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Biomedical subjects

D Allan

Publications and source records attributed to D Allan.

At least 109 records · Page 6Linked to original sources
PubMed1984

Senile atrophy of the human lacrimal gland: the contribution of chronic inflammatory disease.

Histological examination of 99 human lacrimal glands showed a relationship between atrophy of the secretory acini and secretory duct obstruction, ascending periductal fibrosis, and obliteration of the adjacent blood vessels caused by lymphocytic and polymorphonuclear inflammation. Investigation of the subgroups of the B lymphocytic series by immunohistochemistry did not show any statistical change with age, sex, fibrosis, or lymphocytic inflammation. The concept of senile atrophy occurring as a result of senescent involution of the lacrimal gland is challenged on the basis of the histological findings.

Adolescent↗
PubMed1983

The fatty acid composition of 1,2-diacylglycerol and polyphosphoinositides from human erythrocyte membranes.

The fatty acid compositions of 1,2-diacylglycerol and polyphosphoinositides have been determined in human erythrocyte membranes that have been incubated in the presence or in the absence of Ca2+. The results show that the diacylglycerol that is formed in Ca2+-treated membranes has a fatty acid composition closely similar to that of the inositides, consistent with previous indications that Ca2+ stimulates the activity of a polyphosphoinositide phosphodiesterase in the membranes. In contrast with some previous results, it appears that these plasma-membrane inositides and their derived diacylglycerols are rich in stearic acid and arachidonic acid.

Calcium↗
PubMed1983

Limited breakdown of cytoskeletal proteins by an endogenous protease controls Ca2+-induced membrane fusion events in chicken erythrocytes.

The profound morphological changes which follow the treatment of chicken erythrocytes with the ionophore A23187 and Ca2+ are associated with a concomitant breakdown of certain membrane-associated proteins including alpha-spectrin, goblin and microtubule-associated proteins (MAPS) which undergo a limited proteolysis to give large, well-defined fragments. The Ca2+-sensitive protease responsible for these changes appears to be present in the soluble fraction of the cells. Treatment with TLCK or iodoacetamide inhibits both the major morphological changes and the proteolytic events but these agents do not prevent the dissociation of microtubules or the activation of endogenous sphingomyelinase which occur in cells with raised levels of intracellular Ca2+. It is suggested that the sphingomyelinase is activated as a consequence of a Ca2+-induced loss of phospholipid asymmetry in the plasma membrane.

Animals↗
PubMed1983

Effects of valinomycin, A23187 and repetitive sickling on irreversible sickle cell formation.

The formation of irreversibly sickled red cells has been studied by inducing cell shrinkage, ion loss, Ca2+ accumulation and membrane loss either singly or in combination. Valinomycin, A23187+Ca2+ or hypertonic saline caused shrinkage of the cells with retention of the sickled form after reoxygenation. The cells which had retained the sickle shape after treatment with the ionophores and reoxygenation remained sickled after exposure to hypotonic media. These cells were also osmotically insensitive. Retention of the sickled form was not dependent upon membrane loss as induced by repeated sickle-unsickle cycles or by A23187+Ca2+ treatment although repetitive sickling did give rise to shorter, stubbier spicules. Sickled red cells, either the endogenous irreversibly sickled cells or the sickled cells induced by deoxygenation, did not lose membrane by vesicle or spicule loss as normal cells or oxygenated sickle red cells do. Cell water loss without cell membrane loss appears to be an important factor in the irreversible sickling of red cells.

Anemia, Sickle Cell↗
PubMed1983

Common causes of blindness and visual handicap in the west of Scotland.

An analysis of blind registration forms was made to determine the commonest causes of blindness in the west of Scotland. It was found that the leading causes of blindness in order of frequency of incidence were senile macular degeneration, glaucoma, cataract, diabetic retinopathy, and myopic degeneration. Diabetic retinopathy was the leading cause of blindness among persons of working age.

Adolescent↗
PubMed1983

Some morphological consequences of uncoupling the lipid bilayer from the plasma membrane skeleton in intact erythrocytes.

Various procedures which achieve the local separation of the lipid bilayer portion of the plasma membrane from the membrane skeleton cause a destabilisation of the lamellar form of the bilayer and release of bilayer microvesicles containing encapsulated cytosol. These procedures can give us information concerning the composition of the bilayer, the nature of its interaction with the membrane skeleton and the mechanism of the membrane fusion events which are involved in vesiculation. Bilayer microvesicles appear to retain the phospholipid orientation of the original cells, suggesting that spectrin is not essential for the maintenance of lipid asymmetry.

Anemia, Sickle Cell↗
PubMed1982

Microvesiculation and sphingomyelinase activation in chicken erythrocytes treated with ionophore A23187 and Ca2+.

Treatment of chicken erythrocytes with ionophore A23187 and Ca2+ leads to the disappearance of the marginal band of microtubules and to a release of the constraints which normally maintain the nucleus in a central position in the cells. The consequent close apposition of the nucleus to the plasma membrane may allow nuclear-plasma membrane fusion to occur and subsequently results in the release of microvesicles from the hybrid surface membrane. The remnant cells are spherical, and have nuclei which appear to be partly exocytosed. Concomitant with these morphological changes, there is a breakdown of 20-30% of the total cell sphingomyelin by an endogenous sphingomyelinase which does not require Ca2+ and which releases phosphorylcholine only into the cell interior. It is suggested that the pool of sphingomyelin which is broken down as a consequence of Ca2+ entry into the cells is present in the nuclear membrane and that it becomes available to the plasma membrane sphingomyelinase as a result of the close apposition of nucleus and plasma membrane induced by Ca2+.

Animals↗
PubMed1982

Immune recognition of Echinococcus granulosus. 1. Parasite-activated, primary transformation by normal murine lymph node cells.

Culture of murine lymph node cells together with living protoscolices of Echinococcus granulosus is described. The presence of the parasite induced potent blastic transformation in lymphocytes of unimmunized mice as indicated by tritiated thymidine incorporation. The response was markedly reduced by killing the parasite immediately prior to culture. No blastogenic activity was detectable in supernatants from living parasites cultured alone. Protoscolices from artificially infected syngeneic mice were effective stimuli, as were protoscolices from naturally infected horse and sheep. Stimulation was not detectably reduced by maintenance of the parasite in vitro for 72 h at 37 degrees C or for 46 days at 4 degrees C prior to culture. It is concluded that unprimed lymphocytes are stimulated to transform by surface contact with a stimulator synthesized, but not secreted, by the parasite. The biological significance of the reaction and its possible contribution to immunosuppression are discussed.

Animals↗
PubMed1982

Colour perception in pseudophakia.

Minor differences in colour perception between pseudophakic, phakic, and spectacle aphakic eyes were identified by the Pickford-Nicholson anomaloscope and the Farnsworth-Munsell 100-hue test. The results suggest that pseudophakic eyes are more sensitive to red and less sensitive to blue than aphakic eyes corrected with spectacles. Spectrophotometer measurements reveal that the Rayner-Pearce posterior chamber intraocular lens used in this study transmits an evenly balanced colour spectrum, whereas an aphakic spectacle lens exhibits significant colour distortion, reducing the red and enhancing the blue transmission. This distortion may possibly be attributed to the increased chromatic aberration in the spectacle lens compared with the intraocular lens.

Aged↗
PubMed1982

A modified procedure for thin-layer chromatography of phospholipids.

We have found that when lipid samples from a variety of tissues are run on EDTA-impregnated plates in a solvent system which contains a reduced amount of acetic acid and water compared with that used by Skipski et al. (1964. Biochem. J. 90: 374-378), there is a clear separation among sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, and phosphatidate. This modified procedure appears to offer significant advantages over the original method described by Skipski et al. particularly for studies of the metabolism of anionic phospholipids.

Animals↗
PubMed1981

Ca2+-induced biochemical changes in human erythrocytes and their relation to microvesiculation.

1. Human erythrocytes were treated with Ca2+ and ionophore A23187 and measurements were made of K+ efflux, polyphosphoinositide breakdown, 1,2-diacylglycerol accumulation, phosphatidate synthesis, changes in membrane polypeptide pattern and release of microvesicles. 2. It was shown that neither transamidase-mediated protein cross-linking, proteolysis of polypeptides 2.1 (ankyrin) or 4.1, nor accumulation of diacylglycerol or phosphatidate appeared to be necessary for microvesiculation to occur. 3. Microvesicles were released only under conditions where KCl efflux leading to cell shrinkage occurred and where polyphosphoinositides were broken down. These circumstances were sufficient to cause microvesiculation only in the presence of increased intracellular concentrations of Ca2+.

Calcimycin↗
PubMed1981

The effects of Ca2+ and Sr2+ on Ca2+-sensitive biochemical changes in human erythrocytes and their membranes.

1. The Ca2+-dependency of K+ efflux, microvesiculation and breakdown of polyphosphoinositides and of ankyrin have been measured in intact human erythrocytes exposed to ionophore A23187 and HEDTA [N'-(2-hydroxyethyl)ethylenediamine NNN'-triacetate]-Ca2+ buffers. Half-maximal responses were observed at pCa values of 6.4, 4.1, 5.0 and 4.8 respectively. 2. The Ca2+ dependencies of K+ efflux and breakdown of polyphosphoinositides and ankyrin measured in erythrocyte ghosts without addition of ionophore showed almost identical values with those seen in whole cells treated with ionophore. 3. We conclude that ionophore A23187 is able to cause rapid equilibration of extracellular and intracellular [Ca2+] in intact cells and that in the presence of a suitable Ca2+ buffer, ionophore A23187 can be used to precisely fix the intracellular concentration of Ca2+ in erythrocytes. 4. The relatively high concentration of Ca2+ required to produce microvesiculation in intact cells may indicate that microvesiculation could be at least partly dependent on a direct interaction of Ca2+ with phospholipid. 5. Results obtained with Sr2+ paralleled those with Ca2+, although higher Sr2+ concentrations were required to achieve the same effects as Ca2+. Mg2+ produced none of the changes seen with Ca2+ or Sr2+.

Ankyrins↗