Low-Temperature X-ray Crystal Structure Analysis of the Cage-Structured Compounds MBe13 (M = La, Sm, and U)

The beryllides MBe13 (M = rare earths and actinides) crystallize in a NaZn13-type cubic structure, which can be categorized as a cage-structured compound. In this study, powder X-ray diffraction measurements have been performed on LaBe13, SmBe13, and UBe13 in the temperature range between 7 and 300 K in order to investigate their crystallographic characteristics systematically. They keep the NaZn13-type cubic structure down to the lowest temperature. We estimated their Debye temperature to be 600 - 750 K from analyses of the temperature dependence of a lattice parameter, being in good agreement with the values reported previously. Rietveld refinements on the obtained powder patterns revealed that the M atom in the 8a site is located in an almost ideal snub cube formed by 24 Be atoms in the 96i site, whose caged structure is unchanged even at the low temperatures. In addition, it is argued from the temperature variation of an isotropic mean-square displacement parameter that the MBe13 compounds commonly have a low-energy phonon mode, which can be described by a model assuming an Einstein oscillation of the M atom with a characteristic temperature of ~ 160 K.Comment: 8 pages with 6 figures and 2 table

Neutron Diffraction Study on Single-crystalline UAu2{_2}Si2_2

Magnetic structure of tetragonal UAu$_2$Si$_2$ was investigated by single-crystal neutron diffraction experiments. Below $T_{\rm N}$ = 20 K it orders antiferromagnetically with a propagation vector of $k = (2/3, 0, 0)$ and magnetic moments of uranium ions pointing along the tetragonal $c$-axis. Weak signs of the presence of a ferromagnetic component of magnetic moment were traced out.Taking into account a group theory calculation and experimental results of magnetization and $^{29}$Si-NMR, the magnetic structure is determined to be a squared-up antiferromagnetic structure, with a stacking sequence ($+ + -$) of the ferromagnetic $ac$-plane sheets along the $a$-axis. This result highlights similar magnetic correlations in UAu$_2$Si$_2$ and isostructural URu$_2$Si$_2$.Comment: 7 pages, 7 figure

Data supporting the regulation of FOXC2 in podocyte dysfunction

Abstract This data article shows the expression levels of specific podocyte injury markers and podocyte slit diaphragm protein nephrin in obese and lean Zucker rat glomeruli. It also contains information on the effect of the overexpression of transcription factor FOXC2 on the ratio of F- and G-actin and the expression level of ZO-1 in differentiated human podocytes. The article also shows data on the effect of treatments of differentiated podocytes with various factors associated with obesity and diabetes on the expression level of FOXC2. The detailed interpretation of these data and other aspects of podocyte injury mediated by upregulation of FOXC2 can be found in “Overexpression of transcription factor FOXC2 in cultured human podocytes upregulates injury markers and increases motility [1].Peer reviewe

Overexpression of transcription factor FOXC2 in cultured human podocytes upregulates injury markers and increases motility

Obesity and diabetes-related kidney diseases associate with renal failure and cardiovascular morbidity, and represent a major health issue worldwide. However, the molecular mechanisms leading to their development remain poorly understood. We observed increased expression of transcription factor FoxC2 in the podocytes of obese Zucker rats that are insulin resistant and albuminuric. We also found that depletion of adiponectin, an adipocyte-derived hormone whose secretion is decreased in obesity, up regulated FOXC2 in differentiated human podocytes in vitro. Overexpression of FOXC2 in cultured human podocytes led to increased nuclear expression of FOXC2 associated with a change of cellular morphology. This was accompanied by upregulation of vimentin, a key mesenchymal marker, and active beta-catenin, associated with podocyte injury. We also observed re-organization of the actin cytoskeleton, disrupted localization of the tight junction protein ZO-1, and increased motility of podocytes overexpressing FOXC2. These data indicate that the expression of FOXC2 in podocytes needs to be tightly regulated, and that its overexpression induces a chain of cellular events leading to podocyte dysfunction. These changes may lead to podocyte detachment and depletion ultimately contributing to albuminuria. We also suggest a novel molecular mechanism linking obesity-induced decrease in adiponectin to podocyte dysfunction via upregulation of FOXC2. (C) 2015 Elsevier Inc. All rights reserved.Peer reviewe

MFH-1 is required for bone morphogenetic protein-2-induced osteoblastic differentiation of C2C12 myoblasts

AbstractMesenchyme forkhead-1 (MFH-1), a winged helix/forkhead transcription factor, is expressed in developing cartilaginous tissues, kidney and arch arteries, and is essential for the normal development of the axial skeleton and aortic arch formation of mice. To investigate the possible role of MFH-1 in osteogenesis and osteoblast differentiation, we examined expression of MFH-1 induced by bone morphogenetic protein-2 (BMP-2) in C2C12 myoblasts, and found that MFH-1 protein and also MFH-1 mRNA increased markedly in C2C12 cells after treatment with BMP-2. To confirm the hypothesis that BMP-2 induced osteoblastic differentiation of C2C12 cells by increasing MFH-1 expression, we lowered the endogenous MFH-1 level by stably transfecting C2C12 cells with antisense MFH-1 sequence, and found that in antisense MFH-1 cell lines, both alkaline phosphatase (ALP) activity and production of osteocalcin induced by BMP-2 decreased markedly in comparison with control cell lines. Our results suggest that the BMP-2-induced MFH-1 protein may play a key role in regulating the commitment to osteoblastic differentiation of C2C12 myoblasts and production of osteoblast markers including ALP and osteocalcin

P4‐426: Waist Circumference And Domain‐Specific Cognitive Function Among The Non‐Demented Japanese Elderly: Results From The Takashima Study

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/152729/1/alzjjalz2019064098.pd