Forschungsprojekte: Innere Medizin
Validation of ICF Core Sets for Obesity
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Dr. A. Stucki
Background: The first version of the ICF Core Sets of Obesity will be tested from the patients’ point of view. Functioning is explored in different subsets of patients. For example, it is not clear whether patients with severe obesity (BMI>40) may simply have more severe problems or whether the profile of problems differs.
Collaboration: ICF Research Branch of the WHO Collaborating Centre for the Family of International Classifications at the German Institute of Medical Documentation and Information (DIMDI), IMBK, Ludwig-Maximilian University, Munich, Germany
ausgewählte Publikationen:
1. Stucki, A., P. Daansen, M. Fuessl, A. Cieza, E. Huber, R. Atkinson, N. Kostanjsek, G. Stucki, and J. Ruof. 2004. ICF Core Sets for obesity. J Rehabil Med(44 Suppl):107-13.
2. Stucki, A., M. Borchers, G. Stucki, A. Cieza, E. Amann, and J. Ruof. 2006. Content comparison of health status measures for obesity based on the international classification of functioning, disability and health. Int J Obes (Lond).
Development of ICF Core Sets for Sleep
Dr. A. Stucki
Background: Functioning is increasingly being taken into account for evaluating the impact of sleep disturbances on the individual and the effectiveness of treatments. With the International Classification of Functioning, Disability and Health (ICF), we can now rely on a globally-agreed-upon framework and system for classifying the typical spectrum of problems in functioning of persons given the environmental context in which they live. ICF Core Sets are subgroups of ICF items selected to capture those aspects of functioning that are most likely to be affected by sleep disturbances.
Grant: Privat
Collaboration: ICF Research Branch of the WHO Collaborating Centre for the Family of International Classifications at the German Institute of Medical Documentation and Information (DIMDI), IMBK, Ludwig-Maximilian University, Munich, Germany
ausgewählte Publikationen:
1. Stucki, A., A. Cieza, and E. Amann. 2005. Content Comparison of Obstructive-Sleep-Apnea-Targeted health Status Measures in Relation to the International Classification of Functioning, Disability and Health (ICF). Proceedings of the World Association of Sleep Medicine 1st Congress:119-124.
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The master transcription factor PU.1 is essential for normal hematopoiesis: Analysis of PU.1 alterations in acute myeloid leukemia (AML).
Dr. med. Beatrice U. Müller, Gruppenleiterin, Departement für Klinische Forschung, Universität Bern
The transcription factor PU.1 is expressed at highest levels in granulocytic cells and plays a crucial role during myeloid differentiation; furthermore, pu.1-/- mice lack mature myeloid cells. We recently reported that mutations of the PU.1 gene are found in some patients with AML and that decreased pu.1 expression induces leukemia in mice. Here we investigate regulatory elements which direct the expression of PU.1.
Research grants: Oncosuisse Grant to BUM.
Collaborations: Prof. D.G. Tenen, Harvard University, Boston, Dr. Thomas Pabst, Institute for Medical Oncology, Prof. N. Asou, University of Kumamoto, Prof. G. Gilliland, Harvard University Boston.
ATRA resolves the differentiation block in acute promyelocytic leukemia by restoring PU.1 expression.
Dr. med. Beatrice U. Müller, Gruppenleiterin, Departement für Klinische Forschung, Universität Bern
Acute promyelocytic leukemia (APL) harbors in 98% the translocation t(15;17), fusing a part of the PML gene to the retinoic acid receptor a (RARA) gene to encode PML-RARA. ATRA treatment together with chemotherapy is considered to represent a standard therapy for APL patients. The response to ATRA induces differentiation of t(15;17) blasts, presumably through degradation of the PML-RARA fusion protein. PML-RARA interacts with transcriptional co-repressors in an ATRA sensitive manner, blocking the activation of RARA target genes. However, this hypothesis so far has hardly connected PML-RARA with transcription factors which are known to be critical for granulocytic differentiation. We found that expression of PU.1 is suppressed in human PML RARA leukemic cells, and that treatment of these cells with ATRA restores PU.1 expression and induces neutrophil differentiation. In primary t(15;17) patient cells, PU.1 was markedly upregulated after treatment with ATRA. Restoring PU.1 in PML RARA leukemic cells overcame the differentiation block and was necessary and sufficient to trigger neutrophil differentiation. These studies demonstrate that restoration of PU.1 expression is critical to induce differentiation of PML-RARA cells. We are currently investigating further regulatory mechanisms in ATRA induced differentiation.
Research grants: Swiss National Science Foundation SF 3100A0-100445 to BUM.
Collaborations: , Prof. N. Asou, University of Kumamoto, Prof. D.G. Tenen, Harvard University, Boston. Prof. N. Timchenko, Houston, TX
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Dopplersonographische bestimmung des Resistenz-Index (RI) an arteriellen Nierengefäßen bei Patienten mit Leberzirrhose
PD Dr. med. Uwe Schiemann
Untersuchung der Nierenperfusion (Gefäßwiderstände) in Bezug zum Schweregrad der Leberzirrhose (mit oder ohne Aszitesbildung) und Vergleich der Perfusionsmuster bei Patienten mit anderen Hepatopathien (Fettleber, chronische Hepatitis), RI-Erhöhung als Risikofaktor für die Entwicklung eines hepatorenales Syndroms
Kooperation: Medizinische Klinik Innenstadt, Gastroenterolog. Abteilung (Prof. Dr. W.med. Heldwein), Ludwig-Maximilians-Universität München
Grant: Friedrich-Baur-Stiftung München
Sonographie von Pankreastransplantaten bei Typ I-Diabetikern: Verbesserung der Darstellung durch den Einsatz des Tissue Harmonic Imaging
PD Dr. med. Uwe Schiemann
Optimierung der Detektion und Organbeschreibung von Pankreastransplantaten mit dem Ziel der differentialdiagnostischen Abklärung Abstoßungsreaktion vs. Transplantat-Pankreatitis vs. Infektion vs. ischämische Organschädigung.
Kooperation: Medizinische Klinik Innenstadt, Gastroenterolog. Abteilung (Prof. Dr. W. med. Heldwein), Ludwig-Maximilians-Universität München
Grant: Friedrich-Baur-Stiftung München
Erweiterte Mikrosatellitenanalyse beim hereditären nicht polypösen kolorektalen Karzinom (HNPCC)
PD Dr. med. Uwe Schiemann
Analyse eines selektionierten Patientenkollektivs von Amsterdam positiven, mikrosatellitenstabilen oder nur schwach instabilen HNPCC-Tumoren, die keine Mutationen in den klassischen, kausalen Mismatch-Reparaturgenen aufweisen. Detektion zusätzlicher Instabilitäten in anderen Mikrosatelliten, Reklassifikation der Tumoren und Korrelation mit klinischen Merkmalen.
Kooperation: Medizinische Klinik Innenstadt, Humangenetisches Institut (PD Dr. med. dipl.-chem. E. Holinski-Feder), Ludwig-Maximilians-Universität München
Grant: Verbundprojekt der Deutschen Krebshilfe e.V.
Detektion und Charakterisierung von fokalen Leberläsionen durch Kontrastmittelsonographien
PD Dr. med. Uwe Schiemann
Dokumentation und Auswertung von Kontrastmiitelsonographien im Hinblick auf Indikationen und Aussagefähigkeit im Vergleich mit anderen bildgebenden Verfahren, Einsatz bei Kontraindikationen für CT und MRT (z.B. Niereninsuffizienz, Hyperthyreose)
Kooperation: Institut für Interventionelle, Diagnostische und Pädiatrische Radiologie (Prof. Dr. med. Vock), Inselspital Bern
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