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To systematically explore the effects of polynuclear complexes on the removal of chromium pollutants, a new three-dimensional (3D) microporous metal-organic compound [Cd 3 (HCO 2) 2 (dpa) 4 (bpp) 3 ] n (dpa ​= ​diphenic acid, bpp ​= ​1,3-bi(4-pyridyl)propane) (1) was prepared through hydrothermal synthesis. The structure was characterized by X-ray single crystal diffraction, elemental analysis, and Fourier transform infrared spectroscopy. The results indicate that complex 1 based on Cd(II) clusters is monoclinic and consists of the C 2/ c space group. It exhibits a new 2-nodal (3,5)-connected 3D framework with a Schläfli symbol of {43}{45, 65}. The thermogravimetric analysis (TGA) reveals complex 1 has high thermal stability (stable until 490 ​°C). The photoluminescence shows the emission wavelength of the fluorescence is red-shifted (30 ​nm), and the intensity is significantly increased compared to the free ligand. Adsorption analysis shows that the Cd(II) compound demonstrates significant adsorption towards the dichromate anion (Cr 2 O 7 2−). Its adsorption isotherm is consistent with the Langmuir model and its adsorption kinetics follows a pseudo-second-order model. 3D polynuclear Cd(II) complexes exhibit photo-fluorescent property and adsorption towards the dichromate anion. Image 1 • A new polynuclear coordination polymer [Cd 3 (HCO 2) 2 (dpa) 4 (bpp) 3 ] n has been prepared and characterized. • Cd(II) clusters with 1D+2D→3D framework and a new 2-nodal (3,5)-connected topology. • Robust microporous 1D channel for dichromate removal in an aqueous solution. [ABSTRACT FROM AUTHOR]

The crucial effect of vascular endothelial growth factor (VEGF)-induced vascular angiogenesis has been well known in corneal neovascularization (CNV). This research aimed to determine the underlying value and mechanism of Meg3 on CNV in vivo and in vitro. In an alkali-burned mouse model, length and area of new vessels were increased along with thinning of corneal epithelium, accompanied by the overexpression of Meg3. Notably, subconjunctival injection of shMeg3 suppressed the degree of injury in cornea, causing expression of the angiogenesis markers--VEGF-A and CD31 decreased. In VEGF-induced human umbilical vein endothelial cells (HUVECs), knockdown of Meg3 antagonized the enhancement of viability, proliferation, wound healing ability and angiogenesis by VEGF. The proteins expression of VEGF-A, CD31, SDF-1/CXCR4 as well as phosphoraylation-Smad2/3 pathways, which were related to angiogenesis, were reduced with Meg3 deficiency. Overall, knockdown of Meg3 alleviated formation of neovascularization in alkali-burned corneas and reduced VEGF-induced angiogenesis by inhibiting SDF-1/CXCR4 and Smad2/3 signaling in vitro. • Meg3 has a time-dependent relationship with corneal neovascularization(CNV). • Knockdown of Meg3 alleviated pathological changes and angiogenic responses in CNV. • SiMeg3 reduced VEGF-induced proliferation, migration and angiogenesis in HUVEC. • SiMeg3 inhibited expression of SDF-1/CXCR4 and Smad2/3 in VEGF-induced HUVEC. [ABSTRACT FROM AUTHOR]