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Electric hot incremental sheet forming, which is used to form hard-to-form sheet metal, is viewed as the one of rapid prototyping manufacturing technologies. However, the non-uniform stress distribution of forming regions would cause an initial contact loss phenomenon between the tool and the sheet, and an electric arc burn of the part surface is obtained due to the contact loss. In this work, a control method of axial pressure response was proposed to judge the stability of the initial contact between forming the tool and the sheet. A power supply on-off device was designed for electric hot incremental forming, and the calculation model of the initial axial force was established during deformation. Meanwhile, two response pressure values were proposed to control the power supply starting and the current intervention and to ensure the stability of the power supply during the forming process. In addition to this, the axial force and the surface of part were analyzed further in electric hot incremental sheet forming.

Aluminium alloy thick plate is widely used in field of aerospace and automobile industry for its light weight, high strength, good corrosion resistance and formability. Hot rolling is the key process of preparation for thick plates, however, the conventional symmetrical rolling process causes large deformation on the surface and small deformation in the central portion of the thick plate, resulting in inhomogeneous deformation, microstructure and property distributions through the thickness direction of the plate. Asynchronous rolling is beneficial for deformation permeation into the central part of thick plate with introduction of strong shear strain due to velocity asymmetry of two work rolls. However, the plate will bend towards the slower roll due to deformation asymmetry at upper and lower surface of the plate and serious bending is bad for multi-pass rolling process. Asymmetrical shear rolling with velocity asymmetry and geometry asymmetry is adopted in this study. Compared to asynchronous rolling, there is a horizontal offset distance of upper roll in outlet direction. A moment will be applied to the plate in the opposite direction of bending towards the slower roll by an offset distance of the slower roll. The comparisons of distributions of equivalent strain, temperature, DRX fraction and average grain size between symmetrical rolling and asymmetrical shear rolling are studied. The effects of velocity asymmetry and offset distance on microstructure variation and microstructure distribution at different positions of the plate are studied. Due to larger velocity of lower work roll, larger equivalent strain and higher temperature appear at lower layer of the plate, which results in higher DRX fraction and finer grain size. The speed ratio contributes greatly to sufficient DRX process and finer grain size; while the ascending offset distance decreases the DRX fraction. Therefore, speed ratio plays significant role in deformation permeation and grain refinement in asymmetrical shear rolling and the offset distance is mainly used to decrease the bending behaviour of the plate. This study can provide guidance to thick plate preparation with good properties in asymmetrical rolling process.

Abstract Background The regulation of growth and apoptosis in K562 cells by human bone marrow mesenchymal stem cells (MSCs) from leukemia patients was investigated. Methods K562 cells were cocultured with leukemic MSCs under serum deprivation. Cell Counting Kit-8 (CCK-8), PI staining, Annexin V/PI binding and FACS assays were used to investigate cell proliferation, cell cycle status, and apoptosis of K562 cells cultures in the presence or absence of 10% serum. Western blotting was used to determine the levels of Akt, phosphorylated Akt (p-Akt), the BCL-2 family member Bad, and phosphorylated Bad (p-Bad) proteins in K562 cells after coculturing with MSCs. The effects of LY294002 (a specific inhibitor of PI3K) on protein expression were also determined. Results K562 cell proliferation was inhibited by coculture with MSCs and the dominant cell cycle was the G0-G1 phase. The proportion of apoptotic K562 cells was decreased and the levels of p-Akt and p-Bad were upregulated after exposing K562 cells to MSCs. However, when LY294002 was used, p-Akt and p-Bad proteins inK562 cells showed a significant reduction, while no distinct variation was seen in the nonphosphorylated Akt and Bad protein levels. Conclusion Leukemic MSCs can inhibit K562 cell expansion and modulate the cell cycle to a state of relative quiescence. This allows the K562 cells to endure adverse conditions such as serum starvation. The PI3K-Akt-Bad signaling pathway may be involved in this antiapoptotic process via phosphorylation of the Akt and Bad proteins. Blocking MSC-induced transduction of the PI3K-Akt-Bad pathway may be a potential strategy for a targeted therapy to combat leukemia.