Papers by Aurelia Aurelia
Naunyn-schmiedebergs Archives of Pharmacology, 1975
In the eye of rats the long-lasting specific desensitization induced by local or systemic capsaic... more In the eye of rats the long-lasting specific desensitization induced by local or systemic capsaicin treatment is characterized by three phases: 1. complete insensitivity, 2. decreased sensitivity and a tendency to rapid adaptation, 3. normal initial sensitivity with a tendency to rapid adaptation to chemical pain stimuli. A low density of microvesicles and swollen mitochondria were found after local capsaicin treatment in certain nerve endings of the cornea of rats, but no signs of axonal degeneration or alteration in fine structure of non-neural elements were seen. Systemic capsaicin desensitization induced selective mitochondrial swelling in B type of neurons of the trigeminal ganglion which was demonstrable even 60 days after the pretreatment. Actinomycin-D, 8-azaguanine, 6-azauracil, aminopterin, mannomustin or cycloheximide in high doses did not alter the desensitizing effect of systemic capsaicin treatment. However, pretreatment of rats with colchicine or vinblastine prolonged the desensitizing effect of local capsaicin application, probably by inhibiting the axonal flow. It is concluded that capsaicin is a specific sensory neuron blocking agent having a practically irreversible effect in rats and guineapigs.
Intensive Care Medicine, 2005
Objective To construct and validate an update of the Simplified Acute Physiology Score II (SAPS I... more Objective To construct and validate an update of the Simplified Acute Physiology Score II (SAPS II) for the evaluation of clinical performance of Intensive Care Units (ICU). Design and setting Retrospective analysis of prospectively collected multicenter data in 32 ICUs located in the Paris area belonging to the Cub-Rea database and participating in a performance evaluation project. Patients 33,471 patients treated between 1999 and 2000. Measurements and results Two logistic regression models based on SAPS II were developed to estimate in-hospital mortality among ICU patients. The second model comprised reevaluation of original items of SAPS II and integration of the preadmission location and chronic comorbidity. Internal and external validation were performed. In the two validation samples the most complex model had better calibration than the original SAPS II for in-hospital mortality but its discrimination was not significantly higher (area under ROC curve 0.89 vs. 0.87 for SAPS II). Second-level customization and integration of new items improved uniformity of fit for various categories of patients except for diagnosis-related groups. The rank order of ICUs was modified according to the model used. Conclusions The overall performance of SAPS II derived models was good, even in the context of a community cohort and routinely gathered data. However, one-half the variation of outcome remains unexplained after controlling for admission characteristics, and uniformity of prediction across diagnostic subgroups was not achieved. Differences in case-mix still limit comparisons of quality of care.
Journal of Lipid Research, 2005
Mitochondrial cytopathy has been associated with modifications of lipid metabolism in various sit... more Mitochondrial cytopathy has been associated with modifications of lipid metabolism in various situations, such as the acquisition of an abnormal adipocyte phenotype observed in multiple symmetrical lipomatosis or triglyceride (TG) accumulation in muscles associated with the myoclonic epilepsy with ragged red fibers syndrome. However, the molecular signaling leading to fat metabolism dysregulation in cells with impaired mitochondrial activity is still poorly understood. Here, we found that preadipocytes incubated with inhibitors of mitochondrial respiration such as antimycin A (AA) accumulate TG vesicles but do not acquire specific markers of adipocytes. Although the uptake of TG precursors is not stimulated in 3T3-L1 cells with impaired mitochondrial activity, we found a strong stimulation of glucose uptake in AA-treated cells mediated by calcium and phosphatidylinositol 3-kinase/Akt1/glycogen synthase kinase 3  , a pathway known to trigger the translocation of glucose transporter 4 to the plasma membrane in response to insulin. TG accumulation in AA-treated cells is mediated by a reduced peroxisome proliferator-activated receptor ␥ activity that downregulates muscle carnitine palmitoyl transferase-1 expression and fatty acid  -oxidation, and by a direct conversion of glucose into TGs accompanied by the activation of carbohydrate-responsive element binding protein, a lipogenic transcription factor. Taken together, these results could explain how mitochondrial impairment leads to the multivesicular phenotype found in some mitochondria-originating diseases associated with a dysfunction in fat metabolism. -Vankoningsloo, S., M. Piens, C. Lecocq, A. Gilson, A. De Pauw, P. Renard, C. Demazy, A. Houbion, M. Raes, and T. Arnould. Mitochondrial dysfunction induces triglyceride accumulation in 3T3-L1 cells: role of fatty acid  -oxidation and glucose. J. Lipid Res. 2005. 46: 1133-1149.
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Papers by Aurelia Aurelia