Sleep disorder as a clinical risk factor of major depression: associated with cognitive impairment.

BACKGROUND: This research aims explored the sleep disorder (SD) role in major depressive disorder (MDD), and the SD influencing their cognition. METHODS: 372 MDD patients and 457 healthy controls (HCs) were enrolled. RESULTS: Patients increased a 38.88 times SD risk compared with HCs. In patients, visuospatial/constructional score was lower in SD than non-SD, and PSQI score was negatively associated with visuospatial/constructional score of SD. In SD and non-SD, RBANS scores were lower in MDD than HCs, excepted for visuospatial/constructional in non-SD. CONCLUSION: The SD as a MDD risk factor, has more serious visuospatial/constructional impairment alleviated via improving sleep/depression in patients.

Identification of hub genes associated with postmenopausal osteoporosis by Gibbs sampling method.

Underlying pivotal pathways were identified to reveal potential key genes correlated with postmenopausal osteoporosis (PMOP). The pathways were enriched by Kyoto Encyclopedia of Genes and Genomes (KEGG) with genes intersection greater than 5 based on gene expression profile data, and the acquired pathways were then transformed to Markov chain (MC). Gibbs sampling was conducted to obtain a new MC. Moreover, the average probabilities of each pathway in normal and PMOP were computed via an MC Monte Carlo (MCMC) algorithm, and differential pathways were identified based on probabilities more than 0.7. In addition, frequencies of appearance of pathway genes were counted via MCMC and the hub genes were achieved with the probabilities of gene expression efficiencies in two states. Judging by the gene intersection more than 5, overall 280 pathways were determined. After Gibbs sampling, 2 differential pathways were obtained on the basis of probabilities more than 0.7. Moreover, the hub genes comprising TNNC1, MYL2, and TTN were achieved according to probabilities more than 0.7. The identified pathways and the three hub genes probably are useful for developing approaches for the diagnosis and treatment of PMOP in future preclinical and clinical applications.

Theoretical study of Ni+ assisted C-C and C-H bond activations of propionaldehyde in the gas phase.

The reactions of Ni+ with propionaldehyde in the gas phase have been systematically investigated using density functional theory at the B3LYP/def2-TZVP level. The decomposition reaction mechanism has been identified. Our calculations indicated that Ni+ can assist decomposition of propionaldehyde to form Ni+CO and C2H6 through two types of reaction channel: C-C bond activation and C-H bond activation. In addition, charge decomposition analysis (CDA) was carried out to obtain a deeper understanding for orbital interaction of the initial complex. The bonding properties of the species involved were discussed by means of diverse analysis methods including electron localization function (ELF) and atoms in molecules (AIM).

Increased elimination of paclitaxel by magnesium isoglycyrrhizinate in epithelial ovarian cancer patients treated with paclitaxel plus cisplatin: a pilot clinical study.

Magnesium isoglycyrrhizinate (MI) has been complementarily used for restoring the hepatic impairments caused by taxol plus platinum based chemotherapies in China. Due to the hepatic dependence of paclitaxel elimination, this pilot clinical study aimed to investigate the influence of MI on the pharmacokinetics of paclitaxel in epithelial ovarian cancer patients. During the standard chemotherapy of intravenous paclitaxel (125 mg/m(2) infused over a 3-h period) and intraperitoneal cisplatin (60 mg/m(2)) for patients with FIGO stage II epithelial ovarian cancer, 9 each of total 18 patients were respectively treated with intravenous MI (100 mg) or vehicle control for 4 days. Plasma paclitaxel was analyzed by HPLC and the pharmacokinetic parameters were calculated with non-compartmental analysis. The hematological, hepatic and renal status was monitored before and 3 days after paclitaxel administration. It was observed the terminal t 1/2 and MRT of paclitaxel were significantly (p = 0.002 and 0.001) reduced by MI, respectively, from 11.0 ± 2.2 and 5.6 ± 1.0 h to 7.7 ± 1.7 and 4.0 ± 0.3 h. Hematological toxicity indicated by platelet count and hepatic events marked with ALT, AST and γ-GT were significant in both groups. In spite of the insignificance of decreased system exposure of paclitaxel and recovered hepatic function by MI, they did correlate with each other. It was therefore deduced that the liver toxicities of paclitaxel plus cisplatin chemotherapy potentially decrease hepatic elimination and increase system exposure of paclitaxel, and the recovery of liver function by MI helps to restore hepatic clearance of paclitaxel. The clinical significance of this pharmacokinetic interaction requires further studies with larger population size.