| 1. |
- Eriksson, Therese, et al.
(författare)
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Complex magnetic properties of Mn3Ni20P6 and ferromagnetic structure of the new isostructural compound Mn3Pd20P6
- 2007
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Ingår i: Journal of Magnetism and Magnetic Materials. - : Elsevier BV. - 0304-8853 .- 1873-4766. ; 308:2, s. 203-209
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Tidskriftsartikel (refereegranskat)abstract
- A new compound, Mn3Pd20P6, has been synthesized and the crystal and magnetic structures have been determined by neutron powder diffraction. The crystal structure is cubic, with a = 11.9563(2) angstrom, space group Fm (3) over barm, and is isostructural to Mn3Ni20P6, a ternary ordering variant of the Cr23C6-type structure. The magnetic properties of Mn3Pd20P6 and Mn3Ni20P6 were studied by magnetization measurements. For Mn3Pd20P6 a transition, suggested to be of first order, to a ferromagnetic structure takes place at 110 K, whereas the saturation magnetization shows unusual temperature dependence. Magnetization vs. field loops show very weak coercivity, and the magnitude of the saturation magnetization agrees well with parallel Mn magnetic moments on two different sublattices of 4.24(8) mu(B), and 2.88(8) mu(B), respectively, found by neutron powder diffraction at 10 K. Magnetization vs. temperature measurements for Mn3Ni20P6 do not show a well-defined transition temperature, but show signatures of magnetic order with small excess magnetic moments aligned by the applied field below about 240 K. Further, signatures of a spin reorientation process at around 30 K are noted.
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| 2. |
- Kindblom, Jenny, 1971, et al.
(författare)
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Increased adipogenesis in bone marrow but decreased bone mineral density in mice devoid of thyroid hormone receptors.
- 2005
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Ingår i: Bone. - : Elsevier BV. - 8756-3282. ; 36:4, s. 607-16
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Tidskriftsartikel (refereegranskat)abstract
- Mice deficient for all known thyroid hormone receptors, TRalpha1-/-beta-/- mice, display a clear skeletal phenotype characterized by growth retardation, delayed maturation of long bones and decreased trabecular and total bone mineral density (BMD; -14.6 +/- 2.8%, -14.4 +/- 1.5%). The aim of the present study was to investigate the molecular mechanisms behind the skeletal phenotype in TRalpha1-/-beta-/- mice. Global gene expression analysis was performed on total vertebrae from wild-type (WT) and TRalpha1-/-beta-/- mice using DNA microarray and the results were verified by real-time PCR. The mRNA levels of six genes (AdipoQ, Adipsin, Fat-Specific Protein 27 (FSP 27), lipoprotein lipase (LPL), retinol-binding protein (RBP) and phosphoenolpyruvate carboxykinase (PEPCK)) expressed by mature adipocytes were increased in TRalpha1-/-beta-/- compared with WT mice. An increased amount of fat (225% over WT) due to an increased number but unchanged mean size of adipocytes in the bone marrow of TRalpha1-/-beta-/- mice was revealed. Interestingly, the mRNA levels of the key regulator of osteoclastogenesis, receptor activator of NF-varkappab ligand (RANKL), were dramatically decreased in TRalpha1-/-beta-/- mice. In conclusion, TRalpha1-/-beta-/- mice demonstrated increased expression of adipocyte specific genes and an increased amount of bone marrow fat. Thus, these mice have increased adipogenesis in bone marrow associated with decreased trabecular bone mineral density (BMD). One may speculate that these effects either could be caused by an imbalance in the differentiation of the osteoblast and the adipocyte lineages at the expense of osteoblastogenesis, or by independent effects on the regulation of both osteoblastogenesis and adipogenesis.
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