Localization landscape theory of disorder in semiconductors. III. Application to carrier transport and recombination in light emitting diodes

This paper introduces a novel method to account for quantum disorder effects into the classical drift-diffusion model of semiconductor transport through the localization landscape theory. Quantum confinement and quantum tunneling in the disordered system change dramatically the energy barriers acting on the perpendicular transport of heterostructures. In addition they lead to percolative transport through paths of minimal energy in the 2D landscape of disordered energies of multiple 2D quantum wells. This model solves the carrier dynamics with quantum effects self-consistently and provides a computationally much faster solver when compared with the Schr\"odinger equation resolution. The theory also provides a good approximation to the density of states for the disordered system over the full range of energies required to account for transport at room-temperature. The current-voltage characteristics modeled by 3-D simulation of a full nitride-based light-emitting diode (LED) structure with compositional material fluctuations closely match the experimental behavior of high quality blue LEDs. The model allows also a fine analysis of the quantum effects involved in carrier transport through such complex heterostructures. Finally, details of carrier population and recombination in the different quantum wells are given.Comment: 14 pages, 16 figures, 6 table

Determination of bioavailable phosphorus in water samples using bioassay methods.

The total phosphorus analyte (TP) has a long history of use in monitoring and regulatory applications relating to management of cultural eutrophication in freshwaters. It has become apparent, however, that the fraction of the TP analyte ultimately available to support algal growth varies significantly spatially (within a system), seasonally, and among systems. The algal bioassay methods described here provide an approach for determining the bioavailable fraction of the three operationally defined components of TP: soluble reactive phosphorus (SRP), dissolved organic phosphorus (DOP), and particulate phosphorus (PP) in effluents and tributaries discharging to lakes and reservoirs. Application of the technique facilitates a quantitative ranking and targeting of bioavailable phosphorus sources for management.•One congruent method to fractionate particulate and soluble phosphorus (found in aquatic samples) into bioavailable and unavailable fractions was developed based on compilation, adaptation and expansion of two methods from the late 1970s and early 1980s.•Detailed descriptions for culturing phosphorus-starved algae, sub-sampling schedules, kinetics determination, and data presentation are provided•Reproducibility is demonstrated by replication and closure of a mass balance on phosphorus

Localization landscape theory of disorder in semiconductors. II. Urbach tails of disordered quantum well layers

International audienc

Inflammasome-Dependent Induction of Adaptive NK Cell Memory

Monobenzone is a pro-hapten that is exclusively metabolized by melanocytes, thereby haptenizing melanocyte-specific antigens, which results in cytotoxic autoimmunity specifically against pigmented cells. Studying monobenzone in a setting of contact hypersensitivity (CHS), we observed that monobenzone induced a long-lasting, melanocyte-specific immune response that was dependent on NK cells, yet fully intact in the absence of T- and B cells. Consistent with the concept of "memory NK cells," monobenzone-induced NK cells resided in the liver and transfer of these cells conferred melanocyte-specific immunity to naive animals. Monobenzone-exposed skin displayed macrophage infiltration and cutaneous lymph nodes showed an inflammasome-dependent influx of macrophages with a tissue-resident phenotype, coinciding with local NK cell activation. Indeed, macrophage depletion or the absence of the NLRP3 inflammasome, the adaptor protein ASC or interleukin-18 (IL-18) abolished monobenzone CHS, thereby establishing a non-redundant role for the NLRP3 inflammasome as a critical proinflammatory checkpoint in the induction of hapten-dependent memory NK cell

Immune Cell-Poor Melanomas Benefit from PD-1 Blockade after Targeted Type I IFN Activation

Infiltration of human melanomas with cytotoxic immune cells correlates with spontaneous type I IFN activation and a favorable prognosis. Therapeutic blockade of immune-inhibitory receptors in patients with preexisting lymphocytic infiltrates prolongs survival, but new complementary strategies are needed to activate cellular antitumor immunity in immune cell-poor melanomas. Here, we show that primary melanomas in Hgf-Cdk4(R24C) mice, which imitate human immune cell-poor melanomas with a poor outcome, escape IFN-induced immune surveillance and editing. Peritumoral injections of immunostimulatory RNA initiated a cytotoxic inflammatory response in the tumor microenvironment and significantly impaired tumor growth. This critically required the coordinated induction of type I IFN responses by dendritic, myeloid, natural killer, and T cells. Importantly, antibody-mediated blockade of the IFN-induced immune-inhibitory interaction between PD-L1 and PD-1 receptors further prolonged the survival. These results highlight important interconnections between type I IFNs and immune-inhibitory receptors in melanoma pathogenesis, which serve as targets for combination immunotherapies. SIGNIFICANCE: Using a genetically engineered mouse melanoma model, we demonstrate that targeted activation of the type I IFN system with immunostimulatory RNA in combination with blockade of immune-inhibitory receptors is a rational strategy to expose immune cell-poor tumors to cellular immune surveillance. (C) 2014 AACR

Overview of pattern recognition receptors and corresponding ligands used in this project.

<p>Overview of pattern recognition receptors and corresponding ligands used in this project.</p

Comparison of cytokines induced by LPS and R848 in PBMC and in a human WBA.

<p>a – PBMC were incubated in 96 well with increasing concentrations of LPS. After 48 h supernatant was analyzed for TNF-α and IL-6 using ELISA. Results of eight donors are shown as mean +/− SD. b–c – Whole blood anticoagulated either with Heparin, EDTA or Hirudin was incubated in 96 wells with increasing concentrations of LPS and after 48 h supernatant was checked for IL-6 (b), TNF-α (c). Mean of six donors is shown +/− SD. d – Done as described in (a) but R848 was used for stimulation and supernatant was analyzed for IFN-α, TNF-α and IL-6. Mean of eight donors (three for IFN-α) is shown +/− SD. e–g – Done as described for (b) but R848 was used for stimulation and IFN-α (e), TNF-α (f) and IL-6 (g) were measured in supernatant. Results of four (IFN-α) and six donors are shown as mean +/− SD.</p

RNA ligands for TLR7 and RIG-I induce IFN-α in Hirudin-whole blood assay.

<p>a – Whole blood was anticoagulated with Heparin, EDTA or Hirudin and stimulated with 0.8 µg/ml 3p-dsRNA, 9.2s-RNA or A20-RNA (negative control) delivered with Lipofectamine2000 or DOTAP. After 48 h supernatant was analyzed for IFN-α induction by ELISA. Graph shows percentage of induced IFN-α compared to 3p-dsRNA and 9.2s-RNA respectively (induced IFN-α concentrations: 3p-dsRNA: 2641 pg/ml; 9.2s-RNA: 1438 pg/ml). Results of four donors are shown as mean +/− SD. b – 3p-dsRNA was incubated with Lipofectamine2000 and 9.2s-RNA with DOTAP with or without addition of Heparin or Hirudin. Complexes were digested by RNase and subsequently analyzed by gel electrophoresis. c – Whole blood of three different donors anticoagulated with Hirudin was stimulated at two different time points with 0.8 µg/ml 3p-dsRNA, 9.2s-RNA or A20-RNA (negative control). After 48 h supernatant was analyzed for IFN-α using ELISA. Mean of duplicates +/− SD are shown for each timepoint. d – Whole blood was anticoagulated with Hirudin and stimulated with increasing concentrations of 3p-dsRNA and 9.2s-RNA. Results of eight donors are shown as mean +/− SD. e – Done as described for (d) but Protamine (Prot) and poly-L-Arginine (pArg) were used as delivery agents for increasing concentrations of 9.2s-RNA. Results of eight donors are shown as mean +/− SD. f – Done as described for (d) but polyethylenimine (PEI) was used to deliver increasing concentrations of 3p-dsRNA. Results of six donors are shown as mean +/− SD. g – Done as described for (d) but 0.8 µg/ml of dAdT was used to stimulate the cells. Results show mean of IFN-α and IP-10 induction of six donors +/− SD.</p