993 resultados para Line loss


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Wheat yield and grain nitrogen concentration (GNC; mg N/g grain) are frequently negatively correlated. In most growing conditions, this is mainly due to a feedback process between GNC and the number of grains/m2. In Mediterranean conditions, breeders may have produced cultivars with conservative grain set. The present study aimed at clarifying the main physiological determinants of grain nitrogen accumulation (GNA) in Mediterranean wheat and to analyse how breeding has affected them. Five field experiments were carried out in north-eastern Spain in the 2005/06 and 2006/ 07 growing seasons with three cultivars released at different times and an advanced line. Depending on the experiment, source-sink ratios during grain filling were altered by reducing grain number/m2 either through pre-anthesis shading (unshaded control or 0.75 shading only between jointing and anthesis) or by directly trimming the spikes after anthesis and before the onset of the effective grain filling period (un-trimmed control or spikes halved 7–10 days after anthesis). Grain nitrogen content (GN content ; mg N/grain) decreased with the year of release of the genotypes. As the number of grains/m2 was also increased by breeding there was a clear dilution effect on the amount of nitrogen allocated to each grain. However, the increase in GN content in old genotypes did not compensate for the loss in grain nitrogen yield (GNY) due to the lower number of grains/m2. GN content of all genotypes increased (increases ranged from 0.13 to 0.40 mg N/grain, depending on experiment and genotype) in response to the post-anthesis spike trimming or pre-anthesis shading. The degree of source-limitation for GNA increased with the year of release of the genotypes (and thus with increases in grain number/m2) from 0.22 (mean of the four manipulative experiments) in the oldest cultivar to 0.51 (mean of the four manipulative experiments) in the most modern line. It was found that final GN content depended strongly on the source-sink ratio established at anthesis between the number of grains set and the amount of nitrogen absorbed at this stage. Thus, Mediterranean wheat breeding that improved yield through increases in grain number/m2 reduced the GN content by diluting a rather limited source of nitrogen into more grains. This dilution effect produced by breeding was further confirmed by the reversal effect produced by grain number/m2 reductions due to either pre-anthesis shading or post-anthesis spike trimming.

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Lipin proteins (lipin 1, 2, and 3) regulate glycerolipid homeostasis by acting as phosphatidic acid phosphohydrolase (PAP) enzymes in the TG synthesis pathway and by regulating DNA-bound transcription factors to control gene transcription. Hepatic PAP activity could contribute to hepatic fat accumulation in response to physiological and pathophysiological stimuli. To examine the role of lipin 1 in regulating hepatic lipid metabolism, we generated mice that are deficient in lipin-1-encoded PAP activity in a liver-specific manner (Alb-Lpin1(-/-) mice). This allele of lipin 1 was still able to transcriptionally regulate the expression of its target genes encoding fatty acid oxidation enzymes, and the expression of these genes was not affected in Alb-Lpin1(-/-) mouse liver. Hepatic PAP activity was significantly reduced in mice with liver-specific lipin 1 deficiency. However, hepatocytes from Alb-Lpin1(-/-) mice had normal rates of TG synthesis, and steady-state hepatic TG levels were unaffected under fed and fasted conditions. Furthermore, Alb-Lpin1(-/-) mice were not protected from intrahepatic accumulation of diacylglyerol and TG after chronic feeding of a diet rich in fat and fructose. Collectively, these data demonstrate that marked deficits in hepatic PAP activity do not impair TG synthesis and accumulation under acute or chronic conditions of lipid overload.

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MAF1 is a global repressor of RNA polymerase III transcription that regulates the expression of highly abundant noncoding RNAs in response to nutrient availability and cellular stress. Thus, MAF1 function is thought to be important for metabolic economy. Here we show that a whole-body knockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver disease by reducing food intake and increasing metabolic inefficiency. Energy expenditure in Maf1(-/-) mice is increased by several mechanisms. Precursor tRNA synthesis was increased in multiple tissues without significant effects on mature tRNA levels, implying increased turnover in a futile tRNA cycle. Elevated futile cycling of hepatic lipids was also observed. Metabolite profiling of the liver and skeletal muscle revealed elevated levels of many amino acids and spermidine, which links the induction of autophagy in Maf1(-/-) mice with their extended life span. The increase in spermidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associated with obesity resistance. Consistent with this, NAD(+) levels were increased in muscle. The importance of MAF1 for metabolic economy reveals the potential for MAF1 modulators to protect against obesity and its harmful consequences.

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For more than a decade scientists tried to develop methods capable of dating ink by monitoring the loss of phenoxyethanol (PE) over time. While many methods were proposed in the literature, few were really used to solve practical cases and they still raise much concern within the scientific community. In fact, due to the complexity of ink drying processes it is particularly difficult to find a reliable ageing parameter to reproducibly follow ink ageing. Moreover, systematic experiments are required in order to evaluate how different factors actually influence the results over time. Therefore, this work aimed at evaluating the capacity of four different ageing parameters to reliably follow ink ageing over time: (1) the quantity of solvent PE in an ink line, (2) the relative peak area (RPA) normalising the PE results using stable volatile compounds present in the ink formulation, (3) the solvent loss ratio (R%) calculated from PE results obtained by the analyses of naturally and artificially aged samples, (4) a modified solvent loss ratio version (R%*) calculated from RPA results. After the determination of the limits of reliable measurements of the analytical method, the repeatability of the different ageing parameters was evaluated over time, as well as the influence of ink composition, writing pressure and storage conditions on the results. Surprisingly, our results showed that R% was not the most reliable parameter, as it showed the highest standard deviation. Discussion of the results in an ink dating perspective suggests that other proposed parameters, such as RPA values, may be more adequate to follow ink ageing over time.

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Mutations in Sigma 1 receptor (SIGMAR1) have been previously identified in patients with amyotrophic lateral sclerosis and disruption of Sigmar1 in mouse leads to locomotor deficits. However, cellular mechanisms underlying motor phenotypes in human and mouse with disturbed SIGMAR1 function have not been described so far. Here we used a combination of in vivo and in vitro approaches to investigate the role of SIGMAR1 in motor neuron biology. Characterization of Sigmar1(-/-) mice revealed that affected animals display locomotor deficits associated with muscle weakness, axonal degeneration and motor neuron loss. Using primary motor neuron cultures, we observed that pharmacological or genetic inactivation of SIGMAR1 led to motor neuron axonal degeneration followed by cell death. Disruption of SIGMAR1 function in motor neurons disturbed endoplasmic reticulum-mitochondria contacts, affected intracellular calcium signalling and was accompanied by activation of endoplasmic reticulum stress and defects in mitochondrial dynamics and transport. These defects were not observed in cultured sensory neurons, highlighting the exacerbated sensitivity of motor neurons to SIGMAR1 function. Interestingly, the inhibition of mitochondrial fission was sufficient to induce mitochondria axonal transport defects as well as axonal degeneration similar to the changes observed after SIGMAR1 inactivation or loss. Intracellular calcium scavenging and endoplasmic reticulum stress inhibition were able to restore mitochondrial function and consequently prevent motor neuron degeneration. These results uncover the cellular mechanisms underlying motor neuron degeneration mediated by loss of SIGMAR1 function and provide therapeutically relevant insight into motor neuronal diseases.

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Natural Killer (NK) cells use germ line encoded receptors to detect diseased host cells. Despite the invariant recognition structures, NK cells have a significant ability to adapt to their surroundings, such as the presence or absence of MHC class I molecules. It has been assumed that this adaptation occurs during NK cell development, but recent findings show that mature NK cells can also adapt to the presence or absence of MHC class I molecules. Here, we summarize how NK cells adjust to changes in the expression of MHC class I molecules. We propose an extension of existing models, in which MHC class I recognition during NK cell development sequentially instructs and maintains NK cell function. The elucidation of the molecular basis of the two effects may identify ways to improve the fitness of NK cells and to prevent the loss of NK cell function due to persistent alterations in their environment.

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We recently showed that a heavy quark moving sufficiently fast through a quark-gluon plasma may lose energy by Cherenkov-radiating mesons [1]. Here we review our previous holographic calculation of the energy loss in N=4 Super Yang-Mills and extend it to longitudinal vector mesons and scalar mesons. We also discuss phenomenological implications for heavy-ion collision experiments. Although the Cherenkov energy loss is an O(1/Nc) effect, a ballpark estimate yields a value of dE/dx for Nc=3 which is comparable to that of other mechanisms.

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We recently showed that a heavy quark moving sufficiently fast through a quark-gluon plasma may lose energy by Cherenkov-radiating mesons [1]. Here we review our previous holographic calculation of the energy loss in N=4 Super Yang-Mills and extend it to longitudinal vector mesons and scalar mesons. We also discuss phenomenological implications for heavy-ion collision experiments. Although the Cherenkov energy loss is an O(1/Nc) effect, a ballpark estimate yields a value of dE/dx for Nc=3 which is comparable to that of other mechanisms.

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Operatiivisen tiedon tuottaminen loppukäyttäjille analyyttistä tarkastelua silmällä pitäen aiheuttaa ongelmia useille yrityksille. Diplomityö pyrkii ratkaisemaan ko. ongelman Teleste Oyj:ssä. Työ on jaettu kolmeen pääkappaleeseen. Kappale 2 selkiyttää On-Line Analytical Processing (OLAP)- käsitteen. Kappale 3 esittelee muutamia OLAP-tuotteiden valmistajia ja heidän arkkitehtuurejaan sekä tyypillisten sovellusalueiden lisäksi huomioon otettavia asioita OLAP käyttöönoton yhteydessä. Kappale 4, tuo esille varsinaisen ratkaisun. Teknisellä arkkitehtuurilla on merkittävä asema ratkaisun rakenteen kannalta. Tässä on sovellettu Microsoft:n tietovarasto kehysrakennetta. Kappaleen 4 edetessä, tapahtumakäsittelytieto muutetaan informaatioksi ja edelleen loppukäyttäjien tiedoksi. Loppukäyttäjät varustetaan tehokkaalla ja tosiaikaisella analysointityökalulla moniulotteisessa ympäristössä. Vaikka kiertonopeus otetaan työssä sovellusesimerkiksi, työ ei pyri löytämään optimaalista tasoa Telesten varastoille. Siitä huolimatta eräitä parannusehdotuksia mainitaan.