Spelling suggestions: "subject:"[samma]glutamyl transpeptidase"" "subject:"[samma]γglutamyl transpeptidase""
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Étude de la distribution, de la clonalité et caractérisation des campylobacters isolés de poulets à griller et d'humainsNadeau, Éric January 2003 (has links)
Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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Synthèse et études cinétiques de substrats analogues et d'inhibiteurs de l'étape d'acylation de la [gamma]-glutamyl transpeptidaseLherbet, Christian January 2003 (has links)
Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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The Design and Synthesis of Small Molecule Protein Inhibitors as Potential Cancer TherapeuticsRegan, Nicholas Bauman 20 July 2011 (has links)
No description available.
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Transsulfuration Pathway Defects and Increased Glutathione Degradation in Severe Acute Pancreatitis.Rahman, S.H., Srinivasan, Asha R., Nicolaou, Anna January 2009 (has links)
No / Glutathione depletion is a consistent feature of the progression of mild to severe acute pancreatitis. In this study, we examined the temporal relationship between cysteine, homocysteine, and cysteinyl-glycine levels; total reduced erythrocyte glutathione; gamma-glutamyl transpeptidase activity; and disease severity. Initially, cysteine concentration was low, at levels similar to those of healthy controls. However, glutathione was reduced whilst cysteinyl glycine and gamma-glutamyl transpeptidase activity were increased in both mild and severe attacks. As the disease progressed, glutathione and cysteinyl glycine were further increased in mild attacks and cysteine levels correlated with homocysteine (r = 0.8, P < 0.001) and gamma-glutamyl transpeptidase activity (r = 0.75, P < 0.001). The progress of severe attacks was associated with glutathione depletion, reduced gamma-glutamyl transpeptidase activity, and increased cysteinyl glycine that correlated with glutathione depletion (r = 0.99, P = 0.01). These results show that glutathione depletion associated with severe acute pancreatitis occurs despite an adequate cysteine supply and could be attributed to heightened oxidative stress coupled to impaired downstream biosynthesis.
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