Dr. Baumann is currently resident of the Department of Obstetrics and Gynecology at the University Hospital of Bern, Switzerland (Prof. Daniel Surbek). He also works at the Research Laboratory for Prenatal Medicine at the Department of Clinical Research at University of Bern. Following studies at the Medical Schools in Geneva, Switzerland, he studied at the Medical School in Zurich, Switzerland, where he also graduated.

He investigated traumatic spinal cord lesions in mice at the Brain Research Institute of the Univerity of Zurich; Thesis supervised by Prof. Martin Schwab. He worked as a post-doc fellow in the maternofetal medicine group at the Department of Obstetrics and Gynecology of UMDNJ (University of Medicine and Dentistry of New Jersey, U.S.A.; Prof. Nick Illsley). Following residencies in Bern, Biel as well as a followship in St.-Imier he specialized in Obstetrics and Gynecology at the University Hospital of Bern.

Intrauterine growth restriction (IUGR), hypertensive disorders including preeclampsia, and gestational diabetes are common in pregnancy and have a major impact on perinatal morbidity and mortality of both the mother and its child. Furthermore children, compromised by these pregnancy-specific diseases, have an increased risk for cardiovascular disease or diabetes later in life. This phenomenon is known as “fetal programming”. Placental membrane transporters and their regulation play a crucial role in this process since they have key impact on the environment of the fetus.

Dr.  Baumann has extensive expertise in placental transport protein expression and their regulations under pathophysiological conditions. He investigated the expression of various transporters, such as the Glucose transporter-1 (GLUT1) and -3 (GLUT3) the transferring receptor (TfR), upon hypoxia. Further, he established a large placental tissue bank, with focus on preeclampsia and IUGR. This enables to investigate placental protein expression in such diseases, which are commonly associated with fetal hypoxia. As recently reported he observed altered serum protein levels in pregnancies with later preeclampsia, indicating that these proteins might serve as potential serum markers for the prediction of subsequent preeclampsia. Whether these proteins play a role in the pathogenesis of preeclampsia or affect “fetal programming” remains to be investigated.

Understanding the underlying regulation mechanisms of placental membrane transport proteins and their impact on fetal programming will help to develop prophylactic strategies to prevent the long-term consequences of these pregnancy-specific diseases and, thus, to decrease their devastating impact on society.

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