Ascorbate Biosynthesis during Early Fruit Development Is the Main Reason for Its Accumulation in Kiwi

Background: Ascorbic acid (AsA) is a unique antioxidant as well as an enzyme cofactor. Although it has multiple roles in plants, it is unclear how its accumulation is controlled at the expression level, especially in sink tissues. Kiwifruit (Actinidia) is well-known for its high ascorbate content. Our objective was to determine whether AsA accumulates in the fruits primarily through biosynthesis or because it is imported from the foliage. Methodology/Principal Findings: We systematically investigated AsA levels, biosynthetic capacity, and mRNA expression of genes involved in AsA biosynthesis in kiwi (A. deliciosa cv. Qinmei). Recycling and AsA localization were also monitored during fruit development and among different tissue types. Over time, the amount of AsA, with its capacity for higher biosynthesis and lower recycling, peaked at 30 days after anthesis (DAA), and then decreased markedly up to 60 DAA before declining more slowly. Expression of key genes showed similar patterns of change, except for L-galactono-1,4-lactone dehydrogenase and L-galactose-1-phosphate phosphatase (GPP). However, GPP had good correlation with the rate of AsA accumulation. The expression of these genes could be detected in phloem of stem as well as petiole of leaf and fruit. Additionally, fruit petioles had greater ascorbate amounts, although that was the site of lowest expression by most genes. Fruit microtubule tissues also had higher AsA. However, exogenous applications of AsA to those petioles did not lead to its transport into fruits, and distribution of ascorbate was cell-specific in the fruits, with more accumulation occurring in large

Resolution of sickle cell disease-associated inflammation and tissue damage with 17R-resolvin D1.

Resolvins (Rvs), endogenous lipid mediators, play a key role in the resolution of inflammation. Sickle cell disease (SCD), a genetic disorder of hemoglobin, is characterized by inflammatory and vaso-occlusive pathologies. We document altered proresolving events following hypoxia/reperfusion in humanized SCD mice. We demonstrate novel protective actions of 17R-resolvin D1 (17R-RvD1; 7S, 8R, 17R-trihydroxy-4Z, 9E, 11E, 13Z, 15E, 19Z-docosahexaenoic acid) in reducing ex vivo human SCD blood leukocyte recruitment by microvascular endothelial cells and in vivo neutrophil adhesion and transmigration. In SCD mice exposed to hypoxia/reoxygenation, oral administration of 17R -RvD1 reduces systemic/local inflammation and vascular dysfunction in lung and kidney. The mechanism of action of 17R-RvD1 involves (1) enhancement of SCD erythrocytes and polymorphonuclear leukocyte efferocytosis, (2) blunting of NF-\u3baB activation, and (3) a reduction in inflammatory cytokines, vascular activation markers, and E-selectin expression. Thus, 17R-RvD1 might represent a new therapeutic strategy for the inflammatory vasculopathy of SCD

Euclid: The reduced shear approximation and magnification bias for Stage IV cosmic shear experiments

Context: Stage IV weak lensing experiments will offer more than an order of magnitude leap in precision. We must therefore ensure that our analyses remain accurate in this new era. Accordingly, previously ignored systematic effects must be addressed. / Aims: In this work, we evaluate the impact of the reduced shear approximation and magnification bias on information obtained from the angular power spectrum. To first-order, the statistics of reduced shear, a combination of shear and convergence, are taken to be equal to those of shear. However, this approximation can induce a bias in the cosmological parameters that can no longer be neglected. A separate bias arises from the statistics of shear being altered by the preferential selection of galaxies and the dilution of their surface densities in high-magnification regions. / Methods: The corrections for these systematic effects take similar forms, allowing them to be treated together. We calculated the impact of neglecting these effects on the cosmological parameters that would be determined from Euclid, using cosmic shear tomography. To do so, we employed the Fisher matrix formalism, and included the impact of the super-sample covariance. We also demonstrate how the reduced shear correction can be calculated using a lognormal field forward modelling approach. / Results: These effects cause significant biases in Ωm, σ8, ns, ΩDE, w0, and wa of −0.53σ, 0.43σ, −0.34σ, 1.36σ, −0.68σ, and 1.21σ, respectively. We then show that these lensing biases interact with another systematic effect: the intrinsic alignment of galaxies. Accordingly, we have developed the formalism for an intrinsic alignment-enhanced lensing bias correction. Applying this to Euclid, we find that the additional terms introduced by this correction are sub-dominant