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The environmental pollution that accompanies economic growth has always been of widespread concern. The chemical industry is a highly energy-consuming industry in China, and the pollution this industry causes to the environment cannot be ignored. The paper is based on the Porter hypothesis and uses data from different regions of China. In this paper, we investigate the mediating role of different types of environmental regulation (divided into command-controlled, market-incentive, and voluntary environmental regulation) in positively affecting sustainability performance through green technology innovation (divided into green product innovation, green process innovation, and end-of-line management innovation). The results show that different versions of the Porter hypothesis can be accepted in Chinese chemical enterprises. This finding demonstrates that environmental regulation positively impacts both green technology innovation and sustainability performance. Green technology innovation plays a mediating role between environmental regulation and sustainability performance, especially in East China. However, the mediating effect of green product innovation is not significant. Further study shows that command-controlled environmental regulation has a more significant positive effect on sustainability performance. This suggests that the market-incentive and voluntary environmental regulation tools do not fully play their functional roles. Thus, the paper demonstrates the developmental shortcomings of environmental regulation, green technology innovation, and sustainability performance. This is more conducive to chemical enterprises improving green technology innovation and achieving long-term development and ecological environment protection.

Right detection of anaplastic lymphoma kinase (ALK) gene rearrangement is pivotal to selection of patients with lung adenocarcinoma for ALK-targeted therapy. We explored the potential of combination of immunohistochemistry (IHC) screening and fluorescence in situ hybridization (FISH) as an affordable practice. We analyzed 410 unselected lung adenocarcinomas by ALK IHC (D5F3 clone) and FISH. Some equivocal cases were further analyzed by RT-PCR. The EGFR mutation was detected by pyrosequencing assay. In total 368 cases which got all IHC, FISH, EGFR mutation results were eligible for analysis. Cases were evaluated as IHC score 3+ (n = 26), score 2+ (n = 9), score 1+ (n = 51), and score 0 (n = 282), respectively. 23 of 26 IHC 3+ and 5 of 9 IHC 2+ cases were FISH positive, whereas 3 of 26 IHC 3+, 4 of 9 IHC 2+ and all 333 IHC 1+/0 cases were FISH negative. If considering FISH as the standard, the sensitivity and specificity of ALK IHC 3+/2+ as ALK positive were 100% and 97.9%, respectively. Three IHC 3+ cases reported as FISH \"negative\" were actually ALK positive confirmed by ALK RT-PCR or re-detected. Based on the final classify, ALK IHC 3+/2+ was 100% sensitive and 98.8% specific. However, FISH was 90.3% sensitive and 100% specific. IHC 2+ was regarded as equivocal and need to be confirmed by FISH or RT-PCR. In the 368 cases, 8.4% cases had ALK positive, 52.2% cases had EGFR mutation, and only one case had a coexisting. Manually semiquantitative ALK IHC (primary antibody D5F3 coupled with secondary DAKO Envision system) used as the initial screening combined with auxiliary FISH confirmation is a reliable, economical approach to identify ALK positive lung adenocarcinoma. The IHC can find some ALK positive cases which would be missed by FISH only.

The antitumor efficacy of adoptively transferred T cells is limited by their poor persistence, in part due to exhaustion, but the underlying mechanisms and potential interventions remain underexplored. Here, we show that targeting histone demethylase LSD1 by chemical inhibitors reshapes the epigenome of in vitro activated and expanded CD8 + T cells, and potentiates their antitumor efficacy. Upon T cell receptor activation and IL-2 signaling, a timely and transient inhibition of LSD1 suffices to improve the memory phenotype of mouse CD8 + T cells, associated with a better ability to produce multiple cytokines, resist exhaustion, and persist in both antigen-dependent and -independent manners after adoptive transfer. Consequently, OT1 cells primed with LSD1 inhibitors demonstrate an enhanced antitumor effect in OVA-expressing solid tumor models implanted in female mice, both as a standalone treatment and in combination with PD-1 blockade. Moreover, priming with LSD1 inhibitors promotes polyfunctionality of human CD8 + T cells, and increases the persistence and antitumor efficacy of human CD19-CAR T cells in both leukemia and solid tumor models. Thus, pharmacological inhibition of LSD1 could be exploited to improve adoptive T cell therapy. Phenotypic changes in exhausted T cells are linked to chromatin remodeling. Here the authors show that pharmacological inhibition of the H3K4me1/2 demethylase LSD1 promotes the persistence and enhances the therapeutic activity of adoptively transferred T cells for cancer therapy.

Green economy requires enterprises to comply with environmental regulations, which increases the enterprises risk-taking level and ultimately affects the investment decision of enterprises. By constructing multiple linear regression equations with four dimensions of enterprise risk-taking level as dependent variables and three types of environmental regulations as independent variables, the data of listed chemical companies in China are used for the empirical test. Empirical results show that command environmental regulation has a significant promoting effect on the risk-taking level of capital, talent, and product, but has no significant impact on the technology risk-taking level. Market environmental regulation can effectively enhance the risk-taking level of capital and talent, but has no significant impact on the risk-taking level of technology and product. Voluntary environmental regulation only has a significant effect on enhancing the capital risk-taking level. The existing environmental regulation system can be optimized, focusing on the driving function of environmental regulation on the technology risk-taking level, activating the role of voluntary environmental regulation, and ultimately improving the enterprise risk-taking level.

Background Mucosal-associated invariant T (MAIT) cells have been reported to regulate tumor immunity. However, the immune characteristics of MAIT cells in non-small cell lung cancer (NSCLC) and their correlation with the treatment efficacy of immune checkpoint inhibitors (ICIs) remain unclear. Patients and methods In this study, we performed single-cell RNA sequencing (scRNA-seq), flow cytometry, and multiplex immunofluorescence assays to determine the proportion and characteristics of CD8+MAIT cells in patients with metastatic NSCLC who did and did not respond to anti-PD-1 therapy. Survival analyses were employed to determine the effects of MAIT proportion and C-X-C chemokine receptor 6 (CXCR6) expression on the prognosis of patients with advanced NSCLC. Results The proportion of activated and proliferating CD8+MAIT cells were significantly higher in responders-derived peripheral blood mononuclear cells (PBMCs) and lung tissues before anti-PD-1 therapy, with enhanced expression of cytotoxicity-related genes including CCL4, KLRG1, PRF1, NCR3, NKG7, GZMB, and KLRK1. The responders’ peripheral and tumor-infiltrating CD8+MAIT cells showed an upregulated CXCR6 expression. Similarly, CXCR6+CD8+MAIT cells from responders showed higher expression of cytotoxicity-related genes, such as CST7, GNLY, KLRG1, NKG7, and PRF1. Patients with ≥15.1% CD8+MAIT cells to CD8+T cells ratio and ≥35.9% CXCR6+CD8+MAIT cells to CD8+MAIT cells ratio in peripheral blood showed better progression-free survival (PFS) after immunotherapy. The role of CD8+MAIT cells in lung cancer immunotherapy was potentially mediated by classical/non-classical monocytes through the CXCL16-CXCR6 axis. Conclusion CD8+MAIT cells are a potential predictive biomarker for patients with NSCLC responding to anti-PD-1 therapy. The correlation between CD8+MAIT cells and immunotherapy sensitivity may be ascribed to high CXCR6 expression.

Reversed halo sign (RHS) is characterized by a central ground-glass opacity surrounded by a crescentic or ring-shaped consolidation. It was originally described as a pathognomonic imaging feature of cryptogenic organizing pneumonia (COP), but has subsequently been observed in a wide variety of pulmonary disorders, including infectious and non-infectious diseases. Although RHS is currently considered as a non-specific and non-pathognomonic sign, a careful analysis of its radiologic characteristics together with clinical features can greatly facilitate the differential diagnosis. The paper presents a state-of-the-art review of RHS, we retrospectively review the definition of RHS in chronological order and comprehensively summarize the spectrum of pulmonary diseases associated with RHS. In addition, the radiologic–pathologic correlations of RHS in different disease entities are systemically discussed and an integrated approach is proposed to establish the differential diagnosis of RHS.

Background Advances in molecular subtype classification have improved the understanding of extensive-stage small cell lung cancer (ES-SCLC). However, immune landscape differences across ES-SCLC subtypes remain poorly defined. This study aimed to characterize ES-SCLC immune profiles and explore their association with response to immunotherapy. Methods Tumor samples from 135 patients with ES-SCLC were analyzed for molecular subtyping using immunohistochemical markers. Immune profiling of peripheral blood mononuclear cells was performed using cytometry by time-of-flight (CyTOF) and flow cytometry, and tumor tissues were assessed through multiplex immunofluorescence for immune cell subset characterization and distribution. Results Molecular subtyping of the 135 ES-SCLC cases identified 54.1%, 20.0%, 7.4%, and 18.5% as ASCL1-dominant, NEUROD1-dominant, POU2F3-dominant, and inflamed SCLC-I subtypes, respectively. CyTOF indicated a distinct enrichment of CD161 + CD127 + CD8 + T cells in SCLC-I,with flow cytometry validating significantly higher proportions. These cells exhibited elevated cytotoxic markers (GZMB and GNLY) and reduced exhaustion markers (PD-1, TIGIT, and LAG-3) compared with those of other subtypes( P  < 0.05). Multiplex immunofluorescence confirmed higher intratumoral infiltration of CD161 + CD127 + CD8 + T cells in SCLC-I. The intratumoral and peripheral levels of this subset were strongly correlated( r  = 0.669, P  < 0.0001). Patients with a CD161 + CD127 + CD8 + T/CD8 + T cell ratio of ≥ 2.7% had a significantly prolonged progression-free survival (PFS, 11.0 vs. 7.0 months, P  = 0.0196). Conclusions The SCLC-I subtype exhibited a distinct immune profile characterized by enrichment of CD161 + CD127 + CD8 + T cells in both peripheral blood and tumor tissue, which was associated with PFS following anti–PD-L1 therapy. These findings highlight the significance of subtype-specific immune profiling and the potential of CD161 + CD127 + CD8 + T cells as a predictive biomarker to guide precision immunotherapy in ES-SCLC.

Background Pembrolizumab has been approved as a first-line treatment for non-small cell lung cancer (NSCLC) patients. However, a percentage of patients discontinue immunotherapy due to immune-related adverse events (irAE). Among these events, immune-related endocrine toxicities (E-irAE) represents the most common form, though their etiology, risk factors, and impact on patient outcomes remain poorly understood. Materials and methods This retrospective cohort study was conducted across 5 multiple centers to investigate the outcomes of NSCLC patients who received pembrolizumab treatment between October 1, 2019, and September 30, 2023. E-irAE can occur on the thyroid, pituitary, adrenal glands, pancreas, and parathyroid. So thyroid function, adrenocorticotropic hormone, cortisol, sex hormone and glycaemia were measured at baseline and at regular intervals after the initiation of pembrolizumab treatment. Results Our study included a total of 380 NSCLC patients treated with pembrolizumab, 114 patients (30.00%) developed E-irAE. Among them, 107 patients (93.86%) developed immune-related thyroid dysfunction (irTD) (5 cases of combined immune-related hypophysitis (IH)), 4 patients (3.51%) only developed IH, and 3 patients (2.63%) developed type 1 diabetes mellitus. IrTD was found to be independently associated only with monocyte-to-lymphocyte ratio (MLR) (odds ratios ( OR ) = 0.060, 95% CI 0.000-0.375; p  = 0.015) and anti-thyroglobulin antibody (TGAb) ( OR  = 31.898, 95% CI 1.516-671.367; p  = 0.026). Kaplan-Meier Survival Analysis showed that the progression-free survival (PFS) was significant longer in stage IV NSCLC patients with irTD than in those who did not (44.72 weeks vs. 27.79 weeks; hazard ratio ( HR ) = 0.645, 95% CI 0.440–0.946; p  = 0.025), particularly in the subgroup of subclinical hypothyroidism ( HR  = 0.567, 95% CI 0.324–0.994; p  = 0.047). We also found that sex ( HR  = 0.493, 95% CI 0.291–0.834; p  = 0.008) was identified as an independent factor associated with better PFS. Conclusion E-irAE are recognized as prevalent common irAE with various phenotypic manifestations. Low MLR and positive TGAb at baseline have been identified as risk factors that increase the likelihood of developing irTD. Sex and the occurrence of irTD were independently associated with improved PFS.

Introduction Previous studies have reported inconsistent findings regarding the associationbetween ALK and ROS1 rearrangements in lung cancer and thromboembolic risk. This retrospective study aimed to investigate this association in advanced lung adenocarcinoma patients with ALK, ROS1, RET rearrangements, and EGFR mutations. Materials and Methods We retrospectively collected information on patients with advanced lung adenocarcinoma in the First Affiliated Hospital of Zhejiang University School of Medicine from January 2013 to March 2021. All patients with confirmed ALK, ROS1, or RET rearrangements, as well as a comparison cohort of those with EGFR mutation, were included. Clinical characteristics were analyzed, and the association between driver genes and TE risks was analyzed using competing risk and logistic regression. Results A total of 546 patients were included in the study. Among them, those with ROS1 rearrangements exhibited the highest cumulative incidence of thromboembolic events (TEs), reaching 17.5% ± 0.2% during the peri‐diagnostic period (within 6 months following diagnosis). Regardless of the entire follow‐up or the peri‐diagnostic period, ROS1 rearrangements were significantly associated with an increased risk of TEs. Multivariate analysis revealed ROS1 rearrangements, the number of comorbidities, the size of mediastinal lymph nodes, and elevated C‐reactive protein (CRP) levels as TE risk factors during the peri‐diagnostic period. Throughout the follow‐up period, ROS1 rearrangements and hypertension were independent TE risk factors. In addition, the development of TE significantly affected the overall survival of patients with EGFR mutations. Conclusion ROS1 rearrangements were significantly associated with an increased risk of TE. In this retrospective study of 546 lung adenocarcinoma patients with four different driver genes, ROS1 rearrangements were associated with the increased risk of thromboembolic events (TEs), particularly during the peri‐diagnostic period (6 months before and after diagnosis). Risk factors of TEs during the peri‐diagnostic period included ROS1 rearrangements, multiple comorbidities, enlarged mediastinal lymph nodes, and elevated CRP levels.

Background The incidence of small cell lung cancer (SCLC) among Asian patients is on the rise. Nevertheless, there remains a deficiency in precise prognostic models tailored to the specific needs of this patient population. It is imperative to develop a novel nomogram aimed at forecasting the prognosis of Asian SCLC patients. Methods The SEER database supplied data on 661 Asian SCLC patients, who were then divided into training and internal validation sets through a random selection process. In addition, we identified 212 patients from a Chinese medical institution for the purpose of creating an external validation cohort. To forecast survival, we employed both univariate and multivariate analyses. The performance of our nomogram was assessed through calibration plots, the concordance index (C‐index), and decision curve analysis (DCA). Results Five independent prognostic factors were determined and integrated into the nomogram. C‐index values for the training and internal validation cohorts were 0.774 (95% confidence interval [CI] = 0.751–0.797) and 0.731 (95%CI = 0.690–0.772), respectively. In the external validation cohort, the C‐index is 0.712 (95% CI = 0.655–0.7692). Calibration curves demonstrated highly accurate predictions. When compared to the AJCC staging system, our model exhibited improved net benefits in DCA. Furthermore, the risk stratification system effectively differentiated patients with varying survival risks. Conclusion We have created a novel nomogram for predicting the survival of Asian patients with SCLC. This nomogram has been subjected to external validation and has shown its superiority over the conventional TNM staging system. It offers a more precise and reliable means of forecasting the prognosis of Asian SCLC patients. We have created a novel nomogram for predicting the survival of Asian patients with small cell lung cancer (SCLC). This nomogram has been subjected to external validation and has shown its superiority over the conventional TNM staging system. It offers a more precise and reliable means of forecasting the prognosis of Asian SCLC patients.