Efficient and recyclable sericin-derived carbon aerogel for oils and organic solvents adsorption.

Sericin, an industrial waste of the silk industry, is a promising precursor for adsorbent preparation. In this work, an efficient and novel sericin-derived carbon aerogel (SCA) was used to improve the adsorption efficiency of oils and organic solvents. The SCA demonstrated a high-efficiency sorption capacity of not only soybean oil (adsorption capacity reached up to 167.69 times its weight) but also chloroform and methylene chloride (adsorption capacity of 193.67 g/g and 173.25 g/g respectively). It is observed that SCA could be regenerated multiple times through combustion and after five cycles, its adsorbability to ethanol, dimethyl sulfoxide, and soybean oil remained high at 59.08 g/g, 59.34 g/g, and 137.36 g/g, respectively. The physical and chemical characteristics of sericin and SCA were analyzed using Scanning electron microscopy (SEM), Brunauer-Emmett-Teller (BET), X-ray diffraction (XRD), Raman spectra and Fourier transform infrared spectroscopy (FTIR) analysis. The results suggest that SCA is an adsorbent with excellent properties and can significantly increase the adsorption capacity of oils and organic solvents. The overall results indicate that SCA is effectively used as an adsorbent for the adsorption of oils and organic solvents, which will contribute to reduce the discharge of sericin-containing wastewater and alleviate pollution caused by oil and organic solvent leakage.

TIPE3 is a regulator of cell apoptosis in glioblastoma.

Tumor necrosis factor alpha-induced protein 8-like 3 (TIPE3) is closely related to tumourigenesis and development. However, its role in human glioblastoma (GBM) and the underlying mechanisms remain unclear. In this study, we demonstrate that TIPE3 is upregulated in GBM, and its high expression predicts poor prognosis. TIPE3 depletion induces GBM cell apoptosis both in vitro and in vivo. Mechanism studies reveal that TIPE3 inhibits p38 phosphorylation and negatively regulates the p38 MAPK pathway. TIPE3 associates with p38. The nuclear translocation of p38 is blocked by TIPE3 overexpression. And p38 phosphorylation could regulate TIPE3-mediated p38 nuclear-cytopalsmic translocation but does not affect TIPE3-p38 association. Rescue experiments confirm that TIPE3 inhibits GBM cell apoptosis via the p38 MAPK pathway. In conclusion, TIPE3 inhibits p38 phosphorylation and blocks p38 nuclear translocation. This action thus negatively regulates the p38 MAPK pathway and results in GBM cell survival.