Practice automation: an essential, not luxury, tool.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K M Wood.
Explore the source record for details and available documents.
This study examined immediate memory processes in specific reading disability subtypes. Three subgroups (n = 15 in each subgroup) of reading disabled children were examined: (a) perceptual-motor disorder, (b) verbal disorder-general, and (c) verbal disorder-specific (memory). The three groups were matched for age and full scale IQ. All children received a memory-for-colors task (Color Span Test) designed to evaluate intra- and intermodal serial memory functioning. Comparison of memory profiles for the three reading disability subtypes revealed that patterns varied depending on mode of stimulus presentation or response. Although all three groups performed considerably below normative levels on each of the four subtests of the Color Span Test, all subjects performed significantly better on verbally presented items than on visually presented items. The findings were interpreted to suggest that these reading disabled children may not consistently utilize verbal strategies for coding or retrieval of information when stimuli are visually presented.
Sertraline, a new selective 5-HT uptake inhibitor showed a mixed pattern of inhibition of human platelet 5-HT uptake with a Ki value of 2.5 nM and K'i value of 25 nM. Imipramine and alaproclate were found to be fully competitive inhibitors of 5-HT uptake with Ki values of 8 and 130 nM respectively. Sertraline was a fully competitive inhibitor of high-affinity [3H]imipramine binding to platelet membranes with a Ki value of 1.3 nM, as was alaproclate and 5-HT with Ki values of 170 and 800 nM respectively. Both sertraline and imipramine, at a concentration of 10 microM caused a fast monophasic dissociation of [3H]imipramine from platelet membranes in contrast to serotonin which caused a slow monophasic dissociation.
A small group of patients who had been successfully treated with lithium for a number of years were treated with zimeldine in order to determine whether this antidepressant could be substituted for lithium in patients with a bipolar affective illness. The proposed treatment period of 6 months was not reached by any patient due to depression, hypomania, mania or unusual adverse symptoms. The results of this pilot study suggest that bipolar patients being treated with lithium should not then be treated by antidepressants including those which are potent and selective inhibitors of 5-HT uptake.
Clonal subpopulations of lymphosarcoma P1798 have been subjected to glucocorticoid selection in vivo and in culture and the glucocorticoid binding and responsiveness of the resistant variants have been compared with those of the parental lines. Cell populations that are resistant to the cytolytic effects of glucocorticoids in vivo exhibit a slightly reduced level of glucocorticoid binding, although nuclear translocation of the hormone-receptor complex is not reduced. Sensitive and resistant tumors exhibit similar kinetics of hormone uptake and dissociation following a single injection of dexamethasone. Selection for glucocorticoid resistance in vivo does not result in an increase in the modal number of chromosomes. Cells that are resistant to the cytolytic effects of glucocorticoids in vivo are completely sensitive to the antiproliferative effects of glucocorticoids in culture. Moreover, dexamethasone increases the expression of mouse mammary tumor provirus in cytolysis-resistant and sensitive cells both in vivo and in culture. Selection for glucocorticoid resistance in culture yields variants with decreased glucocorticoid binding and/or nuclear translocation of the hormone-receptor complex. These cells appear to express classical receptor-defective phenotypes. Nevertheless, cells that are resistant to glucocorticoids in culture undergo cytolysis when treated with glucocorticoids in vivo. These data indicate that, under certain circumstances, different mechanisms may be involved in loss of glucocorticoid responsiveness in vivo and in culture.
Apparent specific binding of [3H]imipramine to human platelet membranes at high concentrations of imipramine showed deviation from that expected of a single binding site, a result consistent with a low-affinity binding site. The deviation was due to displaceable, saturable binding to the glass fibre filters used in the assays. Imipramine, chloripramine, desipramine, and fluoxetine inhibited binding to filters whereas 5-hydroxytryptamine and ethanol were ineffective. Experimental conditions were developed that eliminated filter binding, allowing assay of high- and low-affinity binding to membranes. Failure to correct for filter binding may lead to overestimation of binding parameters, Bmax and KD for high-affinity binding to membranes, and may also be misinterpreted as indicating a low-affinity binding component in both platelet and brain membranes. Low-affinity binding (KD less than 2 microM) of imipramine to human platelet membranes was demonstrated and its significance discussed.
This paper describes experiments designed to test the hypothesis that DNA sequences upstream from the mouse rRNA promoter are transcribed in vivo or in vitro. Plasmid pB28 contains a SalI restriction fragment that extends from -169 to -1,894 base pairs, with respect to the origin of transcription of pre-rRNA. Labeled RNA synthesized in intact cells does not hybridize to this region. Neither S1 nuclease mapping nor RNA dot blot hybridization revealed the presence of sequences complementary to this region. Transcriptional studies carried out in vitro indicated that this region is not transcribed under conditions that are optimal for utilization of the authentic rRNA promoter. Moreover, this region does not appear to form stable transcription complexes with RNA polymerase I transcription components. These data indicate that the mouse rDNA repeating unit differs from those of Xenopus spp. and Drosophila melanogaster in that reduplicated RNA polymerase I promoters are not found in the mouse rDNA spacer region.
Explore the source record for details and available documents.
Five patients with intercostobrachial nerve entrapment syndrome are reported. The pain in this syndrome has three aspects: somatic stimulus, perceptual surround, and behavioral response. Each must be dealt with appropriately. The distribution of the pain, its anatomic basis, and its treatment are discussed.
The degradation of intravenously administered chondroitin sulphate-peptide, obtained by trypsin digestion of rat cartilage preparations labelled in vitro with 35S (and, in some cases, with 3H), was studied in rats. As with free chains of chondroitin sulphate, the major site of accumulation and degradation in the body was the liver, although peptide-linked chains were taken up more rapidly than free chains. In the first 2h after intravenous injection of a chondroitin sulphate-peptide fraction, labelled macromolecular components were excreted in the urine. These were shown to be chondroitin sulphate-peptide of the same degree of sulphation but of smaller average size than the injected material. A similar observation was made when free chains of chondroitin sulphate from the same source were administered intravenously. An isolated perfused rat kidney failed to de-sulphate circulating chondroitin sulphate-peptide, but a component of lower average molecular weight was excreted in the urine. When a chondroitin sulphate-peptide fraction of relatively larger hydrodynamic volume was administered, very little chondroitin sulphate appeared in the urine in the first 2h. It was concluded that, depending on size and/or peptide content, the chondroitin sulphate-peptide released from connective tissues into the circulation would probably be subjected to one of two alternative fates. The smaller fragments are more likely to be excreted in the urine, whereas the larger ones are taken up by the liver and there degraded to inorganic sulphate and undefined carbohydrate components.
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.
The degradation of chondroitin 4-[(35)S]sulphate isolated from chick-embryo cartilage was studied in the rat by experiments on free-range animals, on wholly anaesthetized animals with ureter cannulae, by perfusion of isolated liver, by whole-body radioautography and by isolation of liver lysosomes. After injection into rats 68% of the radioactivity was recovered in the urine after 24h, approximately one-half of this being in the form of low-molecular-weight material, chiefly inorganic sulphate. Cannulation experiments demonstrated that the proportion of low-molecular-weight components excreted in the urine increased with time until, after 12h, virtually all was inorganic sulphate. Whole-body radioautography identified the liver as the major site of radioisotope accumulation after injection of labelled polysaccharide. Perfusion through isolated liver indicated that this organ has the ability to metabolize the polymer with the release of low-molecular-weight products, principally inorganic sulphate. Incubation of a lysosomal fraction prepared from rat liver after injection of chondroitin 4-[(35)S]sulphate gave rise to degradation products of low molecular weight, and experiments in vitro with rat liver lysosomes confirmed that these organelles are capable of the entire degradative process from chondroitin sulphate to free inorganic sulphate.