![]() ![]() These experimental relations usually exhibit certain variability. When simulations of muscle tissue are concerned, stress/strain relations for both passive and active behavior are required. more In the field of computational biomechanics, the experimental evaluation of the material properties is crucial for the development of computational models that closely reproduce real organ systems. In the field of computational biomechanics, the experimental evaluation of the material propertie. El análisis estadístico de los datos obtenidos en 98 animales demostró que la presencia del fragmento C de la toxina tetánica no int. Mediante la inyección intramuscular de ADN desnudo que codificaba para la proteína de fusión se comprobó que la molécula de fusión es capaz de expresarse en el músculo y que, gracias al fragmento C de la toxina tetánica, es capaz de salir del músculo y alcanzar centros nerviosos superiores manteniendo la actividad enzimática que va fusionada a él. Tras demostrar que la molécula es capaz de alcanzar el córtex motor, consideramos que si la proteína era producida de forma continua y en pequeñas dosis la respuesta inmunitaria se vería disminuida. Para dicho estudio se ha utilizado la molécula de fusión β-galactosidasa-TTC. more En el presente trabajo de investigación se pretenden conocer las posibilidades del fragmento C de la toxina tetánica (TTC) para su utilización como vector de terapia génica en enfermedades que cursan con degeneración de las motoneuronas. iNOS is a main target to prevent liver mitochondrial impairment during sepsis, and melatonin represents an efficient antagonist of these iNOS-dependent effects whereas it may boost mitochondrial respiration to enhance liver survival.Įn el presente trabajo de investigación se pretenden conocer las posibilidades del fragmento C de. These effects were unrelated to the presence or absence of nNOS. Melatonin administration counteracted iNOS activation and mitochondrial damage and enhanced the expression of the respiratory complexes above the control values. Moreover, the nNOS gene did not modify the expression and the effects of iNOS here shown. The absence of the iNOS, but not nNOS, gene absolutely prevented mitochondrial impairment during sepsis. We detected strongly elevated iNOS mRNA expression and protein levels in liver cytosol and mitochondria of septic mice, which were related to enhanced oxidative and nitrosative stress, and with fewer changes in respiratory complexes. To achieve this goal, the determination of messenger RNA (mRNA) expression and protein content of iNOS in cytosol and mitochondria, the mitochondrial respiratory complex content, and the levels of nitrosative and oxidative stress (by measuring 3-nitrotyrosine residues and carbonyl groups, respectively) were examined in the liver of control and septic mice. We induced sepsis by LPS administration to inducible nitric oxide synthase (iNOS(-/-)) and neuronal nitric oxide synthase (nNOS(-/-)) mice and their respective wild-type controls to examine the contribution of iNOS to mitochondrial failure in the absence of nNOS. more NOS isoform activation is related to liver failure during sepsis, but the mechanisms driving mitochondrial impairment remain unclear. NOS isoform activation is related to liver failure during sepsis, but the mechanisms driving mito. ![]()
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