1,230 research outputs found

    Anthocyanin pigments in strawberry

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    The anthocyanin composition was analysed in strawberry fruits from five different cultivars (cv. Eris, Oso Grande, Carisma, Tudnew and Camarosa). Twenty-five defined anthocyanin pigments were detected, most of them containing Pelargonidin (Pg) as aglycone; some cyanidin (Cy) derivatives were also found. Glucose and rutinose were the usual substituting sugars, although arabinose and rhamnose were also tentatively identified; some minor anthocyanins showed acylation with aliphatic acids. A relevant aspect was the detection of anthocyanin-derived pigments, namely 5-carboxypyranopelargonidin-3-glucoside and four condensed pigments containing C–C linked anthocyanin (Pg) and flavanol (catechin and afzelechin) residues. Total anthocyanin content ranged between 200 and 600mg/kg, with Pg 3-gluc constituting 77–90% of the anthocyanins in the strawberry extracts followed by Pg 3-rut (6–11%) and Cy 3-gluc (3–10%). A notable variability was found among the anthocyanin concentrations in samples of a same variety and harvest, indicating a strongly influence of the degree of maturity, edaphic-climatic factors and post-harvest storage

    Synapse efficiency diverges due to synaptic pruning following over-growth

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    In the development of the brain, it is known that synapses are pruned following over-growth. This pruning following over-growth seems to be a universal phenomenon that occurs in almost all areas -- visual cortex, motor area, association area, and so on. It has been shown numerically that the synapse efficiency is increased by systematic deletion. We discuss the synapse efficiency to evaluate the effect of pruning following over-growth, and analytically show that the synapse efficiency diverges as O(log c) at the limit where connecting rate c is extremely small. Under a fixed synapse number criterion, the optimal connecting rate, which maximize memory performance, exists.Comment: 15 pages, 16 figure

    Extracting Br(omega->pi^+ pi^-) from the Time-like Pion Form-factor

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    We extract the G-parity-violating branching ratio Br(omega->pi^+ pi^-) from the effective rho-omega mixing matrix element Pi_{rho omega}(s), determined from e^+e^- -> pi^+ pi^- data. The omega->pi^+ pi^- partial width can be determined either from the time-like pion form factor or through the constraint that the mixed physical propagator D_{rho omega}^{mu nu}(s) possesses no poles. The two procedures are inequivalent in practice, and we show why the first is preferred, to find finally Br(omega->pi^+ pi^-) = 1.9 +/- 0.3%.Comment: 12 pages (published version

    Simplifying the Welfare Quality assessment protocol for broilers = Vereenvoudiging van het Welfare Quality protocol voor het meten van welzijn bij vleeskuikens

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    This report describes the results of a study to simplify the Welfare Quality® assessment protocol for broiler chickens

    Expanding the proteome of an RNA virus by phosphorylation of an intrinsically disordered viral protein

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    The human proteome contains myriad intrinsically disordered proteins. Within intrinsically disordered proteins, polyproline-II motifs are often located near sites of phosphorylation. Wehave used an unconventional experimental paradigm to discover that phosphorylation by protein kinase A (PKA) occurs in the intrinsically disordered domain of hepatitis C virus nonstructural protein 5A (NS5A) on Thr-2332 near one of its polyproline-II motifs. Phosphorylation shifts the conformational ensemble of the NS5A intrinsically disordered domain to a state that permits detection of the polyproline motif by using 15N-, 13C-based multidimensional NMR spectroscopy. PKA-dependent proline resonances were lost in the presence of the Src homology 3 domain of c-Src, consistent with formation of a complex. Changing Thr-2332 to alanine in hepatitisCvirus genotype 1b reduced the steady-state level of RNA by 10-fold; this change was lethal for genotype 2a. The lethal phenotype could be rescued by changing Thr-2332 to glutamic acid, a phosphomimetic substitution. Immunofluorescence and transmission electron microscopy showed that the inability to produce Thr(P)-2332-NS5A caused loss of integrity of the virus-induced membranous web/replication organelle. An even more extreme phenotype was observed in the presence of small molecule inhibitors of PKA. We conclude that the PKA-phosphorylated form of NS5A exhibits unique structure and function relative to the unphosphorylated protein. We suggest that post-translational modification of viral proteins containing intrinsic disorder may be a general mechanism to expand the viral proteome without a corresponding expansion of the genome
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