MODELING OF BONE INJURIES IN ANIMAL EXPERIMENTS

In this review, we discuss the advantages and disadvantages of the existing bone defect animal models and tissue engineering techniques applied in studying novel bone defect regenerative approaches. The paper suggests the requirements for an optimal animal model, as well as analyzes in vivo bone injury models widely used in testing. The authors briefly review the methods of experimentally produced lesions of long bones, calvarial bones, mandibular bones in different animals. This review also describes the standardization techniques allowing one to evaluate the process of osteogenesis and bone-implant interactions. That will help researchers thoroughly plan and conduct experiments according to the bioethical principles

\b{eta}-delayed three-proton decay of 31Ar

The beta decay of 31Ar, produced by fragmentation of a 36Ar beam at 880 MeV/nucleon, was investigated. Identified ions of 31Ar were stopped in a gaseous time projection chamber with optical readout allowing to record decay events with emission of protons. In addition to \b{eta}-delayed emission of one and two protons we have clearly observed the beta-delayed three-proton branch. The branching ratio for this channel in 31Ar is found to be 0.07(2)%.Comment: 5 pages, 3 figures, submitted to Physical Rev.

Biochemical aspects of magnesium-enhanced bone regeneration

Current research is focused on practical implications of magnesium-based implants largely due to their biodegradability and ability to promote bone healing and formation. However, the mechanism underlying the osteogenesis regulation by magnesium is still unclear.We describe cellular and molecular mechanisms underlying the effect of magnesium ions (Mg2+) on bone growth following the device implantation. The presented data demonstrate magnesium-induced activation of canonical Wnt/β-catenin signaling pathway in human bone marrow stromal cells resulting in their differentiation into osteoblasts, osteogenic effect and recovery of bone defects. We describe the role of the molecular mechanisms responsible for osteopromotive properties of Mg2+ and associated with unique transient receptor potential melastatin 7 (TRPM7) cation channels mediating the Mg2+ influx. TRPM7-mediated Mg2+ influx is important for platelet-derived growth factor (PDGF)-induced proliferation, adhesion, and migration of human osteoblasts, as well as for promotion of Mg2+-associated bone regeneration.We discuss the effect of Mg2+ on intracellular signaling processes, expression of the vascular endothelial growth factor (VEGF), hypoxia-inducible factor-2α, and peroxisome proliferator-activated receptor-γ coactivator 1α. Mg2+ can promote bone regeneration by enhancing the production of type X collagen and VEGF by osteogenic cells in bone marrow