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The green credit is one of the effective tools to save energy and reduce pollution, which mainly applies in industry. Thus, this paper explores the impact of green credit on the upgrading of China’s industrial structure from the perspective of industrial sectors, by means of a dynamic panel model with the dada from 2005 to 2016. The upgrading of industrial structure is divided into three dimensions to be analyzed—rationalization of industrial structure (RIS), advancement of industrial structure (AIS), and greenization of industrial structure (GIS). The empirical results are also explained by four influence mechanisms—resource allocation, technological innovation, credit catalysis, and policy guidance mechanism. This paper finds that on the national level, green credit has a positive impact on the upgrading of China’s industrial structure and plays a significant role in promoting the greenization and advancement of industrial structure. However, on the regional level, the effect of green credit is more complex. First, green credit has a significant positive effect on the GIS in the eastern, central, and western regions of China, which suggests that green credit is conductive to the cleaner production of industry across the country. Second, green credit also has a positive impact on the AIS in these three regions, but the effect is only significant in the eastern region. Third, in terms of the RIS, the effect of green credit is positive but not significant in the eastern and central regions. However, it is negative, not significant as well, in the western region, which can be explained from the perspective of the resource allocation and technological innovation mechanism. In addition, there is a significant positive correlation between the previous period and the current value of RIS, AIS, and GIS, which indicates that there is a significant positive inertia dynamic feature in the upgrading of China’s industrial structure.

In recent years, lipid nanoparticles (LNPs) have attracted extensive attention in tumor immunotherapy. Targeting immune cells in cancer therapy has become a strategy of great research interest. mRNA vaccines are a potential choice for tumor immunotherapy, due to their ability to directly encode antigen proteins and stimulate a strong immune response. However, the mode of delivery and lack of stability of mRNA are key issues limiting its application. LNPs are an excellent mRNA delivery carrier, and their structural stability and biocompatibility make them an effective means for delivering mRNA to specific targets. This study summarizes the research progress in LNP delivery carrier-assisted targeted controlled release mRNA vaccines in tumor immunity. The role of LNPs in improving mRNA stability, immunogenicity, and targeting is discussed. This review aims to systematically summarize the latest research progress in LNP delivery carrier-assisted targeted controlled release mRNA vaccines in tumor immunity to provide new ideas and strategies for tumor immunotherapy, as well as to provide more effective treatment plans for patients.

The proteins encoded by the excision repair cross-complementing (ERCC) family are pivotal in DNA damage repair and maintaining genome stability. However, the precise role of the ERCC family in tumor prognosis and the effectiveness of immune checkpoint inhibitors (ICI) therapy remain uncertain. This study aimed to explore the connection between ERCC mutations and prognosis as well as the response to ICI. We observed that patients with ERCC mutations exhibited enhanced progression-free survival (PFS) and overall survival (OS) in two independent pan-cancer cohorts. Furthermore, this mutant subgroup showed higher tumor mutation burden (TMB) compared to the wild-type subgroup. Notably, ERCC mutations were associated with better OS (HR 0.54, 95% CI 0.42–0.70; P < 0.001) in pan-cancer patients who underwent ICI therapy (N = 1661). These findings were validated in a separate cohort, where patients in the ERCC mutant subgroup demonstrated improved clinical outcomes (HR 0.56, 95% CI 0.37–0.84; P = 0.03) and higher response rates (51.9% vs. 26.8%) than the wild-type subgroup. Further analysis revealed that patients with ERCC mutations displayed elevated tumor neoantigen burden (TNB) levels and increased infiltration of immune-response cells. Our study suggests that ERCC mutations are linked to enhanced immunogenicity and improved ICI efficacy, thus potentially serving as a biomarker for ICI therapy.

As the advanced functional materials, silver nanoparticles are potentially useful in various fields such as photoelectric, bio-sensing, catalysis, antibacterial and other fields, which are mainly based on their various properties. However, the properties of silver nanoparticles are usually determined by their size, shape, and surrounding medium, which can be modulated by various synthesis methods. In this review, the fabrication methods for synthesizing silver nanoparticles of different shapes and specific size are illustrated in detail. Besides, the corresponding properties and applications of silver nanoparticles are also discussed in this paper.

Detection and treatment of lung cancer still remain a clinical challenge. This study aims to validate exosomal microRNA‐96 (miR‐96) as a serum biomarker for lung cancer and understand the underlying mechanism in lung cancer progression. MiR‐96 expressions in normal and lung cancer patients were characterized by qPCR analysis. Changes in cell viability, migration and cisplatin resistance were monitored after incubation with isolated miR‐96‐containing exosomes, anti‐miR‐96 and anti‐miR negative control (anti‐miR‐NC) transfections. Dual‐luciferase reporter assay was used to study interaction between miR‐96 and LIM‐domain only protein 7 (LMO7). Changes induced by miR‐96 transfection and LMO7 overexpression were also evaluated. MiR‐96 expression was positively correlated with high‐grade and metastatic lung cancers. While anti‐miR‐96 transfection exhibited a tumour‐suppressing function, exosomes isolated from H1299 enhanced cell viability, migration and cisplatin resistance. Potential miR‐96 binding sites were found within the 3′‐UTR of wild‐type LMO7 gene, but not of mutant LMO7 gene. LMO7 expression was inversely correlated with lung cancer grades, and LMO7 overexpression reversed promoting effect of miR‐96. We have identified exosomal miR‐96 as a serum biomarker of malignant lung cancer. MiR‐96 promotes lung cancer progression by targeting LMO7. The miR‐96‐LMO7 axis may be a therapeutic target for lung cancer patients, and new diagnostic or therapeutic strategies could be developed by targeting the miR‐96‐LMO7 axis.

Objective: The RNA-binding protein RBM10 can regulate apoptosis during the proliferation and migration of pancreatic cancer, endometrial cancer, and osteosarcoma cells; however, the molecular mechanism underlying lung adenocarcinoma is rarely reported. Recent studies have detected multiple truncated and missense mutations in RBM10 in lung adenocarcinoma, but the role of RBM10 in lung adenocarcinoma is unclear. This study mainly explored the immune regulation mechanism of RBM10 in the development of lung adenocarcinoma and its influence on sensitivity to targeted therapy drugs. Methods: The transcriptome data of CGAP were used to analyze the RNA-seq data of lung adenocarcinoma patients from different subgroups by using the CIBERSORT algorithm to infer the relative proportion of various immune infiltrating cells, and Spearman correlation analysis was performed to determine the gene expression and immune cell content. In addition, this study utilized drug trial data from the GDSC database. The IC50 estimates for each specific targeted therapy were obtained by using a regression method, and the regression and prediction accuracy were tested via ten cross-validations with the GDSC training set. An immunohistochemical test was performed on the samples of 20 patients with lung adenocarcinoma in the subcomponent analysis of immune cells, and the protein expression of RBM10 in lung adenocarcinoma tissues was verified by cellular immunofluorescence assays. Nucleic acids were extracted at low temperatures, and qRT-PCR was used to verify the expression levels of the mRNA of RBM10 in lung adenocarcinoma tissues and normal tissues (p < 0.05). Results: After screening and inclusion using a machine language, the results showed that RBM10 was significantly highly expressed in the lung adenocarcinoma tissues. The related signaling pathways were mainly concentrated in ncRNA processing, rRNA metabolic processes, ribosome biogenesis, and the regulation of translation. The qRT-PCR for 20 lung adenocarcinoma tissues showed that the expression of RBM10 in these tissues was significantly different from that in normal tissues (p = 0.0255). Immunohistochemistry analysis and cell immunofluorescence staining also confirmed that RBM10 was involved in the immune regulation of lung adenocarcinoma tissues, and the number of immune cell aggregations was significantly higher than that of the control group. RBM10 regulates B cell memory-CIBERSORT (p = 0.042) and B cell memory-CIBERSOTRT-abs (p = 0.027), cancer-associated fibroblast-EPIC (p = 0.001), cancer-associated fibroblast- MCPCounter (p = 0.0037), etc. The risk score was significantly associated with the sensitivity of patients to lapatinib (p = 0.049), nilotinib (p = 0.015), pazopanib (p = 0.001), and sorafenib (p = 0.048). Conclusions: RBM10 can inhibit the proliferation and invasion of lung adenocarcinoma cells through negative regulation and promote the apoptosis of lung adenocarcinoma cells through immunomodulatory mechanisms. The expression level of RBM10 affects the efficacy of targeted drug therapy and the survival prognosis of lung adenocarcinoma patients, which has a certain guiding significance for the clinical treatment of these patients.

Background Cancer‐associated fibroblasts (CAFs) are potential targets for cancer therapy. Due to the heterogeneity of CAFs, the influence of CAF subpopulations on the progression of lung cancer is still unclear, which impedes the translational advances in targeting CAFs. Methods We performed single‐cell RNA sequencing (scRNA‐seq) on tumour, paired tumour‐adjacent, and normal samples from 16 non‐small cell lung cancer (NSCLC) patients. CAF subpopulations were analyzed after integration with published NSCLC scRNA‐seq data. SpaTial enhanced resolution omics‐sequencing (Stereo‐seq) was applied in tumour and tumour‐adjacent samples from seven NSCLC patients to map the architecture of major cell populations in tumour microenvironment (TME). Immunohistochemistry (IHC) and multiplexed IHC (mIHC) were used to validate marker gene expression and the association of CAFs with immune infiltration in TME. Results A subcluster of myofibroblastic CAFs, POSTN+ CAFs, were significantly enriched in advanced tumours and presented gene expression signatures related to extracellular matrix remodeling, tumour invasion pathways and immune suppression. Stereo‐seq and mIHC demonstrated that POSTN+ CAFs were in close localization with SPP1+ macrophages and were associated with the exhausted phenotype and lower infiltration of T cells. POSTN expression or the abundance of POSTN+ CAFs were associated with poor prognosis of NSCLC. Conclusions Our study identified a myofibroblastic CAF subpopulation, POSTN+ CAFs, which might associate with SPP1+ macrophages to promote the formation of desmoplastic architecture and participate in immune suppression. Furthermore, we showed that POSTN+ CAFs associated with cancer progression and poor clinical outcomes and may provide new insights on the treatment of NSCLC. POSTN+ CAFs were enriched in advanced NSCLC tumours and presented gene expression signatures related to extracellular matrix remodeling, tumour invasion and immune suppression. POSTN+ CAFs were in close localization with SPP1+ macrophages and associated with the exhausted phenotype and lower infiltration of T cells. POSTN expression and POSTN+ CAFs were prognostic factors for NSCLC.

[Objective] Using multi-omics research methods to explore cytolytic activity-related genes through the immunoregulatory factors HAVCR2 (TIM3) affecting the survival and prognosis of lung adenocarcinoma. [Methods] We combined Cox single factor regression and lasso regression feature selection algorithm to screen out the key genes of cytolytic activity in lung adenocarcinoma, and applied multi-omics research to explore the clinical predictive value of the model, including onset risk, independent prognosis, clinical relevance, signal transduction pathways, drug sensitivity, and the correlation of immune regulatory factors, etc. TCGA data are used as the experimental group, and GEO data is used as the external data control group to verify the stability of the model. The survival curve was generated by the Kaplan–Meier method and compared by log-rank, and the Cox proportional hazard model was used for multivariate analysis. In this study, 10 fresh tissue samples of lung adenocarcinoma were collected for cellular immunohistochemical experiments to analyze the expression of immunoregulatory factors in cancer tissues, and the key immunoregulatory factors were verified and screened out. [Results] A total of 450 genes related to cytolytic activity were differentially expressed, of which 273 genes were up-regulated and 177 genes were down-regulated. A total of 91 key genes related to cytolytic activity related to the prognosis of lung adenocarcinoma were screened through Cox single factor regression. The ROC curve results showed that the AUC values of 1, 3, and 5 years in the training set and test set were all greater than 0.7, indicating that the model has a valid verification. The level of risk score is significantly related to the sensitivity of patients to AKT inhibitor VIII, Lenalidomide, and Tipifarnib. In addition, our study also found that receptor and MHC genes related to immunomodulatory, and chemokines, including HAVCR2, are more highly expressed in the low-risk group. [Conclusions] HAVCR2 (TIM3) immunoregulatory factors affect the expression of key genes that affect cytolytic activity in lung adenocarcinoma cells, and to some extent indirectly affect the survival and prognosis of patients with lung adenocarcinoma.

Chimonobambusa rigidula bamboo shoots are an important health-promoting vegetable. This study aims to identify the primary environmental factors influencing the quality of bamboo shoots across various regions, thereby providing a scientific foundation and theoretical support for managing this plant and enhancing shoot quality. The results indicate that the minimum and maximum temperatures in September, along with total soil phosphorus content, soil pH, and total soil nitrogen content, are the five critical factors affecting bamboo shoot quality and should be prioritized during the site selection process for bamboo shoot cultivation. The cumulative variation explanation rate for bamboo quality concerning environmental factors was found to be 90.22%. The appearance, morphology, and taste of bamboo shoots from Muchuan and Pingshan are superior to those from Mabian. Notably, bamboo shoots from Mabian exhibit the highest content of essential amino acids, while bamboo shoots from Muchuan contain the highest levels of mineral elements. This study provides new insights into the interactions between plant environments and Chimonobambusa rigidula bamboo shoot nutrition, offering actionable strategies for region-specific cultivation that align with consumer demand for healthier bamboo-based products.

Lung adenocarcinoma (LUAD) is a prevalent and aggressive form of lung cancer with poor prognosis, largely due to late-stage diagnosis and limited therapeutic options. Recent studies suggest that long noncoding RNAs (lncRNAs) play critical roles in cancer progression and immune modulation, emerging as potential therapeutic targets. In this study, we investigated the expression and functional role of LINC00892 in LUAD using RNA sequencing data from The Cancer Genome Atlas (TCGA) and functional assays in vitro and in vivo. We found that LINC00892 is significantly downregulated in LUAD tissues compared to normal tissues, and lower LINC00892 expression correlates with poorer overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI), particularly in younger patients and those with early-stage disease. Bioinformatic analyses revealed that LINC00892 expression is positively correlated with immune cell infiltration, including CD4+ and CD8+ T cells, and negatively correlated with tumor-promoting Th2 cells, suggesting its role in shaping the tumor immune microenvironment. In vitro functional assays showed that LINC00892 overexpression inhibits LUAD cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, LINC00892 upregulation was found to suppress epithelial–mesenchymal transition (EMT) by increasing E-cadherin expression and decreasing levels of N-cadherin, vimentin, and slug. Additionally, in an in vivo mouse xenograft model, LINC00892 overexpression suppressed tumor growth and metastasis, accompanied by enhanced immune cell infiltration such as CD4+ and CD8+ T cells. Collectively, these findings suggest that LINC00892 acts as a tumor suppressor in LUAD by modulating immune infiltration and EMT, highlighting its potential as a prognostic biomarker and therapeutic target.