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Coronary artery disease (CAD) is a leading cause of death world-wide, and most cases have a complex, multifactorial aetiology that includes a substantial heritable component. Identification of new genes involved in CAD may inform pathogenesis and provide new therapeutic targets. The PROCARDIS study recruited 2,658 affected sibling pairs (ASPs) with onset of CAD before age 66 y from four European countries to map susceptibility loci for CAD. ASPs were defined as having CAD phenotype if both had CAD, or myocardial infarction (MI) phenotype if both had a MI. In a first study, involving a genome-wide linkage screen, tentative loci were mapped to Chromosomes 3 and 11 with the CAD phenotype (1,464 ASPs), and to Chromosome 17 with the MI phenotype (739 ASPs). In a second study, these loci were examined with a dense panel of grid-tightening markers in an independent set of families (1,194 CAD and 344 MI ASPs). This replication study showed a significant result on Chromosome 17 (MI phenotype; p = 0.009 after adjustment for three independent replication tests). An exclusion analysis suggests that further genes of effect size lambda(sib) > 1.24 are unlikely to exist in these populations of European ancestry. To our knowledge, this is the first genome-wide linkage analysis to map, and replicate, a CAD locus. The region on Chromosome 17 provides a compelling target within which to identify novel genes underlying CAD. Understanding the genetic aetiology of CAD may lead to novel preventative and/or therapeutic strategies.

Background: Age-adjusted morbidity and mortality rates from coronary heart disease (CHD) are higher in men than in women. Androgens are suspected to be responsible for the male disadvantage. The genomic effect of androgens is mediated by the androgen receptor (AR), which has a polymorphic CAG repeat in exon 1. The number of repeats is inversely related to the transcriptional activity of the AR on target genes. Methods: We investigated the association of this CAG repeat polymorphism with CHD and myocardial infarction (MI) in 2 independent case–control studies involving 544 Caucasian men. Results: The number of CAG repeats in the AR gene correlated significantly with HDL-cholesterol (HDL-C) in controls (r = 0.21; P = 0.015). This effect was independent of triglycerides, body mass index, alcohol intake, smoking, and age in a multiple regression model (R2 = 50%). Despite decreased HDL-C, lower CAG repeat numbers were not associated with increased risk for CHD (odds ratio = 0.82; 95% confidence interval, 0.50–1.36; P = 0.44) or MI in carriers of AR genes with lower CAG repeat numbers (odds ratio = 0.72; 95% confidence interval, 0.37–1.39; P = 0.33). Conclusions: Shorter, more androgenic AR alleles with fewer CAG repeats are associated with lower HDL-C, but not with an increased risk for CHD or MI, which argues against a detrimental androgen effect on cardiovascular risk under physiologic conditions.

[...]the expected 61% reduction in events of ischaemic heart disease from cholesterol lowering by using statins is about twice that yet seen in any trial.

Coronary artery disease (CAD) is a leading cause of death world-wide, and most cases have a complex, multifactorial aetiology that includes a substantial heritable component. Identification of new genes involved in CAD may inform pathogenesis and provide new therapeutic targets. The PROCARDIS study recruited 2,658 affected sibling pairs (ASPs) with onset of CAD before age 66 y from four European countries to map susceptibility loci for CAD. ASPs were defined as having CAD phenotype if both had CAD, or myocardial infarction (MI) phenotype if both had a MI. In a first study, involving a genome-wide linkage screen, tentative loci were mapped to Chromosomes 3 and 11 with the CAD phenotype (1,464 ASPs), and to Chromosome 17 with the MI phenotype (739 ASPs). In a second study, these loci were examined with a dense panel of grid-tightening markers in an independent set of families (1,194 CAD and 344 MI ASPs). This replication study showed a significant result on Chromosome 17 (MI phenotype; p = 0.009 after adjustment for three independent replication tests). An exclusion analysis suggests that further genes of effect size lambda(sib) > 1.24 are unlikely to exist in these populations of European ancestry. To our knowledge, this is the first genome-wide linkage analysis to map, and replicate, a CAD locus. The region on Chromosome 17 provides a compelling target within which to identify novel genes underlying CAD. Understanding the genetic aetiology of CAD may lead to novel preventative and/or therapeutic strategies.

Doing the right things in a given situation at the right time is the underlying formula for the achievements of every business. But what are \"the right things\"? On what foundation can good and solid decisions be based upon? Most companies have vision and mission statements which guide them in their daily and / or strategic decision making processes. These statements embody a company's fundamental convictions and values - its core of being. The vision statement typically is future oriented outlining a clear picture about a superior state or goal that a company wants to achieve. In this context, the paper presented shows an approach to the development of a vision statement in a workshop framework with help of the LEGO® SERIOUS PLAY® method (LSP). LSP can be described as a perfect tool for enabling and enhancing communication within a workshop framework. In detail, it will be shown how LSP made a valuable contribution to the development of a vision statement. For this, the paper provides a real application example: The development of a vision statement for an automotive competence center that is organized as a public private partnership. [PUBLICATION ABSTRACT]

Zwischen 1979 und 1991 wurden 16 288 Männer und 7 328 Frauen im Alter von 16-65 Jahren in die Prospective Cardiovascular Münster (PROCAM-)Studie aufgenommen.Ergebnis: Der Bodymass-Index (BMI) bei der Eingangsuntersuchung betrug bei Männern 25,6 ± 3,3 kg/m2 Körperoberfläche (KOF) und bei Frauen 23,8 ± 4,1 kg/m2 KOF. Er stieg in beiden Geschlechtern mit dem Alter an, bei Frauen ausgeprägter als bei Männern. Die altersstandardisierten Werte von Gesamt- und LDL-Cholesterin, den Triglyceriden, dem Nüchternblutzucker, der Harnsäure und dem Blutdruck korrelierten positiv, der HDL-Cholesterinspiegel negativ zum BMI. In dem Teilkollektiv der männlichen Teilnehmer an der PROCAM-Studie im mittleren Lebensalter, die 8 Jahre lang nachbeobachtet wurden, traten 258 schwerwiegende koronare Ereignisse auf. Die Inzidenz stieg mit zunehmendem BMI an. In einer multivariaten Auswertung erwies sich der BMI jedoch nicht als unabhängiger Risikofaktor. Die Beziehung ist indirekt; mit steigendem relativen Körpergewicht verschlechtert sich das Profil der Risikofaktoren und damit steigt das koronare Risiko an.