Effects of mitochondrial lipid molecules on release of ROS and beef muscle oxidation: a perspective on membrane system.

A facile route for tuning the asymmetric pore structure of PMIA UF membranes with high water permeance by adjusting the content of LiCl & H2O co-additives

How receptor conformation depends on lipid nanodisc size: Adenosine A2A receptor and implications for class-A GPCR proteins.

Antimicrobial peptides (AMPs) are hoped to complement classical antibiotics in view of increasing microbial resistance. We investigated two members of a family of designed cyclic AMPs with different activity and selectivity. The cyclic hexapeptides are rich in arginine and tryptophan and have been shown previously to target cell membranes and to affect model membranes differently depending on the lipid membrane composition. To better understand their mechanisms of membrane perturbation, we investigated the interactions of cyclic RRRWWW and cyclic RWRWRW with various model membranes containing lipids commonly found in either bacterial or eukaryotic membranes. Using 31P and 2H solid-state NMR methods, we systematically analyzed the interactions between the peptides and lipid membranes at the molecular level. When POPE/POPG model membranes are investigated the two peptides exhibit distinct interactions with the PE and PG components, reflected in a different decrease in lipid chain order parameters. This decrease in deuterium order parameters and deformation of the vesicle shapes indicate disturbance of the lipid membrane structure by the peptides. Our study provides new insights into the molecular mechanisms of AMP-membrane interactions and can contribute to the understanding and development of novel antimicrobial agents.

A semi-analytical formula for the morphological analysis of air-supported membrane structures considering the effect of cables

Proteomic analysis of outer membrane vesicles derived from Vibrio parahaemolyticus causing translucent post-larvae disease.

Comparative proteomic analysis of donkey milk extracellular vesicles isolated by ultracentrifugation and ultrafast isolation systems.

A silicon carbide (SiC) X-ray beam position monitor is presented, based on a resistive charge-division principle derived from lateral-effect photodiodes and specifically adapted for synchrotron radiation applications. This device, referred to as a resistive X-ray beam position monitor (rXBPM), exploits a free-standing SiC membrane combined with a resistive p+-doped layer, enabling transmission-mode operation while preserving high radiation hardness and mechanical robustness. In contrast to conventional segmented X-ray beam position monitors, whose response depends strongly on the beam spot size and is typically limited to narrow linear regions, the resistive architecture of the rXBPM provides an intrinsically beam-footprint-independent position signal with an extended linear response region. The detector was fabricated using selective electrochemical etching to realize a thin membrane structure and was experimentally characterized at the microfocus beamline (MiFo) in the PTB laboratory at the BESSY II synchrotron facility using 5.4 keV X-rays. An average transmission of approximately 61% was measured, with good spatial uniformity across the membrane area. Raster-scan measurements demonstrate a linear position response over ranges of ±500 µm and ±1 mm around the detector center, with position sensitivities exceeding 0.157 mm-1 and estimated upper-limit noise-equivalent positions of a few micrometres. Three-dimensional COMSOL simulations were used to model charge transport and lateral charge division in the real device geometry, showing excellent agreement with experimental results and confirming the independence of the position sensitivity from the beam spot size over a wide range of operating conditions. These results establish SiC rXBPMs as a compact, beam spot size calibration-free and radiation-hard solution for beam diagnostics at modern synchrotron light sources, with particular relevance for applications requiring large active areas, extended linearity and minimal beam perturbation.

Intracellular membrane structures establish highly heterogeneous microenvironments that are essential for regulating organelle function and intracellular signaling. Among the physicochemical parameters governing these processes, weakly alkaline pH microdomains have remained difficult to interrogate owing to the lack of fluorescent probes that combine high sensitivity, selectivity, and compatibility with biological imaging. Here, we report CAlkM, a membrane-anchored fluorescent probe engineered for imaging weakly alkaline intracellular environments. Through rational modulation of the coumarin scaffold, CAlkM exhibits a pKa of 8.24 and shows a sensitive fluorescence response across the biologically relevant weakly alkaline pH range of 7.0-9.0. The probe enables selective detection of weakly alkaline conditions in aqueous systems and can be readily integrated into gel- and paper-based platforms for portable pH sensing. In living cells, stimulated emission depletion (STED) microscopy and molecular docking analysis indicate that CAlkM can localize in intracellular membrane-associated regions through a membrane-anchoring mode, including organelle-associated membranous and vesicle-like structures, enabling high-resolution in situ visualization of membrane-related local weakly alkaline pH changes. Furthermore, CAlkM displays clear pH-dependent fluorescence responses in zebrafish larvae, demonstrating its applicability for pH-responsive fluorescence imaging in living organisms. Together, these results establish a molecular design strategy for membrane-anchored weakly alkaline pH sensing and provide a versatile platform for investigating pH-regulated physiological and pathological processes across complex biological systems.

In recent years, with the rapid progress in bioinspired and self-assembly technologies, vesicles that mimic cell membranes have attracted growing research interest. Among them, polymersomes prepared from natural or biodegradable polymers have emerged as a key focus in biomedicine due to their excellent stability, superior biocompatibility, and low immunogenicity. In particular, permeable polymersomes, as highly biomimetic systems, possess a double-layered membrane structure that enables efficient substance and energy exchange with the external environment, closely resembling natural cell membranes. The entanglement of polymer chains combined with the permeable membrane structure confers outstanding mechanical stability and enhanced permeability, allowing small molecules to pass through while retaining macromolecules inside the vesicle cavity. These unique properties endow permeable polymersomes with broad application potential in drug delivery, diagnostic imaging, and nanoreactors. Given this background, this review summarizes the preparation methods of permeable polymersomes and their recent advances in biomedical applications.

Saturated cardiolipins are potent disruptors of inner mitochondrial membrane structure and function.

The incidence of colorectal cancer (CRC) continues to rise, with colorectal adenoma(CRA) being its primary precancerous lesion. Recent studies suggest that hyperlipidemia may promote adenoma development by influencing cell membrane structure, cholesterol metabolism, and inflammatory responses. However, its independent role in the adenoma stage remains unclear. To investigate the association between hyperlipidemia and colorectal adenoma(CRA) risk and to evaluate the dose-response relationship based on lipoprotein profile stratification. This single-center retrospective case-control study included 180 patients with colorectal adenoma(CRA) and 80 colonoscopy-negative controls. An additional 80 patients with pathologically confirmed colorectal adenocarcinoma (CRAC) were included as a secondary exploratory comparison group. Demographic characteristics and lipid parameters, including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), were collected. Univariate and multivariable unconditional logistic regression analyses were performed to evaluate associations between lipid abnormalities and colorectal adenoma, with adjustment for age, sex, BMI, smoking, alcohol consumption, and family history of colorectal cancer. Variance inflation factors were calculated to assess multicollinearity. Quartile stratification and restricted cubic spline models were used to explore dose-response patterns, and E-value analysis was performed to assess the potential impact of unmeasured confounding. High TC, high TG, high LDL-C, and low HDL-C were significantly associated with the overall presence of CRA in univariate analysis. After adjustment for potential confounders, these associations remained statistically significant. Quartile stratification showed that higher levels of TC, TG, and LDL-C were associated with progressively higher odds of colorectal adenoma, whereas HDL-C showed an inverse association. The RCS models suggested steeper increases in adenoma odds at higher TC and LDL-C levels, while HDL-C showed an approximately linear inverse association. Although high TG was associated with overall adenoma occurrence, TG levels did not differ significantly across adenoma histological subtypes. Subgroup analyses suggested that smoking, obesity, and family history may modify the associations between dyslipidemia and colorectal adenoma. Hyperlipidemia was independently associated with CRA in this retrospective case-control study. A comprehensive dyslipidemic pattern, characterized by elevated TC, TG, and LDL-C and reduced HDL-C, was observed among patients with CRA. Lipoprotein profiles may serve as accessible clinical indicators for colorectal adenoma risk stratification. However, because of the retrospective case-control design, causal inference and temporal relationships cannot be established, and the possibility of reverse causality should be considered.

To observe the effect of acupoint injection on olfactory function, olfactory mucosa structure, olfactory mucosa apoptosis and apoptosis-related protein expression in rats with olfactory dysfunction of allergic rhinitis (AR), so as to explore its mechanisms underlying improvement of AR olfactory dysfunction. Thirty-six SD rats were used in the present study. Nine of them were randomly selected to be used as the normal group, and the rest of the rats were used to prepare the AR olfactory dysfunction model by ovalbumin sensitization. After successful modeling, the AR model rats were allocated to the model, non-meridian non-acupoint injection, and acupoint injection groups, with 9 rats in each group. For rats of the acupoint injection group, an isotonic mixture (0.05 mL/point) of dexamethasone and lidocaine was injected into the bilateral "Yingxiang" (LI20) once every 3 days, for a total of 4 times. For rats of the non-meridian non-acupoint injection group, the same mixture solution (0.05 mL/point) was injected into the midpoint of the line connecting "Houhai" (GV1) and "Huantiao"(GB30) on both sides. The frequency and course of treatment were the same as those of the acupoint injection group. The rats' nasal symptoms were observed and scored, the olfactory function was evaluated by buried food pellet test (BFPT). The histopathological changes and ultrastructure of the olfactory mucosa were observed by H.E. staining and transmission electron microscopy. The contents of serum interleukin (IL) 4, IL-5, IL-13 and IL-17 were detected by ELISA. The expression of olfactory marker protein (OMP) in the olfactory mucosa was detected by immunofluorescence method, and apoptosis of olfactory mucosal cells was detected by TUNEL method. The expression levels of cysteine aspartate protease-3 (Caspase-3), B lymphoblastoma-2 related gene X protein (Bax), and B lymphoblastoma-2 gene (Bcl-2) proteins of the nasal mucosa were detected by Western blot. The histopathological and ultrastructural observations showed that in the model group, the olfactory mucosal epithelium was severely shed, and the intrinsic layer cells were degenerated and necrotic with inflammatory infiltration;the outer mitochondrial membrane was blurred and broken, and the cristae structure dissolved and disappeared. But compared with the model group, the acupoint injection group had an apparent improvement in the structure of the olfactory mucosa, and a relatively complete and unambiguous structure in the outer mitochondrial membrane and cristae of the inner membrane. Compared with the normal group, the model group had a significant increase in the nasal symptom score, search time for food goblet, apoptosis rate of olfactory mucosal cells, contents of serum IL-4, IL-5, IL-13 and IL-17, and expression of Caspase-3 and Bax proteins in the nasal mucosa (P<0.01), and a notable decrease in the immunofluorescence density of OMP and expression of Bcl-2 in the olfactory mucosa tissue (P<0.01). After non-meridian non-acupoint injection and acupoint injection, both the increase and decrease of the indexes mentioned above were all reversed (P<0.05, P<0.01). Comparison between the two injection groups showed that the effects of the acupoint injection group were significantly superior to those of the non-meridian non-acupoint injection group in all indexes (P<0.01). Acupoint injection can significantly improve olfactory function and olfactory mucosal damage in rats with AR olfactory dysfunction, which may be related to its functions in inhibiting the inflammatory damage and reducing cell apoptosis of the olfactory mucosa.

Atomistic studies of plant cell surfaces have typically focused either on plasma membranes or on individual cell wall polymers, such as cellulose and hemicellulose, rather than on combined plasma membrane-cell wall models. Here, we present an atomistic model of the Arabidopsis thaliana cell membrane that explicitly includes both the plasma membrane and the primary cell wall. Simulations reveal that cell wall interactions thin the plasma membrane, especially in the upper leaflet facing the wall, increase lipid area per molecule, and increase the acyl chain disorder. Lipid-cellulose interactions were quantified, showing that phosphate headgroups dominate binding and that lipid species differ in interaction strength. These results provide a molecular-level description of how the cell wall modifies plasma membrane structure and dynamics, establishing a framework for modeling more complex plant cell surfaces.

Lipid rafts are ordered membrane domains composed of sphingomyelin (SM) and cholesterol (chol). They serve as platforms for membrane-based signal transduction. To date, the structural properties of lipid rafts have been investigated using SM/chol/unsaturated-lipid ternary bilayers, which undergo phase separation into SM/chol-rich liquid-ordered (Lo) and unsaturated-lipid-rich liquid-disordered (Ld) phases. Although some previous studies have suggested structural heterogeneity within the Lo phase, the internal organization of lipid-raft-mimetic Lo phases has been largely unexplored owing to the lack of methodologies capable of probing the local membrane structure. Recently, we developed a low-flux electron diffraction (LFED) technique and disclosed the local structures of lipid monolayers. In this study, we examined the local structure within the Lo phase by using LFED. We first tested the applicability of a previously developed rapid-freezing and sublimation protocol to lipid bilayers and successfully prepared dehydrated bilayers with minimal perturbation of lipid chain packing. Next, we optimized the electron beam flux and acquired diffraction patterns from the lipid bilayers in a minimally invasive manner. Finally, we directly examined local chain-packing structures within the Lo phase using LFED for the first time. As a result, sharp-ring and pseudohexagonal-spot diffractions were observed at some locations in the Lo phase. Notably, these diffraction patterns were identical with those observed in pure SM bilayers (gel phase). Hence, these results suggest that subdomains with gel-phase-like lipid packing are formed in the Lo phase and that subdomains consist of almost-pure SM. These results provide experimental evidence for structural heterogeneity within the Lo phase and a new physical basis for understanding the organization and functional versatility of lipid rafts.

Parasitic extracellular vesicles (EVs) play crucial roles in the growth and development of parasites. However, we remain unaware of the EVs from the plerocercoids of Spirometra mansoni. In this study, firstly, the plerocercoids of S. mansoni were cultured in vitro to enrich EVs, which were then characterized using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting. Next, the protein components and miRNAs of EVs were subsequently analysed using data-independent acquisition (DIA) and high-throughput sequencing, respectively. The results showed that EVs derived from the plerocercoids exhibit a typical double-layered membrane structure as spherical or elliptical vesicles ranging from 80 to 150nm in diameter. The molecular markers HSP70, TSG101, HSP90, CD81, and β-Actin were significantly expressed in these EVs. Micro-proteomic analysis revealed 2,729 proteins, with functional annotation indicating that EV proteins are enriched primarily in pathways such as intracellular transport/secretion, cellular processes, and signal transduction. High-throughput miRNA sequencing revealed that the identified EVs contained 37 known miRNAs and 118 novel miRNAs. Functional enrichment analysis indicated that miRNAs primarily participate in host interactions by regulating DNA integration, apoptosis, cholesterol metabolism, and cAMP signaling pathways. Immunological analysis demonstrated that the antiserum against EVs elicited a mixed Th1/Th2 immune response, which was predominantly Th1-type. In this study, S. mansoni plerocercoid-derived EVs were successfully isolated and characterized. Systematic profiling of EV components via microproteomics and high-throughput miRNA sequencing provides a foundation for further investigations into the functional mechanisms of EVs.

Lipid-protein interactions are ubiquitous in biology, where they are fundamental to membrane structure, cell signaling, immunology, and metabolism. Despite the availability of thousands of experimentally determined lipid-protein structures, the molecular basis for lipid recognition and specificity across the lipid-protein interactome remains incompletely understood. Here, we report a systematic analysis of 113,782 annular and nonannular lipid-protein complexes spanning the eight lipid classes. Pairwise atomic interactions are linked to lipid and protein physicochemical properties and binding geometries. Hydrophobic contacts, hydrogen bonds, and salt bridges contributed to over 99% of lipid-protein interactions. Lipid class-, protein sublocalization-, protein function-, and protein fold-dependent trends were identified. Protein pockets were finely tuned for lipid size, shape, and polarity: fatty acyls associated with narrow, moderately hydrophobic pockets; saccharolipids and glycerophospholipids bound to larger, polar cavities; and sterols and prenols preferentially occupied compact hydrophobic sites. Global analysis across different protein families identified similarities in interaction profiles, while also highlighting protein-specific recognition adapted to biochemical function. Lipid-protein interaction maps were projected onto lipid structures to uncover conserved and divergent hotspots and coldspots across lipid classes. The heatmaps imply that recognition and specificity are mediated by tailored anchoring of polar head groups and varying interaction with hydrophobic tails. Together, the data establish nature's principles governing lipid binding, lipid selectivity, and complex stability, and collectively provide a molecular atlas of the lipid-protein interactome. The work enables the elucidation of lipid biology at scale and establishes guiding principles for the rational design of chemical probes and therapeutics targeting lipid biology.

BackgroundAflatoxin B1 (AFB1), a potent mycotoxin, commonly contaminates feeds like maize and soybean, jeopardizing animal reproduction. Although AFB1 exposure is known to cause oxidative stress, immune activation, and cell death in oocytes and early embryos of several species, its effects on sheep remain unclear. This study aimed to investigate AFB1-induced damage in ovine oocytes and its underlying mechanisms. Quercetin (QT), a cost-effective flavonoid with antioxidant and anti-inflammatory properties, is potential to improve this damage. The mechanisms may involve non-canonical ferroptosis, an iron-dependent, lipid peroxidation-driven cell death pathway independent of canonical regulators GPX4 and TFR1.Methods4D Fast DIA-based micro-scale quantitative proteomics was conducted to identify the target proteins, and then immunofluorescence, qPCR, and parallel reaction monitoring (PRM) were conducted for the expression validation of the target proteins, and a series of analyses combined with the inhibitor experiments were conducted for the functional validation of the target proteins, including assessments of mitochondrial function (membrane potential ΔΨm, distribution, ATP levels), mitochondrial morphology observation by transmission electron microscopy (TEM), lipid peroxidation detection (LPO imaging, ROS and GSH detection), Fe2+ detection, endoplasmic reticulum staining, and early apoptosis signaling detection.ResultsOPA1 and ACSL4 are screened as the target proteins by micro-scale quantitative proteomics analysis, and immunofluorescence, qPCR and PRM validate their expression. Molecular docking reveals that there is an interaction of OPA1 and ACSL4, and QT exhibits stronger binding affinity to both OPA1 and ACSL4 than AFB1. AFB1 induces aberrant upregulation of OPA1 and ACSL4, disrupting mitochondrial cristae and membrane structure, impairing mitochondrial function and energy metabolism (including decreased mitochondrial membrane potential, abnormal distribution, and reduced ATP synthesis), promoting lipid peroxidation and Fe2+ accumulation, exacerbating endoplasmic reticulum stress and altering ROS/GSH levels, ultimately leading to ferroptosis in oocytes. Addition of QT ameliorates the AFB1-induced abnormal expression of OPA1 and ACSL4.ConclusionsQT alleviates AFB1-induced damage on ovine oocytes by suppressing non-canonical ferroptosis via the OPA1/ACSL4 pathway. These findings elucidate a novel mechanism underlying AFB1-mediated reproductive toxicity and provide a theoretical foundation for applying QT to mitigate AFB1-induced reproductive impairment and improve livestock health.Graphical Supplementary InformationThe online version contains supplementary material available at 10.1186/s40104-026-01454-3.

MOF-derived carbon membranes for catalytic ozonation: Site-dependent evolution of surface atomic oxygen enables efficient water purification.

Alzheimer's disease (AD) is a leading cause of death among the elderly, with no existing treatment. The development of therapies is further hindered by a limited understanding of the molecular pathogenesis and the absence of reliable early-detection biomarkers. Neuroimaging and lipidomic studies reveal structural and biochemical alterations in both gray and white matter in AD patients, including disruptions in membrane organization and neuronal signaling pathways. In the present work, we employed lipidomics-guided modeling of membranes in gray and white matter regions under healthy and diseased (AD) conditions, and used all-atom molecular dynamics (MD) simulations to examine how AD-associated alterations in lipid composition influence the structure, spatial organization, and micro-heterogeneity of neuronal plasma membranes. The data suggest that Alzheimer's disease-associated lipid alterations in gray matter (GM) and white matter (WM) impact membrane thickness and microdomain distribution, highlighting the critical role of lipid composition in maintaining neuronal membrane homeostasis and function. Higher-order cholesterol-ceramide-sphingomyelin-enriched domains are more abundant in the neuronal membranes of the GM region under diseased conditions. Under AD-mimicking conditions, lipidomic analyses demonstrate that neuronal membranes in GM experience more substantial compositional and structural remodeling than those in WM. Our results show significant changes in membrane microdomain distribution across the lipid bilayers, and, interestingly, these changes are more pronounced in the gray matter than in the white matter. This study establishes a framework for modeling the tissue-specific lipidomics data to understand how disease-driven compositional changes affect the structure, organization, and dynamics of biological membranes.