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Polarized ethylenes having both electron‐donating (an amino or a methylthio group) and electron‐accepting (cyano, carbamoyl, methyl ester) groups on the adjacent two olefinic carbon atoms were prepared by the condensation of S‐alkylthioamidinium salts or methyl dithiocarboxylates with the corresponding active methylene compounds in good yields. These polarized ethylenes were alternatively synthesized by the reaction of thioamides or methyl dithiocarboxylates with tetracyanoethylene oxide in good yields. Reactions of these polarized ethylenes with hydrazine or guanidine derivatives occurred smoothly to give the corresponding pyrazole and pyrimidine derivatives in good yields. The synthesis of 5‐aza[2.2.3]cyclazine derivatives using polarized ethylenes is also described.

The allyl(trimethoxy)silanes (I) react with catechol (II) in the presence of triethylamine (III) to form the siliconates (IV) mentioned in the title.

Vitellogenin (VTG) is a useful biomarker for detecting the estrogenic activity of chemicals in aquatic environments. However, little information is available on the regulatory mechanisms of the expression of each VTG subtype, particularly the relationship between expression patterns of VTG1/2 and estrogen receptor (ER) subtypes, such as ERα and ERβ. In this paper, we measured VTG1 and VTG2 mRNA induction in male medaka liver, which was treated with ERα-selective ligand, (17α, 20E)-3-hydroxy-17,20-[(1-methoxyethylidene)bis(oxy)]-19-norpregna-1,3,5(10),20-tetraene-21-carboxylic acid, methyl ester or ERβ-selective ligand, 2-(4-hydroxyphenyl)-5-hydroxy-1,3-benzoxazole and investigated the characteristics of ER subtype function in VTG1 and VTG2 inductions. Hepatic VTG1 mRNA was induced by ERα-selective ligands at even low concentration and maximum increases were the same as for E2. VTG2 mRNA was also increased, but its levels were very low. On the other hand, ERβ-selective ligands significantly increased VTG2 mRNA in the presence of ERα agonists. These results indicate that the expression of each VTG subtype is regulated by unique ER subtypes. VTG1 expression is only regulated by the action of ERα. In contrast, VTG2 expression is regulated by both ERα and ERβ, with ERα being essential for VTG2 gene expression and ERβ being essential for enhancement.