Tetra­kis(μ-naphthalene-1-acetato-κ2 O:O′)bis­[(N,N-dimethyl­formamide-κO)copper(II)]

The asymmetric unit of the title compound, [Cu2(C12H9O2)4(C3H7NO)2], contains two independent centrosymmetric dinuclear copper(II) complexes. The central paddle-wheel units are formed by four bridging bidentate naphthalene-1-acetate ligands with two dimethyl­formamide ligands in the axial positions. The unique CuII ions have slightly distorted square-pyramidal coordination geometries. One of the naphthalene rings is disordered over two sets of sites, with refined occpancies of 0.535 (4) and 0.465 (4)

Effective grain size refinement of an Fe-24Ni-0.3C metastable austenitic steel by a modified two-step cold rolling and annealing process utilizing the deformation-induced martensitic transformation and its reverse transformation

Metastable austenitic steels having ultrafine grained (UFG) microstructures can be fabricated by conventional cold rolling and annealing processes by utilizing the deformation-induced martensitic transformation during cold rolling and its reverse transformation to austenite upon annealing. However, such processes are not applicable when the austenite has high mechanical stability against deformation-induced martensitic transformation, since there is no sufficient amount of martensite formed during cold rolling. In the present study, a two-step cold rolling and annealing process was applied to an Fe-24Ni-0.3C metastable austenitic steel having high mechanical stability. Prior to the cold rolling, a repetitive subzero treatment and reverse annealing treatment were applied. Such a treatment dramatically decreased the mechanical stability of the austenite and greatly accelerated the formation of deformation-induced martensite during the following cold rolling processes. As a result, the grain refinement was significantly promoted, and a fully recrystallized specimen with a mean austenite grain size of 0.5 μm was successfully fabricated, which exhibited both high strength and high ductility

{3,3′-Bis[(anthracen-9-yl)meth­yl]-1,1′-[(ethane-1,2-diyldi­oxy)bis­(ethane-1,2-di­yl)]bis­(imidazol-2-yl­idene)}mercury(II) bis­(hexa­fluoridophosphate) acetonitrile disolvate

In the title compound, [Hg(C42H38N4O2)](PF6)2·2CH3CN, the HgII cation lies on a twofold axis which is also the inter­nal symmetry element of the complete cationic complex. The HgII cation is coordinated by two symmetry-related C(carbene) atoms [Hg—C = 2.058 (9) Å] in a nearly linear geometry, with a C—Hg—C angle of 175.8 (5)°. There are weak inter­molecular C—H⋯F inter­actions in the crystal packing between an F atom of a hexa­fluoridophosphate anion and a –CH2– group of the bis-N-heterocyclic carbene ligand

A network pharmacology-based study on the anti-hepatoma effect of Radix Salviae Miltiorrhizae

This work is licensed under a Creative Commons Attribution 4.0 International License.Background Radix Salviae Miltiorrhizae (RSM), a well-known traditional Chinese medicine, has been shown to inhibit tumorigenesis in various human cancers. However, the anticancer effects of RSM on human hepatocellular carcinoma (HCC) and the underlying mechanisms of action remain to be fully elucidated. Methods In this study, we aimed to elucidate the underlying molecular mechanisms of RSM in the treatment of HCC using a network pharmacology approach. In vivo and in vitro experiments were also performed to validate the therapeutic effects of RSM on HCC. Results In total, 62 active compounds from RSM and 72 HCC-related targets were identified through network pharmacological analysis. RSM was found to play a critical role in HCC via multiple targets and pathways, especially the EGFR and PI3K/AKT signaling pathways. In addition, RSM was found to suppress HCC cell proliferation, and impair cancer cell migration and invasion in vitro. Flow cytometry analysis revealed that RSM induced cell cycle G2/M arrest and apoptosis, and western blot analysis showed that RSM up-regulated the expression of BAX and down-regulated the expression of Bcl-2 in MHCC97-H and HepG2 cells. Furthermore, RSM administration down-regulated the expression of EGFR, PI3K, and p-AKT proteins, whereas the total AKT level was not altered. Finally, the results of our in vivo experiments confirmed the therapeutic effects of RSM on HCC in nude mice. Conclusions We provide an integrative network pharmacology approach, in combination with in vitro and in vivo experiments, to illustrate the underlying therapeutic mechanisms of RSM action on HCC

Human Hemoglobin Subunit Beta Functions as a Pleiotropic Regulator of RIG-I/MDA5-Mediated Antiviral Innate Immune Responses

Hemoglobin is an important oxygen-carrying protein and plays crucial roles in establishing host resistance against pathogens and in regulating innate immune responses. The hemoglobin subunit beta (HB) is an essential component of hemoglobin, and we have previously demonstrated that the antiviral role of the porcine HB (pHB) is mediated by promoting type I interferon pathways. Thus, considering the high homology between human HB (hHB) and pHB, we hypothesized that hHB also plays an important role in the antiviral innate immunity. In this study, we characterized hHB as a regulatory factor for the replication of RNA viruses by differentially regulating the RIG-I- and MDA5-mediated antiviral signaling pathways. Furthermore, we showed that hHB directly inhibited MDA5-mediated signaling by reducing the MDA5-double-stranded RNA (dsRNA) interaction. Additionally, hHB required hHB-induced reactive oxygen species (ROS) to promote RIG-I-mediated signaling through enhancement of K63-linked RIG-I ubiquitination. Taken together, our findings suggest that hHB is a pleiotropic regulator of RIG-I/MDA5-mediated antiviral responses and further highlight the importance of the intercellular microenvironment, including the redox state, in regulating antiviral innate immune responses. IMPORTANCE Hemoglobin, the most important oxygen-carrying protein, is involved in the regulation of innate immune responses. We have previously reported that the porcine hemoglobin subunit beta (HB) exerts antiviral activity through regulation of type I interferon production. However, the antiviral activities and the underlying mechanisms of HBs originating from other animals have been poorly understood. Here, we identified human HB (hHB) as a pleiotropic regulator of the replication of RNA viruses through regulation of RIG-I/MDA5-mediated signaling pathways. hHB enhances RIG-I-mediated antiviral responses by promoting RIG-I ubiquitination depending on the hHB-induced reactive oxygen species (ROS), while it blocks MDA5-mediated antiviral signaling by suppressing the MDA5-dsRNA interaction. Our results contribute to an understanding of the crucial roles of hHB in the regulation of the RIG-I/MDA5-mediated signaling pathways. We also provide novel insight into the correlation of the intercellular redox state with the regulation of antiviral innate immunity

Field demonstration of distributed quantum sensing without post-selection

Distributed quantum sensing can provide quantum-enhanced sensitivity beyond the shot-noise limit (SNL) for sensing spatially distributed parameters. To date, distributed quantum sensing experiments have been mostly accomplished in laboratory environments without a real space separation for the sensors. In addition, the post-selection is normally assumed to demonstrate the sensitivity advantage over the SNL. Here, we demonstrate distributed quantum sensing in field and show the unconditional violation (without post-selection) of SNL up to 0.916 dB for the field distance of 240 m. The achievement is based on a loophole free Bell test setup with entangled photon pairs at the averaged heralding efficiency of 73.88%. Moreover, to test quantum sensing in real life, we demonstrate the experiment for long distances (with 10-km fiber) together with the sensing of a completely random and unknown parameter. The results represent an important step towards a practical quantum sensing network for widespread applications.Comment: 8 pages, 5 figure