92,807 tirzepatide; 41,065 semaglutide), AKI was listed in 432 (0.47%) and 440 (1.07%) cases, respectively. The ROR for tirzepatide versus semaglutide was 0.44 (95% CI, 0.38–0.50), suggesting a lower reporting frequency for AKI with tirzepatide. Conclusions: In this real-world pharmacovigilance analysis, semaglutide but not tirzepatide showed a disproportionality signal for AKI. While causality cannot be confirmed, clinicians should ensure hydration and renal monitoring when initiating GLP-1 RAs, particularly semaglutide. Semaglutide showed a higher AKI reporting rate than tirzepatide, though these findings should be interpreted cautiously given reporting bias and potential confounders. Both agents appear safe, with low AKI frequency in practice. Further studies should determine if differences reflect biological or reporting effects. These findings support the need for larger epidemiologic studies to define risk modifiers and optimize clinical safety strategies. Full article

Bats are widely recognized as reservoirs of diverse bacterial pathogens with important implications for human health. Recent zoonotic disease outbreaks have intensified interest in bat microbiomes, with high-throughput sequencing increasingly used to assess microbial diversity. In this article, we review literature from the past five years on bacterial species associated with bats and their potential clinical relevance. Using automated searches and manual filtering, we extracted data from 47 peer-reviewed studies. Most research has focused on guano samples, though interest in skin microbiomes is rising, particularly in relation to Pseudogymnoascus destructans, the agent of white-nose syndrome. China leads in the number of publications, followed by the United States, and amplicon sequencing remains the predominant metagenomic method. Across studies, 4700 bacterial species were reported, including several known human pathogens capable of aerosol transmission or opportunistic infections in immunocompromised individuals. Many of these taxa are classified as global priority targets for antimicrobial drug development by the World Health Organization and the U.S. Centers for Disease Control and Prevention. Given the clinical severity of diseases linked to some species, bats should be integrated into epidemiological surveillance systems. However, the lack of standardized reporting practices significantly limits the comparability and utility of bat microbiome data for robust ecological and epidemiological analyses. Full article

Micro- and nanoplastics (MNPs) are emerging environmental immunotoxins with widespread human exposure through ingestion, inhalation, and dermal contact. Detected in the placenta, lungs, blood, bone marrow, and brain, MNPs accumulate in immune organs where they disrupt innate and adaptive cell functions. This review aims to provide a comprehensive summary of the current knowledge on how MNPs affect the immune system at the cellular and molecular levels. Experimental evidence shows that MNPs impair macrophage phagocytosis, skew dendritic cell maturation, trigger neutrophil extracellular traps, and alter T and B cell responses. Mechanistically, these effects are driven by oxidative stress, mitochondrial dysfunction, and activation of key inflammatory signaling pathways, including NF-κB, MAPK, and NLRP3 inflammasome, leading to apoptosis, pyroptosis, and chronic low-grade inflammation. Furthermore, MNP-induced disruption of epithelial barriers and gut microbiota composition undermines immune tolerance and contributes to the pathogenesis of autoimmune conditions. Preclinical models provide evidence linking MNP exposure to exacerbation of diseases such as systemic lupus erythematosus, inflammatory bowel disease, and rheumatoid arthritis. However, human epidemiological data remain limited, highlighting the urgent need for standardized exposure protocols, advanced omics technologies, and longitudinal cohort studies are urgently needed to establish causal links and inform public health strategies. Full article

Background: Lyme borreliosis (LB) constitutes a major challenge for Public Health, particularly in regions where surveillance and diagnostic systems are underdeveloped or fragmented. Despite its potential as a hotspot for tick-borne diseases, Sardinia (Italy) remains poorly explored in terms of LB epidemiology. Methods: A sero-prevalence study was conducted on serum samples stored in the biobank of a hospital in Northern Sardinia. The serum library consisted of serum samples collected on the basis of a diagnostic hypothesis of rheumatic disease. Serological testing for antibodies against Borrelia was performed using the indirect immunofluorescence assay (IFA) and enzyme-linked immunosorbent assays (ELISA), followed by confirmation by Western blot for positive results. The study analyzed 58 serum samples from patients selected based on clinical symptoms compatible with Borrelia spp. infection. Results: Among the 58 patients, 9 (15.5%) yielded positive results, with absorbance values higher than those of the positive control, suggesting that the pathogen is widespread but poorly recognized in Sardinia. The results are in line with broader trends in the Mediterranean, indicating that Sardinia can no longer be considered a marginal area for Borrelia spp. circulation. Conclusions: The status of Sardinia as a sentinel territory underlines the need for enhanced epidemiological surveillance within the One Health approach, including human, animal and environmental health. Full article

Background/Objectives: Dementia is a growing public health concern in rapidly aging Japan. Dietary factors, including dairy products, have been proposed as modifiable influences on cognitive health, although findings across studies remain inconsistent. This study aimed to examine the association between habitual cheese consumption and incident dementia in a large, population-based cohort of older Japanese adults, and to provide epidemiological evidence regarding its potential preventive role in populations with low baseline dairy intake. Methods: We analyzed data from the Japan Gerontological Evaluation Study (JAGES) 2019–2022 cohort, linking survey responses to long-term care insurance (LTCI) certification records. Participants aged ≥65 years without prior LTCI certification were included. Cheese consumption was assessed at baseline and categorized as ≥1 time/week vs. non-consumers. Propensity score matching (PSM) was applied on sociodemographic and health-related covariates. Cox proportional hazards models estimated hazard ratios (HRs) for incident dementia over three years. Results: After PSM, 7914 participants were analyzed (3957 consumers; 3957 non-consumers). Baseline covariates were well-balanced. Over 3 years, 134 consumers (3.4%) and 176 non-consumers (4.5%) developed dementia, corresponding to an absolute risk difference of 1.06 percentage points. Cheese consumption was associated with a lower hazard of dementia (HR = 0.76, 95% CI 0.60–0.95, p = 0.015). Conclusions: Habitual cheese consumption (≥1 time/week) was modestly associated with a reduced 3-year incidence of dementia in older Japanese adults. While the absolute risk reduction was small, these findings are consistent with prior observational evidence linking dairy intake to cognitive health. Further research is warranted to clarify dose–response relationships, cheese subtypes, and underlying mechanisms. Full article

Plant viruses can significantly influence the behavior and performance of their insect vectors, with profound implications for viral epidemiology. However, studies on the effects of co-infection with multiple plant viruses on vector feeding behavior remain scarce, despite its frequent occurrence in nature and potential for altered transmission outcomes. Bemisia tabaci MED, a key vector insect, is closely linked to the rapid spread of tomato chlorosis virus (ToCV) and tomato yellow leaf curl virus (TYLCV) in China. In this study, the electrical penetration graph (EPG) technique was employed to investigate and compare the indirect (via infected plants) and direct (via viruliferous insects) effects of ToCV alone and ToCV and TYLCV co-infection on the feeding behaviors of B. tabaci MED. The results revealed that whiteflies on ToCV-infected or ToCV&TYLCV co-infected plants exhibited significantly longer non-probing durations compared to those on un-infected plants. The intracellular puncture activity of whiteflies was markedly reduced on virus-infected plants, and ToCV infection particularly shortened the duration of phloem sap ingestion. Moreover, viruliferous whiteflies (carrying ToCV or both viruses) spent less time in the intercellular pathway phase. Specifically, ToCV-viruliferous whiteflies had a shorter first-probe duration than non-viruliferous ones. The time from the first probe to the first E phase was also shorter in viruliferous whiteflies, especially in those carrying both ToCV and TYLCV. Furthermore, a significant difference was observed in the total duration of phloem sap ingestion between ToCV-viruliferous and ToCV&TYLCV-viruliferous whiteflies. These findings indicate that both ToCV infection and ToCV&TYLCV co-infection can modulate whitefly feeding behaviors through indirect and direct manners, with co-infection eliciting unique behavioral changes. These insights are valuable for elucidating the negative impact of ToCV-infected and ToCV&TYLCV co-infected tomato plants on whitefly performance, and for uncovering the mechanisms underlying the epidemics of these viruses. Full article

Acinetobacter baumannii is a multidrug-resistant opportunistic pathogen that poses critical challenges in hospital settings due to its environmental resilience and high resistance to antibiotics. Genomic surveillance has become essential for identifying transmission patterns, guiding antimicrobial stewardship, and informing infection control policies. We conducted whole-genome sequencing on 44 A. baumannii isolates collected between 2022 and 2023 from diverse wards in an Italian hospital. Illumina-based sequencing was followed by a comprehensive bioinformatics pipeline, including genome assembly, taxonomic validation, MLST, SNP-based phylogeny, pan-genome analysis, antimicrobial resistance (AMR) gene profiling, and virulence factor prediction. Most isolates were classified as ST2; SAMPLE-34 was ST1 and genetically distinct. Phylogenetic analysis revealed four clonal clusters with cluster-specific AMR and accessory gene content. The pan-genome included 5050 genes, with notable variation linked to hospital ward origin. ICU and internal medicine strains carried higher loads of AMR genes, especially against aminoglycosides, β-lactams, and quinolones. Virulence profiling highlighted widespread immune evasion mechanisms; “Acenovactin” was predominant, while some isolates lacked key adhesion or toxin factors. Our findings underscore the clinical relevance of integrating genomic epidemiology into routine hospital surveillance. Identifying clonal clusters and resistance signatures supports real-time outbreak detection, risk stratification, and targeted infection prevention strategies. Full article

Evidence-based medicine (EBM) supplies the best available data, yet clinicians still face low-value care, surrogate-driven reversals, and pseudoscientific claims. We propose Semi-Imperative Evidentialism (SIE), a normative framework that links evidential warrant to proportionate professional duties while preserving patient autonomy. Using a targeted narrative review in philosophy of science, bioethics, and clinical epidemiology, we distilled six binary attributes to classify activities as Science, Pseudoscience, or Non-science. Scientific items enter a two-tier ladder—Tier 1 (established clinical evidence) or Tier 2 (emerging or preclinical evidence)—with status re-scored as randomized trials, living meta-analyses, and post-marketing safety signals accrue. SIE maps tiers to action: Tier 1 should be offered or strongly recommended, with reasons documented if declined; Tier 2 should be discussed with explicit consent, preferably within trials or registries; Pseudoscience should be refused or discontinued with corrective education; Non-science may be acknowledged as contextual support when safe and non-substitutive. Worked examples—antiarrhythmic suppression post–myocardial infarction (CAST) and “complementary cancer cures”—illustrate earlier and more transparent course-correction. SIE provides a fallibilist bridge from evidence to duty, constraining discretion without eroding autonomy; prospective audits and cluster trials should test its impact on prescribing and consent. Full article