Nurse education: objectively speaking.
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Biomedical subjects
Publications and source records attributed to J Barrett.
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Three homologous toxic peptides which cause postsynaptic inhibition at the vertebrate neuromuscular junction have been purified from the venom of the marine snail Conus geographus. Their amino acid sequences are: (formula see text) The biologically active peptides are monomeric, with internal disulfide bonds.
Symptomatic volunteers (SVs) are increasingly used as subjects for clinical research studies. A total of 362 SVs were recruited, psychiatric diagnoses were made according to Research Diagnostic Criteria (RDC), and standard symptom scale scores on the Hopkins Symptom Check list (HSCL) for the individual diagnostic categories were computed. Of these subjects, 221 were classified as having a depressive disorder (three categories), 112 as having an anxiety disorder (three categories), and 29 as having some other RDC disorder. The HSCL scale scores for the depressive- and anxiety-disorder subject groups were consistent with those for actual patient groups. There were significant differences in HSCL scores for some RDC categories within the broader depressive- or anxiety-disorder groupings. Individual RDC categories should be kept separate in reporting treatment results for depressive or anxiety disorders.
Neither phosphagens nor phosphagen phosphotransferase activity could be detected in Fasciola hepatica, Hymenolepis diminuta, Moniezia expansa or in the plerocercoids of Ligula intestinalis. The plerocercoids of Schistocephalus solidus, however, possess an active taurocyamine phosphotransferase, although it too contains no detectable phosphagens. The taurocyamine phosphotransferase of S. solidus has an absolute requirement for a divalent metal ion and ATP could not be replaced by ITP, GTP, CTP or UTP as the phosphate donor. The role of phosphagens in helminths is discussed.
To study the effects of calcium on the release of human placental lactogen (hPL), placental explants were exposed to media containing lower or higher concentrations of calcium than normally available to the placenta. Explants exposed for 2 h to calcium-poor medium or medium containing either 2 mM EDTA or 2 mM EGTA released 160, 248, and 253% more hPL, respectively, than control explants. In contrast, explants exposed to medium containing higher than normal calcium concentrations released the same amounts of hPL as the control explants. At lower than normal extracellular calcium concentrations, the increased hPL release was inversely proportional to the calcium concentration. The increased release in calcium-poor medium was inhibited by subsequent exposure of the explants to medium containing calcium and was prevented by either barium or magnesium. Changes in barium or magnesium concentrations, however, had no effects on hPL release in the presence of normal extracellular calcium concentrations. Methoxyverapamil (D 600), an inhibitor of calcium flux, stimulated hPL release. Because low extracellular calcium and methoxyverapamil both inhibit calcium influx, these experiments suggest that calcium influx inhibits hPL release. The role of calcium in the regulation of hPL release therefore appears to be different from that reported in other release systems.
Human decidual explants exposed for 4 h to 150 microM arachidonic acid synthesized and secreted 30.4% (P less than 0.001) and 36.4% (P less than 0.001) less 35S-PRL, respectively, than control explants. Over a 5-h period, the inhibition of PRL secretion was directly proportional to the arachidonic acid concentration at concentrations between 30 and 300 microM (r = 0.91; P less than 0.001). Phospholipase A2 at concentrations of 0.11 and 11.1 U/ml, also inhibited PRL secretion by 46.2 +/- 2.4% (P less than 0.001) and 63.9 +/- 1.4% (P less than 0.001), respectively. Likewise, the fatty acid precursors of arachidonic acid, i.e. linoleic, gamma-linolenic, and dihomo-gamma-linolenic acids, inhibited PRL secretion, but palmitic, oleic, and 11,14,17-icosatrienoic acids and the detergents deoxycholic acid and Triton X-100 had no effects, even at concentrations as high as 300 microM. In contrast, prostaglandins E1, E2, and F2 alpha (3 X 10(-5)-10(12) M each) had no effects on PRL secretion, and the prostaglandin synthetase (cyclooxygenase) inhibitors indomethacin (5 and 25 micrograms/ml) and flufenamic acid (5 micrograms/ml) had no effects on either basal PRL secretion or the inhibitory action of arachidonic acid. These results suggest that arachidonic acid may be involved in the regulation of the synthesis and secretion of decidual PRL. The effect of arachidonic acid, however, does not appear to be mediated by a cyclooxygenase product of arachidonic metabolism.
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Acrocarpia paniculata thylakoids were fragmented with Triton X-100 and the pigment-protein complexes so released were isolated by sucrose density gradient centrifugation. Three main chlorophyll-carotenoid-protein complexes with distinct pigment compositions were isolated. (1) A P-700-chlorophyll a-protein complex, with a ratio of 1 P-700: 38 chlorophyll a: 4 beta-carotene molecules, had similar absorption and fluorescence characteristics to the chlorophyll-protein complex 1 isolated with Triton X-100 from higher plants, green algae and Ecklonia radiata. (2) an orange-brown complex had a chlorophyll a : c2 : fucoxanthin molar ratio of 2 : 1 : 2. this complex had no chlorophyll c1 and contained most of the fucoxanthin present in the chloroplasts. This pigment complex is postulated to be the main light-harvesting complex of brown seaweeds. (3) A green complex had a chlorophyll a : c1 : c2 : violaxanthin molar ratio of 8 : 1 : 1. This also is a light-harvesting complex. the absorption and fluorescence spectral characteristics and other physical properties were consistent with the pigments of these three major complexes being bound to protein. Differential extraction of brown algal thylakoids with Triton X-100 showed that a chlorophyll c2-fucoxanthin-protein complex was a minor pigment complex of these thylakoids.
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1. In rats, intra-arterial metoclopramide, a dopamine antagonist, resulted in an elevation of plasma aldosterone at 5 min and plasma renin activity at 10 min and peak aldosterone and renin responses at 10 and 30 min respectively. 2. Pre-administration of L-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. 3. Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, saralasin, as well as bilateral nephrectomy did not significantly affect the aldosterone response to metoclopramide, Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. 4. Modulating effects of dopamine on plasma aldosterone are probably mediated by direct effects as well as by interaction with other factors influencing aldosterone secretion at the adrenal zona glomerulosa.
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Evidence obtained in this study indicates that computer simulations can be a successful method of teaching foods or can replace laboratory experiences. For nine of eleven attitudinal test items, students' attitudes became more positive concerning the value of the course in which computer simulations were used. On the achievement test, seventeen of the twenty-five questions revealed that significant learning (p of less than or equal to 0.05) occurred when the simulations were integrated into a foods course. These students seemed to do well and to like this method of instruction. The advantages of these computer simulations are that students can be motivated to learn and solve problems.
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A membrane-bound monoamine oxidase (EC 1.4.3.4) was demonstrated in homogenates of Hymenolepis diminuta. The enzyme oxidized a variety of biologically active amines (in decreasing order: dopamine, adrenaline, noradrenaline, tryptamine, tyramine, octopamine), there was, however, no activity with 5-hydroxytryptamine or benzylamine. No diamine oxidase (EC 1.4.3.6.) could be detected in H. diminuta (using histamine, cadaverine or putrescine as substrates). The monoamine oxidase from H. diminuta was not inhibited by azide, hydroxylamine or semicarbazide, but was inhibited by cupferron, alpha-alpha dipyridyl and iodoacetamide, and by the specific monoamine oxidase inhibitors pargyline, nialamide and iproniazid. Several anthelmintics were also found to be inhibitors of monoamine oxidase. The possible roles of monoamine oxidase in H. diminuta are discussed.