Nanocrystal quantum dots (QDs) have been applied to molecular biology because of their greater and longer fluorescence. Here we report the potential cytotoxicity of our characterized QDs modified with various molecules. Surface modification of QDs changed their physicochemical properties. In addition, the cytotoxicity of QDs was dependent on their surface molecules. These results suggested that the properties of QDs are not related to those of QD-core materials but to molecules covering the surface of QDs.

., 48(12), [985][986][987][988][989][990][991][992][993][994] 2004 Abbreviations: MPA, 3-mercaptopropanoic acid; QD, quantum dot; TOPO, n-trioctylphosphine oxide.

Population pharmacokinetic parameters of vancomycin (VCM) in Japanese adult patients infected with methicillin-resistant Staphylococcus aureus (MRSA) were estimated using 1253 items of serum concentration data from 190 patients obtained in routine drug monitoring. The two-compartment linear model was adopted, and VCM clearance (CL) was correlated with the creatinine clearance (CLcr), which was observed or estimated by the Cockcroft-Gault equation. The population pharmacokinetic analysis program NONMEM with first-order conditional estimation method was used. The results showed VCM clearance to be linearly correlated with CLcr (CL [ml/min] = 0.797 x CLcr) when the estimated CLcr was <85 ml/min, but no linear relationship at higher than this level because of the lack of accuracy in the CLcr estimates. The interindividual variability of CL was 38.5%; K12 and K21 were 0.525 hr(-1) and 0.213 hr(-1), respectively. The distribution volume at steady state (V[SS]) was 60.71, with no significant dependence on the actual body weight. The interindividual variability of Vss was 25.4%. The calculated half-life (t1/2,beta) in a typical patient with CLcr of 85 ml/minute was 12.8 hours. Residual variability was 23.7%. These results were compared to those of healthy volunteers, and guidelines for dosage adjustment in VCM therapy are discussed.

Chemokines are characterized by the homing activity of leukocytes to targeted inflammation sites. Recent research indicates that chemokines play more divergent roles in various phases of pathogenesis as well as immune reactions. The chemokine receptor, CCR1, and its ligands are thought to be involved in inflammatory bone destruction, but their physiological roles in the bone metabolism in vivo have not yet been elucidated. In the present study, we investigated the roles of CCR1 in bone metabolism using CCR1-deficient mice. Chemokines are initially identified as small cytokines that direct the homing of circulating leukocytes into sites of inflammation (1). Chemokines are now recognized to be major factors in inflammation and immune development as well as tumor growth, angiogenesis, and osteolysis. Chemokine receptors are expressed in a well organized spatiotemporal manner in various types of leukocytes, including lymphocytes, granulocytes, and macrophages. They facilitate the recruitment of these cells into inflammatory sites during the appropriate phase of inflammation.Recent findings indicate that chemokine receptors, including CCR1 7 and its related chemokines, CCL3 and CCL9, are involved in the pathogenesis of a variety of diseases. In particular, CCL3 (also called MIP-1␣), a major pro-inflammatory chemokine produced at inflammatory sites, appears to play a crucial role in pathological osteoclastogenesis (2, 3). In osteolytic bone inflammation (e.g. rheumatoid arthritis-associated bone destruction), CCL3 induces ectopic osteoclastogenesis (4) * This work was supported in part by Grant H19-nano-012 from the Ministry of Health, Labor and Welfare (to K. Y.) and by a research fellowship from the Japan Society for the Promotion of Science for Young Scientists (2007Scientists ( -2009 ( The abbreviations used are: CCR, C-C chemokine receptor; M-CSF, macrophage-colony stimulation factor; BALP, bone-specific alkaline phosphatase; CCL, C-C chemokine ligand; MCP-1, macrophage chemoattractant protein-1; MIP-1, macrophage inflammatory protein-1; CT, computed tomography; PTX, pertussis toxin from Bordetella pertussis; RANK, receptor activator of NF-B; RANKL, receptor activator of NF-B ligand; RANTES, regulated upon activation normal T expression and secreted; TRAP, tartrate-resistant acid phosphatase; NTx, N-telopeptides.