966 resultados para Sweet, Elnathan, 1837-1903.
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Microfilm. Valencia: BV, ca. 1990
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Leptin acts as a potent inhibitory factor against obesity by regulating energy expenditure, food intake, and adiposity. The obese diabetic db/db mouse, which has defects in leptin receptor, displays enhanced neural responses and elevated behavioral preference to sweet stimuli. Here, we show the effects of leptin on the peripheral taste system. An administration of leptin into lean mice suppressed responses of peripheral taste nerves (chorda tympani and glossopharyngeal) to sweet substances (sucrose and saccharin) without affecting responses to sour, salty, and bitter substances. Whole-cell patch-clamp recordings of activities of taste receptor cells isolated from circumvallate papillae (innervated by the glossopharyngeal nerve) demonstrated that leptin activated outward K+ currents, which resulted in hyperpolarization of taste cells. The db/db mouse with impaired leptin receptors showed no such leptin suppression. Taste tissue (circumvallate papilla) of lean mice expressed leptin-receptor mRNA and some of the taste cells exhibited immunoreactivities to antibodies of the leptin receptor. Taken together, these observations suggest that the taste organ is a peripheral target for leptin, and that leptin may be a sweet-sensing modulator (suppressor) that may take part in regulation of food intake. Defects in this leptin suppression system in db/db mice may lead to their enhanced peripheral neural responses and enhanced behavioral preferences for sweet substances.
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Biochemical and genetic studies have implicated α-gustducin as a key component in the transduction of both bitter or sweet taste. Yet, α-gustducin-null mice are not completely unresponsive to bitter or sweet compounds. To gain insights into how gustducin mediates responses to bitter and sweet compounds, and to elicit the nature of the gustducin-independent pathways, we generated a dominant-negative form of α-gustducin and expressed it as a transgene from the α-gustducin promoter in both wild-type and α-gustducin-null mice. A single mutation, G352P, introduced into the C-terminal region of α-gustducin critical for receptor interaction rendered the mutant protein unresponsive to activation by taste receptor, but left its other functions intact. In control experiments, expression of wild-type α-gustducin as a transgene in α-gustducin-null mice fully restored responsiveness to bitter and sweet compounds, formally proving that the targeted deletion of the α-gustducin gene caused the taste deficits of the null mice. In contrast, transgenic expression of the G352P mutant did not restore responsiveness of the null mice to either bitter or sweet compounds. Furthermore, in the wild-type background, the mutant transgene inhibited endogenous α-gustducin's interactions with taste receptors, i.e., it acted as a dominant-negative. That the mutant transgene further diminished the residual bitter and sweet taste responsiveness of the α-gustducin-null mice suggests that other guanine nucleotide-binding regulatory proteins expressed in the α-gustducin lineage of taste cells mediate these responses.
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Este trabajo se inscribe en un proyecto de investigación, que también integran María Sierra y María Antonia Peña, sobre la idea de la representación política en la España liberal (1845-1890), del Ministerio de Ciencia y Tecnología con financiación FEDER (BHA2002-01007).
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En la primera parte del artículo se aborda el problema que ha de afrontar el estadista Antonio Maura al convertirse en el jefe del gobierno español, a finales de 1903 y consistente en concluir el proceso de negociación sobre Marruecos entablado con Francia desde 1901. Se resalta el carácter continuista del ideario colonial de Maura con respecto al del anterior líder conservador, Silvela, y la preponderancia de cuestiones como la seguridad nacional como motivadoras de dicho ideario. En la segunda parte, se explica la apelación del gobierno maurista a una ayuda por parte de Alemania, en función de movimientos previos de la diplomacia germana que se había interesado por controlar una parte del Marruecos español, o por conseguir compensaciones en Fernando Po. Finalmente se analiza el intento de Berlín de instrumentalizar al gobierno Maura en el curso de las conversaciones hispano-francesas sobre el Imperio jerifiano.
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This memoir, written by White in 1837, describes his undergraduate years at Harvard from 1793 to 1797. It contains lengthy passages about a wide variety of experiences White had as a student. He wrote about his classes and professors, student life, American politics, politics in the world at large, food, his classmates, and many other topics. The memoir includes passages from a diary that White seems to have kept as a student, as well as reflections clearly written later in life. White wrote this memoir in 15 separate notebooks, each embossed with "Platner & Porter, Congress" in the upper left-hand corner. Platner & Porter was the manufacturer of the notebooks.
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Printed copy of the 1833 abstract of laws and regulations with the admittatur of undergraduate Samuel F. McCleary signed by President Josiah Quincy on August 28, 1837.
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Novitates zoologicae. Vol. IX. Supplement, v. 2