32 research outputs found
Investigation of the velocity- and Q-structure of the lowermost mantle using PcP/P amplitude ratios from arrays at distances of 70°-84°
Investigations of the core reflection PcP at distances in the neighbourhood of the core shadow zone are especially appropriate for the study of isolated regions of D" because PcP for these distances has a large angle of incidence at the core-mantle boundary and is strongly influenced by the structure immediately above the core. A striking result of this investigation of PcP in the distance range 70°–84° is that PcP could be detected only in four cases (from a total of 16 earthquakes and 29 nuclear explosions) in the NORSAR- and GRF-array beams for PcP. This result is found although the P-wave-coda noise levels in the PcP beams are very low, mostly below the amplitude level of PcP predicted by standard Earth models. In the cases where PcP could not be identified, the PcP/P amplitude ratio, which is estimated from the beams with the aid of a cross-correlation procedure, must be regarded as an upper limit for the actual PcP/P ratio. The interpretation of the PcP/P amplitude ratios with one radially symmetric, elastic model proved to be impossible. The generally small PcP/P ratios can be explained by lateral variations in seismic wave absorption within D". Qα values for short-period P waves in D", between 800 (below Usbekistan) and 100 (below the northern Hudson Bay and Central Siberia), were found. Several recent seismological investigations of the P- and S-wave velocity of the lowermost mantle have suggested velocity models with first-order discontinuities (with velocity increases of the order of 1.5%–3.0%) 150–300 km above the core-mantle boundary. Through the calculation of synthetic short-period seismograms and comparison with the array data compiled for the main part of this study, it is shown that such models are very unlikely to be a global feature if the P velocity jump is of the order of 2.5%–3.0%. Even models with reduced P velocity jumps of 1.3% produce clear onsets in short-period seismograms. They are not observed for P waves with ray paths bottoming beneath Central Siberia.
ARK: https://n2t.net/ark:/88439/y055861
Permalink: https://geophysicsjournal.com/article/215
 
Comment on “Wave propagation effects and the Earth's structure in the lower mantle”
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95270/1/grl3604.pd
Terminal Ligand and Packing Effects on Slow Relaxation in an Isostructural Set of [Dy(Hdapp)X]+ Single Molecule Magnets**
Three new dysprosium complexes with a pentadentate ligand occupying five equatorial sites differ only in the nature of the axial ligands. These help tune the relaxation properties as judged by an analysis of the AC susceptibility data. More in depth analysis by using two recently suggested fitting equations lead to similar outcomes for all three systems. As a further contribution to the relaxation pathway involving the phonon bath it is concluded that a short nitrate-nitrate interaction between molecules helps dampen the spin phonon coupling.
We report three structurally related single ion Dy compounds using the pentadentate ligand 2,6-bis((E)-1-(2-(pyridin-2-yl)-hydrazineylidene)ethyl)pyridine (Hdapp) [Dy(Hdapp)(NO)]NO (1), [Dy(Hdapp)(OAc)]Cl (2) and [Dy(Hdapp)(NO)]Cl(NO) (3). The (Hdapp) occupies a helical twisted pentagonal equatorial arrangement with two anionic ligands in the axial positions. Further influence on the electronic and magnetic structure is provided by a closely associated counterion interacting with the central N−H group of the (Hdapp). The slow relaxation of the magnetisation shows that the anionic acetates give the greatest slowing down of the magnetisation reversal. Further influence on the relaxation properties of compounds1 and 2 is the presence of short nitrate-nitrate intermolecular ligand contact opening further lattice relaxation pathways
Growth differentiation factor 15 deficiency protects against atherosclerosis by attenuating CCR2-mediated macrophage chemotaxis
The TGF-β family member GDF-15 promotes lesion formation and plaque instability in atherosclerosis-prone LDLr-deficient mice
Regulation of GDF-15, a distant TGF-β superfamily member, in a mouse model of cerebral ischemia
GDF-15 is a novel distant member of the TGF-β superfamily and is widely distributed in the brain and peripheral nervous system. We have previously reported that GDF-15 is a potent neurotrophic factor for lesioned dopaminergic neurons in the substantia nigra, and that GDF-15-deficient mice show progressive postnatal losses of motor and sensory neurons. We have now investigated the regulation of GDF-15 mRNA and immunoreactivity in the murine hippocampal formation and selected cortical areas following an ischemic lesion by occlusion of the middle cerebral artery (MCAO). MCAO prominently upregulates GDF-15 mRNA in the hippocampus and parietal cortex at 3 h and 24 h after lesion. GDF-15 immunoreactivity, which is hardly detectable in the unlesioned brain, is drastically upregulated in neurons identified by double-staining with NeuN. NeuN staining reveals that most, if not all, neurons in the granular layer of the dentate gyrus and pyramidal layers of the cornu ammonis become GDF-15-immunoreactive. Moderate induction of GDF-15 immunoreactivity has been observed in a small number of microglial cells identified by labeling with tomato lectin, whereas astroglial cells remain GDF-15-negative after MCAO. Comparative analysis of the size of the infarcted area after MCAO in GDF-15 wild-type and knockout mice has failed to reveal significant differences. Together, our data substantiate the notion that GDF-15 is prominently upregulated in the lesioned brain and might be involved in orchestrating post-lesional responses other than the trophic support of neurons
GDF-15 is abundantly expressed in plexiform lesions in patients with pulmonary arterial hypertension and affects proliferation and apoptosis of pulmonary endothelial cells
<p>Abstract</p> <p>Background</p> <p>Growth-differentiation factor-15 (GDF-15) is a stress-responsive, transforming growth factor-β-related cytokine, which has recently been reported to be elevated in serum of patients with idiopathic pulmonary arterial hypertension (IPAH). The aim of the study was to examine the expression and biological roles of GDF-15 in the lung of patients with pulmonary arterial hypertension (PAH).</p> <p>Methods</p> <p>GDF-15 expression in normal lungs and lung specimens of PAH patients were studied by real-time RT-PCR and immunohistochemistry. Using laser-assisted micro-dissection, GDF-15 expression was further analyzed within vascular compartments of PAH lungs. To elucidate the role of GDF-15 on endothelial cells, human pulmonary microvascular endothelial cells (HPMEC) were exposed to hypoxia and laminar shear stress. The effects of GDF-15 on the proliferation and cell death of HPMEC were studied using recombinant GDF-15 protein.</p> <p>Results</p> <p>GDF-15 expression was found to be increased in lung specimens from PAH patients, com-pared to normal lungs. GDF-15 was abundantly expressed in pulmonary vascular endothelial cells with a strong signal in the core of plexiform lesions. HPMEC responded with marked upregulation of GDF-15 to hypoxia and laminar shear stress. Apoptotic cell death of HPMEC was diminished, whereas HPMEC proliferation was either increased or decreased depending of the concentration of recombinant GDF-15 protein.</p> <p>Conclusions</p> <p>GDF-15 expression is increased in PAH lungs and appears predominantly located in vascular endothelial cells. The expression pattern as well as the observed effects on proliferation and apoptosis of pulmonary endothelial cells suggest a role of GDF-15 in the homeostasis of endothelial cells in PAH patients.</p