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Biomedical subjects

J M Boyle

Publications and source records attributed to J M Boyle.

At least 91 records · Page 5Linked to original sources
PubMed1981

Severe aortic stenosis in a patient with recurrent gastrointestinal bleeding: replacement of the aortic valve with a porcine xenograft.

Patients with aortic stenosis are subject to recurrent episodes of gastrointestinal bleeding of uncertain cause. How such patients should be handled when aortic valve replacement is required is not established. This report deals with such a patient who underwent successful aortic valve replacement with a porcine xenograft without anticoagulation. The patient has had no recurrent gastrointestinal bleeding since the valve replacement. The use of the now widely available porcine xenograft for aortic valve replacement avoids the need for anticoagulants in patients with a history of recurrent gastrointestinal bleeding. This case and limited data from the medical literature suggest that recurrent gastrointestinal bleeding after aortic valve replacement may be uncommon.

Aortic Valve Stenosis↗
PubMed1979

Rescue of marker phenotypes: effects of BUdR sensitization, hypoxia and high LET.

The survival curve of colony-forming ability of Chinese hamster wg3h cells has been compared with the dose-response curve for the expression of an active thymidine kinase (TK) gene from these cells. The TK+ phenotype was measured by hybrid colony formation after fusion of wg3h (TK+) cells with Chinese hamster A23 (TK-) cells. The TK+ survival data fitted a multi-target curve up to 3 krad of 137 Cs irradiation, when a highly resistant fraction of hybrid colonies was seen at about 1 per cent survival. The Do of TK+ survival for the multi-target region was 3.1-4.0 times greater, than that of wg3h survival, even when the Do for cell survival varied between 136 and 545 rad by 14 MeV neutrons and hypoxia respectively. This parallel modification of cell and TK+ sensitivities suggests that the lesions causing cell inactivation are of the same type as those that cause marker inactivation. Using 14 MeV neutron data the approximate target size for TK inactivation was calculated to be 0.54-0.91 per cent of the DNA content of the cell (or about one-fifth to one-tenth of a chromosome). The data support the idea that marker inactivation results primarily from damage occurring outside the marker gene. BUdR labelling of wg3h cells before irradiation caused slight toxicity (30 per cent reduction in plating efficiency) and a twofold increase in cell sensitivity. However, the sensitivity of the TK+ phenotype increases by only 30 per cent. The increased cell sensitivity thus appeared to result from synergism between increased sensitivity of DNA to strand breakage and metabolic toxicity, the latter being largely overcome by fusion with normal cells.

Animals↗
PubMed1977

Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels.

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.

Gastric Juice↗
PubMed1977

Rescue of marker phenotypes mediated by somatic cell hybridization.

The effect of irradiation prior to virus-induced cell fusion on the frequency of hybrid production has been measured as a function of radiation dose. The Chinese hamster line wg3h (HGPRT-) was crossed with the TK- mutants; Chinese hamster A23 or mouse 3T34E, and hybrids were selected in HAT medium. Irradiation of one (marker rescue) or both (mutual rescue) partners before fusion yielded qualitatively different results. After X-irradiation marker rescue curves were of single-hit type, with D0 values about five-fold greater than the irradiated parent cell. Mutual rescue curves were of the multi-hit type, with zero-dose extrapolation value (n) greater than that of the more resistant partner, but no significant alteration in D0. Qualitatively similar results were obtained after U.V.-irradiation, but the probability of rescue per surviving parent cell was higher after U.V. than after X-rays. With both forms of radiation, reciprocal marker rescue curves were not significantly different. Control experiments showed that mutual rescue was not an artefact either of sensitization of parent cells due to TK- or HGPRT- mutations, or of the enhancement of recovery by feeder layers resulting from high-density mutant populations killed with graded radiation doses and HAT selection. Analysis of heterokaryon frequencies within 18 hours of fusion demonstrated that radiation doses up to four lethal hits, given to one or both parents of the cross wg3h x A23, did not increase heterokaryon formation.

Cell Fusion↗
PubMed1977

Characteristics of dimer formation, excision and DNA strand growth in Yoshida sensitive and resistant cells after ultraviolet irradiation.

The sedimentation properties of the nascent DNA of Yoshida sarcoma cells, sensitive and resistant to methylene dimethane sulphonate and cross-resistant to U.V. light, have been studied after irradiation with U.V. light at 11 and 22J/m2. It has been shown that the DNA formed immediately after irradiation with 11J/m2 is some eight to nine times longer than the calculated inter--dimer distance in both cell-lines. Differences were, however, observed between the two cell-lines, in that the absence of excision of dimers in the sensitive cells was accompanied by the formation of a DNA component of low molecular weight, whereas excision in the resistant line was not so accompanied. There are some similarities between the Yoshida tumour line sensitive to methylene dimethane sulphonate and the U.V.-sensitive line of Xeroderma pigmentosum.

Animals↗
PubMed1976

Biological and biochemical characterisation of purine analogue resistant clones of V79 Chinese hamster cells.

Purine analogue resistant clones have been selected from the closely related Chinese hamster lines V79A and V79S. Clones were of either spontaneous origin or induced by EMS or ultraviolet light. The majority of clones selected in 8-azaguanine showed stable cross resistance to 6-thioguanine. Clones derived from V79A and selected for 6-thioguanine resistance were cross resistant to 8-azaguanine: however a group of 6-thioguanine resistant mutants selected from V79S cells were 8-azaguanine sensitive. All clones except two were unable to grow in HAT medium. The two exceptions were 8-azaguanine resistant, showed partial sensitivity to 6-thioguanine, and also differed in other biochemical characteristics. HGPRT activity was measurable in extracts of all clones under standard conditions. In many clones, HGPRT activity increased as the hypoxanthine concentration was reduced. Whole cell uptake of [14C] hypoxanthine was low in all cases examined and was not modified by incubation in the presence of amethopterin. The heat sensitivity and electrophoretic mobility of HGPRT in extracts of some clones was compared to that in wild-type extracts. All clones tested except one, which was consistently HAT positive, showed enhanced heat sensitivity and reduced electrophoretic mobility. None of the mutants reverted spontaneously at detectable frequency but some could be induced to revert by EMS. The presence of measurable enzyme with altered properties in all clones suggests that these revertable drug resistant clones represent missense mutants.

Animals↗
PubMed1976

Factors affecting the growth of Chinese hamster cells in HAT selection media.

Factors affecting the efficiency of selection of "revertants" of salvage pathway mutants in media containing amethopterin have been examined. Our V79 Chinese hamster cell line was found to require a significantly higher level of thymidine for optimal growth in such media than has been reported for other cell lines. Hypoxanthine (but not glycine) was also required for reversal of amethopterin toxicity, but levels did not differ significantly from those reported elsewhere. Growth in HAT was also dependent on plating density and serum batch. Our modification (VHAT) was compared with published HAT recipies in back selection reconstruction experiments. A sharp fall in EOR (efficiency of recovery) of wild type cells from mixtures with mutants at plating densities greater than 3500 cells/cm2 (10(5) cells/6 cm dish) was observed for VHAT. EOR with other HAT recipes was lower still, and was affected also by the particular mutant used in the mixture. EMS induced "revertants" were isolated from three 8AZr mutants by plating in VHAT. All revertants were however amethopterin resistant, they were also 8AZ resistant and the mobility of residual HGPRT (as measured by polyacrylamide gel electrophoresis) was similar to that of their 8AZr parents i.e. dissimilar from that in wild type. The modal chromosome number of V79 wild type cells was 21. No significant deviation from this mode was detected in any of the mutant lines examined. The data indicate that the recovery of colonies in HAT from 8AZr mutants does not necessarily indicate that a back mutation in the structural gene for HGPRT has occurred. Thus, the frequency of HAT+ colonies cannot be taken as a direct indication of reversion frequencies.

Animals↗
PubMed1974

Sequence of events mediating the effect of cholera toxin on rat thymocytes.

We have found that in rat thymocytes binding of [(125)I]choleragen is followed by cellular accumulation of cyclic 3',5'-AMP which, in turn, is followed by stimulation of amino acid transport. Binding of cholera toxin was complete by 30 min and remained constant for the subsequent 150 min. After stimulation by choleragen, cellular cyclic 3',5'-AMP became maximal by 30 min, after which it declined steadily so that by 90 min of incubation, cellular cyclic nucleotide levels were only 20% of those seen at 30 min. Stimulation of amino acid transport, although detectable by 15 min, did not become maximal until 120 min (by which time cellular cyclic 3',5'-AMP had decreased by more than 80%). We have also used this system to delineate the step at which various pharmacologic agents and hormones act to alter the sequence of events mediating the response of rat thymocytes to cholera toxin. The ability of cycloheximide to abolish choleragen-stimulated amino acid influx without reducing [(125)I]choleragen binding or cellular cyclic 3',5'-AMP suggests that cyclic nucleotide stimulation of amino acid transport includes a step involving protein synthesis.

Aminoisobutyric Acids↗