Search Results (2,894)

Biofilms rapidly form on medical devices such as urinary catheters and surgical materials. These biofilms compromise patient safety and undermine infection prevention and control (IPC). Biofilms also reduce the effectiveness of antibiotics and disinfectants. As a result, they increase healthcare-associated infections and increase costs through device failure and the need for maintenance or replacement. Researchers are increasingly exploring biosurfactants (BSs) as surface coatings and cleaning additives to prevent microbial attachment and disrupt early biofilm formation on medical devices and healthcare-related surfaces. This review examines the translational potential of biosurfactants as preventive, disruptive, and adjunctive antibiofilm agents for medical devices and healthcare-related surfaces. Literature evidence on glycolipids (rhamnolipids, sophorolipids) and lipopeptides (surfactin) from static, flow-based, and microfluidic in vitro models that used clinically relevant materials, such as silicone and polydimethylsiloxane (PDMS), were examined. In our literature search, we focused on pathogens central to IPC, such as Staphylococcus aureus, Pseudomonas aeruginosa, Enterococcus spp., and Candida spp., and it was generally noted that BSs reduced microbial adhesion and delayed early biofilm formation on medical devices and healthcare-related surfaces. Significant evidence also suggests that they partially disrupt biofilms and improve antimicrobial penetration when co-applied, mainly through membrane disruption, destabilization of extracellular substances, interfering with quorum sensing, and synergistic and/or antagonistic interactions with other molecules. Their performance varied with class, formulation, hydrodynamic conditions, and microbial composition. BSs function better as preventive and adjunctive IPC tools than stand-alone antimicrobial agents and can help to reduce biofilm formation on devices and improve surface disinfection. However, translating this promise into practice demands more robust data on long-term safety, stability, and product quality. Full article

With the shortage of natural aggregates and the massive accumulation of iron tailings (ITs) solid waste restricting the sustainable development of asphalt pavement engineering, replacing natural aggregates with ITs has become a promising low-carbon solution with prominent economic and social benefits. However, the poor interfacial adhesion between ITs and asphalt severely restricts the engineering application of tailings, and the micro-interaction mechanism at their interface still lacks systematic clarification, which is the key research gap addressed in this work. Different from conventional macro road performance tests, this study innovatively combined molecular dynamics (MD) simulation with microscopic characterization, including Fourier transform infrared spectroscopy (FT-IR) and atomic force microscopy (AFM), to comprehensively reveal the interfacial interaction mechanism between ITs and asphalt at the molecular and microscales. The results indicate that asphalt molecules exhibit higher aggregation concentration and diffusivity on Al₂O₃ and Fe₂O₃ surfaces than on SiO₂ surfaces, proving stronger interfacial interaction between asphalt and iron-rich oxide minerals. Moderate temperature optimizes the adhesion performance of asphalt with Al₂O₃ and Fe₂O₃, while the interfacial bonding of asphalt on CaCO₃ and SiO₂ weakens as temperature rises. The silane coupling agent KH-550 can effectively react with acidic minerals, SiO₂ minerals in ITs, which significantly increases the concentration, diffusion coefficient, and distribution uniformity of asphalt molecules at the interface. FT-IR results verify that the combination of ITs and asphalt mainly relies on physical adsorption without generating new chemical bonds. AFM tests further confirm that alkaline minerals improve the surface roughness of asphalt mastic, and KH-550 greatly enhances the micro-adhesion force of the interface. The novelty of this work lies in clarifying the mechanism of typical mineral components in ITs and revealing the modification enhancement law of silane coupling agent and alkali minerals at the micro level. This study provides a scientific theoretical support for the high-value engineering utilization of ITs in asphalt pavement, and offers a reference for optimizing the interfacial modification design of solid waste aggregate. Full article

This study systematically elucidated the developmental characteristics and molecular regulatory mechanisms of the testis during the critical period of sexual maturation in Kazakh horses by combining histological observation of one- and two-year-old testicular tissues with transcriptomic sequencing. In the testes of one-year-old horses, no obvious lumen was observed, and the interior is mainly comprising supporting cells and spermatogonia on the basement membrane; in contrast, in the testes of two-year-old horses, the tubular lumen was complete with spermatogonia, spermatocytes, and spermatozoa, indicating that spermatogenic function had approached maturity. Transcriptome profiling identified 979 differentially expressed genes (DEGs), with 209 up-regulated genes, including CYP11A1 and CATSPER2, and 770 down-regulated genes, including CD9. Gene Ontology (GO) annotation indicated primary enrichment of DEGs in biological processes related to multicellular organism development, cell membrane composition, and ion binding. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed significant enrichment of DEGs in the calcium signaling pathway, cell adhesion molecules, and neuroactive ligand–receptor interaction, among other key pathways. Protein–protein interaction (PPI) network analysis further highlighted core genes, including TNF, CATSPER2, and CDH13. Validation by RT-qPCR confirmed the reliability of the RNA-Seq data. Our findings reveal the dynamics of testicular development in Kazakh horses through histological and molecular analyses, thereby providing a theoretical framework and candidate genes to further elucidate regulatory mechanisms and guide genetic improvement in reproductive traits. Full article

Invasive candidiasis is a fungal infection characterized by a high mortality rate. Carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family receptors play a crucial role in regulating innate responses of both leukocytes and epithelia. Human CEACAM3, CEACAM5 and CEACAM6 receptors recognize Candida albicans and are expressed in transgenic CEABAC10 mice. In a murine C. albicans infection model, CEABAC10 mice exhibited a shortened survival period attributed to an early cytokine storm, an exacerbated acute phase response, and heightened systemic inflammation compared to their wild-type littermates. The livers and kidneys of CEABAC10 mice displayed intensified purulent necrotizing inflammation, accompanied by increased infiltration of neutrophils and macrophages. Our in vivo and in vitro data indicated that the expression of CEACAM6 on monocytes of CEABAC10 mice caused the elevated cytokine levels and the subsequent exacerbation of the acute phase response upon C. albicans infection, resulting in decreased survival. Full article

Polysialic acid (PSA), a highly negatively charged glycan attached mainly to the neural cell adhesion molecule (NCAM), is emerging as a critical but underrecognized extracellular regulator of glutamatergic neurotransmission. While previous literature has focused on PSA’s developmental roles, increasing evidence indicates that PSA–NCAM also contributes to synaptic plasticity mechanisms in the mature brain. This review integrates evidence from structural biophysics, single-channel electrophysiology, and disease models to explain how PSA modulates glutamate receptor gating to control learning and memory. We synthesize findings from biochemical reconstitution, electrophysiological recordings, and in vivo studies to show that PSA can modulate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor open probability, burst duration, and cooperative gating without affecting conductance, thereby promoting long-term potentiation. Conversely, PSA selectively suppresses GluN2B-containing extrasynaptic N-methyl D-Aspartate (NMDA) receptor activity by lowering open probability and calcium influx, maintaining an optimal balance between potentiation and depression while providing neuroprotection. Disruption of PSA–NCAM signaling in developmental and disease models, including prenatal cannabinoid exposure and neurodegeneration, produces cognitive deficits reversible by PSA restoration. Notably, much of the current evidence derives from in vitro systems, with relatively few studies conducted in vivo, and studies employing PSA mimetics mostly, which should be considered when interpreting physiological relevance. Collectively, the available evidence suggests that PSA functions as an extracellular modulator linking synaptic glycans to glutamate receptor regulation and plasticity related signaling pathways, highlighting the potential importance of extracellular glycan mechanisms in the control of synaptic function. Full article

Inflammatory bowel disease (IBD) is increasingly recognized as a systemic inflammatory disorder associated with elevated long-term risk of ischemic stroke, even among younger individuals without traditional vascular risk factors. Although chronic inflammation, endothelial dysfunction, and hypercoagulability partially explain this association, the biological mechanisms linking intestinal inflammation to cerebral vascular injury remain incompletely defined. Extracellular vesicles (EVs), membrane-bound particles released by epithelial, immune cells and platelets, have emerged as potent mediators of intercellular communication in inflammatory states. In IBD, circulating EVs are enriched with pro-inflammatory cytokines, microRNAs, adhesion molecules, tissue factors, which are capable of promoting endothelial activation, blood–brain barrier disruption, immune-thrombosis and neuroinflammation. This review summarizes epidemiologic, vascular, and EV biology literature to propose a mechanistic framework in which EV-mediated signaling integrates intestinal inflammation with cerebrovascular vulnerability along the gut–vascular–brain axis. While direct causal evidence remains limited, converging mechanistic data supports biological plausibility and defines priorities for future experimental and translational investigation. Full article

Perfluorooctane sulfonate (PFOS) is a persistent environmental pollutant associated with potential hepatoxic effects and other health risks. Despite its widespread distribution, the mechanisms underlying its toxicities remain to be fully understood. To investigate PFOS toxicology, our study utilized HepG2 and THLE-2 human hepatic cell models to replicate conditions reflecting PFOS accumulation in the liver. Cell viability, cell stress, and cell death assays were conducted to assess the toxicological influence of the chemical on both cell lines. Total RNA extraction was performed, followed by cDNA sequencing, and rt-qPCR. The XTT viability assay revealed a dose-dependent decrease in the number of viable cells when incubated with increasing concentrations of PFOS. The inhibitory concentration (${IC}_{50}$) values were approximately 100 micromolar, which led to morphological changes, elevated reactive oxygen species (ROS), and induced early apoptosis in liver cells after 6 h. Based on the transcriptomic analysis for HepG2 cells, mitochondrial genes involved in oxidative phosphorylation were downregulated, including COX, ND, and the ATP synthase family. Additionally, significant alterations of transcripts implicated in cell adhesion molecules (CAMs) were observed. In conclusion, PFOS inhibited cell growth, induced oxidative stress, and elevated apoptotic levels via transcriptomic alteration, including gene transcripts required for mitochondrial activity and cell adhesion. Full article

Fine migration is widely recognized as a primary cause of production decline in unconsolidated sandstone reservoirs. Migrated fines may accumulate within pore throats and obstruct flow channels, or they may be transported into the wellbore with the produced fluids, leading to operational issues such as wellbore plugging, pump sticking, and equipment abrasion. Despite extensive studies on fine migration, the role of particle wettability has received limited attention. In this study, the mineralogical composition of formation particles was first characterized using X-ray diffraction (XRD) and quantitative clay analysis. Surface modification experiments were then conducted to investigate the effect of hexadecylamine (HDA) on particle wettability and to determine the optimal reaction conditions. Surface characterization techniques were employed to elucidate the modification mechanism. Subsequently, sand-packed tube displacement experiments were performed to evaluate the influence of wettability alteration on fine migration behavior. The underlying mechanisms were further interpreted through interfacial thermodynamic analysis. Two potential field application schemes are proposed to facilitate practical implementation in oilfield operations. The results indicate that the water contact angle of formation particles increased from 0° to 150° when treated with 0.8 wt% HDA for 24 h. Surface characterization confirms that HDA molecules were physically adsorbed onto the particle surfaces. Displacement experiments demonstrate that the permeability reduction rate decreases significantly with increasing particle hydrophobicity. Thermodynamic analysis suggests that the work of adhesion on the modified particle surface was reduced by 93.3%, thereby weakening fluid–particle interfacial coupling and suppressing fine mobilization. This study provides a wettability-based approach for mitigating permeability damage caused by fine migration in unconsolidated sandstone reservoirs. Full article

Surface-enhanced Raman spectroscopy (SERS) amplifies Raman scattering by placing molecules in the near-field of plasmonic nanostructures, enabling label-free molecular fingerprinting. While attractive for living cell phenotyping, many cellular SERS works rely on internalized colloidal nanoparticles, leading to variable uptake/localization, aggregation-driven hotspot fluctuations, and potential cellular perturbation. Here, we report a chip-like Au/SiO₂ nanolaminate SERS substrate that supports direct culture and label-free measurements of living cells on spatially defined hotspots without nanoparticle uptake. The periodic nanolaminate forms dense nanogaps and is engineered for 785 nm excitation, providing uniform enhancement over a large, culture-compatible area with high hotspot uniformity. By engineering the cell–substrate nano–bio interface, the platform enables reproducible acquisition of intrinsic cellular vibrational fingerprints under physiological conditions without Raman tags. Using MCF-7 and MDA-MB-231 breast cancer cells, we collected hundreds of spectra per line, and MDA-MB-231 exhibited broader spectral variations, indicating greater heterogeneity. Principal component analysis and linear discriminant analysis achieved 99% classification accuracy for MCF-7 and MDA-MB-231, and bright-field imaging confirmed preserved adhesion and canonical morphologies. This chip-based, label-free living cell SERS platform enables scalable, nonperturbative phenotyping and may support rapid malignancy classification and treatment response screening across subtle cancer states. Full article

Pregnancy represents a dynamic immunological state in which the maternal immune system must balance tolerance toward the semi-allogeneic fetus while maintaining antimicrobial defense. Cytomegalovirus (CMV) infection is highly prevalent worldwide and profoundly shapes immune cell differentiation and long-term activation in adults. However, its interaction with pregnancy-associated immune remodeling remains incompletely defined. In this prospective longitudinal study, we comprehensively analyzed immune profiles of healthy pregnant women across all three trimesters and age-matched nonpregnant controls, stratified by CMV IgG serostatus. Multiparametric flow cytometry characterized T and B cell subsets and cytokine production following in vitro stimulation, while circulating cytokines and adhesion molecules were quantified using multiplex immunoassay. Gestational age was the primary determinant of leukocyte dynamics. Nevertheless, CMV-seropositive pregnant women showed enhanced activation and differentiation of CD4⁺ and, more prominently, CD8⁺ T cell subsets, changes not observed in nonpregnant women. Despite pronounced cellular differences, serum cytokine and adhesion molecule levels were largely comparable between CMV-seropositive and CMV-seronegative participants in both pregnant and nonpregnant groups. Functionally, CMV-seropositive women exhibited enrichment of IFN-γ– and IL-21–producing T cells, whereas B cell responses remained predominantly IL-10–dominated. These findings indicate selective alterations in maternal lymphocyte activation and function during pregnancy in CMV-seropositive women, without evidence of systemic inflammation. Full article

Background/Objectives: Breast cancer (BC) is the most commonly diagnosed cancer in women, and metastasis is the leading cause of BC-related death. Circulating tumor cells (CTCs) are a prerequisite for metastasis. This study examined the diagnostic and prognostic value of CTCs for assessing metastatic risk and recurrence in BC. Methods: The Chiline CATCH^® Circulating Target Cell Enrichment System, an automated negative selection platform, was used to enrich and enumerate CTCs from the peripheral blood of patients with BC. Epithelial cell adhesion molecule (EpCAM) and cell-surface Vimentin (CSV) were used as markers for CTC identification. Results: CSV⁺ CTC counts, but not EpCAM⁺ CTC counts, were increased in patients with BC at higher metastatic risk. A cut-off of >4.5 CSV⁺-CTCs/2 mL blood yielded a sensitivity of 0.56 and specificity of 0.92 for identifying patients at high metastatic risk. CSV⁺-CTCs outperformed conventional serum tumor markers, including cancer antigen 15-3 (CA 15-3), cancer antigen 125 (CA 125), and carcinoembryonic antigen (CEA), in identifying patients with high metastatic risk, and their combined use further improved risk stratification. An elevated CSV⁺-CTC count (≥5 cells/2 mL blood) was significantly associated with worse progression-free survival in patients with BC. Conclusions: These findings suggest that CSV⁺-CTCs may serve as a biomarker for metastatic risk stratification and recurrence monitoring in BC when measured using an automated negative selection platform. Full article

Lactate dehydrogenase (LDH) is a key glycolytic enzyme that catalyzes the interconversion of pyruvate and lactate, with LDHA gaining particular attention for its overexpression in various malignancies and pivotal role in the Warburg effect-driven metabolic reprogramming. Elevated LDHA activity supports rapid ATP production under hypoxic conditions, maintains NAD⁺ regeneration, and promotes lactate accumulation, creating an acidic tumor microenvironment (TME) that favors invasion and immune evasion. Accumulating evidence demonstrates that LDHA is essential for primary tumor growth and critically involved in circulating tumor cell (CTC) survival, anoikis resistance, and metastatic spread. These functions are mediated by its regulation of adhesion molecules, cytoskeletal remodeling, and energy adaptation that enable CTCs to withstand mechanical shear stress and immune surveillance in the bloodstream. Pharmacological inhibition of LDHA, particularly via sodium oxamate (oxamate), has shown substantial potential in reducing metastasis and enhancing chemotherapy sensitivity in preclinical models. Oxamate has emerged as a promising candidate for metabolic cancer therapy due to its unique double effects on tumor metabolism and anti-tumor immunity, which are an advantage rarely highlighted in broader LDHA-focused reviews. This review synthesizes the molecular mechanisms through which LDHA drives tumor progression, dissects its context-specific functions in CTC biology, and evaluates the translational potential of LDHA-targeted strategies, with a focused emphasis on oxamate, as a transformative anti-metastatic therapeutic paradigm. By filling a critical gap in synthesizing oxamate’s distinct metabolic–immune regulatory actions, this work addresses an unmet need in the management of advanced, treatment-refractory cancers. Full article

Background/Objectives. The actin-binding protein EPLIN (epithelial protein lost in neoplasm), also known as LIMA1, contributes to the maintenance of cytoskeleton structure and dynamic. This protein, which interacts with multiple partners to regulate cell adhesion and migration, has been implicated in the progression of solid tumors and in tumor metastasis. Consequently, small molecules binding to EPLIN are actively searched. EPLIN has been characterized as a molecular target for the antitumor antibiotic albacarcin V which affects the cytoskeletal structure and induces cell growth arrest. Methods. We have modeled the binding of albacarcin and naturally occurring derivatives to EPLIN conformers, in order to locate the drug-binding site and to identify additional EPLIN binders. Nineteen compounds were studied, including albacarcins V (vinyl) and M (methyl), five gilvocarcins, four ravidomycins, two chrysomycins, and six related products (including polycarcin and fucomycin). Results. The modeling analysis confirmed the capacity of albacarcin V to bind to EPLIN and identified a few better binders. In particular, ravidomycin V bearing a dimethylamino sugar unit were identified as the best binders in the series, along with the two related anticancer natural products FE35A-B. Structure-binding relationships are discussed. The drug-binding site has been localized near the central residue Asn34 in the conformationally constrained domain between the two zinc-binding regions. Conclusions. This study provides guidance to the design of EPLIN inhibitors based on the ravidomycin core structure. Full article

Background/Objectives: Alloantigen H is one of thirteen systems in the chicken. Little is known about this system which has two serological alleles. The objectives of this study were (1) to identify the genetic region encoding the chicken alloantigen H, and (2) to develop DNA detection-based methods to aid H system allele identification. Methods: SNP genotypes from Axiom chicken SNP arrays were established for samples with known H system serological types. Sources of DNA included two elite Hy-Line White Leghorn lines segregating for alloantigen H, non-pedigreed samples from the Northern Illinois University (NIU) DNA bank, plus inbred line samples. Sequence information was also available for the commercial and inbred lines. Results: GWAS results from the elite Hy-Line lines and NIU DNA bank samples showed a very strong peak in the same 4.20–4.30 Mbp region on chromosome 24. Predicted cell membrane expression and the presence of non-synonymous SNP were criteria to identify candidate genes. Seven genes in this region have membrane-associated products: MCAM (CD146), THY1, MFRP, CLDN25, KCNJ14L, ABCG4, and PDZD3. However, only MCAM had an SNP variation that matched the serological haplotypes. Lines known to be segregating for the H system had concordance rates between serological results and SNP haplotype of 95% for both the elite HYL lines and 99% for the NIU samples, indicating that the MCAM (CD146) gene encodes the chicken H blood system. Conclusions: The gene product is a cell adhesion molecule affecting multiple activities including angiogenesis, development, cell differentiation, cell migration, signaling transduction, and immune responses. Long, short, and soluble isoforms are found in chickens. The described DNA-based typing methods facilitate future investigations to examine H haplotype frequencies in lines with identified differential responses such as growth or immune responses. Determining H haplotype association with egg production, feed conversion, and other traits with economic importance will aid in determining the significance of this immune-related gene in overall poultry health. Full article

Acoustic divergence is widely recognized as a key driver of speciation and niche differentiation in vocal animals. In echolocating horseshoe bats (Rhinolophus), the larynx is specialized for producing high-duty-cycle signals used in foraging, navigation, and species recognition. While the ecological role of echolocation is established, the molecular mechanisms regulating laryngeal frequency remain unclear. We compared the laryngeal transcriptomes of three closely related, sympatric Rhinolophus species with distinct resting frequencies (RFs): R. episcopus (~46 kHz), R. siamensis (~66 kHz), and R. osgoodi (~85 kHz). This comparison identified 511 differentially expressed genes. High-frequency species upregulated genes involved in cytoskeletal dynamics and muscle contraction, such as cell adhesion molecules and motor proteins, while low-frequency species upregulated genes related to cellular homeostasis and metabolic maintenance. Weighted gene co-expression network analysis revealed two RF-correlated modules: a high-frequency module enriched in aerobic respiration and carbon metabolism and a low-frequency module enriched in lipid metabolism. Protein–protein interaction analysis identified ACTC1, vital for muscle contraction, as a hub gene. Evolutionary analysis showed that ACTC1 is highly conserved, with no significant positive selection, indicating that transcriptional regulation, rather than coding-sequence divergence, is the primary driver of the observed functional differences. These findings suggest that RF variation likely results from transcriptional remodeling in laryngeal superfast muscles. This study provides the first transcriptomic evidence linking laryngeal gene expression with acoustic divergence and offers new insights into the genetic basis of bat echolocation. Full article