Magnolia denudata is characterized by floral thermogenesis and blooms in the cold early spring. However, the specific thermogenic tissues and molecular signals that modulate thermogenesis remain elusive. Here, we categorized the developmental process of M. denudata into five stages with stage 2 being the thermogenic peak stage, and identified the thermogenic region as the lateral tissue of gynoecium by integrating infrared (IR) imaging and multispectral imaging (MSI). The optimized integration of these imaging techniques not only distinguished the gynoecium of the non-thermogenic and thermogenic stages but also revealed compound differences between the lateral and central tissues at the thermogenic stage. Moreover, we unveiled the in situ distribution of calcium in thermogenic organs using micro X-ray fluorescence imaging (μ-XRF), and its distribution pattern closely matched the heat distribution. The increased rate of Ca2+ influx both into the cytosol and mitochondria aligns with the upregulation of genes related to mitochondrial Ca2+ transport at the thermogenic stage. Additionally, changes in respiratory capacity caused by altering cytosolic Ca2+ concentration further demonstrated that Ca2+ regulates mitochondrial respiratory metabolism. This study comprehensively utilized multiscale imaging to distinguish the thermogenic tissue within the complex-structured thermogenic organ of M. denudata, revealing the close relationship between Ca2+ and thermogenesis.

Whether and how ovarian hormone fluctuations mediate the skeletal muscle response to ageing in females remains to be elucidated. We examined a tightly controlled, cross-sectional cohort of 96 females 18-80years of age to map the functional and molecular trajectory of muscle ageing and determine its relationship with female sex hormones. Across every decade, we quantified body composition (using dual-energy X-ray absorptiometry), muscle morphology (using peripheral quantitative computed tomography), and voluntary and evoked muscle function. Circulating sex hormone concentrations were measured with GC-MS and immunoassays. Morphology and gene expression of vastus lateralis muscle samples were assessed with immunohistochemical staining and RNA sequencing, respectively. Age was negatively associated with muscle mass, strength and muscle fibre size, and positively associated with hybrid type I/IIa fibre prevalence and fibrosis. We found 37 unique patterns of gene expression across individual decades of age. Immune signalling, cellular adhesion and extracellular matrix organization pathways were the most upregulated with age, whilst mitochondrial function pathways were the most downregulated. Independently of age, circulating oestradiol and progesterone, but not testosterone, concentrations were positively associated with lean mass and negatively associated with hybrid muscle fibres across the lifespan. Oestrogen receptor binding sites were significantly enriched in upregulated genes in pre- versus post-menopausal muscle, suggesting a reduction in the translation of oestrogen target genes after menopause. Altogether, sex hormone fluctuations across the female lifespan may contribute to age-related muscle wasting, although longitudinal and interventional studies are needed to determine the causal nature of the relationship. KEY POINTS: Females live longer than males but experience worse disability in the later decades of life, highlighting the need to study female-specific patterns of ageing. This study mapped female body composition, muscle morphology, function and gene expression across every decade from 18 to 80years of age in tightly controlled conditions and examined the relationships with circulating sex hormones. Unique patterns of muscle gene expression across ageing showed an overall increase in immune signalling and a decrease in mitochondrial respiration pathways, but limited associations with circulating sex hormones. Independently of age, circulating oestradiol and progesterone, but not testosterone, were associated with muscle mass and morphology across the lifespan, after adjusting for influential lifestyle factors (protein intake and physical activity). Fluctuations in female sex hormones across the lifespan should be considered when developing therapies to mitigate age-related muscle wasting and improve the female health span.

Background: Osteoporosis is a major public health concern worldwide. As the predominant and long-lived bone cells, osteocytes serve as key regulators of bone remodeling and mechanotransduction. However, the molecular mechanisms underlying their regulatory roles remain poorly understood. The roles of talin1, a key focal adhesion protein linking integrins to the cytoskeleton, in regulation of osteocyte function and skeletal homeostasis remain unclear.Methods: Osteocyte-specific talin1 conditional knockout (cKO) mice were established, and their skeletal phenotypes were assessed through micro-CT, histomorphometry, and biomechanical analyses. Osteocyte senescence and molecular signaling were assessed by RNA sequencing analysis, immunostaining, and biochemical assays. Talin1-p53 interactions were characterized by co-immunoprecipitation and pull-down assay. Rescue experiments were performed using talin1 and p53 double KO mice.Results: Talin1 expression in osteocytes was markedly reduced during skeletal aging in mice and humans. Osteocyte-specific deletion of talin1 disrupted FA integrity and dendritic networks, leading to severe osteopenia in weight-bearing bones and impaired bone mechanical properties. Talin1 deficiency altered the bone marrow microenvironment, suppressing osteoblast differentiation while enhancing adipogenesis. Mechanistically, talin1 bound and sequestered p53 in the cytoplasm for proteasomal degradation. Thus, talin1 loss enhanced p53 nucleotranslocation, inducing upregulation of p16 and p21 and osteocyte senescence. Importantly, genetic ablation of p53 in osteocytes rescued the low bone mass phenotype, defective bone formation, and excessive senescence caused by talin1 loss.Conclusions: This study identifies talin1 as a key factor governing osteocyte senescence and bone mass. We define a novel talin1-p53 axis that links impaired focal adhesion signaling to osteocyte senescence and bone loss, highlighting potential therapeutic targets for aging-related osteoporosis.

Chemical residues in food pose a global health challenge, which necessitates sensitive and reliable detection methods. Current techniques (e.g., chromatography and immunoassays) remain limited by operational complexity, insufficient sensitivity, and poor adaptability for on-site use. Click chemistry has emerged as a novel solution, offering rapid, specific, and ultrasensitive detection of food chemical residues, such as pesticides, antibiotics, and hormones-contaminants that pose significant health threats through chronic exposure. This review outlines the principles and classifications of click reactions, emphasizing their selectivity, mild reaction conditions, and modular design. Integrating biosensors enhances molecular recognition and signal amplification, enabling on-site screening in complex food matrices. We critically evaluate recent click chemistry-based sensors, detailing their design strategies (e.g., probe functionalization and nanomaterial engineering) and optimization via advanced transduction mechanisms. Key challenges-including matrix interference, reagent stability, and cost-are addressed through molecular imprinting, microfluidic miniaturization, and AI-driven system refinement. Future advancements will focus on integrating green chemistry to reduce environmental impact, developing multiplexed platforms for high-throughput detection, and expanding applications to emerging contaminants such as microplastics and biotoxins. These innovations promise to redefine food safety standards with scalable, next-generation analytical tools.

Acrylamide molecule detection by surface-enhanced infrared absorption spectroscopy using resonant nanoantennas.

Mechanism of Houttuynia cordata in treating acute lung injury based on network pharmacology.

A cellular and molecular perspective on organotypic lymphatic (dys)function.

Macelignan mitigates oxidative and inflammatory damage in hypoxic neurons through PPARγ-dependent pathways: implications for Alzheimer's disease.

Ultrasound molecular imaging of antibody-mediated rejection with CD16a-targeted probes in a complement-independent pathway.

Phosphodiesterase: insight from molecular targets for glycolipid metabolism.

Purpose: Early diagnosis of prostate cancer is critical for improving prognosis, but current detection techniques face limitations such as low sensitivity, high cost, and radiation risks. Prostate-specific membrane antigen (PSMA) is a transmembrane protein highly expressed in prostate cancer cells and a promising diagnostic and prognostic indicator. This study aims to develop a PSMA-targeted ultrasound contrast agent based on nanobody-modified gas vesicles (GVs) for early diagnosis of prostate cancer. Materials and Methods: GVs were extracted from Halobacterium NRC-1 (Halo). PSMA-targeting nanobodies (Nb-PSMA) were synthesized by Escherichia coli. PSMA-targeted gas vesicles (PSMA-GVs) were prepared by coupling Nb-PSMA to GVs via the intermediate coupling agent Mal-PEG2000-NHS. Control vesicles were prepared similarly. The targeting specificity of PSMA-GVs towards prostate cancer cells was assessed by flow cytometry and confocal microscopy using PSMA-positive PC-3 cells. In vivo contrast-enhanced ultrasound imaging of PSMA-GVs was performed in prostate cancer-bearing mice at early and advanced stages. The biocompatibility of PSMA-GVs was assessed by hemolysis tests, CCK8 cytotoxicity assays, serum biochemical assays and HE staining. Results: PSMA-GVs exhibited a uniform size, with a hydrodynamic diameter of 267.73 ± 2.86 nm, and showed a high specific binding ability to PC3 cells. In vivo ultrasound imaging of prostate cancer-bearing mice showed that PSMA-GVs had significantly slower tumor signal attenuation than Con-GVs. Our in vitro and in vivo experiments demonstrated that PSMA-GVs could bind to prostate cancer cells with higher specificity, generating stronger and longer-lasting molecular imaging signals in tumors, which presented significant advantages over Con-GVs. Immunofluorescence confirmed that PSMA-GVs crossed the vascular wall, entered the peritumoral vascular space, bound to tumor cells, and enabled PSMA-targeted molecular imaging. Additionally, PSMA-GVs showed good biocompatibility. Conclusion: Our study provides a new strategy for early ultrasound molecular imaging diagnosis of prostate cancer.

13th Tuscany Retreat on Cancer Research and Apoptosis: Genetic profiling, resistance mechanisms and novel treatment concepts in cancer and neurodegeneration.

Detecting the circular dichroism (CD) spectra of chiral molecules in the deep ultraviolet (DUV) region is of significant research importance in the biomedical field, as it can reflect not only enantiomer concentration but also molecular structural information. Although low-loss dielectric materials in the ultraviolet region can avoid the photothermal effects of traditional plasmonic materials, their poor electromagnetic field localization limits their application in molecular signal enhancement. Here, we designed a diamond nanostructure array. By exciting the collective lattice resonance (CLR) modes with non-local field distribution characteristics and introducing the coupling between the electric and magnetic CLRs, the optical chirality enhancement in the gap region between the diamond nanostructures is increased to a maximum of more than 150, with an average of over 52 at DUV wavelengths. Such characteristics allow the largely enhanced spatial superposition between the superchiral near field and the target chiral analytes. Moreover, simulation results demonstrate a 22-fold enhancement in the DUV CD signals of chiral molecules, with the enhanced CD intensity exhibiting a linear dependence on molecular concentration. Our results could be potentially used for ultrasensitive detection of chiral biomolecules, which is of interest in biopharmaceutical research applications such as rapid detection of chiral drug molecules at ultra-low concentrations.

BDNF and adenosine A2A receptor interaction regulates oligodendrogenesis from postnatal neural stem cells.

Advanced integrated human in vitro approach to explore gut-brain barrier interactions with gut microbiota metabolites and pesticides.

Fulvic acids act as chemical eustressors driving redox and hormonal reprogramming in rice roots.

Indole-3-propionic acid function through PXR and AhR, molecular signaling pathways, and antitoxic role in underlying diseases.

Traditional Mongolian medicine Batri-7 exhibits chemopreventive activity in colitis-associated colorectal cancer through microbiota modulation and NLRP3 inflammasome targeting.

Regenerative dentistry is shifting clinical practice from mechanical repair to biologically driven restoration of dental tissues. Advances in stem cell biology, biomaterials, and molecular signaling now support regeneration of enamel, dentin, pulp, periodontal ligament, and alveolar bone. Dental derived mesenchymal stem cells show strong differentiation,angiogenic,and immunomodulatory capabilities,while modern biomaterials like hydrogels, nanocomposites, bioactive glasses, and smart adhesives enhance remineralization and tissue integration.Biologics such as enamel matrix derivatives, platelet concentrates, and growth factors enable predictable pulp revitalization, and stem cell scaffold constructs promote regeneration of the pulp dentin complex. Periodontal regeneration benefits from photobiomodulation, advanced grafts, hydrogels, and hyaluronan-based systems, with emerging roles for mesenchymal stem cells derived micro RNAs.Rapid developments in 3D bioprinting, decellularized scaffolds, nanodelivery platforms, exosome-based therapies, and AI-driven design are accelerating translation into patient-specific solutions. Together, these innovations outline a paradigm shift toward therapies capable of restoring natural tooth form and function, potentially reducing reliance on traditional fillings, root canals, and periodontal surgery.

Objective: To evaluate the effects of atorvastatin and rosuvastatin on glucose regulation and insulin sensitivity in rats, focusing on biochemical, histological, and molecular changes. Methods: Thirty male albino rats were randomised into three groups (n=10 each): control, atorvastatin (80 mg/kg), and rosuvastatin (40 mg/kg). Treatments were given orally for 30 days. Serum insulin, homeostatic model assessment of insulin resistance (HOMA-IR), oral glucose tolerance test (OGTT), and fasting blood glucose (FBG) were measured. Pancreatic tissue was examined histologically. The molecular signalling pathway was studied by measuring the gene expression of protein kinase B (AKT) and Insulin-responsive glucose transporter type 4 (GLUT4) in adipose tissue and skeletal muscle. Results: [Atorvastatin treatment was associated with an initial reduction in fasting blood glucose and improvement in insulin sensitivity. However, by day 30, this group showed reduced glucose tolerance, increased insulin resistance, and β-cell alterations. These metabolic changes were accompanied by a transient early upregulation of AKT and GLUT4 expression in adipose tissue, which declined by the end of the study. In contrast, rosuvastatin treatment was associated with early improvement in glycaemic markers and preserved glucose tolerance, with histological changes observed in pancreatic tissue. Molecular analysis in this group showed a modest early upregulation of AKT and GLUT4 in skeletal muscle. Conclusion: Atorvastatin and rosuvastatin exert distinct effects on glucose metabolism. While rosuvastatin showed a more stable metabolic profile, prolonged high-dose atorvastatin was associated with insulin resistance and β-cell changes.