Análise da expressão diferencial de genes de raízes de Arachis stenosperma Krapov. & W.C. Gregory infectadas com o fitonematóide Meloidogyne arenaria (Neal) Chitwood raça 1.

bitstream/CENARGEN/29401/1/bp172.pd

Scale Invariance without Inflation?

We propose a new alternative mechanism to seed a scale invariant spectrum of primordial density perturbations that does not rely on inflation. In our scenario, a perfect fluid dominates the early stages of an expanding, non-inflating universe. Because the speed of sound of the fluid decays, perturbations are left frozen behind the sound horizon, with a spectral index that depends on the fluid equation of state. We explore here a toy model that realizes this idea. Although the model can explain an adiabatic, Gaussian, scale invariant spectrum of primordial perturbations, it turns out that in its simplest form it cannot account for the observed amplitude of the primordial density perturbations.Comment: 6 two-column pages, 1 figure. Uses RevTeX4. v2: References added and number of required e-folds refine

Vacuum Choices and the Predictions of Inflation

In the presence of a short-distance cutoff, the choice of a vacuum state in an inflating, non-de Sitter universe is unavoidably ambiguous. The ambiguity is related to the time at which initial conditions for the mode functions are specified and to the way the expansion of the universe affects those initial conditions. In this paper we study the imprint of these uncertainties on the predictions of inflation. We parametrize the most general set of possible vacuum initial conditions by two phenomenological variables. We find that the generated power spectrum receives oscillatory corrections whose amplitude is proportional to the Hubble parameter over the cutoff scale. In order to further constrain the phenomenological parameters that characterize the vacuum definition, we study gravitational particle production during different cosmological epochs.Comment: 10 two-column pages, 1 figure; uses RevTeX

Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR

Erratum in : Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR. [Cell. 2019]International audienceInnate immune responses are intricately linked with intracellular metabolism of myeloid cells. Toll-likereceptor (TLR) stimulation shifts intracellular metabolism toward glycolysis, while anti-inflammatorysignals depend on enhanced mitochondrial respiration. How exogenous metabolic signals affect theimmune response is unknown. We demonstrate that TLR-dependent responses of dendritic cells (DC)are exacerbated by a high fatty acid (FA) metabolic environment. FA suppress the TLR-inducedhexokinase activity and perturb tricarboxylic acid cycle metabolism. These metabolic changesenhance mitochondrial reactive oxygen species (mtROS) production and, in turn, the unfolded proteinresponse (UPR) leading to a distinct transcriptomic signature, with IL-23 as hallmark. Interestingly,chemical or genetic suppression of glycolysis was sufficient to induce this specific immune response.Conversely, reducing mtROS production or DC-specific deficiency in XBP1 attenuated IL-23expression and skin inflammation in an IL-23-dependent model of psoriasis. Thus, fine-tuning of innateimmunity depends on optimization of metabolic demands and minimization of mtROS-induced UPR

Statefinder diagnostic and w−w′w-w^{\prime} analysis for interacting polytropic gas dark energy model

The interacting polytropic gas dark energy model is investigated from the viewpoint of statefinder diagnostic tool and $w-w^{\prime}$ analysis. The dependency of the statefinder parameters on the parameter of the model as well as the interaction parameter between dark matter and dark energy is calculated. We show that different values of the parameters of model and different values of interaction parameter result different evolutionary trajectories in $s-r$ and $w-w^{\prime}$ planes. The polytropic gas model of dark energy mimics the standard $\Lambda$CDM model at the early time.Comment: 17 pages, 4 figures, ijtp accepte

Effects of adaptation to sea water, 170% sea water and to fresh water on activities and subcellular distribution of branchial Na + −K + -ATPase, low- and high affinity Ca ++ -ATPase, and ouabain-insensitive ATPase in Gillichthys mirabilis

1. Branchial activities of Na + −K + -ATPase, ouabain-insensitive ATPase, (Mg ++ -ATPase) and Ca ++ -ATPase were measured in Gillichthys mirabilis after adaptation to salinities ranging from 170% SW to FW. Stabilities of these activities against freezing and deoxycholate solubilization and the temperature-dependence of activity rates were also investigated. Subcellular distribution and some kinetic properties of these activities, and of SDH were compared in branchial tissues of fish adapted to 170% SW and to FW.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47126/1/360_2004_Article_BF00782593.pd

Cell cycle-independent phospho-regulation of Fkh2 during hyphal growth regulates Candida albicans pathogenesis.

The opportunistic human fungal pathogen, Candida albicans, undergoes morphological and transcriptional adaptation in the switch from commensalism to pathogenicity. Although previous gene-knockout studies have identified many factors involved in this transformation, it remains unclear how these factors are regulated to coordinate the switch. Investigating morphogenetic control by post-translational phosphorylation has generated important regulatory insights into this process, especially focusing on coordinated control by the cyclin-dependent kinase Cdc28. Here we have identified the Fkh2 transcription factor as a regulatory target of both Cdc28 and the cell wall biosynthesis kinase Cbk1, in a role distinct from its conserved function in cell cycle progression. In stationary phase yeast cells 2D gel electrophoresis shows that there is a diverse pool of Fkh2 phospho-isoforms. For a short window on hyphal induction, far before START in the cell cycle, the phosphorylation profile is transformed before reverting to the yeast profile. This transformation does not occur when stationary phase cells are reinoculated into fresh medium supporting yeast growth. Mass spectrometry and mutational analyses identified residues phosphorylated by Cdc28 and Cbk1. Substitution of these residues with non-phosphorylatable alanine altered the yeast phosphorylation profile and abrogated the characteristic transformation to the hyphal profile. Transcript profiling of the phosphorylation site mutant revealed that the hyphal phosphorylation profile is required for the expression of genes involved in pathogenesis, host interaction and biofilm formation. We confirmed that these changes in gene expression resulted in corresponding defects in pathogenic processes. Furthermore, we identified that Fkh2 interacts with the chromatin modifier Pob3 in a phosphorylation-dependent manner, thereby providing a possible mechanism by which the phosphorylation of Fkh2 regulates its specificity. Thus, we have discovered a novel cell cycle-independent phospho-regulatory event that subverts a key component of the cell cycle machinery to a role in the switch from commensalism to pathogenicity