Eur Urol. 2025 Apr 26:S0302-2838(25)00210-6. doi: 10.1016/j.eururo.2025.04.008. Online ahead of print.

ABSTRACT

BACKGROUND AND OBJECTIVE: Divergent differentiation and histologic subtypes are common findings in urothelial carcinoma (UC). Clinically relevant genomic alterations and oncogenic drivers of individual subtypes remain poorly defined. We characterized surgical outcomes and the genomic landscape of UC with aberrant histology (UCAH), with a focus on biomarkers and targetable alterations.

METHODS: The clinical cohort comprised 3052 patients who underwent radical cystectomy (RC) with or without neoadjuvant chemotherapy. Targeted exon sequencing was performed for a genomic cohort of 1060 bladder tumors from RC or transurethral resection specimens. We characterized the frequency of oncogenic mutations and targetable alterations, and the tumor mutational burden (TMB) of each subtype. We defined the clonal relatedness of morphologically distinct regions of tumors with mixed histology.

KEY FINDINGS AND LIMITATIONS: Patients with plasmacytoid, micropapillary, sarcomatoid, or mixed-histology tumors had worse cancer-specific survival than patients with pure urothelial histology. ERBB2, FGFR3, and PTEN alterations were most frequent in micropapillary, nested/squamous, and sarcomatoid UC, respectively. TMB was highest in plasmacytoid, neuroendocrine, and micropapillary tumors. Regions of mixed histology had shared clonal origins, but exceptions were observed. The retrospective design and potential for selection bias are limitations of our study.

CONCLUSIONS AND CLINICAL IMPLICATIONS: UCAH tumors have distinct patterns of genomic alterations, which may be targetable via novel therapies and have implications for clinical trial inclusion. Biomarker-driven systemic therapy should be explored in patients with histologic subtypes that are associated with worse clinical outcomes.

PMID:40288936 | DOI:10.1016/j.eururo.2025.04.008

J Affect Disord. 2025 Apr 25:S0165-0327(25)00721-9. doi: 10.1016/j.jad.2025.04.146. Online ahead of print.

ABSTRACT

BACKGROUND: The complexity of the pathogenesis hinders the diagnosis and treatment of bipolar disorder (BD). Despite studies finding a correlation between immune function and BD, the causative relationship between the two remains poorly explained.

METHODS: We investigated the causative relationships between BD (41,917 cases and 371,549 controls) and levels of six types of white blood cells and further evaluated the causative relationships between BD and 731 immune cell traits) using a two-sample Mendelian randomization method, prioritizing the inverse variance weighted approach, based on publicly available GWAS data. Sensitivity analysis was based on MR-Egger intercept method and Cochran's Q test.

RESULTS: We did not find a significant causative relationship between BD and 6 white blood cell traits (FDR > 0.05). However, we found 38 immune cell traits had a causal effect to BD. Among them, 26 immune cell traits increased the risk of BD (OR: 1.01-1.07), including CD4+/CD28+ T cells and CD20+/CD27+ B cells. The remaining 12 including had a protective effect on BD (OR: 0.92-0.99). The backward MR results showed that BD had negative causal effects on 23 immune cell traits (n = 23, OR: 0.79-0.89), which included monocyte, majority of CD4+ T cells, and CD20+ B cells. BD had Positive causal effects 10 immune cell traits (OR: 1.13-1.19), especially CD19+ B cells. The overall causal effect of BD on immune cell traits was significantly higher than the inverse effect (0.011 ± 0.049 vs. 0.001 ± 0.016, p < 0.001).

CONCLUSION: A complex network of bidirectional causative relationships exists between BD and various phenotypic features of immune cells. These findings provide new insights into the diagnosis and treatment of BD from an immunotherapeutic perspective.

PMID:40288451 | DOI:10.1016/j.jad.2025.04.146

Food Chem. 2025 Apr 21;484:144448. doi: 10.1016/j.foodchem.2025.144448. Online ahead of print.

ABSTRACT

The casein-derived bitter peptide VAPFPEVF has been shown to stimulate proton secretion in human parietal cells (HGT-1) via bitter taste receptor TAS2R16, confirmed by siRNA knockdown. Since literature evidence is inconclusive, we hypothized that VAPFPEVF binds to TAS2R16, and investigated its effects on G protein-coupled signaling pathways. Exposure of HGT-1 cells to VAPFPEVF altered cAMP signaling without inducing a calcium response. An atomic force microscopy (AFM)-based approach was employed to demonstrate peptide binding to TAS2R16 in cellular and cell-free environments using TAS2R16-reconstituted proteoliposomes. Increased binding events were observed, reduced by the addition of salicin and TAS2R16 antagonist probenecid. AlphaFold multimer and molecular dynamics simulations suggest VAPFPEVF binds the orthosteric site of TAS2R16. These findings reveal (i) VAPFPEVF interacts with TAS2R16 to modulate cAMP levels without triggering calcium mobilization and (ii) the AFM approach as a valuable tool for studying peptide binding to TAS2R16 and possibly other G-protein coupled transmembrane receptors.

PMID:40288211 | DOI:10.1016/j.foodchem.2025.144448

Cell Rep. 2025 Apr 25;44(5):115623. doi: 10.1016/j.celrep.2025.115623. Online ahead of print.

ABSTRACT

Tissue-resident macrophages (TRMs) populate throughout various tissues, and their homeostatic metabolism is heavily influenced by these microenvironments. Peroxisomes are organelles that contribute to lipid metabolism. However, the involvement of these organelles in the bioenergetics of TRMs remains undetermined. We conducted a developmental screen of TRMs using a conditional peroxisomal biogenesis factor 5 (Pex5) knockout mouse model that lacks functional peroxisomes in all immune cell subsets. Pulmonary alveolar macrophages (AMs) appeared as the only subset of TRMs that required functional peroxisomes for their development. Pex5 deficiency resulted in reduced AM survival due to increased sensitivity to lipotoxicity, in line with an excess accumulation of ceramides. The absence of peroxisomes had a significant effect on overall mitochondrial fitness and altered their metabolic program, allowing them to engage in glycolysis in addition to oxidative phosphorylation. Our results revealed that AMs have a unique metabolic regulation, where peroxisomes play a central role in their homeostatic development and maintenance.

PMID:40287943 | DOI:10.1016/j.celrep.2025.115623

Hum Mol Genet. 2025 Apr 27:ddaf033. doi: 10.1093/hmg/ddaf033. Online ahead of print.

ABSTRACT

Biobanks are innovative biomedical research infrastructures that play a crucial role in advancing cancer research by supporting investigations into the etiology, progression, and therapeutic interventions of the disease. Biobanks have significantly contributed to personalized medicine by providing high-quality bio specimen resources and expertise in tissue handling, essential for understanding the interplay of genetic, ecological, and lifestyle factors on cancer biology, human health, and mortality. By linking bio specimens with clinical, pathological, and epidemiological data, biobanks are central in the discovery and development of cancer therapeutics through biomarkers. In this review, the importance of managing biobanks as integral parts of data generation and analytics continuum driving precision medicine is pointed out. The advent of multi-OMICS analytics, combined with artificial intelligence, systems biology, and deep machine learning, has elevated the importance of bio banking human bio specimens as not only a biological resource but also an informatics asset. Here, we examine the impact of bio banking in facilitating translational, bench-to-bedside cancer research, with a focus on multi-OMICS data-driven biomarker discovery and precision oncology. In addition, we discuss one of the major innovations in biobank management: the hub-and-spoke model. This centralized system leverages core expertise and resources while collecting bio specimens from diverse geographic regions, thereby capturing the heterogeneity of cancer biology. The hub-and-spoke approach is particularly advantageous for countries like India, characterized by vast geographic and demographic diversity. It ensures complete coverage of the different types of cancers, disease stages, and population groups in addressing the complexity and diversity of cancer biology.

PMID:40287834 | DOI:10.1093/hmg/ddaf033

Nucleic Acids Res. 2025 Apr 26:gkaf350. doi: 10.1093/nar/gkaf350. Online ahead of print.

ABSTRACT

Circular dichroism (CD) spectroscopy is an established biophysical technique to study chiral molecules. CD allows investigating conformational changes under varying experimental conditions and has been used to understand secondary structure, folding, and binding of proteins and nucleic acids. Here, we present ChiraKit, a user-friendly, online, and open-source tool to process raw CD data and perform advanced analysis. ChiraKit features include the calculation of protein secondary structure with the SELCON3 and SESCA algorithms, estimation of peptide helicity using the helix-ensemble model, the fitting of thermal/chemical unfolding or user-defined models, and the decomposition of spectra through singular value decomposition or principal component analysis. ChiraKit can be accessed at https://spc.embl-hamburg.de/.

PMID:40287821 | DOI:10.1093/nar/gkaf350

BMC Genomics. 2025 Apr 26;26(1):408. doi: 10.1186/s12864-025-11590-1.

ABSTRACT

BACKGROUND: Enterobacter hormaechei is of increasing concern as both an opportunistic and nosocomial pathogen, exacerbated by its evolving multidrug resistance. However, its taxonomy remains contentious, and little is known about its pathogenesis and the broader context of its resistome. In this study, a comprehensive comparative genomic analysis was undertaken to address these issues.

RESULTS: Phylogenomic analysis revealed that E. hormaechei represents a complex, comprising three predicted species, E. hormaechei, E. hoffmannii and E. xiangfangensis, with the latter putatively comprising three distinct subspecies, namely oharae, steigerwaltii and xiangfangensis. The species and subspecies all display open and distinct pan-genomes, with diversification driven by an array of mobile genetic elements including numerous plasmid replicons and prophages, integrative conjugative elements (ICE) and transposable elements. These elements have given rise to a broad, relatively conserved set of pathogenicity determinants, but also a variable set of secretion systems. The E. hormaechei complex displays a highly mutable resistome, with most taxa being multidrug resistant.

CONCLUSIONS: This study addressed key issues pertaining to the taxonomy of the E. hormaechei complex, which may contribute towards more accurate identification of strains belonging to this species complex in the clinical setting. The pathogenicity determinants identified in this study could serve as a basis for a deeper understanding of E. hormaechei complex pathogenesis and virulence. The extensive nature of multidrug resistance among E. hormaechei complex strains highlights the need for responsible antibiotic stewardship to ensure effective treatment of these emerging pathogens.

PMID:40287657 | DOI:10.1186/s12864-025-11590-1

Cell Death Dis. 2025 Apr 26;16(1):344. doi: 10.1038/s41419-025-07565-5.

ABSTRACT

Chaperone proteins constitute a molecular machinery that controls proteostasis. HSPA2 is a heat shock-non-inducible member of the human HSPA/HSP70 family, which includes several highly homologous chaperone proteins. HSPA2 exhibits a cell type-specific expression pattern in the testis, brain, and multilayered epithelia. It is a crucial male fertility-related factor, but its role in somatic cells is poorly understood. Previously, we found that HSPA2 deficiency can impair epidermal keratinocyte differentiation. In this study, we confirmed the crucial role of HSPA2 in keratinocyte differentiation by investigating immortalized keratinocytes cultured in a reconstructed human epidermis model. Moreover, we uncovered the influence of HSPA2 on immunomodulation. Transcriptomic analysis revealed that the total loss of HSPA2 affected the expression of genes related to keratinocyte differentiation and interleukin- and interferon-mediated signaling. The functional analysis confirmed bidirectional changes associated with the loss of HSPA2. The HSPA2 knockout in HaCaT and Ker-CT keratinocytes, but not HSPA2 overproduction, impaired granular layer development as evidenced by reduced levels of late keratinocyte differentiation markers, filaggrin and involucrin, along with structural abnormalities in the upper epidermal layer. Differentiation defects were accompanied by increased mRNA expression and extracellular secretion of keratinocyte-derived pro-inflammatory IL-6 cytokine and CCL2, CCL8, CXCL1, CXCL6, and CXCL10 chemokines. The loss of HSPA2 also led to increased expression of extracellular HSPA1 and interferon-stimulated genes and secretion of immune cell modulator SLAMF7. Knocking down HSPA1 expression in keratinocytes decreased the secretion of IL-6 and CCL5 release, suggesting extracellular HSPA1's role in the HSPA2-regulated molecular network. To summarize, we uncovered the complex homeostatic role of HSPA2 in epidermal keratinocytes. Our results suggest that dysfunction in HSPA2 activity could be an important pathogenicity factor and potential therapeutic target for inflammatory cutaneous diseases.

PMID:40287440 | DOI:10.1038/s41419-025-07565-5

Life Sci. 2025 Apr 24:123658. doi: 10.1016/j.lfs.2025.123658. Online ahead of print.

ABSTRACT

AIMS: Obesity cardiomyopathy (OCM) is associated with mitochondrial dysfunction caused by altered mitochondrial dynamics. Extracellular mitochondria (exMito) are released following tissue injury under various conditions. While the excessive mitochondrial fission-mediated release of exMito as a mechanism for mitochondrial quality control in several inflammatory disorders, its role in OCM remains unclear. The present work aimed to determine if excessive mitochondrial fission and associated exMito mediate the chronic inflammatory response and cardiac remodeling in OCM.

MATERIALS AND METHODS: H9c2 cardiomyoblasts were treated with 200 μM palmitate (PA) to induce lipotoxicity. C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce OCM. P110, a peptide inhibitor of Drp1/Fis1 interaction, was used to evaluate the impact of excessive mitochondrial fission on cardiac mitochondrial function, quality, and quantity of exMito, systemic inflammatory response, and cardiac contractile function in both models of OCM.

KEY FINDINGS: PA induced excessive mitochondrial fission, increased oxidative stress, decreased ATP level, and damaged exMito release in vitro. Exposure of naïve cardiomyoblasts to exMito isolated from PA treated cells resulted in mitochondrial dysfunction and a pro-inflammatory response. In vivo, HFD induced cardiac mitochondrial and contractile dysfunction, exMito release, and a pro-inflammatory response. Inhibition of Drp1/Fis1 interaction with P110 attenuated the observed effects both in vitro and in vivo.

SIGNIFICANCE: P110 limited lipid-induced mitochondrial dysfunction and decreased exMito release, subsequently improving the inflammatory state and contractile function in our OCM model. Drp1/Fis1 dependent fission and associated exMito release might serve as a therapeutic target for obesity induced cardiomyopathy.

PMID:40287058 | DOI:10.1016/j.lfs.2025.123658

Sci Total Environ. 2025 Apr 25;979:179484. doi: 10.1016/j.scitotenv.2025.179484. Online ahead of print.

ABSTRACT

Environmental stressors in the modern world can fundamentally affect human physiology and health. Exposure to stressors like air pollution, heat, and traffic noise has been linked to a pronounced increase in non-communicable diseases. Specifically, aircraft noise has been identified as a risk factor for cardiovascular and metabolic diseases, such as arteriosclerosis, heart failure, stroke, and diabetes. Noise stress leads to neuronal activation with subsequent stress hormone release that ultimately activates the renin-angiotensin-aldosterone system, increases inflammation and oxidative stress thus substantially affecting the cardiovascular system. However, despite the epidemiological evidence of a link between noise stress and metabolic dysfunction, the consequences of exposure at the molecular, metabolic level of the cardiovascular system are largely unknown. Here, we use a murine model system of short-term aircraft noise exposure to show that noise stress profoundly alters heart metabolism. Within 4 days of noise exposure, the heart proteome and metabolome bear the hallmarks of reduced potential for generating ATP from fatty-acid beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain. This is accompanied by the increased expression of glycolytic metabolites, including the end-product, lactate, suggesting a compensatory shift of energy production towards anaerobic glycolysis. Intriguingly, the metabolic shift is reminiscent of what is observed in failing and ischaemic hearts. Mechanistically, we further show that the metabolic rewiring is likely driven by reactive oxygen species (ROS), as we can rescue the phenotype by knocking out NOX-2/gp91phox, a ROS inducer, in mice. Our results suggest that within a short exposure time, the cardiovascular system undergoes a fundamental metabolic shift that bears the hallmarks of cardiovascular disease. These findings underscore the urgent need to comprehend the molecular consequences of environmental stressors, paving the way for targeted interventions to mitigate health risks associated with chronic noise exposure in modern, environments heavily disturbed by noise pollution.

PMID:40286622 | DOI:10.1016/j.scitotenv.2025.179484

JACC Adv. 2025 Mar 26;4(5):101663. doi: 10.1016/j.jacadv.2025.101663. Online ahead of print.

ABSTRACT

BACKGROUND: Cardiac output (CO) is a quintessential property of the cardiovascular system, one whose estimation is vital to patient care in critical illness. The most common techniques for assessing CO, thermodilution (TD) and the estimated Fick (eFick) approximation, force tradeoffs that motivate a need for new methods.

OBJECTIVES: The purpose of this study was to novel CO estimators to fill key gaps in critical care medicine.

METHODS: Machine learning was used to estimate CO from physiology measurements made during routine clinical care in the intensive care unit (ICU) or cardiac catheterization lab. Models were trained and validated using a curated set of 13,172 ground-truth measurements of TD-CO from 4,825 patients. Model performance was evaluated using regression metrics, trajectory analysis, classification accuracy, and ΔCO tracking.

RESULTS: Three established eFick models all performed poorly in the ICU because their static estimates of oxygen consumption could not track the dynamics of critical illness. In the postcardiac surgery intensive care unit, the best eFick model erred in its CO predictions by 30% (mean absolute percentage error [MAPE]) with a coefficient of determination (R2) of -1.5. The best model derived here, labeled CORE (Catheter Optimized caRdiac output Estimation), predicted CO with an MAPE of 14% (P < 0.001 vs eFick) and an R2 of 0.58. These estimates could be calculated from measurements obtained with either a pulmonary artery catheter or a central venous catheter. The CORE model was also robust to the presence of moderate or severe tricuspid regurgitation, achieving an MAPE of 16% and R2 of 0.65 relative to a ground-truth determined by the direct Fick technique with measured oxygen consumption.

CONCLUSIONS: CO models that account for dynamic physiology in ICU patients were more accurate than widely used eFick models and more versatile than TD. The performance of these models combined with their adaptation to vascular access, broad applicability, ease of use, and ease of deployment should enable them to benefit patients across diverse ICU settings.

PMID:40286350 | DOI:10.1016/j.jacadv.2025.101663

Proteomics. 2025 Apr 26:e202400417. doi: 10.1002/pmic.202400417. Online ahead of print.

ABSTRACT

The accurate construction of computational models in systems biology heavily relies on the availability of quantitative proteomics data, specifically, absolute protein abundances. However, the complex nature of proteomics data analysis necessitates specialised expertise, making the integration of this data into models challenging. Therefore, the development of software tools that ease the analysis of proteomics data and bridge between disciplines is crucial for advancing the field of systems biology. We developed an open access Python-based software tool available either as downloadable library or as web-based graphical user interface (GUI). The pipeline simplifies the extraction and calculation of protein abundances from unprocessed proteomics data, accommodating a range of experimental approaches based on label-free quantification. Our tool was conceived as a versatile and robust pipeline designed to ease and simplify data analysis, thereby improving reproducibility between researchers and institutions. Moreover, the robust modular structure of Alpaca allows its integration with other software tools.

PMID:40285550 | DOI:10.1002/pmic.202400417

Vet Sci. 2025 Apr 9;12(4):347. doi: 10.3390/vetsci12040347.

ABSTRACT

Milk fever, or periparturient hypocalcemia, in dairy cows has traditionally been addressed as an acute calcium deficiency, leading to interventions like supplementation and adjustments in dietary cation-anion balance. Although these measures have improved clinical outcomes, milk fever remains a widespread and economically significant issue for the dairy industry. Emerging findings demonstrate that a narrow emphasis on blood calcium concentration overlooks the complex interactions of immune, endocrine, and metabolic pathways. Inflammatory mediators and bacterial endotoxins can compromise hormone-driven calcium regulation and induce compensatory calcium sequestration, thereby worsening both clinical and subclinical hypocalcemia. Recent insights from systems biology illustrate that milk fever arises from nonlinear interactions among various physiological networks, rather than a single deficiency. Consequently, this review contends that a holistic strategy including integrating nutrition, immunology, microbiology, genetics, and endocrinology is vital for comprehensive management and prevention of milk fever. By embracing a multidisciplinary perspective, producers and veterinarians can develop more robust, customized solutions that not only safeguard animal well-being but also bolster profitability. Such an approach promises to meet the evolving demands of modern dairy operations by reducing disease prevalence and enhancing overall productivity. Tackling milk fever through integrated methods may unlock possibilities for improved herd health and sustainable dairy farming.

PMID:40284849 | DOI:10.3390/vetsci12040347

Polymers (Basel). 2025 Apr 18;17(8):1101. doi: 10.3390/polym17081101.

ABSTRACT

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers worldwide due to its resistance to conventional therapies that is attributed to its dense and acidic tumor microenvironment. Chemotherapy based on gemcitabine usually lacks efficacy due to poor drug penetration and the metabolic characteristics of the cells adapted to grow at a more acidic pHe, thus presenting a more aggressive phenotype. In this context, photodynamic therapy (PDT) offers a promising alternative since it generally does not suffer from the same patterns of cross-resistance observed with chemotherapy drugs. In the present work, a novel bromine-substituted heptamethine-cyanine dye (BrCY7) was synthesized, loaded into PEG-PLGA NPs, and tested on the pancreatic ductal adenocarcinoma cell line cultured under physiological (PANC-1 CT) and acidic (PANC-1 pH selected) conditions, which promotes the selection of a more aggressive phenotype. The cytotoxicity of BrCY7-PEG-PLGA is dose-dependent, with an IC50 of 2.15 µM in PANC-1 CT and 2.87 µM in PANC-1 pH selected. Notably, BrCY7-PEG-PLGA demonstrated a phototoxic effect against PANC-1 pH selected cells but not on PANC-1 CT, which makes these findings particularly relevant since PANC-1 pH selected cells are more resistant to gemcitabine as compared with PANC-1 CT cells.

PMID:40284366 | DOI:10.3390/polym17081101

Plants (Basel). 2025 Apr 20;14(8):1256. doi: 10.3390/plants14081256.

ABSTRACT

Castor bean (Ricinus communis L.) can tolerate long periods of dehydration, allowing the investigation of gene circuits involved in drought tolerance. Genes from gibberellins, jasmonates, and auxin signaling are important for crosstalk in the developmental and environmental adaptation process to drought conditions. However, the genes related to these signals, as well as their transcription profiles under drought, remain poorly characterized in the castor bean. In the present work, genes from gibberellins, jasmonates, and auxin signaling were identified and molecularly characterized. These analyses allowed us to identify genes encoding receptors, inhibitory proteins, and transcription factors from each signaling pathway in the castor bean genome. Chromosomal distribution, gene structure, evolutionary relationships, and conserved motif analyses were performed. Expression analysis through RNA-seq and RT-qPCR revealed that gibberellins, jasmonates, and auxin signaling were modulated at multiple levels under drought, with notable changes in specific genes. The gibberellin receptor RcGID1c was downregulated in response to drought, and RcDELLA3 was strongly repressed, whereas its homologues were not, reinforcing the suggestion of a nuanced regulation of gibberellin signaling during drought. Considering jasmonate signaling, the downregulation of the transcription factor RcMYC2 aligned with the drought tolerance observed in mutants lacking this gene. Altogether, these analyses have provided insights into hormone signaling in the castor bean, unveiling transcriptional responses that enhance our understanding of high drought tolerance in this plant. This knowledge opens avenues for identifying potential candidate genes suitable for genetic manipulation in biotechnological approaches.

PMID:40284144 | DOI:10.3390/plants14081256

Biology (Basel). 2025 Apr 16;14(4):426. doi: 10.3390/biology14040426.

ABSTRACT

Runs of homozygosity (ROH) are key elements of the genetic structure of populations, reflecting inbreeding levels, selection history, and potential associations with phenotypic traits. This study proposes a novel approach to ROH analysis through visualization and classification using convolutional neural networks (CNNs). Genetic data from Large White (n = 568) and Duroc (n = 600) pigs were used to construct ROH maps, where each homozygous segment was classified by length and visualized as a color-coded image. The analysis was conducted in two stages: (1) classification of animals by breed based on ROH maps and (2) identification of the presence or absence of a phenotypic trait (limb defects). Genotyping was performed using the GeneSeek® GGP SNP80x1_XT chip (Illumina Inc., San Diego, CA, USA), and ROH segments were identified using the software tool PLINK v1.9. To visualize individual maps, we utilized a modified function from the HandyCNV package. The results showed that the CNN model achieved 100% accuracy, sensitivity, and specificity in classifying pig breeds based on ROH maps. When analyzing the binary trait (presence or absence of limb defects), the model demonstrated an accuracy of 78.57%. Despite the moderate accuracy in predicting the phenotypic trait, the high negative predictive value (84.62%) indicates the model's reliability in identifying healthy animals. This method can be applied not only in animal breeding research but also in medicine to study the association between ROH and hereditary diseases. Future plans include expanding the method to other types of genetic data and developing mechanisms to improve the interpretability of deep learning models.

PMID:40282291 | DOI:10.3390/biology14040426

Biology (Basel). 2025 Apr 7;14(4):379. doi: 10.3390/biology14040379.

ABSTRACT

This study evaluates the chemical composition, fatty acid profiles, and bioactive properties of ethanolic (SPE), methanolic (SPM), and acetonic (SPA) extracts of Arthrospira platensis. The chemical analysis revealed a high protein content (72.08%), moderate lipid levels (6.49%), and a diverse fatty acid profile, dominated by polyunsaturated fatty acids. Antibacterial testing showed that SPE exhibited the strongest activity against Gram-negative bacteria, including Escherichia coli (ATCC 25922), Enterobacter cloacae (ATCC 49141), Proteus mirabilis (ATCC 25933), Salmonella typhi (ATCC 6539), Salmonella typhimurium (ATCC 14028), Salmonella enteritidis (ATCC 13076), Salmonella gallinarum (ATCC 9184), and Pseudomonas aeruginosa (ATCC 27853). The anticoccidial activity was also significant, with SPE reducing Eimeria sp. oocyst counts in poultry intestines and ceca. Antioxidant activity was highest in SPM, which also had the highest phenolic content. LC-MS/MS profiling of the methanolic extract revealed various bioactive compounds, including phenolic acids, flavonoids, carotenoids, chlorophylls, and phycobiliproteins. These results suggest that A. platensis has great potential as a nutraceutical supplement in poultry farming, offering a sustainable alternative to synthetic additives.

PMID:40282245 | DOI:10.3390/biology14040379

Biology (Basel). 2025 Mar 25;14(4):338. doi: 10.3390/biology14040338.

ABSTRACT

Endosymbiosis can be considered a regressive or degenerative evolutionary process characterized at the genomic level by genome erosion and degeneration due to high mutational pressure toward AT (adenine and thymine) bases. The genomic and biological complexity of endosymbionts must be lower than that of the free-living bacteria from which they evolved. In the present work, we contrasted whether two proposed metrics for measuring genomic complexity in both types of bacteria, GS and BB, reflect their complexity, expecting higher values in free-living bacteria than in endosymbionts. On the other hand, we endeavored to delve into the factors that contribute to the reduction in metric values in endosymbionts, as well as their eventual relationship with six genomic parameters associated with functionality. This study aimed to test the robustness of these proposed metrics in a well-known biological scenario, such as the endosymbiosis process.

PMID:40282203 | DOI:10.3390/biology14040338

BMC Cancer. 2025 Apr 25;25(1):780. doi: 10.1186/s12885-025-14193-x.

ABSTRACT

BACKGROUND: This study aimed to classify dysplastic and healthy oral epithelial histopathological images, according to WHO and binary grading systems, using the Vision Transformer (ViT) deep learning algorithm-a state-of-the-art Artificial Intelligence (AI) approach and compare it with established Convolutional Neural Network models (VGG16 and ConvNet).

METHODS: A total of 218 histopathological slide images were collected from the Department of Oral and Maxillofacial Pathology at Tehran University of Medical Sciences archive and combined with two online databases. Two oral pathologists independently labeled the images based on the 2022 World Health Organization (WHO) grading system (mild, moderate and severe), the binary grading system (low risk and high risk), including an additional normal tissue class. After preprocessing, the images were fed to the ViT, VGG16 and ConvNet models.

RESULTS: Image preprocessing yielded 2,545 low-risk, 2,054 high-risk, 726 mild, 831 moderate, 449 severe, and 937 normal tissue patches. The proposed ViT model outperformed both CNNs with the accuracy of 94% (VGG16:86% and ConvNet: 88%) in 3-class scenario and 97% (VGG16:79% and ConvNet: 88%) in 4-class scenario.

CONCLUSIONS: The ViT model successfully classified oral epithelial dysplastic tissues with a high accuracy, paving the way for AI to serve as an adjunct or independent tool alongside oral and maxillofacial pathologists for detecting and grading oral epithelial dysplasia.

PMID:40281456 | DOI:10.1186/s12885-025-14193-x

BMC Plant Biol. 2025 Apr 25;25(1):544. doi: 10.1186/s12870-025-06563-1.

ABSTRACT

BACKGROUND: Plasma-activated water (PAW) is a recently developed cutting-edge technology that is increasingly gaining interest for its applications in medicine, food industry and agriculture. In plant biology, PAW has been shown to enhance seed germination, plant growth, and plant resilience against biotic and abiotic stresses. Despite increasing knowledge of the beneficial effects exerted by PAW on plants, little information is currently available about how this emerging technology may affect mutualistic plant-microbe interactions in the rhizosphere.

RESULTS: In this work we investigated the impact of irrigation with PAW, generated by a plasma torch, on arbuscular mycorrhizal (AM) symbiosis. Roots of the model legume Lotus japonicus expressing the bioluminescent Ca2+ reporter aequorin responded to treatment with PAW 5' (obtained by 5 min water exposure to plasma) with the immediate induction of cytosolic and nuclear Ca2+ signals, indicating that Ca2+-mediated signalling is one of the earliest cellular responses to PAW. The long-lasting elevations in intracellular Ca2+ levels were not found to alter cell viability. Quantitative analyses of AM fungal accommodation in the host plant roots along with phosphate accumulation in leaves, as well as chemical analysis of N, C, S in shoots, showed that treatments with PAW play a modulatory role on plant AM symbiotic performance, in a manner dependent on the time interval of water exposure to the plasma and on the duration of plant treatment with PAW. In particular, irrigation with PAW 5' increased fungal colonization after 4 weeks, leading to a significant increase in leaf phosphate content after 7 weeks.

CONCLUSIONS: Our findings reveal that PAW enhances AM symbiosis by facilitating early fungal accommodation in roots and subsequently increasing phosphate content in leaves at later stages. A better understanding of the mechanisms underlying the effects of PAW on the plant microbiome may drive research towards a fine-tuning of this novel green technology to maximize its beneficial effects in the context of a more sustainable agriculture.

PMID:40281400 | DOI:10.1186/s12870-025-06563-1