Au, Ag, and Au/Ag colloidal nanoparticles coated with the J-aggregate of an anionic cyanine dye, 3,3′disulfopropyl-5,5′-dichlorothiacyanine sodium salt (TC), have been prepared for the first time. The absorption spectrum of TC-coated Au colloidal nanoparticles is not a simple sum of the contributions of colloidal gold and TC but is characterized by an evident absorption dip at the position corresponding to the J-band of TC. These spectral features are reproduced by the simulation based on the Maxwell-Garnett-type treatment of Gao et al. The alternate adsorption technique allowed us to deposit dye-coated Au/Ag composite nanoparticles at the surface of a cationic polymer, poly(diallyldimethylammonium chroride).

Avenanthramides are characteristic constituents of oat seeds. We analyzed the methanol extract of oat seeds by HPLC and detected three compounds 1, 2, and 3 eluted at retention times similar to avenanthramides. The three compounds were purified by column chromatography and HPLC. Spectroscopic analyses of 1, 2, and 3 suggested that they are amides of 4,5-dihydroxyanthranilic acid with caffeic, p-coumaric, and ferulic acids, respectively. Their identities were confirmed by comparing spectra and chromatographic behavior with compounds synthesized from 4,5-dihydroxyanthranilic acid and N-hyrdroxysuccinimide esters of hydroxycinnamic acids. LC-MS/MS analysis with multiple reaction monitoring showed that the amounts of 1, 2, and 3 were 16.5-26.9% of corresponding avenanthamides with 5-hydroxyanthranilic acid. Compounds 1, 2, and 3 showed stronger 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical-scavenging activity than the corresponding avenanthramides with 5-hydroxyanthranilic acid, indicating the involvement of 4,5-dihydroxyanthranilic acid moiety in the scavenging of DPPH radicals.

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Background-We reported that phospholipase C (PLC)-␦1 activity was enhanced 3-fold in patients with coronary spastic angina. We detected variant PLC-␦1 with replacement of arginine 257 by histidine (R257H) showing increased enzymatic activity. We tested the hypothesis that increased PLC-␦1 activity causes enhanced coronary vasomotility. Methods and Results-We generated transgenic (TG) mice with human R257H variant PLC-␦1 in vascular smooth muscle cells. PLC enzymatic activity in the coronary artery was increased by 2.57 and 1.89 times, respectively, in homozygous and heterozygous TG compared with wild-type (WT) mice. ST elevation after ergometrine occurred in 17 of 18 homozygous TG, 6 of 20 heterozygous TG, and 3 of 22 WT mice (PϽ0.01, homozygous TG versus WT; PϽ0.05, homozygous TG versus heterozygous TG; PϭNS, heterozygous TG versus WT). ST elevation was associated with bradyarrhythmias in homozygous TG mice. Focal coronary artery narrowing was documented with the microvascular filling technique in 3 of 5 homozygous TG mice after ergometrine but not in any of 7 WT mice (PϽ0.05). In the isolated Langendorff hearts, coronary perfusion pressure was increased after ergometrine in homozygous TG mice (PϽ0.01) but not in heterozygous TG or WT mice. Coronary perfusion pressure increase after prostaglandin F 2␣ was similar among homozygous TG, heterozygous TG, and WT mice. Cultured rat aortic smooth muscle cells transfected with variant PLC-␦1 showed a higher PLC activity than those with WT PLC-␦1 (PϽ0.05) and furthermore showed greater intracellular Ca 2ϩ response to acetylcholine in variant than in WT PLC-␦1 (PϽ0.05). Conclusions-Increased PLC-␦1 activity enhances coronary vasomotility such as that seen in patients with coronary spastic angina.

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