999 resultados para Pro Huerta


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Nd(i-PrO)_2Cl-AlEt_3均相二元催化剂异戊二烯聚合动力学──Ⅲ.AlEt_3的链转移作用蔡小平,龚志,王佛松朱行洁,李秀华(中国科学院长春应用化学研究所长春130022)(吉林化工集团公司研究院吉林)关键词异戊二烯,聚合动力学,均相催化...

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catena-Poly[{pentaaqua(L-proline-O)-erbium-mu-(L-proline-O:O')} trichloride], {[Er(C5H9-NO2)2(H2O)5]Cl3}n, M(r) = 594.0, monoclinic, P2(1), a = 8.294 (1), b = 10.981 (3), c = 11.934 (3) angstrom, beta = 107.04 (2)degrees, V = 1039.2 (4) angstrom3, Z = 2, D(x) = 1.90 g cm-3, lambda(Mo Kalpha) = 0.71069 angstrom, mu = 45.2 cm-1, F(000) = 586, T = 298 K, R = 0.0244 for 1711 unique reflections [I > 3 sigma(I(o))]. The crystal consists of one-dimensional chains of infinite length in which one L-proline ligand bridges two neighboring Er ions, the other L-proline ligand being monodentate.

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On a reversed phase Hypersil BDS C-18 (200 mm x 4. 6 mm, 5 mu m) column, 20 amino acids, which were derivatized using 2-(11H-benzo [a] carbazol-11-yl) ethyl carbonochloridate (BCEC-Cl) as pre-column derivatization reagent, were separated in conjunction with a gradient elution. Optimum derivatization was obtained by reacting of amino acids with BCEC-Cl at room temperature for 5 min in the presence of sodium borate catalyst in acetonitrile solvent. The fluorescence excitation and emission wavelengths were 279 nm and 380 nm respectively. The identification of amino acid derivatives from hydrolyzed bovine serum albumin and bee pollen was carried out by post-column mass spectrometry with electrospray ion source in positive ion mode. Linear correlation coefficients of the amino acid derivatives were > 0.9990, and detection limits (at signal to noise of 3:1) were 1.49 - 19.74 fmol for the labeled amino acids.

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Estudo do impacto ambiental do manejo sobre a floresta nativa da Amazonia central, executado pela Mil-Madeireira Itacoatiara Ltda, em Itacoatiara, Amazonas, Brasil.

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van Someren KA, Howatson G, Nunan D, Thatcher R, Shave R., Comparison of the Lactate Pro and Analox GM7 blood lactate analysers, Int J Sports Med. 2005 Oct;26(8):657-61. RAE2008

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Perfusion experiments on an isolated, canine lateral saphenous vein segment preparation have shown that noradrenaline causes potent, flow dependent effects, at a threshold concentration comparable to that of plasma noradrenaline, when it stimulates the segment by diffusion from its microcirculation (vasa vasorum). The effects caused are opposite to those neuronal noradrenaline causes in vivo and that, in the light of the principle that all information is transmitted in patterns that need contrast to be detected – star patterns need darkness, sound patterns, quietness – has generated the hypothesis that plasma noradrenaline provides the obligatory contrast tissues need to detect and respond to the regulatory information encrypted in the diffusion pattern of neuronal noradrenaline. Based on the implications of that hypothesis, the controlled variable of the peripheral noradrenergic system is believed to be the maintenance of a set point balance between the contrasting effects of plasma and neuronal noradrenaline on a tissue. The hypothalamic sympathetic centres are believed to monitor that balance through the level of afferent sympathetic traffic they receive from a tissue and to correct any deviation it detects in the balance by adjusting the level of efferent sympathetic input it projects to the tissue. The failure of the centres to maintain the correct balance, for reasons intrinsic or extrinsic to themselves, is believed to be responsible for degenerative and genetic disorders. When the failure causes the balance to be polarised in favour of the effect of plasma noradrenaline that is believed to cause inflammatory diseases like dilator cardiac failure, renal hypertension, varicose veins and aneurysms; when it causes it to be polarised in favour of the effect of neuronal noradrenaline that is believed to cause genetic diseases like hypertrophic cardiopathy, pulmonary hypertension and stenoses and when, in pregnancy, a factor causes the polarity to favour plasma noradrenaline in all the maternal tissues except the uterus and conceptus, where it favours neuronal noradrenaline, that is believed to cause preeclampsia.

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BACKGROUND: Scythe/BAT3 is a member of the BAG protein family whose role in apoptosis has been extensively studied. However, since the developmental defects observed in Bat3-null mouse embryos cannot be explained solely by defects in apoptosis, we investigated whether BAT3 is also involved in cell-cycle progression. METHODS/PRINCIPAL FINDINGS: Using a stable-inducible Bat3-knockdown cellular system, we demonstrated that reduced BAT3 protein level causes a delay in both G1/S transition and G2/M progression. Concurrent with these changes in cell-cycle progression, we observed a reduction in the turnover and phosphorylation of the CDK inhibitor p21, which is best known as an inhibitor of DNA replication; however, phosphorylated p21 has also been shown to promote G2/M progression. Our findings indicate that in Bat3-knockdown cells, p21 continues to be synthesized during cell-cycle phases that do not normally require p21, resulting in p21 protein accumulation and a subsequent delay in cell-cycle progression. Finally, we showed that BAT3 co-localizes with p21 during the cell cycle and is required for the translocation of p21 from the cytoplasm to the nucleus during the G1/S transition and G2/M progression. CONCLUSION: Our study reveals a novel, non-apoptotic role for BAT3 in cell-cycle regulation. By maintaining a low p21 protein level during the G1/S transition, BAT3 counteracts the inhibitory effect of p21 on DNA replication and thus enables the cells to progress from G1 to S phase. Conversely, during G2/M progression, BAT3 facilitates p21 phosphorylation by cyclin A/Cdk2, an event required for G2/M progression. BAT3 modulates these pro- and anti-proliferative roles of p21 at least in part by regulating cyclin A abundance, as well as p21 translocation between the cytoplasm and the nucleus to ensure that it functions in the appropriate intracellular compartment during each phase of the cell cycle.

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La emergencia de la Agricultura Urbana (AU) en Rosario, Santa Fe, surge como alternativa productiva en un contexto de crisis económica para la inclusión social posibilitando el acceso a los alimentos a familias en situación de vulnerabilidad; evolucionando en algunos casos hacia redes solidarias de producción, transformación y comercialización. El presente trabajo indaga la potencialidad agroecológica de la AU rosarina mediante un estudio de caso. Se plantearon dos objetivos: (1) conocer y caracterizar la dinámica de los procesos sociales y productivos que dieron origen al Programa de AU y a la emergencia del Parque Huerta Molino Blanco como caso estudiado; (2) indagar la presencia de elementos que den cuenta de un desarrollo agroecológico. La interpretación que, desde la Agroecología, se hace sobre la potencialidad de la AU introduce la articulación dialéctica entre lo básicamente descriptivo y la complejidad epistemológica de la diversidad sociocultural y ecológica utilizando para ello una metodología de investigación participativa, donde se entremezclan las tres perspectivas de investigación y su correlato con las dimensiones de indagación agroecológica (distributiva, estructural y dialéctica). Los métodos y técnicas empleados son caracterizados a través del discurso de los huerteros/as. La síntesis del proceso histórico de Rosario da cuenta de los elementos mencionados como característicos de un proceso de agroecologízación, institucionalización y consolidación de la AU como política pública. Los Parques Huerta como estrategia de uso de suelo constituyen una novedad y un potencial en la construcción y consolidación de modelos alternativos de AU erigiendo espacios productivos multifuncionales (productivos, educativos, recreativos y paisajísticos). Podemos decir que la consolidación de sistemas agroalimentarios locales y las políticas de desarrollo endógeno son fenómenos estrechamente asociados al desarrollo agroecológico donde se prioriza la articulación de diversos actores locales en un proyecto político que apunta a la transformación social en los territorios.

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Definición de la etapa de crisis del aparato cinematográfico franquista, llamada aquí “Período Oscuro” (1969-1975), discusión de la etiqueta de subgéneros aplicada al cinema bis de la época, y caracterización histórica del thriller español y de sus corrientes estéticas y conceptuales internas en dicho período. La acotación del período 1969-1975 es clarificada previamente ante el vacío historiográfico al respecto. Se caracteriza la crisis que tiene lugar en el “Período Oscuro”, desde su comienzo oficial en 1969, que supuso el definitivo cierre de las políticas proteccionistas emprendidas por el Director General de Cinematografía García Escudero en 1962. Después se define y discute la etiqueta de subgéneros aplicada tradicionalmente al cine español de género de bajo presupuesto. Luego, se especifican, definen y analizan las diversas categorías dentro del thriller español de 1969-1975: se trata de categorías temáticas y argumentales, estéticas, o bien relacionadas con corrientes internacionales del policíaco europeo. Por último, se extraen las conclusiones pertinentes.

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AIMS/HYPOTHESIS: This study examined the biological effects of the GIP receptor antagonist, (Pro3)GIP and the GLP-1 receptor antagonist, exendin(9-39)amide.

METHODS: Cyclic AMP production was assessed in Chinese hamster lung fibroblasts transfected with human GIP or GLP-1 receptors, respectively. In vitro insulin release studies were assessed in BRIN-BD11 cells while in vivo insulinotropic and glycaemic responses were measured in obese diabetic ( ob/ ob) mice.

RESULTS: In GIP receptor-transfected fibroblasts, (Pro(3))GIP or exendin(9-39)amide inhibited GIP-stimulated cyclic AMP production with maximal inhibition of 70.0+/-3.5% and 73.5+/-3.2% at 10(-6) mol/l, respectively. In GLP-1 receptor-transfected fibroblasts, exendin(9-39)amide inhibited GLP-1-stimulated cyclic AMP production with maximal inhibition of 60+/-0.7% at 10(-6) mol/l, whereas (Pro(3))GIP had no effect. (Pro(3))GIP specifically inhibited GIP-stimulated insulin release (86%; p<0.001) from clonal BRIN-BD11 cells, but had no effect on GLP-1-stimulated insulin release. In contrast, exendin(9-39)amide inhibited both GIP and GLP-1-stimulated insulin release (57% and 44%, respectively; p<0.001). Administration of (Pro(3))GIP, exendin(9-39)amide or a combination of both peptides (25 nmol/kg body weight, i.p.) to fasted (ob/ob) mice decreased the plasma insulin responses by 42%, 54% and 49%, respectively (p<0.01 to p<0.001). The hyperinsulinaemia of non-fasted (ob/ob) mice was decreased by 19%, 27% and 18% (p<0.05 to p<0.01) by injection of (Pro3)GIP, exendin(9-39)amide or combined peptides but accompanying changes of plasma glucose were small.

CONCLUSIONS/INTERPRETATION: These data show that (Pro(3))GIP is a specific GIP receptor antagonist. Furthermore, feeding studies in one commonly used animal model of obesity and diabetes, (ob/ob) mice, suggest that GIP is the major physiological component of the enteroinsular axis, contributing approximately 80% to incretin-induced insulin release.