National Association of Orthopaedic Nurses.
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Humans↗
Biomedical subjects
S C Taylor
Publications and source records attributed to S C Taylor.
The Association of Operating Room Nurses, Inc.
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Humans↗
Pea early browning virus RNA1 encodes four polypeptides including a putative zinc-finger protein.
We have determined the complete nucleotide sequence of RNA1 of the tobravirus pea early browning virus [PEBV] from an overlapping series of cDNA clones. The 7073 nucleotide sequence contains four open reading frames [ORFs]. The 5' proximal ORF encodes a 141K polypeptide, and readthrough of the opal [UGA] termination codon of this ORF would lead to the synthesis of a second, 201K polypeptide. Both of these polypeptides have extensive amino acid homology with the putative replicase proteins of tobacco rattle virus [TRV] and tobacco mosaic virus [TMV]. The third ORF encodes a 30K polypeptide which has homology with the TRV 29K and TMV 30K putative cell-to-cell spread proteins. The fourth, 3' proximal ORF encodes a 12K polypeptide which has extensive homology with the TRV 16K protein whose function is unknown. Examination of the amino acid sequences of the 12K and 16K gene products reveals in each the presence of two multiple-cysteine/histidine motifs, a finding which suggests that these proteins might have zinc and/or nucleic acid-binding properties.
Amino Acid Sequence↗
AACN: the critical care nurses.
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Certification↗
Projected incidence of cardiovascular disease in male firefighters based on current risk factor prevalence.
The projected incidence of cardiovascular disease (CVD) in male firefighters was determined by the prevalence of current CVD risk factors and the use of the Framingham Study general cardiovascular risk profile in a probability sample of firefighters from two municipal fire departments. Hypercholesterolemia (60.9%) and obesity (56.0%) were the most prevalent risk factors. Significant age-related trends were observed for the prevalence of all CVD risk factors, except glucose intolerance (P = .21) and an abnormal resting electrocardiogram (P = .07). The projected incidence of CVD in firefighters did not differ from that of the general male population (relative risk, 1.0; 95% confidence interval, 0.7 to 1.4); similar risk estimates were observed in age-specific analyses. These findings are in accord with previous incidence and mortality studies that used circulatory diseases as an end point. The present method should be viewed primarily as a hypothesis-generating tool because of its limitations in assessing cause and effect.
Adolescent↗
Links with special interest groups. The American Public Health Association.
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Humans↗
Changes in benzodiazepine/GABA receptor complex function in benzodiazepine-tolerant mice.
Mice were given flurazepam, 40 mg k-1, IP, once daily for 7 consecutive days. Twenty-four and forty-eight hours after the last injection measurements were made of the effects on convulsion threshold, body temperature and locomotor activity, of drugs acting on the GABA receptor complex. Significant decreases were seen in the hypothermic and hypomobility effects of progabide at 48 h, but no significant changes were seen in the effects of pentylenetetrazol or pentobarbitone. The actions of picrotoxin in all three types of test and the convulsant action of bicuculline (IP) were significantly decreased at 24 h but not at 48 h. The convulsive, but not the hypothermic, effects of picrotoxin were increased at the 48 h interval. These results may suggest that the chronic benzodiazepine treatment decreased some aspects of GABA receptor function at 48 h after the last dose; however, such an effect probably does not explain the previously reported increases in the effects of inverse agonists following chronic agonist treatment.
Animals↗
Chronic benzodiazepine treatment increases the effects of the inverse agonist FG7142.
A schedule of treatment with the benzodiazepine, flurazepam, in mice for 7 days caused a significant enhancement of the convulsive effects of the partial inverse agonist FG7142. Full convulsions were seen with FG7142 after the chronic administration of flurazepam, although this compound does not cause convulsions in normal mice of the strain used. The change appeared to be maximal at 24 hr after the last dose of flurazepam and lasted for up to a week. The chronic treatment with flurazepam caused tolerance to the effects of flurazepam, but the tolerance was of shorter duration than the increase in the effects of FG7142. When the benzodiazepine antagonist, Ro 15-1788, was given with the flurazepam, the incidence of convulsions induced by FG7142 was no longer significant. Repeated administration of midazolam also slightly increased the effects of FG7142. Single doses of flurazepam or midazolam did not significantly alter the effects of FG7142, although some convulsions were seen.
Animals↗
Kindling with the beta-carboline FG7142 suggests separation between changes in seizure threshold and anxiety-related behaviour.
The aim of this paper was to determine whether the prolonged decrease in seizure threshold produced by chemical kindling was accompanied by behavioural changes in tests of anxiety and aggression. The responses of rats in five tests were examined after chronic treatment with the benzodiazepine inverse agonist FG7142. This treatment caused chemical kindling, so that the originally proconvulsant drug caused full seizures. This effect is very long-lasting, and our previous work with mice had suggested that it might be accompanied by an increase in anxiety-related behavior. In the present work no significant differences were found between the behaviour of FG7142-kindled rats and vehicle-treated controls in social interaction test, elevated plus maze, or the Vogel conflict test of anxiety or in tests of home cage aggression or startle responses. The results therefore show that prolonged changes in seizure threshold can occur without alterations in the apparent level of anxiety.
Aggression↗
Chronic desipramine treatment prevents the upregulation of cortical beta-receptors caused by a single dose of the benzodiazepine inverse agonist FG7142.
The beta-carboline FG7142 is a partial inverse agonist at benzodiazepine receptors. We have shown previously that a single dose of this drug causes an upregulation of cortical beta-adrenoceptor numbers in mouse cerebral cortex. This rise was seen seven days, but not 15-30 min or 24 h after FG7142 administration. We now report that two weeks pretreatment with the tricyclic antidepressant desipramine prevented the beta-adrenoceptor upregulation after a single dose of FG7142, although desipramine alone did not alter beta-adrenoceptor number. We also studied the effects of desipramine pretreatment on other pharmacological effects of FG7142 to see which of these effects might be related to the beta-adrenoceptor changes. Desipramine pretreatment caused a small, but significant, decrease in the depression of locomotor activity, but no change in the hypothermic action of FG7142. The possibility that upregulation of beta-adrenoceptors by FG7142 may be related to the behavioural actions of this compound is discussed.
Animals↗
A single dose of FG 7142 causes long-term increases in mouse cortical beta-adrenoceptors.
There is evidence that central monoamines are involved in the actions of benzodiazepines. We have investigated the effects of a single dose of the benzodiazepine partial inverse agonist, FG 7142, on radioligand binding to alpha 2- and beta-adrenoceptors in mouse cerebral cortex. We found that seven days after a single injection of FG 7142 there was a large increase in the density of beta-adrenoceptors. This rise was not detectable either 15-30 min, or 24 h after the injection and no statistically significant changes in alpha 2-adrenoceptor binding were found at any of these times. Administration of the benzodiazepine antagonist Ro 15-1788 at the same time as FG 7142 prevented the rise in beta-adrenoceptor density. We discuss the possibility that the beta-adrenoceptor upregulation is related to the behavioural effects of FG 7142.
Animals↗
Selective changes in the in vivo effects of benzodiazepine receptor ligands after chemical kindling with FG 7142.
It has recently been demonstrated that kindling occurs with repeated administration of the benzodiazepine "inverse agonist" FG 7142. The present study was an investigation of the effects of other ligands for the benzodiazepine receptor in mice kindled with FG 7142. It was shown that over a range of doses the lowering effects of FG 7142 on the seizure threshold were greater in kindled animals than in control. In contrast, the hypothermic effect of FG 7142 was unaltered. The effects of the partial inverse agonist CGS 8216 were unaltered. The effects of the full inverse agonist DMCM were unchanged except for an enhancement of its convulsant effect when infused at a concentration of 100 mu gm 1-1. Studies with the full agonist benzodiazepine, flurazepam and the full agonist beta-carboline, ZK 93423, showed small but significant reductions in their hypothermic effects. The sedative and anticonvulsant effects of flurazepam were unaltered, whereas the anticonvulsant effects of ZK 93423 were decreased in animals kindled with FG 7142. There was a pronounced reduction in the anticonvulsant and hypothermic effects of the partial agonist beta-carboline, ZK 91296. These data do not fit any simple explanation of kindling being due to a change in the function of benzodiazepine receptors, although they may offer some support for the idea that kindling with FG 7142 produces a change in the effects of all beta-carboline compounds which act at the benzodiazepine receptor.
Animals↗
Bidirectional effects of chronic treatment with agonists and inverse agonists at the benzodiazepine receptor.
We have studied in rodents the effects of beta-carboline inverse agonists on chronic treatment and after repeated administration of benzodiazepine agonists. Chronically, the inverse agonist FG 7142 caused chemical kindling, i.e., a decrease in the threshold to the convulsive effects of the drug. This change was accompanied by decreases in the effects of beta-carboline but not benzodiazepine agonists. In addition the effects of GABA receptor agonists were decreased and the effects of GABA antagonists marginally increased. The GABA stimulated benzodiazepine binding was lower after FG 7142 kindling. Some evidence was found in mice to suggest that these changes were accompanied by behavioural alterations, but studies in rats did not show any changes. Repeated administration of benzodiazepine agonists, sufficient to cause tolerance to their pharmacological actions and to those of beta-carboline agonists, increased all of the effects of the partial inverse agonists and some of the actions of the full inverse agonists. We suggest that this is due not to precipitation of withdrawal but to a "withdrawal shift" in the coupling at the receptor inophore. This would increase the intrinsic properties of inverse agonists and decrease those of agonists. Evidence for this hypothesis is summarised.
Animals↗
pWW174: a large plasmid from Acinetobacter calcoaceticus encoding benzene catabolism by the beta-ketoadipate pathway.
Acinetobacter calcoaceticus RJE74 contains a large transmissible catabolic plasmid, pWW174, of about 200 kb, which encodes its ability to grow on benzene (Bzn+). pWW174 was unstable in Acinetobacter hosts and was lost at high frequency in the absence of selection for Bzn+. The catabolic pathway appeared to be via benzene cis-glycol, catechol and the beta-ketoadipate (ortho) pathway. pWW174 encodes a catechol 1,2-oxygenase which is significantly more thermolabile than the chromosomally determined enzyme. pWW174 was able to complement all cat mutants (catechol to central metabolites) of A. calcoaceticus ADP1 (BD413) tested. Two regions of the plasmid were cloned, one carrying catA, the gene for catechol 1,2-oxygenase, and another carrying catBCDE, the subsequent four enzymes of the beta-ketoadipate pathway: these two regions appeared to be separated by at least 10 kbp. Hybridization indicated homology between the plasmid cat genes and the corresponding chromosomal genes of ADP1.
Acinetobacter↗