New funding strategy for housing for people with mental disabilities.
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Biomedical subjects
Publications and source records attributed to L B James.
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High affinity D-[3H]aspartate and [3H]GABA uptake, and amino acid concentrations were examined in synaptosome-enriched preparations of rat periaqueductal gray matter 6-7 days following N-methyl-D-aspartate lesions confined to medial prefrontal cortex. Specific reductions were observed in the high affinity uptake of D-[3H]aspartate (78% of control, p less than 0.025), but not of [3H]GABA. Concentrations of glutamate, aspartate, GABA, glycine and alanine were not significantly reduced in lesioned animals. These results suggest the presence of glutamatergic and/or aspartatergic projections from medial prefrontal cortex to periaqueductal grey matter.
A mutant strain of Escherichia coli carrying a mutation in the uncE gene which codes for the c-subunit of the F1F0-ATPase has been isolated and examined. The mutant allele, designated uncE513, results in alanine at position 25 of the c-subunit being replaced by threonine. The mutant F1F0-ATPase appears to be fully assembled and is partially functional with respect to oxidative phosphorylation. The ATPase activity of membranes from the mutant strain is resistant to the inhibitor dicyclohexylcarbodiimide, but this is due to the F1-ATPase being lost from the membranes in the presence of the inhibitor. Mutant membranes from which the F1-ATPase has been removed have a greatly reduced proton permeability compared with similarly treated normal membranes. The results are discussed in relation to a previously proposed mechanism of oxidative phosphorylation.
High affinity D-[3H]aspartate uptake and amino acid concentrations were examined in synaptosome-enriched preparations of microdissected rat ventral tegmental area 6-7 days following N-methyl-D-aspartate lesions confined to medial prefrontal cortex. Specific reductions were observed in the high affinity uptake of D-[3H]aspartate (59% of control, P less than 0.005) and concentrations of L-aspartate (79% of control, P less than 0.05) in the ventral tegmental area suggesting the presence of an aspartatergic projection from medial prefrontal cortex to this area.
High-affinity uptake of neurotransmitter substrates in synaptosome-containing homogenates and tissue concentrations of amino acids were examined in subcortical areas 5-6 days after bilateral N-methyl-D-aspartate lesions confined to rat medial prefrontal cortex. D-[3H]Aspartate (32% of control) and [3H] gamma-aminobutyric acid ( [3H]GABA) (60% of control) uptakes were significantly reduced in medial prefrontal cortex, whereas [3H]choline (110% of control) uptake was unchanged, suggesting the production of axon-sparing lesions. The uptake of D-[3H]aspartate (76% of control), but not of [3H]GABA or [3H]choline, was significantly reduced in nucleus accumbens, with no concomitant reduction in amino acid concentrations. When examined in serial coronal sections, reduced D-[3H]aspartate uptake was confined to the most anterior 500 micron of nucleus accumbens (67% of contralateral sample). No significant reductions of uptake or amino acid concentrations were observed in caudate putamen or ventral tegmental area. These results suggest a role for glutamate or aspartate as neurotransmitters in projections from medial prefrontal cortex to anterior nucleus accumbens. Medial prefrontal cortex may represent the major excitatory cortical input to the nucleus accumbens.
The uncE410 allele differs from the normal uncE gene in that C leads to T base changes occur at nucleotides 190 and 191, resulting in proline at position 64 in the c-subunit of the F1F0-ATPase being replaced by leucine. Two partial-revertant strains were isolated in which alanine-20 of the c-subunit was replaced by proline, owing to a G leads to C base change at nucleotide 58. These c-subunits, coded for by the uncE501 and uncE502 alleles, therefore contained two amino acid changes, namely proline-64 leads to leucine, and alanine-20 leads to proline. Membranes prepared from the partial-revertant strains lacked ATP-dependent atebrin-fluorescence-quenching activity but were able to carry out oxidative phosphorylation. The ATPase activity of the F1-ATPase was inhibited when bound to membranes from strains carrying the uncE410, uncE501 and uncE502 alleles. It is concluded that a bend in the helix axis in one of the arms of the c-subunit hairpin structure is required for integration of the c-subunit into a functional F1F0-ATPase.
The amino acid substitutions in the mutant c-subunits of Escherichia coli F1F0-ATPase coded for by the uncE429, uncE408 and uncE463 alleles affect the incorporation of these proteins into the cell membrane. The DNA sequence of the uncE429 allele differed from normal in that a G leads to A base change occurred at nucleotide 68 of the uncE gene, resulting in glycine being replaced by aspartic acid at position 23 in the c-subunit. The uncE408 and uncE463 mutant DNA sequences were identical and differed from normal in that a C leads to T base change occurred at nucleotide 91 of the uncE gene, resulting in leucine being replaced by phenylalanine at position 31 in the c-subunit. An increased gene dosage of the uncE408 or uncE463 alleles resulted in the incorporation into the membranes of the mutant c-subunits. The results are discussed in terms of the 'Helical Hairpin Hypothesis' of Engelman & Steitz [(1981) Cell 23,411-422].
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This study compared children's performance on two tests of articulation. Children ranging in age from five years, four months to eleven years, six months were administered the Deep Test of Articulation and the Arizona Articulation Proficiency Scale: Revised. Comparisons between the tests were made of performance on individual sounds, total test performance, and differences in children identified as potentially in need of remediation. Results revealed differences in performance across tests on 15 of 21 sounds tested. Performance of almost 83% of the subjects varied across tests on at least one sound. Although some individual sounds displayed considerable variation between tests, total test performance and conclusions were similar. The data indicated, however, that the AAPS may fail to identify some children with consistent errors on relatively few sounds. The results are related to previous research, and clinical implications are discussed.