Cascaded signal amplification strategy for ultra-specific, ultra-sensitive, and visual detection of Shigella flexneri.

Pathogen infections including Shigella flexneri have posed a significant threat to human health for numerous years. Although culturing and qPCR were the gold standards for pathogen detection, time-consuming and instrument-dependent restrict their application in rapid diagnosis and economically less-developed regions. Thus, it is urgently needed to develop rapid, simple, sensitive, accurate, and low-cost detection methods for pathogen detection. In this study, an immunomagnetic beads-recombinase polymerase amplification-CRISPR/Cas12a (IMB-RPA-CRISPR/Cas12a) method was built based on a cascaded signal amplification strategy for ultra-specific, ultra-sensitive, and visual detection of S. flexneri in the laboratory. Firstly, S. flexneri was specifically captured and enriched by IMB (Shigella antibody-coated magnetic beads), and the genomic DNA was released and used as the template in the RPA reaction. Then, the RPA products were mixed with the pre-loaded CRISPR/Cas12a for fluorescence visualization. The results were observed by naked eyes under LED blue light, with a sensitivity of 5 CFU/mL in a time of 70 min. With no specialized equipment or complicated technical requirements, the IMB-RPA-CRISPR/Cas12a diagnostic method can be used for visual, rapid, and simple detection of S. flexneri and can be easily adapted to monitoring other pathogens.

Peripheral nerve injury associated with JEV infection in high endemic regions, 2016-2020: a multicenter retrospective study in China.

ABSTRACTPreviously, we have reported a cohort of Japanese encephalitis (JE) patients with Guillain-Barré syndrome. However, the evidence linking Japanese encephalitis virus (JEV) infection and peripheral nerve injury (PNI) remains limited, especially the epidemiology, clinical presentation, diagnosis, treatment, and outcome significantly differ from traditional JE. We performed a retrospective and multicenter study of 1626 patients with JE recorded in the surveillance system of the Chinese Center for Disease Control and Prevention, spanning the years 2016 to 2020. Cases were classified into type 1 and type 2 JE based on whether the JE was combined with PNI or not. A comparative analysis was conducted on demographic characteristics, clinical manifestations, imaging findings, electromyography data, laboratory results, and treatment outcomes. Among 1626 laboratory confirmed JE patients, 230 (14%) were type 2 mainly located along the Yellow River in northwest China. In addition to fever, headache, and disturbance of consciousness, type 2 patients experienced acute flaccid paralysis of the limbs, as well as severe respiratory muscle paralysis. These patients presented a greater mean length of stay in hospital (children, 22 years [range, 1-34]; adults, 25 years [range, 0-183]) and intensive care unit (children, 16 years [range, 1-30]; adults, 17 years [range, 0-102]). The mortality rate was higher in type 2 patients (36/230 [16%]) compared to type 1 (67/1396 [5%]). The clinical classification of the diagnosis of JE may play a crucial role in developing a rational treatment strategy, thereby mitigating the severity of the disease and potentially reducing disability and mortality rates among patients.

Analysis of Microbial Diversity and Community Structure of Rhizosphere Soil of Three Astragalus Species Grown in Special High-Cold Environment of Northwestern Yunnan, China.

Astragalus is a medicinal plant with obvious rhizosphere effects. At present, there are many Astragalus plants with high application value but low recognition and resource reserves in the northwestern area of Yunnan province, China. In this study, metagenomics was used to analyze the microbial diversity and community structure of rhizosphere soil of A. forrestii, A. acaulis, and A. ernestii plants grown in a special high-cold environment of northwestern Yunnan, China, at different altitudes ranging from 3225 to 4353 m. These microbes were taxonomically annotated to obtain 24 phyla and 501 genera for A. forrestii, 30 phyla and 504 genera for A. acaulis, as well as 39 phyla and 533 genera for A. ernestii. Overall, the dominant bacterial phyla included Proteobacteria, Actinobacteria, and Acidobacteria, while the dominant fungal ones were Ascomycota and Basidiomycota. At the genus level, Bradyrhizobium, Afipia, and Paraburkholderia were the most prevalent bacteria, and Hyaloscypha, Pseudogymnoascus, and Russula were the dominant fungal genera. Some of them are considered biocontrol microbes that could sustain the growth and health of host Astragalus plants. Redundancy analysis revealed that pH, TN, and SOM had a significant impact on the microbial community structures (p < 0.05). Finally, triterpene, flavonoid, polysaccharide, and amino acid metabolisms accounted for a high proportion of the enriched KEGG pathways, which possibly contributed to the synthesis of bioactive constituents in the Astragalus plants.

FAM20A-Associated Amelogenesis Imperfecta: Gene Variants with Functional Verification and Histological Features.

OBJECTIVE: To investigate FAM20A gene variants and histological features of amelogenesis imperfecta and to further explore the functional impact of these variants. METHODS: Whole-exome sequencing (WES) and Sanger sequencing were used to identify pathogenic gene variants in three Chinese families with amelogenesis imperfecta. Bioinformatics analysis, in vitro histological examinations and experiments were conducted to study the functional impact of gene variants, and the histological features of enamel, keratinised oral mucosa and dental follicle. RESULTS: The authors identified two nonsense variants c. 406C > T (p.Arg136*) and c.826C > T (p.Arg176*) in a compound heterozygous state in family 1, two novel frameshift variants c.936dupC (p.Val313Argfs*67) and c.1483dupC (p.Leu495Profs*44) in a compound heterozygous state in family 2, and a novel homozygous frameshift variant c.530_531insGGTC (p.Ser178Valfs*21) in family 3. The enamel structure was abnormal, and psammomatoid calcifications were identified in both the gingival mucosa and dental follicle. The bioinformatics and subcellular localisation analyses indicated these variants to be pathogenic. The secondary and tertiary structure analysis speculated that these five variants would cause structural damage to FAM20A protein. CONCLUSION: The present results broaden the variant spectrum and clinical and histological findings of diseases associated with FAM20A, and provide useful information for future genetic counselling and functional investigation.

JCAD deficiency delayed liver regenerative repair through the Hippo-YAP signalling pathway.

BACKGROUND AND AIMS: Liver regeneration retardation post partial hepatectomy (PH) is a common clinical problem after liver transplantation. Identification of key regulators in liver regeneration post PH may be beneficial for clinically improving the prognosis of patients after liver transplantation. This study aimed to clarify the function of junctional protein-associated with coronary artery disease (JCAD) in liver regeneration post PH and to reveal the underlying mechanisms. METHODS: JCAD knockout (JCAD-KO), liver-specific JCAD-KO (Jcad△Hep) mice and their control group were subjected to 70% PH. RNA sequencing was conducted to unravel the related signalling pathways. Primary hepatocytes from KO mice were treated with epidermal growth factor (EGF) to evaluate DNA replication. Fluorescent ubiquitination-based cell cycle indicator (FUCCI) live-imaging system was used to visualise the phases of cell cycle. RESULTS: Both global and liver-specific JCAD deficiency postponed liver regeneration after PH as indicated by reduced gene expression of cell cycle transition and DNA replication. Prolonged retention in G1 phase and failure to transition over the cell cycle checkpoint in JCAD-KO cell line was indicated by a FUCCI live-imaging system as well as pharmacologic blockage. JCAD replenishment by adenovirus reversed the impaired DNA synthesis in JCAD-KO primary hepatocyte in exposure to EGF, which was abrogated by a Yes-associated protein (YAP) inhibitor, verteporfin. Mechanistically, JCAD competed with large tumour suppressor 2 (LATS2) for WWC1 interaction, leading to LATS2 inhibition and thereafter YAP activation, and enhanced expression of cell cycle-associated genes. CONCLUSION: JCAD deficiency led to delayed regeneration after PH as a result of blockage in cell cycle progression through the Hippo-YAP signalling pathway. These findings uncovered novel functions of JCAD and suggested a potential strategy for improving graft growth and function post liver transplantation. KEY POINTS: JCAD deficiency leads to an impaired liver growth after PH due to cell division blockage. JCAD competes with LATS2 for WWC1 interaction, resulting in LATS2 inhibition, YAP activation and enhanced expression of cell cycle-associated genes. Delineation of JCADHippoYAP signalling pathway would facilitate to improve prognosis of acute liver failure and graft growth in living-donor liver transplantation.

TGF-ß1/SMAD3-driven GLI2 isoform expression contributes to aggressive phenotypes of hepatocellular carcinoma.

Hedgehog signaling is activated in response to liver injury, and modulates organogenesis. However, the role of non-canonical hedgehog activation via TGF-ß1/SMAD3 in hepatic carcinogenesis is poorly understood. TGF-ß1/SMAD3-mediated non-canonical activation was found in approximately half of GLI2-positive hepatocellular carcinoma (HCC), and two new GLI2 isoforms with transactivating activity were identified. Phospho-SMAD3 interacted with active GLI2 isoforms to transactivate downstream genes in modulation of stemness, epithelial-mesenchymal transition, chemo-resistance and metastasis in poorly-differentiated hepatoma cells. Non-canonical activation of hedgehog signaling was confirmed in a transgenic HBV-associated HCC mouse model. Inhibition of TGF-ß/SMAD3 signaling reduced lung metastasis in a mouse in situ hepatic xenograft model. In another cohort of 55 HCC patients, subjects with high GLI2 expression had a shorter disease-free survival than those with low expression. Moreover, co-positivity of GLI2 with SMAD3 was observed in 87.5% of relapsed HCC patients with high GLI2 expression, indicating an increased risk of post-resection recurrence of HCC. The findings underscore that suppressing the non-canonical hedgehog signaling pathway may confer a potential strategy in the treatment of HCC.

Accelerating the Phase Formation Kinetics of Alluaudite Sodium Iron Sulfate Cathodes via Ultrafast Thermal Shock.

Alluaudite sodium iron sulfate (NFS) exhibits great potential for use in sodium-ion battery cathodes due to its elevated operating potential and abundant element reserves. However, conventional solid-state methods demonstrate a low heating/cooling rate and sluggish reaction kinetics, requiring a long thermal treatment to effectively fabricate NFS cathodes. Herein, we propose a thermal shock (TS) strategy to synthesize alluaudite sodium iron sulfate cathodes using either hydrous or anhydrous raw materials. The analysis of the phase formation process reveals that TS treatment can significantly facilitate the removal of crystal water and decomposition of the intermediate phase Na2Fe(SO4)2 in the hydrous precursor. In the case of the anhydrous precursor, the kinetics of the combination reaction between Na2SO4 and FeSO4 can be also accelerated by TS treatment. Consequently, pure NFS phase formation can be completed after a substantially shorter time of post-sintering, thereby saving significant time and energy. The TS-treated NFS cathode derived from hydrous precursor exhibits higher retention after 200 cycles at 1C and better rate capability than the counterpart prepared by conventional long-term tube furnace sintering, demonstrating the great potential of this novel strategy.

Role of C/EBP Homologous Protein in Vascular Stenosis After Carotid Artery Injury.

The study aims to explore the fluctuating expression of C/EBP Homologous Protein (CHOP) following rat carotid artery injury and its central role in vascular stenosis. Using in vivo rat carotid artery injury models and in vitro ischemia and hypoxia cell models employing human aortic endothelial cells (HAECs) and vascular smooth muscle cells (T/G HA-VSMCs), a comprehensive investigative framework was established. Histological analysis confirmed intimal hyperplasia in rat models. CHOP expression in vascular tissues was assessed using Western blot and immunohistochemical staining, and its presence in HAECs and T/G HA-VSMCs was determined through RT-PCR and Western blot. The study evaluated HAEC apoptosis, inflammatory cytokine secretion, cell proliferation, and T/G HA-VSMCs migration through Western blot, ELISA, CCK8, and Transwell migration assays. The rat carotid artery injury model revealed substantial fibrous plaque formation and vascular stenosis, resulting in an increased intimal area and plaque-to-lumen area ratio. Notably, CHOP is markedly elevated in vessels of the carotid artery injury model compared to normal vessels. Atorvastatin effectively mitigated vascular stenosis and suppresses CHOP protein expression. In HAECs, ischemia and hypoxia-induced CHOP upregulation, along with heightened TNFα, IL-6, caspase3, and caspase8 levels, while reducing cell proliferation. Atorvastatin demonstrated a dose-dependent suppression of CHOP expression in HAECs. Downregulation of CHOP or atorvastatin treatment led to reduced IL-6 and TNFα secretion, coupled with augmented cell proliferation. Similarly, ischemia and hypoxia conditions increased CHOP expression in T/G HA-VSMCs, which was concentration-dependently inhibited by atorvastatin. Furthermore, significantly increased MMP-9 and MMP-2 concentrations in the cell culture supernatant correlated with enhanced T/G HA-VSMCs migration. However, interventions targeting CHOP downregulation and atorvastatin usage curtailed MMP-9 and MMP-2 secretion and suppressed cell migration. In conclusion, CHOP plays a crucial role in endothelial injury, proliferation, and VSMCs migration during carotid artery injury, serving as a pivotal regulator in post-injury fibrous plaque formation and vascular remodeling. Statins emerge as protectors of endothelial cells, restraining VSMCs migration by modulating CHOP expression.

A Comprehensive Prognostic and Immune Infiltration Analysis of RBM4 in Pan-Cancer.

BACKGROUND: Aberrant splicing has been closely associated with human cancer, though the precise underlying mechanisms linking the two remain not fully understood. Investigating the role of splicing factors in cancer progression may aid in the development of targeted therapies for dysregulated splicing, thereby opening up new avenues for cancer treatment. RNA-binding motif 4 (RBM4) has been identified as a critical participant in the condensin II complex, which is involved in chromosome condensation and stabilization during mitosis. Its significance in tumors is currently gaining attention. The genetic characteristics of RBM4 suggest its potential to elucidate the malignant progression of tumors in a broader context, encompassing various types of cancer, known as pan-cancer. METHODS: This study aims to comprehensively explore the potential function of RBM4 in pan-cancer by leveraging existing databases such as The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx). RESULTS: RBM4 is found to be overexpressed in almost all tumors and exhibits significant prognostic and diagnostic efficacy. The correlation between RBM4 and immune signatures, including immune cell infiltration and immune checkpoint genes, indicates that RBM4 could serve as a guiding factor for immunotherapy. CONCLUSIONS: As a member of the pan-oncogene, RBM4 has the potential to become a biomarker and therapeutic target for various malignant tumors, offering novel possibilities for precision medicine.

Soil health hazards of di(2-ethylhexyl) phthalate: New perspectives on earthworms from different ecological niches DNA damage, gut microbial disruption and soil enzyme changes.

Di(2-ethylhexyl) phthalate (DEHP) is perceived an emerging threat to terrestrial ecosystem, however, clear and accurate studies to fully understander ecotoxicity and underlying mechanisms of DEHP on the soil fauna remain poorly understood. Therefore, this study conducted a microcosm experiment of two earthworm ecotypes to investigate the ecological hazards of DHEP from multiple perspectives. The results showed that DEHP significantly increased the 8-hydroxy-deoxyguanosine (8-OHdG) content both in Eisenia foetida (13.76-133.0%) and Metaphire guillelmi (11.01-49.12%), leading to intracellular DNA damage. Meanwhile, DEHP negatively affected the expression of functional genes (ATP-6, NADH1, COX), which may be detrimental to mitochondrial respiration and oxidative stress at the gene level. The two earthworm guts shared analogous dominant bacteria however, the incorporation of DEHP drastically suppressed the homogeneity and diversity of the gut microbes, which further disrupted the homeostasis of the gut microbial ecological network. The keystone species in the gut of E. foetida decreased under DEHP stress but increased in the gut of M. guillelmi. Moreover, DEHP presented detrimental effects on soil enzyme activity, which is mainly associated with pollutant levels and earthworm activity. Collectively, the findings expand the understanding of soil ecological health and reveal the underlying mechanisms of the potential exposure risk to DEHP.

Optimizing potassium polysulfides for high performance potassium-sulfur batteries.

Potassium-sulfur batteries attract tremendous attention as high-energy and low-cost energy storage system, but achieving high utilization and long-term cycling of sulfur remains challenging. Here we show a strategy of optimizing potassium polysulfides for building high-performance potassium-sulfur batteries. We design the composite of tungsten single atom and tungsten carbide possessing potassium polysulfide migration/conversion bi-functionality by theoretical screening. We create two ligand environments for tungsten in the metal-organic framework, which respectively transmute into tungsten single atom and tungsten carbide nanocrystals during pyrolysis. Tungsten carbide provide catalytic sites for potassium polysulfides conversion, while tungsten single atoms facilitate sulfides migration thereby significantly alleviating the insulating sulfides accumulation and the associated catalytic poisoning. Resultantly, highly efficient potassium-sulfur electrochemistry is achieved under high-rate and long-cycling conditions. The batteries deliver 89.8% sulfur utilization (1504 mAh g-1), superior rate capability (1059 mAh g-1 at 1675 mA g-1) and long lifespan of 200 cycles at 25 °C. These advances enlighten direction for future KSBs development.

Rapid High-Temperature Liquid Shock Synthesis of High-Entropy Alloys for Hydrogen Evolution Reaction.

High-entropy-alloy nanoparticles (HEA-NPs) show great potential as electrocatalysts for water splitting, fuel cells, CO2 conversion, etc. However, fine-tuning the surface, morphology, structure, and crystal phase of HEA remains a great challenge. Here, the high-temperature liquid shock (HTLS) technique is applied to produce HEA-NPs, e.g., PtCoNiRuIr HEA-NPs, with tunable elemental components, ultrafine particle size, controlled crystal phases, and lattice strains. HTLS directly applied Joule heating on the liquid mixture of metal precursors, capping agents, and reducing agents, which is feasible for controlling the morphology and structure such as the atomic arrangement of the resulting products, thereby facilitating the rationally designed nanocatalysts. Impressively, the as-obtained PtCoNiRuIr HEA-NPs delivered superior activity and long-term stability for the hydrogen evolution reaction (HER), with low overpotentials at 10 mA cm-2 and 1 A cm-2 of only 18 and 408 mV, respectively, and 10000 CV stable cycles in 0.5 M H2SO4. Furthermore, in the near future, by combining the HTLS method with artificial intelligence (AI) and theoretical calculations, it is promising to provide an advanced platform for the high-throughput synthesis of HEA nanocatalysts with optimized performance for various energy applications, which is of great significance for achieving a carbon-neutral society with an effective and environmentally friendly energy system.

Primary acinic cell carcinoma of the breast: A case report and review of literature.

BACKGROUND: In the current World Health Organization classification, acinic cell carcinoma (AcCC) of the breast is considered a rare histological subtype of triple-negative breast cancer. Because of the few reports in the literature, data concerning clinical outcomes are limited. Here, we report a case of AcCC of the breast in a 48-year-old woman. CASE SUMMARY: A 48-year-old woman with a mass in her right breast came to our hospital for further diagnosis. Mammography and an ultrasound (US) scan showed a mass in the upper inner side of the right breast. She then underwent surgery to resect the mass in her right breast. Postoperative pathological examination revealed that the tumor had abundant acinar-like structures formed by tumor cells with prominent eosinophilic granules in the cytoplasm, consistent with acinar cell carcinoma. The results of immunohistochemical analysis supported the diagnosis of breast acinar cell carcinoma. Two months later, she underwent breast-conserving surgery and sentinel lymph node biopsy. The pTNM stage was T2N0M0. After surgery, the patient received 30 radiotherapy sessions. The patient was followed up for a period of one year, and no recurrence was found. CONCLUSION: AcCC of the breast is a rare type of malignant tumor. Because it is usually asymptomatic and can be detected by imaging studies, routine breast US or mammograms are important. However, there are no characteristic diagnostic imaging findings or clinical manifestations, so immunohistochemical examination is critical for an accurate diagnosis of AcCC of the breast.

Expanding the insight of ecological risk on the novel chiral pesticide mefentrifluconazole: Mechanism of enantioselective toxicity to earthworms (Eisenia fetida).

Continued application of new chiral fungicide mefentrifluconazole (MFZ) increases its risk to soil ecosystem. However, the toxicity of MFZ enantiomers to soil fauna and whether stereoselectivity exists remains poorly elucidated. Based on multilevel toxicity endpoints and transcriptomics, we investigated the negative effects of racemic, R-(-)-, and S-(+)-MFZ on Eisenia fetida. After exposure to S-(+) configuration at 4 mg/kg for 28 day, its reactive oxygen species levels were elevated by 15.4% compared to R-(-) configuration, inducing enantiospecific oxidative stress and transcriptional aberrations. The S-(+) isomer induced more severe cell membrane damage and apoptosis than the R-(-) isomer, and notably, the selectivity of apoptosis is probably dominated by the mitochondrial pathway. Mechanistically, differential mitochondrial stress lies in: S-(+) isomer specifically up-regulated mitochondrial cellular component compared to R-(-) isomer and identified more serious mitochondrial fission. Furthermore, S-(+) conformation down-regulated biological processes associated with ATP synthesis and metabolism, with specific inhibition of mitochondrial respiratory electron transport chain complex I and IV activity resulting in more severe electron flow disturbances. These ultimately mediated enantioselective ontogenetic process disorders, which were supported at phenotypic (weight loss), genetic, and protein (reverse modulate TCTP and Sox2 expression) levels. Our findings offer an important reference for elucidating the enantioselective toxicological mechanism of MFZ in soil fauna.

JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis.

BACKGROUND/AIMS: Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet. METHODS: Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation. RESULTS: In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL. CONCLUSION: JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.

Guanosine diphosphate-mannose suppresses homologous recombination repair and potentiates antitumor immunity in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor prognosis. TNBCs with high homologous recombination deficiency (HRD) scores benefit from DNA-damaging agents, including platinum drugs and poly(ADP-ribose) polymerase (PARP) inhibitors, whereas those with low HRD scores still lack therapeutic options. Therefore, we sought to exploit metabolic alterations to induce HRD and sensitize DNA-damaging agents in TNBCs with low HRD scores. We systematically analyzed TNBC metabolomics and identified a metabolite, guanosine diphosphate (GDP)-mannose (GDP-M), that impeded homologous recombination repair (HRR). Mechanistically, the low expression of the upstream enzyme GDP-mannose-pyrophosphorylase-A (GMPPA) led to the endogenous up-regulation of GDP-M in TNBC. The accumulation of GDP-M in tumor cells further reduced the interaction between breast cancer susceptibility gene 2 (BRCA2) and ubiquitin-specific peptidase 21 (USP21), which promoted the ubiquitin-mediated degradation of BRCA2 to inhibit HRR. Therapeutically, we illustrated that the supplementation of GDP-M sensitized DNA-damaging agents to impair tumor growth in both in vitro (cancer cell line and patient-derived organoid) and in vivo (xenograft in immunodeficient mouse) models. Moreover, the combination of GDP-M with DNA-damaging agents activated STING-dependent antitumor immunity in immunocompetent syngeneic mouse models. Therefore, GDP-M supplementation combined with PARP inhibition augmented the efficacy of anti-PD-1 antibodies. Together, these findings suggest that GDP-M is a crucial HRD-related metabolite and propose a promising therapeutic strategy for TNBCs with low HRD scores using the combination of GDP-M, PARP inhibitors, and anti-PD-1 immunotherapy.

Review of Carbon Support Coordination Environments for Single Metal Atom Electrocatalysts (SACS).

This topical review focuses on the distinct role of carbon support coordination environment of single-atom catalysts (SACs) for electrocatalysis. The article begins with an overview of atomic coordination configurations in SACs, including a discussion of the advanced characterization techniques and simulation used for understanding the active sites. A summary of key electrocatalysis applications is then provided. These processes are oxygen reduction reaction (ORR), oxygen evolution reaction (OER), hydrogen evolution reaction (HER), nitrogen reduction reaction (NRR), and carbon dioxide reduction reaction (CO2 RR). The review then shifts to modulation of the metal atom-carbon coordination environments, focusing on nitrogen and other non-metal coordination through modulation at the first coordination shell and modulation in the second and higher coordination shells. Representative case studies are provided, starting with the classic four-nitrogen-coordinated single metal atom (MN4 ) based SACs. Bimetallic coordination models including homo-paired and hetero-paired active sites are also discussed, being categorized as emerging approaches. The theme of the discussions is the correlation between synthesis methods for selective doping, the carbon structure-electron configuration changes associated with the doping, the analytical techniques used to ascertain these changes, and the resultant electrocatalysis performance. Critical unanswered questions as well as promising underexplored research directions are identified.

Construction of Bi/BiOI/BiOCl Z-scheme photocatalyst with enhanced tetracycline removal under visible light.

Bi/BiOI/BiOCl composite photocatalyst was constructed by one-step stirring approach at ambient environment to remove of tetracycline (TC) antibiotics via photodegradation in aqueous medium. A systematic discussion of the architecture, composition, formation, photochemical performance and photocatalytic activity of Bi/BiOI/BiOCl was carried out. By adjusting the experimental conditions, it was found that the Bi/BiOI/BiOCl photocatalyst obtained by using 0.7 mmol NaBH4, I/Cl = 5% and reacting for 6 h had the greatest removal performance. Under visible light irradiation, the photocatalytic degradation efficiency of TC reached 90.3% within 60 min, surpassing that of single BiOCl and BiOI. Through the active species removal experiment, it was determined that •O2- made a primary contribution to the photocatalytic degradation process. Moreover, the formation of Z-scheme heterojunction in Bi/BiOI/BiOCl was discussed, analyzing the photocatalytic mechanism and TC degradation pathway. The ecological toxicity of TC solution before and after degradation to rice seedlings was preliminarily tested. This study provides an idea for one-step synthesis of bismuth-based composite photocatalysts, with potential applications in the photocatalytic degradation of antibiotics.

Photocatalytic degradation of butyl benzyl phthalate by S-scheme Bi/Bi2O2CO3/Bi2S3 under simulated sunlight irradiation.

As a kind of plasticizer, butyl benzyl phthalate (BBP) presents a serious hazard to the ecosystem. Therefore, there is a strong need for an effective technique to eliminate the risk of BBP. In this work, a new photocatalyst of Bi/Bi2O2CO3/Bi2S3 with an S-scheme heterojunction was synthesized using Bi(NO3)3 as the Bi source, Na2S as the S source, and DMF as the carbon source and reductant. Numerous techniques have been used to characterize Bi/Bi2O2CO3/Bi2S3, such as scanning electron microscopy, high-resolution transmission electron microscopy, X-ray diffraction, and X-ray photoelectron spectroscopy. The improved photoactivity of Bi/Bi2O2CO3/Bi2S3 was evaluated by photoelectrochemical response, electrochemical impedance spectroscopy, photoluminescence, UV-Vis diffuse reflectance spectroscopy, and electrochemical Mott Schottky spectroscopy. The enhanced photocatalytic activity of this composite for BBP degradation under simulated sunlight irradiation could be attributed to the surface plasmon resonance effect of Bi metal and the heterojunction structure of Bi2O2CO3 and Bi2S3. The degradation rate of Bi/Bi2O2CO3/Bi2S3 was 85%, which was 4.52 and 1.52 times that of Bi2O2CO3 and Bi2S3, respectively. The prepared photocatalyst possessed good stability and reproducibility in eliminating BBP. The improved photocatalytic activity of Bi/Bi2O2CO3/Bi2S3 was demonstrated with the formation of an S-scheme heterojunction, and the degradation mechanism was discussed with a liquid chromatograph mass spectrometer.