Quasi-Brittle Fracture Modeling of Preflawed Bitumen Using a Diffuse Interface Model

Fundamental understandings on the bitumen fracture mechanism are vital to improve the mixture design of asphalt concrete. In this paper, a diffuse interface model, namely, phase-field method is used for modeling the quasi-brittle fracture in bitumen. This method describes the microstructure using a phase-field variable which assumes one in the intact solid and negative one in the crack region. Only the elastic energy will directly contribute to cracking. To account for the growth of cracks, a nonconserved Allen-Cahn equation is adopted to evolve the phase-field variable. Numerical simulations of fracture are performed in bituminous materials with the consideration of quasi-brittle properties. It is found that the simulation results agree well with classic fracture mechanics

State Observer Synchronization Used in the Three-Dimensional Duffing System

Synchronization of chaotic systems has attracted extensive concern in the past few years. In this study, we investigate a new structure of Duffing system by the variable decomposition method. Then, we analyze the state observer synchronization based on the new Duffing system. It is proved theoretically that the designed observer can keep synchronization with Duffing chaotic system in transmitter. The design is presented reasonably with the conditional Lyapunov exponents, and its effectiveness is clearly shown in simulation results

N6-Methyladenosine Methyltransferase METTL3 Alleviates Diabetes-Induced Testicular Damage through Modulating TUG1/Clusterin Axis

Background The present study investigated the regulatory effects of N6-methyladenosine (m6A) methyltransferase like-3 (METTL3) in diabetes-induced testicular damage. Methods In vivo diabetic mice and high glucose (HG) treated GC-1 spg cells were established. The mRNA and protein expressions were determined by real-time quantitative polymerase chain reaction, Western blot, immunofluorescence and immunohistochemistry staining. Levels of testosterone, blood glucose, cell viability, and apoptosis were detected by enzyme-linked immunosorbent assay, MTT, and flow cytometry, respectively. Molecular interactions were verified by RNA immunoprecipitation and RNA pull-down assay. Histopathological staining was performed to evaluate testicular injury. Results METTL3 and long non-coding RNA taurine up-regulated 1 (lncRNA TUG1) were downregulated in testicular tissues of diabetic mice and HG-treated GC-1 spg cells. METTL3 overexpression could reduce the blood glucose level, oxidative stress and testicular damage but enhance testosterone secretion in diabetic mouse model and HG-stimulated GC-1 spg cells. Mechanically, METTL3-mediated m6A methylation enhanced the stability of TUG1, then stabilizing the clusterin mRNA via recruiting serine and arginine rich splicing factor 1. Moreover, inhibition of TUG1/clusterin signaling markedly reversed the protective impacts of METTL3 overexpression on HG-stimulated GC-1 spg cells. Conclusion This study demonstrated that METTL3 ameliorated diabetes-induced testicular damage by upregulating the TUG1/clusterin signaling. These data further elucidate the potential regulatory mechanisms of m6A modification on diabetes-induced testicular injury

1,4-Bis(2-pyridylmethyl­eneamino­meth­yl)benzene

The asymmetric unit of the centrosymmetric title compound, C20H18N4, contains one half-mol­ecule. The pyridine and benzene rings are oriented at a dihedral angle of 77.21 (7)°

Propionate Ameliorates Dextran Sodium Sulfate-Induced Colitis by Improving Intestinal Barrier Function and Reducing Inflammation and Oxidative Stress

Propionate is a short chain fatty acid and abundant as butyrate in the gut and blood. However, propionate has been studied less extensively than butyrate in the treatment of colitis. The present study was to investigate the effects of sodium propionate on intestinal barrier function, inflammation and oxidative stress in dextran sulfate sodium (DSS)-induced mice. Animals in DSS group received drinking water from 1 to 6 days and DSS (3% (w/v) dissolved in double distilled water) instead of drinking water from 7 to 14 days. Animals in DSS+Prop group were given 1% sodium propionate for 14 consecutive days and supplemented with 3% DSS solution on day 7-14. Intestinal barrier function, proinflammatory factors, oxidative stress, and signal transducer and activator of transcription 3 (STAT3) signaling pathway in the colon were determined. It was found that sodium propionate ameliorated body weight loss, colon-length shortening and colonic damage in colitis mice. Sodium propionate significantly inhibited the increase of FITC-dextran in serum and the decrease of zonula occludens-1 (ZO-1), occludin and E-cadherin expression in the colonic tissue. It also inhibited the expression of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) mRNA and phosphorylation of STAT3 in colitis mice markedly, reduced the myeloperoxidase (MPO) level, and increased the superoxide dismutase (SOD) and catalase (CAT) level in colon and serum compared with DSS group. Sodium propionate inhibited macrophages with CD68 marker infiltration into the colonic mucosa of colitis mice. These results suggest that oral administration of sodium propionate could ameliorate DSS-induced colitis mainly by improving intestinal barrier function and reducing inflammation and oxidative stress via the STAT3 signaling pathway