Immense magnetic response of exciplex light emission due to correlated spin-charge dynamics

As carriers slowly move through a disordered energy landscape in organic semiconductors, tiny spatial variations in spin dynamics relieve spin blocking at transport bottlenecks or in the electron-hole recombination process that produces light. Large room-temperature magnetic-field effects (MFE) ensue in the conductivity and luminescence. Sources of variable spin dynamics generate much larger MFE if their spatial structure is correlated on the nanoscale with the energetic sites governing conductivity or luminescence such as in co-evaporated organic blends within which the electron resides on one molecule and the hole on the other (an exciplex). Here we show that exciplex recombination in blends exhibiting thermally-activated delayed fluorescence (TADF) produces MFE in excess of 60% at room temperature. In addition, effects greater than 4000% can be achieved by tuning the device's current-voltage response curve by device conditioning. These immense MFEs are both the largest reported values for their device type at room temperature. Our theory traces this MFE and its unusual temperature dependence to changes in spin mixing between triplet exciplexes and light-emitting singlet exciplexes. In contrast, spin mixing of excitons is energetically suppressed, and thus spin mixing produces comparatively weaker MFE in materials emitting light from excitons by affecting the precursor pairs. Demonstration of immense MFE in common organic blends provides a flexible and inexpensive pathway towards magnetic functionality and field sensitivity in current organic devices without patterning the constituent materials on the nanoscale. Magnetic fields increase the power efficiency of unconditioned devices by 30% at room temperature, also showing that magnetic fields may increase the efficiency of the TADF process.Comment: 12 pages, PRX in pres

Predicting Convection Configurations in Coupled Fluid-Porous Systems

A ubiquitous arrangement in nature is a free-flowing fluid coupled to a porous medium, for example a river or lake lying above a porous bed. Depending on the environmental conditions, thermal convection can occur and may be confined to the clear fluid region, forming shallow convection cells, or it can penetrate into the porous medium, forming deep cells. Here, we combine three complementary approaches - linear stability analysis, fully nonlinear numerical simulations and a coarse-grained model - to determine the circumstances that lead to each configuration. the coarse-grained model yields an explicit formula for the transition between deep and shallow convection in the physically relevant limit of small Darcy number. Near the onset of convection, all three of the approaches agree, validating the predictive capability of the explicit formula. the numerical simulations extend these results into the strongly nonlinear regime, revealing novel hybrid configurations in which the flow exhibits a dynamic shift from shallow to deep convection. This hybrid shallow-to-deep convection begins with small, random initial data, progresses through a metastable shallow state and arrives at the preferred steady state of deep convection. We construct a phase diagram that incorporates information from all three approaches and depicts the regions in parameter space that give rise to each convective state

Multiscale simulations in simple metals: a density-functional based methodology

We present a formalism for coupling a density functional theory-based quantum simulation to a classical simulation for the treatment of simple metallic systems. The formalism is applicable to multiscale simulations in which the part of the system requiring quantum-mechanical treatment is spatially confined to a small region. Such situations often arise in physical systems where chemical interactions in a small region can affect the macroscopic mechanical properties of a metal. We describe how this coupled treatment can be accomplished efficiently, and we present a coupled simulation for a bulk aluminum system.Comment: 15 pages, 7 figure

Thalidomide ameliorates portal hypertension via nitric oxide synthase independent reduced systolic blood pressure

AIM: Portal hypertension is a common complication of liver cirrhosis and significantly increases mortality and morbidity. Previous reports have suggested that the compound thalidomide attenuates portal hypertension (PHT). However, the mechanism for this action is not fully elucidated. One hypothesis is that thalidomide destabilizes tumor necrosis factor α (TNFα) mRNA and therefore diminishes TNFα induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO). To examine this hypothesis, we utilized the murine partial portal vein ligation (PVL) PHT model in combination with endothelial or inducible NOS isoform gene knockout mice. METHODS: Wild type, inducible nitric oxide synthase (iNOS)-/- and endothelial nitric oxide synthase (eNOS)-/- mice received either PVL or sham surgery and were given either thalidomide or vehicle. Serum nitrate (total nitrate, NOx) was measured daily for 7 d as a surrogate of NO synthesis. Serum TNFα level was quantified by enzyme-linked immunosorbent assay. TNFα mRNA was quantified in liver and aorta tissue by reverse transcription-polymerase chain reaction. PHT was determined by recording splenic pulp pressure (SPP) and abdominal aortic flow after 0-7 d. Response to thalidomide was determined by measurement of SPP and mean arterial pressure (MAP). RESULTS: SPP, abdominal aortic flow (Qao) and plasma NOx were increased in wild type and iNOS-/- PVL mice when compared to sham operated control mice. In contrast, SPP, Qao and plasma NOx were not increased in eNOS-/- PVL mice when compared to sham controls. Serum TNFα level in both sham and PVL mice was below the detection limit of the commercial ELISA used. Therefore, the effect of thalidomide on serum TNFα levels was undetermined in wild type, eNOS-/- or iNOS-/- mice. Thalidomide acutely increased plasma NOx in wild type and eNOS-/- mice but not iNOS-/- mice. Moreover, thalidomide temporarily (0-90 min) decreased mean arterial pressure, SPP and Qao in wild type, eNOS-/- and iNOS-/- PVL mice, after which time levels returned to the respective baseline. CONCLUSION: Thalidomide does not reduce portal pressure in the murine PVL model by modulation of NO biosynthesis. Rather, thalidomide reduces PHT by decreasing MAP by an undetermined mechanism