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\"Featuring more than 30 artists, Line, Form, Qi highlights contemporary works that range from the traditional to the deeply experimental. The publication features predominantly Chinese artists, along with Vietnamese, Taiwanese, Japanese and Korean artists working mainly with Chinese characters. The themes reflect significant trends and innovations in contemporary calligraphic art, including abstraction of the character, performance and phenomenological practice, and the exploration of alternative or nontraditional materials and calligraphy methods such as incense burn drawing and lithography. This publication also addresses different through lines from premodern calligraphy to contemporary practice, reflecting the evolution of the Chinese language from pictograph to ideograph and beyond.\"-- description from https://www.artbook.com/9781636811581.html, accessed 20250604.

In the context of global climate change, green development has become the main goal of smart city construction. Most existing research suggests that smart cities will enhance the level of the green total factor productivity (GTFP) in cities. However, this study found that smart cities will reduce the level of green total factor production in the short term and increase it in the long term. Based on this, this article selects three batches of smart cities in China from 2013 to 2019, and uses the Malmquist index model, common frontier function, and panel data method to analyze the GTFP model in the early stage of smart city construction in China. The study found that: (1) the GTFP of the three batches of smart cities in the early stage of construction was less than 1 and showed a downward trend, indicating that smart cities will reduce the GTFP level of cities in the short term. (2) Technical efficiency is the main reason for the decline of GTFP in the early stage of smart city construction and the rise of GTFP in the medium and long term. Specifically, there is a U-shaped relationship between the technological efficiency of smart cities and their GTFP. For every 1% increase in technical efficiency in the later stages of smart cities, GTFP increases by 47.3%. (3) The GTFP in the process of smart city construction shows a trend of decreasing in the early stage and increasing in the middle and later stages. The GTFP level in the later stage of smart cities is greater than 1 and shows a fluctuating upward trend, indicating that smart cities will improve the city’s GTFP level in the long run. In view of this, we should attach importance to ecological protection in the early stage of smart city construction and take effective measures to reduce carbon emissions during this period. During this period, policies such as taxation can be implemented to encourage companies to adopt cleaner production technologies, strengthen the exchange of green technologies between cities, accelerate the flow of green knowledge, reduce redundant construction of information infrastructure, and thus minimize the decline in GTFP in the early stages of smart city construction. This study provides policy recommendations and decision-making references for further promoting the construction of new green and smart cities worldwide.

Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA‐373‐3p (miR‐375‐3p) in CRC remains unclear. The current study aimed to explore the potential function of miR‐375‐3p in 5‐fluorouracil (5‐FU) resistance. MicroRNA‐375‐3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5‐FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR‐375‐3p, and TYMS knockdown exerted similar effects as miR‐375‐3p overexpression on the CRC cellular response to 5‐FU. Lipid‐coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5‐FU and miR‐375‐3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR‐375 + 5‐FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR‐375‐3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5‐FU. Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Our results suggest that the restoration of microRNA‐375‐3p levels could be a future novel therapeutic strategy to modulate and enhance chemosensitivity to 5‐fluorouracil treatment in CRC.

Fusarium graminearum is a destructive wheat pathogen. No fully resistant cultivars are available. Knowledge concerning the molecular weapons of F. graminearum to achieve infection remains limited. Here, we report that deletion of the putative secondary metabolite biosynthesis gene cluster fg3_54 compromises the pathogen’s ability to infect wheat through cell-to-cell penetration. Ectopic expression of fgm4 , a pathway-specific bANK-like regulatory gene, activates the transcription of the fg3_54 cluster in vitro. We identify a linear, C- terminally reduced and d -amino acid residue-rich octapeptide, fusaoctaxin A, as the product of the two nonribosomal peptide synthetases encoded by fg3_54 . Chemically-synthesized fusaoctaxin A restores cell-to-cell invasiveness in fg3_54 -deleted F. graminearum , and enables colonization of wheat coleoptiles by two Fusarium strains that lack the fg3_54 homolog and are nonpathogenic to wheat. In conclusion, our results identify fusaoctaxin A as a virulence factor required for cell-to-cell invasion of wheat by F. graminearum . Fusarium graminearum is a fungal pathogen of wheat and other cereals. Here the authors identify a gene cluster in F. graminearum encoding the production of a non-ribosomal peptide that is required for infection of wheat through cell-to-cell penetration.

Oilfield data is characterized by complex types, large volumes, and significant noise interference, so data cleansing has become a key procedure for improving data quality. However, the traditional data cleansing process needs to deal with multiple types of problems, such as outliers, duplicate data, and missing values in turn, and the processing steps are complex and inefficient. Therefore, an integrated data cleansing and function fitting method is established. The fine-mesh data density analysis method is utilized to cleanse outliers and duplicate data, and the automated segmented fitting method is used for missing data imputation. For the real-time data generated during drilling or well logging, data cleansing is realized through grid partitioning and data density analysis, and the cleansing ratio is controlled by data density threshold and grid spacing. After data cleansing, based on similar standards, the cleansed data is segmented, and the fitting function type of each segment is determined to fill in the missing data, and data outputs with any frequency can be obtained. For the analysis of the hook load data measured by sensors at the drilling site and obtained from rig floor monitors or remote centers, the data cleansing percentage reaches 98.88% after two-stage cleansing, which still retains the original trend of the data. After data cleansing, the cleansed data are modeled through the automated segmented fitting method, with Mean Absolute Percentage Errors (MAPEs) less than 3.66% and coefficient of determination (R2) values greater than 0.94. Through the integrated data processing mechanism, the workflow can synchronously eliminate outliers and redundant data and fill in the missing values, thereby dynamically adapting to the data requirements of numerical simulation and intelligent analysis and significantly improving the efficiency of on-site data processing and decision-making reliability in the oilfield.

A disturbance of reactive oxygen species (ROS) homeostasis may cause the pathogenesis of many diseases. Inspired by natural photosynthesis, this work proposes a photo-driven H 2 -evolving liposomal nanoplatform (Lip NP) that comprises an upconversion nanoparticle (UCNP) that is conjugated with gold nanoparticles (AuNPs) via a ROS-responsive linker, which is encapsulated inside the liposomal system in which the lipid bilayer embeds chlorophyll a (Chl a ). The UCNP functions as a transducer, converting NIR light into upconversion luminescence for simultaneous imaging and therapy in situ. Functioning as light-harvesting antennas, AuNPs are used to detect the local concentration of ROS for FRET biosensing, while the Chl a activates the photosynthesis of H 2 gas to scavenge local excess ROS. The results thus obtained indicate the potential of using the Lip NPs in the analysis of biological tissues, restoring their ROS homeostasis, possibly preventing the initiation and progression of diseases. Hydrogen can be used to reduce the concentration of reactive oxygen species (ROS), but its delivery to diseased tissues is challenging due to its low solubility. Here the authors develop a photosynthesis-inspired FRET nanocomplex to detect and scavenge local excess of ROS in the tissue using photocatalytic hydrogen production.

Autoimmunity in plants has been found in numerous hybrids as a form of hybrid necrosis and mutant panels. Uncontrolled cell death is a main cellular outcome of autoimmunity, which negatively impacts growth. Its occurrence highlights the vulnerable nature of the plant immune system. Genetic investigation of autoimmunity in hybrid plants revealed that extreme variation in the immune receptor repertoire is a major contributor, reflecting an evolutionary conundrum that plants face in nature. In this review, we discuss natural variation in the plant immune system and its contribution to fitness. The value of autoimmunity genetics lies in its ability to identify combinations of a natural immune receptor and its partner that are predisposed to triggering autoimmunity. The network of immune components for autoimmunity becomes instrumental in revealing mechanistic details of how immune receptors recognize cellular invasion and activate signaling. The list of autoimmunity-risk variants also allows us to infer evolutionary processes contributing to their maintenance in the natural population. Our approach to autoimmunity, which integrates mechanistic understanding and evolutionary genetics, has the potential to serve as a prognosis tool to optimize immunity in crops

Severe fever with thrombocytopenia syndrome (SFTS), an emerging tick-borne infectious disease caused by a novel phlebovirus (SFTS virus, SFTSV), was listed among the top 10 priority infectious diseases by the World Health Organization due to its high fatality of 12%–50% and possibility of pandemic transmission. Currently, effective anti-SFTSV intervention remains unavailable. Here, by screening a library of FDA-approved drugs, we found that benidipine hydrochloride, a calcium channel blocker (CCB), inhibited SFTSV replication in vitro. Benidipine hydrochloride was revealed to inhibit virus infection through impairing virus internalization and genome replication. Further experiments showed that a broad panel of CCBs, including nifedipine, inhibited SFTSV infection. The anti-SFTSV effect of these two CCBs was further analyzed in a humanized mouse model in which CCB treatment resulted in reduced viral load and decreased fatality rate. Importantly, by performing a retrospective clinical investigation on a large cohort of 2087 SFTS patients, we revealed that nifedipine administration enhanced virus clearance, improved clinical recovery, and remarkably reduced the case fatality rate by >5-fold. These findings are highly valuable for developing potential host-oriented therapeutics for SFTS and other lethal acute viral infections known to be inhibited by CCBs in vitro.

Metformin, an ancient drug commonly used for treating type II diabetes, has been associated to anti-cancer capacity in a variety of developing cancers, though the mechanism remains elusive. Here, we aimed to examine the inhibitory effect of metformin in osteosarcoma. Herein, we demonstrated that metformin treatment blocked proliferation progression by causing accumulation of G2/M phase in U2OS and 143B cells. Furthermore, metformin treatment triggered programmed cell death process in osteosarcoma cell lines. Further research indicated the induction of apoptosis and autophagy triggered by metformin could remarkably attenuate after the treatment of ROS scavenger NAC and JNK inhibitor SP600125. Additionally, our results showed that NAC-suppressed JNK/c-Jun signaling pathway could have been activated through metformin treatment. Lastly, metformin could inhibit osteosarcoma growth under safe dose . Thus, we propose that metformin could induce cell cycle arrest as well as programmed cell death, including apoptosis and autophagy, through ROS-dependent JNK/c-Jun cascade in human osteosarcoma. This metformin-induced pathway provides further insights into its antitumor potential molecular mechanism and illuminates potential cancer targets for osteosarcoma.

Summary Pattern recognition receptors (PRRs) sense microbial patterns and activate innate immunity against attempted microbial invasions. The leucine‐rich repeat receptor kinases (LRR‐RK) FLS2 and EFR, and the LRR receptor protein (LRR‐RP) receptors RLP23 and RLP42, respectively, represent prototypical members of these two prominent and closely related PRR families. We conducted a survey of Arabidopsis thaliana immune signaling mediated by these receptors to address the question of commonalities and differences between LRR‐RK and LRR‐RP signaling. Quantitative differences in timing and amplitude were observed for several early immune responses, with RP‐mediated responses typically being slower and more prolonged than those mediated by RKs. Activation of RLP23, but not FLS2, induced the production of camalexin. Transcriptomic analysis revealed that RLP23‐regulated genes represent only a fraction of those genes differentially expressed upon FLS2 activation. Several positive and negative regulators of FLS2‐signaling play similar roles in RLP23 signaling. Intriguingly, the cytoplasmic receptor kinase BIK1, a positive regulator of RK signaling, acts as a negative regulator of RP‐type immune receptors in a manner dependent on BIK1 kinase activity. Our study unveiled unexpected differences in two closely related receptor systems and reports a new negative role of BIK1 in plant immunity.