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Biomedical subjects

J Ivey

Publications and source records attributed to J Ivey.

7 recordsLinked to original sources
PubMed1995

A new probability mapping method to describe the development of atherosclerotic lesions in cholesterol-fed rabbits.

A new probability mapping method was developed to quantify the size and location of lesions near aortic orifices. The precise location of any part of the lesion could be compared between rabbits. Colour photographs of lesions were projected onto a digitizing tablet, and coded as lesion or non-lesion. Next the orifices were warped onto a standard orifice, and then the lesion mapped to maintain the original length and angular location of the lesion from the edge of the orifice. This method, unlike the previously used polar mapping method, excludes neither absent lesions nor ones which surround more than one orifice. In contrast to other probability mapping methods it warps the orifice rather than the artery wall containing the lesion, and so is easier to use for correlation with histological studies. The eventual aim is to use the probability maps as a tool to estimate the age of various positions of the lesion and to identify areas for histological sampling. The method was used to describe the distribution of lesions in 21 rabbits fed a diet with cholesterol levels declining from 0.5% during the first week, to 0.25% during the next two weeks, to 0.125% for weeks 3-10, to 0.1% for weeks 11-24. This feeding protocol produces fatty lesions which are transformed into fibro-fatty and fibrous lesions with time.

Algorithms↗
PubMed1992

Cysteamine protects gastric epithelial cell monolayers against drug induced damage: evidence for direct cellular protection by sulphydryl compounds.

The sulphydryl containing drug cysteamine protects gastric mucosa in vivo against acute injury. It is not known whether this protection includes a direct effect on gastric cells. Using gastric epithelial cell monolayers derived from a well differentiated human cell line, we evaluated whether cysteamine protects against taurocholate or indomethacin induced damage in conditions which completely exclude the influence of vascular, hormonal, and neural factors. The effect of cysteamine on prostaglandin production by monolayer cells in vitro was also assessed. Cysteamine decreased damage brought about by sodium taurocholate and indomethacin by 40% (p less than 0.01) and 50% (p less than 0.01) respectively. The sulphydryl blocker iodoacetamide prevented the protective effect of cysteamine. Pretreatment with indomethacin, which inhibited prostaglandin E2 output by 60%, did not prevent protection by cysteamine; incubation with cysteamine decreased prostaglandin E2 production by cultured cells. We conclude that (i) cysteamine directly protected gastric epithelial cells in vitro (ii) this protection occurred with indomethacin, which interferes with cellular metabolism of prostaglandins, and taurocholate, whose damaging action at neutral pH is unrelated to interference with prostanoid metabolism, (iii) cysteamine protection in vitro is unrelated to endogenous prostaglandins and is probably mediated by endogenous sulphydryl compounds.

Cell Line↗
PubMed1986

Prostaglandin production in cultured gastric mucosal cells: role of cAMP on its modulation.

The effect of cAMP on prostaglandin production may depend on cell types. To clarify the relationship between PG and cAMP, we examined arachidonate's effects on PG synthesis and intracellular cAMP accumulation in monolayers of rat gastric mucosal cells. These cells produced PGE2, PGI2 and thromboxaneA2 (TXA2) in amounts of 316 +/- 18, 100 +/- 7 and 30 +/- 5 pg per 10(5) cells in 10 min, respectively, in response to 10 microM arachidonic acid (AA). The production of these PG, however, leveled off subsequently. Cells initially exposed to AA responded poorly to a subsequent stimulation by AA. AA simultaneously stimulated intracellular cAMP accumulation; this stimulatory effect on cAMP production was abolished by the pretreatment with indomethacin. Nevertheless, the pretreatments with dibutyryl cAMP (0.1-5 mM) did not alter the amount of subsequent AA-induced PGE2 production. Furthermore, the preincubation with 1mM isobutyl methyl xanthine also failed to affect PGE2 synthesis, while it increased intracellular cAMP accumulation. Our studies suggest AA stimulates intracellular cAMP formation in cultured gastric mucosal cells, linked with conversion of AA to cyclooxygenase metabolites, AA-induced PG production is limited in these cells, and it seems, however, unlikely that intracellular cAMP modulates AA metabolism to PG.

Animals↗
PubMed1982

Coupling factor.

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Animals↗
PubMed1981

Continuing medical education: viewpoints of Canadian psychiatric residents.

Continuing Medical Education (CME), relicensure and recertification are controversial issues for physicians today. The viewpoints of 142 Canadian psychiatric residents from 12 training centres across Canada were surveyed. The majority (73%) of the residents did not think that CME would pose a problem for them after certification. In fact, a large majority (77%) felt CME should be required after certification. Close to half of the residents favoured monitoring of CME by the Canadian Psychiatric Association. In contrast to these results, few favoured mandatory recertification. A formal relicensure examination was strongly repudiated. Individual reading and self-assessments as well as clinically oriented courses and workshops were the favoured methods of CME. Our recommendations arising from this survey are threefold. CME should remain a voluntary activity. The Canadian Psychiatric Association should be the monitoring body for CME for psychiatrists, and finally, individual readings and self-assessments should be used increasingly in providing CME.

Attitude of Health Personnel↗