In this study, twenty-five yeast strains were isolated from soil samples collected in the gold mining ore in Gia Lai, Vietnam. Among them, one isolate named GL1 T could highly tolerate Cu 2+ up to 10 mM, and the isolates could also grow in a wide range of pH (3–7), and tem perature (10–40 ℃). Dried biomass of GL1 was able to remove Cu 2+ effectively up to 90.49% with a maximal biosorption capacity of 18.1 mg/g at pH 6, temperature 30 ℃, and incuba tion time 60 min. Sequence analysis of rDNA indicated this strain was closely related to Rhodotorula mucilaginosa but with 1.53 and 3.46% nucleotide differences in the D1/D2 domain of the 28S rRNA gene and the ITS1-5.8S rRNA gene-ITS2 region sequence, respect ively. Based on phylogenetic tree analysis and the biochemical characteristics, the strain appears to be a novel Rhodotorula species, and the name Rhodotorula aurum sp. nov. is pro posed. This study provides us with more information about heavy metal-tolerant yeasts and it may produce a new tool for environmental control and metal recovery operations.

Objective: To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia. Methods: The in vitro antiinflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The level of NO produced in the culture media was determined by Griess method. The iNOS and COX-2 protein expressions were analyzed by Western blot. The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. Mice mortality was monitored for 5 days after injection of LPS. The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques. Results: The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vivo models. The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions. In the septic shock model, ELA dose-dependently protected mice from LPS-induced mortality. Further study on the isolated components of ELA indicated that 9,10-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract. Conclusions: These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS, and COX-2 and protects mice from LPS-induced mortality in septic shock model.