997 resultados para element concentration


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Magdeburg, Univ., Fak. für Maschinenbau, Diss., 2012

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This paper deals with the mineral composition fresh and dry matter production of different organs of 4, 5 old guava (Psidium guajava L.) growth on sandy soil (Savanna) without fertilizer. The data obtained for fresh and dry matter productior are present in table 2 (in Portuguese). The concentration of the elements are presented in table 3 (in Portuguese). Finally, the total amounts of elements absorbed by guava are given in the following table: Element Plant (grams) Fruits (grams) Nitrogen (N) 42,55 20,4 Phosphorus (P) 3,84 2,3 Potassium (K) 52,01 31,3 Calcium (Ca) 47,81 0,2 Magnesium (Mg) — 2,4

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Magdeburg, Univ., Fak. für Mathematik, Diss., 2014

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In order to obtain the following informations: a) dry matter production and extraction of nutrients by the fruits at different ages; b) dry matter production and extraction of nutrient by the leaves and "trunk + branches" collected at the flowering stage; c) dry matter production and export of nutrients by pruning (leaves and branches) at the begining dormant stage; A trial was conducted on Latossolo Vermelho Escuro Orto group (Orthox) at Buri, São Paulo State, Brazil. The material was collected from 'Ohio Beauty' and 'Brazil' apples grafted on 'Doucin' 1-2; 3-4; 4-5 and 6-7 years old. The main conclusions were as follows: a) differences were observed on dry matter production by two varieties at the different stages of growth; b) differences were also observed between the two varieties on the matter production in the leaves and "trunk + branches" at the flowering stage, as well as by the leaves and branches pruned at the begining of dormant stages; c) differences were observed betwen the two varieties concerning to nutrient concentration (on dry matter basis) on the fruits collected at different stages of growth. Same results were observed on leaves and "trunk + branches" collected at flowering period; d) differences were observed on the exportation of the nutrients referring to growth period of fruit; e) at the flowering and dormant period, differences were observed on the contents of nutrients in the leaves, 'trunk + branches', on the two varieties; f) the nutrient exportation by the fruits obyed the following order: K>N>P>S>Ca>Mg>Fe>B > Cu > Mn > Zn > Mo; g) the nutrient extration by the aerial part the apple trees obyed the following order: N > K > Ca > Mg > P > S > Fe > B > Cu = Mn = Zn.

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On an apple grove situated at Buri, State of São Paulo, fruits were collected from trees 1-2; 3-4; 4-5, and 6 - 7 years old. The fruits were analysed for N, P, K, Ca, Mg, S, B, Cu, Fe, Mn and Zn. The authors concluded: a) the concentrations of the nutrients in the fruits differ according to the variety, age of the tree and age of the fruit; b) the concentrations of nutrients decrease with aging of the fruits; c) the concentrations of the macronutrients obey the following order: N>K>P>Ca>S> Mg; d) for the micronutrients, the following order was ob -served: Fe > B > Mn > Cu > Zn.

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Eukaryotic cells generate energy in the form of ATP, through a network of mitochondrial complexes and electron carriers known as the oxidative phosphorylation system. In mammals, mitochondrial complex I (CI) is the largest component of this system, comprising 45 different subunits encoded by mitochondrial and nuclear DNA. Humans diagnosed with mutations in the gene NDUFS4, encoding a nuclear DNA-encoded subunit of CI (NADH dehydrogenase ubiquinone Fe-S protein 4), typically suffer from Leigh syndrome, a neurodegenerative disease with onset in infancy or early childhood. Mitochondria from NDUFS4 patients usually lack detectable NDUFS4 protein and show a CI stability/assembly defect. Here, we describe a recessive mouse phenotype caused by the insertion of a transposable element into Ndufs4, identified by a novel combined linkage and expression analysis. Designated Ndufs4(fky), the mutation leads to aberrant transcript splicing and absence of NDUFS4 protein in all tissues tested of homozygous mice. Physical and behavioral symptoms displayed by Ndufs4(fky/fky) mice include temporary fur loss, growth retardation, unsteady gait, and abnormal body posture when suspended by the tail. Analysis of CI in Ndufs4(fky/fky) mice using blue native PAGE revealed the presence of a faster migrating crippled complex. This crippled CI was shown to lack subunits of the "N assembly module", which contains the NADH binding site, but contained two assembly factors not present in intact CI. Metabolomic analysis of the blood by tandem mass spectrometry showed increased hydroxyacylcarnitine species, implying that the CI defect leads to an imbalanced NADH/NAD(+) ratio that inhibits mitochondrial fatty acid β-oxidation.

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Projecte de recerca elaborat a partir d’una estada al Laboratory of Archaeometry del National Centre of Scientific Research “Demokritos” d’Atenes, Grècia, entre juny i setembre 2006. Aquest estudi s’emmarca dins d’un context més ampli d’estudi del canvi tecnològic que es documenta en la producció d’àmfores de tipologia romana durant els segles I aC i I dC en els territoris costaners de Catalunya. Una part d’aquest estudi contempla el càlcul de les propietats mecàniques d’aquestes àmfores i la seva avaluació en funció de la tipologia amforal, a partir de l’Anàlisi d’Elements Finits (AEF). L’AEF és una aproximació numèrica que té el seu origen en les ciències d’enginyeria i que ha estat emprada per estimar el comportament mecànic d’un model en termes, per exemple, de deformació i estrès. Així, un objecte, o millor dit el seu model, es dividit en sub-dominis anomenats elements finits, als quals se’ls atribueixen les propietats mecàniques del material en estudi. Aquests elements finits estan connectats formant una xarxa amb constriccions que pot ser definida. En el cas d’aplicar una força determinada a un model, el comportament de l’objecte pot ser estimat mitjançant el conjunt d’equacions lineals que defineixen el rendiment dels elements finits, proporcionant una bona aproximació per a la descripció de la deformació estructural. Així, aquesta simulació per ordinador suposa una important eina per entendre la funcionalitat de ceràmiques arqueològiques. Aquest procediment representa un model quantitatiu per predir el trencament de l’objecte ceràmic quan aquest és sotmès a diferents condicions de pressió. Aquest model ha estat aplicat a diferents tipologies amforals. Els resultats preliminars mostren diferències significatives entre la tipologia pre-romana i les tipologies romanes, així com entre els mateixos dissenys amforals romans, d’importants implicacions arqueològiques.

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Background: Leptin is produced primarily by adipocytes. Although originally associated with the central regulation of satiety and energy metabolism, increasing evidence indicates that leptin may be an important factor for congestive heart faire (CHF). In the study, we aimed to test the hypothesis that leptin may influence CHF pathophysiology via a pathway of increasing body mass index (BMI). Methods: We studied 2,389 elderly participants aged 70 and older (M; 1161, F: 1228) without CHF and with serum leptin measures at the Health Aging, and Body Composition study. We analyzed the association between serum leptin level and risk of incident CHF using Cox hazard proportional regression models. Elevated leptin level was defined as more than the highest quartile (Q4) of leptin distribution in the total sample for each gender. Adjusted-covariates included demographic, behavior, lipid and inflammation variables (partially-adjusted models), and further included BMI (fully-adjusted models). Results: In a mean 9-year follow-up, 316 participants (13.2%) developed CHF. The partially-adjusted models indicated that men and women with elevated serum leptin levels (>=9.89 ng/ml in men and >=25 ng/ml in women) had significantly higher risks of developing CHF than those with leptin level of less than Q4. The adjusted hazard ratios (95%CI) for incident CHF was 1.49 (1.04 -2.13) in men and 1.71 (1.12 -2.58) in women. However, these associations became non-significant after adjustment for including BMI for each gender. The fully-adjusted hazard ratios (95%CI) were 1.43 (0.94 -2.18) in men and 1.24 (0.77-1.99) in women. Conclusion: Subjects with elevated leptin levels have a higher risk of CHF. The study supports the hypothesis that the influence of leptin level on risk of CHF may be through a pathway related to increasing BMI.

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Third instar larvae of Stomoxys calcitrans (L.) were treated with precocene II, ecdysone and juvenile hormone. The larvae were allowed to develop until pupation and when it occurred, determination of glycogen levels was assayed. The administration of those three substances have interfered on the clycogen concentration. the precocene II causing a decrease whereas the ecdysone and juvenile hormone causing an increase. The ecdysone administered together withprecocene II reverses the effect of the latter. This does not happen when precocene II is administered together with the juvenile hormone. Ecdysone administered together with juvenilehormone causes reduction of the glycogen concentration.

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During the past few decades, numerous plasmid vectors have been developed for cloning, gene expression analysis, and genetic engineering. Cloning procedures typically rely on PCR amplification, DNA fragment restriction digestion, recovery, and ligation, but increasingly, procedures are being developed to assemble large synthetic DNAs. In this study, we developed a new gene delivery system using the integrase activity of an integrative and conjugative element (ICE). The advantage of the integrase-based delivery is that it can stably introduce a large DNA fragment (at least 75 kb) into one or more specific sites (the gene for glycine-accepting tRNA) on a target chromosome. Integrase recombination activity in Escherichia coli is kept low by using a synthetic hybrid promoter, which, however, is unleashed in the final target host, forcing the integration of the construct. Upon integration, the system is again silenced. Two variants with different genetic features were produced, one in the form of a cloning vector in E. coli and the other as a mini-transposable element by which large DNA constructs assembled in E. coli can be tagged with the integrase gene. We confirmed that the system could successfully introduce cosmid and bacterial artificial chromosome (BAC) DNAs from E. coli into the chromosome of Pseudomonas putida in a site-specific manner. The integrase delivery system works in concert with existing vector systems and could thus be a powerful tool for synthetic constructions of new metabolic pathways in a variety of host bacteria.

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Proyecto de investigación realizado a partir de una estancia en el Centro Internacional de Métodos Computacionales en Ingeniería (CIMEC), Argentina, entre febrero y abril del 2007. La simulación numérica de problemas de mezclas mediante el Particle Finite Element Method (PFEM) es el marco de estudio de una futura tesis doctoral. Éste es un método desarrollado conjuntamente por el CIMEC y el Centre Internacional de Mètodos Numèrics en l'Enginyeria (CIMNE-UPC), basado en la resolución de las ecuaciones de Navier-Stokes en formulación Lagrangiana. El mallador ha sido implementado y desarrollado por Dr. Nestor Calvo, investigador del CIMEC. El desarrollo del módulo de cálculo corresponde al trabajo de tesis de la beneficiaria. La correcta interacción entre ambas partes es fundamental para obtener resultados válidos. En esta memoria se explican los principales aspectos del mallador que fueron modificados (criterios de refinamiento geométrico) y los cambios introducidos en el módulo de cálculo (librería PETSc, algoritmo predictor-corrector) durante la estancia en el CIMEC. Por último, se muestran los resultados obtenidos en un problema de dos fluidos inmiscibles con transferencia de calor.

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L'insuline est une hormone qui diminue la concentration de sucre dans le sang et qui est produite par la cellule β du pancréas. Un défaut de production de cette hormone est une des causes principales du diabète. Cette perte de production d'insuline est la conséquence à la fois, de la réduction du nombre de cellules β et du mauvais fonctionnement des cellules β restantes. L'inflammation, en activant la voie de signalisation «c-Jun N-terminal Kinase» (JNK) contribue au déclin de ces cellules. Cette voie de signalisation est activée par des protéines telles que des kinases qui reçoivent le signal de stress. Dans ce travail de thèse nous nous sommes intéressés à étudier le rôle de «Dual leucine zipper bearing kinase» (DLK) comme protéine capable de relayer le stress inflammatoire vers l'activation de la voie JNK dans les cellules β-pancréatiques. Nous montrons que DLK est présente dans les cellules β-pancréatiques et qu'elle agit effectivement comme un activateur de la voie de signalisation de JNK. En outre, DLK joue un rôle clé dans le contrôle de l'expression de l'insuline, de la sécrétion de l'insuline en réponse au glucose et au maintien de la survie des cellules β. Si l'expression de cette protéine diminue, la cellule produit moins d'insuline et sera plus sensible à la mort en réponse au stress inflammatoire. A l'inverse si l'expression de DLK est augmentée, la cellule β produit et secrète plus d'insuline. Des variations de l'expression de DLK sont par ailleurs, associées à l'état de santé de la cellule β. Chez la ratte en gestation ou la souris obèse, dans lesquelles la cellule β produit plus d'insuline, l'expression de DLK est augmentée. En revanche dans les cellules β des patients diabétiques, l'expression de DLK est diminuée par rapport aux cellules non malades. En résumé, DLK est nécessaire pour le bon fonctionnement de la cellule β-pancréatique et son expression corrèle avec le degré de santé des cellules, faisant que cette protéine pourrait être une cible thérapeutique potentiel. Les cellules β-pancréatiques ont la capacité de réguler la sécrétion d'insuline en s'adaptant précisément au stimulus et à la glycémie. La fonction de la cellule β est cruciale dans l'homéostasie du glucose puisque sa dysfonction et sa mort mènent au développement des diabètes de type 1 et 2. De nombreuses études suggèrent que l'inflammation pourrait avoir un rôle dans la dysfonction et la destruction de ces cellules dans le diabète de type 2. L'excès chronique de cytokines proinflammatoires accélère le dysfonctionnement de la cellule β pancréatique par un mécanisme qui implique la voie de signalisation «c-Jun N-terminal Kinase» (JNK). L'activation de cette voie est organisée par des protéines d'échafaudages. Elle se fait par trois étapes successives de phosphorylation impliquant une «Mitogen Activated Protein Kinase Kinase Kinase» (MAP3K), une MAP2K et JNK. Dans ce travail de thèse nous montrons l'expression abondante et spécifique de la MAP3K «Dual Leucine Zipper Bearing Kinase» (DLK) dans les cellules β pancréatiques. Cela est la conséquence de l'absence du répresseur transcriptionnel «Repressor Element 1 Silencing Transcription». Nous montrons également que DLK régule l'activation de JNK et qu'il s'avère nécessaire pour la fonction et la survie de la cellule β pancréatique par un mécanisme impliquant le facteur de transcription PDX-1. L'invalidation de l'expression de DLK diminue l'expression de l'insuline et potentialise l'apoptose induite par des cytokines proinflammatoires. A l'inverse, la surexpression de DLK augmente l'expression et la sécrétion d'insuline induites par le glucose. Par conséquent des niveaux d'expression appropriés de DLK sont déterminants pour la fonction et la survie de la cellule β pancréatique. L'obésité et la grossesse sont caractérisées par une hyperinsulinémie qui résulte d'une augmentation de la production et de la sécrétion de l'insuline. L'expression de DLK est augmentée dans des îlots de rattes gestantes et des souris obèses comparés à leurs contrôles respectifs. A l'inverse, dans des sujets diabétiques, l'expression de DLK est diminuée. Ensemble ces résultats montrent l'importance de DLK dans l'adaptation des îlots par un mécanisme qui pourrait impliquer la voie de signalisation de JNK. Des défauts dans cette voie régulée par DLK pourraient contribuer au dysfonctionnement et la mort de la cellule β pancréatique et par conséquent au développement du diabète. L'étude détaillée du mécanisme par lequel DLK active la voie de signalisation JNK et régule la fonction de la cellule β pancréatique pourrait ouvrir la voie des nouvelles thérapies ciblant l'amélioration de la fonction de la cellule β dans le diabète. - Pancreatic β-cells are evidently plastic in their ability to regulate insulin secretion. The quantity of insulin released by these cells varies according to the stimulus, and the prevailing glucose concentration, β-cell function is pivotal in glucose homeostasis, as their dysfunction, and death can lead to development of type 1 and type 2 diabetes. There are numerous reports so far underlying the role of inflammation in dysfunction, and destruction of β-cells, in both type 1 and type 2 diabetes. Chronic excess of pro¬inflammatory cytokines promotes a β-cell decline, via induction of the c-Jun N-terminal Kinase (JNK) pathway. The activation of the JNK pathway is organized by a scaffold protein-mediated module in which, a three-step phosphorylation cascade occurs. The latter includes, Mitogen activated protein kinase kinase kinase (MAP3K), MAP2K and JNK. In this thesis, we unveil that the MAP3K Dual Leucine Zipper Bearing Kinase (DLK) is selectively, and highly expressed in pancreatic β-cells, as the result from the absence of the transcriptional repressor named, Repressor Element 1 Silencing Transcription (REST). We show that DLK regulates activation of JNK, and is required for β-cell function and survival by modulating the PDX-1 transcription factor. Silencing of DLK expression diminishes insulin expression, and potentiated cytokine-mediated apoptosis. Conversely, overexpression of DLK increased insulin expression, and glucose-induced insulin secretion. Therefore, an appropriate level of DLK is critical for β-cell function and survival. Obesity and pregnancy are characterized by hyperinsulinemia resulting from an increased production and secretion of insulin. In isolated islets of pregnant rats, and obese mice, the expression of DLK was elevated when compared to their respective controls. However, decreased expression of DLK was observed in islets of individuals with diabetes. Taken together, we highlight the importance of DLK in islet adaptation, and describe a mechanism that may involve the JNK signaling. Deficiency in the JNK pathway regulated by DLK may contribute to β-cell failure and death, and thereby development of diabetes. Unraveling the mechanism whereby DLK activates the JNK pathway, and β-cell function, may pave the way for the design of novel therapies, aiming to improve β-cell function and survival in diabetes in general.