3 resultados para Mocho odontológico - Apoio frontal

em Université de Montréal, Canada


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There is increasing evidence that central noradrenaline (NA) transport mechanisms are implicated in the central nervous system complications of acute liver failure. In order to assess this possibility, binding sites for the high affinity NA transporter ligand [3H]-nisoxetine were measured by quantitative receptor autoradiography in the brains of rats with acute liver failure resulting from hepatic devascularization and in appropriate controls. In vivo microdialysis was used to measure extracellular brain concentrations of NA. Severe encephalopathy resulted in a significant loss of [3H]-nisoxetine sites in frontal cortex and a concomitant increase in extracellular brain concentrations of NA in rats with acute liver failure. A loss of transporter sites was also observed in thalamus of rats with acute liver failure. This loss of NA transporter sites could result from depletion of central NA stores due to a reserpine-like effect of ammonia which is known to accumulate to millimolar concentrations in brain in ischemic liver failure. Impaired NA transport and the consequent increase in synaptic concentrations and increased stimulation of neuronal and astrocytic noradrenergic receptors could be implicated in the pathogenesis of the encephalopathy and brain edema characteristic of acute liver failure.

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It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-1 was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT-1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.

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Among the external manifestations of scoliosis, the rib hump, which is associated with the ribs' deformities and rotations, constitutes the most disturbing aspect of the scoliotic deformity for patients. A personalized 3-D model of the rib cage is important for a better evaluation of the deformity, and hence, a better treatment planning. A novel method for the 3-D reconstruction of the rib cage, based only on two standard radiographs, is proposed in this paper. For each rib, two points are extrapolated from the reconstructed spine, and three points are reconstructed by stereo radiography. The reconstruction is then refined using a surface approximation. The method was evaluated using clinical data of 13 patients with scoliosis. A comparison was conducted between the reconstructions obtained with the proposed method and those obtained by using a previous reconstruction method based on two frontal radiographs. A first comparison criterion was the distances between the reconstructed ribs and the surface topography of the trunk, considered as the reference modality. The correlation between ribs axial rotation and back surface rotation was also evaluated. The proposed method successfully reconstructed the ribs of the 6th-12th thoracic levels. The evaluation results showed that the 3-D configuration of the new rib reconstructions is more consistent with the surface topography and provides more accurate measurements of ribs axial rotation.