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A novel macrocyclic spermine alkaloid incasine C' (1), along with a known compound incasine C (2), were isolated from the whole plants of Incarvillea sinensis, and their structures were elucidated on the basis of chemical and spectroscopic evidence.

Using a sol-gel method, rare earth element europium (Eu) doped lead zirconate titanate (Pb0.925Eu0.05(Zr0.52Ti0.48)O3, denoted as PEZT) films were obtained. A novel method was proposed to measure the PEZT film's local piezoelectric properties by piezoresponse force microscope tip utilizing wire bonding through which external electric field was applied. Relative piezoelectric coefficient (“d33”) and the strain behavior (butterfly loop) of the PEZT films described as the function of electric field were obtained by using this method. The oscillation amplitude against the ac voltage curve is linear, revealing a slope of 3.78 × 10− 5 V/V, and the coercive field estimated from the butterfly loop has a mean value of 27.5 kV/cm. The butterfly loops obtained from different places can be used to describe the transfer and attenuation of the domain vibration in PEZT films.

In an attempt to study potential feedback regulation of the neu oncogene, we have found that the neu oncogene product specifically represses its own promoter activity. Deletion analysis indicated a 140-bp region (nucleotides -312 to -173 relative to the ATG initiation codon) in the rat neu promoter responsible for neu autorepression. Gel shift assays and methylation interference analysis further demonstrated that a GGTGGGGGGG sequence (nucleotides -243 to -234 relative to the ATG initiation codon) in this 140-bp region interacts with specific protein complexes. The GGTGGGGGGG sequence (GTG element), which functions as an enhancer, is sufficient to cause neu-mediated repression in a heterologous promoter. Furthermore, it produces different gel shift patterns with nuclear extracts from neu-transformed cell lines and their parental lines, suggesting that a transcriptional factor(s) interacting with this enhancer element has been perturbed by the introduction of neu. Taken together, the data presented in this report show that (i) the neu oncogene product autorepresses its own promoter, (ii) the neu promoter contains a novel enhancer, and (iii) neu autorepression is mediated through this enhancer, likely by inhibition of the enhancer activity.