A feeding experiment was conducted to examine the potential of a commercial steam-processed-feather meal (SPFM) and feathers enzymatically hydrolysed for 60 or 120 min (EHF60 and EHF120) as substitutes for ®shmeal (FM) in diets for white shrimp juveniles. Enzymatically hydrolised feathers or SPFM were blended through an extruder with soyabean meal (SBM) in a 1:1 ratio (EHF-SBM, SPFM-SBM). Isoproteic and isolipidic diets were formulated to contain 9% EHF60-SBM, 9% EHF120-SBM and 18% EHF60-SBM. These diets were compared with a diet containing 13.7% SPFM-SBM and a control diet designed to contain 18.4% FM and no feather. Quadruplicate groups of 15 shrimp (0.33 g initialbody weight) were fed twice a day on each diet for 4 weeks. The weight gain of shrimp fed on the three EHF-SBM diets did not dier from that of shrimp fed on the FM-control diet; however, shrimp fed on the SPFM-SBM diet gained less weight. The EHF60 and EHF120 coextruded with SBM in a 2:1 ratio were evaluated in a commercial rearing pond. Both ingredients included at 20% in the test diets were compared with a control diet containing 17.8% FM. Triplicate groups of juvenile shrimp (3.4 g initial-mean weight), randomly allocated in 1 m 3 plastic cages, were fed with the test diets during 30 days. Growth (weight gain, speci®c-growth rate (SGR)) and nutritional value of the diets, food conversion ratio (FCR), protein-eciency ratio (PER), digestibility were similar. In summary, these results indicate that white shrimp can be fed with a practical diet containing 20% EHF-SBM (2:1) without impairing growth or food conversion. The use of 20% EHF-SBM (2:1) allowed the ®sh-meal portion to be reduced by nearly by 55%.
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These data suggest that cf-DNA when analyzed using NGS is a reliable approach for detecting molecular abnormalities in MDS and should be used to determine if bone marrow aspiration and biopsy are necessary.
Sphingopyxis granuli TFA is a contaminant degrading alphaproteobacterium that responds to adverse conditions by inducing the General Stress Response (GSR), an adaptive response that controls the transcription of a variety of genes to overcome adverse conditions. The GSR triggered by TFA is driven by two extracytoplasmic function σ factors (ECFs), EcfG1 and EcfG2, whose functional differences have been addressed previously, being EcfG2 the main activator. Upstream in this cascade, NepR anti-s factors directly inhibit EcfG activity under non-stress conditions, whereas PhyR response regulators sequester the NepR elements upon stress sensing to relieve EcfG inhibition. These elements, which are essential mediators of the GSR regulation, are duplicated in TFA, being NepR1 and NepR2, and PhyR1 and PhyR2. Here, based on multiple genetic, phenotypical and biochemical evidences including in vitro transcription assays, we have assigned distinct functional features to each of these paralogs and assessed their contribution to the GSR regulation, dictating its timing and the intensity. We show that different stress signals are differentially integrated into the GSR by PhyR1 and PhyR2, therefore producing different levels of GSR activation. We demonstrate in vitro that both NepR1 and NepR2 bind EcfG1 and EcfG2, although NepR1 produces a more stable interaction than NepR2. Conversely, NepR2 interacts with phosphorylated PhyR1 and PhyR2 more efficiently than NepR1. We propose an integrative model where NepR2 would play a dual negative role: it would directly inhibit the s factors upon activation of the GSR and it would modulate the GSR activity indirectly by titrating the PhyR regulators.
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