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Biomedical subjects

C E Rowe

Publications and source records attributed to C E Rowe.

At least 19 recordsLinked to original sources

The concept of resistance in self psychology.

Self psychology views resistances as protecting a vulnerable self. Resistances are seen as efforts to maintain levels of organization that patients have achieved within the context of their traumatic life situation. Patients feel able to move forward in the treatment when the importance of their need to maintain their developmental position is understood. This view is in contrast to the traditional view of resistances as treatment interferences that must be overcome as they defend against awareness of impulses and allow for unconscious instinctual gratification.

Adult

'Neurosis' and the personal social environment. The effects of a time-limited course of intensive day care.

The Interview Schedule for Social Interactions (ISSI) was used to assess the social environment of 65 British inner-city patients suffering from severe neurotic disorder; all patients were offered a 12-week course of intensive day treatment with an educational and psychodynamic basis. Compared with a general population in Canberra, the neurosis sufferers had lower (morbid) scores on the ISSI for the extent and quality of their social relationships. Of the 34 subjects who completed treatment and attended for the post-treatment investigation, 21 attained a PSE score below the level for 'caseness'. Twenty-five subjects who attended for follow-up at 18-24 months had improved significantly on all four of the standard ISSI measures, although they had not done so immediately after treatment. This suggests that although symptoms may improve at the time of treatment, social relationships improve only over several months.

Adult

Intraoral effects of a fluoride-releasing device on acid-softened enamel.

Among the anticaries benefits of fluorides is the remineralization of incipient carious lesions. There is increasingly convincing evidence that low-potency fluoride agents applied frequently are effective in remineralizing early carious lesions. This study of in vivo remineralization used an intraoral appliance with demineralized enamel slabs mounted in the appliance and an innovative method of fluoride delivery, the fluoride-releasing device, which releases a controlled amount of fluoride (0.3 mg fluoride every 24 hours) on exposure to saliva. After control and treatment periods of 7 and 30 days, the enamel specimens were removed from the appliance and evaluated for microhardness, acid resistance, and fluoride uptake. The treated specimens significantly exceeded the values of their corresponding controls in all parameters measured, indicating that considerable remineralization of the treated enamel had occurred at both 7 and 30 days. Although the longer period of treatment produced greater results, considerable effects were observed after 7 days. This model system provided for an in vivo environment to study the effects of treatment of the FRD and allowed for subsequent recovery of the enamel specimens for evaluation. The results of this study are encouraging with respect to the efficacy of a fluoride-releasing device but indicate that subsequent clinical testing of the effects of FRDs on incipient carious lesions in the natural dentition of human subjects is necessary.

Adult

The intracellular location of a Ca2+-stimulated phospholipase A1 in rat brain.

Rat brain contains a phospholipase A1 which hydrolyzes phosphatidylethanolamine with a pH optimum of 9.5. The enzyme is stimulated by CaCl2 and inhibited by sodium taurocholate and Triton X-100. The subcellular distibution of the enzyme is similar to that of lactate dehydrogenase indicating the location of the phospholipase in the soluble cytoplasm in vitro.

Animals

The acylation of lysophosphatidylcholine by subcellular fractions of guinea-pig cerebral cortex.

The acylation of lysophosphatidylcholine by isolated subcellular fractions of guinea-pig cerebral cortex has been determined. The microsomal fraction contained the highest acylation activity, in terms of both specific and total activity. In all particulate fractions, including synaptic plasma membrane and mitochondria, there was a high correlation (correlation coefficient r = 0.90; P less than 0.001) between acylation and the activity of the microsomal enzyme, NADPH-cytochrome c reductase. No correlation existed between acylation and the activities of (Na+ + K+)-ATPase, acetylcholinesterase or succinate dehydrogenase. Acyl-CoA synthetase and lysophosphatidylcholine/acyltransferase, the individual enzymes responsible for acylation were enriched in the microsomal fraction. The activities of both enzymes in subcellular fractions correlated well with those of NADPH-cytochrome c reductase, with the exception that acyl-CoA synthetase activity in the mitochondrial fraction was largely independent of endoplasmic reticulum. Neither synaptic plasma membranes nor mitochondria appeared to possess significant amounts of acyltransferase activity. The results indicate that the acylation of lysophosphatidylcholine is confined to the endoplasmic reticulum, and that activity present in the synaptic plasma membrane or mitochondrial fraction is attributable to microsomal contamination.

1-Acylglycerophosphocholine O-Acyltransferase

Net activity of phospholipase A2 in brain and the lack of stimulation of the phospholipase A2-acylation stem.

Certain observations reported previously from this laboratory have not proved reproducible. These are (1) the relatively rapid hydrolysis of added phosphatidylcholine by phospholipase A2 of tissue from the cerebral cortex of the guinea pig and (2) the stimulation by 10 micron-noradrenaline and by 1.0nM-cyclic AMP of the phospholipase A2-acylation system of isolated synaptic membranes.

Retraction Notice

The stimulation by transmitter substances and putative transmitter substances of the net activity of phospholipase A2 of synaptic membranes of cortex of guinea-pig brain.

1. The distribution of the hydrolyses of phosphatidylcholine by phospholipase A2 and phospholipase A1, and the hydrolysis of lysophosphatidylcholine by lysophospholipase, in subcellular and subsynaptosomal fractions of cerebral cortices of guinea-pig brain, was determined. 2. Noradrenaline stimulated hydrolysis by phospholipase A2 in whole synaptosomes, synaptic membranes and fractions containing synaptic vesicles. 3. Stimulation of hydrolysis by phospholipase A2 in synaptic membranes by noradrenaline was enhanced by CaCl2, and by a mixture of ATP and MgCl2. The optimum concentration of CaCl2, in the presence of ATP and MgCl2, for stimulation by 10 muM-noradrenaline was in the range 1-10muM. The optimum concentration for ATP-2MgCl2 in the presence of 1 muM-CaCl2 was in the range 0.1-1mM. 4. Hydrolysis by phospholipase A2 of synaptic membranes was also stimulated by acetylcholine, carbamoylcholine, 5-hydroxytryptamine, dopamine (3,4-dihydroxyphenethylamine), histamine, psi-aminobutyric acid, glutamic acid and aspartic acid. With appropriate concentrations of cofactors, sigmoidal dose-response curves were obtained, half-maximum stimulations being obtained with concentrations of stimulant in the range 0.1-1muM. 5. Taurine also stimulated hydrolysis of phosphatidylcholine by phospholipase A2. There were only slight stimulations with methylamine, ethylenediamine or spermidine. No stimulation was obtained with glucagon.

Acetylcholine

The stimulation by synaptic transmitters of the incorporation of oleate into the phospholipid of synaptic membranes.

Noradrenaline stimulated the incorporation of oleate into choline glycerophospholipids of guinea-pig brain synaptic membranes incubated in sodium phosphate buffer. In the presence of 1 mm-NaF, noradrenaline stimulated the incorporation of oleate into the choline glycerophospholipids, phosphatidylinositol, ethanolamine glycerophospholipids, phosphatidylserine and phosphatidic acid of synaptic membranes incubated in 10 mm-Tris-HCl buffer. In Tris-CHl containing 1 mm-NaF, stimulation of incorporation of oleate into choline glycerophospholipids by noradrenaline was enhanced by ATP, CaCl2, MgCl2 and CoA plus dithiothreitol. The optimum concentration of CaCl2 for stimulation by 10 mum-noradrenaline was 10 mum. In the presence of CaCl2, the optimum concentration of ATP-2MgCl2 was in the range 0.1-1 mm. Acetylcholine, carbamoylcholine, 5-hydroxytryptamine, dopamine, histamine and gamma-aminobutyric acid also stimulated the incorporation of oleate into choline glycerophospholipids of synaptic membranes. Sigmoidal dose-response curves were obtained, similar to those obtained previously for stimulation by the same agonists of the hydrolysis of phosphatidylcholine by phospholipase A2 (Gullis & Rowe, 1975a). The initial rate of transfer of oleate from oleoyl-CoA to choline glycerophospholipid was similar to the initial rate of transfer from oleate-albumin, stimulated by noradrenaline. Transfer of oleate from oleoyl-CoA was not appreciably stimulated by noradrenaline, but was stimulated by ATP and MgCl2.

Adenosine Triphosphate

The stimulation of the phospholipase A2-acylation system of synaptic membranes of brain by cyclic nucleotides.

Hydrolysis of phosphatidylcholine by phospholipase A2 of synaptic membranes i n Tris-CHl buffer was stimulated by cyclic AMP, cyclic GMP, cyclic CMP, cyclic UMP and adenosine (0.1 mm). In the presence of 1 mm-NaF and cofactors, the same cyclic nucleotides and adenosine (10 mm) stimulated the incorporation of added oleate into the choline glycerophospholipids of synaptic membranes. Cyclic AMP and noradrenaline stimulated the incorporation of added oleate into position 2 of choline glycerophospholipid. Stimulation of net acylation was increased by preincubation in conditions which stimulated hydrolysis of phosphatidylcholine. Cyclic AMP only slightly stimulated the transfer of oleate from oleoyl-CoA into choline glycerophospholipid. The optimum concentration of CaCl2 for the stimulation of hydrolysis by phospholipase A2 by cyclic AMP was 1 mum. Stimulation of the incorporation of added oleate was maximal in the CaCl2 concentration range 1 mum-1mm. MgCl2 also enhanced stimulations, maximum effects being obtained with concentrations of 10 mum and 0.5 mm for hydrolysis by phospholipase A2 and incorporation of added oleate respectively. ATP enhanced the stimulation of incorporation of oleate but had no effect on the cyclic nucleotide stimulation of hydrolysis of added phosphatidylcholine by phospholipase A2. Adenosine, guanosine, ADP and 5'-AMP (all at 1 mm) inhibited the stimulation of incorporation of oleate by cyclic nucleotides and inhibited the transfer of oleate from oleoyl-CoA to phospholipid. They did not inhibit the stimulation of hydrolysis of added phosphatidylcholine (by phospholipase A2) by cyclic nucleotides, but inhibited the stimulation by noradrenaline, acetylcholine, 5-hydroxytryptamine, dopamine (3,4-dihydroxyphenethylamine) and histamine. Preincubation of synaptic membranes in the water or buffer increased the net activity of phospholipase A2. Preincubation with a mixture of ATP and MgCl2 increased the initial rate of acylation of membrane lipid.

Acylation