Tetra­kis(μ2-5-methyl­pyrazine-2-carboxyl­ato)-1:2κ3 N 1,O:O;2:3κ3 O:N 1,O;1:2κ2 O:O′;3:4κ2 O:O′-octa­octyl-1κ2 C,2κ2 C,3κ2 C,4κ2 C-di-μ3-oxido-1:2:3κ3 O;1:3:4κ3 O-tetra­tin(IV)

The title compound, [Sn4(C8H17)8O2(C6H5N2O2)4], is a tetra­nuclear SnIV complex, built up by inversion symmetry around the central Sn2O2 ring. The SnIV coordination geometries are distorted SnO3C2 trigonal-bipyramidal and distorted SnO4C2 octa­hedral. The three-coordinate μ3-oxido bridging O atom in the Sn2O2 ring is attached to three Sn atoms. All non-H atoms, with the exception of the Sn-bonded octyl groups, lie approximately on a non-crystallographic mirror plane

Bis(2,2′-bipyridine-κ2 N,N′)chloridocobalt(II) perchlorate

In the cation of the title compound, [CoCl(C10H8N2)2]ClO4, the CoII atom displays a distorted trigonal-bipyramidal coordination geometry. The two pyridine rings in each 2,2′-bipyridine ligand form dihedral angles of 10.75 (12) and 4.28 (13)°. The crystal packing is stabilized by inter­ionic C—H⋯O hydrogen bonds, C—H⋯π inter­actions and aromatic π–π stacking inter­actions, with centroid–centroid distances of 3.616 (7) Å

The Differentiation Balance of Bone Marrow Mesenchymal Stem Cells Is Crucial to Hematopoiesis.

Bone marrow mesenchymal stem cells (BMSCs), the important component and regulator of bone marrow microenvironment, give rise to hematopoietic-supporting stromal cells and form hematopoietic niches for hematopoietic stem cells (HSCs). However, how BMSC differentiation affects hematopoiesis is poorly understood. In this review, we focus on the role of BMSC differentiation in hematopoiesis. We discussed the role of BMSCs and their progeny in hematopoiesis. We also examine the mechanisms that cause differentiation bias of BMSCs in stress conditions including aging, irradiation, and chemotherapy. Moreover, the differentiation balance of BMSCs is crucial to hematopoiesis. We highlight the negative effects of differentiation bias of BMSCs on hematopoietic recovery after bone marrow transplantation. Keeping the differentiation balance of BMSCs is critical for hematopoietic recovery. This review summarises current understanding about how BMSC differentiation affects hematopoiesis and its potential application in improving hematopoietic recovery after bone marrow transplantation

Association of Lumican Gene with Susceptibility to Pathological Myopia in the Northern Han Ethnic Chinese

Pathological myopia is a severe hereditary ocular disease leading to blindness. It is urgent and very important to find the pathogenesis and therapy for this disease. The purpose of the study is to analyze sequences of lumican and decorin genes with pathological myopia(PM) and control subjects to verify the relationship between lumican, decorin genes and PM in Northern Han Chinese. We collected and analyzed the blood samples of 94 adults (including 12 pedigree cases and 82 sporadic cases) with PM and 90 controls in the northern Han ethnic Chinese. Genotyping was performed by direct sequencing after polymerase chain reaction(PCR) amplification and allele frequencies were tested for Hardy-Weinberg equilibrium. Univariate analysis revealed significant differences between two groups for three SNPs: rs3759223 (C → T) and rs17853500 (T → C) of the lumican gene and rs74419 (T → C) of decorin gene with (P < .05) for all their genotype distribution and allele frequency. There is no significant difference for incidence of these mutations between pedigree and sporadic group (P > .05). The results suggested that the sequence variants in 5′-regulatory region of lumican gene and 3'UTR of decorin gene were associated significantly with PM in Northern Han Chinese. Further studies are needed to confirm finally whether the two genes are the virulence genes of PM

Crif1 Promotes Osteoporosis in Mice after Radiation

Abstract Radiation induces rapid bone loss and enhances bone resorption and RANKL expression. RANKL provides the crucial signal to induce osteoclast differentiation and plays an important role in bone resorption. However, the mechanisms of radiation-induced osteoporosis are not fully understood. Here, we show that Crif1 expression increases in bone marrow cells after radiation. Conditional Crif1 deletion in bone marrow cells causes decreases in RANKL expression and the RANKL/OPG ratio, and relieves bone loss after radiation in mice. We further demonstrated in vitro that Crif1 promotes RANKL secretion via the cAMP/PKA pathway. Moreover, protein-protein docking screening identified five compounds as Crif1 inhibitors; these compounds dramatically suppressed RANKL secretion and CREB phosphorylation when cells were exposed to forskolin. This study enriches current knowledge of the pathogenesis of osteoporosis and provides insights into potential therapeutic strategies for osteoporosis treatment