Formation of nanocluster {Dy12} containing Dy-exclusive vertex-sharing [Dy4(µ3-OH)4] cubanes via simultaneous multitemplate guided and step-by-step assembly.

The formation of high-nuclearity clusters of lanthanide usually involves many complicated self-assembly processes. Thus, tracking the formation process is extremely difficult and research on the assembly mechanism is very rare. In this study, a Dy-exclusive nanocluster containing vertex-sharing [Dy4(µ3-OH)4] cubanes, denoted as [Dy12(L)8(OH)16(CH3O)8(H2O)8]·(CH3O)4 (Dy12, L = quinoline-2-carboxylate), was designed and synthesized from L and DyCl3·6H2O. Eight quinoline-2-carboxylate ligands were encapsulated on the periphery of the Dy12 cluster, which served to stabilize the core. The high stability of the Dy12 cluster core was further confirmed by high-resolution electrospray-ionization mass spectrometry (HRESI-MS). With increased ion-source energy, only CH3O- and OH- bridging ligands were replaced inside the Dy12 cluster. Notably, eight intermediate fragments were successfully observed from the Dy12 cluster formation by time-dependent HRESI-MS. First, ligand L captured Dy3+ to give Dy1, which further formed Dy2 through µ2-O bridging. The Dy12 cluster was constructed in one step with four Dy2 and four Dy3+ as templates: L → Dy1→ Dy2→ Dy12. Moreover, a series of Dy3-Dy6 fragment peaks with relatively weak intensities were observed, and an alternative stepwise-assembly route was proposed: L → Dy1→ Dy2→ Dy3→ Dy4→ Dy5→ Dy6→ Dy12. On comparing the two different assembly methods, the multitemplate guided assembly formed Dy12 was found to be dominant. To the best of our knowledge, this study was the first to propose the involvement of two self-assembly mechanisms in the construction of lanthanide clusters, as further confirmed by HRESI-MS. Magnetic studies further showed that Dy12 clusters exhibited field-induced single-molecule magnet behavior.

Semi-volatile organic compounds in infant homes: Levels, influence factors, partitioning, and implications for human exposure.

While infants are developing, they are easily affected by toxic chemicals existing in their environments, such as semi-volatile organic compounds (SVOCs): phthalates, polycyclic aromatic hydrocarbons (PAHs), polybrominated diphenyl ethers (PBDEs), and organophosphate esters (OPEs). However, the specific living environment of infants, including increased plastic products and foam floor mats, may increase the presence of these chemicals. In this study, 68 air, dust, and window film samples were collected from homes, with 3- to 6-month-old infant occupants, to analyze phthalates, PAHs, PBDEs, and OPEs. High detection rates and concentrations suggest that these SVOCs are widespread in infant environments and are associated with cooking methods, smoking habits, the period of time after decoration, and room floors. The partitioning behavior of SVOCs indicates that the logarithms of the dust/gas-phase air partition coefficient (logKD) and the window film/gas-phase air partition coefficient (logKF) in homes are not at an equilibrium state when the logarithm of the octanol/air partition coefficient (logKOA) is less than 8 or greater than 11. Considering the 3 exposure routes, ingestion and dermal absorption have become the main routes of infant exposure to phthalates and OPEs, and ingestion and inhalation have become the dominant routes of exposure to PAHs and PBDEs. The total carcinogenic risk of SVOCs, which have carcinogenic toxicities, via ingestion and dermal absorption for infants in homes exceeds the acceptable value, suggesting that the current levels of these SVOCs in homes might pose a risk to infant health.

Impact of the tissue factor pathway inhibitor gene on apoptosis in human vascular smooth muscle cells.

Tissue factor pathway inhibitor (TFPI) plays a vitally important role in the blood coagulation pathway. Recent studies indicated that TFPI induces apoptosis in vascular smooth-muscle cells (VSMCs) in animals. The present study investigated whether the TFPI gene could also induce apoptosis in human vascular smooth-muscle cells (hVSMCs). Such cells were isolated from human umbilical arteries and subsequently transfected with pIRES-TFPI plasmid (2 µg/mL). MTT assaying and cell counting were applied to measure cell viability and proliferation, RT-PCR was utilized to analyze TFPI gene expression in the cells. Apoptosis was analyzed by fluorescence activated cell sorting (FACS). Several key proteins involved in apoptosis were examined through Western blotting. It was shown that TFPI gene transfer led to its increased cellular expression, with a subsequent reduction in hVSMC proliferation. Further investigation demonstrated that TFPI gene expression resulted in lesser amounts of procaspase-3, procaspase-8 and procascase-9, and an increased release of mitochondrial cytochrome c (cyt-c) into cytoplasm, thereby implying the involvement of both extrinsic and intrinsic pathways in TFPI gene-induced apoptosis in hVSMCs.

Impact of the tissue factor pathway inhibitor gene on apoptosis in human vascular smooth muscle cells

Tissue factor pathway inhibitor (TFPI) plays a vitally important role in the blood coagulation pathway. Recent studies indicated that TFPI induces apoptosis in vascular smooth-muscle cells (VSMCs) in animals. The present study investigated whether the TFPI gene could also induce apoptosis in human vascular smooth-muscle cells (hVSMCs). Such cells were isolated from human umbilical arteries and subsequently transfected with pIRES-TFPI plasmid (2 μg/mL). MTT assaying and cell counting were applied to measure cell viability and proliferation, RT-PCR was utilized to analyze TFPI gene expression in the cells. Apoptosis was analyzed by fluorescence activated cell sorting (FACS). Several key proteins involved in apoptosis were examined through Western blotting. It was shown that TFPI gene transfer led to its increased cellular expression, with a subsequent reduction in hVSMC proliferation. Further investigation demonstrated that TFPI gene expression resulted in lesser amounts of procaspase-3, procaspase-8 and procascase-9, and an increased release of mitochondrial cytochrome c (cyt-c) into cytoplasm, thereby implying the involvement of both extrinsic and intrinsic pathways in TFPI gene-induced apoptosis in hVSMCs.