Adsorption properties and mechanism of ginkgo biloba leaf-based materials for Cd (II) in aqueous solution.

The cheap and efficient heavy metal adsorbents were developed with the forestry and agricultural residues. In this study, three kinds of adsorbents, original ginkgo leaf (GL), NaOH modified ginkgo leaf (NaOH-GL), and KMnO4-modified ginkgo leaf (KMnO4-GL), were prepared and used to adsorb Cd (II) in aqueous solution respectively. The effects of the concentration of Cd (II), absorption time, the dosage of absorbent, and pH of solution on the adsorption process were explored by adsorption experiments. The results showed that the maximum adsorption capacity of Cd (II) by GL, NaOH-GL, and KMnO4-GL was 10.20 mg/g, 39.99 mg/g, and 48.82 mg/g, respectively, under the conditions of room temperature, adsorbent dosage 1g/L, adsorption time 300 min, and pH 6.0. The adsorption of Cd (II) by the three adsorbents accorded with the pseudo-second-order kinetic model and Langmuir isothermal adsorption model, which indicated that the rate-limiting step in the adsorption process was chemical adsorption process and mainly monolayer adsorption. The reason why NaOH-GL and KMnO4-GL could effectively adsorb Cd (II) was that the surface of the modified adsorbent was rough and porous, the number of active groups on the surface increased, and Na and Mn elements could promote the precipitation of Cd (II). The mechanism analysis of KMnO4-GL, which had the best adsorption effect, showed that the adsorption mechanism of Cd (II) might be surface adsorption, ion exchange, and complexing precipitation.

Targeting autophagy is a promising therapeutic strategy to overcome chemoresistance and reduce metastasis in osteosarcoma.

Osteosarcoma (OS) is the most common primary bone malignancy, mainly affecting children and adolescents. Currently, surgical resection combined with adjuvant chemotherapy has been standardized for OS treatment. Despite great advances in chemotherapy for OS, its clinical prognosis remains far from satisfactory; this is due to chemoresistance, which has become a major obstacle to improving OS treatment. Autophagy, a catabolic process through which cells eliminate and recycle their own damaged proteins and organelles to provide energy, can be activated by chemotherapeutic drugs. Accumulating evidence has indicated that autophagy plays the dual role in the regulation of OS chemoresistance by either promoting drug resistance or increasing drug sensitivity. The aim of the present review was to demonstrate thatautophagy has both a cytoprotective and an autophagic cell death function in OS chemoresistance. In addition, methods to detect autophagy, autophagy inducers and inhibitors, as well as autophagy­mediated metastasis, immunotherapy and clinical prognosis are also discussed.