The surfaces of cyclo-olefin polymer (COP) were treated using vacuum ultraviolet (VUV) light at 172 nm in wavelength in order to improve its wettability and adhesion properties. The effect of the VUV-light treatment with variable conditions was studied, and then the condition was 2 optimized. The chemical and physical properties of the sample was examined by using water contact angle measurements, X-ray photoelectron spectroscopy, fourier transform infrared spectroscopy, and atomic force microscopy. The VUV treatment of an COP sample was carried out by placing the sample in air and then irradiating the sample surface with a Xe-excimer lamp. At that time, The surface terminal groups were oxidized into the functional groups (detected as CO , C=O, and COO components) readily on COP surfaces. The introduction of oxygen functional groups formed hydrophilic COP surfaces. We investigated how the oxygen functional groups are formed on the COP surface from the viewpoint of different distances between the lamp and the sample. The dependence of oxygenation extent on different experimental parameters of VUV irradiation distance or treatment duration is measured by atomic ratio O1s / C1s of XPS spectra and [C=O]/[C-H] area ratio of FTIR-ATR spectra. It was shown that the surface property of COP samples, such as hydrophilicity and functionalization, were improved 3 remarkably after VUV treatment with suitable conditions. A much higher concentration of oxygen functional groups was observed for distance 5 mm than for the corresponding distance 30 mm at the same extent of VUV-light treatment. VUV-light treatment also has a more obvious effect on the short irradiation distance. In both cases, however, the concentration of oxygen functional groups changes remarkably. It was concluded that VUV treatment is a promising technique to modify COP surface property.

The chemical conversion of the top surface of n-octadecyltrimethoxy silane self-assembled monolayers (ODS-SAMs) on oxide-covered Si substrates using active oxygen species generated from atmospheric oxygen molecules irradiated with vacuum ultraviolet (VUV) light at 172 nm in 2 wavelength has been studied on the basis of water contact angle measurements, ellipsometry, X-ray photoelectron spectroscopy, and atomic force microscopy. An ODS-SAM whose water contact angle was 104˚ on average was prepared using chemical vapor deposition with substrate and vapor temperatures of 150 ˚C. The VUV treatment of an ODS-SAM sample was carried out by placing the sample in air and then irradiating the sample surface with a Xe-excimer lamp. The distance between the lamp and the sample was regulated so that the VUV light emitted from the lamp was almost entirely absorbed by atmospheric oxygen molecules to generate active oxygen species, such as ozone and atomic oxygen before reaching the sample surface. Hence, the surface chemical conversion of the ODS-SAM was primarily promoted through chemical reactions with the active oxygen species. Photochemical changes in the ODS-SAM were found to be the generation of polar functional groups, such as-COOH,-CHO, and-OH, on the surface and the subsequent etching of the monolayer. Irradiation parameters, such as 3 irradiation time, were optimized to achieve a better functionalization of the SAM top surface while minimizing the etching depth of the ODS-SAM. The ability to graft another SAM onto the modified ODS-SAM bearing polar functional groups was demonstrated by the formation of alkylsilane bilayers.

Hepatocellular carcinoma (HCC)3 is a leading cause of mortality in patients with liver cirrhosis (1). In the United States, the incidence of HCC has risen during the last few decades from 1.3/100,000 population between 1978 and 1980 to 3.3/100,000 population between 1998 and 2001 (2, 3). This is likely to continue, primarily due to progressive liver diseases attributable to the hepatitis C virus in individuals infected a few decades ago (4). However, as hepatitis B virus infection is more prevalent globally than hepatitis C virus, hepatitis B virus remains the single most important cause of HCC worldwide, and is particularly high in Asia and Africa (5). Treatment of HCC is clinically difficult, as HCC expresses multidrug-resistance genes and is insensitive to current chemotherapeutic agents (6). HCC cells are characterized by high cellular levels of cyclin-dependent kinases (Cdks). Up-regulation of Cdks results from the inactivation of p16 Ink4, p21Waf1 and p27 Kip1 , Cdk inhibitory proteins, and abnormal activation of cyclins (7-10). For this reason, Cdk inhibitors are strong candidates for the treatment of HCC, and some (e.g. olomoucine, roscovitine and flavopiridol) have been tested in clinical trials (11).Cdks regulate two biological processes essential for cancer cell survival: cell cycle progression and gene transcription (12). They control entry into each stage of the cell cycle by phosphorylating key substrates such as pRb (13,14). Cdks usually form heterodimers with cyclins to create active complexes and, because cyclin levels oscillate throughout the cell cycle, this contributes to the temporal activation of specific Cdks. Cdks also regulate transcription by phosphorylating the carboxylterminal domain (CTD) of the large subunit of RNA polymerase II (15). In humans, the CTD contains 52 heptapeptide (YSPTSPS) repeats that can be phosphorylated on serines, threonines, and tyrosines (15). A number of Cdks phosphorylate these sites, including Cdk7/cyclin H/Mat1 (part of the TFIIH complex that initiates transcription) (16) and Cdk9/cyclin T (also called P-TEFb), which activates transcriptional elongation (17-21).Mcl-1, an anti-apoptotic member of the Bcl-2 family (22), was first identified as a protein up-regulated in a human carcinoma cell line induced to differentiate along the monocyte lineage (23), and is essential for the survival of carcinoma cells (24 -27). Mcl-1 is thought to act by antagonizing pro-apoptotic proteins such as Bim (28). Inhibitor of apoptosis protein (IAP) is a family of proteins that regulates cell death; X-linked IAP (XIAP) and survivin are two important members of this family in mammals. Both inhibit caspases and block apoptosis (29).Ibulocydine, ((2S,3S,4S,5S)-5-(4-amino-6-bromo-5-carbamoyl-1H-pyrrolo [2,3-d]pyrimidin-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl isobutyrate, is an isobutyrate ester prodrug of a novel synthetic Cdk inhibitor, BMK-Y101 (4-amino-6-bromo-1-((2S,3S,4S,5S)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)-1H-pyrrolo[2,3-d]pyrimidine-5-carboxamide) ...

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