RESUMEN
Two new complexes [Cu(I)(3)(L1)I(3)](n) (1, L1 = 2,5-bis(4-pyridyl)-1,3,4-oxadiazole) and [Cu(I)(3)(L2)I(2)](n) (2, L2 = 2,5-bis(4-pyridyl)-1,2,4-triazolate) are controllably formed by using aqueous ammonia to regulate the pH value of the reaction involving CuI and L1. Interestingly, L2 of 2 is in situ generated from the ring transform of L1 when increase the pH value of the reaction. 1 exhibits 2-D layer, while 2 shows 3-D MOFs with a novel 3-nodal 4,4,5-connected net topology of an unprecedented Point (Schlafli) symbol: (4·5(2)·6(2)·7)(5(4)·8(2))(4(3)·5·6(6)). Although both 1 and 2 are built of CuI and similar ligands, different arrangements of CuI chains and ligands endow them with different physical properties. 1 displays a strong pure red luminescence emission, while 2 is nonluminescent and shows a broad absorption band covering the whole UV-vis-NIR spectrum range. The emissive excited states of 1 and the charge transitions of the optical absorption for 2 are solved by DFT calculations.
RESUMEN
Three novel microporous three-dimensional (3-D) metal-organic framework materials [ML](n) [M = Ni, Co, Cd; L = N,N'-bis(4-picolinoyl)hydrazine] were obtained from hydrothermal reactions. The organic ligand L was formed through the in situ ring-opening hydrolysis reaction of 2,5-bis(4-pyridyl)-1,3,4-oxadiazole with the assistance of metal ions. Single-crystal X-ray diffraction studies reveal that complexes 1-3 adopt 6-connected 3-D networks of distorted alpha-Po topology, which are built from non-interpenetrated (4,4) grids cross-linked by zigzag chains. These isomorphic complexes are all of high thermal stability, but some other physical properties are quite different because of their different metal centers. Antiferromagnetic exchange was observed between Ni(II) centers of complex 1, while ferromagnetic for Co(II) centers of complex 2. Complex 3 exhibits strong fluorescence emission.
RESUMEN
The resistance of breast cancer to radiotherapy remains a major obstacle to successful cancer management. Radiotherapy may result in DNA damage and activate breast cancer stem cells. DNA damage may lead to activation of the checkpoint kinase (CHK) signaling pathway, of which debromohymenialdisine (DBH) is a specific inhibitor. Radiotherapy also increases the expression of phosphorylated CHK1/2 (pCHK1/2) in the breast cancer cell line, MCF-7, in vitro in a dose-dependent manner. DBH is a relatively stable effective inhibitor that significantly reduces pCHK1/2 expression and MCF-7 proliferation. Low-dose radiotherapy combined with DBH resulted in a higher MCF-7 inhibition rate compared with high-dose radiation alone. This result indicates that the inhibition of the CHK1/2 signal pathway may significantly reduce DNA damage within radiated cells. Radiotherapy may also regulate the proportion of CD44+/CD24- MCF-7 cancer stem cells in a dose- and time-dependent manner. However, the stem cell proportion of MCF-7 cells was significantly reduced by treatment with DBH. The inhibition is relatively stable and time dependent. Significant reductions were observed after 3 days of culture (P<0.01). The results of the present study indicate that the DBH-induced downregulation of CHK may provide a novel method of enhancing the effect of radiotherapy and reducing stem cell survival in the MCF-7 cell line.