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Precise control of the crystal field and local symmetry around the paramagnetic spin center is crucial for the design and synthesis of single-molecule magnets (SMMs). Herein, three mononuclear Dy(III)-based complexes, [Dy(LN6)(CH3COO)2](BPh4)(CH2Cl2) (1), [Dy(LN6)(2,6-Cl-4-NO2-PhO)(H2O)2]2(PF6)2(H2O)(2,6-Cl-4-NO2-PhO)2 (2) and [Dy(LN6)(2,6-Cl-4-NO2-PhO)2](BPh4)(CH2Cl2)2 (3) (LN6 = N6-hexagonal plane accomplished by a neutral Schiff base ligand formed from 2,6-diacetylpyridine and ethylenediamine), are successfully isolated. In these complexes, the Dy(III) centers are coordinated with six neutral N atoms from a nonrigid equatorial ligand, while different oxygen-bearing ligands are arranged at the axial positions of the central ions by gradual regularization of the axial ligands. As a result, Dy(III) ions in the three complexes exhibit various coordination geometries, forming a ten-coordinate tetradecahedron for 1, a nine-coordinate muffin configuration for 2 and a distorted eight-coordinate hexagonal bipyramid for 3. Magnetic studies reveal that all complexes exhibit no SIM behaviour under zero dc field, due to the predominant quantum tunneling of magnetization (QTM), which can be effectively suppressed by additional dc fields. Experiments, coupled with theoretical calculations, demonstrate that varying local symmetries and coordination geometries are synergistically responsible for the disparities of QTM and uniaxial anisotropy, resulting in notably different magnetic properties. [ABSTRACT FROM AUTHOR]

Background/Aims: The mechanistic target of rapamycin (mTOR) signaling pathway is essential for angiogenesis and embryonic development. DEP domain-containing mTOR-interacting protein (DEPTOR) is an mTOR binding protein that functions to inhibit the mTOR pathway In vitro experiments suggest that DEPTOR is crucial for vascular endothelial cell (EC) activation and angiogenic responses. However, knowledge of the effects of DEPTOR on angiogenesis in vivo is limited. This study aimed to determine the role of DEPTOR in tissue angiogenesis and to elucidate the molecular mechanisms. Methods:Cre/loxP conditional gene knockout strategy was used to delete the Deptor gene in mouse vascular ECs. The expression or distribution of cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1 alpha (HIF-1α) were detected by immunohistochemical staining or western blot. Tube formation assay was used to measure angiogenesis in vitro. Results:Deptor knockdown led to increased expression of CD31, VEGF and HIF-1α in heart, liver, kidney and aorta. After treatment with rapamycin, their expression was significantly down regulated. In vitro, human umbilical vein endothelial cells (HUVECs) were transfected with DEPTOR-specific small interfering RNA (siRNA), which resulted in a significant increase in endothelial tube formation and migration rates. In contrast, DEPTOR overexpression markedly reduced the expression of CD31, VEGF and HIF-1α. Conclusions: Our findings demonstrated that deletion of the Deptor gene in vascular ECs resulted in upregulated expression of CD31 and HIF-1α, and further stimulated the expression of VEGF which promoted angiogenesis, indicating that disruption of normal angiogenic pathways may occur through hyperactivation of the mTORC1/HIF-1α/VEGF signaling pathway. [ABSTRACT FROM AUTHOR]