Current technologies for removing heavy metal ions are typically metal ion specific. Herein we report the development of a broad-spectrum heavy metal ion trap by incorporation of ethylenediaminetetraacetic acid into a robust metal-organic framework. The capture experiments for a total of 22 heavy metal ions, covering hard, soft, and borderline Lewis metal ions, show that the trap is very effective, with removal efficiencies of >99% for single-component adsorption, multi-component adsorption, or in breakthrough processes. The material can also serve as a host for metal ion loading with arbitrary selections of metal ion amounts/types with a controllable uptake ratio to prepare well-dispersed single or multiple metal catalysts. This is supported by the excellent performance of the prepared Pd2+-loaded composite toward the Suzuki coupling reaction. This work proposes a versatile heavy metal ion trap that may find applications in the fields of separation and catalysis.

Higher hydrocarbons in natural gas must be removed for safe storage, transport, and application of natural gas. Considering C3H8 and CH4 are nonpolar molecules, electrostatic interactions between C3 and MOFs are relatively weak, while they could be sensitive to the van der Waals interactions. Thus, it is an effective method to greatly enhance the separation performance by improving the van der Waals interactions through tuning the pore size of MOFs. Herein, we synthesized a series of isostructural Zr-MOFs with different pore sizes, and the separation performances of these materials for C3/C1 were systematically studied. The results indicate that pore size plays an important role in the C3 storage and C3/C1 separation in MOFs. Specifically, Zr-BPDC with large surface area and pore volume has the highest C3H8 and C3H6 adsorption capacity (159.2 cc/g and 161.5 cc/g at 298 K 1 bar, respectively), while Zr-FUM with the smallest surface area and pore volume has the highest adsorption heat for C3 as well as C3/C1 selectivities (292.0 and 242.2 at 298 K and 1 bar for C3H8/CH4 and C3H6/CH4, respectively) among the five Zr-MOFs. In addition, a defective structure in MOFs can largely improve C3 adsorption capacity for its higher surface area and pore volume, while functional groups in Zr-MOF will not obviously affect the C3 adsorption and C3/C1 separation performance. This work shows that van der Waals interactions in MOFs are predominantly for C3 adsorption and C3/C1 separation, and it can be efficiently tuned by changing the surface area and pore volume in MOFs. More importantly, this information could help design and synthesize a novel adsorbent to separate C3/C1 mixtures.

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The pathogenesis of gastric cancer is not completely understood. Tumor necrosis factor-α-induced protein-8 like-2 (TIPE2) has recently been identified as a novel negative regulator gene of the immune system, and studies in mice and humans have suggested its inhibitory action in both inflammation and cancer. In this study, we examined the expression levels of TIPE2 in human gastric cancer tissues and also samples of paraneoplastic control tissue, and found that TIPE2 expression was reduced in gastric cancer. To investigate the role of TIPE2 in gastric cell carcinogenesis, a TIPE2 plasmid was introduced into gastric cell lines and TIPE2 function was examined. Colony-forming assays showed that restoration of TIPE2 expression in gastric cells significantly suppressed cell proliferation. Analysis by flow cytometry showed that the number of cells in the S phase of the cell cycle was reduced concomitant with TIPE2 expression, and cell apoptosis was maintained at a low level. Microarray and western blot analyses revealed that TIPE2 selectively up-regulated N-ras and p27 expression. The role of p27 in mediating TIPE2-associated cell growth inhibition was verified by a p27 siRNA interference assay. In this study, we proved that TIPE2 is an inhibitor of gastric cancer cell growth, and suggest that TIPE2 might promote a p27-associated signaling cascade that leads to restored control of the cell cycle and cell division. Our results provide a new molecular mechanism by which TIPE2 may regulate proliferation of gastric cells.