Integrated urban water management by coupling iron salt production and application with biogas upgrading.

Integrated urban water management is a well-accepted concept for managing urban water. It requires efficient and integrated technological solutions that enable system-wide gains via a whole-of-system approach. Here, we create a solid link between the manufacturing of an iron salt, its application in an urban water system, and high-quality bioenergy recovery from wastewater. An iron-oxidising electrochemical cell is used to remove CO2 (also H2S and NH3) from biogas, thus achieving biogas upgrading, and simultaneously producing FeCO3. The subsequent dose of the electrochemically produced FeCO3 to wastewater and sludge removes sulfide and phosphate, and enhances sludge settleability and dewaterability, with comparable or superior performance compared to the imported and hazardous iron salts it substitutes (FeCl2, and FeCl3). The process enables water utilities to establish a self-reliant and more secure supply chain to meet its demand for iron salts, at lower economic and environmental costs, and simultaneously achieve recovery of high-quality bioenergy.

UBE2O ubiquitinates PTRF/CAVIN1 and inhibits the secretion of exosome-related PTRF/CAVIN1.

BACKGROUND: Exosomes are small vesicles released by cells, which have crucial functions in intercellular communication. Exosomes originated from cell membrane invagination and are released followed by multivesicular bodies (MVBs) fused with the cell membrane. It is known that Polymerase I and Transcript Release Factor (PTRF, also known as Caveolin-associated Protein-1, CAVIN1) plays an important role in caveolae formation and exosome secretion. And PTRF in exosomes has been identified as a potential biomarker in multiple malignancies such as glioma and renal cell carcinoma. However, the mechanisms of how to regulate the secretion of exosome-related PTRF remain unknown. METHODS: We performed exogenous and endogenous immunoprecipitation assays to investigate the interaction between ubiquitin-conjugating enzyme E2O (UBE2O) and PTRF. We identified UBE2O ubiquitinated PTRF using ubiquitination assays. Then, exosomes were isolated by ultracentrifugation and identified by transmission electronic microscopy, western blot and nanoparticle tracking analysis. The effect of UBE2O on the secretion of exosome-related PTRF was analyzed by western blot, and the effect of UBE2O on exosome secretion was evaluated by exosome markers and the total protein content of exosomes. RESULTS: Here, we showed that UBE2O interacts with PTRF directly and ubiquitinates PTRF. Functionally, we found that UBE2O inhibited the effects of PTRF on exosome secretion via decreasing caveolae formation. Importantly, UBE2O decreased exosome secretion, resulting in downregulating PTRF secretion via exosomes. Our study also identified Serum Deprivation Protein Response (SDPR, also known as Caveolin-associated Protein-2, CAVIN2) interacted with both UBE2O and PTRF. Furthermore, we found that SDPR promotes PTRF expression in exosomes. Interestingly, even in the presence of SDPR, UBE2O still inhibited the secretion of exosome-related PTRF. CONCLUSIONS: Our study demonstrated that UBE2O downregulated exosome release and controlled the secretion of exosome-related PTRF through ubiquitinating PTRF. Since exosomes play an important role in malignant tumor growth and PTRF included in exosomes is a biomarker for several malignant tumors, increasing UBE2O expression in cells has the potential to be developed as a novel approach for cancer treatment. Video Abstract.

Impact of reactive iron in coal mine dust on oxidant generation and epithelial lung cell viability.

Coal workers' pneumoconiosis (CWP) is a preventable occupational lung disease caused by the chronic inhalation of coal mine dust. The inhalation of coal mine dusts can result in the development of a range of lung diseases termed coal mine dust lung diseases, which is not limited to CWP and includes silicosis, bronchitis, emphysema and cancer. For decades, the presence of elemental Fe, C and Si has been proposed to be the causal factors underlying CWP. The recent resurgence of CWP globally with examination of cases in the United States suggesting a potential but inconclusive role of Fe(II)-sulfide minerals. To obtain a better understanding of Australian coals, the existence and potential adverse impacts of iron minerals were examined using 24 representative Australian coal samples. The results of this work revealed that reduced iron minerals were widely distributed within samples obtained from Australian coal mines with pyrite and siderite being particularly abundant. Compared with carbon and crystalline silica, the presence of these specific iron minerals were negatively correlated to the viability of both alveolar macrophages (NR8383) and human lung epithelial cells (A549) (R2 = 0.689) under scenarios reflecting biologically-relevant inflammatory response conditions. Further analysis using Welch's unpaired t-test indicated that the presence of reduced iron minerals statistically enhanced acellular oxidant production (90% CI [0.74 to 2.55]) and inflammatory response (90% CI [0.15 to 36.96]). Compared with Fe(II)-hydroxide, Fe(II)- and Fe(III)-(phyllo)silicate and Fe(II)-sulfate mineralogies, pyrite and siderite bearing dusts are likely to have greater adverse impacts on epithelial lung cells under inflammatory response conditions in view of both their iron content and reactivity.

Establishment of a congenital tooth agenesis related gene MSX1 knockout human embryonic stem cell lines by CRISPR-Cas9 technology.

Human MSX1 gene is mapped to chromosome 4 and encodes a 303aa homeobox protein MSX1. MSX1 expression appears during early tooth development of vertebrate embryogenesis. Mutations in this protein are related to human tooth anomalie, cleft lip and palate and congenital ectodermal dysplasia syndrome. Most of the confirmed pathogenic mutations are located in exon2 encoded homeobox domain. Here, we report the establishment of MSX1 gene knockout human embryonic stem (hES) cell lines by CRISPR-Cas9 technology. These cell lines provide good materials for further studies of the roles MSX1 plays in human tooth development and congenital tooth agenesis.