Efficacy of Vitaflo 280 to control soil- and seed-borne diseases of pea and lentil, and compatibility with rhizobium inoculants

Non-Peer ReviewedLentil (Lens culinaris Medikus) and pea (Pisum sativum L.) have the ability to fix dinitrogen (N2) from the atmosphere. Rhizobium inoculants are applied to the seed to ensure effective N2 fixation. In addition, fungicidal seed treatments are recommended to control extremely aggressive diseases such as Ascochyta, Botrytis, Fusarium, and Rhizoctonia seedling blight. To determine the efficacy of Vitaflo 280 to control seedling blight of pea and lentil caused by Botrytis cinerea, Mycosphaerella pinodes (Ascochyta blight), Rhizoctonia solani and Fusarium spp. experiments were established at several locations and years in western Canada. To determine the effect of Crown, Allegiance FL, Vitaflo 280, and Apron Maxx on the ability of Rhizobium inoculants to nodulate and fix N2 from the atmosphere experiments were established at two locations in Saskatchewan in 2002. Vitaflo 280 at the recommended rates effectively controls seedling blight of lentil caused by seed-borne Botrytis cinerea and soil-borne Fusarium spp and Rhizoctonia solani. Vitaflo 280 at the recommended rates effectively controls seedling blight of pea caused by seed-borne Mycosphaerella pinodes and soil-borne Fusarium spp and Rhizoctonia solani. In addition, Allegiance FL, Crown, Vitaflo 280, and Apron Maxx at the recommended rates have no effect on visual nodulation or the ability of the Rhizobium to fix N2 from the atmosphere

Effects of Crown (carbathiin and thiabendazole), Allegiance FL (metalaxyl), Vitaflo 280 (carbathiin and thiram), and Apron Maxx (fluodioxonil and metalaxyl) on N2 fixation of chickpea, dry bean, lentil, and pea

Non-Peer Reviewe

Proximity Effects and Nonequilibrium Superconductivity in Transition-Edge Sensors

We have recently shown that normal-metal/superconductor (N/S) bilayer TESs (superconducting Transition-Edge Sensors) exhibit weak-link behavior.1 Here we extend our understanding to include TESs with added noise-mitigating normal-metal structures (N structures). We find TESs with added Au structures also exhibit weak-link behavior as evidenced by exponential temperature dependence of the critical current and Josephson-like oscillations of the critical current with applied magnetic field. We explain our results in terms of an effect converse to the longitudinal proximity effect (LoPE)1, the lateral inverse proximity effect (LaiPE), for which the order parameter in the N/S bilayer is reduced due to the neighboring N structures. Resistance and critical current measurements are presented as a function of temperature and magnetic field taken on square Mo/Au bilayer TESs with lengths ranging from 8 to 130 {\mu}m with and without added N structures. We observe the inverse proximity effect on the bilayer over in-plane distances many tens of microns and find the transition shifts to lower temperatures scale approximately as the inverse square of the in- plane N-structure separation distance, without appreciable broadening of the transition width. We also present evidence for nonequilbrium superconductivity and estimate a quasiparticle lifetime of 1.8 \times 10-10 s for the bilayer. The LoPE model is also used to explain the increased conductivity at temperatures above the bilayer's steep resistive transition.Comment: 10 pages, 8 figure

Genetic Inhibition of Phosphorylation of the Translation Initiation Factor eIF2alpha Does Not Block Abeta-Dependent Elevation of BACE1 and APP Levels or Reduce Amyloid Pathology in a Mouse Model of Alzheimer's Disease

beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) initiates the production of beta-amyloid (Abeta), the major constituent of amyloid plaques in Alzheimer's disease (AD). BACE1 is elevated approximately 2-3 fold in AD brain and is concentrated in dystrophic neurites near plaques, suggesting BACE1 elevation is Abeta-dependent. Previously, we showed that phosphorylation of the translation initiation factor eIF2alpha de-represses translation of BACE1 mRNA following stress such as energy deprivation. We hypothesized that stress induced by Abeta might increase BACE1 levels by the same translational mechanism involving eIF2alpha phosphorylation. To test this hypothesis, we used three different genetic strategies to determine the effects of reducing eIF2alpha phosphorylation on Abeta-dependent BACE1 elevation in vitro and in vivo: 1) a two-vector adeno-associated virus (AAV) system to express constitutively active GADD34, the regulatory subunit of PP1c eIF2alpha phosphatase; 2) a non-phosphorylatable eIF2alpha S51A knockin mutation; 3) a BACE1-YFP transgene lacking the BACE1 mRNA 5' untranslated region (UTR) required for eIF2alpha translational regulation. The first two strategies were used in primary neurons and 5XFAD transgenic mice, while the third strategy was employed only in 5XFAD mice. Despite very effective reduction of eIF2alpha phosphorylation in both primary neurons and 5XFAD brains, or elimination of eIF2alpha-mediated regulation of BACE1-YFP mRNA translation in 5XFAD brains, Abeta-dependent BACE1 elevation was not decreased. Additionally, robust inhibition of eIF2alpha phosphorylation did not block Abeta-dependent APP elevation in primary neurons, nor did it reduce amyloid pathology in 5XFAD mice. We conclude that amyloid-associated BACE1 elevation is not caused by translational de-repression via eIF2alpha phosphorylation, but instead appears to involve a post-translational mechanism. These definitive genetic results exclude a role for eIF2alpha phosphorylation in Abeta-dependent BACE1 and APP elevation. We suggest a vicious pathogenic cycle wherein Abeta42 toxicity induces peri-plaque BACE1 and APP accumulation in dystrophic neurites leading to exacerbated Abeta production and plaque progression

Development of Transition Edge Sensor Detectors Optimized for Single-Photon Spectroscopy in the Optical and Near-Infrared

The search for biosignatures in the atmospheres of exoplanets will be a key focus of future space telescopes that operate in the ultraviolet, visible, and near-infrared bands. Detection of biosignatures requires an instrument with moderate spectral resolving power ($R \sim 100$) and a large bandwidth ($\sim 400$ nm -- $\sim 1.8$ $\mu$m). Additionally, biosignature detection is a photon-starved science; instruments designed for these measurements would ideally combine high optical efficiency with quantum-limited photon detectors (i.e., detectors that exhibit zero dark current). In this work, we report on our efforts to develop energy resolving transition edge sensor (TES)-based detectors designed for biosignature detection. TESs operated as microcalorimeters are compelling detectors for this application. Unlike semiconductor detectors, TESs eliminate the need for dispersive optics and are truly single photon detectors -- fundamental TES noise yields uncertainty in the energies of detected photons, not in the number of detected photons. We introduce TESs designed for this application and discuss the path toward realizing a TES-based dispersionless spectrometer optimized for biosignature detection

Longitudinal Proximity Effects in Superconducting Transition-Edge Sensors

We have found experimentally that the critical current of a square superconducting transition-edge sensor (TES) depends exponentially upon the side length L and the square root of the temperature T. As a consequence, the effective transition temperature T(sub c) of the TES is current-dependent and at fixed current scales as 1/L(sup 2). We also have found that the critical current can show clear Fraunhofer-like oscillations in an applied magnetic field, similar to those found in Josephson junctions. The observed behavior has a natural theoretical explanation in terms of longitudinal proximity effects if the TES is regarded as a weak link between superconducting leads. We have observed the proximity effect in these devices over extraordinarily long lengths exceeding 100 microns