Microstructure and Mechanical Properties of Laser-Welded DP Steels Used in the Automotive Industry.

The aim of this work was to investigate the microstructure and the mechanical properties of laser-welded joints combined of Dual Phase DP800 and DP1000 high strength thin steel sheets. Microstructural and hardness measurements as well as tensile and fatigue tests have been carried out. The welded joints (WJ) comprised of similar/dissimilar steels with similar/dissimilar thickness were consisted of different zones and exhibited similar microstructural characteristics. The trend of microhardness for all WJs was consistent, characterized by the highest value at hardening zone (HZ) and lowest at softening zone (SZ). The degree of softening was 20 and 8% for the DP1000 and DP800 WJ, respectively, and the size of SZ was wider in the WJ combinations of DP1000 than DP800. The tensile test fractures were located at the base material (BM) for all DP800 weldments, while the fractures occurred at the fusion zone (FZ) for the weldments with DP1000 and those with dissimilar sheet thicknesses. The DP800-DP1000 weldment presented similar yield strength (YS, 747 MPa) and ultimate tensile strength (UTS, 858 MPa) values but lower elongation (EI, 5.1%) in comparison with the DP800-DP800 weldment (YS 701 MPa, UTS 868 MPa, EI 7.9%), which showed similar strength properties as the BM of DP800. However, the EI of DP1000-DP1000 weldment was 1.9%, much lower in comparison with the BM of DP1000. The DP800-DP1000 weldment with dissimilar thicknesses showed the highest YS (955 MPa) and UTS (1075 MPa) values compared with the other weldments, but with the lowest EI (1.2%). The fatigue fractures occurred at the WJ for all types of weldments. The DP800-DP800 weldment had the highest fatigue limit (348 MPa) and DP800-DP1000 with dissimilar thicknesses had the lowest fatigue limit (<200 MPa). The fatigue crack initiated from the weld surface.

Characteristics of poly-silicate aluminum sulfate prepared by sol method and its application in Congo red dye wastewater treatment.

A novel method for synthesizing poly-silicate aluminum sulfate coagulant (PSAS) using a silica-alumina sol was reported. Herein, two modalities (nSiO2/nNa2O: 1.11 and 3.27) of self-made water glasses were used as the silica source for synthesizing the sol precursor. Then, the PSAS1.11 and PSAS3.27 with different basicity were obtained by controlling the Al molar ratio of precursor to aluminum sulfate. The results showed that the PSAS1.11 coagulant prepared with low modulus water glass (LMWS, 1.11) has low turbidity and good stability. Using low modulus water glass, the effect of the Al molar ratio of precursor to aluminum sulfate on the basicity and stability of PSAS1.11 with Al/Si of 20 and the effect of the molar ratio of aluminum to silicon on the basicity and stability of PSAS1.11 were studied, respectively. Based on XRD and Fourier infrared (FTIR) characterization of the sol precursor and PSAS1.11, the synthesis mechanism of PSAS by the silica-alumina sol method was discussed. Al species distribution of PSAS1.11 was determined using the Al-Ferron timed spectrophotometric method. Moreover, the performance of PSAS1.11 coagulant was examined, regarding its efficiency towards color removal of Congo red. The results showed that PSAS1.11 coagulant with Al/Si of 20 and Al molar ratio of 1/12 exhibits excellent performance, and the color removal rate reached 98.6% at an initial pH of 11 and coagulant dosage of 40 mg L-1 (Al mg L-1). Finally, the PSAS coagulant mechanism was discussed in detail through infrared characterization, 27Al NMR, Raman, morphology and mapping of the flocs.

Cullin3/KCTD5 induces monoubiquitination of ΔNp63α and impairs its activity.

Potassium channel tetramerization domain containing 5 (KCTD5) was previously documented as a component of the Cullin3-RING ligase (CRL3). It has been reported that KCTD5 can induce enrichment of polyubiquitinated proteins, and KCTD5-based CRL3 destabilizes several proteins. In our present study, we report that KCTD5 may physically interact with ΔNp63α, which is a member of the p53 family. Our further investigation revealed that Cullin3/KCTD5 can induce monoubiquitination of ΔNp63α. Cullin3/KCTD5 downregulates the DNA-binding affinity of ΔNp63α, impairing either its transactivity or its transinhibitory activity. Functionally, Cullin3/KCTD5 abates the proproliferation activity of ΔNp63α. These findings suggest that KCTD5-based CRL3 may mediate monoubiquitination and is a novel regulator of ΔNp63α.

p53 and p73 Regulate Apoptosis but Not Cell-Cycle Progression in Mouse Embryonic Stem Cells upon DNA Damage and Differentiation.

Embryonic stem cells (ESCs) are fast proliferating cells capable of differentiating into all somatic cell types. In somatic cells, it is well documented that p53 is rapidly activated upon DNA damage to arrest the cell cycle and induce apoptosis. In mouse ESCs, p53 can also be functionally activated, but the precise biological consequences are not well characterized. Here, we demonstrated that doxorubicin treatment initially led to cell-cycle arrest at G2/M in ESCs, followed by the occurrence of massive apoptosis. Neither p53 nor its target gene p73 was required for G2/M arrest. Instead, p53 and p73 were fully responsible for apoptosis. p53 and p73 were also required for differentiation-induced apoptosis in mouse ESCs. In addition, doxorubicin treatment induced the expression of retinoblastoma protein in a p53-dependent manner. Therefore, both p53 and p73 are critical in apoptosis induced by DNA damage and differentiation.

Insulin-like growth factor-1 regulates the SIRT1-p53 pathway in cellular senescence.

Cellular senescence, which is known to halt proliferation of aged and stressed cells, plays a key role against cancer development and is also closely associated with organismal aging. While increased insulin-like growth factor (IGF) signaling induces cell proliferation, survival and cancer progression, disrupted IGF signaling is known to enhance longevity concomitantly with delay in aging processes. The molecular mechanisms involved in the regulation of aging by IGF signaling and whether IGF regulates cellular senescence are still poorly understood. In this study, we demonstrate that IGF-1 exerts a dual function in promoting cell proliferation as well as cellular senescence. While acute IGF-1 exposure promotes cell proliferation and is opposed by p53, prolonged IGF-1 treatment induces premature cellular senescence in a p53-dependent manner. We show that prolonged IGF-1 treatment inhibits SIRT1 deacetylase activity, resulting in increased p53 acetylation as well as p53 stabilization and activation, thus leading to premature cellular senescence. In addition, either expression of SIRT1 or inhibition of p53 prevented IGF-1-induced premature cellular senescence. Together, these findings suggest that p53 acts as a molecular switch in monitoring IGF-1-induced proliferation and premature senescence, and suggest a possible molecular connection involving IGF-1-SIRT1-p53 signaling in cellular senescence and aging.