Disturbances in peripheral O extraction can be produced in dogs treated with 2 endotoxin and thereby provide an opportunity to test theories for the origin of pathological O supply dependency or to try different treatment modalities. The 2 most serious deficiency in the current animal models is the inability to mimic the increased O demand that is observed in patients at 02 delivery rates in excess of 2 normal. A particular feature of this increased O demand is that it apparently does 2 not stimulate increased 02 extraction, although the limitation in O extraction has 2 not been explored in patients by lowering 02 supply, for obvious reasons. At least two possibilities to account for increased 02 demand could be investigated in animal models, however. The amount of 02 that is utilized in extramitochondrial pathways, which is normally on the order of 10%, may be greatly increased in ARDS and sepsis by O radical formation. There is presently no information 2 concerning how much 02 might be used in this way. Another strong possibility is that mitochondrial injury, perhaps as a result of 02 radical formation, uncouples oxidative phosphorylation. Some evidence presently in the literature supports this idea [19]. Indeed, the association of increased blood lactate levels with higher than expected 02 demands makes uncoupling a very attractive hypothesis that warrants further investigation in animal models using such agents as 2,4-dinitrophenol. References 1.

Disturbances in peripheral O extraction can be produced in dogs treated with 2 endotoxin and thereby provide an opportunity to test theories for the origin of pathological O supply dependency or to try different treatment modalities. The 2 most serious deficiency in the current animal models is the inability to mimic the increased O demand that is observed in patients at 02 delivery rates in excess of 2 normal. A particular feature of this increased O demand is that it apparently does 2 not stimulate increased 02 extraction, although the limitation in O extraction has 2 not been explored in patients by lowering 02 supply, for obvious reasons. At least two possibilities to account for increased 02 demand could be investigated in animal models, however. The amount of 02 that is utilized in extramitochondrial pathways, which is normally on the order of 10%, may be greatly increased in ARDS and sepsis by O radical formation. There is presently no information 2 concerning how much 02 might be used in this way. Another strong possibility is that mitochondrial injury, perhaps as a result of 02 radical formation, uncouples oxidative phosphorylation. Some evidence presently in the literature supports this idea [19]. Indeed, the association of increased blood lactate levels with higher than expected 02 demands makes uncoupling a very attractive hypothesis that warrants further investigation in animal models using such agents as 2,4-dinitrophenol. References 1.

¿Notás que te cuesta administrar tu dinero? ¿Sentís que no sabés cuánto gastás cada mes? No quiero ser millonario, solo quiero llegar a fin de mes presenta una mirada simple y eficaz sobre el gran desafío que se nos presenta hoy a la hora de manejar nuestra economía personal, tanto para que los números nos cierren, como para no llevarnos sorpresas."No quiero ser millonario, solo quiero llegar a fin de mes" aporta un diagnóstico y numerosas ideas de muy fácil aplicación, con efectos concretos y medibles.  Escrito por dos ciudadanos comunes en un lenguaje sencillo, nos lleva por un camino de autoconocimiento, para ver cómo nos llevamos con nuestra economía personal, cómo fuimos educados, contemplando los cambios que venimos experimentando silenciosamente, que nos ubican en esta época de hiperconsumo, colmada de nuevos gastos por afrontar. Desde ese punto, los autores nos llevan por un sinnúmero de situaciones cotidianas, ideas, recursos -tanto para administrar nuestros gastos como para aumentar nuestros ingresos- y reflexiones, para que formemos hábitos sencillos, que nos reconcilien y ordenen con nuestro presupuesto, en la firme convicción de que ese abordaje nos brinda un protagonismo único para actuar en forma positiva, y mejorar este aspecto que, al final del día, impacta en nuestra calidad de vida.Los autores son también socios fundadores de E8 (e-8.online), una consultora dedicada a la capacitación, la formación y el asesoramiento en temas de administración de la economía personal y del hogar. Todos son bienvenidos a visitar su sitio web y seguir en contacto con ellos. Las experiencias laborales, profesionales y personales de ambos autores fueron de gran ayuda para elaborar el contenido de este libro.

Disturbances in peripheral O extraction can be produced in dogs treated with 2 endotoxin and thereby provide an opportunity to test theories for the origin of pathological O supply dependency or to try different treatment modalities. The 2 most serious deficiency in the current animal models is the inability to mimic the increased O demand that is observed in patients at 02 delivery rates in excess of 2 normal. A particular feature of this increased O demand is that it apparently does 2 not stimulate increased 02 extraction, although the limitation in O extraction has 2 not been explored in patients by lowering 02 supply, for obvious reasons. At least two possibilities to account for increased 02 demand could be investigated in animal models, however. The amount of 02 that is utilized in extramitochondrial pathways, which is normally on the order of 10%, may be greatly increased in ARDS and sepsis by O radical formation. There is presently no information 2 concerning how much 02 might be used in this way. Another strong possibility is that mitochondrial injury, perhaps as a result of 02 radical formation, uncouples oxidative phosphorylation. Some evidence presently in the literature supports this idea [19]. Indeed, the association of increased blood lactate levels with higher than expected 02 demands makes uncoupling a very attractive hypothesis that warrants further investigation in animal models using such agents as 2,4-dinitrophenol. References 1.

Disturbances in peripheral O extraction can be produced in dogs treated with 2 endotoxin and thereby provide an opportunity to test theories for the origin of pathological O supply dependency or to try different treatment modalities. The 2 most serious deficiency in the current animal models is the inability to mimic the increased O demand that is observed in patients at 02 delivery rates in excess of 2 normal. A particular feature of this increased O demand is that it apparently does 2 not stimulate increased 02 extraction, although the limitation in O extraction has 2 not been explored in patients by lowering 02 supply, for obvious reasons. At least two possibilities to account for increased 02 demand could be investigated in animal models, however. The amount of 02 that is utilized in extramitochondrial pathways, which is normally on the order of 10%, may be greatly increased in ARDS and sepsis by O radical formation. There is presently no information 2 concerning how much 02 might be used in this way. Another strong possibility is that mitochondrial injury, perhaps as a result of 02 radical formation, uncouples oxidative phosphorylation. Some evidence presently in the literature supports this idea [19]. Indeed, the association of increased blood lactate levels with higher than expected 02 demands makes uncoupling a very attractive hypothesis that warrants further investigation in animal models using such agents as 2,4-dinitrophenol. References 1.

¿Notás que te cuesta administrar tu dinero? ¿Sentís que no sabés cuánto gastás cada mes? No quiero ser millonario, solo quiero llegar a fin de mes presenta una mirada simple y eficaz sobre el gran desafío que se nos presenta hoy a la hora de manejar nuestra economía personal, tanto para que los números nos cierren, como para no llevarnos sorpresas."No quiero ser millonario, solo quiero llegar a fin de mes" aporta un diagnóstico y numerosas ideas de muy fácil aplicación, con efectos concretos y medibles.  Escrito por dos ciudadanos comunes en un lenguaje sencillo, nos lleva por un camino de autoconocimiento, para ver cómo nos llevamos con nuestra economía personal, cómo fuimos educados, contemplando los cambios que venimos experimentando silenciosamente, que nos ubican en esta época de hiperconsumo, colmada de nuevos gastos por afrontar. Desde ese punto, los autores nos llevan por un sinnúmero de situaciones cotidianas, ideas, recursos -tanto para administrar nuestros gastos como para aumentar nuestros ingresos- y reflexiones, para que formemos hábitos sencillos, que nos reconcilien y ordenen con nuestro presupuesto, en la firme convicción de que ese abordaje nos brinda un protagonismo único para actuar en forma positiva, y mejorar este aspecto que, al final del día, impacta en nuestra calidad de vida.Los autores son también socios fundadores de E8 (e-8.online), una consultora dedicada a la capacitación, la formación y el asesoramiento en temas de administración de la economía personal y del hogar. Todos son bienvenidos a visitar su sitio web y seguir en contacto con ellos. Las experiencias laborales, profesionales y personales de ambos autores fueron de gran ayuda para elaborar el contenido de este libro.