The changes in the dielectric constant of perovskite BiMnO 3 at about T C , which are induced by the magnetic ordering as well as by the application of magnetic fields, indicate that coupling exists between the magnetism and the dielectric properties. The soft-mode theory based on the single-well potential model and the molecular-field approximation to the Heisenberg model are successfully applied to the electric and magnetic subsystems coexisting in the perovskitetype ferroelectromagnet BiMnO 3 , respectively. By adding an appropriate coupling term, which is related to a combination of electrical polarization and spin correlation, we investigate the inherent coupling between the ferroelectric and ferromagnetic orders, and find that the application of magnetic fields induces a fairly large suppression of χ p around T C , and the field-induced change in the magnetocapacitance effect becomes maximal at T C , which are in good agreement with experimental data in ferroelectromagnetic BiMnO 3 .

Cerebral amyloid angiopathy (CAA) is a critical factor in the pathogenesis of Alzheimer’s disease (AD). In the clinical setting, nearly 98% AD patients have CAA, and 75% of these patients are rated as severe CAA. It is characterized by the deposition of the β-amyloid peptide (mainly Aβ40) in the walls of cerebral vessels, which induces the degeneration of vessel wall components, reduces cerebral blood flow, and aggravates cognitive decline. Platelets are anuclear cell fragments from bone marrow megakaryocytes and their function in hemostasis and thrombosis has long been recognized. Recently, increasing evidence suggests that platelet activation can also mediate the onset and development of CAA. First, platelet activation and adhesion to a vessel wall is the initial step of vascular injury. Activated platelets contribute to more than 90% circulating Aβ (mainly Aβ1-40), which in turn activates platelets and results in the vicious cycle of Aβ overproduction in damaged vessel. Second, the uncontrolled activation of platelets leads to a chronic inflammatory reaction by secretion of chemokines (eg, platelet factor 4 [PF4], regulated upon activation normal T-cell expressed and presumably secreted [RANTES], and macrophage inflammatory protein [MIP-1α]), interleukins (IL-1β, IL-7, and IL-8), prostaglandins, and CD40 ligand (CD40L). The interaction of these biological response modulators with platelets, endothelial cells, and leukocytes establishes a localized inflammatory response that contributes to CAA formation. Finally, activated platelets are the upholder of fibrin clots, which are structurally abnormal and resistant to degradation in the presence of Aβ42. Thus, opinion has emerged that targeting blood platelets may provide a new avenue for anti-AD therapy.

No abstract

A liquid-core metal-cladding waveguide structure of millimeter scale is designed to enhance Raman signal via the excitation of Fabry-Perot-like resonance. Theoretically, an oscillating field distribution covering the whole guiding layer is generated by the multireflection at the two metal interfaces. The large detection area covers the whole sample chamber because of the oscillating nature of excited high order modes with concentrated intensity. By adding metal nanoparticles, the Fabry-Perot-like resonance can be combined with local surface plasmons resonance to further enhance the light-matter interaction with the target molecules, which is also confirmed by the experimental results.

Current antiplatelet drugs mainly focus on prevention rather than the more clinically relevant issue of clearance of an existing thrombus. We recently described a novel and effective therapeutic strategy for dissolution of preexisting platelet thrombus in a murine ischemic stroke model with a bifunctional platelet GPIIIa49-66 ligand (Single-chain antibody Linked first Kringle 1 of plasminogen, named SLK), which homes to newly deposited fibrin strands tangled of platelet thrombus and induces aggregated platelet fragmentation. In this study, we perform in-depth analysis of the effect of SLK on myocardial ischemia-reperfusion (IR) injury in rats. We show that SLK dose-dependently reduces lactate dehydrogenase (LDH) release as well as mean infarction size of left ventricle. Histological observation demonstrates that the arterial thrombi in coronary arteries of rat almost disappear after SLK injection. Optimal dose of SLK (37.5 μg/ individual) provides the myocardial protection at 2 hours post-infusion. However, there are no significant protective effects if SLK was given at 4 or 8 hours post-infusion. The combined application of SLK and urokinase (UK) demonstrates greater myocardial protection than UK alone at 2 hours post-infusion. Thus, SLK could be used as a thrombolytic alternative in other arterial vascular beds associated with thrombosis to enhance fibrinolysis.