We demonstrate a simple fabrication method to produce randomly stacked graphene chemiresistors using surfactant-assisted exfoliation of graphite. We analyze the sensitivity of such chemiresistors as a function of vacuum filtration volume and temperature. At low vacuum filtration volumes (<∼5 mL) the sensors exhibit superior sensitivity towards target molecules compared to previously developed polycrystalline graphene, polycrystalline graphene microribbon, and carbon nanotube chemical sensors. Temperature dependent measurements, transmission electron microscopy and scanning electron microscopy suggest the improved sensitivity in the randomly stacked graphene chemiresistors is due to 2-dimensional charge carrier hopping through edge defects.

In displaying accelerated oxygen diffusion along extended defects, (La,Sr)MnO 3+δ is an atypical acceptor-doped perovskite-type oxide. In this study, 18 O/ 16 O diffusion experiments on epitaxial thin films of La 0.8 Sr 0.2 MnO 3+δ and molecular dynamics (MD) simulations are combined to elucidate the origin of this phenomenon for dislocations: Does diffusion occur along dislocation cores or along space-charge tubes? Transmission electron microscopy studies of the films revealed dislocations extending from the surface. 18 O penetration profiles measured by secondary ion mass spectrometry indicated (slow) bulk diffusion and faster diffusion along dislocations. Oxygen tracer diffusivities obtained for temperatures 873 ≤ T [K] ≤ 973were over two orders of magnitude higher for dislocations than for the bulk. The activation enthalpy of oxygen diffusion along dislocations, of (2.95 ± 0.21) eV, is surprisingly high relative to that for bulk diffusion, (2.67 ± 0.13) eV. This result militates against fast diffusion along dislocation cores. MD simulations confirmed no accelerated migration of oxide ions along dislocation cores. Faster diffusion of oxygen along dislocations in La 0.8 Sr 0.2 MnO 3+δ is thus concluded to occur within space-charge tubes in which oxygen vacancies are strongly accumulated. Reasons for and the consequences of space-charge zones at extended defects in manganite perovskites are discussed.

Reactive sintering of dual phase composites for the use as oxygen transport membrane is a promising method enabling lower sintering temperatures as well as low cost raw materials. Ce0.8Gd0.2O2−δ -...

Dexmedetomidine (DXM) is a selective α2-adrenoceptor (α2-AR) and imidazoline receptor (IR) agonist that has been reported to regulate inflammatory responses mediated by diverse signaling pathways through α2-AR. The majority of the reported receptors or downstream molecules have been demonstrated to locate with caveolin-1, a protein suggested to participate in regulating Toll-like receptor 4 (TLR4)-mediated inflammatory responses and the pathogen endocytosis capability of macrophages. The present study hypothesized that DXM may influence these pathways by regulating the expression of caveolin-1 and mediating the subsequent effects. Using a cecal-ligation and puncture-induced rat sepsis model, it was initially observed that pre-emptive DXM is able to upregulate and stabilize the amount of caveolin-1 expression, which may be partly antagonized by both α2-AR and the IR antagonist atepamezole (APZ). The pathophysiological parameters indicated that DXM is able to inhibit secondary lung injury, in addition to the rise of body temperature and arterial lactate accumulation, however it marginally increased arterial glucose and the murine sepsis score, which can be largely antagonized by APZ. The overall effect was beneficial and improved the 24-h cumulative survival rate of rats with sepsis. In conclusion, preemptive clinical sedative doses of DXM may upregulate the expression of caveolin-1 downregulated by sepsis, which may contribute to the inhibition of inflammatory pathways such as TLR4-mediated pathways. Furthermore, DXM may favor the improvement of short-term outcomes by the regulation of other metabolic pathways.