Suppression of mid-infrared plasma resonance due to quantum confinement in delta-doped silicon

The classical Drude model provides an accurate description of the plasma resonance of three-dimensional materials, but only partially explains two-dimensional systems where quantum mechanical effects dominate such as P:$\delta$-layers - atomically thin sheets of phosphorus dopants in silicon that induce novel electronic properties beyond traditional doping. Previously it was shown that P:$\delta$-layers produce a distinct Drude tail feature in ellipsometry measurements. However, the ellipsometric spectra could not be properly fit by modeling the $\delta$-layer as discrete layer of classical Drude metal. In particular, even for large broadening corresponding to extremely short relaxation times, a plasma resonance feature was anticipated but not evident in the experimental data. In this work, we develop a physically accurate description of this system, which reveals a general approach to designing thin films with intentionally suppressed plasma resonances. Our model takes into account the strong charge density confinement and resulting quantum mechanical description of a P:$\delta$-layer. We show that the absence of a plasma resonance feature results from a combination of two factors: i), the sharply varying charge density profile due to strong confinement in the direction of growth; and ii), the effective mass and relaxation time anisotropy due to valley degeneracy. The plasma resonance reappears when the atoms composing the $\delta$-layer are allowed to diffuse out from the plane of the layer, destroying its well-confined two-dimensional character that is critical to its novel electronic properties

Albany: Using Component-based Design to Develop a Flexible, Generic Multiphysics Analysis Code

Abstract: Albany is a multiphysics code constructed by assembling a set of reusable, general components. It is an implicit, unstructured grid finite element code that hosts a set of advanced features that are readily combined within a single analysis run. Albany uses template-based generic programming methods to provide extensibility and flexibility; it employs a generic residual evaluation interface to support the easy addition and modification of physics. This interface is coupled to powerful automatic differentiation utilities that are used to implement efficient nonlinear solvers and preconditioners, and also to enable sensitivity analysis and embedded uncertainty quantification capabilities as part of the forward solve. The flexible application programming interfaces in Albany couple to two different adaptive mesh libraries; it internally employs generic integration machinery that supports tetrahedral, hexahedral, and hybrid meshes of user specified order. We present the overall design of Albany, and focus on the specifics of the integration of many of its advanced features. As Albany and the components that form it are openly available on the internet, it is our goal that the reader might find some of the design concepts useful in their own work. Albany results in a code that enables the rapid development of parallel, numerically efficient multiphysics software tools. In discussing the features and details of the integration of many of the components involved, we show the reader the wide variety of solution components that are available and what is possible when they are combined within a simulation capability. Key Words: partial differential equations, finite element analysis, template-based generic programmin

Study on the Cellular Anti-Inflammatory Effect of Torularhodin Produced by <i>Sporidiobolus pararoseus</i> ZQHL Isolated from Vinegar Fungus

The red stretcher bacterium Sporidiobolus pararoseus is a high producer of carotenoids such as torularhodin, but its presence in vinegar has not been detected. Moreover, torularhodin has several biological activities, but its effect on the LPS-induced RAW 264.7 inflammatory cell model has also yet to be elucidated. In this study, S. pararoseus was identified in different vinegar samples from China by ITS sequencing. Meanwhile, one of the strains was deeply resolved by whole genome sequencing and functional annotation and named S. pararoseus ZQHL. Subsequently, the antioxidant effect of the fungal carotenoid torularhodin was investigated using in vitro DPPH, ABTS, and cellular models. Finally, LPS-induced RAW 264.7 cells were used as an inflammation model to assess torularhodin’s protective effect on inflammatory cells and to determine whether the TLR4 pathway is associated with this process. The results indicate that torularhodin has good free radical scavenging ability in vitro and can contribute to cell viability. More importantly, torularhodin alleviated LPS-induced cellular inflammatory damage and reduced the expression of inflammatory factors such as TLR4, MyD88, and TNF-a. The mechanism may attenuate the cellular inflammatory response by inhibiting the TLR4 inflammatory pathway. In conclusion, torularhodin produced by S. pararoseus fungi in vinegar samples significantly scavenged free radicals in vitro and alleviated RAW 264.7 cellular inflammation by modulating the TLR4 pathway

Study on the Cellular Anti-Inflammatory Effect of Torularhodin Produced by Sporidiobolus pararoseus ZQHL Isolated from Vinegar Fungus

The red stretcher bacterium Sporidiobolus pararoseus is a high producer of carotenoids such as torularhodin, but its presence in vinegar has not been detected. Moreover, torularhodin has several biological activities, but its effect on the LPS-induced RAW 264.7 inflammatory cell model has also yet to be elucidated. In this study, S. pararoseus was identified in different vinegar samples from China by ITS sequencing. Meanwhile, one of the strains was deeply resolved by whole genome sequencing and functional annotation and named S. pararoseus ZQHL. Subsequently, the antioxidant effect of the fungal carotenoid torularhodin was investigated using in vitro DPPH, ABTS, and cellular models. Finally, LPS-induced RAW 264.7 cells were used as an inflammation model to assess torularhodin&rsquo;s protective effect on inflammatory cells and to determine whether the TLR4 pathway is associated with this process. The results indicate that torularhodin has good free radical scavenging ability in vitro and can contribute to cell viability. More importantly, torularhodin alleviated LPS-induced cellular inflammatory damage and reduced the expression of inflammatory factors such as TLR4, MyD88, and TNF-a. The mechanism may attenuate the cellular inflammatory response by inhibiting the TLR4 inflammatory pathway. In conclusion, torularhodin produced by S. pararoseus fungi in vinegar samples significantly scavenged free radicals in vitro and alleviated RAW 264.7 cellular inflammation by modulating the TLR4 pathway

R-(+)-WIN55212-2 protects pericytes from ischemic damage and restores retinal microcirculatory patency after ischemia/reperfusion injury

Background and purpose: Cannabinoids are vasoactive substances that act as key regulators of arterial tone in the blood vessels supplying peripheral tissues and the central nervous system. This study aimed to investigate the potential of R-(+)-WIN55212-2 (WIN), a cannabinoid receptor 1 agonist (CB1), as a treatment for retinal ischemia/reperfusion (I/R) injury. Experimental approach: Male Wistar rats were subjected to retinal I/R injury by increasing intraocular pressure in the anterior chamber. The rats were randomly divided into four groups: normal control, I/R, vehicle (pre-treated with dimethyl sulfoxide [DMSO] via intraperitoneal injection), and experimental (pre-treated with WIN at a dose of 1 ml/kg via intraperitoneal injection). The rats were sacrificed at different time points of reperfusion (1 hour, 3 hours, 6 hours, and 1 day) after inducing retinal I/R injury, and their retinas were collected for analysis. Oxygen-glucose deprived/reperfusion (OGD/R) was performed by initially perfusing the retinas with oxygenated artificial cerebrospinal fluid (ACSF), then switching to an OGD solution to simulate ischemia, followed by another perfusion with ACSF. Pericyte contraction and the ''no-reflow'' phenomenon were observed using infrared differential interference contrast (IR-DIC) microscopy and immunohistochemistry. Western blot, enzyme-linked immunosorbent assay (ELISA), and nitric oxide (NO) detection were used to explore the potential mechanism. Key results: In both the OGD/R and I/R models, retinal pericytes exhibited persistent contraction even after reperfusion. The ability of WIN to regulate the tone of retinal pericytes and capillaries was specifically blocked by the BKCa inhibitor iberiotoxin (100 nM). WIN demonstrated a protective effect against retinal I/R injury by preserving blood flow in vessels containing pericytes. Pretreatment with WIN alleviated the persistent contraction and apoptosis of retinal pericytes in I/R-induced rats, accompanied by a reduction in intracellular calcium ion (Ca2+) concentration. The expression of CB1 decreased in a time-dependent manner in the I/R group. After I/R injury, endothelium-derived nitric oxide (eNOS) levels were reduced at all time points, which was successfully reversed by WIN therapy except for the 1 day group. Additionally, the downregulation of cyclic guanosine monophosphate (cGMP) and BKCa expression at 3 hours, 6 hours, and 1 day after I/R injury was restored by pretreatment of WIN. Conclusions &amp; implications: WIN exerted its protective effects on retinal I/R injury by inhibiting the contraction and apoptosis of pericytes through the CB1-eNOS-cGMP-BKCa signaling pathway, thus ameliorated the occlusion of retinal capillaries