Baicalin induces ferroptosis in cervical squamous cell carcinoma via the NRF2/SLC7A11/GPX4 signaling axis.

Extracellular vesicles co-delivery of Tangeretin to mitigate sepsis-induced acute lung injury by inhibiting macrophage ferroptosis via ALOX5/ACSL4 signaling pathway.

Weathering of scorodite by root exudates: Arsenic dissolution and solid-phase speciation.

DNM1L-related disorders are rare mitochondrial diseases characterized by defective fission dynamics, often presenting with severe neurological manifestations. Current diagnostic and prognostic challenges stem from incomplete knowledge of domain-specific genotype-phenotype correlations and limited clinical data. We report a novel GTPase effector domain (GED) variant (p.Val687del) and conduct a systematic analysis of 80 reported DNM1L cases with variants in the GTPase, Middle, or GED domains. Clinical, genetic, and survival data were extracted and analyzed to evaluate associations between mutation localization and clinical outcomes. Statistical comparisons of phenotypic severity, survival, and hotspot prevalence were performed. Functional validation of the novel variant was performed through invitro overexpression, Western blot, immunofluorescence, and transmission electron microscopy. A novel GED deletion (p.Val687del) associated with peripheral neuropathy was identified, expanding the mutational spectrum. Invitro functional studies confirmed that this variant impairs DRP1 mitochondrial localization and induces severe ultrastructural damage, including fragmentation, swelling, and vacuolation. The preserved protein expression level excludes haploinsufficiency, consistent with a dominant-negative mechanism. Within the total cohort of 81 patients (including our case), de novo variants were predominant (74.1%), with R403C representing a major mutational hotspot (28.4%). Middle domain mutations conferred the most severe prognosis, manifesting high frequencies of developmental delay (90.7%), epilepsy (83.7%), abnormal muscle tone (67.4%), abnormal EEG findings (74.4%), and cerebral atrophy (73.2%). In contrast, GTPase domain mutations primarily affected sensory pathways, with optic atrophy (57.6%) and peripheral neuropathy (27.3%) as hallmark features. Carriers of the R403C variant exhibited a 3.9-year delay in disease onset compared to non-carriers. This study establishes that mutation location in DNM1L dictates clinical severity, with Middle domain variants defining a severe encephalopathic subtype, while GTPase domain mutations predominantly target sensory pathways, leading to optic atrophy and peripheral neuropathy. These findings provide a framework for precision prognostication and targeted therapeutic strategies in DNM1L-related disorders.

Electroacupuncture modulates P300-mediated STAT6/PPARγ binding to promote M2 polarization of microglia following cerebral ischemic injury.

Diabetic nephropathy (DN), a major complication of diabetes mellitus (DM), is characterized by severe clinical manifestations, impaired quality of life, and a high risk of progression to end-stage renal disease, underscoring the urgent need for effective therapeutic interventions. Mesenchymal stromal cell-derived exosomes (MSC-Exo) have emerged as promising candidates for mitigating inflammatory injury in DN due to their immunomodulatory properties, and exosomes derived from MSCs pretreated with inflammatory factors such as TNF-α and IFN-γ may possess enhanced therapeutic potential. In this study, exosomes isolated from human umbilical cord MSCs were characterized by transmission electron microscopy, nanoparticle tracking analysis, and western blotting. Their therapeutic effects were evaluated in diabetic mice, focusing on renal inflammation and macrophage polarization. Both normal MSC-Exo (Norm-Exo) and TNF-α&IFN-γ-pretreated MSC-Exo (TNF-α&IFN-γ-Exo) effectively ameliorated kidney injury and promoted M2 macrophage polarization, with TNF-α&IFN-γ-Exo showing superior efficacy. High-glucose-stimulated RAW264.7 cells were used to explore the underlying mechanisms, and high-throughput RNA sequencing identified inhibitor of DNA binding 3 (ID3) as a molecule involved in MSC-Exo-regulated macrophage polarization. Loss-of-function experiments confirmed that ID3 knockdown alone recapitulated the effects of exosomes, promoting M2 polarization and suppressing M1 markers. Conversely, ID3 overexpression attenuated exosome efficacy. Mechanistically, ID3 partially mediated exosome-induced inhibition of the NF-κB pathway. The translational relevance of these findings was further validated in PMA-differentiated THP-1 human macrophages. Collectively, these findings demonstrate that MSC-Exo-particularly TNF-α&IFN-γ-Exo-attenuate diabetic renal injury by modulating macrophage polarization through ID3 regulation, highlighting a novel cell-free immunomodulatory approach for DN therapy.

Fenton-like biotransformation of graphene by Pseudomonas sp. W4: Structural alteration, metabolites and genetic determinants.

Three-way photocatalytic redox conversions: Removal of organic contaminant and Cr(VI) with concurrent H2 production achieved in aerated condition.

Mechanistic insights into electrocoagulation-driven removal of polystyrene nanoplastics from urban treated wastewater.

Molecular-level fractionation and transformation of dissolved organic matter by schwertmannite during photo-aging: Implications for the carbon cycle in acid mine drainage environments.

The production of 5-hydroxymethylfurfural (HMF) from glucose is a reaction of considerable interest in biomass conversion into platform molecules. This reaction suffers, however, in general from low selectivity and the generation of undesirable polymeric byproducts (humins). Herein, we describe the preparation of phosphate-terminated Nb2C MXene (Nb2C-PO4) as a novel heterogenous water-tolerant acid catalyst, able to afford high yields of HMF, while minimizing humin formation. The phosphate-modified Nb2C has been extensively characterized (X-ray diffractometry (XRD), high resolution transmission electron microscopy (HRTEM), scanning transmission electron microscopy(STEM-EDS), X-ray photoelectron spectroscopy (XPS)) in order to prove the retention of the MXene structure and the presence of phosphate groups on the surface, and the acid-base properties have been assessed by NH3- and CO2-TPD and pyridine-DRIFTS. Apparently, the effect of phosphate is to mask less selective acid sites, while the remaining ones are more selective to promote HMF formation from glucose. This proposal is also supported by the contrasting behavior of pyridine and 2,6-di-tert-butylpyridine as quenchers of acid sites. Under optimized conditions, 64% yield of HMF can be obtained at 150°C in a monophasic THF/water mixture, using a high glucose concentration (5% w/w) and a low Nb2C-PO4 loading (S/C = 10 w/w), reaching a TOF of 3077 h-1.

A heterojunction photocatalyst composed of single-atom, atomically dispersed Ni sites on g-C3N4/TiO2 was developed for sacrificial-agent-free CO2-to-CO reduction under simulated solar irradiation. The optimized catalyst, containing 0.78 wt% Ni and 46 wt% g-C3N4, delivered 70% selectivity to CO over H2 and exhibited 16-fold enhancement in activity compared with bare g-C3N4/TiO2 and Ni-single-atom catalysts supported on either g-C3N4 or TiO2 alone. High-resolution transmission electron microscopy (HRTEM) revealed intimate interfacial coupling within the g-C3N4/TiO2 heterojunction, while atomically dispersed Ni species were predominantly anchored on g-C3N4 nanosheets coating the TiO2 surface. X-ray photoelectron spectroscopy revealed pronounced interfacial electronic redistribution following heterojunction formation and Ni incorporation, indicating strong electronic communication between the semiconductor components. Electrochemical impedance spectroscopy (EIS) and steady-state photoluminescence measurements showed significantly suppressed charge recombination, whereas transient absorption spectroscopy revealed that isolated Ni sites act as efficient electron traps, extracting photogenerated electrons and directing them toward catalytic reduction centers. Combined with the comparative photocatalytic performance of individual components, these findings identify the Ni-Nx moieties on g-C3N4 as active sites for CO2-to-CO conversion and support the S-scheme charge-transfer pathway, in which TiO2 preferentially consumes holes while highly reducing electrons accumulate on the g-C3N4-supported Ni single-atom sites to drive selective CO2 reduction in water.

Establishment of a novel model of depression caused by olfactory dysfunction through intranasal administration of 3-methylindole.

Establishment and characterization of an immortalized porcine gastric epithelial cell line and identification of NPC1 as a key mediator of aflatoxin B1 toxicity.

Engineered EV-mediated delivery of an anti-amyloid peptide provides neuroprotection in an in vitro Alzheimer's disease model.

Impact of natural antimicrobials on survival behavior and cell morphology of acid-stressed pathogens in ready-to-eat rice.

Bicelles stabilize a compact conformation of opsin with enhanced α-helical packing.

Krabbe Disease (KD) is a lysosomal leukodystrophy characterized by the production of psychosine in oligodendrocytes, leading to neurodegeneration and ultimately death. The only treatment modality currently available for this disease is hematopoietic stem cell transplantation (HSCT), a procedure with high morbidity, highlighting the need for further therapies to be developed. In this study, we established and characterized GALC knockout MO3.13 cells, a cell line derived from human oligodendrocytes, as a model for KD. Clonal MO3.13 cells with GALC KO were obtained via CRISPR/Cas9-mediated gene editing. GALC activity was measured by a 4-methylumbellyferyl (4-MU)-based assay, and morphology analyses were performed using light microscopy and transmission electron microscopy. Psychosine was measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The GALC KO cells have elevated levels of psychosine and an increased number of autophagosomes, autolysosomes, and cytoplasmic granules on transmission electron microscopy. Glycogen abundance was decreased in GALC KO cells compared to controls. After administration of BMN-S202, a ceramide galactosyltransferase inhibitor, psychosine levels in GALC KO cells were reduced back to WT levels. In conclusion, we demonstrated that the GALC KO MO3.13 cell line recapitulates the KD phenotype and biochemical response to SRT and may be a useful KD model for mechanistic studies and therapeutic development for KD.

This study investigates the mechanism of the TRPV1 channel in neuropathic pain (NP), focusing on the c/EBPβ/Uchl3/TRPV1 axis and mitochondrial dynamics. Using male rats chronic constriction injury (CCI) model and an LPS-induced dorsal root ganglion (DRG) cell model, we measured paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL), assessed expression changes of related molecules via Real-time quantitative reverse transcription PCR (RT-qPCR) and Western blot, observed mitochondrial fission via transmission electron microscopy (TEM) and Tomm20 immunofluorescence, evaluated mitochondrial function via JC-1 and MitoSOX, and examined neuronal excitability via calcium imaging. Co-immunoprecipitation (Co-IP) confirmed Uchl3-TRPV1 binding, and ubiquitination assay combined with Cycloheximide (CHX) chase and proteasome inhibition assays demonstrated that Uchl3 inhibits TRPV1 degradation via deubiquitination. Luciferase and Chromatin immunoprecipitation (ChIP) assays verified c/EBPβ as a transcriptional activator of Uchl3. Results showed that TRPV1 activation promoted mitochondrial fission, dysfunction, and neuronal excitability, driving NP. Uchl3 stabilized TRPV1 by removing its ubiquitination, altering mitochondrial dynamics. c/EBPβ transcriptionally upregulated Uchl3, forming a regulatory cascade. Intrathecal si-c/EBPβ in CCI rats downregulated c/EBPβ, Uchl3, and TRPV1, restored mitochondrial homeostasis, and alleviated pain behavior. In conclusion, the c/EBPβ/Uchl3/TRPV1 pathway regulates NP through mitochondrial dynamics in male rats, presenting a novel therapeutic target for NP treatment.

Elastic and inelastic interactions of electrons in transmission electron microscopy.