Semi-artificial photosynthesis that merges biocatalytic specificity with engineered materials enables sustainable solar fuel production, yet it remains constrained by low solar-to-chemical efficiency and limited scalability. Here, we present a supramolecular strategy by programmatically integrating photocatalysts, biocatalysts, and cofactors on a single protein scaffold, and realize the coupling of photocatalytic CO2-to-CH4 conversion with enzymatic biomass upgrading. A rationally designed molecular hub-comprising switchable μ-oxo-bridged bis(FeIII-porphyrin) units and NADH mimics-drives deep CO2 reduction to CH4 at rates up to 32 000 µmol g-1 h-1 with >99% selectivity and a total apparent quantum efficiency of 1.82%. Modular tethering of diverse dehydrogenases activates inert C(sp3)─H bonds, delivering C2─C6 chemicals, including enantioenriched compounds (ee >96%). This programmable platform establishes a redox-balanced strategy for solar-driven synthesis of fuels and fine chemicals from CO2 and low-value feedstocks, unifying abiotic and biotic catalysis within a single framework.

Timely vascular access is critical in neurological emergencies, where delays in treatment may worsen secondary brain injury and functional outcomes. Intraosseous access offers a rapid alternative when intravenous cannulation is difficult, delayed, or unsuccessful, but its role in neurocritical care remains incompletely defined. PubMed, ScienceDirect, and Scopus were searched from inception through August 2025, with a targeted evidence update through 10 September 2026. This critical narrative review examines the feasibility, pharmacologic considerations, safety, evidence quality, and research gaps surrounding intraosseous access across acute ischemic and hemorrhagic stroke, status epilepticus, traumatic brain injury, neurological infections, metabolic encephalopathy, pediatric neurological emergencies, and cardiac arrest as an indirect neurologic outcome model. Available evidence supports intraosseous access as a technically feasible emergency route in selected scenarios, particularly when vascular access delay may postpone time-sensitive therapy. However, most data are derived from case reports, animal pharmacokinetic studies, heterogeneous emergency cohorts, or extrapolation from resuscitation and trauma literature. Direct evidence demonstrating improved neurologic outcomes remains very limited and varies substantially by condition. Intravenous access should remain preferred when rapidly obtainable, while intraosseous access should be viewed as a temporary rescue bridge rather than a routine early intervention. Prospective condition-specific studies are needed to evaluate drug delivery, timing, insertion site, complications, workflow integration, and meaningful neurologic outcomes before neuro-focused intraosseous protocols can be broadly recommended.

Ocular drug delivery remains a major challenge due to anatomical, physiological, and pathological barriers that limit drug penetration and retention. Liposomes offer a promising strategy to address these constraints; however, their effectiveness depends on physicochemical properties such as size, surface charge, and interfacial functionality, which govern transport across ocular tissues. Microfluidic technology provides a powerful platform to achieve precise control over these properties through tunable flow conditions and controlled self-assembly, enabling the reproducible fabrication of liposomes with tailored characteristics. In this context, this review establishes a barrier-informed framework that links ocular transport limitations to liposome design requirements and microfluidic processing strategies. In this review, we systematically examine microfluidic mixer geometries, including hydrodynamic flow, Dean-flow-based designs, and chaotic advection mixers, and discuss their impact on liposome formation. Methods for evaluating mixing performance are reviewed alongside the advantages and limitations of different chip materials and fabrication approaches. In addition, strategies for tuning liposome properties, including size, polydispersity, lamellarity, and stability, are critically analyzed in relation to ocular delivery requirements. Finally, emerging directions such as integrated single-step platforms, hybrid and 3D-printed systems, machine learning-assisted process control, solvent-free fabrication, and non-spherical liposomes are discussed. Collectively, this review provides a conceptual and engineering framework for the rational design of microfluidic platforms for liposome-based ocular drug delivery, bridging transport physics with translational applications.

Current diagnostic approaches to oral disease have limitations, highlighting the need for rapid, sensitive, and accessible technologies for routine clinical use. Biosensors can evaluate a wide range of biomarkers in oral conditions, including periodontal diseases, oral cancer, dental caries, oral infections, and peri-implant diseases.

Bioactivation and clearance of anticancer agents are crucial factors in the efficacy and toxicity of anticancer drugs. Exosomes are membrane-bound vesicles secreted by tumor cells and the tumor microenvironment. These vesicles contain drug-metabolizing enzymes, transporters, and RNA. Exosomes can be non-invasively collected from the blood. This article has been prepared by combining the evidence of the role of exosomal cytochrome P450 isoforms, such as cytochrome P450 family 2 subfamily C member 19, cytochrome P450 family 2 subfamily D member 6, and cytochrome P450 family 3 subfamily A member 5, in the oxidation of anticancer drugs in the first phase of drug metabolism. Exosomal UDP-glucuronosyltransferase 1A1 has been found to help in the conjugation of anticancer drugs in the second phase of drug metabolism. Exosomal ATP-binding cassette transporters, P-glycoprotein, multidrug resistance-associated protein 1, and breast cancer resistance protein have been found to act as intercellular conveyors of drug efflux capacity. These transporters can modulate the efficacy of chemotherapy. Exosomal microRNAs, such as microRNA-21, microRNA-155, and microRNA-1246, have been found to modulate apoptosis, DNA repair, metabolic adaptation, and chemotherapy resistance through the PI3K/AKT pathway, EZH2/STAT3 pathway, and PDCD4 pathway. Long non-coding RNAs, such as UCA1 and HOXA antisense RNA, can reprogram the chromatin structure. These long non-coding RNAs can suppress tumor suppressor genes, thus leading to chemotherapy resistance. Bioinformatics pipelines have been designed to bridge the gap between exosomal RNA and protein levels in the profile of dynamic metabolic states. The challenges in the field of exosomal therapy drug monitoring have been discussed in the article. The article has recommended the use of artificial intelligence in the integration of omics with microfluidic technology for the improvement of exosomal therapy drug monitoring.

Long-term standardized surveys are the cornerstone of our ability to measure changes in populations. Throughout North America, the North American Breeding Bird Survey (BBS) has been instrumental in documenting population changes on a broad scale. However, individual survey routes are often far apart, posing a challenge to assessing population dynamics at a fine spatial scale or to address responses to local land-use change. Community science efforts like eBird have helped to fill this gap by expanding spatial coverage, but the lack of standardized survey effort limits its suitability for evaluating trends. To bridge this gap, we present the North Carolina Mini Breeding Bird Survey (NCMBBS), a long-term, standardized breeding bird surveying program designed to provide high spatial resolution data for three counties in central North Carolina. The NCMBBS has been conducted annually since 1999 and has so far surveyed 208,366 individuals of 119 bird species as of 2025. The temporal extent of the NCMBBS enables analysis of long-term population change, while the spatial coverage supports study of local drivers of change. The NCMBBS complements large-scale programs such as the BBS by enabling multi-scale analyses of standardized data. The data are available for reuse under the MIT License, and users should cite this data paper if they make use of the NCMBBS and acknowledge the contributions of the volunteers who conduct our surveys.

Sustainable cellulose textiles are promising for wearable protection, yet integrating durable superamphiphobicity, fire safety, and environmental remediation within a single cellulose substrate remains challenging. Herein, a silane-mediated stabilized organic-inorganic interface was constructed on cotton fabric through hierarchical interfacial engineering. First, a bio-based phytic acid/L-lysine interlayer was introduced to impart phosphorus-nitrogen synergistic flame retardancy. Subsequently, a molecularly designed poly(perfluorodecyl acrylate-co-butyl acrylate-co-methacryloxypropyl trimethoxysilane) acted as an interfacial bridge coupling the cellulose substrate with fluorinated TiO2 nanoparticles to form a robust hierarchical micro/nano-structure. Benefiting from this chemically coupled and structurally stabilized architecture, the fabric exhibited durable superamphiphobicity with water and oil contact angles above 150° even after washing, abrasion, tape-peeling, ultrasonication, corrosive media exposure, and prolonged ultraviolet irradiation. It also displayed excellent flame retardancy with a limiting oxygen index of 33.2%, while enabling efficient formaldehyde degradation for photocatalytic air purification, achieving removal efficiencies of 75.15% and 82.10% under static and dynamic conditions, respectively. These results demonstrate that silane-mediated interfacial coupling and polymer-assisted nanoparticle immobilization suppressed nanoparticle detachment and stabilizes the hierarchical architecture, enabling long-term synergistic liquid repellency, fire safety, and photocatalytic activity. Overall, this strategy offers a versatile route to durable multifunctional cellulose textiles for wearable protection and environmental remediation.

The transition from nursing education to professional practice is marked by rapid professional development, increasing responsibility, psychological strain, and uncertainty. In Oman, the one-year Enhancement Training Program (ETP) was introduced to support early career nurses (ECNs) in bridging the gap between academic preparation and clinical practice.

Fuel cells represent the core components of next-generation high-efficiency electrochemical energy conversion technologies. The performance of the cathode oxygen reduction reaction (ORR) catalyst determines battery efficiency and lifespan. Thus, developing efficient, cost-effective ORR single-atom catalysts is essential for fuel cell commercialization. However, the symmetrical metal with a four-nitrogen (MN4) coordination and its electronic structure hinder the adsorption and conversion of oxygen intermediates, resulting in insufficient intrinsic activity and poor structural stability, which limits the efficiency of the ORR. To address this issue, several strategies have been proposed to improve catalytic performance and stability. This review introduces the mechanism of ORR and analyzes the effects of coordination engineering and substrate modification on the electronic structure, coordination environment, and geometric configuration of active sites in transition metal-nitrogen-carbon (M-N-C) catalysts, based on representative experimental results and theoretical calculations. Particular emphasis is placed on the relationship between the microenvironment and intrinsic activity. Subsequently, this review analyzes the origins of discrepancies between theoretical calculations and electrochemical experiments and summarizes optimization strategies to bridge this gap. Furthermore, the value of in situ characterization techniques is highlighted in investigating the microscale coordination and interfacial microenvironment of active sites, thereby promoting an understanding of catalytic mechanisms.

Drug resistance remains the first and most significant barrier to long-term curative benefits in lung cancer patients. Traditional resistance mechanisms focused on oncogenic driver mutations are inadequate to explain reversible tumor phenotypic plasticity under therapeutic stress. Increasing evidence has placed mitochondrial metabolic rewiring as the core signaling hub bridging energy homeostasis to nuclear epigenetic reprogramming; however, a comparative review of this metabolic-transcriptional axis in lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), and small cell lung cancer (SCLC) remains underrepresented. Here, this review integrates the published preclinical and translational data, dissecting how mitochondrial dysfunction, including altered oxidative phosphorylation (OXPHOS), TCA metabolite accumulation, ROS imbalance, and defective mitochondrial quality control, establishesdrug-tolerant persister (DTP) states. Subsequently, we elaborate on the conserved and subtype-specific genetic and epigenetic cascades induced by mtDNA variants, oncogenes (MYC/RAS), tumor suppressors (p53/LKB1), and oncometabolites (α-ketoglutarate, succinate, fumarate) that remodel chromatin landscapes and further initiate lineage plasticity, epithelial-mesenchymal transition, and immune evasion. We summarize promising mitochondrial-targeted interventions from OXPHOS inhibitors, fatty acid oxidation blockers, ROS modulators, and epigenetic agents and propose combinatorial therapeutic regimens according to the three lung cancer subtypes. This work establishes a unified metabolic-resilience framework and highlights multi-omics integrated profiling as a new paradigm in precision medicine to forecast resistance risk and reverse therapeutic failure in lung cancer.

The title compound, {[CdCl2(C6H8N2)2]·H2O} n (C6H8N2 = 2,3-di-methyl-pyrazine) was prepared by the reaction of cadmium chloride with 2,3-di-methyl-pyrazine in water. The asymmetric unit consists of two crystallographically independent cadmium cations that are situated on a twofold rotation axis, two crystallographically independent chloride anions and 2,3-di-methyl-pyrazine ligands as well as one water mol-ecule that are all located in general positions. The cadmium cations are octa-hedrally coordinated by two terminally N-bonded 2,3-di-methyl-pyrazine ligands and four chloride anions and are linked by pairs of μ-1,1 bridging chloride anions into chains that propagate in the crystallographic b-axis direction. These chains are connected into layers via the water mol-ecule of crystallization by inter-chain O-H⋯N hydrogen bonding. Powder X-ray diffraction (PXRD) indicates that a pure phase has been obtained. Thermogravimetry (TG) coupled to differential thermal analysis (DTA) indicates that the water mol-ecules are removed in the first step and that the 2,3-di-methyl-pyrazine ligands are lost in the subsequent two steps, leading to a compound with the composition [CdCl2(C6H8N2)].

The title compounds μ-oxido-bis-[(2-{[2-(3-meth-oxy-2-oxido-benzyl-idene-amino)-phenyl-imino]-meth-yl}-6-meth-oxy-phenolato)iron(III)] penta-hydrate, [Fe2(C22H18N2O4]·5H2O or {[(FeIII(L)](μ2-O)[FeIII(L)]}·5H2O (2), and di-chlorido-bis-(μ-2-{[2-(3-meth-oxy-2-oxido-benzyl-idene-amino)-phenyl-imino]-meth-yl}-6-meth-oxy-phenolato)diiron(III)potassium(I) nitrate, [KFe2(C22H18N2O4)2Cl2]NO3 or {[(FeIII(L)(Cl)](K)[FeIII(L)(Cl)]}·NO3 (3), were formed from the reaction of the metallo-ligand [FeII(L)]·(H2O) (H2 L is 2-{[2-(2-hy-droxy-3-meth-oxy-benzyl-idene-amino)-phenyl-imino]-meth-yl}-6-meth-oxy-phenol, C22H20N2O4) with yttrium acetate and potassium nitrate, respectively. In complex 2, the FeIII ions, which presumably arise through aerial oxidation from FeII, have a distorted square-pyramidal environment and are bridged by a μ2 oxo oxygen atom with an Fe-O-Fe angle of 137.97 (5)°. In complex (3) the environment around the FeIII ions is a distorted square pyramid. All four phenoxo oxygen atoms link the FeIII ions to a potassium atom (site symmetry 2), yielding two four-membered Fe/O/K/O rings. The K+ ion is linked also to four meth-oxy oxygen atoms.

The coordination co-crystal (4-bromo-2-{[(2-hy-droxy-eth-yl)imino]-meth-yl}pheno-lolato-κ3 O,N,O')(thio-cyanato-κN)copper(II)-5-bromo-2-hy-droxy-benz-alde-hyde-water (2/1/1), [Cu(C9H9BrNO2)(NCS)]·0.5C7H5BrO2·0.5H2O or [Cu(HL)(SCN)]2·C7H5BrO2·H2O, crystallizes in the monoclinic space group P21/c. The asymmetric unit contains two mononuclear units of the complex, each consisting of one deprotonated ligand, one thio-cyanate anion (SCN-) coordinated through its nitro-gen atom, one free water mol-ecule, and one free 5-bromo-salicyl-aldehyde mol-ecule, forming a co-crystal. The copper atom is four-coordinate, adopting a slightly distorted square-planar geometry defined by the tridentate ligand and the nitro-gen atom of the thio-cyanate anion. Bond length values show that the thio-cyanate ion has a linear S-C≡N arrangement, typical of a terminal, N-bound iso-thio-cyanate group. The water mol-ecule plays a key role in linking the two complex units through O-H⋯O hydrogen bonds. In the crystal, C-H⋯O and C-H⋯Br hydrogen bonds allow the free 5-bromo-salicyl-aldehyde mol-ecule to form a bridge between two adjacent layers. Additional O-H⋯O, C-H⋯S, O-H⋯S, and C-H⋯N inter-actions further consolidate the overall structure.