Search Results (2,996)

Conventional needle-based vaccination may cause tissue injury and increase the risk of cross-contamination between animals. This study evaluated the immunological effects of delivering an inactivated porcine circovirus type 2 (PCV2) vaccine using a needle-free jet injection system compared with needle injection in pigs. Immune responses were assessed using enzyme-linked immunosorbent assay (ELISA) for PCV2-specific antibody levels on days 7, 14, and 28 post-vaccination. Cellular architecture at injection sites and differential gene expression were analyzed using immunohistochemistry and transcriptome sequencing. Results showed that pigs receiving needle-free vaccination at 0.50 mL and 0.75 mL injection volumes exhibited higher PCV2-specific antibody responses than pigs receiving 1.0 mL needle injection. Needle-free vaccination also preserved dermal collagen fiber architecture, altered antigen-presenting cell distribution, and was associated with distinct activation of immune-related pathways, particularly those involved in leukocyte migration and cytokine-cytokine receptor interactions. These findings indicate that needle-free vaccination was associated with distinct PCV2-specific antibody responses and local immune microenvironment changes, supporting its potential as an alternative vaccine delivery strategy for swine PCV2 vaccination. Full article

The effects of biostimulants on raspberry remain insufficiently understood, particularly in relation to cultivar-specific responses and the potential of remote sensing for treatment evaluation. The aim of this study was to assess the impact of foliar-applied biostimulants on yield and physiological responses of two floricane raspberry cultivars, Glen Ample and Przehyba, using UAV-based multispectral imaging under field conditions. Five treatment variants were tested, including a control and four biostimulant formulations based on animal-derived amino acids, plant-derived amino acids, seaweed extract, and seaweed extract combined with animal-derived amino acids. Biostimulant application significantly affected yield and fruit number per plant, whereas fruit weight remained unchanged. The highest yield values per plant regardless of cultivar were associated with treatments based on plant-derived amino acids (2578.78 g) and seaweed-containing (2483.36–2544.49 g) formulations, while the lowest values were recorded in the control (2335.66 g) and after the application of animal-derived amino acids (2351.80 g). Multispectral analysis revealed treatment-dependent temporal changes in vegetation indices, with clearer trends emerging after aggregation of relative percentage changes across measurement intervals. These results indicate that biostimulant effectiveness in floricane raspberry is strongly dependent on cultivar, formulation type, and temporal context. UAV-based multispectral imaging proved to be a promising non-destructive tool for tracking physiological responses to biostimulation under field conditions. Full article

Bioactive peptides are an important source of therapeutic molecules and molecular scaffolds involved in defense, signaling, and immune regulation. Despite the extraordinary diversity of Coleoptera, the structural landscape of beetle-derived bioactive peptides remains largely unexplored, limiting our understanding of their evolutionary diversity and biotechnological potential. Here, we performed a large-scale structural survey of predicted toxin-like peptide scaffolds across publicly available Coleoptera transcriptomes by integrating transcriptome mining, peptide maturation prediction, physicochemical characterization, AlphaFold 3 structural modeling, structural similarity analyses, and interpretable machine learning. We identified 291 candidate peptides, of which 155 contained canonical signal peptides and 273 produced mature peptides within the expected size range of known bioactive peptides. Structural analyses revealed that, despite extensive sequence diversity, many candidates were organized into a comparatively restricted repertoire of compact cysteine-rich architectures, indicating that structural similarity is retained across peptides exhibiting substantial primary-sequence variation. Comparative structural analyses further identified recurrent protein architectures shared across multiple beetle lineages, while machine learning prioritization integrated structural and biochemical descriptors to identify high-confidence candidates for future functional characterization. These analyses establish the first structural atlas of predicted toxin-like peptides across Coleoptera and demonstrate that structure-guided transcriptome mining provides a powerful framework for uncovering recurrent bioactive peptide scaffolds that would remain largely undetected using sequence-based approaches alone. Beyond expanding our understanding of peptide evolution in beetles, this resource is a foundation for future structural, functional, and biotechnological exploration of bioactive peptides in underexplored animal groups. Full article

Background/Objectives: Retinal imaging has considerable potential for monitoring Alzheimer’s disease (AD) neurodegeneration, as retinal ganglion cell dendritic atrophy within the inner plexiform layer (IPL) is an early event. We tested whether quantitative optical coherence tomography (OCT) speckle texture analysis combined with supervised machine learning could discriminate AD-related IPL alterations without exogenous contrast agents in a mouse model. Methods: Retinal explants from triple-transgenic AD mice (n = 7, aged 12 months) and C57BL/6 controls (n = 3, aged 15 months) were imaged ex vivo using a custom 1040 nm spectral-domain OCT system. Five grey-level co-occurrence matrix (GLCM) features were extracted from IPL volumes of interest (VOIs) and classified using a linear support vector machine (SVM). Results: AD and control IPL textures formed two completely separable clusters in a two-dimensional feature space defined by contrast and entropy (0°), achieving 100% VOI-level classification accuracy (95% CI: 96.4–100%). However, given the small sample size, VOI-level rather than animal-level validation, lack of histological confirmation, non-interleaved image acquisition, and differences in age/strain between groups, these results represent exploratory dataset separability rather than a validated diagnostic test. Conclusions: These findings demonstrate the feasibility of the ligand-free, texture-based OCT discrimination of IPL alterations, indicating a strong underlying optical signal. Adequately powered, in vivo longitudinal studies with matched controls, interleaved acquisition, animal-level cross-validation, and histological validation are required before any clinical translation. Full article

Lying behaviour reflects cattle welfare response. This study aimed to investigate changes in salivary profiles and production variables based on lying time in dairy cows to identify potential biomarkers of rest-related changes. Over a three-month period, lying time was monitored in 15 healthy commercial dairy cows using accelerometric collars. Saliva samples were analyzed for relevant biomarkers. The LMM showed that salivary cortisol (β = 0.481, 95% CI: 0.204–0.758, p = 0.001) and total adenosine deaminase (tADA, β = 0.011, 95% CI: 0.005–0.017, p < 0.001) were positively associated with daily lying time, whereas creatinine kinase (CK) was negatively associated with daily lying time (β = −0.015, 95% CI: −0.030 to −0.001, p = 0.035). Metabolic stress can drive cows to prioritize lying, revealing a coping response to sub-optimal welfare. Increased salivary tADA reflects inflammatory conditions that alter animal behaviour by enhancing lying time. Increasing CK indicates muscle tissue injury, and physical strain may be due to acute restlessness or sustained standing. The findings suggest that changes in lying behaviour may be associated with changes in salivary analytes. The results are encouraging but require validation in larger and more diverse populations before routine application in dairy welfare assessment. Full article

Nanomaterials are increasingly used in manufacturing, medicine, consumer products, and environmental technologies due to their unique physicochemical properties. Although these materials offer substantial technological and societal benefits, their widespread use has raised concerns about potential health risks. Of particular importance is exposure during pregnancy, as certain nanoparticles can cross the placental barrier and reach the developing embryo. Fetal tissues are highly sensitive to environmental insults, so maternal exposure to nanoparticles may disrupt normal development and increase the risk of abnormal pregnancy outcomes. This review examines the current understanding of nanoparticle-induced developmental toxicity, with a focus on the vulnerability of the maternal–fetal unit. We discuss the structure and function of the placental barrier and the mechanisms that enable nanoparticle transfer from mother to fetus. Particular attention is given to how nanoparticle characteristics, including size, shape, composition, and surface chemistry, influence biodistribution, placental transport, tissue accumulation, and toxicity. We summarize the major molecular and cellular mechanisms implicated in fetotoxicity, highlighting oxidative stress, apoptosis, autophagy, and DNA damage as recurring pathways identified across experimental studies. These interconnected processes contribute to placental dysfunction, impaired fetal growth, developmental abnormalities, and adverse pregnancy outcomes. We also compare findings across different classes of nanoparticles, including metal, metal oxide, carbon-based, and polymeric nanomaterials, identifying both shared toxicological mechanisms and material-specific effects. Evidence from animal models demonstrates that susceptibility varies according to nanoparticle properties, exposure conditions, and species, underscoring the complexity of nanoparticle–biological interactions and the limitations of extrapolating experimental findings directly to humans. Overall, the available evidence indicates that nanoparticle exposure during pregnancy represents a potential risk to fetal health, although important knowledge gaps remain regarding human exposure and long-term developmental outcomes. A better understanding of the mechanisms underlying nanoparticle-induced fetotoxicity is essential for improving human health risk assessment, refining experimental models, informing regulatory policies, and supporting the safe-by-design development of nanomaterials. Such knowledge will help ensure the responsible application of nanotechnology while minimizing potential risks during pregnancy. Finally, this review is distinguished by its integrated analysis of how the chemical characteristics of nanoparticles govern placental transfer and the mechanistic pathways of fetotoxicity across multiple nanomaterial classes, providing a unified framework that connects material properties with their potential for abnormal fetal development and adverse pregnancy outcomes. Full article

Stroke remains one of the leading causes of death and long-term neurological disability worldwide, while currently available therapeutic strategies are limited by narrow treatment windows and incomplete neuroprotection. In this context, plant-derived polyphenols have attracted increasing attention as potential adjunctive agents because of their multimodal biological activity. This review focuses on resveratrol and curcumin, two of the most extensively investigated polyphenols, and evaluates their potential role in the prevention and treatment of ischaemic and haemorrhagic stroke. Evidence from in vitro studies, animal models, and early clinical trials indicates that both compounds may attenuate key mechanisms involved in stroke-related brain injury, including oxidative stress, neuroinflammation, mitochondrial dysfunction, apoptosis, autophagy dysregulation, blood–brain barrier disruption, and microglial activation. Emerging evidence further suggests that interactions with the gut microbiota and modulation of the gut–brain axis may contribute to their biological effects by influencing intestinal barrier integrity, microbial metabolite production, systemic inflammation, and vascular risk. Preclinical studies show that resveratrol and curcumin can reduce infarct volume, limit cerebral oedema, preserve neuronal viability, promote angiogenesis and neurogenesis, and improve neurological and cognitive outcomes. Their beneficial effects have been reported both when administered before stroke onset and after cerebral injury, suggesting potential relevance for both prevention and post-stroke therapy. However, interpretation of these findings requires consideration of the translational limitations of experimental stroke models, which do not fully reproduce the heterogeneity, comorbidities, age profile, and variable reperfusion patterns characteristic of human stroke. Although commonly used models such as middle cerebral artery occlusion provide important mechanistic and therapeutic insights, preclinical efficacy should therefore not be regarded as a direct predictor of clinical benefit. Resveratrol and curcumin may also complement established and emerging treatment strategies, including thrombolysis, endovascular interventions, antihypertensive therapy, and stem cell-based approaches. Nevertheless, their clinical translation remains limited by poor solubility, low bioavailability, rapid metabolism, and insufficient clinical evidence. Novel formulations, including nanoparticles, exosome-based delivery systems, and structurally modified analogues, may help overcome these barriers by improving brain targeting and therapeutic efficacy. Overall, resveratrol and curcumin represent promising but still investigational candidates for adjunctive stroke therapy, requiring further well-designed clinical trials to define their optimal dosing, timing, safety, and clinical value. Full article

Background: Microbiome-based mechanisms have emerged as a key area of investigation in epilepsy, given the growing recognition that gut microbial communities can modulate central nervous system (CNS) function through the gut–brain axis. Epilepsy is a common chronic neurological disorder affecting more than 65 million people worldwide, and despite the availability of anti-seizure medications (ASMs), approximately 30% of patients develop drug-resistant epilepsy. Current ASMs primarily suppress seizures rather than prevent disease progression, highlighting the need for alternative therapeutic strategies. In this context, increasing evidence supports a role for microbiota-dependent pathways in modulating seizure activity and treatment responsiveness. However, the mechanistic basis of these interactions remains incompletely understood. Methods: This narrative review synthesizes findings from the existing literature to examine the role of microbiota-derived metabolites, including neurotransmitters, vitamins, and the polyphenol metabolite S-equol, in gut–brain communication relevant to epilepsy. Evidence was drawn from both preclinical animal models and clinical studies to provide an integrated, mechanistic perspective on how these pathways may influence central nervous system function and seizure susceptibility. Emphasis was placed on studies describing molecular, metabolic, and signaling mechanisms linking the gut microbiome to epileptogenesis and treatment response. Results: Current evidence indicates that communication between the gut and CNS occurs through neural pathways, such as the vagus nerve, as well as through circulating microbial metabolites. These metabolites can cross the intestinal barrier and, in some cases, the blood–brain barrier (BBB), serving as key mediators of host–microbiota signaling. Emerging studies suggest that while some microbial metabolites may directly influence neuronal hyperexcitability and seizure susceptibility, others likely exert secondary or modulatory effects through broader metabolic and immune pathways. However, the precise mechanisms underlying these interactions remain incompletely understood. Conclusions: Some microbial-derived metabolites may serve as promising biomarkers and mechanistic mediators of epilepsy; however, further investigation is needed to define the molecular and cellular pathways through which these metabolites influence seizure susceptibility and epileptogenesis. Full article

Olfactory enrichment is recommended for captive felids, but systematic evidence on practical implementation in multiple species and institutions is limited. We evaluated a simple, keeper-safe scent diffuser delivering spice-based odours to captive lions (Panthera leo), tigers (Panthera tigris), jaguars (Panthera onca), leopards (Panthera pardus), cheetahs (Acinonyx jubatus) and pumas (Puma concolor) at two zoological institutions in Johannesburg, South Africa. Behaviour was recorded during baseline and scent-exposure conditions in 23 individuals. Behavioural diversity (number of distinct behaviours per 15-min session) was the primary outcome. Engagement duration, latency to approach and individual response consistency were also quantified. Animals were exposed to a compound spice blend and four component spices (coriander, paprika, black pepper and garlic) and subsequently to decreasing concentrations of their most preferred scent. Behavioural diversity increased significantly during scent exposure at both institutions (1.9 times greater at Lory Park and 1.8 times greater at Johannesburg Zoo), with large effect sizes at both sites (Cohen’s d ≥ 1.2). Spice type did not significantly affect behavioural diversity, but individual animals showed consistent engagement preferences, approach latencies and response profiles during repeated exposures. Full odour concentrations showed significantly longer engagement durations than low concentrations at both institutions (approximately twofold at Lory Park and threefold at Johannesburg Zoo), but behavioural diversity did not differ significantly between concentration levels. No significant species differences were detected, indicating that assessment by individuals is more informative than species level predictions for enrichment planning. Spice-based diffusers provide a practical, low-cost enrichment tool suitable for multi-institutional implementation. Moreover, enrichment programmes should be evaluated and tailored at the individual animal level. Full article

Aflatoxin B1 (AFB1) is a highly toxic mycotoxin which can be carried over into animal products and cause deterioration of livestock productivity when fed to livestock and wildlife. This review proposes a biomarker-guided framework for improving the early assessment of AFB1 exposure and toxicological responses in animal models. Oral exposure leads to the absorption of AFB1, which is bioactivated in the liver to the reactive AFB1-exo-8,9-epoxide that causes DNA and protein adduct formation, inflammation, mitochondrial apoptosis, and other effects. Cytochrome P450 activation and glutathione-dependent detoxification are in balance in determining susceptibility species, and this balance is different for poultry, pigs, ruminants, and rodents. In addition to traditional liver enzymes and histopathology, we highlight mechanistically informative biomarkers such as metabolites of aflatoxin, DNA and albumin adduct, lipid peroxidation products, antioxidant indices, cytokines, apoptotic markers, as well as signals involved in the Nrf2/NFκB pathway. AFB1 also damages the integrity of the intestinal barrier, the maintenance of the intestinal gut microbiota, reproductive function, growth performance, and development, thus creating a gut–liver-systemic toxic cascade. Finally, an assessment of stage-targeted interventions such as aluminosilicate binders, adsorbents derived from yeast, probiotics and nano-enabled interventions is conducted as viable tools for the reduction in exposure and injury. This review offers targeted mitigation strategies for early diagnosis of aflatoxicosis in animal production systems based on a biomarker approach. Full article

Feed efficiency classification based on residual feed intake (RFI) and residual intake and gain (RIG) is widely used to identify biologically efficient animals, yet it remains unclear whether this classification reflects consistent differences in digestive, fermentative, and metabolic processes. This study evaluated the effects of RFI and RIG classification on nutrient intake, apparent digestibility, ruminal fermentation, nitrogen metabolism, microbial protein synthesis, and gaseous emissions in confined lambs. Thirty-eight weaned Texel ewe lambs underwent a 60-day performance test using an automated feed intake system and were classified as high-efficiency, neutral, or low-efficiency based on both indices. Animals were individually housed in respirometric chambers where emissions of methane, carbon dioxide, nitrous oxide, and ammonia were assessed by cavity ring-down spectroscopy; apparent digestibility was determined from total collections of feed, orts, faeces, and urine; microbial protein synthesis was estimated from urinary purine derivatives; and ruminal short-chain fatty acid profiles were determined by gas chromatography. Feed efficiency classification did not significantly affect body weight, nutrient intake, apparent digestibility, ruminal fermentation parameters, nitrogen balance, microbial protein synthesis, or greenhouse gas emissions. Principal component analysis revealed two major biological gradients related to nutrient intake and utilisation (42.9%) and ruminal fermentation and gaseous emissions (23.3%), together explaining 66.2% of total variance, but showing no clear separation among efficiency groups. These findings indicate that the digestive, fermentative, and nitrogen metabolism variables evaluated in this study did not account for the observed variation in feed efficiency. Because the regression underlying RIG explained little additional variation (R² = 0.01), these conclusions primarily reflect feed efficiency as classified by RFI, suggesting that other physiological mechanisms may play a more important role in determining feed efficiency in confined Texel ewe lambs. Full article

This research investigated the extraction and purification of melanin from the Ophiocordyceps sinensis TZ8-1; characterized its structural properties; and evaluated its safety, photoprotective efficacy, and ability to mitigate heavy metals. The results demonstrated that the spectral features of TZ8-1 melanin were consistent with those of synthetic melanin, confirming its classification as typical eumelanin. The safety assessment indicated that TZ8-1 melanin has relatively low toxicity to four types of normal human cells, and based on the results of acute oral toxicity tests, this substance showed high safety for experimental animals. Photoprotection studies showed that TZ8-1 melanin effectively suppressed reactive oxygen species (ROS) generation and significantly improved cell viability post-ultraviolet B (UVB) exposure. Heavy metal mitigation experiments showed that TZ8-1 melanin reduced malondialdehyde (MDA) levels, increased glutathione (GSH) concentrations, and enhanced cell survival rates in heavy metal-exposed conditions. Full article

Persistent racial and ethnic disparities in type 2 diabetes mellitus (T2DM) are incompletely explained by genetic susceptibility, obesity, lifestyle, and socioeconomic factors, suggesting that additional biological mechanisms may link environmental exposures to metabolic disease risk. Increasing evidence indicates that the exposome, encompassing environmental exposures across the life course, may influence long-term metabolic health through molecular mechanisms that integrate environmental signals with host biology. This Review synthesizes epidemiological, experimental, and mechanistic evidence on the gut microbiota–host epigenetic axis and its potential role in linking environmental exposures to population differences in T2DM susceptibility. Gut microbial dysbiosis alters the production and metabolism of short-chain fatty acids, bile acids, and tryptophan-derived metabolites. These microbial metabolites can modulate host signaling and epigenetic processes, including DNA methylation, histone modifications, and non-coding RNA activity, which may influence the expression of genes involved in glucose homeostasis, inflammation, and insulin sensitivity. Conversely, host epigenetic programs may influence intestinal barrier integrity and immune responses, thereby potentially affecting the gut microbial ecosystem, highlighting the reciprocal nature of host–microbiota interactions. We further examine how diet, psychosocial stress, environmental pollutants, and socioeconomic conditions may shape the microbiota–epigenetic axis across diverse populations, providing a framework for understanding differences in metabolic susceptibility without attributing disparities to intrinsic biological variation. However, direct human evidence linking the gut microbiota–host epigenetic axis to racial and ethnic disparities in T2DM risk remains limited, and much of the current framework is based on mechanistic studies, animal models, and associative human data rather than direct causal evidence. Further research in diverse human populations is needed to validate these pathways and establish their contribution to T2DM disparities. This framework may inform biomarker discovery, stratification, precision nutrition, and microbiome-targeted interventions and generate hypotheses for equitable prevention and personalized management of T2DM across diverse populations. Full article

C-C motif chemokine ligand 2 (CCL2) interacts with cytokines, adipokines, miRNAs, and multiple synovial cell populations. Experimental studies indicate that these interactions can form a CCL2-associated inflammatory amplification network across cell types. In cellular and animal models, increased CCL2 is associated with monocyte recruitment, synovial fibroblast activation, osteoclast-related bone remodelling, and vascular responses. Therapeutic strategies targeting the CCL2-centered inflammatory network include antagonists of the CCL2/CCR2 axis, natural products, synthetic compounds, conventional antirheumatic drugs, and emerging delivery-based approaches. Notably, direct CCL2/CCR2 inhibition has shown biological activity in experimental models but has not produced consistent clinical benefit in established rheumatoid arthritis (RA). Although these findings do not establish CCL2 as a dominant causal driver of RA, human observational studies suggest that circulating CCL2 may complement established markers in preclinical RA risk assessment, disease activity and remission classification, estimation of treatment response, and evaluation of RA-related complications such as interstitial lung disease. Of note, no validated concentration cut-off or standardized assay currently supports its routine clinical use. This review examines the CCL2-related inflammatory network in RA and evaluates its cellular mechanisms, therapeutic implications, and potential clinical applications. Full article

Insulin resistance (IR) represents one of the most pressing problems in contemporary public health. Its estimated global prevalence ranges from approximately 15.5% to over 61%, depending on the population studied, the diagnostic criteria applied, and the method used for its assessment. Despite the scale of the problem, IR remains underrecognized and lacks formal definition as a distinct disease entity, even as a growing number of clinicians and researchers worldwide describe it as such. Its asymptomatic or mildly symptomatic course allows it to remain undetected for years, during which it makes a significant contribution to the development of type 2 diabetes, cardiovascular disease (CVD) and metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD), and has been increasingly linked to cellular senescence, certain cancers, neuropsychiatric disorders, and other metabolic conditions. The aim of this review was to summarize current knowledge on the pathophysiology, diagnosis, and clinical implications of insulin resistance, to discuss current challenges in its diagnosis, and to evaluate whether available scientific evidence supports its recognition as a distinct disease entity. This narrative review is based on clinical, epidemiological, and mechanistic data retrieved from PubMed and Google Scholar. Meta-analyses, systematic reviews, clinical and observational studies, clinical guidelines, and expert position statements were analyzed. Animal studies were excluded to maintain a focus on human public health implications. The diagnostic gold standard—the hyperinsulinemic-euglycemic clamp—was discussed, along with surrogate methods used in clinical practice (HOMA-IR, OGTT with insulin measurements, the TyG index, and the TG/HDL-C ratio). Factors potentially contributing to the pathogenesis of IR were examined, including hyperinsulinemia (HI), high-carbohydrate diets, inflammation, stress, and sleep disturbances, as well as conditions in which IR occurs physiologically. The findings indicate that current evidence supports the need for a clearer clinical and diagnostic framework for insulin resistance and suggest that its recognition as a distinct disease entity could facilitate earlier diagnosis, improve the standardization of clinical management, and enable earlier metabolic intervention. Given the steadily rising prevalence of metabolic disease, systemic efforts directed at the early identification and treatment of IR may be a key component of strategies aimed at reducing the population-level burden of metabolic disease and its negative consequences. Full article