Enhanced Adsorption-Photocatalytic Degradation of Organic Pollutants via a ZIF-67-Derived Co-N Codoped Carbon Matrix Catalyst.

Stable and efficient photocatalytic degradation of organic pollutants has been achieved via a ZIF-67-derived Co-embedded N-doped nanoporous carbon material catalyst (Co-N/C). The catalyst features a well-distributed structure, suitable specific surface area, and more active sites according to the various characterization analyses. The photocatalytic activity of Co-N/C was evaluated by the degradation of the target pollutant Rhodamine B (RhB). As a result, RhB could establish an adsorption-desorption equilibrium in the dark within 30 min and was thoroughly degraded into H2O and CO2 by Co-N/C under 500 W visible light irradiation in 40 min. Moreover, radical-quenching experiments and reactive oxygen species monitoring were performed to further probe the plausible photodegradation mechanism of RhB. Co-N/C is also appropriate for other alternative dyes and antibiotics affording ideal removal efficiencies. After the reaction, Co-N/C could be facilely separated by an external magnetic field and reused for eight reaction cycles without obvious deactivation of its photocatalytic properties. This study is expected to provide an instructive guideline for the design of efficient and recyclable composite photocatalysts derived from metal-organic frameworks for a broad range of environmental remediation processes.

miR-19 promotes development of renal fibrosis by targeting PTEN-mediated epithelial-mesenchymal transition.

In recent years, it has been found that miRNA may play an important role in the field of gene regulation; miRNAs can participate in the regulation of various physiologic processes such as cell differentiation, proliferation, apoptosis, metabolism, and insulin secretion by regulation of target genes. The purpose of this study is to observe the relationship between the expression of miR-19 and renal fibrosis, to analyze the regulatory effect of miR-19 on renal tubular EMT, and to reveal its role and working mechanism in renal fibrosis. We found that the expression of miR-19 was significantly increased in peripheral blood of patients with renal fibrosis, in renal tissue of unilateral ureteral occlusion (UUO) mice, and in NRK-52E cells treated with TGF-ß1. Overexpression of miR-19 could decrease the expression of E-cadherin and increase the expression of α-SMA and fibronectin, while inhibition of miR-19 reverses TGF-ß1-induced EMT. Further studies revealed that miR-19 could inhibit its expression by binding to the 3'-UTR of PTEN. MiR-19 inhibitor or Akt inhibitor blocks phospho-Akt by TGF-ß1, and Akt inhibitors block miR-19 mimic-induced EMT. In UUO mice, overexpression of miR-19 promoted the development of renal fibrosis, while inhibition of miR-19 expression produced the opposite result. These results indicate that abnormal expression of miR-19 is associated with renal fibrosis. Moreover, miR-19 activates the Akt signaling pathway by targeting PTEN, and induces EMT in renal tubular epithelial cells, thereby promoting renal fibrosis.

Discovery of novel pyrimidine-based benzothiazole derivatives as potent cyclin-dependent kinase 2 inhibitors with anticancer activity.

To develop novel CDK2 inhibitors as anticancer agents, a series of novel pyrimidine-based benzothiazole derivatives were designed and synthesized. Initial biological evaluation demonstrated some of target compounds displayed potent antitumor activity in vitro against five cancer cell lines. Especially, the analogue 10s exhibited approximately potency with AZD5438 toward four cells including HeLa, HCT116, PC-3, and MDA-MB-231 with IC50 values of 0.45, 0.70, 0.92, 1.80 µM, respectively. More interestingly, the most highly active compound 10s in this study also possessed promising CDK2/cyclin A2 inhibitory activities with IC50 values of 15.4 nM, which was almost 3-fold potent than positive control AZD5438, and molecular docking studies revealed that the analogue bound efficiently with the CDK2 binding site. Further studies indicated that compound 10s could induce cell cycle arrest and apoptosis in a concentration-dependent manner. These observations suggest that pyrimidine-benzothiazole hybrids represent a new class of CDK2 inhibitors and well worth further investigation aiming to generate potential anticancer agents.