This study was undertaken to determine the effectiveness of zero-valent iron (Fe0) and several adsorbent materials in removing uranium (U) from contaminated groundwater and to investigate the rates and mechanisms that are involved in the reactions. Fe0 filings were used as reductants, and the adsorbents included peat materials, iron oxides, and a carbon-based sorbent (Cercona Bone-Char). Results indicate that Fe0 filings are much more effective than the adsorbents in removing uranyl (UO22+) from the aqueous solution. Nearly 100% of U was removed through reactions with Fe0 at an initial concentration up to 76 mM (or 18 000 mg of U/L). Results from the batch adsorption and desorption and from spectroscopic studies indicate that reductive precipitation of U on Fe0 is the major reaction pathway. Only a small percentage (<4%) of UO22+ appeared to be adsorbed on the corrosion products of Fe0 and could be desorbed by leaching with a carbonate solution. The study also showed that the reduced U(IV) species on Fe0 surfaces could be reoxidized and potentially remobilized when the reduced system becomes more oxidized. Results of this research support the application of the permeable reactive barrier technology using Fe0 as a reactive media to intercept U and other groundwater contaminants migrating to the tributaries of Bear Creek at the U.S. Department of Energy's Y-12 Plant located in Oak Ridge, TN.
Background: It has been reported that activation of glutamate kainate receptor subunit 2 (GluK2) subunit-containing glutamate receptors and the following Fas ligand(FasL) up-regulation, caspase-3 activation, result in delayed apoptosis-like neuronal death in hippocampus CA1 subfield after cerebral ischemia and reperfusion. Nitric oxide-mediated S-nitrosylation might inhibit the procaspase activation, whereas denitrosylation might contribute to cleavage and activation of procaspases. Objectives: The study aimed to elucidate the molecular mechanisms underlying procaspase-3 denitrosylation and activation following kainic acid (KA)-induced excitotoxicity in rat hippocampus. Methods: S-nitrosylation of procaspase-3 was detected by biotin-switch method. Activation of procaspase-3 was shown as cleavage of procaspase-3 detected by immunoblotting. FasL expression was detected by immunoblotting. Cresyl violets and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining were used to detect apoptosis-like neuronal death in rat hippocampal CA1 and CA3 subfields. Results: KA led to the activation of procaspase-3 in a dose- and time-dependent manner, and the activation was inhibited by KA receptor antagonist NS102. Procaspase-3 was denitrosylated at 3 h after kainic acid administration, and the denitrosylation was reversed by SNP and GSNO. FasL ASODNs inhibited the procaspase-3 denitrosylation and activation. Moreover, thioredoxin reductase (TrxR) inhibitor auranofin prevented the denitrosylation and activation of procaspase-3 in rat hippocampal CA1 and CA3 subfields. NS102, FasL AS-ODNs, and auranofin reversed the KAinduced apoptosis and cell death in hippocampal CA1 and CA3 subfields. Conclusions: KA led to denitrosylation and activation of procaspase-3 via FasL and TrxR. Inhibition of procaspase-3 denitrosylation by auranofin, SNP, and GSNO played protective effects against KA-induced apoptosis-like neuronal death in rat hippocampal CA1 and CA3 subfields. These investigations revealed that the procaspase-3 undergoes an initial denitrosylation process before becoming activated, providing valuable insights into the underlying mechanisms and possible treatment of excitotoxicity.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Aluminum–bronze coatings are successfully prepared on ductile iron by cold metal transfer (CMT) wire‐arc deposition. Interface characteristics and properties of aluminum–bronze coatings on ductile iron are investigated. The results demonstrate that heat input not only has a significant effect on the dilution rate, but also can affect the microstructure evolution and interface behavior. At low heat input, the dilution rate is close to zero, and incompletely dissolved graphite nodules and a few short cracks are distributed on the fusion line. The γ 2 + α‐Cu eutectic phase is produced along the columnar grain boundaries of the deposited layer, and no Fe‐enriched phase is found. As heat input increases, the interface between aluminum bronze and cast iron changes from a diffusion joint to a metallurgical bond and from a single interface to a double interface. Fe‐enriched phases and Cu‐enriched phases are produced in the deposited layer and fusion zone, respectively. The microstructure of the fusion zone is mainly austenite, martensite, and ledeburite, resulting in the highest hardness near the interface. The interfacial bond strength of high heat input deposited layer is significantly higher than that of low heat input, and the latter has higher wear resistance than the former.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Mesenchymal stem cells (MSCs) derived from induced pluripotent stem cells (iPSCs) represent a promising alternative source of MSCs for effective periodontal regeneration. Scientific evidence has demonstrated that growth/differentiation factor‑5 (GDF‑5) supports regeneration of periodontal tissues and has a key role in MSC differentiation. The present study investigated the effects of recombinant human GDF‑5 (rhGDF‑5) on periodontal specific differentiation of iPSC‑derived MSCs (iPSC‑MSCs) and bone marrow mesenchymal stem cells (BMSCs). rhGDF‑5 treatment in vitro significantly enhanced the expression levels of marker genes associated with osteogenesis (OCN), fibrogenesis (periostin) and cementogenesis (CAP) in the iPSC‑MSCs compared with untreated controls (all P<0.05). Interestingly, the rhGDF‑5‑treated BMSCs failed to exhibit overexpression of periostin and CAP despite highly upregulated expression of OCN. In the presence of rhGDF‑5, both the iPSC‑MSCs and BMSCs demonstrated marked formation of mineralized nodules. Notably, rhGDF‑5 greatly promoted periodontal specific differentiation of the iPSC‑MSCs encapsulated in hyaluronic acid (HA) hydrogels in vivo as determined by immunohistochemical and immunofluorescence staining. The majority of the PKH67‑labeled iPSC‑MSCs implanted with rhGDF‑5 exhibited strong expression of OCN, periostin and CAP. In conclusion, iPSC‑MSCs demonstrate high periodontal specific differentiation potential in response to rhGDF‑5 both in vitro and in vivo. The delivery of iPSC‑MSCs and rhGDF‑5 with HA hydrogel may have beneficial effects in regenerative periodontal therapy.
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