Biomedical subjects
Publications and source records attributed to T Moran.
The inanimate, little 1.5-g pieces of matter carry far more import than they should. Worse, they tend to multiply, like aggressive malignancies, to form paperwork--that dreaded, colossal barrier between physicians and weightier matters. Growing mounds of it demand physicians' attention and steal time away from healing the sick and saving the dying.
The 1997 Texas Legislature directed the Office of Public Insurance Counsel (OPIC) to issue annual report cards comparing Texas health maintenance organizations (HMOs). OPIC released its first statewide consumer survey in August, conducted by The University of Texas Office of Survey Research.
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Neuronal regulation of glutamate homeostasis is mediated by high-affinity sodium-dependent and highly hydrophobic plasma membrane glycoproteins which maintain low levels of glutamate at central synapses. To further elucidate the molecular mechanisms that regulate glutamate metabolism and glutamate flux at central synapses, a monoclonal antibody was produced to a synthetic peptide corresponding to amino acid residues 161-177 of the deduced sequence of the human neuron-specific glutamate transporter III (EAAC1). Immunoblot analysis of human and rat brain total homogenates and isolated synaptosomes from frontal cortex revealed that the antibody immunoreacted with a protein band of apparent Mr approximately 70 kDa. Deglycosylation of immunoprecipitates obtained using the monoclonal antibody yielded a protein with a lower apparent Mr (approximately 65 kDa). These results are consistent with the molecular size of the human EAAC1 predicted from the cloned cDNA. Analysis of the transfected COS-1 cells by immunocytochemistry confirmed that the monoclonal antibody is specific for the neuron-specific glutamate transporter. Immunocytochemical studies of rat cerebral cortex, hippocampus, cerebellum, substantia nigra and spinal cord revealed intense labeling of neuronal somata, dendrites, fine-caliber fibers and puncta. Double-label immunofluorescence using antibody to glial fibrillary acidic protein as a marker for astrocytes demonstrated that astrocytes were not co-labeled for EAAC1. The localization of EAAC1 immunoreactivity in dendrites and particularly in cell somata suggests that this transporter may function in the regulation of other aspects of glutamate metabolism in addition to terminating the action of synaptically released glutamate at central synapses.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.