Search Results (2,917)

Rhabditis (Rhabditella) axei is a predominantly free-living nematode commonly found in sewage systems and decomposing organic matter. While primarily saprophytic, it has been documented as an opportunistic pathogen in human urinary and gastrointestinal tracts. The Chinese red panda (Ailurus styani), a rare and protected species in China, has not previously been reported as a host for Rhabditis (Rhabditella) spp. infections. This study reports the first documented occurrence of R. axei in red panda feces, unambiguously confirmed through integrative taxonomic approaches combining morphological and molecular analyses. The nematodes exhibited key morphological features consistent with R. axei, including a cylindrical rhabditiform esophagus, sexually dimorphic tail structures, and diagnostic spicule morphology. Molecular analysis based on 18S-ITS-28S rDNA sequencing confirmed their identity, showing >99% sequence similarity to R. axei reference strains (GenBank: PP135624.1, PP135622.1). Phylogenetic reconstruction using 18S rDNA and ITS rDNA sequences placed the isolate within a well-supported R. axei clade, clearly distinguishing it from related species such as R. blumi and R. brassicae. The findings demonstrate the ecological plasticity of R. axei as a facultative parasite capable of infecting non-traditional hosts and further highlight potential zoonotic risks associated with environmental exposure in captive wildlife populations. Our results emphasize the indispensable role of molecular diagnostics in accurately distinguishing morphologically similar nematodes within the Rhabditidae family, while providing essential baseline data for health monitoring in both in situ and ex situ conservation programs for this endangered species. Full article

Microplastics (MPs) can affect fish health by inducing oxidative stress, but their impact on structural coloration remains poorly understood. This study investigated the effects of environmentally relevant concentrations (16 and 160 μg/L) of MPs and nanoplastics (NPs) exposure on growth, oxidative stress and structural coloration in blue strain guppy fish (Poecilia reticulata). Results showed exposure to 160 μg/L MPs significantly reduced specific growth rate of fish compared to controls. Plastic accumulation followed a dose-dependent pattern, especially within gut concentrations. Oxidative stress responses differed between MPs and NPs: 160 μg/L MPs decreased SOD activity in skin and reduced GSH levels, while 160 μg/L NPs increased MDA levels in gut tissues, indicating severe lipid peroxidation. Structural coloration analysis revealed exposure to 160 μg/L MPs decreased lightness and increased yellowness, demonstrating reduced blue coloration. This was accompanied by an increase in skin uric acid content, suggesting that guanine conversion might occur to combat oxidative stress. These findings demonstrate that MPs, particularly at high concentrations, impair growth and induce oxidative stress in guppies. To counteract stress, guanine in iridophores may be converted into uric acid, leading to a decline in structural coloration. This study is the first to reveal that MPs disrupt structural coloration of fish, providing new insights into the ecological risks of plastic pollution on aquatic organisms. Full article

Processed sea sand has emerged as a viable alternative to traditional fine aggregates in the Sri Lankan construction industry. Despite its economic and environmental advantages, concerns over residual seashell content have limited its widespread adoption by local contractors. Residual seashell content, typically ranging from 1% to 3% after processing, has raised concerns about its impact on the performance of concrete. This study systematically investigates the influence of seashell fragments, with a content of up to 5%, on the fresh, mechanical, and durability properties of sea sand concrete and mortar. Experimental results indicate that workability remains stable, with minor variations across the tested range of shell content. Compressive strength remains relatively consistent from 0% to 5% seashells, indicating that seashell content does not significantly impact the strength within this range. Durability tests reveal minimal effects of shell content on concrete performance within the tested shell range, as indicated by results for water absorption, rapid chloride penetration, and acid exposure testing. Accelerated corrosion indicates that the typical shell content does not increase corrosion risk; however, high shell content (>3%) can compromise corrosion durability. Overall, these findings demonstrate that the mechanical and durability performance of sea sand concrete remains uncompromised at typical seashell content levels (1–3%), supporting the use of processed sea sand as a sustainable and viable alternative to traditional fine aggregates in Sri Lankan construction. Full article

As typical environmental hormones, endocrine-disrupting chemicals (EDCs) have become a global environmental health issue of high concern due to their property of interfering with the endocrine systems of organisms. As a commonly used substitute for bisphenol A (BPA), bisphenol E (BPE) has been frequently detected in environmental matrices such as soil and water in recent years. Existing research has unveiled the developmental and reproductive toxicity of BPE; however, only one in vitro cellular experiment has preliminarily indicated potential neurotoxic risks, with its underlying mechanisms remaining largely unelucidated in the current literature. Potential toxic mechanisms and action targets of BPE were predicted using the zebrafish model via network toxicology and molecular docking, with RT-qPCRs being simultaneously applied to uncover neurotoxic effects and associated mechanisms of BPE. A significant decrease (p < 0.05) in the frequency of embryonic spontaneous movements was observed in zebrafish at exposure concentrations ≥ 0.01 mg/L. At 72 hpf and 144 hpf, the larval body length began to shorten significantly from 0.1 mg/L to 1 mg/L, respectively (p < 0.01), accompanied by a reduced neuronal fluorescence intensity and a shortened neural axon length (p < 0.01). By 144 hpf, the motor behavior in zebrafish larvae was inhibited. Through network toxicology and molecular docking, HSP90AB1 was identified as the core target, with the cGMP/PKG signaling pathway determined to be the primary route through which BPE induces neurotoxicity in zebrafish larvae. BPE induces neuronal apoptosis and disrupts neurodevelopment by inhibiting the cGMP/PKG signaling pathway, ultimately suppressing the larval motor behavior. To further validate the experimental outcomes, we measured the expression levels of genes associated with neurodevelopment (elavl3, mbp, gap43, syn2a), serotonergic synaptic signaling (5-ht1ar, 5-ht2ar), the cGMP/PKG pathway (nos3), and apoptosis (caspase-3, caspase-9). These results offer crucial theoretical underpinnings for evaluating the ecological risks of BPE and developing environmental management plans, as well as crucial evidence for a thorough comprehension of the toxic effects and mechanisms of BPE on neurodevelopment in zebrafish larvae. Full article

Environmental risk assessment (ERA) for pesticide approval in the context of predatory insects remains inadequate as it often overlooks the influence of agricultural practices. An increasing number of studies have shown that prolonged and synergistic pesticide exposure can elevate insect mortality. However, such effects remain largely unstudied in non-target predatory carabid beetles. The carabid beetle Platynus assimilis was subjected to repeated oral and continuous contact exposure to low doses of prothioconazole (20 g ha⁻¹), lambda-cyhalothrin (0.4 g ha⁻¹), or their combination over a 64-day period. The food consumption rate, body mass, locomotor activity, and mortality were monitored throughout the experiment. All pesticide-treated groups showed significantly increased final mortality, with median lethal times (LT₅₀) of 51.6 days for prothioconazole, 60.3 days for lambda-cyhalothrin, and 12.2 days for their combination. A significant synergistic effect on mortality was observed in the combined treatment group, with the highest synergistic ratio detected 20 days after the first exposure. Pesticide-treated beetles exhibited significant abnormalities in locomotor activity and body mass compared to the untreated group. These findings demonstrate that both time-cumulative mortality and potential synergistic interactions, reflecting field-realistic conditions, must be considered in ERA. Failure to do so may lead to an underestimation of pesticide toxicity to predatory carabids. Full article

The extensive use of conventional pesticides has been a fundamental strategy in modern agriculture for controlling pests and increasing crop productivity; however, their improper application poses significant risks to human health and environmental sustainability. This review compiles scientific evidence linking pesticide exposure to oxidative stress and genotoxic damage, particularly affecting rural populations and commonly consumed foods, even at levels exceeding the maximum permissible limits in fruits, vegetables, and animal products. Additionally, excessive pesticide use has been shown to alter soil microbiota, negatively compromising long-term agricultural fertility. In response to these challenges, recent advances in nanotechnology offer promising alternatives. This review highlights the development of nanopesticides designed for controlled release, improved stability, and targeted delivery of active ingredients, thereby reducing environmental contamination and increasing efficacy. Moreover, emerging nanobiosensor technologies, such as e-nose and e-tongue systems, have shown potential for real-time monitoring of pesticide residues and soil health. Although pesticides are still necessary, it is crucial to implement stricter laws and promote sustainable solutions that ensure safe and responsible agricultural practices. The need for evidence-based public policy is emphasized to regulate pesticide use and protect both human health and agricultural resources. Full article

Exposure to per- and polyfluoroalkyl substances (PFASs) can cause detrimental health effects. The consumption of contaminated food is viewed as a major exposure pathway for humans, but the relationship between agriculture and PFASs has not been investigated thoroughly, and it is becoming a pressing issue since health advisories are continuously being reassessed. This semi-systematic literature review connects the release, environmental fate, and agriculture uptake of PFASs to enhance comprehension and identify knowledge gaps which limit accurate risk assessment. It focuses on the heavily agricultural state of Minnesota, USA, which is representative of the large Midwestern US Corn Belt in terms of agricultural activities, because PFASs have been monitored in Minnesota since the beginning of the 21st century. PFAS contamination is a complex issue due to the over 14,000 individual PFAS compounds which have unique chemical properties that interact differently with air, water, soil, and biological systems. Moreover, the lack of field studies and monitoring of agricultural sites makes accurate risk assessments challenging. Researchers, policymakers, and farmers must work closely together to reduce the risk of PFAS exposure as the understanding of their potential health effects increases and legacy PFASs are displaced with shorter fluorinated replacements. Full article

Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta cells, resulting in lifelong insulin dependence. While genetic susceptibility—particularly human leukocyte antigen (HLA) class II alleles—is a major risk factor, accumulating evidence implicates viral infections as potential environmental triggers in disease onset and progression. This narrative review synthesizes current findings on the role of viral pathogens in T1DM pathogenesis. Enteroviruses, especially Coxsackie B strains, are the most extensively studied and show strong epidemiological and mechanistic associations with beta-cell autoimmunity. Large prospective studies—including Diabetes Virus Detection (DiViD), The environmental determinans of diabetes in the young (TEDDY), Miljøfaktorer i utvikling av type 1 diabetes (MIDIA), and Diabetes Autoimmunity Study in the Young (DAISY)—consistently demonstrate correlations between enteroviral presence and the initiation or acceleration of islet autoimmunity. Other viruses—such as mumps, rubella, rotavirus, influenza A (H1N1), and SARS-CoV-2—have been investigated for their potential involvement through direct cytotoxic effects, immune activation, or molecular mimicry. Interestingly, certain viruses like varicella-zoster virus (VZV) and cytomegalovirus (CMV) may exert modulatory or even protective influences on disease progression. Proposed mechanisms include direct beta-cell infection, molecular mimicry, bystander immune activation, and dysregulation of innate and adaptive immunity. Although definitive causality remains unconfirmed, the complex interplay between genetic predisposition, immune responses, and viral exposure underscores the need for further mechanistic research. Elucidating these pathways may inform future strategies for targeted prevention, early detection, and vaccine or antiviral development in at-risk populations. Full article

Microplastics are pervasive environmental pollutants that pose risks to human health through ingestion and inhalation. This review synthesizes current practices to reduce exposure and toxicity by examining major exposure routes and dietary interventions. More than 130 papers were analyzed to achieve this aim. The findings show that microplastics contaminate a wide range of food products, with particular concern over seafood, drinking water, plastic-packaged foods, paper cups, and tea filter bags. Inhalation exposure is mainly linked to indoor air quality and smoking, while dermal contact poses minimal risk, though the release of additives from plastics onto the skin remains an area of concern. Recommended strategies to reduce dietary exposure include consuming only muscle parts of seafood, moderating intake of high-risk items like anchovies and mollusks, limiting canned seafood liquids, and purging mussels in clean water before consumption. Avoiding plastic containers, especially for hot food or microwaving, using wooden cutting boards, paper tea bags, and opting for tap or filtered water over bottled water are also advised. To mitigate inhalation exposure, the use of air filters with HyperHEPA systems, improved ventilation, regular vacuuming, and the reduction of smoking are recommended. While antioxidant supplementation shows potential in reducing microplastic toxicity, further research is needed to confirm its effectiveness. This review provides practical, evidence-based recommendations for minimizing daily microplastic exposure. Full article

Chronic kidney disease (CKD) has now reached epidemic proportions in many parts of the world, primarily due to the high incidence of diabetes and hypertension. By 2040, CKD is predicted to be the fifth-leading cause of years of life lost. Developing strategies to prevent CKD and to reduce its progression to kidney failure is thus of great public health significance. Hypertension is known to be both a cause and a consequence of kidney damage and an eminently modifiable risk factor. An increased risk of hypertension, especially among women, has been linked to chronic exposure to the ubiquitous food contaminant cadmium (Cd). The mechanism is unclear but is likely to involve its action on the proximal tubular cells (PTCs) of the kidney, where Cd accumulates. Here, it leads to chronic tubular injury and a sustained drop in the estimated glomerular filtration rate (eGFR), a common sequela of ischemic acute tubular necrosis and acute and chronic tubulointerstitial inflammation, all of which hinder glomerular filtration. The present review discusses exposure levels of Cd that have been associated with an increased risk of hypertension, albuminuria, and eGFR ≤ 60 mL/min/1.73 m² (low eGFR) in environmentally exposed people. It highlights the potential role of 20-hydroxyeicosatetraenoic acid (20-HETE), the second messenger produced in the kidneys, as the contributing factor to gender-differentiated effects of Cd-induced hypertension. Use of GFR loss and albumin excretion in toxicological risk calculation, and derivation of Cd exposure limits, instead of β₂-microglobulin (β₂M) excretion at a rate of 300 µg/g creatinine, are recommended. Full article

Background/Objectives: Urban green space has been increasingly recognized as a determinant of maternal and child health. This study investigated the association between prenatal exposure to different types of green space and the risk of congenital anomalies in South Korea. Methods: We analyzed data from the National Health Insurance Service (N = 142,422). Green space exposure was measured at the area level and categorized into grassland and forest; statistical analysis was performed using generalized estimating equations and generalized additive models to analyze the associations. Additionally, subgroup and sensitivity analyses were performed. Results: GEE analysis showed that a 10% increase in the proportion of grassland in a residential district was associated with a reduced risk of nervous system (adjusted odds ratio [aOR]: 0.77, 95% confidence interval [CI]: 0.63–0.94) and genitourinary system anomalies (aOR: 0.83, 95% CI: 0.71–0.97). The subgroup analysis results showed significance only for male infants, but the difference between the sexes was not significant. In the quartile-based analysis, we found a slightly significant p-value for trend for the effect of forests on digestive system anomalies, but the trend was toward increasing risk. In a sensitivity analysis with different exposure classifications, the overall and nervous system anomalies in built green space showed that the risk decreased as green space increased compared to that in the lowest quartile. Conclusions: Our results highlight the importance of spatial environmental factors during pregnancy and suggest that different types of green spaces differentially impact the offspring’s early health outcomes. This study suggests the need for built environment planning as part of preventive maternal and child health strategies. Full article

Air pollution is linked to childhood mortality and morbidity in low- and middle-income countries globally. There is growing evidence linking air pollution to asthma and other respiratory diseases in children. Studies have shown that children are likely to experience asthma due to their narrow airways and their heightened sensitivity to environmental irritants. This study aims to investigate the relationship between ambient air pollution and respiratory diseases in children under the age of 5. The study will be conducted in the informal township of Alexandra, north of Johannesburg, South Africa. A quantitative approach will be used in this cross-sectional analytical study. Data will be collected using different tools that include a questionnaire to determine the prevalence of asthma and respiratory disease and potential risk factors. While environmental air pollution will be measured using Radiello passive samplers and Gillian pumps. Data will be analyzed using the latest version of the STATANow/MP 19.5 software. Furthermore, health risk assessment will be conducted for lifetime non-carcinogenic and carcinogenic risk estimation following the USEPA framework. The study will identify environmental triggers that exacerbate asthma and other respiratory conditions in other similar community settings and will contribute to the body of knowledge in public health. Ethical approval was obtained from the Research Ethics Committee, Faculty of Health Sciences at the University of Johannesburg. Full article

Background: Patients diagnosed with melanoma are at increased risk of developing multiple primary melanomas (MPMs). Identifying clinical and genetic factors associated with MPM is critical for implementing personalized surveillance strategies. This study aims to describe the clinical, histopathological, and genetic characteristics of patients with MPM managed in a tertiary hospital and to contextualize findings within the current literature. Methods: We conducted a retrospective review of patients diagnosed with two or more primary melanomas between 2010 and 2023 at a tertiary dermatology unit. Demographic data, personal and family cancer history, phototype, melanoma characteristics, genetic testing, staging, treatments, and outcomes were collected. These data were compared with findings from the recent literature. Results: Thirteen patients (ten males, three females; median age: 59 years) were found to have a total of 33 melanomas. Most patients had Fitzpatrick phototype II and no immunosuppression. The number of melanomas per patient ranged from two to five. Synchronous lesions were observed in two patients. Common locations included the trunk and extremities. Histologically, 57% were in situ melanomas, and subsequent melanomas were generally thinner than the index lesion. Two patients showed progression to advanced disease. One patient was positive for MC1R mutation; the rest were negative or inconclusive. Additional phenotypic and environmental risk factors were extracted from patient records and are summarized as follows: Ten patients (76.9%) had Fitzpatrick skin phototype II, and three (23.1%) had phototype III. Chronic occupational sun exposure was reported in four patients (30.8%), while five (38.5%) recalled having suffered multiple sunburns during childhood or adolescence. Eight patients (61.5%) presented with a total nevus count exceeding 50, and five (38.5%) exhibited clinically atypical nevi. None of the patients reported use of tanning beds. Conclusions: Our findings are consistent with the existing literature indicating that patients with MPM often present with thinner subsequent melanomas and require long-term dermatologic follow-up. The inclusion of genetic testing and phenotypic risk factors enables stratified surveillance and supports the application of personalized medicine in melanoma management. Full article

Schizophrenia is a challenging multifactorial neuropsychiatric disease that involves interactions between genetic susceptibility and environmental insults. Increasing evidence implicates viral infections as significant environmental contributors, particularly during sensitive neurodevelopmental periods. This review synthesises current findings on the viral hypothesis of schizophrenia, encompassing a wide array of neurotropic viruses, including influenza viruses, herpesviruses (HSV-1 and 2, CMV, VZV, EBV, HHV-6 and 8), hepatitis B and C viruses, HIV, HERVs, HTLV, Zika virus, BoDV, coronaviruses (including SARS-CoV-2), and others. These pathogens can contribute to schizophrenia through mechanisms such as direct microinvasion, persistent central nervous system infection, immune-mediated neuroinflammation, molecular mimicry, and the disturbance of the blood–brain barrier. Prenatal exposure to viral infections can trigger maternal immune activation, resulting in cytokine-mediated alterations in the neurological development of the foetus that persist into adulthood. Genetic studies highlight the role of immune-related loci, including major histocompatibility complex polymorphisms, in modulating susceptibility to infection and neurodevelopmental outcomes. Clinical data also support the “mild encephalitis” hypothesis, suggesting that a subset of schizophrenia cases involve low-grade chronic neuroinflammation. Although antipsychotics have some immunomodulatory effects, adjunctive anti-inflammatory therapies show promise, particularly in treatment-resistant cases. Despite compelling associations, pathogen-specific links remain inconsistent, emphasising the need for longitudinal studies and integrative approaches such as viromics to unravel causal relationships. This review supports a “multi-hit” model in which viral infections interfere with hereditary and immunological susceptibilities, enhancing schizophrenia risk. Elucidating these virus–immune–brain interactions may facilitate the discovery of biomarkers, targeted prevention, and novel therapeutic strategies for schizophrenia. Full article

Progress in establishing environmental risk factors and, consequently, prophylactic measures for glial tumors, particularly for glioblastomas, is of utmost importance, considering the dismal prognosis and limited treatment options. This report surveyed updates on established and recently identified factors that can predispose a patient to glioma formation while highlighting possible mechanistic links and further research directions. In addition to established factors that increase the risk of glioma, i.e., brain irradiation and several genetic syndromes, another group consists of likely factors contributing to such risks, such as the use of tobacco and those yielding ambiguous results (e.g., UV exposure). Oxidative stress is a common denominator for several types of exposure, and a mechanistic background for other factors remains elusive. Nevertheless, the analysis of clinical and basic research strongly suggests that, apart from the effect of environmental stressors on DNA alterations and mutation burden, the impact of modifying the tumor microenvironment should be considered. Identifying the involvement of environmental hazards in gliomagenesis and glial tumor progression would lower overall risk by modifying clinical practice, patient management, and lifestyle choices. Further verifying the environmental hazards in glioma formation and progression would have far-reaching implications for neurologists, neurosurgeons, and patients. Full article