Bis(μ-2-hydroxy­benozato)-κ3 O,O′:O′;κ3 O:O,O′-bis­[(2-hydroxy­benozato-κ2 O,O′)(1,10-phenanthroline-κ2 N,N′)cadmium(II)]

The dinuclear title compound, [Cd2(C7H5O3)4(C12H8N2)2], is located on a crystallographic rotation twofold axis. The two CdII ions are connected by two tridentate bridging 2-hydroxy­benzoate anions. Each CdII ion is seven-coordinated by five O atoms from three 2-hydroxy­benzoate ligands and two N atoms from 1,10-phenanthroline. The 2-hydroxy­benzoate mol­ecules adopt two kinds of coordination mode, bidentate chelating and tridentate bridging–chelating. Intra­molecular hydrogen bonds between hydr­oxy and carboxyl­ate groups from 2-hydroxy­benzoate groups and π–π stacking interactions between parallel 1,10-phenanthroline ligands [centroid–centroid distances = 3.707 (3) and 3.842 (3) Å] are observed. Furthermore, adjacent benzene rings from 2-hydroxy­benzoate ligands are involved in π–π inter­actions with inter­planar distances of 3.642 (3) Å, thereby forming a chain along the a axis direction

Extraction and Separation of Lanthanum and Actinium by Non-Saponification P507 System

Due to the ineffective separation and removal of actinium during the production process of rare earths, the radioactive of some products in China exceed the exemption values(the total activity of α and β less than 1 Bq/g). Using non-saponified 2-ethylhexyl phosphate mono-2-ethylhexyl ester(P507) as an extractant, diethylenetriamine-N, N, N', N'', N''-pentaacetic acid(DTPA) or N-(2-hydroxyethyl)ethylenediamine-N, N', N'-triacetic acid(HEDTA) as aqueous masking agent, lactic acid as acidity buffer, the extraction and separation of lanthanum-actinium elements was studied respectively in hydrochloric acid and nitric acid media in this work. The results show that the weak acid can effectively buffer the acidity of the aqueous phase and promote the coordination reaction to form organic chelates favorably. The extraction properties of La3+ in the above system is better than in the single saponified P507 system. When pH is 3.0 and the initial La3+ concentration is 0.2 mol/L in hydrochloric acid solution, D(La) can reach 5.0 and SF(La/Ac) value is 3-4. Compared with that，SF(La/Ac) can increase to 5-7 in nitric acid system under the fixed conditions of pH as 2.0-2.5, the DTPA/HEDTA and lactic acid concentrations as 0.02 mol/L and 1.0 mol/L, respectively. In this case, Ac3+ is effectively masked and the maximum D(Ac) is only 0.46. Furthermore, the non-saponification P507 system can also preferentially remove the radioactive Ac3+ from the acidic rare earth wastewater, and SF(Ac/La) value can reach 14 with the increase of lactic acid concentration. The phenomenon can be used to achieve the goal of effective control of radioactive substances in the wastewater of rare earth industry

12CO, 13CO and C18O observations along the major axes of nearby bright infrared galaxies

We present simultaneous observations of CO,13CO and C18O J=1-0 emission in 11 nearby (cz<1000 km/s) bright infrared galaxies. Both 12CO and 13CO are detected in the centers of all galaxies, except for 13CO in NGC 3031. We have also detected C18O, CS J=2-1, and HCO+ J=1-0 emission in the nuclear regions of M82 and M51. These are the first systematical extragalactic detections of 12CO and its isotopes from the PMO 14m telescope. We have conducted half-beam spacing mapping of M82 over an area of 4'*2.5' and major axis mapping of NGC 3627, NGC 3628, NGC 4631, and M51. The radial distributions of 12CO and 13CO in NGC 3627, NGC 3628, and M51 can be well fitted by an exponential profile. The 12CO/13CO intensity ratio,R,decreases monotonically with galactocentric radius in all mapped sources. The average R in the center and disk of the galaxies are 9.9+/-3.0 and 5.6+/-1.9 respectively, much lower than the peculiar R(~24) found in the center of M82. The intensity ratios of 13CO/C18O, 13CO/HCO+ and 13CO/CS (either ours or literature data) show little variations with galactocentric radius, in sharp contrast with the greatly varied R. This supports the notion that the observed gradient in R could be the results of the variations of the physical conditions across the disks. The H_2 column density derived from C18O shows that the Galactic standard conversion factor (X-factor) overestimates the amount of the molecular gas in M82 by a factor of ~2.5. These observations suggest that the X-factor in active star-forming regions (i.e., nuclear regions) should be lower than that in normal star-forming disks, and the gradient in R can be used to trace the variations of the X-factor.Comment: 27 pages, 7 figures, accepted by RA

Activation of PI3K/AKT and MAPK Pathway through a PDGFRβ-Dependent Feedback Loop Is Involved in Rapamycin Resistance in Hepatocellular Carcinoma

Background: Rapamycin is an attractive approach for the treatment and prevention of HCC recurrence after liver transplantation. However, the objective response rates of rapamycin achieved with single-agent therapy were modest, supporting that rapamycin resistance is a frequently observed characteristic of many cancers. Some studies have been devoted to understanding the mechanisms of rapamycin resistance, however, the mechanisms are cell-type-dependent and studies on rapamycin resistance in HCC are extremely limited. Methodology/Principal Findings: The anti-tumor sensitivity of rapamycin was modest in vitro and in vivo. In both human and rat HCC cells, rapamycin up-regulated the expression and phosphorylation of PDGFRb in a time and dose-dependent manner as assessed by RT-PCR and western blot analysis. Using siRNA mediated knockdown of PDGFRb, we confirmed that subsequent activation of AKT and ERK was PDGFRb-dependent and compromised the anti-tumor activity of rapamycin. Then, blockade of this PDGFRb-dependent feedback loop by sorafenib enhanced the anti-tumor sensitivity of rapamycin in vitro and in an immunocompetent orthotopic rat model of HCC. Conclusions: Activation of PI3K/AKT and MAPK pathway through a PDGFRb-dependent feedback loop compromises the anti-tumor activity of rapamycin in HCC, and blockade of this feedback loop by sorafenib is an attractive approach t

Plastome phylogenomics and morphological traits analyses provide new insights into the phylogenetic position, species delimitation and speciation of Triplostegia (Caprifoliaceae)

Background The genus Triplostegia contains two recognized species, T. glandulifera and T. grandifora, but its phylogenetic position and species delimitation remain controversial. In this study, we assembled plastid genomes and nuclear ribosomal DNA (nrDNA) cistrons sampled from 22 wild Triplostegia individuals, each from a separate population, and examined these with 11 recently published Triplostegia plastomes. Morphological traits were measured from herbarium specimens and wild material, and ecological niche models were constructed. Results Triplostegia is a monophyletic genus within the subfamily Dipsacoideae comprising three monophyletic species, T. glandulifera, T. grandifora, and an unrecognized species Triplostegia sp. A, which occupies much higher altitude than the other two. The new species had previously been misidentifed as T. glandulifera, but difers in taproot, leaf, and other characters. Triplotegia is an old genus, with stem age 39.96Ma, and within it T. glandulifera diverged 7.94Ma. Triplostegia grandifora and sp. A diverged 1.05Ma, perhaps in response to Quaternary climate fuctuations. Niche overlap between Triplostegia species was positively correlated with their phylogenetic relatedness. Conclusions Our results provide new insights into the species delimitation of Triplostegia, and indicate that a taxonomic revision of Triplostegia is needed. We also identifed that either rpoB-trnC or ycf1 could serve as a DNA barcode for Triplostegi

The MALATANG Survey : The L GAS-L IR Correlation on Sub-kiloparsec Scale in Six Nearby Star-forming Galaxies as Traced by HCN J = 4 → 3 and HCO + J = 4 → 3

This is an author-created, un-copyedited version of an article published in The Astrophysical Journal. The Version of Record is available online at https://doi.org/10.3847/1538-4357/aac512.We present HCN J = 4→3 and HCO+ J = 4→3 maps of six nearby star-forming galaxies, NGC 253, NGC 1068, IC 342, M82, M83, and NGC 6946, obtained with the James Clerk Maxwell Telescope as part of the MALATANG survey. All galaxies were mapped in the central 2×2 region at 14 (FWHM) resolution (corresponding to linear scales of ∼0.2-1.0 kpc). The LIR-Ldense relation, where the dense gas is traced by the HCN J = 4→3 and the HCO+ J = 4→3 emission, measured in our sample of spatially resolved galaxies is found to follow the linear correlation established globally in galaxies within the scatter. We find that the luminosity ratio, LIR/Ldense, shows systematic variations with LIR within individual spatially resolved galaxies, whereas the galaxy-integrated ratios vary little. A rising trend is also found between LIR/Ldense ratio and the warm-dust temperature gauged by the 70 μm/100 μm flux ratio. We find that the luminosity ratios of IR/HCN (4-3) and IR/HCO+ (4-3), which can be taken as a proxy for the star formation efficiency (SFE) in the dense molecular gas (SFE dense), appear to be nearly independent of the dense gas fraction ( f dense) for our sample of galaxies. The SFE of the total molecular gas (SFEmol) is found to increase substantially with f dense when combining our data with those on local (ultra)luminous infrared galaxies and high-z quasars. The mean LHCN(4-3) LHCO+(4-3) line ratio measured for the six targeted galaxies is 0.9±0.6. No significant correlation is found for the L'HCN(4-3) L'HCO+(4-3) ratio with the star formation rate as traced by L IR, nor with the warm-dust temperature, for the different populations of galaxies.Peer reviewe

Restoration of mutant K-Ras repressed miR-199b inhibits K-Ras mutant non-small cell lung cancer progression

Background: miRNAs play crucial role in the progression of K-Ras-mutated nonsmall cell lung cancer (NSCLC). However, most studies have focused on miRNAs that target K-Ras. Here, we investigated miRNAs regulated by mutant K-Ras and their functions. Methods: miRNAs regulated by mutant K-Ras were screened using miRNA arrays. miR-199b expression levels were measured by qRT-PCR. The protein expression levels were measured using Western blot and immunohistochemistry. The effects of miR-199b on NSCLC were examined both in vitro and in vivo by overexpressing or inhibiting miR-199b. DNA methylation was measured by bisulfite sequencing. Results: An inverse correlation was observed between K-Ras mutation status and miR-199b levels in NSCLC specimens and cell lines. The inhibition of miR-199b stimulated NSCLC growth and metastasis, while restoration of miR-199b suppressed K-Ras mutation-driven lung tumorigenesis as well as K-Ras-mutated NSCLC growth and metastasis. miR-199b inactivated ERK and Akt pathways by targeting K-Ras, KSR2, PIK3R1, Akt1, and Rheb1. Furthermore, we determined that mutant K-Ras inhibits miR-199b expression by increasing miR-199b promoter methylation. Conclusion: Our findings suggest that mutant K-Ras plays an oncogenic role through downregulating miR-199b in NSCLC and that overexpression of miR-199b is a novel strategy for the treatment of K-Ras-mutated NSCLC.This work was supported by the National Natural Science Foundation of China (81672283 to H.J.) and the Startup Fund for Talented Scholars of Daping Hospital and Research Institute of Surgery, Third Military Medical University (to H.J. and C.-X.X).