Portrait of Franz Matthiesen; London Portraits Men

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Portrait of Hans Bernkopf Portraits Men

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Studio portrait of Hans Bernkopf Portraits Men

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Studio portrait of Hans Bernkopf as a young man. Portraits Men

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Freddy Godshaw (Gottschalk) while President of his Rotary Club. Portraits Men

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Walter Godshaw (Gottschalk) riding a motor scooter; Japan(?) Portraits Men

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Studio portrait of Moritz "Mori" Meyerhof. Portraits Men

Verso: Moritz Meyerhof (Mori) Meyerhof (29. April 1867 in Hildesheim?); p. 12 of the Stammtafeln die Familie Meyerhof. Donated by his nephew Hillel (Herbert) Meyerhof.

Portrait of Hirsch Lucas Goldschmidt Portraits men

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Portrait of Sampson Schoenbeck; Hannover, Germany. Portraits men

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Passport photo of Fritz Gottschalk Portraits Men

Photograph from Fritz Gottschalk's Nazi identification papers

Walter Godshaw (Gottschalk) riding a motor scooter; Japan(?) Portraits Men

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Leo Catzenstein seated on an outdoor bench Portraits Men

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Portrait of the engineer and geneologist Robert Goldschmidt Portraits Men

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Julius Pick aged 93 at his grandson Gary Godshaw's Bar Mitzvah; Buffalo, New York Portraits Men

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Candidate gene studies on cardiovascular traits

Cardiovascular diseases (CVD) are a major cause of death and disability in Western countries and a growing health problem in the developing world. The genetic component of both coronary heart disease (CHD) and ischemic stroke events has been established in twin studies, and the traits predisposing to CVD, such as hypertension, dyslipidemias, obesity, diabetes, and smoking behavior, are all partly hereditary. Better understanding of the pathophysiology of CVD-related traits could help to target disease prevention and clinical treatment to individuals at an especially high disease risk and provide novel pharmaceutical interventions. This thesis aimed to clarify the genetic background of CVD at a population level using large Nordic population cohorts and a candidate gene approach. The first study concentrated on the allelic diversity of the thrombomodulin (THBD) gene in two Finnish cohorts, FINRISK-92 and FINRISK-97. The results from this study implied that THBD variants do not substantially contribute to CVD risk. In the second study, three other candidate genes were added to the analyses. The study investigated the epistatic effects of coagulation factor V (F5), intercellular adhesion molecule -1 (ICAM1), protein C (PROC), and THBD in the same FINRISK cohorts. The results were encouraging; we were able to identify several single SNPs and SNP combinations associating with CVD and mortality. Interestingly, THBD variants appeared in the associating SNP combinations despite the negative results from Study I, suggesting that THBD contributes to CVD through gene-gene interactions. In the third study, upstream transcription factor -1 (USF1) was analyzed in a cohort of Swedish men. USF1 was associated with metabolic syndrome, characterized by accumulation of different CVD risk factors. A putative protective and a putative risk variant were identified. A direct association with CVD was not observed. The longitudinal nature of the study also clarified the effect of USF1 variants on CVD risk factors followed in four examinations throughout adulthood. The three studies provided valuable information on the study of complex traits, highlighting the use of large study samples, the importance of replication, and the full coverage of the major allelic variants of the target genes to assure reliable findings. Although the genetic basis of coronary heart disease and ischemic stroke remains unknown, single genetic findings may facilitate the recognition of high-risk subgroups.