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By Jeffery C. Hall

Advances in Genetics raises its specialise in sleek human genetics and its relation to medication with the merger of this long-standing serial with Molecular Genetic medication . This merger affirms theAcademic Press dedication to put up very important reports of the broadest curiosity to geneticists and their colleagues in affiliated disciplines.

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However, if laboratories are not equipped for multiple analyses, patients may be best served by a consortium of laboratories within the area, each performing its own particular test. If no duplication is detected in a patient and there is recorded male-tomale transmission of the disease within the family, then mutation screening of Po and PMP22 should he considered. The most common approach to this involves single-strand conformation polymorphism (SSCP) analysis, which relies on the amplification of a region of interest, and nondenaturing polyacrylamide gel electrophoresis.

Mohajeri, M. , Giese. K. , and Schachner, M. (1995b). Mice doubly deficient in the genes for Po and myelin basic protein show that both proteins contribute t o the formation of the major dense line in peripheral nerve myelin. J. Neurosci. 15:4488-4498. , Neuberg, D. , and Schachner, M. (1996). Mice deficient in the gene for connexin32 show pathological changes in peripheral nerves. 5th Annu. Eur. , London, 1996. , Lensch, M. , Hanemann, C. , Muller, H. , Bird, T. , and Chance, P. F. (1992). 2associated with Charcot-Marie-Tooth 1A.

75:9-12. , and Werner, R. (1991). Cell/cell channel formation involves disulphide exchange. Eur. Biochem. 197:141-144. , and Rabadan-Diehl, C. (1992). Mutational analysis of gap junction formation. Biophys. J. 62:172-182. Davies, D. M. ( 1954). Recurrent peripheral nerve palsies in a family. Lancet 2:266-268. 38 C. Bell and N. Hailes Dehruyne, J.. , and Martin, J . J. (1980). Hereditary pressure sensitive neuropathy. J. Neurol. Sci. 47:385-394. Defesche. 1. , Hoogendijk, J. , Ongerhoer de Visser, B.

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