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With the implementation of the third
C4 professorship at the Institute, the Tropical Medicine Section was founded
to foster disease-oriented research. It combines the pre-existing Departments
of Pathology and Clinical Chemistry with two newly established units, namely
the Department of Molecular Medicine and the Kumasi Centre for Collaborative
Research in Tropical Medicine in Kumasi, Ghana. The activities of the Provisional
Research Unit, Macenta, Guinea, were terminated. They are described by
the Unit’s Head separately.
The Department of Pathology continued
its successful and internationally reputed work on the role of productively
and latently infected cells in HIV infection. An additional study addresses
the contribution of antibodies to the enhancement and neutralization of
lentivirus pathogenicity. One of the outstanding characteristics of the
Department is its intimate engagement in a highly productive network of
international scientific cooperation, which is documented in an impressive
list of collaborating partners. Of critical regional and national importance
are the diagnostic skills of the Department, which make it a reference
centre for the histopathology of tropical as well as other infectious and
exotic diseases.
Research activities of the Department
of Clinical Chemistry like before concentrated on clinical immunology in
the framework of the Institute Programme on Molecular and Cellular Interactions
between Parasite and Host in Onchocerciasis. The projects are summarized
separately in this issue by the Programme Coordinator. To the greater part,
the Department of Clinical Chemistry used to be devoted to diagnostic services
for the Hafenkrankenhaus and the Institute’s Department of Clinical Medicine.
The closing of the Hafenkrankenhaus in February 1997 drastically reduced
the workload in diagnostics, and, subsequently, nearly all of routine clinical
chemistry had to be abandoned for economic reasons.
The Department of Molecular Medicine
arose from the Department of Molecular Genetics when it moved from the
Molecular Biology to the Tropical Medicine Section early during the year.
The move did not affect the research projects, which continued to address
the genetic basis of human and, to a lesser extent, animal disease. Still
the main objective is to identify genes conferring resistance to major
tropical diseases. Human schistosomiasis and bovine trypanosomiasis are
under intense study. A side project on genetic factors influencing the
development of Parkinson´s disease had been started three years ago,
when suitable samples from classical tropical diseases were not available;
it now yielded evidence for an interesting disease locus on chromosome
2. Likewise, a small project disclosed the molecular basis for an inherited
form of severe hearing impairment occurring with an extraordinarily high
prevalence in a village in Ghana. This project provided a fortunate start
for collaborative research with scientists from Kumasi.
Certainly the hallmark of the year
was the founding of the Kumasi Centre for Collaborative Research in Tropical
Medicine, a joint venture of the Bernhard Nocht Institute and the School
of Medical Sciences of the University of Science and Technology in Kumasi.
The Centre is described in greater detail in a separate chapter and commented
upon in the Director’s Report.
| Staff
Prof. Dr. Rolf D. Horstmann,
Prof. Dr. Paul Racz
Privatdozent Dr. Frank W. Tischendorf
Dr. Christoph Hamelmann
Dr. Thomas F. Kruppa
Dr. Zézé Albert
Privatdozent Dr. B. Müller-Myhsok
Visiting Scientists, Department of Pathology and Körber-Laboratory for AIDS-Research Prof. Dr. Michel Huerre, Institut
Pasteur, Paris, France
Doctoral Students Kirsten Arndt
Graduate Students Tanja Kubica
Support Staff Birgit Förster
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Genetic cause for severe neurosensory
hearing ímpairment among inhabitants of the "deaf village" in Ghana.
Two deaf women communicating in the unique sign language developed in their
village and DNA sequence electropherograms showing a C -> T mutation in
the first position of codon 143 of the connexin-26 gene found in a homozygous
form (left) in 17 deaf villagers, and heterozygosity for this mutation
(middle) and wild-type genotypes (right) found in 9 and 2 normally hearing
family members, respectively.
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