No abstract

Hydrophilization of poly(methyl methacrylate) (PMMA) substrates has been demonstrated using a Xe 2 / excimer lamp radiating vacuum ultraviolet (VUV) light of 172 nm in wavelength. In this study, we have particularly focused on the effects of atmospheric pressure during VUV irradiation. Each of the substrates was photoirradiated with VUV light under a pressure of 10, 10 3 , or 10 5 Pa. Although in each case the hydrophobic PMMA surface became hydrophilic, the water-contact angle and photooxidation rate markedly depended on the atmospheric pressure. The sample treated at 10 Pa was less wettable than the samples treated at 10 3 and 10 5 Pa due to the shortage of oxygen molecules in the atmosphere. The minimum water-contact angles of the samples treated at 10, 10 3 , and 10 5 Pa were about 40, 25, and 24°, respectively. Microfabrication of the PMMA substrates was also demonstrated employing a simple mesh-mask contact method using the same excimer lamp. As confirmed by atomic force microscopy, a photoetched groove composed of 25 × 25 µm 2 features was successfully fabricated on the PMMA substrates. Both the spatial resolution and photoetch depth of the microstructures depended on the atmospheric pressure. At 10 and 10 3 Pa, we achieved finely grooved microstructures at etching rates of 13 and 13.2 nm/min, respectively. In comparison, when the pressure was further increased to 10 5 Pa, the etching rate decreased to 6.9 nm/min and patterning resolution became significantly worse. The pressure of 10 3 Pa was determined to be optimum for accurately defining PMMA surfaces both chemically and geometrically.

A number of nuclear complexes modify chromatin structure and operate as functional units. However, the in vivo role of each component within the complexes is not known. ATP-dependent chromatin remodeling complexes form several types of protein complexes, which reorganize chromatin structure cooperatively with histone modifiers. Williams syndrome transcription factor (WSTF) was biochemically identified as a major subunit, along with 2 distinct complexes: WINAC, a SWI/SNF-type complex, and WICH, an ISWI-type complex. Here, WSTF −/− mice were generated to investigate its function in chromatin remodeling in vivo. Loss of WSTF expression resulted in neonatal lethality, and all WSTF −/− neonates and ≈10% of WSTF +/− neonates suffered cardiovascular abnormalities resembling those found in autosomal-dominant Williams syndrome patients. Developmental analysis of WSTF −/− embryos revealed that Gja5 gene regulation is aberrant from E9.5, conceivably because of inappropriate chromatin reorganization around the promoter regions where essential cardiac transcription factors are recruited. In vitro analysis in WSTF −/− mouse embryonic fibroblast (MEF) cells also showed impaired transactivation functions of cardiac transcription activators on the Gja5 promoter, but the effects were reversed by overexpression of WINAC components. Likewise in WSTF −/− MEF cells, recruitment of Snf2h, an ISWI ATPase, to PCNA and cell survival after DNA damage were both defective, but were ameliorated by overexpression of WICH components. Thus, the present study provides evidence that WSTF is shared and is a functionally indispensable subunit of the WICH complex for DNA repair and the WINAC complex for transcriptional control.