For decades, solid solution strengthening with up to 9 wt.% Ni has been the only successful strategy to obtain high strength and high impact toughness in bcc-structured (ferritic or tempered martensitic) cryogenic steels. Until now coherent nano-precipitates, an effective strengthening agent at room temperature, cannot be used to improve properties at cryogenic temperatures. Here, a new type of Mo-rich nano-B2 precipitates formed in a 6.5 wt.% Ni steel upon doping with 0.2 wt.% of Mo is reported. These precipitates are not only fully coherent with the matrix but are also shearable at 77 K. A high precipitate number density in excess of 2 × 10²⁴ m⁻³ has been achieved by an industrially feasible process optimization, which brings both the cryogenic strength and impact toughness of the steel to the same levels as those of 9Ni steels. The Mo-rich B2 precipitation strengthening, therefore, opens a new avenue for the design and development of low-cost high-performance cryogenic steels.

Vink and colleagues capture the transcriptome of the first functional HSCs in mouse by single-cell RNA-seq, index-sorting, and in vivo and invitro hematopoietic analyses. The HSC transcriptome is unique compared to HPCs, and heterogeneous expression of pivotal genes suggests that establishment of functional hematopoietic fate during cell emergence from embryonic aortic endothelium is stochastic.

Hematopoietic stem cells (HSCs) develop from the hemogenic endothelium in cluster structures that protrude into the embryonic aortic lumen. Although much is known about the molecular characteristics of the developing hematopoietic cells, we lack a complete understanding of their origin and the three-dimensional organization of the niche. Here, we use advanced live imaging techniques of organotypic slice cultures, clonal analysis, and mathematical modeling to show the two-step process of intra-aortic hematopoietic cluster (IACH) formation. First, a hemogenic progenitor buds up from the endothelium and undergoes division forming the monoclonal core of the IAHC. Next, surrounding hemogenic cells are recruited into the IAHC, increasing their size and heterogeneity. We identified the Notch ligand Dll4 as a negative regulator of the recruitment phase of IAHC. Blocking of Dll4 promotes the entrance of new hemogenic Gfi1⁺ cells into the IAHC and increases the number of cells that acquire HSC activity. Mathematical modeling based on our data provides estimation of the cluster lifetime and the average recruitment time of hemogenic cells to the cluster under physiologic and Dll4-inhibited conditions.