Optimization of the Post-Process Heat Treatment Strategy for a Near-α Titanium Base Alloy Produced by Laser Powder Bed Fusion.

During the last decades, titanium alloys have been of great interest for lightweight applications due to their high strength in combination with a low material density. Current research activities focus on the investigation of near-α titanium alloys produced by laser powder bed fusion (LPBF). These alloys are known for their superior tensile strength and high creep resistance.

Microstructural evolution of a dual hardening steel during heat treatment.

Dual hardening steels combine precipitation of both secondary hardening carbides and intermetallic phases in a martensitic matrix. Due to this combination, the carbon content necessary to achieve high hardness levels can be reduced, resulting in a decreased amount of large and embrittling carbides. In this study, the influence of different heat treatments on microstructure evolution and secondary hardness is investigated.

Recruitment of ikaros to pericentromeric heterochromatin is regulated by phosphorylation.

Ikaros encodes a zinc finger protein that is involved in heritable gene silencing. In hematopoietic cells, Ikaros localizes to pericentromeric heterochromatin (PC-HC) where it recruits its target genes, resulting in their activation or repression via chromatin remodeling. The function of Ikaros is controlled by post-translational modifications.

Tec kinases mediate sustained calcium influx via site-specific tyrosine phosphorylation of the phospholipase Cgamma Src homology 2-Src homology 3 linker.

Tyrosine phosphorylation of phospholipase Cgamma2 (PLCgamma2) is a crucial activation switch that initiates and maintains intracellular calcium mobilization in response to B cell antigen receptor (BCR) engagement. Although members from three distinct families of non-receptor tyrosine kinases can phosphorylate PLCgamma in vitro, the specific kinase(s) controlling BCR-dependent PLCgamma activation in vivo remains unknown. Bruton's tyrosine kinase (Btk)-deficient human B cells exhibit diminished inositol 1,4,5-trisphosphate production and calcium signaling despite a normal inducible level of total PLCgamma2 tyrosine phosphorylation.