[Periodontal status assessment before orthodontic treatment and opportune moment selection for orthodontic treatment].

The aesthetic demands of teeth by the public have improved with the increase in the living standard. Orthodontics, which is a method of aesthetic dentistry, is becoming increasingly important. Orthodontic treatment mainly involves the application of orthodontic force to the teeth and guides the reconstruction of the periodontal tissue, thereby changing the position of the teeth at the occlusal bone. Orthodontic treatment can also improve the dental occlusion caused by dentition crowding and teeth mobility to achieve long-term stability of periodontal tissue. The number of patients with periodontal disease is high in China, and the number of patients with periodontal disease that are eager to receive orthodontic treatment is increasing. Hence, the periodontal status during the orthodontic therapy should be explored along with periodontal therapy and orthodontic treatment. This article briefly demonstrates the assessment criteria of periodontal status before orthodontic treatment, the opportune moment selection for orthodontic treatment, and the supportive periodontal therapy. This study helps dentists develop individualized treatment programs and win a balanced, stable, and aesthetic impression.

A ß-carboline derivative-based nickel(ii) complex as a potential antitumor agent: synthesis, characterization, and cytotoxicity.

A novel nickel(ii) complex of 6-methoxy-1-pyridine-ß-carboline (4a) was synthesized and characterized. The cytotoxicities of the complex towards six cancer cell lines, including MGC-803, Hep G2, T24, OS-RC-2, NCI-H460, and SK-OV-3, and human normal liver cell line HL-7702 were investigated. The IC50 values for MGC-803, Hep G2, T24, OS-RC-2, NCI-H460 and SK-OV-3 were generally in the micromolar range (3.77-15.10 µM), lower than those of ligand 4 and cisplatin. Furthermore, 4a (6 µM) significantly induced cell cycle arrest at the S phase, and caused the down-regulation of p-AKT, cyclin E, cyclin A and CDK2 and the up-regulation of p27. Various experiments showed that 4a induced apoptosis, activated caspase-3, increased the levels of reactive oxygen species (ROS) and enhanced the intracellular [Ca2+]c levels in MGC-803. In addition, the expression of intrinsic apoptotic proteins, including cytochrome c and apaf-1, increased. Further intrinsic apoptosis was triggered via executive molecular caspase-9 and caspase-3. In short, 4a exerted its cytotoxic activity primarily through inducing cell cycle arrest at the S phase and intrinsic apoptosis.

Preparation of Rhodium(III) complexes with 2(1H)-quinolinone derivatives and evaluation of their in vitro and in vivo antitumor activity.

A series of 2(1H)-quinolinone derivatives and their rhodium (III) complexes were designed and synthesized. All the rhodium (III) complexes exhibited higher in vitro cytotoxicity for Hep G2, HeLa 229, MGC80-3, and NCI-H460 human tumor cell lines than their ligands and cisplatin, and among them complex 9 was found to be selectively cytotoxic to tumor cells. Further investigation revealed that complex 9 caused cell cycle arrest at the G2/M phase and induced apoptosis, and inhibited the proliferation of Hep G2 cells by impeding the phosphorylation of epidermal growth factor receptor (EGFR) and its downstream enzymes. Complex 9 also up-regulated the proapoptotic proteins Bak, Bax, and Bim, which altogether activated caspase-3/9 to initiate cell apoptosis. Notably, complex 9 effectively inhibited tumor growth in the NCI-H460 xenograft mouse model with less adverse effect than cisplatin.