35 research outputs found
Primordial Magnetic Field from Gravitationally Coupled Electrodynamics in Bouncing Scenario
We in this paper study the generation of primordial magnetic field (PMF) in
the non-singular bouncing scenario, through the coupling of the electromagnetic
field to gravity. We adopt an electrodynamic model with a coupling coefficient
as a function of the scale factor , i.e. , with
and being constants. The result implies that in this mechanism,
the power spectrum of PMF today is always blue tilted on large scales from
Mpc to the Hubble length, and the observational constraints favor the
ekpyrotic-bounce scenario. Furthermore, the back reaction of the energy density
of PMF at the bouncing point yields theoretical constraints on the bouncing
model
Selective Formation of Cu Active Sites with Different Coordination States on Pseudospinel CuAl<sub>2</sub>O<sub>4</sub> and Their NO Reduction Catalysis
In the spinel framework,
copper (Cu) in two distinct
coordination
states exhibits catalytic activity for NO reduction through different
mechanisms. However, detailed exploration of their respective catalytic
properties, such as the redox behavior of Cu and substrate molecule
adsorption, has been challenging due to difficulties in their separate
formation. In this study, we present the controlled formation of pseudospinel
CuAl2O4, containing exclusively tetrahedrally
or octahedrally coordinated Cu, achieved by manipulating aging temperature
and O2 concentration. Through these materials, we observed
that in the CO–NO reaction, the step primarily determining
the rate differs: NO reduction dominates with octahedrally coordinated
Cu, whereas carbon monoxide (CO) oxidation is prominent with tetrahedrally
coordinated Cu. The lower coordination number of Cu significantly
benefits NO reduction but negatively impacts the CO–NO reaction,
albeit positively influencing NO reduction in three-way catalytic
reactions
Redox Dynamics of Rh Supported on ZrP<sub>2</sub>O<sub>7</sub> and ZrO<sub>2</sub> Analyzed by Time-Resolved In Situ Optical Spectroscopy
In situ time-resolved
diffuse reflectance spectroscopy was first
applied to supported Rh catalysts (0.4 wt % Rh/ZrO<sub>2</sub> and
Rh/ZrP<sub>2</sub>O<sub>7</sub>) under dynamic three-way catalysis
conditions fluctuating between fuel-lean and fuel-rich gas atmospheres.
The optical absorption at 650 nm was found to decrease upon lean-to-rich
switching of the gas feed, which led to the reduction of Rh oxide
(Rh<sup>3+</sup>) to metallic Rh (Rh<sup>0</sup>), followed by a reversible
increase upon back switching rich-to-lean. The kinetic analysis suggested
that the reduction of Rh<sup>3+</sup> to Rh<sup>0</sup> was faster
than the reoxidation over Rh/ZrP<sub>2</sub>O<sub>7</sub>, whereas
the reduction was comparable with or slower than the reoxidation over
Rh/ZrO<sub>2</sub>. The activation energy of Rh/ZrP<sub>2</sub>O<sub>7</sub> for the reduction, 13.6 kJ mol<sup>–1</sup>, was smaller
than that for the oxidation, 48.7 kJ mol<sup>–1</sup>, which
contrasted with those of Rh/ZrO<sub>2</sub> (21.4 and 34.1 kJ mol<sup>–1</sup>, respectively). These results were closely associated
with the higher NO reduction activity of Rh/ZrP<sub>2</sub>O<sub>7</sub> than Rh/ZrO<sub>2</sub> under a lean-gas atmosphere because Rh was
more active in the metallic state than in the oxide state. Applying
fast lean–rich perturbation of the gas feed with 1 s intervals
led to an immediate and significant drop of the optical absorption
intensity, suggesting that the reduction of Rh substantially penetrated
to deeper layers under the surface. This study provided the first
in situ evidence for the formation of active metallic Rh species under
high-frequency lean–rich oscillations
<i>MiR-376c</i> Down-Regulation Accelerates EGF-Dependent Migration by Targeting <i>GRB2</i> in the HuCCT1 Human Intrahepatic Cholangiocarcinoma Cell Line
<div><p>MicroRNA <i>miR-376c</i> was expressed in normal intrahepatic biliary epithelial cells (HIBEpiC), but was significantly suppressed in the HuCCT1 intrahepatic cholangiocarcinoma (ICC) cell line. The biological significance of the down-regulation of <i>miR-376c</i> in HuCCT1 cells is unknown. We hypothesized that <i>miR-376c</i> could function as a tumor suppressor in these cells. To test this hypothesis, we sought the targets of <i>miR-376c</i>, and characterized the effect of its down-regulation on HuCCT1 cells. We performed proteomic analysis of <i>miR-376c</i>-overexpressing HuCCT1 cells to identify candidate targets of <i>miR-376c</i>, and validated these targets by 3′-UTR reporter assay. Transwell migration assays were performed to study the migratory response of HuCCT1 cells to <i>miR-376c</i> overexpression. Furthermore, microarrays were used to identify the signaling that were potentially involved in the <i>miR-376c</i>-modulated migration of HuCCT1. Finally, we assessed epigenetic changes within the potential promoter region of the <i>miR-376c</i> gene in these cells. Proteomic analysis and subsequent validation assays showed that <i>growth factor receptor-bound protein 2</i> (<i>GRB2</i>) was a direct target of <i>miR-376c</i>. The transwell migration assay revealed that <i>miR-376c</i> significantly reduced epidermal growth factor (EGF)-dependent cell migration in HuCCT1 cells. DNA microarray and subsequent pathway analysis showed that interleukin 1 beta and matrix metallopeptidase 9 were possible participants in EGF-dependent migration of HuCCT1 cells. Bisulfite sequencing showed higher methylation levels of CpG sites upstream of the <i>miR-376c</i> gene in HuCCT1 relative to HIBEpiC cells. Combined treatment with the DNA-demethylating agent 5-aza-2′-deoxycytidine and the histone deacetylase inhibitor trichostatin A significantly upregulated the expression of <i>miR-376c</i> in HuCCT1 cells. We revealed that epigenetic repression of <i>miR-376c</i> accelerated EGF-dependent cell migration through its target <i>GRB2</i> in HuCCT1 cells. These findings suggest that <i>miR-376c</i> functions as a tumor suppressor. Since metastasis is the major cause of death in ICC, microRNA manipulation could lead to the development of novel anti-cancer therapy strategies for ICC.</p></div
Unusual Redox Behavior of Rh/AlPO<sub>4</sub> and Its Impact on Three-Way Catalysis
The
influence of the redox behavior of Rh/AlPO<sub>4</sub> on automotive
three-way catalysis (TWC) was studied to correlate catalytic activity
with thermal stability and metal–support interactions. Compared
with a reference Rh/Al<sub>2</sub>O<sub>3</sub> catalyst, Rh/AlPO<sub>4</sub> exhibited a much higher stability against thermal aging under
an oxidizing atmosphere; further deactivation was induced by a high-temperature
reduction treatment. In situ X-ray absorption fine structure experiments
revealed a higher reducibility of Rh oxide (RhO<sub><i>x</i></sub>) to Rh, and the metal showed a higher tolerance to reoxidation
when supported on AlPO<sub>4</sub> compared with Al<sub>2</sub>O<sub>3</sub>. This unusual redox behavior is associated with an Rh–O–P
interfacial linkage, which is preserved under oxidizing and reducing
atmospheres. Another effect of the Rh–O–P interfacial
linkage was observed for the metallic Rh with an electron-deficient
character. This leads to the decreasing back-donation from Rh <i>d</i>-orbitals to the antibonding π* orbital of chemisorbed
CO or NO, which is a possible reason for the deactivation by high-temperature
reduction treatments. On the other hand, surface acid sites on AlPO<sub>4</sub> promoted oxidative adsorption of C<sub>3</sub>H<sub>6</sub> as aldehyde, which showed a higher reactivity toward O<sub>2</sub>, as well as NO, compared with carboxylate adsorbed on Al<sub>2</sub>O<sub>3</sub>. A precise control of the acid–base character
of the metal phosphate supports is therefore a key to enhance the
catalytic performance of supported Rh catalysts for TWC applications
Downregulation of <i>miR-376c</i> expression levels in bile duct carcinoma cell lines, and proteomic analysis of <i>miR-376c</i>-overexpressing HuCCT1.
<p>(<b>A</b>) Real-time PCR assay of <i>miR-376c</i> in HIBEpiC, HuCCT1, Huh28, IHGGK, TKKK, and TFK1. Expression levels were normalized to <i>RNU6B</i>, and the expression level in HIBEpiC cells was defined as 1. The significance of differences among cells was assessed by ANOVA followed by Tukey's test (*<i>P</i><0.05). (<b>B</b>) Representative 2D-DIGE images of <i>miR-376c</i>-overexpressing HuCCT1 cells. Cells were harvested 72 h after the initiation of transfection of Pre-miR-376c or the Pre-miR-negative control, and subjected to proteomic analysis. A spot downregulated by treatment with Pre-miR-376c is indicated by the arrow, which was later shown by mass spectrometry to be GRB2. (<b>C</b>) Quantitative analysis of the fluorescence intensity of the GRB2 protein spot shown in <b>B</b> (peak outlined in red).</p
The effect of Olig1 deficiency on T cell proliferation capability.
<p>(A) Proliferative responses of MOG-specific T cells isolated from WT and Olig1<sup>−/−</sup> EAE mice (<i>n</i> = 4). (B) RT-PCR analysis of Olig1 expression in brain, spinal cord, lymph node, spleen and thymus of WT mice.</p
Quantification of histopathology of the spinal cords in EAE mice.
<p>Quantitative analysis of the extent of demyelination (A), GFAP-positive (B) and iba1-positive (C) cells in the spinal cord. The areas of demyelinated regions in the white matter were measured by ImageJ 1.43u and expressed as a percentage of the whole area of the white matter. GFAP- and iba1-positive cells were counted per unit area (0.143 mm<sup>2</sup>) in the middle region of the ventral horn. ***<i>P</i><0.001; **<i>P</i><0.01; *<i>P</i><0.05.</p
Validation of <i>GRB2</i> as a <i>miR-376c</i> Target.
<p>(<b>A</b>) Western blotting analysis of GRB2 protein levels in HuCCT1 cells transfected with Pre-miR-376c or the Pre-miR negative control (NC). ACTB was monitored as an internal control. Relative GRB2 expression levels were calculated and are indicated below the bands. (<b>B</b>) <i>GRB2</i> mRNA expression levels in HuCCT1 cells transfected with Pre-miR-376c or the Pre-miR negative control (NC). The <i>GRB2</i> expression level was normalized to <i>GAPDH</i>. The expression level of the NC sample was defined as 1. The significance of differences between means was determined by Student's <i>t</i>-test. (<b>C</b>) The sequences of the mature <i>miR-376c</i> and its putative target site in the 3'-UTR of <i>GRB2</i>. The target site corresponding to the seed sequence of <i>miR-376c</i> was converted via mutation; the mutation introduced into the <i>miR-376c</i> recognition site of <i>GRB2</i> 3'-UTR in the reporter plasmid is also shown. (<b>D</b>) <i>GRB2</i> 3'-UTR luciferase reporter assay. Reporter vector (pMIR-GRB2 [GRB2] or pMIR-GRB2mt [GRB2mt]) and Pre-miR molecule (Pre-miR-376c [376c] or Pre-miR negative control [NC]) were co-transfected into HuCCT1 cells. Renilla luciferase vector pRL-TK was used as an internal control. Luciferase expression levels of Pre-miR negative control (NC) were set to 1.0. The significance of differences between means was determined by Student's <i>t</i>-test.</p
Representative histopathology of the optic nerves in EAE mice.
<p>(A) Optic nerves were stained with luxol fast blue (LFB) and hematoxylin and eosin (HE) (upper two panels) or NF200 and toluidine blue for the semithin transverse sections (lower two panels). The arrows point to the degenerating axons. Scale bar: 100 µm for the first and third panels, 75 µm for the second panels and 15 µm for the lower panels. (B) Quantitative analysis of cell infiltrates in the longitudinal section of the optic nerve. (C) Quantitative analysis of degenerating axons in the transverse section of the optic nerve. *<i>P</i><0.01.</p