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Biomedical subjects

D J Osborne

Publications and source records attributed to D J Osborne.

At least 37 records · Page 2Linked to original sources
PubMed1984

gamma-Hexachlorocyclohexane stimulation of macrophage phospholipid hydrolysis and leukotriene production.

gamma-Hexachlorocyclohexane stimulates arachidonic acid release from macrophage phospholipids. It is also a powerful stimulator of leukotriene C4 production, yet (by comparison with zymosan) produces only a small effect on prostaglandin production. This suggests that synthesis of leukotrienes and prostaglandins can be independently regulated. The most likely mechanism of action of gamma-hexachlorocyclohexane is through its effect on phosphatidylinositol metabolism.

Animals↗
PubMed1984

Concepts of target cells in plant differentiation.

The regeneration of whole plants from fragments of mature organs is compelling evidence that plant cells retain genetic totipotency throughout differentiation. Within the intact plant, however, strict regulatory controls operate to maintain a co-ordinated pattern of growth. Not every cell differentiates along the same developmental pathway. Cell performance is determined by mechanisms that permit subtle discriminations in recognition of and response to an array of environmental and hormonal cues. Much effort is currently directed to understanding these control systems in plants. Certain positionally differentiated cells and tissues have been characterized by their specific signal recognition and their precise responses in gene expression. In a few, the competence to respond to particular signals has been distinguished by the presence of cell-specific protein markers. This article discusses some recent studies that help towards an understanding of the target nature of cells in plant development.

Cell Differentiation↗
PubMed1984

Comparative effects of some non-steroidal anti-inflammatory drugs on the ultrastructural integrity and prostaglandin levels in the rat gastric mucosa: relationship to drug uptake.

Studies were performed in fasted rats to establish if the propensity of 4 non-steroidal anti-inflammatory (NSAI) drugs to elicit varying degrees of gastric mucosal damage following oral administration is related to their rate of absorption by the mucosal and subsequent inhibitory effects on prostaglandin (PG) production in vivo. Aspirin (200 mg/kg p.o.) and indomethacin (10 mg/kg p.o.) produced ultrastructural signs of damage at 10-60 min to the surface mucous cells, parietal cells and endothelial cells of sub-mucosal capillaries coincident with the relatively rapid absorption of the radiolabelled drugs and reduction in the mucosal content of PGE2 and 6-keto PGF1 alpha determined by gas chromatography/mass spectrometry. Azapropazone (100 mg/kg p.o.) failed to elicit mucosal damage either ultrastructurally or even visually up to 23 h after dosing and did not affect the content of PG's even though the drug was present in the mucosa in sufficient concentration to elicit reduction in prostaglandin synthesis in vitro. Benoxaprofen (110 mg/kg p.o.) reduced the content of PGE2 and somewhat variably, that of 6-keto PGF1 alpha, was more slowly absorbed c.f. aspirin and indomethacin, but failed to elicit appreciable mucosal damage. These results show that while reduction in PG synthesis is a factor in the development of damage by ulcerogenic drugs, it appears that the rate of absorption or other biochemical effects (including e.g. influences on the production of oxyradicals or 5-lipoxygenase products of eicosanoid metabolism) may contribute to the relatively low irritancy of drugs such as azapropazone or benoxaprofen.

Animals↗
PubMed1983

The separation of leukotrienes and hydroxyeicosatetraenoic acid metabolites of arachidonic acid by high performance liquid chromatography (HPLC).

The following high performance liquid chromatography system was found suitable for separating most lipoxygenase metabolites of arachidonic acid: Techsphere 5-C18 column, eluting solvent methanol:water:acetic acid (65:35:0.06 v/v), pH 5.3. Comparisons with other packing materials and solvent systems are described. The method could be used to identify lipoxygenase products released from mouse macrophage cells stimulated with gamma-hexachlorocyclohexane. Detection limits between 1 and 10 ng were obtained.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

A rapid method for detecting inhibitors of both cyclo-oxygenase lipoxygenase metabolites of arachidonic acid.

A method for detecting inhibitors of arachidonic acid metabolism is described. Guinea pig peritoneal polymorphonuclear leukocytes incubated with [14C] arachidonic acid were stimulated with calcium ionophore A23187. The radiolabelled products were identified by HPLC and GC/MS as cyclo-oxygenase and lipoxygenase metabolites. A TLC system was utilized to separate these metabolites which were then analysed by automatic quantitative scanning. This method allowed rapid determination of the radiolabel incorporated into each metabolite. This method of analysis was used to study the actions of indomethacin, NDGA, benoxaprofen, and BW775C on the formation of radiolabelled arachidonic acid metabolites.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1982

A comparative study of the physical properties and enzymatic reactions of slow reacting substance of anaphylaxis and some leukotriene D4 isomers.

Eight synthetic isomers of 5-hydroxy-6-S-cysteinylglycine -7,9,11,14-eicosatetraenoic acid were compared with authentic guinea pig SRS-A using UV spectroscopy, high performance liquid chromatography and soybean lipoxygenase. It was found that only the 5S, 6R 7,9trans 11,14cis isomer was similar to SRS-A in all respects. The 5S,6R 7trans, 9,11,14 cis isomer shows similar UV and HPLC characteristics but differs in that it spontaneously undergoes a 1,7 hydride shift reaction and unexpectedly does not react with soybean lipoxygenase.

Animals↗
PubMed1982

Comparison of ochratoxin, aflatoxin, and T-2 toxin for their effects on selected parameters related to digestion and evidence for specific metabolism of carotenoids in chickens.

Aflatoxicosis, ochratoxicosis, and T-2 toxicosis were produced by feeding diets containing graded concentration of the appropriate toxin to broiler chicks from hatching unit 3 weeks of age. Aflatoxin, even at levels not growth inhibitory, produced a malabsorption syndrome characterized by steatorrhea, hypocarotenoidemia, and decreased concentrations of bile salts and pancreatic lipase, trypsin, amylase, and RNase. The T-2 toxin at concentrations higher than required to inhibit growth produced a mild malabsorption syndrome characterized by steatorrhea and decreased levels of pancreatic lipase, trypsin, amylase, and RNase. The only suggestion of malabsorption during ochratoxicosis was a severe hypocarotenoidemia. The following observations indicated a lack of correlation between lipid malabsorption and hypocarotenoidemia. The T-2 toxicosis exhibited lipid malabsorption in the absence of hypocarotenoidemia, ochratoxicosis exhibited hypocarotenoidemia in the absence of lipid malabsorption, and aflatoxicosis exhibited both symptoms. These findings imply that carotenoids are physiologically active compounds with specific metabolic processes and are not inert substances swept along with lipids as is commonly assumed from the ability to grow apparently healthy birds free of carotenoids. The current findings also indicate that great specificities exist in mycotoxicoses despite superficial similarities.

Aflatoxins↗
PubMed1981

Steatorrhea during aflatoxicosis in chickens.

Graded levels of dietary aflatoxin (0, .625, 1.25, 2.5, 5 and 10 microgram/g) were tested for their effect on lipid excretion in feces of young broiler chickens. There was a highly significant (P less than .01) increase at 1.25 microgram/g and above including a threefold increase at 10 microgram/g, while growth rate was decreased only at levels of 2.5 microgram/g and above. Pancreatic lipase, the primary fat digestive enzyme, was decreased significantly (P less than .05) at all levels of aflatoxin and at 10 microgram/g was only 40% of the control value, Bile, which is required for lipid digestion and absorption, was decreased highly significantly (P less than .01) in concentration by all growth inhibition levels of aflatoxin. A slight but significant ( P less than .05) increase in bladder size at growth inhibitory levels of aflatoxin appeared adequate to compensate for decreased bile concentration. A pair feeding technique showed the effect of aflatoxin on fecal lipids and pancreatic lipase occurred in diets low (2%) or high (17%) in fat. The steatorrhea caused by aflatoxin apparently reflects a lipid malabsorption syndrome caused by an impaired ability to digest lipids.

Aflatoxins↗
PubMed1981

Decreased pancreatic digestive enzymes during aflatoxicosis.

Dietary aflatoxin at concentrations of 1.25 microgram/g or above caused in broiler chickens a significant (P less than .05) decrease in the specific activities of pancreatic amylase, trypsin, lipase, RNase, and DNase. These enzymes are the primary enzymes of digestion for starches, protein, lipid, and nucleic acids. At concentrations of 2.5 microgram/g or above there was a compensatory pancreatomegaly that resulted in essentially normal total activity for trypsin, RNase, and DNase. Thus, aflatoxicosis was associated with reduced activity levels of enzymes that digest starch and lipid. This digestive deficiency could account for a malabsorption syndrome observed in field outbreaks of aflatoxicosis.

Aflatoxins↗
PubMed1979

PGE1 metabolism by the perfused rat liver.

The hepatic and biliary metabolites of PGE1 have been isolated and identified after infusions of PGE1 into isolated rat liver preparations. The results demonstrate that in general PGE1 undergoes metabolism similar to that of PGE2 in the rat and reveals the possibility of a selective PG metabolite transport system across the biliary canalicular membrane.

Animals↗
PubMed1978

Modification of prostaglandin and thromboxane release by immunological sensitisation and successive immunological challenges from guinea-pig lumg.

The release of prostaglandins (PGs) and thromboxanes (Txs) from perfused guinea pig lungs was investigated during different immunological states. The major product released from normal lungs perfused with exogenous arachidonic acid was 6-oxo-PGF1a. The procedure of sensitisation to specific antigen resulted in an increase in the release of 15-oxo-13,14-dihydro-TxB2 and a decrease in the release of 6-oxo-PGF1a- and 6,15-dioxo-13,14-dihydro-PGF1a from lungs perfused with arachidonic acid. The relative amount of 15-oxo-13,14-dihydro-TxB2 released progressively increased with the number of immunological challenges with both exogenous and endogenously derived substrate, arachidonic acid. This change in response to successive immunological challenges may represent a protective mechanism to prevent parent Txs and PGs entering the systemic circulation.

Anaphylaxis↗
PubMed1977

Gravity-induced cell elongation.

When the flowering stalks of grasses are displaced from the vertical position they are caused to bend at special gravity perceptive regions, the nodes. Growth of the lower side of the node returns the shoot to its original orientation with respect to gravity, but when this is achieved, growth ceases. Possible mechanisms by which elongation growth is turned on in the lower sides and turned off again once the stalk is vertical are described. The facilities of Spacelab offer a unique opportunity for testing models of gravity perception and response.

Dose-Response Relationship, Drug↗