987 resultados para reduced nicotinamide adenine dinucleotide phosphate oxidase


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Qualitative differences in strategy selection during foraging in a partially baited maze were assessed in young and old rats. The baited and non-baited arms were at a fixed position in space and marked by a specific olfactory cue. The senescent rats did more re-entries during the first four-trial block but were more rapid than the young rats in selecting the reinforced arms during the first visits. Dissociation between the olfactory spatial cue reference by rotating the maze revealed that only few old subjects relied on olfactory cues to select the baited arms and the remainder relied mainly on the visuo-spatial cues.

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For a family of reduced games satisfying a monotonicity property, we introduced the reduced equal split-off set, an extension of the equal split-off set (Branzei et. al, 2006), and study its relation with the core. Regardless of the reduction operation we consider, the intersection between both sets is either empty or a singleton containing the lexmax solution (Arin et al., 2008). We also provide a procedure for computing the lexmax solution for a class of games that includes games with large core (Sharkey, 1982). [JEL Classification: C71]

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Se llevó a cabo un experimento de 406 días en macetas para evaluar el nuevo inhibidor de la nitrificación, 3,4-dimetilpirazol fosfato (DMPP), añadido a purines de cerdo. Se utilizaron macetas que contenían tierra franca calcárea que fueron sujetas a los siguientes tratamientos: sin purín, 73,7; 147,3 y 221 cm3 de purín por maceta, todas con o sin tratamiento de DMPP. A los 18 días las macetas fueron sembradas con Lolium perenne L. El mayor rendimiento (36,3 g maceta-1) se obtuvo para el tratamiento con la dosis superior de purín y DMPP, siendo un 7,4% superior al mismo tratamiento sin inhibidor y un 46,1% superior al tratamiento control. Las plantas tratadas con dosis alta y mediana, más el DMPP, absorbieron el 70% del total del N durante la primera fase del experimento (104 días) mientras que sin inhibidor absorbieron el 55,3 y el 62% respectivamente. Se observó una reducción significativa del 17% en el N lixiviado en los tratamientos sin cultivo al aplicar DMPP. El inhibidor aumentó significativamente la eficiencia agronómica del purín (g materia seca g-1 N aplicado).

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Further genetic gains in wheat yield are required to match expected increases in demand. This may require the identification of physiological attributes able to produce such improvement, as well as the genetic bases controlling those traits in order to facilitate their manipulation. In the present paper, a theoretical framework of source and sink limitation to wheat yield is presented and the fine-tuning of crop development as an alternative for increasing yield potential is discussed. Following a top-down approach, most crop physiologists have agreed that the main attribute explaining past genetic gains in yield was harvest index (HI). By virtue of previous success, no further gains may be expected in HI and an alternative must be found. Using a bottom-up approach, the present paper firstly provides evidence on the generalized sink-limited condition of grain growth, determining that for further increases in yield potential, sink strength during grain filling has to be increased. The focus should be on further increasing grain number per m2, through fine-tuning pre-anthesis developmental patterns. The phase of rapid spike growth period (RSGP) is critical for grain number determination and increasing spike growth during pre-anthesis would result in an increased number of grains. This might be achieved by lengthening the duration of the phase (though without altering flowering time), as there is genotypic variation in the proportion of pre-anthesis time elapsed either before or after the onset of the stem elongation phase. Photoperiod sensitivity during RSGP could be then used as a genetic tool to further increase grain number, since slower development results in smoother floret development and more floret primordia achieve the fertile floret stage, able to produce a grain. Far less progress has been achieved on the genetic control of this attribute. None of the well-known major Ppd alleles seems to be consistently responsible for RSGP sensitivity. Alternatives for identifying the genetic factors responsible for this sensitivity (e.g. quantitative trait locus (QTL) identification in mapping populations) are being considered.

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Background: Experimental evidences demonstrate that vegetable derived extracts inhibit cholesterol absorption in the gastrointestinal tract. To further explore the mechanisms behind, we modeled duodenal contents with several vegetable extracts. Results: By employing a widely used cholesterol quantification method based on a cholesterol oxidase-peroxidase coupled reaction we analyzed the effects on cholesterol partition. Evidenced interferences were analyzed by studying specific and unspecific inhibitors of cholesterol oxidase-peroxidase coupled reaction. Cholesterol was also quantified by LC/MS. We found a significant interference of diverse (cocoa and tea-derived) extracts over this method. The interference was strongly dependent on model matrix: while as in phosphate buffered saline, the development of unspecific fluorescence was inhibitable by catalase (but not by heat denaturation), suggesting vegetable extract derived H2O2 production, in bile-containing model systems, this interference also comprised cholesterol-oxidase inhibition. Several strategies, such as cholesterol standard addition and use of suitable blanks containing vegetable extracts were tested. When those failed, the use of a mass-spectrometry based chromatographic assay allowed quantification of cholesterol in models of duodenal contents in the presence of vegetable extracts. Conclusions: We propose that the use of cholesterol-oxidase and/or peroxidase based systems for cholesterol analyses in foodstuffs should be accurately monitored, as important interferences in all the components of the enzymatic chain were evident. The use of adequate controls, standard addition and finally, chromatographic analyses solve these issues.

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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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The high cost of feed ingredients, the use of non-renewable sources of phosphate and the dramatic increase in the environmental load resulting from the excessive land application of manure are major challenges for the livestock industry. Precision feeding is proposed as an essential approach to improve the utilization of dietary nitrogen, phosphorus and other nutrients and thus reduce feeding costs and nutrient excretion. Precision feeding requires accurate knowledge of the nutritional value of feedstuffs and animal nutrient requirements, the formulation of diets in accordance with environmental constraints, and the gradual adjustment of the dietary nutrient supply to match the requirements of the animals. After the nutritional potential of feed ingredients has been precisely determined and has been improved by the addition of enzymes (e.g. phytases) or feed treatments, the addition of environmental objectives to the traditional feed formulation algorithms can promote the sustainability of the swine industry by reducing nutrient excretion in swine operations with small increases in feeding costs. Increasing the number of feeding phases can also contribute to significant reductions in nutrient excretion and feeding costs. However, the use of precision feeding techniques in which pigs are fed individually with daily tailored diets can further improve the efficiency with which pigs utilize dietary nutrients. Precision feeding involves the use of feeding techniques that allow the provision of the right amount of feed with the right composition at the right time to each pig in the herd. Using this approach, it has been estimated that feeding costs can be reduced by more than 4.6%, and nitrogen and phosphorus excretion can both be reduced by more than 38%. Moreover, the integration of precision feeding techniques into large-group production systems can provide real-time off-farm monitoring of feed and animals for optimal slaughter and production strategies, thus improving the environmental sustainability of pork production, animal well-being and meat-product quality.

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Among adolescents, overweight, obesity and metabolic syndrome are rapidly increasing in recent years as a consequence of unhealthy palatable diets. Animal models of diet-induced obesity have been developed, but little is known about the behavioural patterns produced by the consumption of such diets. The aim of the present study was to determine the behavioural and biochemical effects of a cafeteria diet fed to juvenile male and female rats, as well as to evaluate the possible recovery from these effects by administering standard feeding during the last week of the study. Two groups of male and female rats were fed with either a standard chow diet (ST) or a cafeteria (CAF) diet from weaning and for 8 weeks. A third group of males (CAF withdrawal) was fed with the CAF diet for 7 weeks and the ST in the 8th week. Both males and females developed metabolic syndrome as a consequence of the CAF feeding, showing overweight, higher adiposity and liver weight, increased plasma levels of glucose, insulin and triglycerides, as well as insulin resistance, in comparison with their respective controls. The CAF diet reduced motor activity in all behavioural tests, enhanced exploration, reduced anxiety-like behaviour and increased social interaction; this last effect was more pronounced in females than in males. When compared to animals only fed with a CAF diet, CAF withdrawal increased anxiety in the open field, slightly decreased body weight, and completely recovered the liver weight, insulin sensitivity and the standard levels of glucose, insulin and triglycerides in plasma. In conclusion, a CAF diet fed to young animals for 8 weeks induced obesity and metabolic syndrome, and produced robust behavioural changes in young adult rats, whereas CAF withdrawal in the last week modestly increased anxiety, reversed the metabolic alterations and partially reduced overweight.

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Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional housekeeping protein reported to be a target of several covalent modifications in many organisms. In a previous study we showed that enterohemorragic (EHEC) and enteropathogenic (EPEC) Escherichia coli strains secrete GAPDH and that this protein binds to human plasminogen and fibrinogen. Here we report that GAPDH of these pathogens is ADP-ribosylated either in the cytoplasm or in the extracellular medium. GAPDH catalyzes its own modification which involves Cys149 at the active site. ADP-ribosylation of extracellular GAPDH may play important role in the interaction with the host as it has been proposed in other pathogens.

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Background:Our objective is to determine the activity of the antioxidant defense system at admission in patients with early onset first psychotic episodes compared with a control group. Methods: Total antioxidant status (TAS) and lipid peroxidation (LOOH) were determined in plasma. Enzyme activities and total glutathione levels were determined in erythrocytes in 102 children and adolescents with a first psychotic episode and 98 healthy controls. Results: A decrease in antioxidant defense was found in patients, measured as decreased TAS and glutathione levels. Lipid damage (LOOH) and glutathione peroxidase activity was higher in patients than controls. Our study shows a decrease in the antioxidant defense system in early onset first episode psychotic patients. Conclusions: Glutathione deficit seems to be implicated in psychosis, and may be an important indirect biomarker of oxidative stress in early-onset schizophrenia. Oxidative damage is present in these patients, and may contribute to its pathophysiology.

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The inhibition of phosphatidic acid phosphatase (PAP) activity by propanolol indicates that diacylglycerol (DAG) is required for the formation of transport carriers at the Golgi and for retrograde trafficking to the ER. Here we report that the PAP2 family member lipid phosphate phosphatase 3 (LPP3, also known as PAP2b) localizes in compartments of the secretory pathway from ER export sites to the Golgi complex. The depletion of human LPP3: (i) reduces the number of tubules generated from the ER-Golgi intermediate compartment and the Golgi, with those formed from the Golgi being longer in LPP3-silenced cells than in control cells; (ii) impairs the Rab6-dependent retrograde transport of Shiga toxin subunit B from the Golgi to the ER, but not the anterograde transport of VSV-G or ssDsRed; and (iii) induces a high accumulation of Golgi-associated membrane buds. LPP3 depletion also reduces levels of de novo synthesized DAG and the Golgi-associated DAG contents. Remarkably, overexpression of a catalytically inactive form of LPP3 mimics the effects of LPP3 knockdown on Rab6-dependent retrograde transport. We conclude that LPP3 participates in the formation of retrograde transport carriers at the ER-Golgi interface, where it transitorily cycles, and during its route to the plasma membrane.

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Sucroferric oxyhydroxide (VELPHORO(®)) is a polynuclear iron-based phosphate binder recently approved for the treatment of hyperphosphataemia in patients with chronic kidney disease (CKD). As a number of the available phosphate binders do not provide the optimal combination of good efficacy, adequate tolerability and low pill burden, sucroferric oxyhydroxide constitutes a promising alternative. Among the attributes of an ideal phosphate binder is minimal absorption and, hence, low risk of systemic toxicity. Accordingly, the iron-releasing properties and absorption, distribution, metabolism and excretion (ADME) profile of sucroferric oxyhydroxide, as well as the possibility of iron accumulation and toxicity, were investigated in a series of preclinical studies. The effect of sucroferric oxyhydroxide on the progression of vascular calcification was also investigated. Sucroferric oxyhydroxide exhibited a high phosphate-binding capacity and low iron-releasing properties across the physiological pH range found in the gastrointestinal tract. In the ADME studies, uptake of (59)Fe-radiolabelled sucroferric oxyhydroxide was low in rats and dogs (<1% from a 50 mg Fe/kg bodyweight dose), with the majority of absorbed iron located in red blood cells. Long-term (up to 2 years) administration of sucroferric oxyhydroxide in rats and dogs was associated with modest increases in tissue iron levels and no iron toxicity. Moreoever, in uraemic rats, sucroferric oxyhydroxide was associated with reduced progression of vascular calcification compared with calcium carbonate. In conclusion, sucroferric oxyhydroxide offers a new option for the treatment of hyperphosphataemia, with a high phosphate-binding capacity, minimal iron release, and low potential for iron accumulation and toxicity.