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Biomedical subjects

J Morley

Publications and source records attributed to J Morley.

At least 181 records · Page 10Linked to original sources
PubMed1980

Actions of aspirin and dipyridamole on lymphocyte activation.

The actions of aspirin and dipyridamole on lymphocyte activation in vitro have been studied. Aspirin inhibits lymphocyte activation when measured by protein synthesis or by 3H-thymidine incorporation at therapeutic concentration. Dipyridamole also strongly inhibits 3H-thymidine incorporation, but is a less potent inhibitor of protein synthesis at therapeutic concentrations. Aspirin/dipyridamole combinations did not show synergism as inhibitors of lymphocyte activation. It is concluded that these drugs has dissimilar actions on the lymphocyte and that dipyridamole will not serve as an aspirin-sparing drug in anti-inflammatory therapy.

Animals↗
PubMed1980

An evaluation of cusum analysis in asthma.

It has been claimed that cusum analysis may be a clearer way of expressing trends in serial peak flow (PF) measurements in asthma than visual inspection of peak flow charts. To assess this we have applied cusum analysis to serial PF measurements in patients receiving various forms of treatment for airflow obstruction. We found that cusum analysis usually gave no additional advantage over simple graphs of PF data. In cases in which trends were apparent only by cusum analysis, their dimension was such that they were unlikely to form the basis of decisions on treatment.

Asthma↗
PubMed1980

Somatostatin-like immunoreactivity in the retina.

A substance with somatostatin-like immunoreactivity (SLI) was found in extracts of goldfish, frog, and cow retina. Dilutions of retinal SLI parallel the standard curve for radioimmunoassay obtained with synthetic somatostatin. Chromatography of goldfish retinal extract on Sephadex G-50 revealed two peaks of SLI, one that coeluted with synthetic somatostatin and one that eluted as a larger molecule. Incubation in 8 M urea did not alter the chromatographic pattern of the extract. SLI was present in extracts of frog optic nerve and tectum in concentrations higher than those found in the retina. In goldfish retina, SLI was localized by immunofluorescence to four types of processes in the inner plexiform layer; their origins could be traced to three classes of SLI-containing cell bodies in the proximal row of the inner nuclear layer and one class in the ganglion cell layer. Localization of SLI to cells of the retina and characterizations of the molecular forms of retinal SLI suggest that the retina is a promising model system for studies on the potential neurotransmitter function of somatostatin.

Animals↗
PubMed1980

Anti-allergy properties of PRD-92 Ea in guinea pig and rat.

The effects of PRD-92 Ea were examined on the increased plasma protein extravasation in the skin of guinea pig and rat elicited by specific antigens and spasmogenic mediators. PRD-92 Ea was found to be a potent inhibitor of rat PCA reactions when administered intradermally, intravenously or orally. This compound did not antagonize the local inflammatory responses of histamine, bradykinin or 5HT. This implies that in vivo PRD-92 Ea acts predominantly as an anti-allergy agent rather than a spasmogen antagonist. At high concentrations PRD-92 Ea directly increased vascular permeability when injected intradermally (greater than 250 micrograms/site) or administered by aerosol into the lung (greater than 10%). The importance of investigating such direct irritant actions of similar new drugs is discussed.

Administration, Oral↗
PubMed1979

Prostaglandin and thromboxane production by human and guinea-pig macrophages and leucocytes.

The ability of partially purified human and guinea-pig haematogenous cell populations, when cultured in vitro, to metabolise arachidonic acid (AA) has been studied. Supernatants from 24 hour cell culture have been subjected to analysis for products of AA metabolism by gas chromatography with electron-capture detection. The cell types studied were human peripheral blood monocytes (both glass adherent and non-adherent), neutrophils, eosinophils and leukemia leucocytes; thoracic duct lymphocytes and lung alveolar macrophages. From the guinea-pig, induced and non-induced macrophage or neutrophil enriched peritoneal exudate populations, lymph node cells, peritoneal eosinophils and peripheral blood platelets were examined. Supernatants were assayed for the presence of PGE2, PGD2, PGF2 alpha, TXB2 and 6-keto-PGF1 alpha. In all types studied PGE2 and TXB2 were the major products formed. The identification of PGE2 and TXB2 was confirmed by GC/MS with multiple ion monitoring. The results have been compared with other reports and their possible significance discussed in relation to the proposed role of prostaglandins as mediators and modulators in immunopathology.

Animals↗
PubMed1978

Anti-inflammatory drug actions on allergic responses in guinea-pig skin.

Five non-steroidal anti-inflammatory drugs (indomethacin, naproxen, meclofenamic acid, feprazone and phenylbutazone: NSAIDs) and three glucocorticosteroids (dexamethasone, hydrocortisone and prednisolone) have been tested as local inhibitors of increased vascular permeability in guinea-pig skin. Lesions were induced by histamine or by antigen to evoke type I (passive cutaneous anaphylaxis), type III (reverse passive Arthus) and type IV (delayed hypersensitivity) allergic reactions. NSAIDs and glucocorticosteroids caused either weak, inconsistent inhibition or slight, high-dose inhibition of the response to histamine. None of the drugs tested showed significant inhibition of the type IV response. The NSAIDs caused dose-related inhibition of both type I and type III responses whereas glucocorticosteroids were ineffective. Maximum inhibition with the NSAIDs was never greater than 50--60% Feprazone, meclofenamic acid and indomethacin were the most potent inhibitors of histamine, PCA and Arthus responses respectively. The possible significance of the effects of these anti-inflammatory agents on vascular permeability is discussed.

Animals↗
PubMed1978

Prostaglandins as regulators in cellular immunity.

Guinea-pig peritoneal macrophages have been shown to generate substantial concentrations of E-type prostaglandins during culture in vitro. Partially purified lymphokine preparations stimulate PGE production by macrophages. Exogenous PGE1 and PGE2 are potent inhibitors of lymphocyte activation and secretion of lymphokines causing lymphocyte mitogenesis and macrophage migration inhibition. Also indomethacin augments the secretion of these lymphokines in vitro. It is therefore suggested that production of PGE by macrophages provides a physiological mechanism for the regulation of lymphocyte activation in reactions of delayed hypersensitivity.

Animals↗
PubMed1978

The effect of luteinizing hormone releasing hormone (LRH) on pituitary gonadotropins in male homosexuals.

Basal serum LH and FSH values were found to be within normal limits in 9 homosexual men. The mean LH and FSH responses following the intravenous administration of 100 microgram of LRH were not significantly different from that of heterosexual controls. In addition, the mean basal plasma serum testosterone was similar in the two groups. There is thus no definite implication of endocrine factors in the genesis of male homosexuality.

Adult↗
PubMed1978

Prostaglandins and lymphokines in inflammation.

It is suggested that the inflammatory process in rheumatoid arthritis (RA) results from activation of small lymphocytes to produce lymphokines, whose biological properties are appropriate to a mediator of chronic inflammation. Since prostaglandins (PGs) and allied products of arachidonic acid metabolism have properties pertinent to chronic inflammation, these compounds can also be regarded as potential mediators of chronic inflammation, a viewpoint supported by the capacity of steroids and non-steroidal anti-inflammatory drugs (NSAIDs) to suppress PG formation. Certain observations are inconsistent with PGs fulfilling this role. These anomalies may be resolved by considering PGE2 formation by macrophages to be a device for regulating lymphocyte activation. A defect of lymphocyte reactivity to PGE2 provides a basis for chronicity and has been demonstrated in multiple sclerosis (MS). Alternatively, should lymphocytes in lesions of RA be susceptible to PGE2 inhibition, one consequence of NSAID treatment may be exacerbation of joint destruction.

Animals↗
PubMed1978

Prostaglandin production in arthritis.

Inflammatory cell populations from synovial effusions or synovial villi in rheumatoid arthritis have been cultured in vitro. Prostaglandin productive capacity, measured by radioimmunoassay, showed the polymorphonuclear leucocyte rich populations from synovial effusions to be poor sources of PGE production whereas the synovial fragments produced substantial amounts of PGE activity. It is suggested that the macrophage is the major source of local prostaglandin formation both in gout and rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1978

A comparison of the hematogenous cell infiltrate evoked by lymphokine injection with that of delayed hypersensitivity reactions.

Lymphokine preparations of high potency obtained by in vitro assay were employed in vivo to determine whether they could produce inflammatory responses showing a cellular infiltrate that qualitatively or quantitatively resembled responses of delayed hypersensitivity. Hematogenous cell infiltrates in guinea pig skin were characterized in terms of the number and types of participating cells following intradermal injection of either lymphokines or an antigen (PPD) to which the animals exhibited delayed hypersensitivity. The dose of lymphokine or PPD per skin test site was selected on the basis of comparable ability to enhance vascular permeability. Delayed hypersensitivity responses showed, as expected, a persistent mononuclear cell exudate both in dermis and subcutis, but most notable in the dermis, during the 24 hours following antigen injection. In contrast, the response to lymphokine over the same period was characteristically neutrophilic and principally in the subcutis. There was no pronounced mononuclear cell infiltrate at any time throughout the reaction to lymphokine. It is concluded that preformed lymphokine produces a pattern of increased vascular permeability appropriate to a mediator of delayed hypersensitivity reactions, provided there is sustained secretion of this material. The ability of lymphokine to cause carbon labeling of dermal capillaries is also pertinent to a mediator of delayed hypersensitivity. The absence of significant mononuclear cell accumulation suggests that the in vitro chemotactic activity of lymphokine toward mononuclear cells may be more important for retention of mononuclear cells in the extravascular connective tissue space than for their selective accumulation.

Animals↗
PubMed1977

Carbohydrate metabolism in motor neurone disease.

Eight patients with classical motor neurone disease, and eight control patients with neurological disease and matched for degree of wasting, were studied. Both groups had abnormal glucose tolerance, but the patients with motor neurone disease had a significantly lower insulin response both to oral glucose loading and to intravenous tolbutamide. These results suggest that in patients with motor neurone disease there is an impaired synthesis or release of insulin due to islet cell damage. Blood pyruvate and lactate, and cerebrospinal fluid pyruvate, lactate, and citrate, did not differ significantly from the control group. Blood citrate levels were significantly higher in patients with motor neurone disease compared with the controls. Triglyceride levels were raised in patients with motor neurone disease compared to the control patients. This may be secondary to the increased citrate levels.

Adult↗
PubMed1977

Prostaglandins and the lung.

Evidence exists implicating prostaglandins as mediators of asthma and of chronic inflammation in the lung. In addition to their spasmogenic effects, PGs are also potent in vitro regulators of mediator secretion by basophils, mast cells, or lymphocytes. These regulatory effects of E-series PGs may have considerable significance in drug design and evaluation in both asthma and chronic inflammation.

Asthma↗