Removal Efficiency and Performance Optimization of Organic Pollutants in Wastewater Using New Biochar Composites

The purpose is to optimize the catalytic performance of biochar (BC), improve the removal effect of BC composites on organic pollutants in wastewater, and promote the recycling and sustainable utilization of water resources. Firstly, the various characteristics and preparation principles of new BC are discussed. Secondly, the types of organic pollutants in wastewater and their removal principles are discussed. Finally, based on the principle of removing organic pollutants, BC/zero valent iron (BC/ZVI) composite is designed, among which BC is mainly used for catalysis. The effect of BC/ZVI in removing tetracycline (TC) is comprehensively evaluated. The research results reveal that the TC removal effect of pure BC is not ideal, and that of ZVI is general. The BC/ZVI composite prepared by combining the two has a better removal effect on TC, with a removal amount of about 275 mg/g. Different TC concentrations, ethylene diamine tetraacetic acid (EDTA), pH environment, tert-butanol, and calcium ions will affect the TC removal effect of BC composites. The overall effect is the improvement of the TC removal amount of BC composites. It reveals that BC has a very suitable catalytic effect on ZVI, and the performance of BC composite material integrating BC catalyst and ZVI has been effectively improved, which can play a very suitable role in wastewater treatment. This exploration provides a technical reference for the effective removal of organic pollutants in wastewater and contributes to the development of water resource recycling

S-allylcysteine suppresses ovarian cancer cell proliferation by DNA methylation through DNMT1

Abstract Background The anti-tumor effects of S-allylcysteine (SAC), a water-soluble garlic derivative, on human ovarian cancer cells have been previous studied in vitro and in vivo models but the precise epigenetic molecular mechanisms are still unclear. This study aimed to investigate the epigenetic mechanism of SAC. Methods Human epithelial ovarian cancer cell line A2780 was selected. Cell proliferation and cell cycle was analyzed. DNA methylation, DNA methyltransferase (DNMT) activity, tumor suppressor gene expressions, as well as protein expression were analyzed. Results SAC could inhibit the proliferation of A2780 cells in dose- and time-dependent manners (the IC50 was 16.25 mmol/L and 5.25 mmol/L at 48 h and 72 h). Treatment of A2780 cells with SAC resulted in G1/S phase arrest. SAC treatment decreased global DNA methylation levels in A2780 cells in a dose-dependent manner. SAC decreased the levels of 5-methylcytosine, DNMT activity, messenger RNA (mRNA) and protein levels of DNMT1. Additionally, SAC treatment resulted in re-expression of the mRNA and proteins of silenced tumor suppressor gene CDKN1A accompany with reduced cell division control 2 expression. Conclusion Our data indicated the potential therapeutic effects of SAC on the human ovarian carcinoma cell line A2780 in vitro. The epigenetic mechanism of action of SAC may have important implications for epigenetic therapy

MFN2 deficiency affects calcium homeostasis in lung adenocarcinoma cells via downregulation of UCP4

Mitofusin‐2 (MFN2) is a transmembrane GTPase that regulates mitochondrial fusion and thereby modulates mitochondrial function. However, the role of MFN2 in lung adenocarcinoma remains controversial. Here, we investigated the effect of MFN2 regulation on mitochondria in lung adenocarcinoma. We found that MFN2 deficiency resulted in decreased UCP4 expression and mitochondrial dysfunction in A549 and H1975 cells. UCP4 overexpression restored ATP and intracellular calcium concentration, but not mtDNA copy number, mitochondrial membrane potential or reactive oxygen species level. Furthermore, mass spectrometry analysis identified 460 overlapping proteins after independent overexpression of MFN2 and UCP4; these proteins were significantly enriched in the cytoskeleton, energy production, and calponin homology (CH) domains. Moreover, the calcium signaling pathway was confirmed to be enriched in KEGG pathway analysis. We also found by protein–protein interaction network analysis that PINK1 may be a key regulator of MFN2‐ and UCP4‐mediated calcium homeostasis. Furthermore, PINK1 increased MFN2/UCP4‐mediated intracellular Ca2+ concentration in A549 and H1975 cells. Finally, we demonstrated that low expression levels of MFN2 and UCP4 in lung adenocarcinoma are associated with poor clinical prognosis. In conclusion, our data suggest not only a potential role of MFN2 and UCP4 in co‐regulating calcium homeostasis in lung adenocarcinoma but also their potential use as therapeutic targets in lung cancer

Dnmt3b Deficiency in Myf5+-Brown Fat Precursor Cells Promotes Obesity in Female Mice

Increasing energy expenditure through activation of brown fat thermogenesis is a promising therapeutic strategy for the treatment of obesity. Epigenetic regulation has emerged as a key player in regulating brown fat development and thermogenic program. Here, we aimed to study the role of DNA methyltransferase 3b (Dnmt3b), a DNA methyltransferase involved in de novo DNA methylation, in the regulation of brown fat function and energy homeostasis. We generated a genetic model with Dnmt3b deletion in brown fat-skeletal lineage precursor cells (3bKO mice) by crossing Dnmt3b-floxed (fl/fl) mice with Myf5-Cre mice. Female 3bKO mice are prone to diet-induced obesity, which is associated with decreased energy expenditure. Dnmt3b deficiency also impairs cold-induced thermogenic program in brown fat. Surprisingly, further RNA-seq analysis reveals a profound up-regulation of myogenic markers in brown fat of 3bKO mice, suggesting a myocyte-like remodeling in brown fat. Further motif enrichment and pyrosequencing analysis suggests myocyte enhancer factor 2C (Mef2c) as a mediator for the myogenic alteration in Dnmt3b-deficient brown fat, as indicated by decreased methylation at its promoter. Our data demonstrate that brown fat Dnmt3b is a key regulator of brown fat development, energy metabolism and obesity in female mice

New Insights into the Cellular Toxicity of Carbon Quantum Dots to Escherichia coli

In this study, the cytotoxicity and toxic mechanism of carbon quantum dots (CQDs) to E. coli were evaluated in vitro. The synthetic CQDs were extremely small in size (~2.08 nm) and displayed strong fluorescence. The results demonstrated that CQDs showed good biocompatibility with E. coli within a short culture time. However, when the exposure time exceeded 24 h, the toxicity of CQDs became apparent, and the contents of reactive oxygen species, lactate dehydrogenase, and the crystal violet absorption rate increased significantly. To further explore the cytotoxic mechanism, approaches including confocal laser scanning microscopy, scanning electron microscopy, and biological transmission electron microscopy combined with zeta potential tests, osmotic pressure measurement, and comet assays were performed. On the one hand, the CQDs altered the surface charges of cells and induced lipid peroxidation by adhesion on the surface of E. coli, leading to an increase in the permeability of the cell wall. On the other hand, when the concentration of CQDs reached 200 µg/mL, the osmotic pressure of the extracellular environment was significantly reduced. These are the main factors that lead to cell edema and death. Finally, the comet assays confirmed that CQDs could induce DNA damage, which could inhibit the proliferation of E. coli

Cytotoxic Effect of Graphene Oxide Nanoribbons on Escherichia coli

The biological and environmental toxicity of graphene and graphene derivatives have attracted great research interest due to their increasing applications. However, the cytotoxic mechanism is poorly understood. Here, we investigated the cytotoxic effect of graphene oxide nanoribbons (GORs) on Escherichia coli (E. coli) in an in vitro method. The fabricated GORs formed long ribbons, 200 nm wide. Based on the results of the MTT assay and plate-culture experiments, GORs significantly inhibited the growth and reproduction of E. coli in a concentration-dependent manner. We found that GORs stimulated E. coli to secrete reactive oxygen species, which then oxidized and damaged the bacterial cell membrane. Moreover, interaction between GORs and E. coli cytomembrane resulted in polysaccharide adsorption by GORs and the release of lactic dehydrogenase. Furthermore, GORs effectively depleted the metal ions as nutrients in the culture medium by adsorption. Notably, mechanical cutting by GORs was not obvious, which is quite different from the case of graphene oxide sheets to E. coli

The Hydrological Impact of Extreme Weather-Induced Forest Disturbances in a Tropical Experimental Watershed in South China

Tropical forests are frequently disturbed by extreme weather events including tropical cyclones and cold waves, which can not only yield direct impact on hydrological processes but also produce indirect effect on hydrology by disturbing growth and structures of tropical forests. However, the hydrological response to extreme weather-induced forest disturbances especially in tropical forested watersheds has been less evaluated. In this study, a tropical experimental watershed in Hainan Province, China, was selected to investigate the hydrological responses to extreme weather-induced forest disturbances by use of a single watershed approach and the paired-year approach. Key results are: (1) extreme weather-induced forest disturbances (e.g., typhoon and cold wave) generally had a positive effect on streamflow in the study watershed, while climate variability either yielded a negative effect or a positive effect in different periods; (2) the response of low flows to forest discussion was more pronounced; (3) the relative contribution of forest disturbances to annual streamflow (48.6%) was higher than that of climate variability (43.0%) from 1995 to 2005. Given the increasing extreme weather with climate change and their possible catastrophic effects on tropical forests and hydrology in recent decades, these findings are essential for future adaptive water resources and forest management in the tropical forested watersheds.Arts and Sciences, Irving K. Barber School of (Okanagan)Non UBCEarth, Environmental and Geographic Sciences, Department of (Okanagan)ReviewedFacult

Vegetation cover-another dominant factor in determining global water resources in forested regions

Forested catchments provide critically important water resources. Due to dramatic global forest change over the past decades, the importance of including forest or vegetation change in the assessment of water resources under climate change has been highly recognized by Intergovernmental Panelon Climate Change (IPCC); however, this importance has not yet been examined quantitatively across the globe. Here, we used four remote sensing-based indices to represent changes in vegetation cover in forest-dominated regions, and then applied them to widely used models: the Fuh model and the Choudhury-Yang model to assess relative contributions of vegetation and climate change to annual runoff variations from 2000 to 2011 in forested landscape (forest coverage >30%) across the globe. Our simulations show that the global average variation in annual runoff due to change in vegetation cover is 30.7% +/- 22.5% with the rest attributed to climate change. Large annual runoff variation in response to vegetation change is found in tropical and boreal forests due to greater forest losses. Our simulations also demonstrate both offsetting and additive effects of vegetation cover and climate in determining water resource change. We conclude that vegetation cover change must be included in any global models for assessing global water resource change under climate change in forest-dominant areas

Low-Dose Radiation Induces Cell Proliferation in Human Embryonic Lung Fibroblasts but not in Lung Cancer Cells

Hormesis and adaptive responses are 2 important biological effects of low-dose ionizing radiation (LDR). In normal tissue, LDR induces hormesis as evinced by increased cell proliferation; however, whether LDR also increases tumor cell proliferation needs to be investigated. In this study, cell proliferation was assayed by total cell numbers and the Cell Counting Kit 8 assay. Mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3′ -kinase( PI3K )- Akt (PI3K/AKT) phosphorylation were determined by Western blot analysis. Human embryonic lung fibroblast 2BS and lung cancer NCI-H446 cell lines were irradiated with LDR at different doses (20-100 mGy). In response to 20 to 75 mGy X-rays, cell proliferation was significantly increased in 2BS but not in NCI-H446 cells. In 2BS cells, LDR at 20 to 75 mGy also stimulated phosphorylation of MAPK/ERK pathway proteins including ERK, MEK, and Raf and of the PI3K/AKT pathway protein AKT. To test whether ERK1/2 and AKT pathway activation was involved in the stimulation of cell proliferation in 2BS cells, the MAPK/ERK and PI3K/AKT pathways were inhibited using their specific inhibitors, U0126 and LY294002. U0126 decreased the phosphorylation of ERK1/2, and LY294002 decreased the phosphorylation of AKT; each could significantly inhibit LDR-induced 2BS cell proliferation. However, LDR did not stimulate these kinases, and kinase inhibitors also did not affect cell proliferation in the NCI-H446 cells. These results suggest that LDR stimulates cell proliferation via the activation of both MAPK/ERK and PI3K/AKT signaling pathways in 2BS but not in NCI-H446 cells. This finding implies the potential for applying LDR to protect normal tissues from radiotherapy without diminishing the efficacy of tumor therapy