Electronic Structure and Functions of Carbon Nitride in Frontier Green Catalysis.

ConspectusGraphitic carbon nitride-based materials have emerged as promising photocatalysts for a variety of energy and environmental applications owing to their "earth-abundant" nature, structural versatility, tunable electronic and optical properties, and chemical stability. Optimizing carbon nitride's physicochemical properties encompasses a variety of approaches, including the regulation of inherent structural defects, morphology control, heterostructure construction, and heteroatom and metal-atom doping. These strategies are pivotal in ultimately enhancing their photocatalytic activities. Previous reviews with extensive examples have mainly focused on the synthesis, modification, and application of carbon nitride-based materials in photocatalysis. However, there has been a lack of straightforward and in-depth discussion to understand the electronic characteristics and functions of various engineered carbon nitrides as well as their precise tailoring strategies and ultimately to explain the regularity and specificity of their improved performance in targeted photocatalytic systems. In the past ten years, our group has conducted extensive investigations on carbon nitride-based materials and their application in photocatalysis. These studies demonstrate the close yet intricate relationship between the electronic structure of carbon nitride materials and their photocatalytic reactivity. Understanding the electronic structure and functions of carbon nitride, as well as different engineering strategies, is essential for the improvement of photocatalytic processes from fundamental study to practical applications.To this end, in this Account, we first delve into the nature of the electronic properties of carbon nitride, highlighting the electronic structures, including band structure, density of states, molecular orbitals, and band center, as well as its electronic functions, such as the charge distribution, internal electric field, and external electric force. Subsequently, based on recent research in our group, we present a detailed discussion of the strategic modifications of carbon nitride and the consequential impacts on the physicochemical properties, particularly the optical properties and intrinsic electronic characteristics, for enhancing the photocatalytic performance. These modifications are categorized as follows: (i) component changing, which involves intralayer and interface heterojunctions as well as homojunctions, to modulate the band-edge potentials and reactivity of photoinduced electrons and holes toward surface redox reactions; (ii) dimensional tuning, which engineers the dimensional structure of carbon nitride, to influence the electron transfer direction; (iii) defect and heteroatom modification, which introduces a symmetry break in the carbon nitride framework, to promote charge redistribution for altering the charge density and electronic structure; and (iv) anchoring of single-atom metals to facilitate orbital hybridization and charge transfer enhancement through the unique metal-N coordination configurations. Finally, we propose an appraisal of the prospects and challenges in the precise manipulation and characterization of the electronic structure and functions of carbon nitride. The integration of in situ electronic structure analysis, theoretical calculation based on machine learning, and precise mechanism study may propel its substantial development in the light-driven circular economy. We hope this Account aspires to offer novel insights and perspectives into the operational mechanisms and tailored structure of carbon nitride-based materials in photocatalysis.

AhNPR3 regulates the expression of WRKY and PR genes, and mediates the immune response of the peanut (Arachis hypogaea L.).

Systemic acquired resistance is an essential immune response that triggers a broad-spectrum disease resistance throughout the plant. In the present study, we identified a peanut lesion mimic mutant m14 derived from an ethyl methane sulfonate-mutagenized mutant pool of peanut cultivar "Yuanza9102." Brown lesions were observed in the leaves of an m14 mutant from seedling stage to maturity. Using MutMap together with bulked segregation RNA analysis approaches, a G-to-A point mutation was identified in the exon region of candidate gene Arahy.R60CUW, which is the homolog of AtNPR3 (Nonexpresser of PR genes) in Arabidopsis. This point mutation caused a transition from Gly to Arg within the C-terminal transactivation domain of AhNPR3A. The mutation of AhNPR3A showed no effect in the induction of PR genes when treated with salicylic acid. Instead, the mutation resulted in upregulation of WRKY genes and several PR genes, including pathogenesis-related thaumatin- and chitinase-encoding genes, which is consistent with the resistant phenotype of m14 to leaf spot disease. Further study on the AhNPR3A gene will provide valuable insights into understanding the molecular mechanism of systemic acquired resistance in peanut. Moreover, our results indicated that a combination of MutMap and bulked segregation RNA analysis is an effective method for identifying genes from peanut mutants.

A+T rich interaction domain protein 3a (Arid3a) impairs Mertk-mediated efferocytosis in cholestasis.

BACKGROUND & AIMS: Macrophages are key elements in the pathogenesis of cholestatic liver diseases. Arid3a plays a prominent role in the biologic properties of hematopoietic stem cells, B lymphocytes and tumor cells, but its ability to modulate macrophage function during cholestasis remains unknown. METHODS: Gene and protein expression and cellular localization were assessed by q-PCR, immunohistochemistry, immunofluorescence staining and flow cytometry. We generated myeloid-specific Arid3a knockout mice and established three cholestatic murine models. The transcriptome was analyzed by RNA-seq. A specific inhibitor of the Mertk receptor was used in vitro and in vivo. Promoter activity was determined by chromatin immunoprecipitation-seq against Arid3a and a luciferase reporter assay. RESULTS: In cholestatic murine models, myeloid-specific deletion of Arid3a alleviated cholestatic liver injury (accompanied by decreased accumulation of macrophages). Arid3a-deficient macrophages manifested a more reparative phenotype, which was eliminated by in vitro treatment with UNC2025, a specific inhibitor of the efferocytosis receptor Mertk. Efferocytosis of apoptotic cholangiocytes was enhanced in Arid3a-deficient macrophages via upregulation of Mertk. Arid3a negatively regulated Mertk transcription by directly binding to its promoter. Targeting Mertk in vivo effectively reversed the protective phenotype of Arid3a deficiency in macrophages. Arid3a was upregulated in hepatic macrophages and circulating monocytes in primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). Mertk was correspondingly upregulated and negatively correlated with Arid3a expression in PBC and PSC. Mertk+ cells were located in close proximity to cholangiocytes, while Arid3a+ cells were scattered among immune cells with greater spatial distances to hyperplastic cholangiocytes in PBC and PSC. CONCLUSIONS: Arid3a promotes cholestatic liver injury by impairing Mertk-mediated efferocytosis of apoptotic cholangiocytes by macrophages during cholestasis. The Arid3a-Mertk axis is a promising novel therapeutic target for cholestatic liver diseases. IMPACT AND IMPLICATIONS: Macrophages play an important role in the pathogenesis of cholestatic liver diseases. This study reveals that macrophages with Arid3a upregulation manifest a pro-inflammatory phenotype and promote cholestatic liver injury by impairing Mertk-mediated efferocytosis of apoptotic cholangiocytes during cholestasis. Although we now offer a new paradigm to explain how efferocytosis is regulated in a myeloid cell autonomous manner, the regulatory effects of Arid3a on chronic liver diseases remain to be further elucidated.

Tandem and inverted duplications in haemophilia A: Breakpoint characterisation provides insight into possible rearrangement mechanisms.

INTRODUCTION: Approximately half of patients with severe haemophilia A are caused by structural variants in the F8 gene. Unlike inversions or deletions directly impairing the integrity of F8, some duplications do not completely disrupt the open reading frame or even retain an intact F8 copy. Currently, only a few duplication breakpoints were precisely characterized, and the corresponding rearrangement mechanisms and clinical outcomes remain to be further investigated. AIM: Establishing an effective strategy for breakpoint characterization of duplications and revealing their rearrangement mechanisms. METHODS: AccuCopy is used for the detection of duplications, long-distance PCR for the characterization of tandem duplications, genome walking technique and whole genome sequencing for the characterization of inverted duplications. RESULTS: Four F8 duplication rearrangements were successfully characterized at the nucleotide level: one tandem duplication (exons 7-11) and three inverted duplications (exons 7-22, exons 2-26, and exons 15-22). Two shared features of inverted duplication were found after carefully analysing our results and breakpoint information in the literature: 1, an inverted fragment was inserted into the original chromosome via two junctions; 2, one junction is mediated by a pair of inverted repetitive elements, while the other consists of two breakpoints with microhomology. CONCLUSION: Similar breakpoint features motivated us to propose a DNA replication-based model to explain the formation of duplication rearrangements. Based on our model, we further divide the inverted duplications into three basic types: type I with a DEL-NOR/INV-DUP pattern, type II with a DUP-NOR/INV-DUP pattern and type III with a DUP-TRP/INV-DUP pattern.

Causal effects of inflammatory bowel diseases on the risk of kidney stone disease: a two-sample bidirectional mendelian randomization.

BACKGROUND: Existing epidemiological observational studies have suggested interesting but inconsistent clinical correlations between inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), and kidney stone disease (KSD). Herein, we implemented a two-sample bidirectional Mendelian randomization (MR) to investigate the causal relationship between IBD and KSD. METHODS: Data on IBD and KSD were obtained from Genome-Wide Association Studies (GWAS) summary statistics and the FinnGen consortium, respectively. Strict selection steps were used to screen for eligible instrumental SNPs. We applied inverse variance weighting (IVW) with the fix-effects model as the major method. Several sensitivity analyses were used to evaluate pleiotropy and heterogeneity. Causal relationships between IBD and KSD were explored in two opposite directions. Furthermore, we carried out multivariable MR (MVMR) to obtain the direct causal effects of IBD on KSD. RESULTS: Our results demonstrated that CD could increase the risk of KSD (IVW: OR = 1.06, 95% CI = 1.03-1.10, p < 0.001). Similar results were found in the validation group (IVW: OR = 1.05, 95% CI = 1.01-1.08, p = 0.013) and in the MVMR analysis. Meanwhile, no evidence of a causal association between UC and KSD was identified. The reverse MR analysis detected no causal association. CONCLUSIONS: This MR study verified that CD plays a critical role in developing kidney stones and that the effect of UC on KSD needs to be further explored.

Effects of 14 F9 synonymous codon variants on hemophilia B expression: Alteration of splicing along with protein expression.

There is growing evidence that synonymous codon variants (SCVs) can cause disease through the disruption of different processes of protein production. The aim of the study is to investigate whether the 14 SCVs reported in the F9 variant database were the pathogenic causes of hemophilia B. The impacts of SCVs on splicing and protein expression were detected using a combination of in silico prediction, in vitro minigene splicing assay and cell expression detection. The splicing transcripts were identified and quantified by co-amplification fluorescent PCR. The mechanism of splicing was verified by a modified pU1snRNA and pU7snRNA approach. Aberrant splicing patterns were found in eight SCVs. Five of the 8 SCVs produced almost all aberrant splicing isoforms, which were expected to truncate protein, three of them presented a partial defect on both splicing and protein secretion, the overall effects were consistent with the residual Factor IX activity of the affected cases. Neither the pre-messenger RNA (mRNA) splicing process nor the protein function was impaired in the rest six SCVs. In conclusion, our study firstly revealed the pathogenic mechanism of the 14 F9 SCVs and highlighted the importance of performing mRNA splicing analysis and protein expression studies of SCVs in inherited disorders.

Electric Field-Controlled Damping Switches of Coupled Dirac Plasmons.

For quasiparticle systems, the control of the quasiparticle lifetime is an important goal, determining whether the related fascinating physics can be revealed in fundamental research and utilized in practical applications. Here, we use double-layer graphene with a boron nitride spacer as a model system to demonstrate that the lifetime of coupled Dirac plasmons can be remotely tuned by electric field-controlled damping pathways. Essentially, one of the graphene layers serves as an external damping amplifier whose efficiency can be controlled by the corresponding doping level. Through this damping switch, the damping rate of the plasmon can be actively tuned up to 1.7 fold. This Letter provides a prototype design to actively control the lifetime of graphene plasmons and also broadens our horizon for the damping control of other quasiparticle systems.

Interplay between Lefty and Nodal signaling is essential for the organizer and axial formation in amphioxus embryos.

The organizer is an essential signaling center required for axial formation during vertebrate embryonic development. In the basal chordate amphioxus, the dorsal blastopore lip of the gastrula has been proposed to be homologous to the vertebrate organizer. Lefty is one of the first genes to be expressed in the organizer. The present results show that Lefty overexpression abolishes the organizer; the embryos were severely ventralized and posteriorized, and failed to develop anterior and dorsal structures. In Lefty knockouts the organizer is enlarged, and anterior and dorsal structures are expanded. Different from Lefty morphants in vertebrates, amphioxus Lefty mutants also exhibited left-right defects. Inhibition of Nodal with SB505124 partially rescued the effects of Lefty loss-of-function on morphology. In addition, while SB505124 treatment blocked Lefty expression in the cleavage stages of amphioxus embryos, activation of Nodal signaling with Activin protein induced ectopic Lefty expression at these stages. These results show that the interplay between Lefty and Nodal signaling plays an essential role in the specification of the amphioxus organizer and axes.

Piperine inhibits colorectal cancer migration and invasion by regulating STAT3/Snail-mediated epithelial-mesenchymal transition.

Cancer metastasis is the primary cause of death in patients diagnosed with colorectal cancer. Piperine, an active nontoxic ingredient in pepper, has potent anti-inflammatory and anti-cancer properties. However, little is known about the anti-migratory and anti-invasive effects of piperine on colorectal cancer. We demonstrated piperine inhibited the migration and invasion of colorectal cancer cells. Then, we found piperine reversed the biomarker expression of epithelial-to-mesenchymal transition (EMT), and suppressed the EMT regulator Snail. Furthermore, signal transducers and activators of transcription 3 (STAT3) was downregulated by piperine. Finally, STAT3 inhibitors were applied to observe the role of STAT3 in colorectal cancer migration, invasion and EMT. Collectively, piperine inhibits colorectal cancer migratory and invasive capacities through STAT3/Snail mediated EMT. Therefore, piperine could be applied as a possible therapeutic regimen for the prevention of colorectal cancer metastasis.

Cerberus-Nodal-Lefty-Pitx signaling cascade controls left-right asymmetry in amphioxus.

Many bilaterally symmetrical animals develop genetically programmed left-right asymmetries. In vertebrates, this process is under the control of Nodal signaling, which is restricted to the left side by Nodal antagonists Cerberus and Lefty. Amphioxus, the earliest diverging chordate lineage, has profound left-right asymmetry as a larva. We show that Cerberus, Nodal, Lefty, and their target transcription factor Pitx are sequentially activated in amphioxus embryos. We then address their function by transcription activator-like effector nucleases (TALEN)-based knockout and heat-shock promoter (HSP)-driven overexpression. Knockout of Cerberus leads to ectopic right-sided expression of Nodal, Lefty, and Pitx, whereas overexpression of Cerberus represses their left-sided expression. Overexpression of Nodal in turn represses Cerberus and activates Lefty and Pitx ectopically on the right side. We also show Lefty represses Nodal, whereas Pitx activates Nodal These data combine in a model in which Cerberus determines whether the left-sided gene expression cassette is activated or repressed. These regulatory steps are essential for normal left-right asymmetry to develop, as when they are disrupted embryos may instead form two phenotypic left sides or two phenotypic right sides. Our study shows the regulatory cassette controlling left-right asymmetry was in place in the ancestor of amphioxus and vertebrates. This includes the Nodal inhibitors Cerberus and Lefty, both of which operate in feedback loops with Nodal and combine to establish asymmetric Pitx expression. Cerberus and Lefty are missing from most invertebrate lineages, marking this mechanism as an innovation in the lineage leading to modern chordates.

Quantum Control of Graphene Plasmon Excitation and Propagation at Heaviside Potential Steps.

Quantum mechanical effects of single particles can affect the collective plasmon behaviors substantially. In this work, the quantum control of plasmon excitation and propagation in graphene is demonstrated by adopting the variable quantum transmission of carriers at Heaviside potential steps as a tuning knob. First, the plasmon reflection is revealed to be tunable within a broad range by varying the ratio γ between the carrier energy and potential height, which originates from the quantum mechanical effect of carrier propagation at potential steps. Moreover, the plasmon excitation by free-space photos can be regulated from fully suppressed to fully launched in graphene potential wells also through adjusting γ, which defines the degrees of the carrier confinement in the potential wells. These discovered quantum plasmon effects offer a unified quantum-mechanical solution toward ultimate control of both plasmon launching and propagating, which are indispensable processes in building plasmon circuitry.

Substantially Enhancing Quantum Coherence of Electrons in Graphene via Electron-Plasmon Coupling.

The interplays between different quasiparticles in solids lay the foundation for a wide spectrum of intriguing quantum effects, yet how the collective plasmon excitations affect the quantum transport of electrons remains largely unexplored. Here we provide the first demonstration that when the electron-plasmon coupling is introduced, the quantum coherence of electrons in graphene is substantially enhanced with the quantum coherence length almost tripled. We further develop a microscopic model to interpret the striking observations, emphasizing the vital role of the graphene plasmons in suppressing electron-electron dephasing. The novel and transformative concept of plasmon-enhanced quantum coherence sheds new insight into interquasiparticle interactions, and further extends a new dimension to exploit nontrivial quantum phenomena and devices in solid systems.

The antifouling mechanism and application of bio-inspired superwetting surfaces with effective antifouling performance.

With the rapid development of industries, the issue of pollution on Earth has become increasingly severe. This has led to the deterioration of various surfaces, rendering them ineffective for their intended purposes. Examples of such surfaces include oil rigs, seawater intakes, and more. A variety of functional surface techniques have been created to address these issues, including superwetting surfaces, antifouling coatings, nano-polymer composite materials, etc. They primarily exploit the membrane's surface properties and hydration layer to improve the antifouling property. In recent years, biomimetic superwetting surfaces with non-toxic and environmental characteristics have garnered massive attention, greatly aiding in solving the problem of pollution. In this work, a detailed presentation of antifouling superwetting materials was made, including superhydrophobic surface, superhydrophilic surface, and superhydrophilic/underwater superoleophobic surface, along with the antifouling mechanisms. Then, the applications of the superwetting antifouling materials in antifouling domain were addressed in depth.

Study on peanut protein oxidation and metabolomics/proteomics analysis of peanut response under hypoxic/re-aeration storage.

To better understand the effect of oxygen levels in the storage environment on peanut protein oxidation and explore the mechanism, the functional properties and the oxidation degree of peanut proteins extracted from peanuts under conventional storage (CS), nitrogen modified atmosphere storage (NS, hypoxic) and re-aeration storage (RS) were investigated. Metabolomics and proteomics were employed to analyze peanut's response to hypoxic/re-aeration storage environment. The results showed that NS retarded the decline of the functional properties and the oxidation of peanut proteins, while the process were accelerated after re-aeration. That was the result of the metabolic changes of peanuts under different storage environments. The omics results presented the decreased (NS)/increased (RS) levels of the antioxidant-related proteins acetaldehyde dehydrogenase and glutathione S-transferase, and the inhibition (NS)/activation (RS) of metabolic pathways such as the TCA cycle and the pentose phosphate pathway. This study provided a reference for the re-aeration storage of other agricultural products.

Pleiotropic effects of different exonic nucleotide changes at the same position contribute to hemophilia B phenotypic variation.

BACKGROUND: The disease-causing effects of genetic variations often depend on their location within a gene. Exonic changes generally lead to alterations in protein production, secretion, activity, or clearance. However, owing to the overlap between proteins and splicing codes, missense variants can also affect messenger RNA splicing, thus adding a layer of complexity and influencing disease phenotypes. OBJECTIVES: To extensively characterize a panel of 13 exonic variants in the F9 gene occurring at 6 different factor IX positions and associated with varying severities of hemophilia B (HB). METHODS: Computational predictions, splicing analysis, and recombinant factor IX assays were exploited to characterize F9 variants. RESULTS: We demonstrated that 5 (38%) of 13 selected F9 exonic variants have pleiotropic effects. Although bioinformatic approaches accurately classified effects, extensive experimental assays were required to elucidate and deepen the molecular mechanisms underlying the pleiotropic effects. Importantly, their characterization was instrumental in developing tailored RNA therapeutics based on engineered U7 small nuclear RNA to mask cryptic splice sites and compensatory U1 small nuclear RNA to enhance exon definition. CONCLUSION: Overall, albeit a multitool bioinformatic approach suggested the molecular effects of multiple HB variants, the deep investigation of molecular mechanisms revealed insights into the HB phenotype-genotype relationship, enabling accurate classification of HB variants. Importantly, knowledge of molecular mechanisms allowed the development of tailored RNA therapeutics, which can also be translated to other genetic diseases.

Influence of Nitrogen-Modified Atmosphere Storage on Lipid Oxidation of Peanuts: From a Lipidomic Perspective.

The effect of nitrogen-modified atmosphere storage (NS) on peanut lipid oxidation was investigated in this paper. Non-targeted lipidomics was employed to detect the lipid metabolites in peanuts with the aim of exploring the mechanism of lipid oxidation in peanuts under different storage conditions. The results showed that compared with conventional storage (CS), NS significantly (p < 0.05) delayed the increase in acid value, carbonyl value, and 2-thiobarbituric acid value and the decrease in vitamin E content. However, the storage time has a much greater effect on lipid oxidation than the oxygen level in the storage environment. Lipidomics analysis revealed that there were significant differences in metabolite changes between CS and NS. NS reduced the decline of most glycerophospholipids by regulating lipid metabolism in peanuts. NS maintained higher levels of Diacylglycerol (DAG), sulfoquinovosyl diacylglycerol (SQDG), lysophophatidylcholine (LPC), lysophosphatidylethanolamine (LPE) and phosphatidylinositol (PI) compared to CS. This work provided a basis for the application of NS technology to peanut storage.

Electrostatically induced Furfural-Derived carbon Dots-CdS hybrid for solar Light-Driven hydrogen production.

Carbon dots (CDs) exhibit distinctive optical, electronic, and physicochemical properties, rendering them effective cocatalysts to enhance the photocatalytic performance of light-absorbing materials. The interplay between CDs and substrates is pivotal in manipulating photogenerated charge separation, transfer, and redistribution, significantly influencing overall photocatalytic efficiency. This study introduces a novel electrostatic interaction strategy to interface positively charged CdS nanorods (CdS NRs) with negatively charged furfural-derived CDs. The resulting optimized composite (25-CDs@CdS NRs), showcases photocatalytic hydrogen production at a rate of 1076 µmol g-1h-1. Experimental analyses and theoretical simulations offer insights into the structure-activity relationship, underscoring the crucial role of enhanced electrostatic interaction between CDs and CdS NRs in facilitating efficient charge transfer, activating reaction sites, and improving reaction kinetics. This research establishes an adaptable strategy for integrating CDs with metal-based semiconductors, opening new avenues for developing photocatalytic hybrid assemblies.

Patient-derived organoids in human cancer: a platform for fundamental research and precision medicine.

Cancer is associated with a high degree of heterogeneity, encompassing both inter- and intra-tumor heterogeneity, along with considerable variability in clinical response to common treatments across patients. Conventional models for tumor research, such as in vitro cell cultures and in vivo animal models, demonstrate significant limitations that fall short of satisfying the research requisites. Patient-derived tumor organoids, which recapitulate the structures, specific functions, molecular characteristics, genomics alterations and expression profiles of primary tumors. They have been efficaciously implemented in illness portrayal, mechanism exploration, high-throughput drug screening and assessment, discovery of innovative therapeutic targets and potential compounds, and customized treatment regimen for cancer patients. In contrast to conventional models, tumor organoids offer an intuitive, dependable, and efficient in vitro research model by conserving the phenotypic, genetic diversity, and mutational attributes of the originating tumor. Nevertheless, the organoid technology also confronts the bottlenecks and challenges, such as how to comprehensively reflect intra-tumor heterogeneity, tumor microenvironment, tumor angiogenesis, reduce research costs, and establish standardized construction processes while retaining reliability. This review extensively examines the use of tumor organoid techniques in fundamental research and precision medicine. It emphasizes the importance of patient-derived tumor organoid biobanks for drug development, screening, safety evaluation, and personalized medicine. Additionally, it evaluates the application of organoid technology as an experimental tumor model to better understand the molecular mechanisms of tumor. The intent of this review is to explicate the significance of tumor organoids in cancer research and to present new avenues for the future of tumor research.

Intracellular calcium dysregulation in heart and brain diseases: Insights from induced pluripotent stem cell studies.

The central nervous system (CNS) plays a role in regulating heart rate and myocardial contractility through sympathetic and parasympathetic nerves, and the heart can impact the functional equilibrium of the CNS through feedback signals. Although heart and brain diseases often coexist and mutually influence each other, the potential links between heart and brain diseases remain unclear due to a lack of reliable models of these relationships. Induced pluripotent stem cells (iPSCs), which can differentiate into multiple functional cell types, stem cell biology and regenerative medicine may offer tools to clarify the mechanisms of these relationships and facilitate screening of effective therapeutic agents. Because calcium ions play essential roles in regulating both the cardiovascular and nervous systems, this review addresses how recent iPSC disease models reveal how dysregulation of intracellular calcium might be a common pathological factor underlying the relationships between heart and brain diseases.

Interfacial tuning in FeP/ZnIn2S4 Ohm heterojunction: Enhanced photocatalytic hydrogen production via Zn-P charge bridging.

Interfacial regulation is key to photocatalytic performance, yet modulating interfacial charge transfer in heterostructures remains challenging. Herein, a novel nanoflower-like FeP/ZnIn2S4 Ohm heterostructure is first designed, with Zn atoms in ZnIn2S4 (ZIS) acting as potential anchoring sites around P atoms, forming liganded Zn-P bonds. Combining 1D FeP nanowires and 2D ZIS nanosheets enhances the mobility of photogenerated electrons. The synergistic chain-type "electron pickup" mechanism of the Ohm heterojunction coupled with the Zn-P bond speeds up electron transport at the interface. The Ohm heterojunction initiates an internal electric field, creating a driving force to further transfer photogenerated electrons through the Zn-P rapid electron transport channel to FeP, which acts as a reservoir for active sites to release H2. The optimized FeP/ZIS demonstrates a remarkable H2 evolution rate at 4.36 mmol h-1 g-1, 3.6 times that of pristine ZIS. This work provides novel insights into optimizing photocarrier dynamics via interfacial microenvironment modulation.