Influence of Mg, Ag and Al substitutions on the magnetic excitations in the triangular-lattice antiferromagnet CuCrO2

Magnetic excitations in CuCrO$_{2}$, CuCr$_{0.97}$Mg$_{0.03}$O$_{2}$, Cu$_{0.85}$Ag$_{0.15}$CrO$_{2}$, and CuCr$_{0.85}$Al$_{0.15}$O$_{2}$ have been studied by powder inelastic neutron scattering to elucidate the element substitution effects on the spin dynamics in the Heisenberg triangular-lattice antiferromagnet CuCrO$_{2}$. The magnetic excitations in CuCr$_{0.97}$Mg$_{0.03}$O$_{2}$ consist of a dispersive component and a flat component. Though this feature is apparently similar to CuCrO$_{2}$, the energy structure of the excitation spectrum shows some difference from that in CuCrO$_{2}$. On the other hand, in Cu$_{0.85}$Ag$_{0.15}$CrO$_{2}$ and CuCr$_{0.85}$Al$_{0.15}$O$_{2}$ the flat components are much reduced, the low-energy parts of the excitation spectra become intense, and additional low-energy diffusive spin fluctuations are induced. We argued the origins of these changes in the magnetic excitations are ascribed to effects of the doped holes or change of the dimensionality in the magnetic correlations.Comment: 7 pages, 5 figure

TLR4 (Toll-Like Receptor 4) Mediates the Development of Intracranial Aneurysm Rupture.

Inflammation is emerging as a critical factor in the pathophysiology of intracranial aneurysm. TLR4 (toll-like receptor 4) contributes not only to the innate immune responses but also to the inflammatory processes associated with vascular disease. Therefore, we examined the contribution of the TLR4 pathway to the development of the rupture of intracranial aneurysm. We used a mouse model of intracranial aneurysm. TLR4 inhibition significantly reduced the development of aneurysmal rupture. In addition, the rupture rate and levels of proinflammatory cytokines were lower in TLR4 knockout mice than the control littermates. Macrophage/monocyte-specific TLR4 knockout mice had a lower rupture rate than the control littermate mice. Moreover, the deficiency of MyD88 (myeloid differentiation primary-response protein 88), a key mediator of TLR4, reduced the rupture rate. These findings suggest that the TLR4 pathway promotes the development of intracranial aneurysmal rupture by accelerating inflammation in aneurysmal walls. Inhibition of the TLR4 pathway in inflammatory cells may be a promising approach for the prevention of aneurysmal rupture and subsequent subarachnoid hemorrhage

Vitamin D deficiency promotes intracranial aneurysm rupture.

Intracranial aneurysm rupture causes severe disability and high mortality. Epidemiological studies show a strong association between decreased vitamin D levels and an increase in aneurysm rupture. However, the causality and mechanism remain largely unknown. In this study, we tested whether vitamin D deficiency promotes aneurysm rupture and examined the underlying mechanism for the protective role of vitamin D against the development of aneurysm rupture utilizing a mouse model of intracranial aneurysm. Mice consuming a vitamin D-deficient diet had a higher rupture rate than mice with a regular diet. Vitamin D deficiency increased proinflammatory cytokines in the cerebral arteries. Concurrently, vitamin D receptor knockout mice had a higher rupture rate than the corresponding wild-type littermates. The vitamin D receptors on endothelial and vascular smooth muscle cells, but not on hematopoietic cells, mediated the effect of aneurysm rupture. Our results establish that vitamin D protects against the development of aneurysmal rupture through the vitamin D receptors on vascular endothelial and smooth muscle cells. Vitamin D supplementation may be a viable pharmacologic therapy for preventing aneurysm rupture