Effect of Ligand Coordination on the Structures and Visible-Light Photocatalytic Activity of Manganese Vanadate Hybrids

A new manganese–vanadate hybrid structure, Mn­(H₂O)­(bpy)­V₂O₆ (<b>I</b>; bpy = 2,2′-bipyridine), has been synthesized via hydrothermal methods and characterized by single crystal X-ray diffraction [<i>P</i>2₁/<i>n</i>, <i>Z</i> = 4, <i>a</i> = 6.8557(4) Å, <i>b</i> = 10.4900(6) Å, <i>c</i> = 19.7921(13) Å, β = 96.419(4)°], infrared spectroscopy, thermogravimetric analysis, magnetic susceptibility measurements, and UV–vis diffuse reflectance. The structure is comprised of manganese vanadate layers with 2,2’-bipyridine ligands coordinated to the Mn­(II) cations. The water molecules coordinated to the manganese sites can be reversibly desorbed at ∼190 °C with the formation of a new hybrid structure before then further decomposing to MnV₂O₆ upon heating to 300 °C. Notably, <b>I</b> undergoes a reversible structural transformation to Mn­(bpy)­V₄O₁₁(bpy) (<b>II</b>) under hydrothermal conditions. This structural transformation results from additional bpy-ligand coordination to 1/4 of the vanadium sites. Magnetic data indicate Mn­(II) cations in both <b>I</b> and <b>II</b> are high spin (<i>S</i> = 5/2). The optical bandgap sizes of <b>I</b> and <b>II</b> were measured to be ∼2.2 eV and ∼1.6 eV, respectively, and that are calculated by DFT methods to arise primarily from Mn-to-bpy and Mn-to-V electronic transitions between the valence and conduction bands. Visible-light irradiation of <b>II</b> in aqueous solutions leads to photocatalytic activities for total water splitting at rates of ∼92 μmol H₂/¹/₂O₂ g^–1 h^–1 and ∼21 μmol H₂/¹/₂O₂ g^–1 h^–1 for <b>II</b>, with and without a 1 wt % Pt surface cocatalyst, respectively, but no measurable activity for <b>I</b>. Rates for only H₂ production using aqueous methanol solutions were significantly lower. Results from electronic structure calculations show that the change in ligand coordination from <b>I</b> to <b>II</b> causes the excited electrons to populate slightly lower-energy bpy ligand π* orbitals that are coordinated to V­(V), and thus this structural change in <b>II</b> leads to a better excited-state charge separation within its hybrid structure

Additional file 1 of Comparison of laparoscopic hepatectomy and percutaneous radiofrequency ablation for the treatment of small hepatocellular carcinoma: a meta-analysis

Supplementary Material 1

Glutathione S-transferase P1 suppresses iNOS protein stability in RAW264.7 macrophage-like cells after LPS stimulation

<div><p>Glutathione S-transferase P1 (GSTP1) is a ubiquitous expressed protein which plays an important role in the detoxification and xenobiotics metabolism. Previous studies showed that GSTP1 was upregulated by the LPS stimulation in RAW264.7 macrophage-like cells and GSTP1 overexpression downregulated lipopolysaccharide (LPS) induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Here we show that GSTP1 physically associates with the oxygenase domain of iNOS by the G-site domain and decreases the protein level of iNOS dimer. Both overexpression and RNA interference (RNAi) experiments indicate that GSTP1 downregulates iNOS protein level and increases S-nitrosylation and ubiquitination of iNOS. The Y7F mutant type of GSTP1 physically associates with iNOS, but shows no effect on iNOS protein content, iNOS S-nitrosylation, and changes in iNOS from dimer to monomer, suggesting the importance of enzyme activity of GSTP1 in regulating iNOS S-nitrosylation and stability. GSTM1, another member of GSTs shows no significant effect on regulation of iNOS. In conclusion, our study reveals the novel role of GSTP1 in regulation of iNOS by affecting S-nitrosylation, dimerization, and stability, which provides a new insight for analyzing the regulation of iNOS and the anti-inflammatory effects of GSTP1.</p></div

Sequential Differentiation of Embryonic Stem Cells into Neural Epithelial-Like Stem Cells and Oligodendrocyte Progenitor Cells

<div><p>Background</p><p>Recent advances in stem cell technology afford an unlimited source of neural progenitors and glial cells for cell based therapy in central nervous system (CNS) disorders. However, current differentiation strategies still need to be improved due to time-consuming processes, poorly defined culture conditions, and low yield of target cell populations.</p><p>Methodology/Principle Findings</p><p>This study aimed to provide a precise sequential differentiation to capture two transient stages: neural epithelia-like stem cells (NESCs) and oligodendrocytes progenitor cells (OPCs) derived from mouse embryonic stem cells (ESCs). CHIR99021, a glycogen synthase kinase 3 (GSK-3) inhibitor, in combination with dual SMAD inhibitors, could induce ESCs to rapidly differentiate into neural rosette-like colonies, which facilitated robust generation of NESCs that had a high self-renewal capability and stable neuronal and glial differentiation potentials. Furthermore, SHH combined with FGF-2 and PDGF-AA could induce NESCs to differentiate into highly expandable OPCs. These OPCs not only robustly differentiated into oligodendrocytes, but also displayed an increased migratory activity <i>in vitro</i>.</p><p>Conclusions/Significance</p><p>We developed a precise and reliable strategy for sequential differentiation to capture NESCs and OPCs derived from ESCs, thus providing unlimited cell source for cell transplantation and drug screening towards CNS repair.</p></div

Rapid and robust differentiation of ESCs into NESCs.

<p>(A) Phase-contrast and fluorescence images of mouse ESCs, which express Oct3/4 and SSEA1. (B) Under defined differentiation conditions by adding SB431542, Dorsomorphin, Noggin, and CHIR99021, ESCs made transitions into neural rosette-like colonies expressing Pax6 and Sox1. (C) ESCs-derived-NESCs differentiated into neuroepithelial-like stem cells (NESCs) expressing Pax6 and Sox1. (D) Cumulative curve showing ESCs-derived NESCs could be expanded over 20 passages (Passage denoted P1-P20). *<i>p</i><0.05, passage 20 (P20) versus all other passages. (E, F) qPCR of representative markers during neural differentiation from ESCs to patterned neural rosettes-like colonies (NR) and NESCs showing a rapid downregulation in pluripotency genes such as Oct4 and Nanog and upregulation in genes specific to NR and NESCs such as Pax6 and Nestin. (G) Representative confocal image showing NESCs were highly pure as the percentage of PLZF-positive cells in total cell population was 97% ± 1%, the values significantly higher than those for negative control (cell population stained only with secondary antibody). Nuclei counterstained with Ho (Hoechst 33342 blue). Data were expressed as means ± SEM from 4 chosen fields per slide. Scale bar, 200 μm in phase contrast images and 50 μm in fluorescence images of A, B, C; and scale bar, 25μm in F. *<i>p</i><0.05.</p

Synthesis of New Mixed-Metal Ammonium Vanadates: Cation Order versus Disorder, and Optical and Photocatalytic Properties

Two new ammonium vanadate hydrates, i.e., M₃(H₂O)₂V₈O₂₄­·2NH₄ (M = Mn and Co, <b>I</b> and <b>II</b>, respectively) were synthesized using hydrothermal reaction conditions, and their structures were determined by single crystal X-ray diffraction [<b>I</b>: <i>P</i>2<i>/m</i> (No. 10), <i>Z</i> = 1, <i>a</i> = 8.2011(2) Å, <i>b</i> = 3.5207(1) Å, <i>c</i> = 9.9129(3) Å, β = 110.987(2)°; <b>II</b>: <i>C</i>2<i>/m</i> (No. 12), <i>Z</i> = 2, <i>a</i> = 19.4594(6) Å, <i>b</i> = 6.7554(2) Å, <i>c</i> = 8.4747(3) Å, β = 112.098(2)°]. Interestingly, the two structures are homeotypic, with the structure of <b>I</b> exhibiting an uncommon type of structural disorder between locally-bridging Mn­(H₂O)₂²⁺ (i.e., part of the oxide framework) and nonbridging NH₄⁺ cations over the same site (1:2 ratio), wherein two NH₄⁺ ions occupy the same site as the two H₂O molecules when Mn­(II) is vacant. The amount of Mn­(II) in the formula of <b>I</b> was determined by a combination of techniques, including electron paramagnetic resonance, while the relative amounts of NH₄⁺/H₂O in its structure were determined by combined thermogravimetric-mass spectrometry analyses as well as confirmed by infrared spectroscopy. In contrast, this site disorder is absent in the crystal structure of <b>II</b>, which contains a fully ordered arrangement of locally-bridging Co­(H₂O)₂²⁺ and NH₄⁺ cations that alternate down its <i>c</i>-axis within a larger superstructure related to <b>I</b> by (<i>a</i> → <i>c</i>, <i>b</i> → 2<i>b</i>, <i>c</i> → 2<i>a</i>). Within both structures, the respective Mn²⁺/Co²⁺ cations bridge to neighboring edge-sharing chains of distorted VO₅ square pyramids, forming a three-dimensional network that contains channels of H₂O and NH₄⁺ molecules. Hydrogen bonding distances in <b>I</b> are significantly longer and weaker than in <b>II</b> and leading to the disordered structure of <b>I</b>. Both show the loss of all H₂O and NH₄⁺ molecules, by ∼300 °C for <b>I</b> and a slightly higher ∼325 °C for <b>II</b>, in each case yielding V₂O₅ and MV₂O₆ (M = Co or Ni) as the final products. Both <b>I</b> and <b>II</b> exhibit visible-light bandgap sizes of ∼1.55 and ∼1.77 eV, respectively, owing to low-energy metal-to-metal electronic transitions. Further, <b>I</b> shows a temperature-dependent photocatalytic activity (at 40 °C) for the production of hydrogen from the reduction of water under irradiation by UV–vis or only visible light at respective rates of ∼314 μmol H₂ g^–1 h^–1 and ∼54 μmol H₂ g^–1 h^–1 (irradiant power density of ∼1.0 W/cm²). Thus, these first two known ammonium vanadate hydrates provide new insights into the structural driving forces for ordered versus disordered structures as well as into their resulting physical properties

Efficient differentiation of NESCs-derived OPCs into OLs.

<p>(A) phase contrast image (left) and fluorescence images (right) by marker MBP for OLs. The percentage of MBP positive population among the differentiated OLs was significantly higher than negative control (cell population stained only with secondary antibody) (B) RT-PCR analysis compared NESCs, OPCs, and OLs with representative markers for each population. (C) qPCR profiling, performed during the transition of NESCs-derived OPCs to OLs, showing a rapid down regulation of OPCs genes and up regulation of genes specific to OLs. (D) Phase contrast (left) and immunofluorescence image (right) of astrocytes marked with GFAP differentiated from OPCs, and quantitative analysis revealed that there was significant different between the percentage of GFAP positive astrocytes and negative control marked only with 2° antibody. (p<0.05) (E) Immunofluorescence image of neurons derived from NESCs with a marker of β-tubulin III. Also shown (at the right half) is a magnification of the boxed area in the left half. Scale bar, 100 μm in (A), 200 μm in (D), 100 μm in the left half of (E), and 50 μm in the right half of (E). *<i>p</i><0.05.</p

Schematic diagram showing step-by-step differentiation of ESCs into OLs under influences of a series of developmental signals.

<p>Schematic diagram showing step-by-step differentiation of ESCs into OLs under influences of a series of developmental signals.</p

Comparison of NSCs and NESCs.

<p>(A) Phase contrast of NSCs isolated from mouse embryo cortex and NESCs derived from ESCs, which were both at p1. (B) RT-PCR analysis of NSCs and NESCs at P1 with representative NSC markers (C) According to the expression of representative genes in NESCs and NSCs, as determined by RT-PCR, NESCs shared similar markers as NSCs such as Pax6, Neurod4, Ncam1, Nestin, and Rarb. (D) Immunocytochemistry of NSCs and NESCs at P1 revealed that they shared similar NSC markers such as Sox1, Pax6, Sox9 and CD133. Scale bar, 200 μm in A, and 50 μm in D.</p

Comparison of NESCs at different passages.

<p>(A) Phase contrast of NESCs at P1 and P10. (B) Flow cytometry analysis revealed that percentage of NESC population positive for Nestin and PLZF are over 90% at both p1 and p10. (C) Immunocytochemistry of NESC showed that NESCs at P10 still expressed neuroepithelial stem cell markers, such as Sox1, Sox2, Dach1, PLZF and ZO-1 as in P1. Scale bar, 200 μm in A, and 50 μm in C.</p