Probabilistic optimization of fatigue maintenance for welded components in steel bridges based on LEFM and LCCM

In this paper a probabilistic-based method for fatigue maintenance optimization of steel bridge’s welded joints, combined with linear elastic fracture mechanics (LEFM), the structure reliability, and life cycle cost method(LCCM) is proposed. The probabilistic analysis method can be used with the fatigue maintenance of steel bridges. Weld cracks are classified by its size and maintenance decisions, and are made according to its size classification. Maintenance cost is divided into inspection, repair and failure costs, according to the life cycle cost method. The maintenance optimization strategy is transformed to minimize the expected lifetime total costs with the constraints of the minimum acceptable reliability index to attain the most cost-optimal inspection and repair for the balanced costs between risk and safety. An example concerning the transverse stiffeners of welded components in the main girder of suspension bridge is investigated through the research of some parameters sensitivity. Among all the parameters, the inspection cost is the most remarkable. The optimal time interval of repair will delay based on the increase of the inspection cost. The optimal time interval of repair will advance based on the increase of repair cost. A discount rate can drastically change the value of the total cost, but when the probability of failure is very small, the increase of failure cost has little effect on the optimal time interval of repair. The method presented in this paper can be conducted using the similar maintenance of steel structures

Facile Preparation of Efficient WO 3

Tungsten trioxide (WO3) was surface modified with Cu(II) nanoclusters and titanium dioxide (TiO2) nanopowders by using a simple impregnation method followed by a physical combining method. The obtained nanocomposites were studied by scanning electron microscope, X-ray photoelectron spectroscopy spectra, UV-visible light spectra, and photoluminescence, respectively. Although the photocatalytic activity of WO3 was negligible under visible light irradiation, the visible light photocatalytic activity of WO3 was drastically enhanced by surface modification of Cu(II) nanoclusters and TiO2 nanopowders. The enhanced photocatalytic activity is due to the efficient charge separation by TiO2 and Cu(II) nanoclusters functioning as cocatalysts on the surface. Thus, this simple strategy provides a facile route to prepare efficient visible-light-active photocatalysts for practical application

Long-Term Exposure of Fine Particulate Matter Causes Hypertension by Impaired Renal D1 Receptor-Mediated Sodium Excretion via Upregulation of G-Protein-Coupled Receptor Kinase Type 4 Expression in Sprague-Dawley Rats.

BACKGROUND: Epidemiological evidence supports an important association between air pollution exposure and hypertension. However, the mechanisms are not clear. METHODS AND RESULTS: Our present study found that long-term exposure to fine particulate matter (PM2.5) causes hypertension and impairs renal sodium excretion, which might be ascribed to lower D1 receptor expression and higher D1 receptor phosphorylation, accompanied with a higher G-protein-coupled receptor kinase type 4 (GRK4) expression. The in vivo results were confirmed in in vitro studies (ie, PM2.5 increased basal and decreased D1 receptor mediated inhibitory effect on Na+-K+ ATPase activity, decreased D1 receptor expression, and increased D1 receptor phosphorylation in renal proximal tubule cells). The downregulation of D1 receptor expression and function might be attributable to a higher GRK4 expression after the exposure of renal proximal tubule cells to PM2.5, because downregulation of GRK4 by small-interfering RNA reversed the D1 receptor expression and function. Because of the role of reactive oxygen species on D1 receptor dysfunction and its relationship with air pollution exposure, we determined plasma reactive oxygen species and found the levels higher in PM2.5-treated Sprague-Dawley rats. Inhibition of reactive oxygen species by tempol (4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl) reduced blood pressure and increased sodium excretion in PM2.5-treated Sprague-Dawley rats, accompanied by an increase in the low D1 receptor expression, and decreased the hyperphosphorylated D1 receptor and GRK4 expression. CONCLUSIONS: Our present study indicated that long-term exposure of PM2.5 increases blood pressure by decreasing D1 receptor expression and function; reactive oxygen species, via regulation of GRK4 expression, plays an important role in the pathogenesis of PM2.5-induced hypertension

BCL-xL Regulates ATP Synthase and Synaptic Efficiency

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Characterization and cytotoxicity of PAHs in PM2.5 emitted from residential solid fuel burning in the Guanzhong Plain, China

The emission factors (EFs) of polycyclic aromatic hydrocarbons (PAHs) in PM2.5 were measured from commonly used stoves and fuels in the rural Guanzhong Plain, China. The toxicity of the PM2.5 also was measured using in vitro cellular tests. EFs of PAHs varied from 0.18 mg kg(-1) (maize straw charcoal burning in a clean stove) to 83.3 mg kg(-1) (maize straw burning in Heated Kang). The two largest influencing factors on PAH EFs were air supply and volatile matter proportion in fuel. Improvements in these two factors could decrease not only EFs of PAHs but also the proportion of 3-ring to 5-ring PAHs. Exposure to PM2.5 extracts caused a concentration-dependent decline in cell viability but an increase in reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6). PM2.5 emitted from maize burning in Heated Kang showed the highest cytotoxicity, and EFs of ROS and inflammatory factors were the highest as well. In comparison, maize straw charcoal burning in a clean stove showed the lowest cytotoxicity, which indicated a clean stove and fuel treatment were both efficient methods for reducing cytotoxicity of primary PM2.5. The production of these bioreactive factors were highly correlated with 3-ring and 4-ring PAHs. Specifically, pyrene, anthracene and benzo(a)anthracene had the highest correlations with ROS production (R = 0.85, 0.81 and 0.80, respectively). This study shows that all tested stoves emitted PM2.5 that was cytotoxic to human cells; thus, there may be no safe levels of exposure to PM2,5 emissions from cooking and heating stoves using solid fuels. The study may also provide a new approach for evaluating the cytotoxicity of primary emitted PM2.5 from solid fuel burning as well as other PM2.5 sources. (C) 2018 Elsevier Ltd. All rights reserved

MiR-199a-5P promotes osteogenic differentiation of human stem cells from apical papilla via targeting IFIT2 in apical periodontitis

IntroductionPeriapical alveolar bone loss is the common consequence of apical periodontitis (AP) caused by persistent local inflammation around the apical area. Human stem cells from apical papilla (hSCAPs) play a crucial role in the restoration of bone lesions during AP. Studies have recently identified the critical role of microRNAs (miRNAs) involved in AP pathogenesis, but little is known about their function and potential molecular mechanism, especially in the osteogenesis of hSCAPs during AP. Here, we investigated the role of clinical sample-based specific miRNAs in the osteogenesis of hSCAPs.MethodsDifferential expression of miRNAs were detected in the periapical tissues of normal and patients with AP via transcriptomic analysis, and the expression of miR-199a-5p was confirmed by qRT-PCR. Treatment of hSCAPs with miR-199a-5p mimics while loaded onto beta-tricalcium phosphate (β-TCP) ceramic particle scaffold to explore its effect on osteogenesis in vivo. RNA binding protein immunoprecipitation (RIP) and Luciferase reporter assay were conducted to identify the target gene of miR-199a-5p.ResultsThe expression of miR-199a-5p was decreased in the periapical tissues of AP patients, and miR-199a-5p mimics markedly enhanced cell proliferation and osteogenic differentiation of hSCAPs, while miR-199a-5p antagomir dramatically attenuated hSCAPs osteogenesis. Moreover, we identified and confirmed Interferon Induced Protein with Tetratricopeptide Repeats 2 (IFIT2) as a specific target of miR-199a-5p, and silencing endogenous IFIT2 expression alleviated the inhibitory effect of miR-199a-5p antagomir on the osteogenic differentiation of hSCAPs. Furthermore, miR-199a-5p mimics transfected hSCAPs loaded onto beta-tricalcium phosphate (β-TCP) scaffolds induced robust subcutaneous ectopic bone formation in vivo.DiscussionThese results strengthen our understanding of predictors and facilitators of the key AP miRNAs (miR-199a-5p) in bone lesion repair under periapical inflammatory conditions. And the regulatory networks will be instrumental in exploring the underlying mechanisms of AP and lay the foundation for future regenerative medicine based on dental mesenchymal stem cells