Fabrication, microstructure, friction and wear properties of SiC3D/Al brake disc-graphite/Si C pad tribo-couple for high-speed train

The friction and wear properties of interpenetrating phase composites(IPC) SiC3D/Al sliding against graphite/SiC(G/SiC) composites were investigated using a sub-scale brake dynamometer. The testing conditions included a braking pressure of 1.25 MPa and an initial braking speed(IBS) of 200-350 km/h in a braking process of high-speed train according to the scale-conversion rules. The tribo-couple materials were characterized using scanning electron microscopy(SEM), X-ray diffractometry(XRD), and energy-dispersive X-ray spectrometry(EDS). It is found that the matching tribo-couple features low friction surface temperature, reliable friction factor, and high durability. The continuous lubricating mechanically-mixed layer(MML) forms gradually on the worn surfaces of ring in the friction process. The MML is heterogeneous, which greatly controls wear rate and coefficient of friction(COF) of the composites. The wear mechanism of SiC3D/Al is typically abrasive wear at an IBS of 200-300 km/h. When the IBS increases to 350 km/h, oxidation wear and delamination are observed. The friction behavior of the tribo-couple predicted using Solidwork simulation software agrees well with the experimental results. The tribo-couple meets the requirement of emergency braking of high-speed train.

Synergistic suppression of the PI3K inhibitor CAL-101 with bortezomib on mantle cell lymphoma growth

Objective: To investigate the effects of CAL-101, particularly when combined with bortezomib(BTZ) on mantle cell lymphoma(MCL) cells, and to explore its relative mechanisms.Methods: MTT assay was applied to detect the inhibitory effects of different concentrations of CAL-101. MCL cells were divided into four groups: control group, CAL-101 group, BTZ group, and CAL-101/BTZ group. The expression of PI3K-p110σ, AKT, ERK, p-AKT and p-ERK were detected by Western blot. The apoptosis rates of CAL-101 group, BTZ group, and combination group were detected by flow cytometry. The location changes of nuclear factor kappa-B(NF-κB) of 4 groups was investigated by NF-κB Kit exploring. Western blot was applied to detect the levels of caspase-3 and the phosphorylation of AKT in different groups. Results: CAL-101 dose- and time-dependently induced reduction in MCL cell viability. CAL-101 combined with BTZ enhanced the reduction in cell viability and apoptosis. Western blot analysis showed that CAL-101 significantly blocked the PI3K/AKT and ERK signaling pathway in MCL cells. The combination therapy contributed to the inactivation of NF-κB and AKT in MCL cell lines. However, cleaved caspase-3 was up-regulated after combined treatment. Conclusion: Our study showed that PI3K/p110σ is a novel therapeutic target in MCL, and the underlying mechanism could be the blocking of the PI3K/AKT and ERK signaling pathways. These findings provided a basis for clinical evaluation of CAL-101 and a rationale for its application in combination therapy, particularly with BTZ.