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Biomedical subjects

J E Thompson

Publications and source records attributed to J E Thompson.

At least 253 records · Page 14Linked to original sources
PubMed1981

Effect of membrane lipid perturbers on the temperature dependence of repair of sublethal and potentially lethal radiation damage.

The repair of sublethal radiation damage (SLD) in Chinese hamster (V79) cells was investigated as a function of temperature in the presence and absence of the membrane lipid perturbers, butylated hydroxytoluene (BHT) or adamantanone, which decrease the viscosity of the membrane lipids. Addition of 0.01 mM BHT to the cells significantly increased the amount of repair of SLD over controls from 0 to 25 degrees C but not from 30 to 37 degrees C. The amount of repair of SLD decreased as a function of temperature to about 20 degrees C and remained relatively constant thereafter till about 2.5 degrees C where it began to decrease again. The change in the amount of repair at approximately 20 degrees C coincides with a membrane lipid phase transition, as seen by spin labelling, in these cells. The repair of potentially lethal damage (PLD) was not increased by BHT at the two temperatures investigated (5 and 20 degrees C). In fact, additional PLD was expressed when cells were incubated post-irradiation at these temperatures. The results imply that at least a component of the SLD repair system is membrane associated and that the SLD and PLD repair systems are independent.

Adamantane↗
PubMed1981

Simulation of the effects of leaf senescence on membranes by treatment with paraquat.

Chloroplast and microsomal membranes from the primary leaf of bean acquired increasing proportions of gel phase lipid as the tissue senesced. The lipid-phase transition temperature for microsomes rose from about 25 to 43 C and that for chloroplasts rose from below -30 C to about 52 C within 5 weeks of planting. This was accompanied by large increases (2- to 4-fold) in the sterol to phospholipid ratio of the membranes, which reflected breakdown of phospholipid. Changes in fatty acid saturation were of insufficient magnitude to account for the rise in transition temperature. All of these senescence-related changes in chloroplast and microsomal membranes were also induced by treating young, 2-week-old-plants with 10 milligrams per liter paraquat. Within 48 hours of treatment, the transition temperature rose from 25 to 57 C for microsomes and from below -30 to 24 C for chloroplasts. The membranes sustained only small changes in fatty acid saturation, comparable to those incurred during natural senescence, and there was a selective loss of phospholipid, resulting in augmented sterol to phospholipid ratios. Malondialdehyde, a product of lipid peroxidation, rose by 2- to 3-fold in both senescing and paraquat-treated leaves. Paraquat is known to form cation redicals that react with O(2) to produce O(2) (-) and has been implicated as an agent of lipid peroxidation. Accordingly, these observations suggest that membrane deterioration during natural senescence may be due in part to free radical damage.

Journal Article↗
PubMed1981

Compositional and physical properties of microsomal membrane lipids from regressing rat corpora lutea.

Wide angle x-ray diffraction has revealed that during corpus luteum regression there is a liquid-crystalline to gel phase transition in the phospholipid molecules of the cellular membranes. In the present study we have examined the lipid composition of these membranes and looked for evidence of membrane protein involvement in this change. Lipid analysis of smooth microsomal membranes prepared from rat corpora lutea revealed no significant change in the cholesterol to phospholipid ratio or in the ratio of unsaturated to saturated fatty acids with advancing luteolysis. In addition, there was no clear trend for these changes in the relative proportions of the major fatty acids. Liposomes were prepared from smooth microsomal fractions of regressing rat corpora lutea, and examination of these lipid vesicles by x-ray diffraction revealed that the temperature of the liquid-crystalline to gel phase transition was much lower (approximately 25-30 C) than that for the corresponding microsomes. These observations are consistent with the view that membrane proteins contribute to the ordering of lipid that results in a mixture of liquid-crystalline and gel phases in membranes from regressed corpora lutea.

Animals↗
PubMed1980

Chronic cholelithiasis and decreased bile salt pool size: cause or effect?

The hypothesis that the decreased bile salt pool size observed in humans with chronic cholelithiasis is a result rather than a cause of gallstones was tested in a prairie dog gallstone model. A decrease in bile salt pool size was observed in cholesterol-fed prairie dogs only after the chronic presence of stones had induced physiologic, anatomic and microscopic changes typical of human chronic cholecystitis. These data suggest that the decreased bile salt pool size associated with chronic cholelithiasis is a result rather than a cause of gallstones and that the link between the hepatic secretion of cholelithogenic bile and gallstones is altered gallbladder function.

Animals↗
PubMed1980

Roles of lithogenic bile and cystic duct occlusion in the pathogenesis of acute cholecystitis.

The hypothesis that the elements essential for the induction of acute cholecystitis are the presence of lithogenic bile and cystic duct occlusion was tested in the prairie dog gallstone model. Neither the presence of gallstones alone nor acute cystic duct occlusion alone resulted in acute inflammation of the gallbladder. Acute cholecystitis developed in prairie dog gallbladders containing cholesterol-saturated bile, with or without gallstones, shortly after cystic duct occlusion. These data suggest that the factors essential for the induction of acute cholecystitis are the presence of lithogenic bile and cystic duct occlusion and that gallstones, although frequently present, are not an essential prerequisite to acute inflammation.

Acute Disease↗
PubMed1980

Canine anatomy as assessed by computerized tomography.

Computerized tomographic studies of normal canine anatomy were obtained, using a whole body scanner. The regions of interest were head and neck, thorax, and abdomen and pelvis. Scans were compared with gross transverse sections from one euthanatized dog. Identification and labeling of anatomic structures were aided by reference to recognized texts of canine anatomy.

Animals↗
PubMed1979

Induction of gel-phase lipid in plasma membrane of chick intestinal cells after coccidial infection.

When chickens are infected with the coccidial parasite Eimeria necatrix, the plasma membrane of intestinal cells harbouring second-generation schizonts becomes refractory to mechanical shearing, hypotonic shock and ultrasonication. Plasma membrane from these infected cells was isolated to high purity as judged by enriched levels of ouabain-sensitive (Na+ + K+)-stimulated Mg2-dependent ATPase activity and sialic acid content, the lack of detectable cytochrome oxidase and glucose-6-phosphatase activities and electron microscopic analysis of the final preparation. Wide-angle X-ray diffraction patterns recorded from the isolated membranes revealed that during the later stages of parasite maturation the host cell plasma membrane acquires increasing proportions of gel-phase lipid. By contrast, purified membrane from isolated parasites is in a liquid-crystalline state. The transition temperature of host cell plasmalemma at 100 h postinfection is 61 degrees C, about 20 degrees C above physiological temperature. By contrast, liposomes of plasma membranes from infected cells undergo a thermal transition at about 28 degrees C. The accumulation of gel-phase lipid in the host cell plasma membrane is not attributable either to an increase in the constituent ratio of saturated to unsaturated fatty acids or to a significant change in the cholesterol to phospholipid ratio. During the late stages of infection, the cells become stainable with trypan blue which suggests that the acquisition of crystalline phase lipid disrupts the permeability of the host cell plasmalemma.

Animals↗