THE CREATIVE THINKING DEDUCTION OF TRADITIONAL CHINESE PIANO MUSIC ELEMENTS - TAKING CULTURAL WORKS FROM DIFFERENT PERIODS IN HISTORY AS THE MAIN LINE

In the 70 years since the founding of China, piano music has undergone a unique process of development. In the early years of the founding, piano composers tended to favor folk material, focusing on nationalization and mass. This study explores multiple stages in the evolution of creative thinking about traditional elements of Chinese piano music, using the cultural lineage of piano works from different historical periods as the main thread. Among them, the first stage is 1949-1966, the seventeen years of unprecedented prosperity of piano creation in the early years of the founding of the country. To make piano music more accessible to the masses, the subjects of piano works had regional and mass characteristics, the melodies tended to be folk materials while not using overly complex musical language and the melody was served by form, weave, and harmony. The second stage was from 1967 to 1977, the decade of the Cultural Revolution. Although the subject matter could only be pianistic adaptations of model operas, revolutionary songs, and traditional instrumental pieces, it prompted composers to dig deeper into the musical language and explore the perfect use of folk music patterns, traditional branching vocal weaves, and nationalized harmonies in the piano. The third stage is 1978-2019, the period of diversified development. A variety of modern Western music genres influenced Chinese piano music composition. Composers used and modernized ethnic materials to varying degrees, resulting in different approaches to ethnicized subject matter. Non-traditional tonality and dissonant acoustics are two of the main characteristics of the musical language at this stage. Nationalization and modernization are explored in Chinese piano works in multiple ways, with remarkable achievements

Molecular cloning and characterization of CIDE-3, a novel member of the cell-death-inducing DNA-fragmentation-factor (DFF45)-like effector family.

DNA fragmentation is one of the critical steps in apoptosis, which is induced by DNA fragmentation factor (DFF). DFF is composed of two subunits, a 40 kDa caspase-activated nuclease (DFF40) and a 45 kDa inhibitor (DFF45). Recently a novel family of cell-death-inducing DFF45-like effectors (CIDEs) has been identified. Among CIDEs, two from human (CIDE-A and CIDE-B) and three from mouse (CIDE-A, CIDE-B and FSP27) have been reported. In this study human CIDE-3, a novel member of CIDEs, was identified upon sequence analysis of a previously unidentified cDNA that encoded a protein of 238 amino acids. It was shown to be a human homologue of mouse FSP27, and shared homology with the CIDE-N and CIDE-C domains of CIDEs. Apoptosis-inducing activity was clearly shown by DNA-fragmentation assay of the nuclear DNA of CIDE-3 transfected 293T cells. The expression pattern of CIDE-3 was different from that of CIDE-B. As shown by Northern-blot analysis, CIDE-3 was expressed mainly in human small intestine, heart, colon and stomach, while CIDE-B showed strong expression in liver and small intestine and at a lower level in colon, kidney and spleen. Green-fluorescent-protein-tagged CIDE-3 was revealed in some cytosolic corpuscles. Alternative splicing of the CIDE-3 gene was also identified by reverse transcription PCR, revealing that two transcripts, CIDE-3 and CIDE-3alpha, were present in HepG2 and A375 cells. CIDE-3 comprised a full-length open reading frame with 238 amino acids; in CIDE-3alpha exon 3 was deleted and it encoded a protein of 164 amino acids. Interestingly the CIDE-3alpha isoform still kept the apoptosis-inducing activity and showed the same pattern of subcellular localization as CIDE-3. Consistent with its chromosome localization at 3p25, a region associated with high frequency loss of heterozygosity in many tumours, CIDE-3 may play an important role in prevention of tumorigenesis

Dual promoters control the cell-specific expression of the human cell death-inducing DFF45-like effector B gene

CIDE-B [cell death-inducing DFF45 (DNA fragmentation factor 45)-like effector B] is a member of the CIDE family of apoptosis-inducing factors. The highly restricted pattern of expression of CIDE-B in the liver and spleen suggests that a mechanism exists for the tissue- and cell-specific regulation of transcription of this gene. We have analysed the promoters of the human CIDE-B gene, particularly the mechanism of cell-specific transcription. Expression of CIDE-B is driven by two promoters which are responsible for the synthesis of two types of transcript, and Sp1 and Sp3 are key regulators of basal transcription from both the upstream and the internal promoter, as indicated by EMSAs (electrophoretic mobility-shift assays) and site-directed mutagenesis. Bisulphite sequencing analysis demonstrated that the upstream promoter was hypermethylated in cells that did not express the long transcript of CIDE-B, but was hypomethylated in cells that expressed this transcript. Furthermore, methylation of this region in vitro reduced the promoter activity to ∼5% of the control. Thus methylation at CpG sites in the upstream promoter region appeared to be important for cell-specific synthesis of the long transcript. By contrast, HNF4α (hepatocyte nuclear factor-4α) bound to the internal promoter and enhanced its activity. Moreover, the short transcript of CIDE-B gene was expressed in cells which do not normally express this transcript upon introduction of exogenous HNF4α, demonstrating the involvement of HNF4α in the cell-specific synthesis of the short transcript. Thus our analysis revealed a novel mechanism for the cell-specific transcription of the human CIDE-B gene, which involves epigenetic and genetic control at separate respective promoters