Y.H. Abdulla
Guy's Hospital
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Featured researches published by Y.H. Abdulla.
Journal of Atherosclerosis Research | 1969
Y.H. Abdulla
Summary Evidence is presented for the existence of β-adrenergic receptors effecting disaggregation of clumped platelets. This function is mediated by adenosine 3′-5′ cyclic monophosphate.
Journal of Atherosclerosis Research | 1968
Y.H. Abdulla; C.C. Orton; C. W. M. Adams
Summary In vitro cholesterol esterification by either human or rabbits aorta in the presence of β -fatty acid-labelled lecithin appears to depend on a lecithin:cholesterol fatty acid (acyl) transferase. The activity of this enzyme increases in human fatty atherosclerotic lesions and in atherosclerotic aortas from cholesterol-fed rabbits. Activity decreases in fibrous and calcified human atherosclerotic lesions.
Atherosclerosis | 1978
C. W. M. Adams; Y.H. Abdulla
High density lipoprotein (HDL) was found in vitro to form myelin buds (liposomes) from washed crystals of free cholesterol (commercial or atheroma sources). This activity led to the progressive destruction and solubilization of the crystals. Low density and very low density lipoproteins did not have any effect. Liposome formation and solubilization were accelerated by calcium ions, phospholipase A and polyunsaturated lecithin (Lipostabil). Cholesterol crystals were nearly completely destroyed after 18 h incubation with HDL-Lipostabil.
Journal of Atherosclerosis Research | 1969
Y.H. Abdulla; C. W. M. Adams; R. S. Morgan
Summary Free [ 3 H] cholesterol, various [ 3 H] cholesterol esters and [ 3 H]cholesterol-[ 14 C]linolenate were implanted subcutaneously in rats. Three weeks after implantation [ 3 H] cholesterol linolenate and arachidonate were resorbed to a significantly greater extent than free [ 3 H]cholesterol, [ 3 H] cholesterol linolenate and the more saturated labelled sterol esters. [ 3 H]Cholesterol was more rapidly mobilized than the saturated and monounsaturated [ 3 H] cholesterol esters. The resorption of esterified cholesterol did not appear to depend on rapid hydrolysis of the fatty acid moiety and slow removal of the sterol nucleus, for 3 H and 14 C labels disappeared at nearly equal rates from implants of [ 3 H]cholesterol-[l- 14 C]linolenate. Addition of antioxidants to the polyunsaturated ester implants did not significantly accelerate resorption, even though it did reduce chromolipid formation. We infer that esterification of cholesterol with linolenic or arachidonic acids would accelerate its removal from the normal or atherosclerotic arterial wall.
Journal of Atherosclerosis Research | 1969
Y.H. Abdulla; C. W. M. Adams; O. B. Bayliss
Summary Quantitative histochemical estimation of multiple layers of 6 human coronary arteries shows that the triglycerides in coronary atherosclerosis are mainly derived from contaminating adventitial adipose tissue. Only between 4.6 and 24.1 % of the neutral lipids in atherosclerotic intima are triglycerides; sterols and their esters constitute the remainder.
Atherosclerosis | 1978
Y.H. Abdulla; C. W. M. Adams
Electron microscopy of the reaction product between human pooled high density lipoprotein (HDL) and cholesterol shows that characteristic liposome macromicellar bodies are formed. These bodies vary in size between 30 and 1200 nm. In comparison with HDL, they contain markedly more cholesterol, but less protein and phospholipid. Their phospholipid pattern shows enrichment with sphingomyelin and phosphatidyl serine in comparison with HDL.
Journal of Atherosclerosis Research | 1969
Y.H. Abdulla; C. W. M. Adams; O. B. Bayliss
Summary Cholesterol esterification by lecithin cholesterol fatty acid transferase (acylase) was estimated in multiple layers of atherosclerotic human and rabbit aorta; lecithin- β -[1- 14 C]linoleic acid was used as substrate. Between 5 and 9 layers were obtained from the inside to the outside of the aortas; adjacent samples were examined histologically. Most transferase activity was located in the outer part of the atherosclerotic intima, but some was located in the inner media. Medial transferase activity must be derived from smooth muscle cells. Some activity in the atherosclerotic intima is probably located in lipid phagocytes; such cells are thought to be modified smooth muscle. The high activity in the outer part of the atherosclerotic intima may be partly due to the hyperplastic layer of smooth muscle cells in the zone.
Journal of Atherosclerosis Research | 1965
Y.H. Abdulla; C. W. M. Adams
Summary Quantitative histochemical analyses of multiple layers of the atherosclerotic human aortic wall — cut from the inside to the outside of the vessel — show that (1) the sphingomyelin/lecithin ratio is much higher than that in plasma; (2) this ratio remains relatively constant throughout the various layers of the aorta; (3) there is no falling gradient in phospholipid concentration from the inside to the outside of the vessel wall; and (4) that there is little phospholipid in the innermost layer of the aorta. These results support the view that phospholipid is synthesized within the arterial wall and does not infiltrate there from the plasma. These analyses are consistent with previous qualitative histochemical studies on the distribution and nature of phospholipids in the human aortic wall.
Atherosclerosis | 1971
C. W. M. Adams; Y.H. Abdulla; O. B. Bayliss
Abstract A mixture of doubly labelled cholesterol linolenate and non-radioactive cholesterollinoleate was injected subcutaneously in rats. The lipid implants were separated into predominantly extracellular and intracellular phases by progressive solvent extractions. Chromatography and scintillation counting of the fractions showed that little esterified cholesterol had been hydrolysed in the intracellular phase and little randomization of fatty acids had occurred between radioactive and non-radioactive cholesterol. It is concluded that foam cells (macrophages) can take up cholesterol in esterified form and that preliminary hydrolysis to free cholesterol is not obligatory for uptake by these cells.
Journal of Atherosclerosis Research | 1967
Y.H. Abdulla
Summary A hypothesis is proposed that some platelet aggregating substances act by increasing the ‘ice-likeness’ (ordered structure) of water around platelets. The aggregating action of noble gases, long chain aliphatic alcohols, tetra alkyl ammonium salts and dicarboxylic cholesterol esters is reported. Their action is explained in terms of the hypothesis.