Search

In recent years, with the development of the global economy, water pollution has increased. Pollutants migrate, accumulate, and diffuse in aquatic environments. Most of the pollutants eventually enter aquatic organisms. The accumulation of pollutants affects the development and reproduction of organisms, and many pollutants have teratogenic, carcinogenic, and/or mutagenic effects. Aquatic organisms in estuaries and coastal areas are under pressure due to both salinity and pollutants. Among them, salinity, as an environmental factor, may affect the behavior of pollutants in the aquatic environment, causing changes in their toxic effects on fishes. Salinity also directly affects the growth and development of fishes. Therefore, this paper focuses on metals and organic pollutants and discusses the toxic effects of pollutants on fish under different salinities. This research is of great significance to environmental protection and ecological risk assessment of aquatic environments.

Environmental sciences Europe : ESEU 34, 78 (2022). doi:10.1186/s12302-022-00661-9, Published by Springer, Berlin ; Heidelberg

A composite Mn-Cu-Ce tri-metal oxide supported on γ-Al2O3 (Mn-Cu-Ce/Al2O3) catalyst was prepared by an impregnation-calcination method and investigated in the catalytic ozonation treatment of real coal chemical wastewater (CCW). The catalyst was characterized by XRD, SEM, TEM, XRF, BET, and XPS techniques. The results showed that Mn, Cu, and Ce metal oxides were evenly distributed on the Al2O3 surface and the catalyst maintained a large surface area and a high pore volume compared with the pristine Al2O3. The synergy between Mn, Cu, and Ce oxides greatly enriched the catalytic active sites and enhanced the ozonation performance. The catalytic ozonation process with Mn-Cu-Ce/Al2O3 increased the removal rate of total organic carbon (TOC) by 31.6% compared with ozonation alone. The ketones, aromatic compounds, phenols, and nitrogen-containing heterocyclic compounds in CCW have been effectively degraded and mineralized by Mn-Cu-Ce/Al2O3 catalytic ozonation process, and its biodegradability has also been significantly improved. The experimental results of ∙OH scavengers revealed that the mechanism of Mn-Cu-Ce/Al2O3 catalytic ozonation was to promote the generation of ∙OH radicals. The catalytic activity of Mn-Cu-Ce/Al2O3 was only a slight decrease in six consecutive catalytic ozonation treatments, showing good stability. Therefore, Mn-Cu-Ce/Al2O3 can be used as a candidate catalyst for the advanced treatment of refractory organic wastewaters upon catalytic ozonation.

Ring finger protein 144A (RNF144A), a poorly characterized member of the RING-in-between-RING family of E3 ubiquitin ligases, is an emerging tumor suppressor, but its underlying mechanism remains largely elusive. To address this issue, we used Affymetrix GeneChip Human Transcriptome Array 2.0 to profile gene expression in MDA-MB-231 cells stably expressing empty vector pCDH and Flag-RNF144A, and found that 128 genes were differentially expressed between pCDH- and RNF144A-expressing cells with fold change over 1.5. We further demonstrated that RNF144A negatively regulated the protein and mRNA levels of glial maturation factor γ (GMFG). Mechanistical investigations revealed that transcription factor YY1 transcriptionally activated GMFG expression, and RNF144A interacted with YY1 and promoted its ubiquitination-dependent degradation, thus blocking YY1-induced GMFG expression. Functional rescue assays showed that ectopic expression of RNF144A suppressed the proliferative, migratory, and invasive potential of breast cancer cells, and the noted effects were partially restored by re-expression of GMFG in RNF144A-overexpressing breast cancer cells. Collectively, these findings reveal that RNF144A negatively regulates GMFG expression by targeting YY1 for proteasomal degradation, thus inhibiting the proliferation, migration, and invasion of breast cancer cells.

Prior research on the effects of personality on depression has focused heavily on the Five Factor Model (FFM). However, the FFM has recently been criticized for that it does not capture the “dark side” of personality. To address this research gap, a field study consisting of two waves of survey was conducted to explore the relationships between the Dark Triad (DT) personality traits and depressive symptoms. Results of a path analysis on data collected from a sample of 228 full-time employees from diverse industries in Taiwan showed that Machiavellianism and psychopathy were positively associated with the interpersonal and cognitive dimensions of depressive symptoms, respectively. Narcissism was found to be the strongest predictor of depressive symptoms among the DT traits — It was found to be associated with all four dimensions of depressive symptoms and the relationships were all negative. Overall, these findings provide evidences for the effects of the dark side personality traits on depression, while the pattern of relationships between each DT trait and depressive symptoms were different.

In this study, the hypothesis that Wnt/β-catenin pathway is involved in the arterial calcification by regulating the osteoprotegerin (OPG)/receptor activator of NF-κB ligand (RANKL) system was tested. The β-catenin expression was measured in the warfarin-induced calcified arteries and the osteoblast-like cells differentiating from smooth muscle cells (SMCs) by immunohistochemistry and Western blotting. The Wnt/β-catenin pathway was activated or inhibited by lithium chloride (LiCl) or dickkopf 1 (DKK1) in vitro and in vivo. Then the calcification level was determined by von Kossa staining, Ca2+ content assay, and alkaline phosphatase (ALP) activity assay. The expression levels of osteocalcin, OPG and RANKL were detected by Western blotting or real-time PCR. The results showed that in calcified arteries and OBL cells, the activation of Wnt/β-catenin pathway significantly enhanced the calcification as evidenced by increased von Kossa stains, Ca2+ contents, ALP activities, and osteocalcin expression levels (P

Breast cancer is ranked as the second leading cause of cancer-related deaths among women. Accumulating evidences have revealed that long non-coding RNAs (lncRNAs) are involved in human tumorigenesis owing to the regulation of essential pathways for tumor initiation and progression. Herein, the current study aimed to explore the regulatory mechanism of lncRNA ZFHX4-AS1 in breast cancer in relation to the Hippo signaling pathway. Initially, microarray analysis was conducted to screen out differentially expressed lncRNAs related to breast cancer. Next, the functional role of lncRNA ZFHX4-AS1 in breast cancer was determined using ectopic expression, knockdown, and reporter assay experiments. Subsequently, lncRNA ZFHX4-AS1, TAF4, TAZ, and YAP expressions were determined, followed by verification of the targeting relationship between lncRNA ZFHX4-AS1 and TAF4. Then cell proliferation, invasion, migration, cell cycle, and apoptosis were measured. Lastly, tumor growth and metastasis were detected by tumor xenograft in nude mice. LncRNA ZFHX4-AS1 was found to be highly expressed while FAT4 was poorly expressed in breast cancer tissues. FAT4 was the target gene of lncRNA ZFHX4-AS1, and lncRNA ZFHX4-AS1 silencing increased FAT4 expressions, while decreased YAP and TAZ expressions. In addition, knockdown of lncRNA ZFHX4-AS1 suppressed breast cancer cell proliferation, migration, and invasion as well as tumor growth, blocked cell cycle entry, while promoted cell apoptosis by inhibiting the Hippo signaling pathway. In conclusion, our findings reveal that lncRNA ZFHX4-AS1 silencing exerts an inhibitory effect on breast cancer development by suppressing the activation of the Hippo signaling pathway via FAT4.

Background In order to mitigate the risk of allele dropout (ADO) and ensure the accuracy of preimplantation genetic testing for monogenic disease (PGT-M), it is necessary to construct parental haplotypes. Typically, haplotype resolution is obtained by genotyping multiple polymorphic markers in both parents and a proband or a relative. Sometimes, single sperm typing, or tests on the polar bodies may also be useful. Nevertheless, this process is time-consuming. At present, there was no simple linkage analysis strategy for patients without affected relatives. Method To solve this problem, we established a haplotyping by linked-read sequencing (HLRS) method without the requirement for additional relatives. First, the haplotype of the genetic disease carriers in the family was constructed by linked-read sequencing, and then the informative single nucleotide polymorphisms (SNPs) in upstream and downstream mutation region were selected to construct the embryo haplotype and to determine whether the embryo was carrying the mutation. Two families were selected to validate this method; one with alpha thalassemia and the other with NDP gene disorder. Results The haplotyping by linked-read sequencing (HLRS) method was successfully applied to construct parental haplotypes without recruiting additional family members; the method was also validated for PGT-M. The mutation carriers in these families were sequenced by linked-read sequencing, and their haplotypes were successfully phased. Adjacent SNPs of the mutation gene were identified. The informative SNPs were chosen for linkage analyses to identify the carrier embryos. For the alpha thalassemia family, a normal blastocyst was transferred to the uterus and the accuracy of PGT-M was confirmed by amniocentesis at 16 weeks of gestation. Conclusions Our results suggest that HLRS can be applied for PGT-M of monogenic disorders or de novo mutations where the mutations haplotype cannot be determined due to absence of affected relatives.