Professor Tomas Pexieder (6.6.1941-28.10.1995).

While hiking in the Swiss Alps, Prof T Pexieder tragically lost his life on October 28th, 1995. Tomas Pexieder was born in Prague on the 6.6. 1941, where he undertook his undergraduate studie~ and received his M. D. in 1965 from Charles Universil y. During his last 3 years at medical school, he also dedicated himself to research at the Institute of Anatomy and published his first paper on adipose vascularisation in rab II}. From 1962 to 1965, he worked with Dr Z. Rychtcr :It the Institute of Anatomy, where he investigated the de\clopmenr of aortic arches in the chick embryo. After three \car" at Ihc Institute of Embryology, he moved to the Lund University (Sweden) for one year before joining the Institute of Histology and Embryology in Lausanne in 1969, where he became associated professor in 1977. In August 1995, he became cochairman of the Institute "ad interim" until his death. As one of the pioneers of modern cardiac embryology, Tomas Pexieder attempted to link molecular and cellular events to structure changes of the developing heart. He focused his attention on programmed cell death (now called apoptosis) 25 years before the present large interest in the field [2]. For his research, Tomas Pexieder used the tools of modern investigating morphology, including precise fixation techniques, transmission electron microscopy, scanning electron microscopy, immunohistochemistry and in situ hybridization [3 -14J. His publications were not only scientifically accurate, but also artistically composed. In the process of his morphologic studies, Tomas Pexieder reorganized thc conflicting and confusing terminology of embryonic cardiac morphology [15 -17J. He summarized his particular analysis of the conotruncus in a masterful recent paper [18J, explaining conotruncal defects in the Keeshond dog [19, 20J. He further pioneered the investigation of cardiac phenotype in the trisomy mouse [2/24J and was involved in defining the teratogen effect of trimethadione in the rat and of retinoic acid in the mouse. More recently he became fascinated by the effect of RXRa: genc knock-out (in collaboration with K. R. Chien, P. J. Gruber et aI., La Jolla, USA). His comparative pathogenetic studies lead him to bring new concepts about the pathogenesis of cardiac malformations. He recently attacked the molecular mechanisms of cardiac pathogenesis. His sense of excellence and competence led him to create a "developmental cardiology network" with the above mentioned investigators as well as Drs B. Keller, E. B. Clark (Rochester, USA), R. R. Markwald (Charleston, USA), 1. C. Prados (Madrid), P. S. Jouk (Grenoble, France), I. Ostadalova, V. Pelouch, M. Peterka (Czech Republic) and Y. Shimada (Chiba, Japan). In the course of the years Tomas Pexieder became one of the most prominent forces in the research of cardiovascular development and congenital heart disease keeping this position for more than a quarter century. His contributions ranged from the pioneering description of programmed cell death in the developing heart through nomenclature de scrip-