ISBN-10: 0470513500

ISBN-13: 9780470513507

ISBN-10: 0471910961

ISBN-13: 9780471910961

Many universal human ailments have a multifactorial foundation: they're inspired through a person's genetic predisposition in addition to via elements within the setting. This quantity offers with the appliance of recombinant DNA concepts to the id of illnesses that experience multiple inherited part. concentration is at the polygenic components liable for coronary atherosclerosis. numerous different problems having a polygenic beginning also are mentioned, together with high blood pressure, diabetes mellitus, psychiatric illnesses, and autoimmune (HLA-related) problems. difficulties raised via the examine of alternative households or diverse populations are lined, in addition to the potential of employing molecular concepts to disorder prevention--for instance, via gene treatment. additionally, a number of the moral matters that relate to human gene mapping are in brief explored.


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However, to the extent that it is possible to identify a genetic component to the determination of high fibrinogen levels, the argument can be countered. We are at present collaborating with Dr Humphries to try to sort this out. Humphries: There are several problems about comparing studies done in different countries. The ethnic origins of populations in London, Norway, Denmark or Italy are different and therefore one might expect there to be different associations between a disease and particular RFLPs.

Proc Natl Acad Sci USA 83:7367-7370 Carlsson P, Darnfors C, Oloffson SO, Bjursell G 1986 Analysis of the human apolipoprotein B gene: complete structure of the B-74 region. Gene (Amst) 49:29-51 Funke H, Frossard PM, Coleman RT, Assmann G 1986 Genetic marker for atherosclerosis at the human insulin gene locus. Am J Hum Genet 38:A199 Jowett NI, Williams LG, Hitman GA, Galton DJ 1984a Diabetic hypertriglyceridaemia and related 5' flanking polymorphisms of the human insulin gene. Br Med J 288:96 99 Jowett NI, Rees A, Williams LG et al 1984b Insulin and apolipoprotein A-I/C-I11gene polymorphisms relating to hypertriglyceridaemia and diabetes mellitus.

These are preliminary results. We have deduced the haplotypes of a limited number of people from their offspring, but we are not yet in a position to link haplotypes with lipid levels. Sing: Why are we seeing dominance at the apolipoprotein level? I noticed that the XbaI restriction site was associated with a dominant effect on apoB in your results. Scotf: Perhaps I could answer this. The relative molecular mass ( M , ) of apoB was contentious until the entire sequence became available (Knott et al 1986).

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Ciba Foundation Symposium 130 - Molecular Approaches to Human Polygenic Disease

by Ronald

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