Search PubMed⌕ Search

Biomedical subjects

A Garner

Publications and source records attributed to A Garner.

At least 163 records · Page 9Linked to original sources
PubMed1983

Radiation-induced generation and properties of lipid hydroperoxide in liposomes.

The generation of hydroxyl free radicals in 60Co gamma-irradiation of a dilute aqueous suspension of phosphatidyl choline liposomes, resulted in the rapid accumulation of lipid hydroperoxides (linearly with time), but only small concentrations of malondialdehyde. Incubation of the irradiated liposomes with ferric chloride was found to significantly increase the malondialdehyde, and evidence is presented that this resulted from iron catalysed decomposition of the lipid hydroperoxide. This suggests a role for free iron or iron chelates in the propagation of lipid peroxidation stimulated by other systems.

Air↗
PubMed1983

Prenatal diagnosis of oculocutaneous albinism by electron microscopy of fetal skin.

Oculocutaneous albinism was diagnosed prenatally by electron microscopic examination of fetal skin samples taken during fetoscopy at 20 weeks of gestation. Melanosome development in hair bulb melanocytes progressed no further than stage II, indicating a lack of melanin synthesis. In 4 age-matched control fetuses, numerous stage IV melanosomes, signifying active melanin synthesis, were identified. The diagnosis was confirmed after the pregnancy was terminated at 22 weeks. Examination of the fetal eye showed absence of pigment in the retinal epithelium and uvea at a stage when ocular melanogenesis would normally be active. This study shows that oculocutaneous albinism can be detected in the second trimester using similar techniques to those employed in the prenatal diagnosis of epidermolysis bullosa and ichthyosis.

Adult↗
PubMed1983

Lymphoproliferative disorders of the orbit: an immunological approach to diagnosis and pathogenesis.

A prospective immunological study of patients with proptosis due to intraorbital lesions composed largely or exclusively of lymphoid tissue indicates that the use of antisera to specific heavy and light chain antibody components can be helpful in distinguishing between polyclonal and truly neoplastic monoclonal disorders. On the basis of combined histological and immunological information it is possible to delineate 4 categories of patient: those with unequivocal chronic inflammation, those with a virtually pure lymphoproliferative lesion and a polyclonal profile, and those with a monoclonal lymphomatous disorder which may be histologically comparable to the previous category or, in a fourth group, be unmistakably malignant on cytological grounds. The first of these groups will normally respond to corticosteroid treatment, but the others, including the polyclonal lymphoproliferative masses, need radiotherapy. The finding of reduced numbers of circulating T cells in the presence of low plasma levels of IgA, and of autoantibodies in the serum of a third of the patients, could mean that individuals developing lymphoproliferative lesions in the orbit, whether hyperplastic or neoplastic, are partially immunodeficient.

Adult↗
PubMed1983

Treatment of idiopathic inflammatory orbital pseudotumours by radiotherapy.

Radiotherapy offers an alternative to steroid therapy for idiopathic inflammatory orbital pseudotumours. Twenty-four orbits were treated with radiotherapy, of which 75% responded adequately. There were no significant complications and no recurrences during the average follow-up time of 22.3 months (1-50 months). Biopsy, CT scanning, and steroid response of orbital pseudotumours can be helpful in predicting the response to radiotherapy. An adequate response to radiotherapy can be predicted if lymphocytes with germinal centres are present in biopsy specimens. Polymorphonuclear leucocytes and eosinophils suggest a poor response to radiotherapy. Small, discrete, inflammatory masses respond better than large diffuse masses. Pseudotumours initially responding to steroids were likely to respond to radiotherapy.

Adolescent↗
PubMed1983

Gastric and duodenal HCO3- transport in vivo: influence of prostaglandins.

Gastric and duodenal HCO3- transport was compared in the same mammalian species (cat) in vivo. The most appropriate technique for detecting HCO3- in the lumen of the stomach was measurement of pH and CO2 tension, whereas in the duodenum it was pH-stat titration. For experiments on gastric HCO3- transport, conscious cats prepared with vagally denervated fundic pouches were used; for those on duodenal transport anesthetized animals with in situ perfused segments were studied. When expressed in terms of gross surface area, basal HCO3- output was six times greater in the duodenum than in the stomach (approximately 1.5 cf. approximately 0.25 mumol X cm-2 X 15 min-1). topical application of 16,16-dimethyl prostaglandin E2 (dmPGE2) to duodenal mucosa caused a concentration-dependent increase in HCO3- output and transmucosal electrical potential difference (PD) over the range 0.01-1.0 microgram X ml-1. PGE2 was approximately 200 times less potent than dmPGE2 as a stimulant of duodenal HCO3- transport. Increases in the rate of luminal HCO3- output following application of dmPGE2 were considerably less in the stomach compared with the duodenum (approximately 50% cf. approximately 1,000% at 1 microgram X ml-1). Intravenous dmPGE2 (1 microgram X kg-1 X h-1) had no effect on either gastric or duodenal HCO3- outputs. Indomethacin (5 mg X kg-1 iv) inhibited duodenal HCO3- output by approximately 50% and reduced PD but did not influence gastric HCO3- output. We propose that in the cat duodenum in vivo local prostaglandins regulate HCO3- transport, but in the cat stomach in vivo they have a less important role.

Animals↗
PubMed1982

A simple method for measuring thickness of the mucus gel layer adherent to rat, frog and human gastric mucosa: influence of feeding, prostaglandin, N-acetylcysteine and other agents.

1. A technique has been developed for measuring thickness of the gastric surface mucus gel layer. Mucosal sections (1.6 mm) were cut from frog and rat stomach and human antrum, mounted transversely and viewed by an inverse microscope (x 200 magnification) under dark field illumination or phase contrast. The mucus layer was readily distinguishable and its dimensions could be recorded by means of an eyepiece graticule. 2. Mean mucus gel thickness in rat, frog was 73, 76, 55 and 192 micrometer respectively. However, there was variation in the average thickness of the gel layer between individual mucosae from the same species (up to twofold). Mucus thickness between adjacent regions of the same mucosal section also varied markedly (up to tenfold). 3. Topical administration of 16,16-dimethylprostaglandin E2 by oral intubation caused a significant increase in thickness in both rat and frog at doses of 5 microgram/ml and 0.5 microgram/ml respectively. Feeding and exposure of the mucosa to N-acetylcysteine (10-20%, w/v) produced variable effects whereas pepsin (1 mg/ml) caused a marked reduction in thickness of the surface gel layer in both rat and frog. 4. The technique provides a rapid and simple method for determining gastrointestinal mucus thickness in relation to mucosal morphology. It is ideally suited for studying the control of mucus secretion and effect of drugs.

16,16-Dimethylprostaglandin E2↗
PubMed1982

A low-molecular-weight angiogenic factor in cat retina.

A low-molecular-weight angiogenic factor has been isolated from healthy adult cat retinas. The factor, which has been purified by diethylaminoethyl (DEAE) cellulose chromatography and affinity chromatography, stimulates neovascularisation of the chick chorioallantoic membrane and has a number of properties similar to those previously described for a tumour factor. The finding of an angiogenic factor in healthy retina and its relationship to previously described inhibitors of angiogenesis is discussed.

Angiogenesis Inducing Agents↗
PubMed1982

Corneal graft rejection: a new rabbit model and cyclosporin-A.

In order to test the efficacy of topically applied cyclosporin-A in preventing corneal allograft rejection, existing rabbit models were modified to produce a new model in which the allograft reaction could be consistently initiated solely as a result of corneal transfer without any additional means of sensitisation. With this model, which reflects clinical corneal grafting more closely than many previous models, cyclosporin-A 1% drops applied to the recipient eye 5 times daily for 4 weeks inhibited corneal graft rejection. When cyclosporin-A 1% drops were applied to corneal allografts for 13 weeks, 44% of grafts remained clear 180 days after transplantation. No side effects were observed that could be attributed to topically applied cyclosporin-A.

Animals↗
PubMed1982

Tapetoretinal degeneration in the cerebro-hepato-renal (Zellweger's) syndrome.

Electrophysiological and histopathological study of a baby suffering from Zellweger's syndrome and presenting progressive retinal dysfunction showed this to be related to degenerative changes in the photoreceptor cells and pigment epithelium and to defective myelination of the optic nerve. Disturbances of bile acid and lysine metabolism were also demonstrated, lending support to the concept that Zellweger's syndrome is attributable to a widespread inadequacy of intracellular oxidative function.

Brain Diseases↗
PubMed1982

Gastric and duodenal HCO3- transport in vitro: effects of hormones and local transmitters.

Luminal application of acid was recently shown to stimulate surface epithelial HCO3(-) transport in stomach and duodenum. Effects of some potential transmitters of this response were therefore studied in amphibian gastric fundic and proximal duodenal mucosa in vitro. Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Stimulation by glucagon, but not by prostaglandin E2 (PGE2, 10(-6) M), required Cl- in the luminal solution and was prevented by furosemide (10(-3) M). This suggests that glucagon may affect HCO3(-)-Cl- exchange at the luminal membrane while transport stimulated by prostaglandins may be electrogenic. Stimulatory effects of glucagon and PGE2 were also additive. Gastric HCO3- transport, studied in tissues after inhibition of H+ secretion by histamine H2-antagonists, clearly differed from duodenum in that noradrenaline and GIP were inhibitory and DBcAMP was without effect. Stimulation of gastric HCO3- transport was observed with glucagon (10(-8) M), natural cholecystokinin (CCK, 10(-8) M), and CCK octapeptide (10(-7) M), CCK preparations had no effect in the duodenum. Although tested over a wide range of concentrations, no effect on either duodenal or gastric HCO3- transport was observed with histamine, pentagastrin, tetragastrin, urogastrone, ACTH, bombesin, motilin, secretin, serotonin, somatostatin, substance P, or vasoactive intestinal peptide.

Animals↗
PubMed1982

Gastroduodenal HCO3(-) transport: characteristics and proposed role in acidity regulation and mucosal protection.

Gastric HCO3(-) transport (basal) studied in isolated amphibian mucosa and mammalian stomach in vivo amounts to 2-10% of maximal H+ secretion. Duodenal mucosa, devoid of Brunner's glands, transports HCO3(-) at a greater rate (per unit surface area) than either stomach or jejunum in vitro and in vivo. Gastric (but not duodenal) HCO3(-) transport is stimulated by dibutyryl cGMP, carbachol, and cholecystokinin and duodenal (but not gastric) transport by dibutyryl cAMP and gastric inhibitory peptide. Glucagon and E- and F-type prostaglandins stimulate, whereas histamine, gastrin, and secretin are without effect in both stomach and duodenum. Gastric transport very probably occurs by Cl--HCO3(-) exchange at the luminal membranes of the surface epithelial cells. In addition to this mechanism, the duodenum also transports HCO3(-) electrogenically. Lowering the luminal pH increases transport in both the stomach and duodenum. This response, probably mediated via both local production of prostaglandins and tissue-specific humoral agents, may be important in mucosal protection against acid. Metabolism-dependent transport of HCO3(-), stimulated by acid, seems quantitatively sufficient to account for all of the duodenal and most of the gastric mucosa's ability to remove luminal acid.

Acid-Base Equilibrium↗
PubMed1982

Surface epithelial HCO3(-) transport by mammalian duodenum in vivo.

Duodenal surface epithelial transport of HCO3(-) was measured by direct titration in anesthetized animals. Alkalinization of the lumen occurred in all species, although basal rates varied considerably: rats (approximately 10), cats (approximately 15), pigs (approximately 25), dogs (approximately 25), guinea pigs (approximately 40), and rabbits (approximately 170 mueq.cm-1.h-1). In cats duodenum transported HCO3(-) at a greater basal rate than jejunum (approximately 5 mueq.cm-2.h-1) and developed a higher transmucosal electrical potential difference (PD, lumen negative). Luminal application of 10 mM HCl for 5 min produced a sustained increase in the rate of duodenal HCO3(-) transport that was accompanied by a rise in appearance of E-like prostaglandin immunoreactivity in the lumen and a decrease in DNA release. In cats pretreated with indomethacin (10 mg/kg iv), acid caused only a transient increase in HCO3(-) transport. Exogenous prostaglandin E2 (1-12 microM, luminal) increased basal HCO3(-) transport in cats, rats, and dogs but had no effect on this transport in guinea pigs and rabbits. However, prostaglandin E2 increased HCO3(-) transport and PD in guinea pigs pretreated with inhibitors of tissue cyclooxygenase activity (indomethacin or aspirin) or gastric H+ secretion (cimetidine). Thus the continuous exposure of the duodenum of herbivores to HCl discharged from the stomach may itself stimulate HCO3(-) transport via an increase in endogenous prostaglandin levels and render exogenous prostaglandins ineffective. Secretin (1-15 CU/kg iv) was without effect in both cats and guinea pigs. In guinea pigs, intravenous glucagon (120-360 micrograms.kg-1.h-1) or gastric inhibitory peptide (5 micrograms/kg) both increased HCO3(-) transport but not PD. Hence, prostaglandin-stimulated and hormone-stimulated mechanisms of HCO3(-) transport probably occur in mammalian duodenum as found previously in the isolated amphibian duodenum. The results suggest that epithelial HCO3(-) transport is a major mechanism of acid disposal, and thus mucosal protection, in mammalian duodenum under the control of hormones and endogenous prostaglandins.

Animals↗
PubMed1982

Studies of acid and alkaline secretion by rabbit gastric fundus in vitro: effect of low concentrations of sodium taurocholate.

The effect of low concentrations of sodium taurocholate on the secretory and electrical activity of isolated rabbit fundic mucosa has been studied. Fundic mucosa maintained a stable potential difference (10.2 +/- 0.6 mV, n = 70) and electrical resistance (85 +/- 6 omega . cm-2, n = 70) and the majority of preparations spontaneously secreted acid (2.85 +/- 0.31 mumol . cm-2 . h-1, n = 70). Histamine (10(-5) and 10(-4) M) and carbachol (10-4 M) increased acid secretion, and these responses were prevented by cimetidine (10(-3) M) and atropine (10(-5) M), respectively. Mucosal application of taurocholate (10(-4) and 10(-3) M) increased net acidity without altering electrical activity. This response exhibited tachyphylaxis, was not altered by pretreating the tissues with cimetidine (10(-3) M), atropine (10(-5) M), or somatostatin (10(-6) M), and occurred in mucosas maximally stimulated by histamine. Sodium thiocyanate (6 x 10(-2) M, serosal side) inhibited spontaneous acid secretion revealing net alkalinization (0.83 +/- 0.05 mumol . cm-2 . h-1, n = 58) that was completely inhibited by anoxia and potassium cyanide (10(-2) M) and markedly reduced by 2,4-dinitrophenol (10(-4) M). Some fundic preparations spontaneously secreted alkali (1.20 +/- 0.20 mumol . cm-2 . h-1, n = 6) after an initial period of acid secretion. Mucosal-side taurocholate (10(-3) M) converted net alkali secretion by both thiocyanate-treated and spontaneously-secreting mucosas to acid secretion without affecting electrical conductance. These secretory responses may be implicated in the pathogenesis of gastric mucosal damage by bile salts.

Animals↗