How can open public data promote efficient and equitable green production? Evidence from eco-efficiency in China.

Nowadays, concurrent attention to economic development and ecological issues is becoming an important trend. In this paper, we measure the eco-efficiency of 285 Chinese cities from 2003 to 2019 using a non-radial directional distance function and the data envelopment analysis method, based on which we analyze the club convergence of cities' eco-efficiency using the logt test; we estimate the impact of open public data platforms on eco-efficiency and its convergence using a multi-period difference in difference model and panel-ordered logit model, respectively. We find that, first, open public data platforms improve cities' eco-efficiency by about 6.

Carbon emissions trading schemes and economic growth: New evidence on the Porter Hypothesis from 285 China's prefecture-level cities.

The Chinese government has established carbon emissions trading schemes (CETS) to cope with climate change and reduce carbon emissions. This paper uses the multi-period difference in difference (DID) model to explore the impact of CETS on cities' GDP and GDP growth rates in China based on data from 285 prefecture-level cities from 2008-2019. We find that CETS increase the level of GDP by 3.

Do energy-environmental efficiency benefit from advanced policy zones? Evidence from national new zones of China.

As global climate change aggravates, reducing energy consumption and environmental pollution is essential to sustainable economic development. This paper measures the energy-environmental efficiency of 284 prefecture-level cities in China using a non-radial directional distance function (NDDF) and data envelopment analysis (DEA), and evaluates the impact of the establishment of national new zones on energy-environmental efficiency using the multi-period difference-in-difference model (DID). The results are: first, establishing national new zones improves the energy-environmental efficiency of the prefecture-level cities in which they are located by 13%-25%, and the mechanisms include enhancing the green technical efficiency and scale efficiency.

Gut microbial evidence chain in high-salt diet exacerbates intestinal aging process.

Although excessive salt consumption appears to hasten intestinal aging and increases susceptibility to cardiovascular disease, the molecular mechanism is unknown. In this study, mutual validation of high salt (HS) and aging fecal microbiota transplantation (FMT) in C56BL/6 mice was used to clarify the molecular mechanism by which excessive salt consumption causes intestinal aging. Firstly, we observed HS causes vascular endothelial damage and can accelerate intestinal aging associated with decreased colon and serum expression of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and increased malondialdehyde (MDA); after transplantation with HS fecal microbiota in mice, vascular endothelial damage and intestinal aging can also occur.

MicroRNA-1252-5p, regulated by Myb, inhibits invasion and epithelial-mesenchymal transition of pancreatic cancer cells by targeting NEDD9.

MicroRNAs (miRNAs) are known to be involved in the development and progression of pancreatic cancer (PAC). The expression levels and roles of miR-1252-5p in PAC remain unclear. Quantitative real-time PCR and hybridization were used to detect miR-1252-5p expression in PAC cells and human tissues.

Correlation between Claudin-18 expression and clinicopathological features and prognosis in patients with gastric cancer.

Background: To investigate the correlation between Claudin-18 expression and the clinicopathological features and prognosis of gastric cancer.

Methods: A total of 63 patients who underwent gastric cancer surgery from December 2012 to June 2013 were recruited as the research participants. The clinicopathological data and prognostic information of the participants were collected, and expression levels of Claudin-18 in gastric cancer and adjacent tissues were detected by immunohistochemical (IHC) staining.

CD137 agonist induces gastric cancer cell apoptosis by enhancing the functions of CD8 T cells via NF-κB signaling.

Background: CD137 is a target for tumor immunotherapy. However, the role of CD137 in gastric cancer (GC), especially in inducing GC cell apoptosis, has not been studied.

Methods: Foxp3 and CD8 T cells in GCs were investigated using immunohistochemistry (IHC).

Anti-Proliferative and Apoptosis-Promoting Effect of microRNA-125b on Pancreatic Cancer by Targeting NEDD9 via PI3K/AKT Signaling.

Purpose: The expression of microRNA-125b (miR-125b) is low in a variety of cancers, including gastric, lung, bladder, thyroid, and esophageal cancers. However, its specific mechanism in pancreatic ductal adenocarcinoma (PDAC) remains unclear. This study is aimed to explore the role of miR-125b in PDAC.

6-gingerol alleviates inflammatory injury in DSS-induced ulcerative colitis mice by regulating NF-κB signaling.

Background: The imbalance of Treg/Thl7 cells and inflammatory injury are believed to be involved in the development of ulcerative colitis (UC). Meanwhile, 6-gingerol has been reported to alleviate intestinal inflammatory damage in mice models, but the underlying mechanism remains elusive.

Methods: In this study, dextran sulfate sodium (DSS)-induced colitis mice models were established to examine the effects of 6-gingerol on IL-17 and IL-10 secretion, and the activation of NF-κB signaling was evaluated using enzyme-linked immunosorbent assay (ELISA), Western blotting, and immunohistochemistry.

The effect of 6-gingerol on inflammatory response and Th17/Treg balance in DSS-induced ulcerative colitis mice.

Background: Ulcerative colitis (UC) is a non-specific chronic intestinal inflammatory disease with unclear etiology. Previous studies have suggested that the imbalance of Treg/Thl7 cells may be involved in the development of UC. It was found that 6-gingerol can alleviate the intestinal inflammatory damage and improve the weight loss of colitis mice.

Silencing NEDD9 by lentivirus-delivered shRNA inhibits the growth of BxPC-3 cells and .

Background: Neural precursor cell-expressed, developmentally downregulated protein 9 (NEDD9) is an invasion and metastasis-related gene. It has been proven to be highly expressed and closely associated with tumor proliferation and invasion in several types of human cancers including pancreatic adenocarcinoma. The present study was aimed to investigate and characterize the efficacy of silencing NEDD9 by lentivirus-delivered shRNA in pancreatic cancer (PC) BxPC-3 cells and .

Expression of receptor interacting protein 3 and mixed lineage kinase domain-like protein-key proteins in necroptosis is upregulated in ulcerative colitis.

Background: Ulcerative colitis (UC) is a chronic inflammatory colonic disease strongly associated with intestinal epithelial cell (IEC) death. Necroptosis is characterized by a newly programmed cell death through a caspase-independent pathway. Receptor interacting protein 3 (RIP3) and mixed lineage kinase domain-like protein (MLKL) are very important in the pathway of necroptosis.

NEDD9 expression is correlated with epithelial-to-mesenchymal transition markers in colorectal cancer.

The epithelial-to-mesenchymal transition (EMT) is a critical step in tumor metastasis. NEDD9 has been shown to be an oncogene in colorectal cancer. However, little is known about the relationship between NEDD9 and EMT in colorectal cancer metastasis.

DLC-1 is a candidate biomarker methylated and down-regulated in pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDA) is one of the most aggressive malignancies in humans, and its prognosis is generally poor even after surgery. Many advances have been made to understand the pathogenesis of PDA; however, the molecular mechanisms that lead to pancreatic carcinogenesis are still not clearly understood. The aims of this study were to investigate the relationship between DLC-1 methylation status and clinicopathological characteristics of PDA patients and evaluate the role of DLC-1 methylation status in PDA.