YTHDC2 Retards Cell Proliferation and Triggers Apoptosis in Papillary Thyroid Cancer by Regulating CYLD-Mediated Inactivation of Akt Signaling.

N6-Methyladenosine (m6A) mRNA methylation modification is regarded as an important mechanism involved in diverse physiological processes. YT521-B homology (YTH) domain family members are associated with the tumorigenesis of several cancers. However, the role of YTHDC2 in papillary thyroid cancer (PTC) progression remains unknown. Results showed that YTHDC1, YTHDF1, YTHDF2, and YTHDF3 showed no observable difference in thyroid cancer samples. YTHDC2 was significantly downregulated in thyroid cancer samples and cells. YTHDC2 inhibited cell proliferation in PTC cells. YTHDC2 elicited apoptosis in PTC cells, as demonstrated by the elevated expression of pro-apoptotic factors cl-caspase-3/caspase-3 and Bcl-2-associated (Bax), and the reduced anti-apoptotic B cell lymphoma-2 (Bcl-2) expression. There was a positive correlation between YTHDC2 and cylindromatosis (CYLD) expression based on GEPIA database. YTHDC2 increased CYLD expression in PTC cells. CYLD knockdown abolished the effects of YTHDC2 on PTC cell proliferation and apoptosis. Additionally, YTHDC2 inactivated the protein kinase B (Akt) pathway by increasing CYLD in PTC cells. Overall, YTHDC2 inhibited cell proliferation and induced apoptosis in PTC cells by regulating CYLD-mediated inactivation of Akt pathway.

Iron-nitrogen co-doped carbon nanotubes decorated with Cu2O possess enhanced electronic properties for effective peroxymonosulfate activation.

Exploiting the full potential of copper-based nanoparticles in the activation of peroxymonopersulfate (PMS) is a great challenge due to their insufficient dispersity and electronic properties. We report here a novel iron­nitrogen co-doped carbon nanotube (FNC) modified with a Cu2O nanocomposite (Cu2O/FNC) that exhibits ultrahigh catalytic performance in the activation of PMS to degrade fluconazole (~95%). Catalytic performance evaluation illustrated that Cu2O/FNC also has wide pH applicability (3.0-11.0), long-term stability and excellent adaptability. In addition, luminescent bacteria toxicity tests confirm that Cu2O/FNC/PMS significantly reduced the acute biotoxicity of various recalcitrant pollutants (reduced by 45-83%). By identifying the reactive oxygen species (ROS) and catalytic performance for various pollutants, we propose that pollutants that interact weekly with activators are mostly destroyed by sulfate radicals and hydroxyl radicals, whilst both radical and non-radical routes were involved in the degradation of pollutants that were easily adsorbed. By modifying Cu2O with FNC, several crucial properties such as the specific surface area, surface defects, active sites and the charge transfer rate were significantly improved, leading to excellent catalytic performance for pollutant removal. Finally, a reasonable reaction mechanism is advanced for the fluconazole degradation pathway. This study not only develops a novel PMS oxidation system for fluconazole degradation, but also provides a new strategy to improve the reactivity and applicability of PMS activators by combining radical and non-radical activation pathways.

Biological Sulfur Reduction To Generate H2S As a Reducing Agent To Achieve Simultaneous Catalytic Removal of SO2 and NO and Sulfur Recovery from Flue Gas.

The conventional flue gas treatment technologies require high capital investments and chemical costs, which limit their application in industrial sectors. This study developed a sulfur-cycling technology to integrate sulfide production by biological sulfur reduction and simultaneous catalytic desulfurization and denitrification with H2S (H2S-SCDD) for flue gas treatment and sulfur recovery. In a packed bed reactor, high-rate sulfide production (1.63 ± 0.16 kg S/m3-d) from biological sulfur reduction was achieved using organics in wastewater as electron donors at pH around 5.8. 93% of sulfide in wastewater was stripped out as H2Sg, which can be a low-cost reducing agent in the H2S-SCDD process. Over 90% of both SO2 and NO were removed by the H2S-SCDD process under the test conditions, resulting in the formation of sulfur. 88% of the input S (H2Sg and SO2) were recovered as octasulfur with high purity. Besides partial recycling to produce biogenic sulfide, excessive sulfur can be obtained as a sellable product. The integrated sulfur-cycling technology is a chemical-saving and even profitable solution to the flue gas treatment in industrial sectors with wastewater available.

Endometrial regenerative cells as a novel cell therapy attenuate experimental colitis in mice.

BACKGROUND: Endometrial regenerative cells (ERCs) are mesenchymal-like stem cells that can be non-invasively obtained from menstrual blood and are easily grown /generated at a large scale without tumorigenesis. We previously reported that ERCs exhibit unique immunoregulatory properties in vitro, however their immunosuppressive potential in protecting the colon from colitis has not been investigated. The present study was undertaken to determine the efficacy of ERCs in mediating immunomodulatory functions against colitis. METHODS: Colitis was induced by 4% dextran-sulfate-sodium (DSS, in drinking water) in BALB/c mice for 7 days. ERCs were cultured from healthy female menstrual blood, and injected (1 million/mouse/day, i.v.) into mice on days 2, 5, and 8 following colitis induction. Colonic and splenic tissues were collected on day 14 post-DSS-induction. Clinical signs, disease activity index (DAI), pathological and immunohistological changes, cytokine profiles and cell populations were evaluated. RESULTS: DSS-induced mice in untreated group developed severe colitis, characterized by body-weight loss, bloody stool, diarrhea, mucosal ulceration and colon shortening, as well as pathological changes of intra-colon cell infiltrations of neutrophils and Mac-1 positive cells. Notably, ERCs attenuated colitis with significantly reduced DAI, decreased levels of intra-colon IL-2 and TNF-α, but increased expressions of IL-4 and IL-10. Compared with those of untreated colitis mice, splenic dendritic cells isolated from ERC-treated mice exhibited significantly decreased MHC-II expression. ERC-treated mice also demonstrated much less CD3(+)CD25(+) active T cell and CD3(+)CD8(+) T cell population and significantly higher level of CD4(+)CD25(+)Foxp3(+) Treg cells. CONCLUSIONS: This study demonstrated novel anti-inflammatory and immunosuppressive effects of ERCs in attenuating colitis in mice, and suggested that the unique features of ERCs make them a promising therapeutic tool for the treatment of ulcerative colitis.