Ultrafast evolution and transient phases of a prototype out-of-equilibrium Mott-Hubbard material

The study of photoexcited strongly correlated materials is attracting growing interest since their rich phase diagram often translates into an equally rich out-of-equilibrium behaviour. With femtosecond optical pulses, electronic and lattice degrees of freedom can be transiently decoupled, giving the opportunity of stabilizing new states inaccessible by quasi-adiabatic pathways. Here we show that the prototype Mott-Hubbard material V2O3 presents a transient non-thermal phase developing immediately after ultrafast photoexcitation and lasting few picoseconds. For both the insulating and the metallic phase, the formation of the transient configuration is triggered by the excitation of electrons into the bonding a1g orbital, and is then stabilized by a lattice distortion characterized by a hardening of the A1g coherent phonon, in stark contrast with the softening observed upon heating. Our results show the importance of selective electron-lattice interplay for the ultrafast control of material parameters, and are relevant for the optical manipulation of strongly correlated systems. \ua9 The Author(s) 2017

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Expression of various growth factors for cell proliferation and cytodifferentiation during fracture repair of bone

We examined immunohistochemically the fracture repair process in rat tibial bone using antibodies to PCNA, BMP2, TGF-b 1,-2,-3, TGF-b R1,- R2, bFGF, bFGFR, PDGF, VEGF, and S-100. The peak level of cell proliferation as revealed by PCNA labelling appeared first in primitive mesenchymal cells and inflammatory cells at the fracture edges and neighboring periosteum at 2-days after fracture, followed by the peaks of periosteal primitive fibroblasts and chondroblasts, which appeared at fracture edges at 3- and 4-days after fracture, respectively. BMP2 was weakly positive in primitive mesenchymal cells, osteoblasts and chondroblasts. At 3-days post-fracture, periosteal osteoblasts produced osteoid tissue and callus with marrow spaces lined by osteoblasts and osteoclasts, and all primitive mesenchymal cells and osteoblasts were positive for TGF-b 1,-2,-3, and TGF-b R1,-R2. They were also positive for vascular growth factors bFGF, FGFR and PDGF, but negative for VEGF, and the peak of PCNA labelling of vascular endothelial cells in the marrow space was delayed to 4-days after fracture. Chondroblasts at fracture edges produced hypertrophic chondrocytes at 5-days after fracture and they were positive for TGF-b 1,-2,-3, and TGF-b R1,-R2. Primitive chondroblasts were positive for vascular growth factors VEGF as well as bFGF, FGFR, and the peak of PCNA labelling of vascular endothelial cells in the cartilage was at 5-days after fracture. Hypertrophic chondrocytes were also positive for these growth factors but negative for bFGF and bFGFR. S-100 protein-induced calcification was only positive on chondroblasts and hypertrophic chondrocytes. At 7-days after fracture, bone began to be formed from the cartilage at fracture edges, by a process similar to bone formation in the growth plate. Enchondral ossification established a bridge between both fracture edges and periosteal membranous ossification encompassed the fracture site like a sheath at 14- day after fracture. Our study of fracture repair of bone indicates that this process is complex and occurs through various steps involving various growth factors