The present study was performed to evaluate the effect of steaming ginseng at a temperature over 100 degrees C on its chemical constituents and biological activities. Raw ginseng was steamed at 100, 110, and 120 degrees C for 2 h using an autoclave. The ginseng steamed at 120 degrees C was more potent in its ability to induce endothelium-dependent relaxation. Steaming the raw ginseng at 120 degrees C also remarkably increased the radical-scavenging activity. Ginsenosides F(4), Rg(3), and Rg(5), which were not present in raw ginseng, were produced after steaming. Ginsenosides Rg(3) and Rg(5) were the most abundant ginsenosides in the ginseng steamed at 120 degrees C, accounting for 39% and 19% of all ginsenosides, respectively.

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Our Slc4a11 KO mouse model successfully represents clinical manifestations of human CHED. We were able to show chronological corneal progression for the first time in a knockout mouse model as well as renal abnormalities.

Intravenous (i.v.) busulfan can produce a more consistent pharmacokinetic profile than oral formulations can, but nonetheless, significant interpatient variability is evident. We investigated the influence of polymorphisms of 3 GST isozyme genes (GSTA1, GSTM1, and GSTT1) on i.v. busulfan clearance. Fifty-eight adult patients who received 3.2 mg/kg/day of busulfan as conditioning for hematopoietic cell transplantation were included in this study. Stepwise multiple linear regression demonstrated that GSTA1 variant GSTA1∗B (P = .004), GSTM1/GSTT1 double-null genotype (P = .039), and actual body weight (P = .001) were significantly associated with lower clearance of i.v. busulfan. A trend test analyzing the overall effect of GST genotype on busulfan pharmacokinetics, combining GSTA1 gene polymorphism and the number of GSTM1- and GSTT-null genotypes, showed a significant correlation between GST genotype and busulfan clearance (P = .001). The clearance of i.v. busulfan was similar between patients with GSTA1∗A/∗A and GSTM1/GSTT1 double-null genotypes and those with GSTA1∗A/∗B and GSTM1/GSTT1 double-positive genotypes. In conclusion, a pharmacogenetic approach using GST gene polymorphisms may be valuable in optimizing the i.v. busulfan dosage scheme. Our results also highlight the importance of including polygenic analyses and addressing interactions among isozyme genes in pharmacogenetic studies.