Dioxine. Eine Einfuehrung und Uebersicht zum Kenntnisstand

The state of knowledge on dioxins and furans is reviewed. Subjects: Reaction pathways of dioxin formation, toxicology, production processes and volumes in technical processes, prevention and reduction of dioxin production in technical processes, dispersion and fate in the environment, uptake by humand, routine analysis of dioxins and furans. (orig./SR)Es wird eine Uebersicht ueber den Kenntnisstand zu den Schadstoffen Dioxin und Furan gegeben. Hierbei wird eingegangen auf wichtige Reaktionswege zur Bildung von Dioxinen, Toxikologie, Entstehung und Vorkommen in technischen Prozessen, Vermeidung und Verminderung der Entstehung in technischen Prozessen, Verbreitung und Verhalten in der Umwelt, Aufnahme durch den Menschen und Routineanalytik der Dioxine und Furane. (orig./SR)SIGLEAvailable from TIB Hannover / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekLovar Stiftung fuer Umweltschutz, Luzern (Switzerland)DEGerman

Lack of association between the MEF2A gene and myocardial infarction.

Coronary artery disease (CAD) and myocardial infarction (MI) are caused in part by genetic factors. Recently, the MEF2A gene was linked to MI/CAD in a single pedigree with autosomal-dominant pattern of inheritance. In addition, genetic variants within the gene have been associated with MI in case-control settings, producing inconsistent results. METHODS AND RESULTS: The MEF2A gene was sequenced in MI patients from 23 MI families (> or =5 affected members per family), but no mutation was identified in any of these extended families. Moreover, the Pro279Leu variant in exon 7 was analyzed in 1181 unrelated MI patients with a positive family history for MI/CAD, in 533 patients with sporadic MI, and in 2 control populations (n=1021 and n=1055), showing no evidence for association with MI/CAD. In addition, a (CAG)n repeat in exon 11 was genotyped in 543 sporadic MI patients and in 1190 controls without evidence for association with MI. Finally, analyzing 11 single-nucleotide polymorphisms from the GeneChip Mapping 500K Array, genotyped in 1644 controls and 753 cases, failed to provide evidence for association (region-wide P=0.23). CONCLUSIONS: Studying independent samples of >1700 MI patients, 2 large control populations, and multiple families with apparently mendelian inheritance of the disease, we found no evidence for any linkage or association signal in the MEF2A gene