A coordination polymer of CdII with benzene-1,3-dicarboxyl­ate and 1,4-bis­[1-(2-pyridylmeth­yl)benzimidazol-2-yl]butane

The title CdII coordination polymer, catena-poly[[{1,4-bis­[1-(2-pyridylmeth­yl)benzimidazol-2-yl]butane}cadmium(II)]-μ-benzene-1,3-dicarboxyl­ato], [Cd(C8H4O4)(C30H28N6)]n, was obtained by reaction of CdCO3, benzene-1,3-dicarboxylic acid (H2btc) and 1,4-bis­[1-(2-pyridylmeth­yl)benzimidazol-2-yl]butane (L). The CdII cation is six-coordinated by an N2O4-donor set. L acts as a bidentate ligand and btc anions link CdII centers into a chain propagating parallel to [010]

Multiscale Point Correspondence Using Feature Distribution and Frequency Domain Alignment

In this paper, a hybrid scheme is proposed to find the reliable point-correspondences between two images, which combines the distribution of invariant spatial feature description and frequency domain alignment based on two-stage coarse to fine refinement strategy. Firstly, the source and the target images are both down-sampled by the image pyramid algorithm in a hierarchical multi-scale way. The Fourier-Mellin transform is applied to obtain the transformation parameters at the coarse level between the image pairs; then, the parameters can serve as the initial coarse guess, to guide the following feature matching step at the original scale, where the correspondences are restricted in a search window determined by the deformation between the reference image and the current image; Finally, a novel matching strategy is developed to reject the false matches by validating geometrical relationships between candidate matching points. By doing so, the alignment parameters are refined, which is more accurate and more flexible than a robust fitting technique. This in return can provide a more accurate result for feature correspondence. Experiments on real and synthetic image-pairs show that our approach provides satisfactory feature matching performance

Axin downregulates TCF-4 transcription via β-catenin, but not p53, and inhibits the proliferation and invasion of lung cancer cells

<p>Abstract</p> <p>Background</p> <p>We previously reported that overexpression of Axin downregulates T cell factor-4 (TCF-4) transcription. However, the mechanism(s) by which Axin downregulates the transcription and expression of TCF-4 is not clear. It has been reported that β-catenin promotes and p53 inhibits TCF-4 transcription, respectively. The aim of this study was to investigate whether β-catenin and/or p53 is required for Axin-mediated downregulation of TCF-4.</p> <p>Results</p> <p>Axin mutants that lack p53/HIPK2 and/or β-catenin binding domains were expressed in lung cancer cells, BE1 (mutant p53) and A549 (wild type p53). Expression of Axin or AxinΔp53 downregulates β-catenin and TCF-4, and knock-down of β-catenin upregulates TCF-4 in BE1 cells. However, expression of AxinΔβ-ca into BE1 cells did not downregulate TCF-4 expression. These results indicate that Axin downregulates TCF-4 transcription via β-catenin. Although overexpression of wild-type p53 also downregulates TCF-4 in BE1 cells, cotransfection of p53 and AxinΔβ-ca did not downregulate TCF-4 further. These results suggest that Axin does not promote p53-mediated downregulation of TCF-4. Axin, AxinΔp53, and AxinΔβ-ca all downregulated β-catenin and TCF-4 in A549 cells. Knock-down of p53 upregulated β-catenin and TCF-4, but cotransfection of AxinΔβ-ca and p53 siRNA resulted in downregulation of β-catenin and TCF-4. These results indicate that p53 is not required for Axin-mediated downregulation of TCF-4. Knock-down or inhibition of GSK-3β prevented Axin-mediated downregulation of TCF-4. Furthermore, expression of Axin and AxinΔp53, prevented the proliferative and invasive ability of BE1 and A549, expression of AxinΔβ-ca could only prevented the proliferative and invasive ability effectively.</p> <p>Conclusions</p> <p>Axin downregulates TCF-4 transcription via β-catenin and independently of p53. Axin may also inhibits the proliferation and invasion of lung cancer cells via β-catenin and p53.</p

Multicolor Photometry Study of the Galaxy Cluster A2589: Dynamics, Luminosity Function and Star Formation History

In this paper we present a multicolor photometry for A2589 ($z=0.0414$) with 15 intermediate bands in the Beijing-Arizona-Taiwan-Connecticut (BATC) system which covers an optical wavelength range from 3000 \AA\ to 10000 \AA. The spectral energy distributions (SEDs) for more than 5000 sources are achieved down to {\it V} $\sim$ 20 mag in about 1 deg$^{2}$ field. A2589 has been also covered by the Sloan Digital Sky Survey (SDSS) in photometric mode only. A cross-identification of the BATC-detected galaxies with the SDSS photometric catalog achieves 1199 galaxies brighter than $i=19.5$ mag, among which 68 member galaxies with known spectroscopic redshifts are found. After combining the SDSS five-band photometric data and the BATC SEDs, the technique of photometric redshift is applied to these galaxies for selecting faint member galaxies. The color-magnitude relation is taken as a further restriction of early-type cluster galaxies. As a result, 106 galaxies are newly selected as member galaxies. Spatial distribution of member galaxies shows a north-south elongation which agrees with the X-ray brightness profile and the orientation of central cD galaxy, NGC 7647. No substructures are detected on the basis of positions and radial velocities of cluster galaxies, indicating that A2589 is a well-relaxed system. The luminosity function of A2589 exhibits a peak at $M_{R} \sim -20$ mag and a dip at $M_{R} \sim -19$ mag. The low-density outer regions are the preferred habitat of faint galaxies. With the evolutionary population synthesis model, PEGASE, the environmental effect on the star formation properties for 68 spectroscopically confirmed member galaxies is studied. The outlier faint galaxies tend to have longer time scales of star formation, shorter mean stellar ages, and lower metallicities of interstellar medium, which can be interpreted in the context of hierarchical cosmological scenario.Comment: 2011 Accepted to A

Genetic Variation At 8Q24, Family History Of Cancer, And Upper Gastrointestinal Cancers In A Chinese Population

Genetic variation at 8q24 is associated with prostate, bladder, breast, colorectal, thyroid, lung, ovarian, UADT, liver and stomach cancers. However, a role for variation at 8q24 in familial clustering of upper gastrointestinal cancers has not been studied. In order to explore potential inherited susceptibility, we analyzed epidemiologic data from a population-based case-control study of upper gastrointestinal cancers from Taixing, China. The study population includes 204 liver, 206 stomach, and 218 esophageal cancer cases and 415 controls. Associations between 8q24 rs1447295, rs16901979, rs6983267 and these cancers were stratified by family history of cancer. Odds ratios and 95% confidence intervals were adjusted for potential confounders: age, sex, education, tobacco smoking, alcohol consumption, and BMI at interview. We also adjusted for hepatitis B and aflatoxin (liver cancer) and Helicobacter pylori (stomach cancer). In a dominant model, among those with a family history of cancer, rs1447295 was positively associated with liver cancer (ORadj 2.80; 95% CI 1.15–6.80). Heterogeneity was observed (Pheterogeneity=0.029) with rs6983267 and liver cancer, with positive association in the dominant model among those with a family history of cancer and positive association in the recessive model among those without a family history of cancer. When considered in a genetic risk score model, each additional 8q24 risk genotype increased the odds of liver cancer by two-fold among those with a family history of cancer (ORadj 2.00; 95% CI 1.15–3.47). These findings suggest that inherited susceptibility to liver cancer may exist in the Taixing population and that variation at 8q24 might be a genetic component of that inherited susceptibility