Interaction of composite fume suppression and odor elimination agents with crumb rubber modified asphalt: Inhibition behavior of volatile organic compounds (VOCs) and inorganic fume.

The production and construction of crumb rubber modified asphalt (RMA) at high temperatures can produce a large amount of toxic fume, which is detrimental to human health and environment. In this study, a series of composite fume suppression and odor elimination agents (CSEAs) with both physical adsorption and chemical capture functions were adopted to reduce the emissions of volatile organic compounds (VOCs) and hydrogen sulfide (H2S). The material composition, microstructure, and specific surface area of CSEA were analyzed by using X-ray diffraction (XRD), scanning electron microscopy (SEM), energy dispersive spectroscopy (EDS), and N2 adsorption-desorption isotherm (BET). The inhibitory effects of adding CSEA on toxic fume emissions from RMA at high temperatures were investigated through a combination of fume emission tests, H2S gas detection, gel permeation chromatography (GPC), and gas chromatography-mass spectrometry technology (GC-MS). The adsorption behavior of CSEA on H2S was analyzed through adsorption dynamics. Results showed that the physical and chemical properties of CSEA are stable while chemical adsorption dominates the CSEA's effect on H2S. ZnO and Ca(OH)2 exhibit good crystallization effects on the surface of the carrier by forming mesoporous structures mostly above 3.4 nm in size. The incorporation of CSEA significantly reduced the total emissions of RMA fume and the main components of VOCs in which the average inhibition rate of H2S can reach 44 % at an initial 30 mins.

Drugs targeting CTGF in the treatment of pulmonary fibrosis.

Pulmonary fibrosis represents the final alteration seen in a wide variety of lung disorders characterized by increased fibroblast activity and the accumulation of substantial amounts of extracellular matrix, along with inflammatory damage and the breakdown of tissue architecture. This condition is marked by a significant mortality rate and a lack of effective treatments. The depositing of an excessive quantity of extracellular matrix protein follows the damage to lung capillaries and alveolar epithelial cells, leading to pulmonary fibrosis and irreversible damage to lung function. It has been proposed that the connective tissue growth factor (CTGF) plays a critical role in the advancement of pulmonary fibrosis by enhancing the accumulation of the extracellular matrix and exacerbating fibrosis. In this context, the significance of CTGF in pulmonary fibrosis is examined, and a summary of the development of drugs targeting CTGF for the treatment of pulmonary fibrosis is provided.

The role of molecular chaperone CCT/TRiC in translation elongation: A literature review.

Protein synthesis from mRNA is an energy-intensive and strictly controlled biological process. Translation elongation is a well-coordinated and multifactorial step in translation that ensures the accurate and efficient addition of amino acids to a growing nascent-peptide chain encoded in the sequence of messenger RNA (mRNA). Which undergoes dynamic regulation due to cellular state and environmental determinants. An expanding body of research points to translational elongation as a crucial process that controls the translation of an mRNA through multiple feedback mechanisms. Molecular chaperones are key players in protein homeostasis to keep the balance between protein synthesis, folding, assembly, and degradation. Chaperonin-containing tailless complex polypeptide 1 (CCT) or tailless complex polypeptide 1 ring complex (TRiC) is an essential eukaryotic molecular chaperone that plays an essential role in assisting cellular protein folding and suppressing protein aggregation. In this review, we give an overview of the factors that influence translation elongation, focusing on different functions of molecular chaperones in translation elongation, including how they affect translation rates and post-translational modifications. We also provide an understanding of the mechanisms by which the molecular chaperone CCT plays multiple roles in the elongation phase of eukaryotic protein synthesis.

Identification and validation of a novel prognosis model based on m5C-related long non-coding RNAs in colorectal cancer.

BACKGROUND: The prognosis of tumor patients can be assessed by measuring the levels of lncRNAs (long non-coding RNAs), which play a role in controlling the methylation of the RNA. Prognosis in individuals with colorectal adenocarcinoma (CRC) is strongly linked to lncRNA expression, making it imperative to find lncRNAs that are associated with RNA methylation with strong prognostic value. METHODS: In this study, by analyzing TCGA dataset, we were able to develop a risk model for lncRNAs that are associated with m5C with prognostic significance by employing LASSO regression and univariate Cox proportional analysis. There were a number of methods employed to ensure the model was accurate, including multivariate and univariate Cox regression analysis, Kaplan analysis, and receiver operating characteristic curve analysis. The principal component analysis, GSEA and GSVA analysis were used for risk model analysis. The CIBERSORT instrument and the TIMER database were used to evaluate the link between the immune cells that infiltrate tumors and the risk model. In vitro experiments were also performed to validate the predicted m5C-related significant lncRNAs. RESULTS: The m5c regulators were differentially expressed in colorectal cancer and normal tissue. Based on the screening criteria and LASSO regression, 11 m5c-related lncRNAs were identified for developing the prognostic risk model. Multivariate and univariate Cox regression analysis showed the risk score is a crucial prognostic factor in CRC patients. The 1-year, 3-year, and 5-year AUC curves showed the risk score was higher than those identified for other clinicopathological characteristics. A nomogram using the risk score as a quantitative tool was developed for predicting patients' outcomes in clinical settings. In addition, the risk profile of m5C-associated lncRNAs can discriminate between tumor immune cells' characteristics in CRC. Mutation patterns and chemotherapy were analyzed between high- and low- risk groups of CRC patients. Moreover, TNFRSF10A-AS1 was chosen for the in vitro verification of the m5C-connected lncRNA to demonstrate impressive effects on the proliferation, migration and invasion of CRC cells. CONCLUSION: A risk model including the prognostic value of 11 m5C-associated lncRNAs proves to be a useful prognostic tool for CRC and improves the care of patients suffering from CRC based on these findings.

PFDN2 promotes cell cycle progression via the hnRNPD-MYBL2 axis in gastric cancer.

Gastric cancer (GC) is a major health burden worldwide, but our understanding of GC is limited, and the prognosis is poor. Novel therapeutic strategies and biomarkers are urgently needed to improve GC patient outcomes. Previously, we identified PFDN2 as a novel key gene in gastric cancer based on its differential expression between cancer and normal tissues. However, the role and underlying mechanisms of PFDN2 in GC remain elusive. In this article, we demonstrated that PFDN2 is highly expressed in GC and that upregulation of PFDN2 is associated with the progression of GC. We further found that PFDN2 could promote cell cycle progression by promoting MYBL2 expression. Mechanistically, we demonstrated that PFDN2 could upregulate MYBL2 expression by facilitating the nuclear translocation of hnRNPD, and thus promoting MYBL2 transcriptional program. In conclusion, we found that PFDN2 promotes cell cycle progression via the hnRNPD-MYBL2 axis and may serve as a potential biomarker and therapeutic target for GC.

Single-cell and WGCNA uncover a prognostic model and potential oncogenes in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Single-cell transcriptome sequencing (scRNA-seq) can provide accurate gene expression data for individual cells. In this study, a new prognostic model was constructed by scRNA-seq and bulk transcriptome sequencing (bulk RNA-seq) data of CRC samples to develop a new understanding of CRC. METHODS: CRC scRNA-seq data were downloaded from the GSE161277 database, and CRC bulk RNA-seq data were downloaded from the TCGA and GSE17537 databases. The cells were clustered by the FindNeighbors and FindClusters functions in scRNA-seq data. CIBERSORTx was applied to detect the abundance of cell clusters in the bulk RNA-seq expression matrix. WGCNA was performed with the expression profiles to construct the gene coexpression networks of TCGA-CRC. Next, we used a tenfold cross test to construct the model and a nomogram to assess the independence of the model for clinical application. Finally, we examined the expression of the unreported model genes by qPCR and immunohistochemistry. A clone formation assay and orthotopic colorectal tumour model were applied to detect the regulatory roles of unreported model genes. RESULTS: A total of 43,851 cells were included after quality control, and 20 cell clusters were classified by the FindCluster () function. We found that the abundances of C1, C2, C4, C5, C15, C16 and C19 were high and the abundances of C7, C10, C11, C13, C14 and C17 were low in CRC tumour tissues. Meanwhile, the results of survival analysis showed that high abundances of C4, C11 and C13 and low abundances of C5 and C14 were associated with better survival. The WGCNA results showed that the red module was most related to the tumour and the C14 cluster, which contains 615 genes. Lasso Cox regression analysis revealed 8 genes (PBXIP1, MPMZ, SCARA3, INA, ILK, MPP2, L1CAM and FLNA), which were chosen to construct a risk model. In the model, the risk score features had the greatest impact on survival prediction, indicating that the 8-gene risk model can better predict prognosis. qPCR and immunohistochemistry analysis showed that the expression levels of MPZ, SCARA3, MPP2 and PBXIP1 were high in CRC tissues. The functional experiment results indicated that MPZ, SCARA3, MPP2 and PBXIP1 could promote the colony formation ability of CRC cells in vitro and tumorigenicity in vivo. CONCLUSIONS: We constructed a risk model to predict the prognosis of CRC patients based on scRNA-seq and bulk RNA-seq data, which could be used for clinical application. We also identified 4 previously unreported model genes (MPZ, SCARA3, MPP2 and PBXIP1) as novel oncogenes in CRC. These results suggest that this model could potentially be used to evaluate the prognostic risk and provide potential therapeutic targets for CRC patients.

A Constitutive Model of Plate-Like Entangled Metallic Wire Material in Wide Temperature Range.

Entangled metallic wire material (EMWM) is a kind of porous damping material. To promote the engineering application of EMWM, it is necessary to establish the constitutive model of EMWM to estimate its mechanical properties. In this paper, a series of quasi-static compression experiments for plate-like EMWM specimens made of austenitic stainless steel wire (06Cr19Ni10) with different densities were carried out in the temperature range of 20-500 °C. It was found that the stiffness of the plate-like EMWM would increase with the increases in the ambient temperature. The non-linear characteristics of the force-displacement curve of the plate-like EMWM would be weakened. Taking the spatial structural characteristics of the plate-like EMWM and the influence of the thermal expansion of the structure into account, a new constitutive model for plate-like EMWM was presented by the combination of the Johnson-Cook model and the Sherwood-Frost constitutive framework model. The accuracy of the model was verified by the experimental data under different temperatures. The results show that the calculated results of the model are consistent with the experimental results. This model can provide an effective theoretical basis for predicting the mechanical properties of plate-like EMWM and guiding its design.

Angustifoline inhibits human colon cancer cell growth by inducing autophagy along with mitochondrial-mediated apoptosis, suppression of cell invasion and migration and stimulating G2/M cell cycle arrest.

PURPOSE: The prime objective of the present study was to investigate the anticancer properties of angustifoline against COLO-205 human colon cancer cells. Its effects on cell autophagy, apoptosis, cell invasion and cell migration, and cell cycle arrest were also evaluated in the current study. METHODS: WST-1 assay was used to study cytotoxic effects of the compound on the cell viability. Effects on apoptosis and cell cycle arrest were evaluated by flow cytometry. In vitro wound healing assay and matrigel assay were carried out to study the effects of angustifoline on cell migration and cell invasion respectively. To confirm autophagy, we evaluated the expression of several autophagy-associated proteins using Western blot assay along with transmission electron microscopy (TEM). RESULTS: The findings indicated that angustifoline induced dose- and time-dependent cytotoxicity in COLO-205 human colon cancer cells along with inhibiting cancer cell colony formation. Angustifoline-treated cells exhibited cell shrinkage along with distortion of the normal cell morphology. Angustifoline-treated cells were also arrested in the G2/M phase of the cell cycle, showing strong dose-dependence. The compound also led to inhibition of cell migration and cell invasion. The results showed that treatment of these cells led to generation of autophagic cell vesicles. Furthermore, it was observed that the expression of Beclin-1 and LC3-II proteins was significantly upregulated in the angustifoline-administered COLO-205 cells. CONCLUSIONS: In brief, the present study hints towards the potent anticancer potential of the natural product angustifoline against COLO-205 human colon cancer cells with in depth mechanistic studies.