Microscopic Investigation on Morphologies of Bilayer Gel Structure in the Mixed Polyoxyethylene-Type Nonionic Surfactant Systems

We investigated morphologies of lamellar domains below the Krafft temperature in the mixed polyoxyethylene-type nonionic surfactant, a C₁₆E₆/C₁₆E₇/water system, by using optical microscopy, confocal microscopy, small/wide-angle X-ray scattering, and small-angle neutron scattering. We have found that the morphology discontinuously changes from network structures of lamellar domains to spherical vesicles with increasing mole fraction of C₁₆E₇, via the coexistence region of vesicles and network structures of lamellar domains

Mutation analysis of <it>Rad18 </it>in human cancer cell lines and non small cell lung cancer tissues

Abstract Background Genetic instability is known as a cause of oncogenesis. Though Rad18 is reported to function in a post replication mismatch repair system, the relation between the status of Rad18 and human tumorigenesis has not been described so far. Methods Mutation analysis of 34 human cancer cell lines and 32 non small cell lung cancer (NSCLC) tissues were performed by RT-PCR SSCP. Expression level of Rad18 was measured by real time RT-PCR. Stable transfectant was constructed for in vitro study. Results No mutation was found in both cancer cell lines and NSCLC tissues. A single nucleotide polymorphism (SNP) at codon 302 was detected in 51.5% of the cell lines and 62.5% of NSCLC tissues. Interestingly, Rad18 was homozygously deleted in a pulmonary adenocarcinoma cell line PC3. Furthermore, there was no difference in the expression level of wild type Rad18 and Rad18 with SNP. The growth, cell morphology, sensitivity to anti-cancer drugs and in vitro DNA repair activity between wild type Rad18 and Rad18 with SNP revealed to have no difference in vitro. Conclusion Though the frequency of SNP was tended to be higher in NSCLC patients than healthy volunteers (57.7%), as the difference was not significant, we have concluded that there is no relation between Rad18 SNP and lung cancer development.</p

Mutation analysis of Rad18 in human cancer cell lines and non small cell lung cancer tissues

BACKGROUND: Genetic instability is known as a cause of oncogenesis. Though Rad18 is reported to function in a post replication mismatch repair system, the relation between the status of Rad18 and human tumorigenesis has not been described so far. METHODS: Mutation analysis of 34 human cancer cell lines and 32 non small cell lung cancer (NSCLC) tissues were performed by RT-PCR SSCP. Expression level of Rad18 was measured by real time RT-PCR. Stable transfectant was constructed for in vitro study. RESULTS: No mutation was found in both cancer cell lines and NSCLC tissues. A single nucleotide polymorphism (SNP) at codon 302 was detected in 51.5% of the cell lines and 62.5% of NSCLC tissues. Interestingly, Rad18 was homozygously deleted in a pulmonary adenocarcinoma cell line PC3. Furthermore, there was no difference in the expression level of wild type Rad18 and Rad18 with SNP. The growth, cell morphology, sensitivity to anti-cancer drugs and in vitro DNA repair activity between wild type Rad18 and Rad18 with SNP revealed to have no difference in vitro. CONCLUSION: Though the frequency of SNP was tended to be higher in NSCLC patients than healthy volunteers (57.7%), as the difference was not significant, we have concluded that there is no relation between Rad18 SNP and lung cancer development

Focal Mechanism Solutions of Micro- and Small Earthquakes Occurred in the Western Kanagawa Area Situated in the Izu Collision Zone

Focal mechanism solutions of earthquakes in the western Kanagawa area are compiled and characteristics of fault types in the Izu collision zone are discussed. Reverse, strike-slip, and oblique fault mechanisms are seen in the Izu collision zone. Although only about 10 per cent of micro- and small earthquakes, are associated with strike-slip fault mechanisms, the largest and the second largest earthquakes (M 6.0 and M 5.6) are of that type. It was found that the direction of the P axis is somewhat different in the western and eastern Tanzawa areas : in western Tanzawa the average direction of the P axis is NW-SE, while it is NNW-SSE in eastern Tanzawa. We think this difference in the P axis direction reflects differences in tectonic conditions in those areas. In the Ashigara plain area, mechanism solutions are mostly reverse and oblique faults with the P axis direction between E-W and NNW-SSE