Identification and validation of ferroptosis related markers in erythrocyte differentiation of umbilical cord blood-derived CD34+ cell by bioinformatic analysis.

Ferroptosis has been observed to play an important role during erythrocyte differentiation (ED). However, the biological gene markers and ferroptosis mechanisms in ED remain unknown. We downloaded the datasets of ED in human umbilical cord blood-derived CD34+ cells from the Gene Expression Omnibus database. Using median differentiation time, the sample was categorized into long and short groups. The differentially expressed ferroptosis-related genes (DE-FRGs) were screened using differential expression analysis. The enrichment analyses and a protein-protein interaction (PPI) network were conducted. To predict the ED stage, a logistic regression model was constructed using the least absolute shrinkage and selection operator (LASSO). Overall, 22 DE-FRGs were identified. Ferroptosis-related pathways were enriched using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. Gene Set Enrichment Analysis and Gene Set Variation Analysis revealed the primary involvement of DE-FRGs in JAK-STAT, MAPK, PI3K-AKT-mTORC1, WNT, and NOTCH signaling pathways. Ten-hub DE-FRGs were obtained using PPI analysis. Furthermore, we constructed mRNA-microRNA (miRNA) and mRNA-transcription factor networks. Immune cell infiltration levels differed significantly during ED. LASSO regression analysis established a signature using six DE-FRGs (ATF3, CDH2, CHAC1, DDR2, DPP4, and GDF15) related to the ED stage. Bioinformatic analyses identified ferroptosis-associated genes during ED, which were further validated. Overall, we identified ferroptosis-related genes to predict their correlations in ED. Exploring the underlying mechanisms of ferroptosis may help us better understand pathophysiological changes in ED and provide new evidence for clinical transformation.

Atmospheric deposition of microplastics in a rural region of North China Plain.

Microplastics (MPs) pollution is becoming one of the most pressing environmental issues globally. MPs in the marine, freshwater and terrestrial environments have been fairly well investigated. However, knowledge of the atmospheric-mediated deposition of MPs within rural environments is limited. Here, we present the results of bulk (dry and wet) atmospheric MPs deposition in a rural region of Quzhou County in the North China Plain (NCP). Samples of MPs in the atmospheric bulk deposition were collected for individual rainfall events over a 12-month period from August 2020 to August 2021. The number and size of MPs from 35 rainfall samples were measured by fluorescence microscopy, while the chemical composition of MPs was identified using micro-Fourier transform infrared spectroscopy (µ-FTIR). The results showed that the atmospheric MPs deposition rate in summer (892-75,421 particles/m2/day) was highest compared to 735-9428, 280-4244 and 86-1347 particles/m2/day in spring, autumn, and winter, respectively. Furthermore, the MPs deposition rates in our study were 1-2 orders of magnitude higher than those in other regions, indicating a higher rate of MPs deposition in the rural region of the NCP. MPs with a diameter of 3-50 µm accounted for 75.6 %, 78.4 %, 73.4 % and 66.1 % of total MPs deposition in spring, summer, autumn, and winter, respectively, showing that the majority of MPs in the current study were small in size. Rayon fibers accounted for the largest proportion (32 %) of all MPs, followed by polyethylene terephthalate (12 %) and polyethylene (8 %). This study also found that a significant positive correlation between rainfall volume and MPs deposition rate. In addition, HYSPLIT back-trajectory modelling showed that the farthest source of deposition MPs may have come from Russia.

Construction of a mitochondrial dysfunction related signature of diagnosed model to obstructive sleep apnea.

Background: The molecular mechanisms underlying obstructive sleep apnea (OSA) and its comorbidities may involve mitochondrial dysfunction. However, very little is known about the relationships between mitochondrial dysfunction-related genes and OSA. Methods: Mitochondrial dysfunction-related differentially expressed genes (DEGs) between OSA and control adipose tissue samples were identified using data from the Gene Expression Omnibus database and information on mitochondrial dysfunction-related genes from the GeneCards database. A mitochondrial dysfunction-related signature of diagnostic model was established using least absolute shrinkage and selection operator Cox regression and then verified. Additionally, consensus clustering algorithms were used to conduct an unsupervised cluster analysis. A protein-protein interaction network of the DEGs between the mitochondrial dysfunction-related clusters was constructed using STRING database and the hub genes were identified. Functional analyses, including Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene set enrichment analysis (GSEA), and gene set variation analysis (GSVA), were conducted to explore the mechanisms involved in mitochondrial dysfunction in OSA. Immune cell infiltration analyses were conducted using CIBERSORT and single-sample GSEA (ssGSEA). Results: we established mitochondrial dysfunction related four-gene signature of diagnostic model consisted of NPR3, PDIA3, SLPI, ERAP2, and which could easily distinguish between OSA patients and controls. In addition, based on mitochondrial dysfunction-related gene expression, we identified two clusters among all the samples and three clusters among the OSA samples. A total of 10 hub genes were selected from the PPI network of DEGs between the two mitochondrial dysfunction-related clusters. There were correlations between the 10 hub genes and the 4 diagnostic genes. Enrichment analyses suggested that autophagy, inflammation pathways, and immune pathways are crucial in mitochondrial dysfunction in OSA. Plasma cells and M0 and M1 macrophages were significantly different between the OSA and control samples, while several immune cell types, especially T cells (γ/δ T cells, natural killer T cells, regulatory T cells, and type 17 T helper cells), were significantly different among mitochondrial dysfunction-related clusters of OSA samples. Conclusion: A novel mitochondrial dysfunction-related four-gen signature of diagnostic model was built. The genes are potential biomarkers for OSA and may play important roles in the development of OSA complications.

TMUB1 Correlated with Immune Infiltration Is a Prognostic Marker for Colorectal Cancer.

Background: Transmembrane and ubiquitin-like domain-containing protein 1 (TMUB1) is overexpressed in a large number of liver and esophageal tumors. However, only a few reports on the clinical significance of TMUB1 in colorectal cancer (CRC) exist. Methods: Here, we evaluated the clinical significance and potential biological role of TMUB1 using bioinformatics analysis. Univariate and multivariate analyses were performed to evaluate the relationship of TMUB1 with clinicopathological features. Gene set enrichment analysis (GSEA) was performed to identify the biological function of TMUB1, while any associations between the expression of TMUB1 and the infiltration of 24 immune cells were analyzed using simple-sample GSEA. Results: TMUB1 was significantly overexpressed in CRC tissues compared with normal controls. The high expression of TMUB1 in CRC was associated with T stage, neotype, and residual tumor. Moreover, TMUB1 was identified as an independent factor of poor disease-free survival (DFS) and short overall survival (OS). GSEA demonstrated that TMUB1 was related to hypoxia, angiogenesis, adipogenesis, inflammatory response, IL6-JAK-STAT3 signaling, apoptosis, mitotic spindle, and IL2-STAT5 signaling. The expression of TMUB1 negatively correlated with the abundance of T helper cells, Tcm cells, macrophages, and Th2 cells, whereas it positively correlated with the abundance of several immune cell types, including CD56bright and CD56dim NK cells. Conclusions: The high expression of TMUB1 is closely related to a poor prognosis in patients with CRC. TMUB1 may be a potential prognostic biomarker and be used for therapeutic approaches in CRC.

Influence of Superhydrophobic Coating on the Water Resistance of Foundry Dust/Magnesium Oxychloride Cement Composite.

In this work, magnesium oxychloride cement (MOC) was used to realize the resource use of foundry dust (FD). Portland cement (PC)-based superhydrophobic coating was prepared on the surface of FD/MOC composite to improve the water resistance of the composite. First, the FD/MOC composites with different contents of FD were prepared. The phase structure of the composite was analyzed using X-ray diffraction (XRD). The microstructure of the cross-section and surface of the composite was observed using field emission scanning electron microscope (FE-SEM). The mechanical properties of the FD/MOC composites with different FD contents at different ages were tested and analyzed. Secondly, the superhydrophobic coating was prepared on the surface of MOC composite using silane/siloxane aqueous emulsion as the hydrophobic modifier, PC as the matrix and water as the solvent. The microstructure and chemical composition of the PC-based superhydrophobic coating were tested and analyzed. The results show that FD can significantly improve the early strength of the FD/MOC composite. The 28-day compressive strength of the FD/MOC composite decreases with increasing FD content. When the FD content is 30%, the 28-day compressive strength of the FD/MOC composite is as high as 75.68 MPa. Superhydrophobic coating can effectively improve the water resistance of the FD/MOC composite. The softening coefficient of the FD/MOC composite without superhydrophobic coating is less than 0.26, while that of the composite modified by superhydrophobic coating is greater than 0.81.

Mechanical Properties of Natural Rubber Filled with Foundry Waste Derived Fillers.

The main aim of this study is to evaluate the possibility of applying foundry dust (FD) derived filler for the preparation of natural rubber (NR) based composites by characterizing the mechanical properties. The as-received FD was processed via a simple and low-cost procedure, including sieving, deironing and milling using a variety of industrial equipment. FD powders before and after silane coupling agent (Si 69) modification were used as fillers for NR. NR composites inserted with different content of modified and unmodified FD up to 50 phr were prepared via dry-mixing method. Then, comprehensive mechanical performances were performed on the corresponding vulcanizates. It was demonstrated that NR composite filled with 50 phr of modified FD exhibited optimized comprehensive mechanical performance. Tear strength and hardness is increased by 21.3% and 12.8% than pure NR, respectively. Tensile strength is reduced by 21% and elongation at break remained nearly unchanged. Additionally, the composite showed a large increment of 50.9% for its wet grip property, while exhibited an increment of only 11.9% for its rolling resistance in comparison with the composite containing 10 phr of FD. The findings of this study may provide a new application area for the large amounts of utilization of foundry waste with a high level of value being added.