Publications
429 results found
THOMPSON GR, 1990, HISTORY AND EVOLUTION OF EXTRACORPOREAL LDL ELIMINATION IN SEVERE HYPERCHOLESTEROLEMIA, 2ND INTERNATIONAL SYMP ON TREATMENT OF SEVERE HYPERCHOLESTEROLEMIA IN THE PREVENTION OF CORONARY HEART DISEASE, Publisher: KARGER, Pages: 164-169
Thompson GR, 1990, Mobilisation of tissue cholesterol by apheresis., Prog Clin Biol Res, Vol: 337, Pages: 183-187, ISSN: 0361-7742
THOMPSON GR, 1990, TOWARDS A NEW ERA - IS CORONARY-ARTERY DISEASE REVERSIBLE, 11TH CONGRESS OF EUROPEAN SOC OF CARDIOLOGY : HMG COA ( 3-HYDROXY-3-METHYLGLUTARYL COENZYME-A) REDUCTASE INHIBITORS - NEW HORIZONS IN MANAGEMENT OF HYPERCHOLESTEROLEMIA, Publisher: KARGER, Pages: 66-69, ISSN: 0008-6312
- Author Web Link
- Cite
- Citations: 1
THOMPSON GR, 1990, MOBILIZATION OF TISSUE CHOLESTEROL BY APHERESIS, 2ND INTERNATIONAL CONGRESS OF THE WORLD APHERESIS ASSOC, Publisher: WILEY-LISS, INC, Pages: 183-187
- Author Web Link
- Cite
- Citations: 2
Thompson GR, 1990, Towards a new era: is coronary artery disease reversible?, Cardiology, Vol: 77 Suppl 4, Pages: 66-69, ISSN: 0008-6312
There is increasing evidence that conventional lipid-lowering therapy can arrest the progression of coronary atherosclerosis. Trials are now under way to determine whether more radical reduction of low-density-lipoprotein cholesterol will reverse atherosclerosis and lead to regression of coronary lesions. The ability to effect such reductions has been markedly enhanced by the introduction into clinical practice of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
THOMPSON GR, 1989, SATURATION OF FAT AND CHOLECYSTOKININ RELEASE, LANCET, Vol: 2, Pages: 1338-1338, ISSN: 0140-6736
Thompson GR, 1989, Management of hyperlipidaemia, Prescribers' Journal, Vol: 29, Pages: 221-223, ISSN: 0032-7611
- Cite
- Citations: 3
MAHER VMG, PAPPU A, ILLINGWORTH DR, et al., 1989, PLASMA MEVALONATE RESPONSE IN LOVASTATIN-RELATED MYOPATHY, LANCET, Vol: 2, Pages: 1098-1098, ISSN: 0140-6736
- Author Web Link
- Cite
- Citations: 23
THOMPSON GR, 1989, LIPID RELATED CONSEQUENCES OF INTESTINAL MALABSORPTION, GUT, Vol: 30, Pages: 29-34, ISSN: 0017-5749
- Author Web Link
- Cite
- Citations: 13
Thompson GR, 1989, Current management of hyperlipidaemia., Br J Hosp Med, Vol: 42, Pages: 268-274, ISSN: 0007-1064
Hyperlipidaemia is a major cause of coronary heart disease (CHD) and is especially prevalent in Britain. Prior to lipid-lowering therapy it is necessary to define the type of lipoprotein abnormality present and whether it is primary or secondary. Diet forms the initial treatment but additional drug therapy may be necessary in patients with established CHD or considered to be at high risk of developing CHD or rarely, in the case of severe hypertriglyceridaemia, acute pancreatitis.
THOMPSON GR, 1989, CURRENT MANAGEMENT OF HYPERLIPEMIA, BRITISH JOURNAL OF HOSPITAL MEDICINE, Vol: 42, Pages: 268-&, ISSN: 0007-1064
- Author Web Link
- Cite
- Citations: 9
THOMPSON GR, MAHER V, PAPPU A, et al., 1989, USE OF PLASMA MEVALONATE TO MONITOR HMG COA REDUCTASE INHIBITION, ATHEROSCLEROSIS, Vol: 79, Pages: 96-96, ISSN: 0021-9150
OHRI SK, KEANE PF, SWIFT I, et al., 1989, REAPPRAISAL OF PARTIAL ILEAL BYPASS FOR THE TREATMENT OF FAMILIAL HYPERCHOLESTEROLEMIA, AMERICAN JOURNAL OF GASTROENTEROLOGY, Vol: 84, Pages: 740-743, ISSN: 0002-9270
- Author Web Link
- Cite
- Citations: 9
DAVIS TME, PROBY C, STRONG JA, et al., 1989, EFFECT OF ENPROSTIL ON GLUCOSE AND LIPID-METABOLISM IN TYPE-2 DIABETES, DIABETIC MEDICINE, Vol: 6, Pages: 400-405, ISSN: 0742-3071
- Author Web Link
- Cite
- Citations: 4
WILE DB, BARBIR M, GALLAGHER J, et al., 1989, APOLIPOPROTEIN-A-I GENE POLYMORPHISMS - FREQUENCY IN PATIENTS WITH CORONARY-ARTERY DISEASE AND HEALTHY CONTROLS AND ASSOCIATION WITH SERUM APO-A-I AND HDL-CHOLESTEROL CONCENTRATION, ATHEROSCLEROSIS, Vol: 78, Pages: 9-18, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 42
Utermann G, Hoppichler F, Dieplinger H, et al., 1989, Defects in the low density lipoprotein receptor gene affect lipoprotein (a) levels: multiplicative interaction of two gene loci associated with premature atherosclerosis., Proc Natl Acad Sci U S A, Vol: 86, Pages: 4171-4174, ISSN: 0027-8424
The lipoprotein (a) [Lp(a)] contains two nonidentical protein species, apolipoprotein (apo) B-100 and a specific high molecular weight glycoprotein, apo(a). Lp(a) represents a continuous quantitative genetic trait, the genetics of which are only poorly understood. Genetic variation at the apo(a) locus affects plasma Lp(a) levels and explains at least 40% of the variability of this trait. Lp(a) levels were found to be elevated 3-fold in the plasma from patients with the heterozygous form of familial hypercholesterolemia who have one mutant low density lipoprotein receptor gene. This elevation was not due to a higher frequency of those apo(a) types that are associated with high Lp(a) levels in familial hypercholesterolemia patients. Rather Lp(a) levels were elevated for each of the apo(a) phenotypes examined. The effects of the apo(a) and low density lipoprotein receptor genes on Lp(a) levels are not additive but multiplicative. This is a situation not commonly considered in quantitative human genetics. We conclude that Lp(a) levels in plasma may be determined by variation at more than one gene locus.
MYANT NB, GALLAGHER J, BARBIR M, et al., 1989, RESTRICTION FRAGMENT LENGTH POLYMORPHISMS IN THE APO-B-GENE IN RELATION TO CORONARY-ARTERY DISEASE, ATHEROSCLEROSIS, Vol: 77, Pages: 193-201, ISSN: 0021-9150
- Author Web Link
- Cite
- Citations: 102
BARBIR M, BANNER NR, REID CJ, et al., 1989, INFLUENCE OF LIPID ABNORMALITIES ON THE DEVELOPMENT OF CORONARY ARTERIAL-DISEASE AFTER CARDIAC TRANSPLANTATION, BRITISH HEART JOURNAL, Vol: 61, Pages: 462-462, ISSN: 0007-0769
- Author Web Link
- Cite
- Citations: 4
THOMPSON GR, BARBIR M, OKABAYASHI K, et al., 1989, PLASMAPHERESIS IN FAMILIAL HYPERCHOLESTEROLEMIA, ARTERIOSCLEROSIS, Vol: 9, Pages: I152-I157, ISSN: 0276-5047
- Author Web Link
- Cite
- Citations: 26
Thompson G, Barbir M, Michishita I, et al., 1989, Comparison of plasma exchange and LDL apheresis in the treatment of hypercholesterolemia, Pages: 815-818
- Cite
- Citations: 3
THOMPSON GR, SEED M, NITHTHYANANTHAN S, et al., 1989, GENOTYPIC AND PHENOTYPIC VARIATION IN FAMILIAL HYPERCHOLESTEROLEMIA, ARTERIOSCLEROSIS, Vol: 9, Pages: I75-I80, ISSN: 0276-5047
- Author Web Link
- Cite
- Citations: 23
TAHA TH, BARBIR M, NIHOYANNOPOULOS P, et al., 1989, CORONARY-ARTERY ECTASIA - PREVALENCE, FREQUENCY OF HYPERLIPEMIA, AND INFLUENCE ON MYOCARDIAL PERFUSION, BRITISH HEART JOURNAL, Vol: 61, Pages: 82-83, ISSN: 0007-0769
Thompson GR, 1989, Lipid-lowering therapy and its effect on atherosclerosis., Postgrad Med J, Vol: 65 Suppl 1, Pages: S22-S25, ISSN: 0032-5473
THOMPSON GR, 1989, LIPID-LOWERING THERAPY AND ITS EFFECT ON ATHEROSCLEROSIS, POSTGRADUATE MEDICAL JOURNAL, Vol: 65, Pages: S22-S25, ISSN: 0032-5473
SEED M, REAVELY DA, LUCK V, et al., 1988, LP(A) - A COMPARISON BETWEEN PATIENTS WITH FAMILIAL HYPERCHOLESTEROLEMIA (FH) AND A NORMAL BRITISH-POPULATION, ATHEROSCLEROSIS, Vol: 74, Pages: 253-253, ISSN: 0021-9150
BARBIR M, WILE D, TRAYNER I, et al., 1988, HIGH PREVALENCE OF HYPERTRIGLYCERIDEMIA AND APOPROTEIN ABNORMALITIES IN CORONARY-ARTERY DISEASE, ATHEROSCLEROSIS, Vol: 74, Pages: 254-254, ISSN: 0021-9150
KOIZUMI J, KANO M, OKABAYASHI K, et al., 1988, BEHAVIOR OF HUMAN APOLIPOPROTEIN A-L - PHOSPHOLIPID AND APOHDL - PHOSPHOLIPID COMPLEXES INVITRO AND AFTER INJECTION INTO RABBITS, JOURNAL OF LIPID RESEARCH, Vol: 29, Pages: 1405-1415, ISSN: 0022-2275
- Author Web Link
- Cite
- Citations: 30
BARBIR M, WILE D, TRAYNER I, et al., 1988, HIGH PREVALENCE OF HYPERTRIGLYCERIDEMIA AND APOLIPOPROTEIN ABNORMALITIES IN CORONARY-ARTERY DISEASE, BRITISH HEART JOURNAL, Vol: 60, Pages: 397-403, ISSN: 0007-0769
- Author Web Link
- Cite
- Citations: 111
KANO M, KOIZUMI J, JADHAV A, et al., 1988, COMPARISON OF LDL LOWERING AND HDL RAISING EFFECTS OF LDL APHERESIS AND PLASMA-EXCHANGE IN WHHL RABBITS, ARTIFICIAL ORGANS, Vol: 12, Pages: 355-355, ISSN: 0160-564X
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.