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Biomedical subjects

J Shaw

Publications and source records attributed to J Shaw.

At least 253 records · Page 14Linked to original sources
PubMed1986

Effects of intervention on medication compliance in children with asthma.

We have assessed the effects of intervention on medication compliance in asthmatic children. The intervention comprised both written information about the medications and behavioural strategies effected by the physician. Children were assigned at random to either control (received no intervention) or test (received the intervention) groups. Compliance was assessed by questionnaire. The mean compliance for the test (78.0%; n = 93) and for the control (54.5%; n = 103) groups differed significantly (P less than 0.001; Mann-Whitney U-test). The test group had a better knowledge of asthma and of the medications, and was more satisfied with the physician and with the regimen than was the control group. These variables were also related to good compliance. This study demonstrates that a programme of intervention can significantly improve medication compliance and can be accompanied by increases in the knowledge of, and satisfaction with, treatment.

Asthma↗
PubMed1986

Effects of verapamil on activation of arachidonic acid metabolism in guinea-pig lungs.

The effects of (+/-)-verapamil and its optical isomers on the activation of arachidonic acid (AA) in guinea-pig isolated perfused lungs were investigated. The calcium ionophore A23187 (6-15 nmol), histamine (20-50 nmol) and leukotriene E4 (1-2 nmol) induced the release of thromboxane A2 (TxA2), which was detected by bioassay and by radioimmunoassay of the stable metabolite TxB2. Racemic (+/-)-verapamil (0.4-40 microM) caused concentration-dependent inhibition of A23187-induced release of TxA2 without affecting the conversion of exogenous AA to TxA2. Both (+)-verapamil and (-)-verapamil (1-10 microM) caused concentration-dependent inhibition of histamine-induced release of TxA2. In contrast, racemic (+/-)-verapamil did not inhibit leukotriene E4 (LTE4)-induced release of TxB2. Calcium depletion (with 2 mM ethylenediamine tetra acetate) significantly reduced both histamine-induced release of TxB2 from 8.6 +/- 2.6 to 1.8 +/- 0.8 ng/min (P less than 0.05) and LTE4-induced release of TxB2 from 4.9 +/- 0.9 to 0.5 +/- 0.2 ng/min (mean +/- S.E.M.) (P less than 0.05). Since histamine stimulates phospholipase A2 in guinea-pig lungs, these results suggest that (+/-)-verapamil inhibits phospholipase A2 and that A23187 activates AA metabolism by stimulating phospholipase A2. Although all three agents activate AA metabolism by calcium-dependent processes, LTE4 may stimulate calcium entry via separate mechanisms because it is not inhibited by (+/-)-verapamil.

Animals↗
PubMed1986

Effect of cigarette smoking, pulmonary inflammation, and lung disease on concentrations of carcinoembryonic antigen in serum and secretions.

A specific radioimmunoassay for carcinoembryonic antigen was used to investigate aspects of its measurement in lung disease. The results confirm that serum carcinoembryonic antigen concentrations are higher in healthy smokers and patients with chronic obstructive bronchitis than in healthy non smokers (p less than 0.01). Corticosteroid treatment reduced the concentration in nine patients with bronchitis (p less than 0.05). Other inflammatory lung diseases (bronchiectasis, pneumonia, fibrosing alveolitis) are not associated with a raised serum carcinoembryonic antigen concentration. The sputum concentrations were about 100 times those found in serum and there was a positive correlation (r = 0.611 2p less than 0.01) between the concentrations in sputum and serum in patients with bronchitis. No preferential rise in sputum concentration was found in current smokers or patients with lung carcinoma (n = 16). A higher ratio of carcinoembryonic antigen to albumin concentration (p less than 0.05) was, however, found in lavage fluid obtained from the tumour site than in fluid from "normal" lung in the same patients, suggesting an increase in carcinoembryonic antigen secretion in the vicinity of the tumour. Despite this "local" effect the sputum concentration does not, however, appear to be a useful marker of lung carcinoma and the measurement could not be used as a screening test.

Bronchitis↗
PubMed1985

Teleocidin and phorbol ester tumor promoters exert similar mitogenic effects on human lymphocytes.

The tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate (TPA) affects a wide variety of cellular functions via its binding to protein kinase C (PKC). The TPA molecule contains a diacylglycerol (DAG)-like structure, which may explain its ability to mimic DAG in PKC activation. Teleocidin (TCD) is a different tumor promoter which can compete with TPA in binding to its cell surface receptors even though structurally unrelated to TPA or DAG. Since TCD may use an additional receptor system and/or be distinguished from TPA in its effect on cells, we compared the effects of TPA and TCD on human peripheral blood lymphocytes (PBL). Both tumor promoters preferentially enhanced cell proliferation of sheep erythrocyte-rosetted lymphocytes, which were enriched for T cells. Additionally, TPA and TCD both induced a high density of cell surface receptors for interleukin 2 (IL2) and transferrin, but not synthesis or production of IL2. However, either of the tumor promoters synergized with T cell mitogens to induce high level IL2 production by PBL. In dose response and kinetic studies, matching concentrations of TPA and TCD induced similar effects in PBL. The results thus demonstrate that TPA and TCD are alike in mitogenic capacity, and suggest that structural similarity between the tumor promoter and DAG, the physiological activator of PKC, is not an essential property for promoting tumors or affecting a wide variety of cellular functions.

Cell Division↗
PubMed1985

Mechanisms involved in the vasodilator action of 5-hydroxytryptamine in the dog femoral arterial circulation in vivo.

The possibility that the vasodilator effect of 5-hydroxytryptamine (5-HT) in vivo involves a presynaptic inhibitory effect on sympathetic nerve activity was investigated in the femoral arterial circulation of pentobarbitone-anaesthetized dogs. The vasodilator effect of intraarterial (i.a.) 5-HT was abolished following ganglion blockade with mecamylamine, and remained inhibited after restoration of femoral vascular tone with i.a. ornipressin. These procedures had no effect on the vasodilator response to i.a. acetylcholine. The vasoconstrictor response to i.a. noradrenaline was not inhibited by mecamylamine. These findings suggest that a presynaptic inhibition of sympathetic neurotransmission is responsible for 5-HT-induced vasodilatation in vivo. Pizotifen (0.1-0.4 mg/kg i.v.) inhibited the 5-HT dilator response, but the doses required were too high to be commensurate with an action at 'D' type 5-HT receptors. Ketanserin (0.1-0.4 mg/kg i.v.) specifically inhibited the dilator response to 5-HT; higher doses (1-4 mg/kg i.v.) also inhibited noradrenaline-induced vasoconstriction. Ketanserin, at all doses used, reduced systemic blood pressure and femoral vascular resistance. The effects of the lower doses of ketanserin (0.1-0.4 mg/kg) cannot be due to peripheral alpha-adrenoceptor antagonism; blockade of the dilator effect of 5-HT may simply be due to inhibition of sympathetic nerve activity by ketanserin itself.

Animals↗
PubMed1985

Hypotensive actions of ketanserin in dogs: involvement of a centrally mediated inhibition of sympathetic vascular tone.

The intravenous (i.v.) administration of ketanserin (0.1-0.4 mg/kg) produced immediate and sustained decreases in systemic blood pressure and heart rate in pentobarbitone-anaesthetized dogs. These doses of ketanserin did not inhibit common carotid vasoconstrictor responses to intraarterial (i.a.) noradrenaline, pre-ganglionic stimulation of the sectioned cervical sympathetic nerve, or i.v. nicotine, thus the effects of ketanserin are not due to blockade of vascular alpha-adrenoceptors, adrenergic neurone blockade, or ganglionic blockade. Systemic pressor responses to i.v. nicotine, which produces sympathetic activation by both central and ganglionic stimulating actions, and to common carotid artery occlusion, were inhibited by 0.1-0.4 mg/kg of ketanserin i.v. These results suggest that in the anaesthetized dog, the hypotensive action of ketanserin involves a centrally mediated inhibition of sympathetic tone. Peripheral vascular 5-HT2 receptor blockade does not appear to be responsible for the hypotensive effect of ketanserin in this model, although this does not preclude the involvement of such a mechanism in its clinical antihypertensive action.

Animals↗
PubMed1985

Nucleotide sequence of the birA gene encoding the biotin operon repressor and biotin holoenzyme synthetase functions of Escherichia coli.

A 2.2-kb region of DNA containing the birA gene of Escherichia coli has been sequenced. The birA gene sequence predicts a 35.3-kDal [321 amino acids (aa)] bifunctional protein containing biotin-operon-repressor and biotin-holoenzyme-synthetase activities. Mutations, generated by random insertion of XhoI linkers, defined the extent of the gene. Mutations affecting one or more of five discernable properties of birA [Barker, D. and Campbell, A., J. Bacteriol., 143 (1980) 789-800] were mapped. Three mutations that result in temperature-sensitive (ts) growth, birA85, birA215, and birA879 mapped in the N-terminal two-thirds of the protein. The birA352 mutation, which partially complements birA215 and birA879, maps in the N-terminal third of the protein. Finally, birA361 maps closest to the amino terminus.

Amino Acid Sequence↗
PubMed1985

Evidence for a central component to the hypotensive action of ketanserin in the dog.

The mechanisms responsible for the hypotensive action of ketanserin are controversial. Vascular 5-HT2-receptor blockade, resulting in inhibition of serotonin-induced vasoconstriction and amplification of other vasoconstrictors, has been suggested by some investigators, but others have concluded that vascular alpha-adrenoceptor blockade is responsible. In our experiments using pentobarbitone-anaesthetized dogs, ketanserin (0.1-0.4 mg/kg i.v.) produced immediate and sustained falls in systemic arterial blood pressure and vascular resistance in the common carotid and femoral arterial circulations. Constrictor responses to noradrenaline in these circulations were unaffected by 0.1-0.4 mg/kg i.v. of ketanserin; alpha-adrenoceptor blockade was only produced by higher doses (1-4 mg/kg i.v.). Constrictor responses in the common carotid circulation to preganglionic cervical sympathetic nerve stimulation and to nicotine were not inhibited by 0.1-0.4 mg/kg of ketanserin. The systemic pressor responses to nicotine and common carotid artery occlusion, however, were reduced by these doses of ketanserin. These results suggest that alpha-adrenoceptor blockade is not responsible for the hypotensive action of 0.1-0.4 mg/kg of ketanserin, and that a centrally mediated inhibition of sympathetic nerve activity is involved.

Animals↗
PubMed1985

Analysis of a deleted MC29 provirus: gag sequences are not required for fibroblast transformation.

Recovered avian myelocytomatosis virus HBI is an MC29-related virus that induces lymphoid tumors in chickens rather than the predominant neoplastic disease induced by wild-type MC29 (namely, endotheliomas). An analysis of the structure of the HBI provirus(es) in the tumors demonstrated that the provirus(es) could be either full size or deleted. One tumor was found to be clonal in that it contained a single provirus which had been partially deleted; this raised a question concerning the role of this provirus in the maintenance of tumor growth. To characterize the detailed structure of this provirus and determine its biological activity, it was molecularly cloned from tumor DNA. Sequencing confirmed that the provirus contained a deletion which effectively removed the whole gag gene. However, the provirus was shown to encode a myc-specific protein, presumably initiating from within the myc gene, and to be biologically active when it was transfected onto quail embryo fibroblasts. Our results suggest that myc alone is sufficient to transform quail embryo fibroblasts and to maintain tumor growth in vivo.

Amino Acid Sequence↗
PubMed1985

Beta-adrenoceptor blockade with propranolol and bronchial responsiveness to a number of bronchial provocation tests in non-asthmatic subjects.

The role of beta-adrenoceptors in the mechanisms of bronchial hyperresponsiveness was studied in 20 normal subjects. Propranolol 120 mg b.d. or placebo was taken for one week. Four bronchial provocation tests: exercise, inhalation of nebulised water, histamine, and methacholine, were carried out before and during the last 2 days of the treatments. FEV1 and flow rate at 50% of vital capacity (V50) were measured. Cardio-vascular beta-blockade with propranolol, measured by reduction in exercise heart rate, was shown in 17 subjects. Propranolol enhanced bronchial responsiveness to some tests in some subjects, but there was no consistent pattern. For the group, the only significant increases in response were 1) the maximum fall in V50 on methacholine challenge (P less than 0.05, paired t-test, n = 17), 2) the dose of methacholine giving a 10% fall (PD10 value) in FEV1 (p less than 0.05 n = 11). These results do not support the concept of decreased beta-adrenoceptor responsiveness as a single lesion leading to abnormal bronchial reactivity.

Adolescent↗
PubMed1985

A possible mechanism in the anti-anaphylactic effect of beta-adrenoceptor agonists in guinea-pig lungs.

The anaphylactic mediators, histamine and leukotrienes, stimulate arachidonic acid (AA) metabolism in the guinea-pig lungs, leading to the synthesis and release of thromboxane A2 (TxA2) and other cyclo-oxygenase products. Since TxA2 is a potent bronchoconstrictor, it is possible that the activation of AA metabolism by histamine may contribute to the pulmonary manifestations of anaphylaxis. In the present experiments, histamine-induced release of TxA2 was inhibited by mepyramine (10(-8)-10(-6) M) but not by cimetidine (5 X 10(-5) M) indicating that the release was mediated by H1-receptors. The beta-adrenoceptor agonists, fenoterol (10(-6) M) and isoprenaline (10(-6) M) inhibited the histamine-induced release of TxA2. This effect was partially reversed by propranolol. These results suggest that if histamine-induced TxA2 release is involved in guinea-pig pulmonary anaphylaxis then inhibition of this release may be a factor in the anti-anaphylactic effect of beta-adrenoceptor agonists.

Adrenergic beta-Agonists↗