Ecohydrological indicators and environmental flow assessment in the middle and lower reaches of the Huai River, China.

The vitality of river ecosystems is vital for the sustainable development of river basins, with the assessment of environmental flow (EF) playing a pivotal role in eco-informatics. This study delves into the middle and lower reaches (MLR) of the Huai River basin (HRB) in China, utilizing hydrological data spanning from 1950 to 2020. Its principal objective lies in the selection of ecohydrological indicators to refine the estimation of EF in the HRB. Employing principal component analysis (PCA), ecologically relevant hydrological indicators (ERHIs) were discerned and scrutinized for their hydrological characteristics. The analysis extended to evaluating hydrological shifts at different stations using ERHIs, determining suitable EF in the MLR, and delineating the trajectories of appropriate intra-annual flows in different hydrological years through HEC-RPT. Based on a variety of mutation test methods, the change point of runoff sequence was determined in 1991. The PCA analysis identified eight ERHIs, reflecting hydrological changes of 49.79 % and 56.26 % at Bengbu and Sanhezha, respectively, which indicate a moderate alteration. Based on ERHIs, the other stations in the HRB exhibited hydrological alterations ranging from 33 % to 47 %, notably highlighting substantial changes in maximal 30d flow and flow fall rate. The optimal flood pulse discharge in the middle reaches is 4150 m3/s, 3140 m3/s and 2150 m3/s in wet, dry and dry years, respectively. Downstream, flood pulse flow in wet, normal and dry years should exceed 4070 m3/s, 3110 m3/s and 1980 m3/s, respectively. The research contributes significantly to the management of rivers and the sustainable conservation of the ecological milieu.

Tabersonine enhances cisplatin sensitivity by modulating Aurora kinase A and suppressing epithelial-mesenchymal transition in triple-negative breast cancer.

CONTEXT: Tabersonine has been investigated for its role in modulating inflammation-associated pathways in various diseases. However, its regulatory effects on triple-negative breast cancer (TNBC) have not yet been fully elucidated. OBJECTIVE: This study uncovers the anticancer properties of tabersonine in TNBC cells, elucidating its role in enhancing chemosensitivity to cisplatin (CDDP). MATERIALS AND METHODS: After tabersonine (10 µM) and/or CDDP (10 µM) treatment for 48 h in BT549 and MDA-MB-231 cells, cell proliferation was evaluated using the cell counting kit-8 and colony formation assays. Quantitative proteomics, online prediction tools and molecular docking analyses were used to identify potential downstream targets of tabersonine. Transwell and wound-healing assays and Western blot analysis were used to assess epithelial-mesenchymal transition (EMT) phenotypes. RESULTS: Tabersonine demonstrated inhibitory effects on TNBC cells, with IC50 values at 48 h being 18.1 µM for BT549 and 27.0 µM for MDA-MB-231. The combined treatment of CDDP and tabersonine synergistically suppressed cell proliferation in BT549 and MDA-MB-231 cells. Enrichment analysis revealed that the proteins differentially regulated by tabersonine were involved in EMT-related signalling pathways. This combination treatment also effectively restricted EMT-related phenotypes. Through the integration of online target prediction and proteomic analysis, Aurora kinase A (AURKA) was identified as a potential downstream target of tabersonine. AURKA expression was reduced in TNBC cells post-treatment with tabersonine. DISCUSSION AND CONCLUSIONS: Tabersonine significantly enhances the chemosensitivity of CDDP in TNBC cells, underscoring its potential as a promising therapeutic agent for TNBC treatment.

Sensor Fault Reconstruction Using Robustly Adaptive Unknown-Input Observers.

Sensors are a key component in industrial automation systems. A fault or malfunction in sensors may degrade control system performance. An engineering system model is usually disturbed by input uncertainties, which brings a challenge for monitoring, diagnosis, and control. In this study, a novel estimation technique, called adaptive unknown-input observer, is proposed to simultaneously reconstruct sensor faults as well as system states. Specifically, the unknown input observer is used to decouple partial disturbances, the un-decoupled disturbances are attenuated by the optimization using linear matrix inequalities, and the adaptive technique is explored to track sensor faults. As a result, a robust reconstruction of the sensor fault as well as system states is then achieved. Furthermore, the proposed robustly adaptive fault reconstruction technique is extended to Lipschitz nonlinear systems subjected to sensor faults and unknown input uncertainties. Finally, the effectiveness of the algorithms is demonstrated using an aircraft system model and robotic arm and comparison studies.

Dynamic process of ecosystem water use efficiency and response to drought in the Yellow River Basin, China.

Ecosystem water use efficiency (WUE) is a crucial indicator of the impact of climate change on terrestrial ecosystems, reflecting the balance between biological processes (photosynthesis and transpiration) and physical processes (evapotranspiration). However, the response mechanisms and driving processes of WUE to drought remain to be further understood. In this study, we analyzed the spatial and temporal dynamics and response mechanisms of WUE in the Yellow River Basin (YRB) using data on Gross Primary Productivity (GPP), Evapotranspiration (ET) and Standardized Precipitation Evapotranspiration Index (SPEI), which revealed the cumulative effect of drought on WUE and assessed the ecosystem's resilience. The study results showed that (1) GPP, ET and WUE in the YRB exhibited a significant increasing trend, with 63.04 % of the area showing a marked increase in WUE. (2) GPP was the dominant factor influencing WUE in 65.36 % of the area, particularly in cropland and grassland, while ET was more influential in forested areas. Vapor pressure deficit (VPD) was identified as the principal driver affecting vegetation GPP in semi-arid and semi-humid regions of the YRB. In contrast, soil moisture (SM) was the limiting factor in arid areas. (3) 71.00 % of the WUE in the basin was affected by drought cumulative effects, with an average cumulative duration of 4.5 months. Arid regions experienced the most extended duration of 7.29 months, compared to 3.05 months in semi-humid regions. (4) 74.85 % of the regional ecosystems exhibited ecological resilience to drought, particularly in the source areas of the western basin of the YRB. Shrublands have the highest drought resilience among vegetation types, while grasslands have the lowest. The resilience of each climatic zone was in the order of semi-humid, semi-arid, and arid order. This study comprehensively analyzed of the spatial and temporal dynamics and response mechanisms of WUE in the YRB, offering a new perspective and scientific basis for understanding and predicting the ecosystem response to climate change.

Distinct roles of CD244 expression in cancer diagnosis and prognosis: A pan-cancer analysis.

The abnormal expression of tumor associated genes in pan-cancer is closely related to the clinicopathological features of distinct cancer types. Thus, identifying the role of specific genes in pan-cancer is needed for developing effective anti-cancer strategies. However, the function of CD244 in pan-cancer has not been fully understood. In this study, we explored the CD244 expression profile across 33 tumor types based on The Cancer Genome Atlas project, the Gene Expression Omnibus database, and other bioinformatics tools. We found down-regulated expression levels in seven tumor types and up-regulated expression levels in two tumor types. We subsequently explored the relationship between survival rate and CD244 expression, and found the positive relationship in patients with adrenocortical carcinoma (ACC), head and neck squamous cell carcinoma (HNSC), skin cutaneous melanoma (SKCM), and uterine corpus endometrial carcinoma (UCEC). We further investigated the association between CD244 expression and tumor-infiltrating immune cells, and discovered their positive correlation in different tumors. We found that CD244 expression level was higher in normal samples than in UCEC samples, and was positively associated with CD8+ T cells infiltrating. The mutation status, promoter methylation, CD244-related molecules and signaling pathways were also employed to study the potential function of CD244 in tumor initiation and progression. Our study offers a comprehensive overview of CD244 in human tumors, revealing CD244 as a potential prognostic biomarker and immunotherapeutic target in cancers.

CRABP2 reduces the sensitivity of Olaparib in ovarian cancer by downregulating Caspase-8 and decreasing the production of reactive oxygen species.

Poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors, such as Olaparib, have been pivotal in treating BRCA-deficient ovarian cancer. However, their efficacy is limited in over 40% of BRCA-deficient patients, with acquired resistance posing new clinical challenges. To address this, we employed bioinformatics methods to identify key genes impacting Olaparib sensitivity in ovarian cancer. Through comprehensive analysis of public databases including GEO, CPTAC, Kaplan Meier Plotter, and CCLE, we identified CRABP2 as significantly upregulated at both mRNA and protein levels in ovarian cancer, correlating with poor prognosis and decreased Olaparib sensitivity. Using colony formation and CCK-8 assays, we confirmed that CRABP2 knockdown in OVCAR3 and TOV112D cells enhanced sensitivity to Olaparib. Additionally, 4D label-free quantitative proteomics analysis, GSEA, and GO/KEGG analysis revealed CRABP2's involvement in regulating oxidation signals. Flow cytometry, colony formation assays, and western blotting demonstrated that CRABP2 knockdown promoted ROS production by activating Caspase-8, thereby augmenting Olaparib sensitivity and inhibiting ovarian cancer cell proliferation. Moreover, in xenograft models, CRABP2 knockdown significantly suppressed tumorigenesis and enhanced Olaparib sensitivity, with the effect being reversed upon Caspase-8 knockdown. These findings suggest that CRABP2 may modulate Olaparib sensitivity in ovarian cancer through the Caspase-8/ROS axis, highlighting its potential as a target for Olaparib sensitization.

Suppression of ITPKB degradation by Trim25 confers TMZ resistance in glioblastoma through ROS homeostasis.

Temozolomide (TMZ) represents a standard-of-care chemotherapeutic agent in glioblastoma (GBM). However, the development of drug resistance constitutes a significant hurdle in the treatment of malignant glioma. Although specific innovative approaches, such as immunotherapy, have shown favorable clinical outcomes, the inherent invasiveness of most gliomas continues to make them challenging to treat. Consequently, there is an urgent need to identify effective therapeutic targets for gliomas to overcome chemoresistance and facilitate drug development. This investigation used mass spectrometry to examine the proteomic profiles of six pairs of GBM patients who underwent standard-of-care treatment and surgery for both primary and recurrent tumors. A total of 648 proteins exhibiting significant differential expression were identified. Gene Set Enrichment Analysis (GSEA) unveiled notable alterations in pathways related to METABOLISM_OF_LIPIDS and BIOLOGICAL_OXIDATIONS between the primary and recurrent groups. Validation through glioma tissue arrays and the Xiangya cohort confirmed substantial upregulation of inositol 1,4,5-triphosphate (IP3) kinase B (ITPKB) in the recurrence group, correlating with poor survival in glioma patients. In TMZ-resistant cells, the depletion of ITPKB led to an increase in reactive oxygen species (ROS) related to NADPH oxidase (NOX) activity and restored cell sensitivity to TMZ. Mechanistically, the decreased phosphorylation of the E3 ligase Trim25 at the S100 position in recurrent GBM samples accounted for the weakened ITPKB ubiquitination. This, in turn, elevated ITPKB stability and impaired ROS production. Furthermore, ITPKB depletion or the ITPKB inhibitor GNF362 effectively overcome TMZ chemoresistance in a glioma xenograft mouse model. These findings reveal a novel mechanism underlying TMZ resistance and propose ITPKB as a promising therapeutic target for TMZ-resistant GBM.

Tabersonine Enhances Olaparib Sensitivity through FHL1-Mediated Epithelial-Mesenchymal Transition in an Ovarian Tumor.

Ovarian cancer (OVC) is one of the most aggressive gynecological malignancies worldwide. Although olaparib treatment has shown favorable outcomes against the treatment of OVC, its effectiveness remains limited in some OVC patients. Investigating new strategies to improve the therapeutic efficacy of olaparib against OVC is imperative. Our study identified tabersonine, a natural indole alkaloid, for its potential to increase the chemosensitivity of olaparib in OVC. The combined treatment of olaparib and tabersonine synergistically inhibited cell proliferation in OVC cells and suppressed tumor growth in A2780 xenografts. The combined treatment effectively suppressed epithelial-mesenchymal transition (EMT) by altering the expression of E-cadherin, N-cadherin, and vimentin and induced DNA damage responses. Integrating quantitative proteomics, FHL1 was identified as a potential regulator to modulate EMT after tabersonine treatment. Increased expression of FHL1 was induced by tabersonine treatment, while downregulation of FHL1 reversed the inhibitory effects of tabersonine on OVC cells by mediating EMT. In vivo findings further reflected that the combined treatment of tabersonine and olaparib significantly inhibited tumor growth and OVC metastasis through upregulation of FHL1. Our findings reveal the role of tabersonine in improving the sensitivity of olaparib in OVC through FHL1-mediated EMT, suggesting that tabersonine holds promise for future application in OVC treatment.

Nanomaterial-encapsulated STING agonists for immune modulation in cancer therapy.

The cGAS-STING signaling pathway has emerged as a critical mediator of innate immune responses, playing a crucial role in improving antitumor immunity through immune effector responses. Targeting the cGAS-STING pathway holds promise for overcoming immunosuppressive tumor microenvironments (TME) and promoting effective tumor elimination. However, systemic administration of current STING agonists faces challenges related to low bioavailability and potential adverse effects, thus limiting their clinical applicability. Recently, nanotechnology-based strategies have been developed to modulate TMEs for robust immunotherapeutic responses. The encapsulation and delivery of STING agonists within nanoparticles (STING-NPs) present an attractive avenue for antitumor immunotherapy. This review explores a range of nanoparticles designed to encapsulate STING agonists, highlighting their benefits, including favorable biocompatibility, improved tumor penetration, and efficient intracellular delivery of STING agonists. The review also summarizes the immunomodulatory impacts of STING-NPs on the TME, including enhanced secretion of pro-inflammatory cytokines and chemokines, dendritic cell activation, cytotoxic T cell priming, macrophage re-education, and vasculature normalization. Furthermore, the review offers insights into co-delivered nanoplatforms involving STING agonists alongside antitumor agents such as chemotherapeutic compounds, immune checkpoint inhibitors, antigen peptides, and other immune adjuvants. These platforms demonstrate remarkable versatility in inducing immunogenic responses within the TME, ultimately amplifying the potential for antitumor immunotherapy.

Asymmetric response of vegetation GPP to impervious surface expansion: Case studies in the Yellow and Yangtze River Basins.

Terrestrial gross primary production (GPP) changes due to impervious surfaces significantly impact ecosystem services in watersheds. Understanding the asymmetric response of vegetation GPP to impervious surface expansion is essential for regional development planning and ecosystem management. However, the asymmetric response of vegetation GPP to the impacts of impervious surface expansion is unknown in different watersheds. This paper selected the Yellow River and Yangtze River basins as case studies. We characterized the overall change in GPP based on changes in impervious surface ratio (ISR), determined impervious surface expansion's direct and indirect impacts on GPP in the two watersheds, and further analyzed the asymmetric response of the compensatory effects of indirect influences on the impervious surface expansion in different watersheds. The results showed that: (1) The vegetation GPP decreased with increasing ISR in the Yangtze River Basin, while that in the Yellow River Basin first increased and then reduced. (2) The direct impacts of increased ISR reduced vegetation GPP, while the indirect impacts both had a growth-compensating effect. Growth compensation stabilized at approximately 0.40 and 0.30 in the Yellow and Yangtze River Basins. (3) When the ISR was 0.34-0.56, the growth compensation could offset the reduction of GPP due to direct impact and ensure that the background vegetation GPP was not damaged in the Yellow River Basin. In contrast, the background vegetation GPP was inevitably impaired with increased ISR in the Yangtze River Basin. Therefore, this study suggests that the ISR should be ensured to be between 0.34 and 0.56 to maximize the impervious surface of the Yellow River Basin without compromising the background vegetation GPP. While pursuing impervious surface expansion in the Yangtze River Basin, other programs should be sought to compensate for the loss to GPP.

Nickel-Catalyzed Ligand-Controlled Regioselective Allylic Alkenylation of Allylic Alcohols with Easily Accessible Alkenyl Boronates: Synthesis of 1,4-Dienes.

A nickel-catalyzed direct reaction of allylic alcohols with easily accessible alkenyl boronates has been developed, which provides valuable 1,4-dienes with high regio- and stereoselectivity in good to excellent yields, wide substrate scope, and functional group compatibility. The catalytic system simply consists of Ni(cod)2 as the catalyst and a ligand, without a need for a base and alcohol activator in most cases. The proper choice of ancillary ligands is highly important for this reaction. Depending on the substitution pattern of allylic alcohols and/or alkenyl boronates, different ligands were used for improving the reaction efficiency.

Gold-Catalyzed Oxidative Cyclization/C-C Bond Cleavage of Ynones with External Nucleophiles: Synthesis of Linear Functionalized N-Tosylamides.

A gold-catalyzed oxidative cyclization/nucleophilic addition/C-C bond cleavage reaction of ynones with various nucleophiles has been developed. This methodology allows for the formation of highly functionalized linear N-Ts amides with broad substrate scope, high efficiency, and general tolerance of functional groups. A wide range of nucleophiles such as alcohols, water, and amines including aryl and alkyl amines are compatible with the current method. The C-C triple bond cleavage of the ynone substrate was observed during the process.

Drug metabolism-related gene ABCA1 augments temozolomide chemoresistance and immune infiltration abundance of M2 macrophages in glioma.

Gliomas are the most prevalent primary tumor in the central nervous system, with an abysmal 5-year survival rate and alarming mortality. The current standard management of glioma is maximum resection of tumors followed by postoperative chemotherapy with temozolomide (TMZ) or radiotherapy. Low chemosensitivity of TMZ in glioma treatment eventuates limited therapeutic efficacy or treatment failure. Hence, overcoming the resistance of glioma to TMZ is a pressing question. Our research centered on identifying the drug metabolism-related genes potentially involved in TMZ-treated resistance of glioma through several bioinformatics datasets and cell experiments. One efflux transporter, ATP-binding cassette transporter subfamily A1 (ABCA1), was discovered with an upregulated expression level and signaled poor clinical outcomes for glioma patients. The transcript level of ABCA1 significantly elevated across the TMZ-resistant glioma cells in contrast with non-resistant cells. Over-expressed ABCA1 restrained the drug activity of TMZ, and ABCA1 knockdown improved the treatment efficacy. Meanwhile, the results of molecular docking between ABCA1 protein and TMZ showed a high binding affinity. Additionally, co-expression and immunological analysis revealed that ABCA1 facilitates the immune infiltration of M2 macrophages in glioma, thereby stimulating tumor growth and aggravating the poor survival of patients. Altogether, we discovered that the ABCA1 transporter was involved in TMZ chemoresistance and the immune infiltration of M2 macrophages in glioma. Treatment with TMZ after ABCA1 knockdown enhances the chemosensitivity, suggesting that inhibition of ABCA1 may be a potential strategy for improving the therapeutic efficacy of gliomas.

A Sensor-Fault-Estimation Method for Lithium-Ion Batteries in Electric Vehicles.

In recent years, electric vehicles powered by lithium-ion batteries have developed rapidly, and the safety and reliability of lithium-ion batteries have been a paramount issue. Battery management systems are highly dependent on sensor measurements to ensure the proper functioning of lithium-ion batteries. Therefore, it is imperative to develop a suitable fault diagnosis scheme for battery sensors, to realize a diagnosis at an early stage. The main objective of this paper is to establish validated electrical and thermal models for batteries, and address a model-based fault diagnosis scheme for battery sensors. Descriptor proportional and derivate observer systems are applied for sensor diagnosis, based on electrical and thermal models of lithium-ion batteries, which can realize the real-time estimation of voltage sensor fault, current sensor fault, and temperature sensor fault. To verify the estimation effect of the proposed scheme, various types of faults are utilized for simulation experiments. Battery experimental data are used for battery modeling and observer-based fault diagnosis in battery sensors.

Functional roles of magnetic nanoparticles for the identification of metastatic lymph nodes in cancer patients.

Staging lymph nodes (LN) is crucial in diagnosing and treating cancer metastasis. Biotechnologies for the specific localization of metastatic lymph nodes (MLNs) have attracted significant attention to efficiently define tumor metastases. Bioimaging modalities, particularly magnetic nanoparticles (MNPs) such as iron oxide nanoparticles, have emerged as promising tools in cancer bioimaging, with great potential for use in the preoperative and intraoperative tracking of MLNs. As radiation-free magnetic resonance imaging (MRI) probes, MNPs can serve as alternative MRI contrast agents, offering improved accuracy and biological safety for nodal staging in cancer patients. Although MNPs' application is still in its initial stages, exploring their underlying mechanisms can enhance the sensitivity and multifunctionality of lymph node mapping. This review focuses on the feasibility and current application status of MNPs for imaging metastatic nodules in preclinical and clinical development. Furthermore, exploring novel and promising MNP-based strategies with controllable characteristics could lead to a more precise treatment of metastatic cancer patients.

Ozonated triglyceride protects against septic lethality via preventing the activation of NLRP3 inflammasome. / é ¸åŒ–è„‚è‚ªé ¸é ¯é€šè¿‡æŠ‘åˆ¶NLRP3炎症小体活化减少脓毒症致死（英文）.

OBJECTIVES: Sepsis is a critical dysregulated host response with high mortality and current treatment is difficult to achieve optimal efficacy. Ozone therapy has been revealed to protect infection and inflammation-related diseases due to its role in antibiotic and immunoregulatory effect. Ozonated triglyceride is a key component of ozonated oil that is one of ozone therapy dosage form. However, the potential role of ozonated triglyceride in sepsis remains unclear. This study aims to explore the effect of ozonated triglyceride on septic mouse model and the molecular mechanism. METHODS: Intraperitoneal injection of lipopolysaccharide (LPS), cecal ligation and puncture (CLP) were applied to construct septic mouse model. The mouse serum was obtained for detection of cytokines, and lung tissues were collected for hematoxylin and eosin (HE) staining to evaluate the extent of lung injury in septic mouse with ozonated triglyceride treatment at different time and doses. The survival of septic mice was observed for 96 h and Kaplan-Meier analysis was used to analyze the survival rates. In addition, primary peritoneal macrophages and human acute monocytic-leukemia cell line (THP-1) were treated with inflammasome activators with or without ozonated triglyceride. The level of cytokines was detected by enzyme-linked immunosorbent assay (ELISA). The cleavage of caspase-1 and gasdermin-D (GSDMD) was detected by Western blotting. RESULTS: Ozonated triglyceride at different time and doses reduced the release of inflammasome-related cytokines [interleukin (IL)-1ß and IL-18] (all P<0.05) but not pro-inflammatory cytokines such as IL-6 and tumor necrosis factor-α (TNF-α) in septic mice (all P>0.05). Ozonated triglyceride significantly improved the survival rate of septic mice and reduced sepsis-induced lung injury (all P<0.05). Ozonated triglyceride significantly suppressed the canonical and non-canonical activation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome (all P<0.05) but not affected absent in melanoma 2 (AIM2) and NLR family CARD domain-containing protein 4 (NLRC4) inflammasomes in vitro (all P>0.05). Ozonated triglyceride reduced the cleavage of caspase-1 and the downstream GSDMD. CONCLUSIONS: Ozonated triglyceride presents a protect effect on sepsis lethality via reducing cytokines release and sepsis-related organ injury. The mechanism is that ozonated triglyceride specifically suppresses the activation of NLRP3 inflammasome. Ozonated triglyceride is a promising candidate for sepsis treatment.

Sodium thiosulfate ameliorates atopic dermatitis via inhibiting the activation of NLRP3 inflammasome.

Atopic dermatitis (AD) is a common disease with a considerable impact on the patient's quality of life and limited treatment options. Sodium thiosulfate (STS) is a traditional medicine used in the rescue of cyanide poisoning, and some pruritus dermatosis. However, the exact efficacy and mechanism of its application on AD are not clear. In this work, comparing to other traditional therapy, STS was found to effectively improve the severity of skin lesions and the quality of life in AD patients with a dose-dependent manner. Mechanically, STS downregulated the expression of IL-4, IL-13, IgE in the serum of AD patients, as well as reduce the concentration of eosinophils. Furthermore, in the AD-like mice model triggered by ovalbumin (OVA) and calcitriol, STS was found to reduce the epidermal thickness, scratching times, and the infiltration of dermal inflammatory cells in AD mice, as well as the reactive oxygen species (ROS) production and the expression levels of inflammatory cytokines in the skin tissue. In HacaT cells, STS inhibited the accumulation of ROS and activation of NLRP3 inflammasome and its downstream IL-1ß expression. Therefore, this study revealed that STS plays an important therapeutic role in AD, and the mechanism may be that STS inhibits the activation of NLRP3 inflammasome and the subsequent release of inflammatory cytokines. Thus, the role of STS in treating AD was clarified and the possible molecular mechanism was revealed.

4,5-Dihydro-1,2,4-oxadiazole as a Single Nitrogen Transfer Reagent: Synthesis of Functionalized Isoxazoles Assisted by Sc(OTf)3 or Au(I)/Sc(OTf)3 Synergistic Catalysis.

A five-membered N-O heterocycle, 4,5-dihydro-1,2,4-oxadiazole, was found to act as a single nitrogen atom transfer reagent via elimination of a ketone/aldehyde and a nitrile. This reagent was successfully applied for the synthesis of isoxazoles from ynones promoted by Sc(OTf)3 or through Au(I)/Sc(OTf)3 synergistic catalysis. The efficiency of this protocol was also demonstrated by its application in modifications of structurally complex natural products and pharmaceuticals.

How does coordinated regional digital economy development improve air quality? New evidence from the spatial simultaneous equation analysis.

Countries around the world are increasingly turning towards developing digital economies to find better strategies for tackling the environmental pollution associated with economic growth while also pursuing high-quality economic conditions. This study aims to probe the link between coordinated regional digital economy development (RDEC) and air quality. A province-level RDEC indicator based on city-level data is developed, and air pollution is gauged by annual average PM2.5 concentrations. Furthermore, a spatial simultaneous equation model is employed to examine the causality further. The empirical results indicate that a bilateral causal relationship exists: RDEC improves air quality, and better air quality also facilitates RDEC. This relationship is influenced by spatial spillover effects. Specifically, air quality and RDEC of an area have a negative influence on the RDEC of neighboring regions, while they have a positive impact on neighboring areas' air quality. Further analysis suggests that green total factor productivity, advanced industrial structure, and regional entrepreneurship level can indirectly affect the contribution of RDEC to air quality. Additionally, the impact of air quality on RDEC may be realized through the increase in labor productivity, lower external environmental costs of regional economic development, and enhanced regional foreign economic exchange.