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Transportation infrastructure is crucial to China’s economic growth because it substantially contributes to the holistic development of rural primary, secondary, and tertiary industries. This study innovatively examines transportation infrastructure and urbanization levels to explore, both theoretically and empirically, their relationship with the holistic development of primary, secondary, and tertiary industries in rural China, and the mediating role of urbanization on this relationship. We employed fixed-effects models, the entropy weight approach, mixed regression, and generalized method of moments to analyze the data of 30 provinces across China from 2013 to 2020. The results indicate that the construction of transportation infrastructure directly fosters the collective advancement of such industries in rural areas and that urbanization partially mediates the transportation infrastructure–rural industry integration relationship. However, the western region shows disparities in the integrated development of these sectors. Further analysis reveals that foreign investments amplify the positive influence of transportation infrastructure on rural industry integration. Essentially, the enhancement of rural transportation infrastructure, promotion of urbanization, implementation of strategic planning, and strengthening of support mechanisms are crucial aspects in the comprehensive development of rural industries and the achievement of rural revitalization in China.

OpenStreetMap (OSM) is a voluntary platform designed to provide free and up-to-date geographic data. Since OSM is based on multisource geographic data provided by the public, the quality of the data has become a concern of researchers. In this study, a unified measure for evaluating OSM data quality was constructed, and the entropy weight method (EWM) and Technique for Order Performance by Similarity to Ideal Solution (TOPSIS) model were used to evaluate the quality of multiscale OSM data in China from 2014 to 2020. In addition to evaluating the data quality, the use of OSM data quality index factors in economic modeling at different spatial scales in China was explored by using a geographic information system (GIS) analysis method and a geographically and temporally weighted regression (GTWR) model. Four machine learning models, SVM, RF, XGBoost and CatBoost, were used to simulate the grid-scale GDP, and the effectiveness of these simulations was discussed. The results showed that (1) the weights of OSM data quality indicator factors vary across different spatial scales. (2) From 2014 to 2020, the quality of national-scale OSM data first increased, then decreased and then gradually stabilized. In addition, the quality of OSM data at the provincial and municipal scales is significantly different, and the distribution is affected by the population and geographical environment. (3) Over time, the spatial clustering characteristics of OSM data quality at different spatial scales in China has continuously strengthened. In addition, the quality of Chinese OSM data displays obvious local spatial autocorrelation characteristics, which are dominated by H-H clustering and L-L clustering. (4) The GTWR model performs well in predicting and revealing the spatiotemporal correlation characteristics between GDP and OSM data quality indicators at the provincial and municipal scales in China. The correlations increase with decreasing spatial scale (provincial to municipal). Moreover, the GDP modeling ability is better in economically underdeveloped Northwest China and economically developed East China. (5) Four machine learning models coupled with road network length completeness, relative linear density, road name attribute completeness, POI name attribute completeness, road network accuracy, road network update frequency, POI update frequency, topological consistency and directional similarity yielded the best grid-scale GDP simulation values. Notably, the CatBoost model provided the best accuracy, and the results further verified that it is feasible to use the proposed OSM data quality index system to predict the regional economic development level in China.

The increasingly prominent issue of unfair competition on Internet platforms (IPUC) severely restricts the healthy and sustainable development of the platform economy. Based on the IPUC "multi-agent co-governance" scenario, this paper introduces stochastic disturbances and continuous strategy set to improve the classical binary deterministic evolutionary game system. The results show that after considering stochastic disturbances, the positive state corresponding to the equilibrium point (1,1) is no longer stable, and the required parameter conditions are more stringent. The IPUC "multi-agent co-governance" system under stochastic disturbances exhibits specific vulnerability. In the continuous strategy set evolutionary game system, government departments and Internet platforms can flexibly make optimal decisions based on maximizing expected returns, and strategy selection has better elasticity. Regardless of the evolutionary game scenario, maintaining the participation level of NGOs and the public above a certain threshold while increasing the penalty intensity is conducive to the evolution of the game system toward the positive state. The analysis process and conclusions provide insights and guidance for the governments to design the IPUC regulatory system and frameworks.

Unfair competition on internet platforms (UCIP) has become a critical issue restricting the platform economy's healthy development. This paper applies evolutionary game theory to study how to utilize multiple subjects' synergy to supervise UCIP effectively. First, the "multi-agent co-governance" mode of UCIP is constructed based on the traditional "unitary supervision" mode. Second, the government and internet platform evolutionary game models are built under two supervision modes. Finally, MATLAB is used to simulate and analyze the evolutionary stage and parameter sensitivity. In addition, we match the model's evolutionary stage with China's supervisory process. The results show that (1) the Chinese government's supervision of UCIP is in the transitional stage from "campaign-style" to "normalization." (2) Moderate government supervision intensity is essential to guide the game system to evolve toward the ideal state. If the supervision intensity is too high, it will inhibit the enthusiasm for supervision. If the supervision intensity is too low, it cannot form an effective deterrent to the internet platforms. (3) When the participation of industry associations and platform users is low, it can only slow down the evolutionary speed of the game system's convergence to the unfavorable state. Nevertheless, it cannot reverse the evolutionary result. (4) Maintaining the participation level of industry associations and platform users above a specific threshold value while increasing punishment intensity will promote the transition of government supervision from the "campaign-style" to the "normalization" stage. This paper provides ideas and references for the Chinese government to design a supervision mechanism for UCIP.

Abstract Background Idiopathic pulmonary fibrosis (IPF) is fibrotic lung disease with no effective treatment. It is characterized by destruction of alveolar structure and pulmonary interstitial fibrosis, leading to dyspnea and even asphyxia death of patients. Epithelial-mesenchymal transition (EMT) is considered to be a driving factor in the pathogenesis of IPF. Osteopontin (OPN) is a secreted protein widely present in the extracellular matrix and involved in the occurrence and development of a variety of diseases. Methods The original datasets were obtained from NCBI GEO databases analyzed with the online tool GEO2R and EasyGEO. Bleomycin induced mouse pulmonary fibrosis model and OPN/OPN-biotin treated mouse model were established to investigate the role of OPN in mouse pulmonary fibrosis and the target cells of OPN. A549 cells and HBE cells were used to explore the mechanism of OPN-induced epithelial-mesenchymal transition (EMT) in epithelial cells and mass spectrometry was used to detect OPN downstream receptors. Precision-cut lung slices and lentivirus-treated mice with pulmonary fibrosis were used to examine the therapeutic effect of OPN and its downstream pathways on pulmonary fibrosis. Results We demonstrate that the content of OPN in IPF bronchoalveolar lavage fluid (BALF) is high compared to the normal groups, and its expression level is correlated with prognosis. At the animal level, OPN was highly expressed at all stages of pulmonary fibrosis in mice, and the bronchoalveolar lavage fluid (BALF) could accurately reflect its expression in the lung. Next, we reveal that OPN was mainly expressed by macrophages and the main target cells of OPN were epithelial cells. Mice developed pulmonary fibrosis accompanied after treating the mice with OPN. Both in vitro and in vivo experiments confirmed that OPN could induce EMT of alveolar epithelial cells. Mechanistically, OPN binding triggered phosphorylation of FAK by CD44, thus activating snail1-mediated profibrotic protein synthesis. Inhibition of FAK phosphorylation and its downstream pathways can effectively alleviate pulmonary fibrosis in precision sections of lung tissue (PCLS) assay. OPN knockdown in bleomycin-induced lung fibrosis mice led to significantly less fibrosis. Conclusion Our data suggest that OPN mediates lung fibrosis through EMT, implicating its potential therapeutic target and prognostic indicator role for IPF. OPN may be a target for the diagnosis and treatment of IPF.

Metabolism-related fatty liver disease (MAFLD) is the most common form of chronic liver disease in the world. Its pathogenesis is influenced by both environmental and genetic factors. With the upgrading of gene screening methods and the development of human genome project, whole genome scanning has been widely used to screen genes related to MAFLD, and more and more genetic variation factors related to MAFLD susceptibility have been discovered. There are genetic variants that are highly correlated with the occurrence and development of MAFLD, and there are genetic variants that are protective of MAFLD. These genetic variants affect the development of MAFLD by influencing lipid metabolism and insulin resistance. Therefore, in-depth analysis of different mechanisms of genetic variation and targeting of specific genetic variation genes may provide a new idea for the early prediction and diagnosis of diseases and individualized precision therapy, which may be a promising strategy for the treatment of MAFLD.

Bile acids (BAs) are synthesized in liver tissue from cholesterol and are an important endocrine regulator and signaling molecule in the liver and intestine. It maintains BAs homeostasis, and the integrity of intestinal barrier function, and regulates enterohepatic circulation in vivo by modulating farnesoid X receptors (FXR) and membrane receptors. Cirrhosis and its associated complications can lead to changes in the composition of intestinal micro-ecosystem, resulting in dysbiosis of the intestinal microbiota. These changes may be related to the altered composition of BAs. The BAs transported to the intestinal cavity through the enterohepatic circulation are hydrolyzed and oxidized by intestinal microorganisms, resulting in changes in their physicochemical properties, which can also lead to dysbiosis of intestinal microbiota and overgrowth of pathogenic bacteria, induction of inflammation, and damage to the intestinal barrier, thus aggravating the progression of cirrhosis. In this paper, we review the discussion of BAs synthesis pathway and signal transduction, the bidirectional regulation of bile acids and intestinal microbiota, and further explore the role of reduced total bile acid concentration and dysregulated intestinal microbiota ratio in the development of cirrhosis, in order to provide a new theoretical basis for the clinical treatment of cirrhosis and its complications.

Gastric cancer (GC), a common and high-mortality disease, still occupies an important position in current cancer research, and Helicobacter pylori (H. pylori) infection as its important risk factor has been a hot and challenging research area. Among the numerous pathogenic factors of H. pylori, the virulence protein CagA has been widely studied as the only bacterial-derived oncoprotein. It was found that CagA entering into gastric epithelial cells (GECs) can induce the dysregulation of multiple cellular pathways such as MAPK signaling pathway, PI3K/Akt signaling pathway, NF-κB signaling pathway, Wnt/β-catenin signaling pathway, JAK-STAT signaling pathway, Hippo signaling pathway through phosphorylation and non-phosphorylation. These disordered pathways cause pathological changes in morphology, adhesion, polarity, proliferation, movement, and other processes of GECs, which eventually promotes the occurrence of GC. With the deepening of H. pylori-related research, the research on CagA-induced abnormal signaling pathway has been updated and deepened to some extent, so the key signaling pathways activated by CagA are used as the main stem to sort out the pathogenesis of CagA in this paper, aiming to provide new strategies for the H. pylori infection and treatment of GC in the future.

The incidence of liver cancer is extremely high worldwide and poses a serious threat to human life and health. But at present, apart from radiotherapy, chemotherapy, liver transplantation, and early resection, sorafenib was the main systemic therapy proven to have clinical efficacy for unresectable liver cancer (HCC) until 2017. Despite the emerging immunotherapy in the past decade with immune inhibitors such as PD - 1 being approved and applied to clinical treatment, there are still some patients with no response. This review aims to elucidate the mechanisms underlying the tumor microenvironment of hepatocellular carcinoma and thus analyze the effectiveness of targeting the tumor microenvironment to improve the therapeutic efficacy of hepatocellular carcinoma, including the effectiveness and feasibility of immunotherapy, tumor oncolytic viruses and anti-vascular proliferation therapy.

GNB2L1 and its O-GlcNAcylation has been reported to play roles in gastric cancer metastasis. However, the roles of GNB2L1 in chemoresistance of gastric cancer has never been determined. In the present study, we found that GNB2L1 was downregulated in chemoresistant patients of gastric cancer, and observed the decrease of GNB2L1 in protein levels instead of mRNA levels in different chemoresistant gastric cancer cell lines. Further we proved that this downregulation of GNB2L1 was resulted from its elevated O-GlcNAcylation catalyzed by OGT in both cell lines and patients. Next, we investigate the function of GNB2L1 and its O-GlcNAcylation on gastric cancer metastasis during chemoresistance, and confirmed Ser124 as the major O-GlcNAcylation site on GNB2L1 that regulated its function on metastasis. Furthermore, our data demonstrated that GNB2L1 modulated EMT via regulating the translation of EMT-related proteins in the process of chemoresistance. In summary, this study indicated that GNB2L1 and its O-GlcNAcylation regulated metastasis via modulating the translation of EMT-related proteins in the chemoresistance of gastric cancer.

OBJECTIVE: The aim of the study was to evaluate whether the insertion/deletion polymorphism (rs3783553) locating in the 3' untranslated region (3'UTRs) of IL-1A was related to the risk of gastric cancer (GC) in a Chinese population and explore the possible molecular mechanism. METHODS: Genomic DNA was extracted from peripheral venous blood of 519 GC patients and 536 healthy control individuals. The IL-1A rs3783553 polymorphism was genotyped by using a polymerase chain reaction assay. The vectors containing the insertion or deletion allele were constructed, and luciferase assay was used to detect the effect of the polymorphism on the transcriptional activity of IL-1A. RESULTS: Strong evidence of association was observed between the IL-1A rs3783553 polymorphism and susceptibility to GC in the study. In addition, the 'TTCA' insertion allele of rs3783553 disrupts the binding site for miR-122 and miR-378, thereby increasing transcription of IL-1α in vitro. CONCLUSION: These findings suggest that functional polymorphism rs3783553 in IL-1A could contribute to GC susceptibility, possibly or at least partially through affecting the transcriptional activity of IL-1A. [ABSTRACT FROM AUTHOR]