Search Results (752)

Due to the complex pore structure and strong heterogeneity of carbonate reservoirs, accurately characterizing reservoir properties remains a major challenge. Electrical imaging logs and nuclear magnetic resonance (NMR) logging are the essential techniques for analyzing reservoir pore structures and assessing fluid distribution. However, the high cost of NMR logging often limits its field application, resulting in sparse data coverage. To overcome this limitation, a pore spectrum model was constructed from electrical imaging logs, and corresponding pseudo-echo signals were generated. Through an optimized inversion algorithm, key parameters such as pseudo-NMR total porosity, fracture porosity, and other pore-structure-related parameters were extracted. These parameters, together with acoustic and density logs, as well as other derived logging features, were integrated to develop a comprehensive porosity prediction model based on support vector machines (SVMs). The model was applied to carbonate reservoirs in the Tarim Basin. For Well AT01, the average relative errors of the four-parameter SVM model and the full-parameter SVM model on the independent test set were 43.49% and 9.70%, respectively. The relative error of the full-parameter SVM model ranged from 4.40% to 15.30%, indicating improved prediction accuracy compared with direct use of pseudo-NMR-derived porosity. In addition, the full-parameter SVM model provided porosity estimates that were generally consistent with core-measured porosity in the locally calibrated test interval. These results suggest that integrating pseudo-NMR-derived pore-structure parameters with conventional logging features can improve porosity evaluation in complex carbonate reservoirs, especially when measured NMR logging data are limited. Full article

Although the underlying mechanisms of renal IRI have been extensively studied, the corresponding effective treatments are still lacking. HMGB1, an important nuclear factor that is secreted outside cells when experiencing stress conditions, acts as a DAMP and exerts crucial effects on renal IRI. Many studies have suggested that the effect of HMGB1 on kidney damage is mediated mainly through the interaction of HMGB1 with pattern recognition receptors such as TLR4 and RAGE, which then results in the aggravation of local inflammatory response, increased infiltration of leukocytes, and finally renal tubular damage. Preclinical studies using animal models have demonstrated that inhibition of HMGB1 and downstream signal pathways can attenuate renal injury. This review critically evaluates HMGB1 in renal IRI across redox state, subcellular localization, temporal and cell-specific release, receptor usage, integrated stress pathways, autophagy, and regulated cell death. It also compares direct neutralization, inhibition of release or translocation, epigenetic/RNA-based regulation, and receptor-directed strategies. The evidence is predominantly derived from short-term rodent studies, with one large-animal antibody study and no therapeutic human trials. Accordingly, HMGB1 is best regarded as a biologically compelling but clinically unvalidated target whose therapeutic value will depend on redox- and phase-selective inhibition, kidney-directed delivery, and rigorous pharmacokinetic and safety evaluation. Full article

Chronic myeloid leukemia (CML) is driven by constitutive BCR–ABL1 activity and remains clinically challenging due to disease persistence and resistance to tyrosine kinase inhibitors (TKIs). SIRT1, a NAD⁺-dependent deacetylase, has been implicated in leukemic cell survival and chemoresistance through negative regulation of p53. In this study, we evaluated the antileukemic effects of the Sechium hybrid H387 extract and its impact on the SIRT1–p53 signaling axis in K562 CML cells. Cell proliferation was assessed using a crystal violet assay, while gene and protein expression were analyzed by RT-qPCR, immunofluorescence, and flow cytometry. Apoptosis was determined by Annexin V/7-AAD staining. The extract significantly inhibited K562 cell proliferation and downregulated SIRT1 expression, reducing its nuclear localization. These effects were associated with increased p53 acetylation at lysine 382 (Ac-K382-p53) and enhanced apoptosis. Notably, a higher percentage of apoptotic cells was observed following extract treatment than with imatinib under the experimental conditions used, although the two agents have distinct mechanisms of action. These findings suggest that the antileukemic activity of Sechium hybrid H387 extract is associated with modulation of the SIRT1–p53 axis and induction of apoptosis in K562 cells. Full article

Accurate detection of sub-millimeter defects in reactor core-plate cotter-pin holes is essential for nuclear safety. However, underwater inspection images often suffer from low signal-to-noise ratios, weak boundary responses, and pseudo-edge interference, resulting in unstable localization of defects. Existing deformable and attention-based detectors remain vulnerable to sampling drift and semantic–boundary inconsistency under such conditions. To address these challenges, an Edge-Geometry-Guided Deformable Detection Network (EGD-Net) is proposed for underwater defect detection. EGD-Net introduces an edge-geometry-constrained deformable sampling mechanism that embeds edge-confidence priors into deformable convolution to improve boundary-aware feature sampling. A cross-level semantic–geometric alignment strategy is designed to enhance the interaction between defect semantics and geometric boundary cues, while a top-down feedback recalibration mechanism improves multi-scale response consistency for weak defects. Experiments on the Core-Plate Pin-Hole Defect (CPHD) dataset demonstrate that EGD-Net achieves the highest AP@[0.5:0.95] on both datasets while maintaining competitive or superior Precision, Recall, and F1-score while reducing engineering center error under a fixed operating point. Performance across the two complementary domains suggests its robustness to variations between coupon images and practical underwater inspection scenes. These results indicate that EGD-Net provides a reliable solution for boundary-sensitive localization of underwater sub-millimeter defects in nuclear inspection. Full article

Fusarium sacchari is one of the major pathogenic fungi that cause sugarcane Pokkah Boeng disease (PBD). Effectors play pivotal roles in F. sacchari–sugarcane interaction; thus, characterizing these effectors is essential for elucidating the molecular mechanisms underlying F. sacchari pathogenicity and for developing effective strategies to control PBD. However, only a limited number of effectors have been functionally validated to date. Here, we report FsRGAE1, a candidate effector protein from F. sacchari predicted to encode a rhamnogalacturonan acetylesterase (RGAE). FsRGAE1 exhibits high expression during the early stages of infection and maintains relatively elevated expression levels throughout the F. sacchari–sugarcane interaction. Targeted deletion of the FsRGAE1 gene in F. sacchari had no discernible impact on mycelial growth, conidiation, or carbon-source utilization, yet it significantly attenuated fungal virulence. FsRGAE1 possesses both a signal peptide conferring secretory capacity and a transit peptide enabling its translocation into the host cytoplasm and nucleus. Using the Agrobacterium tumefaciens-mediated transient expression system in Nicotiana benthamiana, FsRGAE1 was confirmed to suppress cell death induced by Bcl-2-associated X protein (BAX), as well as ROS accumulation and callose deposition, and its nuclear localization is indispensable for this immunosuppressive activity. Collectively, these findings indicate that FsRGAE1 promotes F. sacchari virulence by suppressing host immune responses in a nuclear localization-dependent manner, providing new insights into effector-mediated F. sacchari pathogenesis and potential target for resistance breeding in sugarcane. Full article

Nicotinamide adenine dinucleotide (NAD⁺) is a fundamental metabolic cofactor and signaling molecule that supports redox reactions, DNA repair, chromatin regulation, stress adaptation, inflammation, and neuronal maintenance. Age-associated NAD⁺ decline has been implicated in brain aging and neurodegenerative disorders, but the causal node and limiting compartment differ across tissues and disease states. Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) catalyzes the final step in NAD⁺ biosynthesis and represents the major nuclear isoform of the mammalian NMNAT family. Direct human genetic evidence establishes NMNAT-1 as a causal gene in inherited retinal degeneration, whereas evidence linking endogenous NMNAT-1 to broader brain aging or sporadic neurodegeneration is mainly convergent preclinical, preliminary, or indirect. Beyond NAD⁺ synthesis, biochemical and Drosophila studies suggest possible chaperone-like and proteostasis-supporting functions, but a separable NAD⁺-independent function of endogenous mammalian NMNAT-1 has not yet been established in vivo. Here, we review the molecular structure, localization, and regulation of NMNAT-1, emphasizing calibrated distinctions among catalytic nuclear NAD⁺ supply, engineered axonal protection, pathway-adjacent NAD⁺ interventions, and putative non-catalytic protection. We further discuss how NMNAT-1 dysfunction may contribute to aging-associated genomic instability, neuroinflammation, synaptic impairment, retinal degeneration, selected neurodegenerative models, and glioma biology. Finally, we evaluate therapeutic strategies targeting NMNAT-1 and NAD⁺ pathways, noting that no human trial has yet established efficacy for an NMNAT-1-directed neurological therapy. A compartment-aware and evidence-stratified view is therefore essential for translating NMNAT-1 biology into interventions for age-related neural disease. Full article

Immunotherapy can reduce treatment-related side effects but shows limited efficacy in “cold tumors,” whose immunosuppressive tumor immune microenvironment is characterized by abundant M2 macrophages and poor T cell infiltration. Because biopsy-based qualitative assessment of the tumor microenvironment is invasive and conventional imaging lacks functional information, this study aimed to develop an M2 macrophage-targeted theranostic agent enabling non-invasive photoacoustic (PA) imaging and pH-triggered cytotoxicity. A pullulan-based nanogel conjugated with mannose and near-infrared dye (IR-820) was further functionalized with the pH-responsive doxorubicin (DOX) prodrug, Aldoxorubicin, to develop Pullulan-mannose-IR820-Aldoxorubicin (PMID) nanogel. PMID was successfully synthesized, and the resulting self-assembled nanogels (<100 nm) exhibited a highly negative ζ-potential, near-infrared absorption peaks at 780 and 850 nm, and PA contrast comparable to IR-820 at 850 nm excitation. Dialysis studies demonstrated suppressed drug release at neutral pH (~20%) but accelerated release under acidic conditions, reaching ~80% within 48 h at pH 5.5, consistent with hydrazone hydrolysis and supporting tumor/lysosome-activated delivery. In RAW264.7 macrophages, PMID nanogel showed preferential uptake by M2-poralized versus M1-polarized macrophages, outperforming non-mannosylated PID nanogel and IR-820, and produced the strongest PA signal in M2 macrophage pellets. PMID nanogel also induced the highest concentration-dependent cytotoxicity in M2 macrophages, and microscopy indicated lysosomal accumulation of the nanogel with partial nuclear localization of released DOX. These findings support the use of PMID nanogel as M2 macrophage-targeted PA contrast agents and pH-responsive drug carriers with the potential to deplete immunosuppressive macrophages, modulate cold tumor microenvironments, and improve precision cancer theranostics. Full article

Understanding how co-occurring freshwater species respond to the same hydrological landscape is important for interpreting genetic diversity and population connectivity. We compared the population genetic structure of two widespread freshwater fishes, Rutilus rutilus (Linnaeus, 1758) and Perca fluviatilis Linnaeus, 1758, across major Lithuanian river basins using mitochondrial ATP6 and D-loop sequences. Both species exhibited high haplotype diversity but differed markedly in genetic structure. R. rutilus showed weak differentiation, widespread haplotype sharing among basins, and demographic signals compatible with population expansion. By contrast, P. fluviatilis exhibited stronger, more spatially heterogeneous structuring, with less consistent demographic signals and more localized differentiation. Contrary to expectations, genetic variation was not consistently associated with major drainage-basin boundaries in either species. Instead, the observed patterns suggest that species-specific ecological traits, particularly differences in dispersal capacity and habitat use, may play a greater role in shaping population structure than contemporary hydrological boundaries alone. These findings demonstrate that co-occurring freshwater fishes can exhibit contrasting patterns of genetic diversity even within shared hydrological systems. Although nuclear or genome-wide markers would strengthen these mitochondrial inferences, the study highlights the value of comparative approaches for understanding population connectivity and informing freshwater biodiversity conservation and management. Full article

Auxin response factors (ARFs) are key transcription factors regulating plant growth and development, but their functions and molecular mechanisms in stem elongation of cucurbit crops remain unclear. In this study, we identified a nuclear-localized ARF member, ClARF4, in watermelon. ClARF4 knockout lines were generated using CRISPR-Cas9 technology and exhibited significant reductions in plant height, internode number, and internode length. Cytological analysis indicated that the dwarf phenotype resulted from inhibited longitudinal cell elongation in stems. Transcriptome analysis revealed that ClARF4 modulates cell size by regulating the expression of genes involved in auxin signaling and response pathways. Furthermore, using yeast two-hybrid screening, we identified ClPetC, a component of the photosynthetic electron transport chain, as an interacting protein of ClARF4; bimolecular fluorescence complementation (BiFC) assays further confirmed their direct interaction in the plant nucleus. This study not only reveals the key role of ClARF4 in regulating plant height in watermelon, but also provides important insights into the function of chloroplast–nucleus signaling crosstalk in plant architecture establishment by identifying the interaction between ClARF4 and the chloroplast protein ClPetC in the nucleus. Full article

Background: Atopic dermatitis (AD) is a persistent and recurring skin disease characterized by epidermal barrier dysfunction, immune dysregulation, and elevated expression of proinflammatory mediators. We investigated the anti-inflammatory potential of polynucleotides (PN), highly purified DNA biopolymers isolated from salmonid gonads, in keratinocyte and macrophage activation models. Methods: RAW 264.7 macrophages were stimulated with lipopolysaccharide (LPS), whereas HaCaT keratinocytes were stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The effects of PN treatment on the production or expression of inflammatory mediators, cytokines, and chemokines were evaluated. Changes in the phosphorylation of mitogen-activated protein kinases (MAPKs) and Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) and in the nuclear localization of nuclear factor-κB (NF-κB) were also assessed. Results: In LPS-activated RAW 264.7 macrophages, PN treatment significantly suppressed nitric oxide production and downregulated the expression of inducible nitric oxide synthase (iNOS), TNF-α, IL-1β, and IL-8, accompanied by reduced NF-κB nuclear translocation. In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PN treatment markedly decreased the secretion levels of IL-6, IL-1β, and thymic stromal lymphopoietin. Moreover, PN treatment markedly reduced T-cell-recruiting chemokines, including MDC/CCL22, TARC/CCL17, RANTES/CCL5, and IL-8. Signaling analyses demonstrated that PN treatment attenuated the phosphorylation of key MAPKs (ERK, JNK, and p38) and the JAK1/STAT3 axis. Furthermore, PN treatment markedly reduced NF-κB nuclear translocation. Conclusions: These in vitro findings indicate that the anti-inflammatory effects of PN are associated with reduced activation of multiple core signaling pathways governing cytokine and chemokine responses, supporting further investigation of PN in AD and other chronic inflammatory skin diseases. Full article

Solid electrolyte interphase (SEI) characterization is needed to interpret the performance, degradation, and lifetime of graphite and Si-containing carbon-based negative electrodes in lithium-ion batteries. However, SEI claims are often difficult to compare because measured signals, inferred assignments, sample history, and electrode architecture are not always clearly separated. This review presents a claim-bounded framework for SEI characterization that distinguishes direct observables from inferred chemical, molecular, structural, morphological, and functional information. Photoelectron spectroscopy methods provide chemical-state and relative-depth-sensitivity constraints; secondary-ion mass spectrometry methods provide fragment and isotope distributions; vibrational spectroscopies support functional-group and local vibrational evidence; nuclear magnetic resonance and molecular mass spectrometry provide molecular or product-level constraints; and microscopy, tomography, and atomic force microscopy provide morphology, architecture, local thickness, topography, and mechanical response. Across these methods, rinsing, drying, sputtering, beam exposure, extraction, and limited sampling can alter the observable and therefore the defensible claim. The review emphasizes the distinction between native electrode-associated SEI features and extracted, soluble, or electrolyte-phase products, and between morphology-only evidence and chemically assigned morphology. It concludes by proposing claim-driven correlative workflows and reporting guidance for reproducible interpretation on graphite, Si/graphite, Si/C, and carbon-coated Si architectures where directly studied or present. Full article

Although Alternaria gansuense causes yellow stunt and root rot (YSRR)—a destructive disease of the leguminous forage Astragalus adsurgens in northern China—systematic investigations of this pathogen at the protein level remain scarce. In this study, we establish an optimized proteomic workflow for A. gansuense by comparing two protein extraction methods. Using data-independent acquisition (DIA) mass spectrometry with a DIA-NN search against the Alternaria protein database, we construct the first comprehensive proteome reference map of A. gansuense, then perform functional annotation via Gene Ontology, KOG, KEGG, InterPro domain, and subcellular localization analyses. A total of 5052 proteins were identified from vegetative mycelia, and the proteome was found to be predominantly composed of proteins involved in primary metabolism, signal transduction, secondary metabolism, and stress responses. Notably, a set of putative pathogenicity-associated proteins, including two-component regulators (SSK1p), protein kinases, cytochrome P450 enzymes, and ABC transporters, was identified. These proteins are homologs of well-characterized virulence factors in other pathogenic fungi, suggesting a potential coordinated signaling—metabolism—defense network that may contribute to fungal virulence. Subcellular localization further shows that cytoplasmic and nuclear proteins together account for over 50% of the annotated proteome. This study presents the first comprehensive proteomic reference map for A. gansuense, providing a valuable resource for functional genomics. Subsequent experimental validation of the bioinformatically predicted candidate molecular targets presented here may help to dissect the pathogenic mechanisms of YSRR and enable the development of novel disease management strategies. Full article

The renin–angiotensin–aldosterone system (RAAS) is a fundamental regulator of blood pressure, electrolyte balance, fluid homeostasis, and tissue remodeling. The discovery of the prorenin receptor (PRR), the protein encoded by the ATP6AP2 gene, has substantially expanded the classical RAAS paradigm by demonstrating that prorenin possesses biological activity beyond its proteolytic conversion to renin. Binding of renin or prorenin to PRR enhances local angiotensin II (Ang II) generation while simultaneously initiating Ang II-independent intracellular signaling pathways, including ERK1/2, mitogen-activated protein kinases, PI3K/Akt, transforming growth factor-β, and nuclear factor-κB, thereby promoting inflammation, oxidative stress, fibrosis, cellular proliferation, and extracellular matrix accumulation. Beyond its receptor function, PRR serves as an essential accessory component of the vacuolar H+-ATPase (V-ATPase) complex, regulating vesicular acidification, lysosomal function, autophagy, protein trafficking, cellular metabolism, and Wnt/β-catenin signaling. These diverse functions explain its indispensable role in embryonic development, cell differentiation, and tissue homeostasis, as evidenced by the embryonic lethality associated with ATP6AP2 gene deficiency. PRR is predominantly localized to intracellular organelles, including the endoplasmic reticulum, Golgi apparatus, endosomes, lysosomes, and autophagic vesicles, although membrane-bound and soluble forms also contribute to physiological and pathological processes. Increasing evidence implies dysregulated PRR signaling in the development and progression of hypertension, cardiovascular disease, chronic kidney disease, diabetes, obesity, and other metabolic disorders. This review summarizes current advances in PRR and soluble PRR biology, discusses unresolved mechanistic and translational questions, and evaluates the potential of PRR as a biomarker and therapeutic target for cardiovascular, renal, and metabolic diseases. Full article

Redox regulation plays an important role in plant stress responses. Our previous study revealed that rice GLUTATHIONE PEROXIDASE 1 (GPX1) acts as a redox sensor and transducer and promotes osmotic stress tolerance by transfer of cytosolic oxidative signals to transcription factor BASIC LEUCINE ZIPPER 68 (bZIP68). However, the mechanisms governing GPX1 activity and nuclear localization remain unclear. Here, we show that osmotic stress increases GPX1 acetylation. Peroxidase activity and subcellular localization assay indicated that the effects of acetylation on GPX1 function are site-specific, as the acetylation of K94 and K121 enhances GPX1 enzymatic activity, whereas the C-terminal K159/K162/K163 cluster is required for its nuclear translocation. Transgenic complementation and physiological assays confirmed that substitution of K159/K162/K163 sites into arginine abolished GPX1-mediated osmotic stress tolerance and the activation of bZIP68 target genes. Furthermore, we discovered that HISTONE DEACETYLASE 15 (HDA15) interacts with and deacetylates GPX1. HDA15-mediated deacetylation reduced enzymatic activity, nuclear translocation and subsequently the interaction with bZIP68 of GPX1. Accordingly, HDA15-overexpressing rice showed greater membrane damage, weaker induction of bZIP68-regulated genes and increased sensitivity to osmotic stress. These results identify HDA15-mediated GPX1 deacetylation as a negative regulatory mechanism that connects redox enzyme activity, protein localization and stress-responsive transcription in rice. Full article

Accurate binarization of phase-detection probe signals (gas vs. liquid) is necessary for the estimation of local void fraction, interfacial velocity, and bubble statistics in gas–liquid flows, particularly in nuclear thermal–hydraulic experiments. Classical threshold-based methods—single or double level—perform well on clean laboratory signals but degrade under realistic industrial conditions where noise, baseline drift, and clustered (slug-like) events challenge fixed rules. This work investigates whether deep learning (DL) models trained exclusively on synthetic data can deliver robust, generalizable binarization on real probe measurements. We (i) build a parametric generator of realistic time series from bubbly pulse templates, extended to clusters/slug patterns and perturbed with controlled noise, drift, and oscillatory baselines; (ii) train four lightweight DL architectures—one-dimensional U-Net (UNET-1D), Temporal Convolutional Network (TCN), a minimal one-dimensional Convolutional Neural Network (CNN-1D), and a Bidirectional Long-Short Memory network (BiLSTM)—only on synthetic signals; and (iii) evaluate them against classical threshold methods using event-level and sample-level metrics. On synthetic signal evaluation, UNET-1D and TCN achieve near-perfect event detection and sub-millisecond onset errors. On real bubbly and slug flow sensor data, classical threshold-based methods remain highly competitive on clean sensor signals, while DL models retain advantages under non-stationary baselines and clustered events, yielding accurate void and timing with no hand-tuned assumptions. Results support DL as a practical, data-driven complement to fixed algorithms, particularly in noisy or drift-dominated measuring conditions typical of nuclear thermal–hydraulic loops and safety-relevant test facilities. Full article