Search

As a fission product in high‐level radioactive nuclear waste, Mo has low solubility in borosilicate glass. Fe2O3 is not only a prevalent transition metal element but also a major corrosion product in high‐level radioactive nuclear waste. Against this backdrop, the effect of Fe2O3 content on the structure and chemical durability of typical molybdenum‐containing sodium borosilicate glasses for nuclear waste immobilization are studied. The results show that the samples containing more than 3.85 mol% Fe2O3, a completely homogenous amorphous glass sample is obtained. Moreover, the mechanism of the effect of Fe2O3 on the solubility of Mo is discussed in detail. In this work, a portion of Fe3+ is reduced to Fe2+ and enters into the glasses as a charge compensation ion as Fe2+O6. Concurrently, Fe3+ ions contribute to the formation of the glass networks as Fe3+O4. Iron incorporation can improve the chemical durability of the sample. [ABSTRACT FROM AUTHOR]

The effect of substitution of Li2O for Na2O on the solubility, crystallization of Mo in an aluminoborosilicate glass, and their aqueous durability were investigated. The results show that the substitution of Li2O for Na2O improves the depolymerization degree of the glass network by transferring part of [4]Al to [5]Al and [6]Al. When the Na2O is all replaced by Li2O, the solubility of Mo in the glass reaches 5 mol%. From the structural analysis, with the increase of the solubility of Mo in the glass, the depolymerization degree of the glass and the average modified cations field strength in the depolymerization region are also increased. After 28 days, the normalized leaching rates of Mo and B of all samples are about ~10−4 g·m−2·d−1 and ~10−3 g·m−2·d−1, respectively, and the normalized leaching rates of Mo decrease with the substitution of Li2O for Na2O. The results provide researchers and engineers with a potential way to improve the solubility of Mo in nuclear waste glasses. [ABSTRACT FROM AUTHOR]

Background: Large-scale normative studies of pancreatic stiffness and potential influences have yet to be pursued via magnetic resonance elastography (MRE).Purpose: To determine normative MRE-based pancreatic stiffness values and to examine related influential factors.Study Type: Prospective.Subjects: In all, 361 volunteers (men, 199; women, 162) with a median age of 54.0 years and a median body mass index (BMI) of 22.86 kg/m2 were prospectively recruited. Those with no histories of smoking, alcohol abuse, and diabetes mellitus (DM) were grouped as healthy volunteers, designating all others as positive controls.Field Strength/sequence: Each volunteer underwent 3.0T pancreatic MRI at a frequency of 40 Hz.Assessment: Pancreatic stiffness values, pancreatic width and volume, waist circumference, and wave distance were measured in all subjects.Statistical Tests: Multiple linear regression analyses were performed to determine variables that influence MRE-determined stiffness.Results: The mean pancreatic stiffness in all volunteers was 1.20 ± 0.16 kPa. Stiffness levels in positive control volunteers proved significantly greater than levels in healthy volunteers (1.29 ± 0.17 kPa vs. 1.14 ± 0.13 kPa; P < 0.001). In multiple linear regression analysis, sex (P = 0.004), BMI (P < 0.001), pancreatic width (P = 0.005), smoking (P < 0.001), alcohol abuse (P < 0.001), and DM (P = 0.001) emerged as significant independent factors impacting pancreatic stiffness. Smoking, alcohol abuse, DM, and wide pancreas were associated with greater pancreatic stiffness (coefficients = 0.202, 0.183, 0.149, and 0.160, respectively), while reduced pancreatic stiffness corresponded with female sex and larger BMI (coefficient = -0.155 and -0.192, respectively).Data Conclusion: MRE-based pancreatic stiffness values are impacted by sex, BMI, pancreatic width, smoking, alcohol abuse, and DM. Reference values are essential for future clinical studies.Level Of Evidence: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2020;52:448-458. [ABSTRACT FROM AUTHOR]

In this article, design, fabrication, and testing of SiC/SiC turbine blisk with the fiber’s preform of Spider Web Structure (SWS) subjected to different load spectrums at elevated temperature are conducted. Micro-CT scans are conducted to show the fibers preform and defects inside the SWS-SiC/SiC turbine blisk. For 2D plain-woven SiC/SiC composite under monotonic tensile loading at an elevated temperature of T = 900°C in air atmosphere, the composite ultimate tensile strength is σ uts = 200 MPa with the fracture strain ε f = 0.36%. For SWS-SiC/SiC turbine blisk under the rotation testing, the first and second order natural frequency of the SWS-SiC/SiC turbine blisk are tested using the laser vibration meter. Relationships between the rotation speed, internal damage, and the natural frequency degradation of the SWS-SiC/SiC turbine blisk are established. Under the maximum rotation speed of n = 17,000 rpm at the exhaust temperature of T = 930°C, no damage occurred in the SWS-SiC/SiC turbine blisk. However, multiple coating spalling occurred due to the thermal-chemical coupling failure of the coating under flame impingement. The first natural frequency of the SWS-SiC/SiC turbine blisk decreases by 5% with the increase in the rotating speed from n max = 85,000 rpm to n max = 105,000 rpm, which indicates that there is an internal damage in the SWS-SiC/SiC turbine blisk, which leads to the decrease in the stiffness of the blisk.

Homeostasis of Smad phosphorylation at its C-terminal SXS motif is essential for transforming growth factor beta (TGFbeta) signaling. Whereas it is known that TGFbeta signaling can be terminated by phosphatases, which dephosphorylate R-Smads in the nucleus, it is unclear whether there are any cytoplasmic phosphatase(s) that can attenuate R-Smad phosphorylation and nuclear translocation. Here we demonstrate that myotubularin-related protein 4 (MTMR4), a FYVE domain-containing dual-specificity protein phosphatase (DSP), attenuates TGFbeta signaling by reducing the phosphorylation level of R-Smads in early endosomes. Co-immunoprecipitation experiments showed that endogenous MTMR4 interacts with phosphorylated R-Smads, and that this interaction is correlated with dephosphorylation of R-Smads. Further analysis showed that overexpression of MTMR4 resulted in the sequestration of activated Smad3 in the early endosomes, thus reducing its nuclear translocation. However, both point mutations at the conserved catalytic site of the phosphatase (MTMR4-C407S) and small interference RNA of endogenous Mtmr4 expression led to sustained Smad3 activation. This work therefore suggests that MTMR4 plays an important role in preventing the overactivation of TGFbeta signaling by dephosphorylating activated R-Smads that have been trafficked to early endosomes.