scispace - formally typeset
D

David J. Galton

Researcher at St Bartholomew's Hospital

Publications -  191
Citations -  4457

David J. Galton is an academic researcher from St Bartholomew's Hospital. The author has contributed to research in topics: Adipose tissue & Lipoprotein lipase. The author has an hindex of 35, co-authored 191 publications receiving 4402 citations. Previous affiliations of David J. Galton include University Hospital of Wales & Hammersmith Hospital.

Papers
More filters
Journal ArticleDOI

A DNA Variant at the Angiotensin-Converting Enzyme Gene Locus Associates With Coronary Artery Disease in the Caerphilly Heart Study

TL;DR: The DD genotype is a linkage marker for an etiologic mutation at or near the ACE gene that may confer risk of CAD detectable in subjects previously unidentifiable with "classic" risk factors, however, this risk may be quantitatively small among the general male population.
Journal ArticleDOI

Apolipoprotein B gene variants are involved in the determination of serum cholesterol levels: a study in normo- and hypelipidaemic individuals

TL;DR: This study suggests that variations in the gene for apo B are associated with the determination of serum cholesterol and triglyceride levels both in patients with type III hyperlipidaemia and in the normal population.
Journal ArticleDOI

DNA variants at the LPL gene locus associate with angiographically defined severity of atherosclerosis and serum lipoprotein levels in a Welsh population.

TL;DR: The data suggest that the H2 allele may be a linkage marker for an etiologic mutation for dyslipidemia and the severity and development of atherosclerosis; this is not the Ser447-Ter mutation.
Journal ArticleDOI

Deoxyribonucleic acid polymorphism in the apolipoprotein A-1-C-III gene cluster. Association with hypertriglyceridemia.

TL;DR: A DNA sequence polymorphism, shown to be located in or close to the 3' noncoding region of the apolipoprotein C-III gene, is found in significantly increased prevalence in Caucasian hypertriglyceridemic subjects compared with race-matched controls, and its distribution in normal individuals of differing racial origins is reported.