By K. Kitagawa, D. R. Colman (auth.), S. Salvati (eds.)
The ailments that fall less than the generalized workforce of demyelinating illnesses -Multiple Sclerosis, Leukodystrophyes, Encephalomyelitis-are the focal point of globally obstacle. This quantity comprises papers awarded through best scientists who attended the NATO complex examine Workshop held on the Istituto Superiore di SanitA, Rome, March 1-4, 1993. This publication is an replace of the former one released in 1987 of the learn mentioned at the same assembly held in 1986. It used to be determined to carry this 2d assembly considering the fact that there was nice development within the advances in figuring out the myelinogenesis approach within the final 5 years. The workshop accrued jointly scientists from many fields akin to mobile and molecular biology, immunology, pathology, virology and naturally medical neurology. Stimulating principles have been exchanged within the desire that extra wisdom of demyelinating illnesses can result in new theraupetic ways. even though the workshop used to be customarily just like the former one, this time there has been extra emphasis on experimental versions and medical facets. within the former using animal and mobile versions as instruments for knowing the pathological mechanisms associated with human affliction have been mentioned; within the latter the clinicians defined the filtering down of uncomplicated learn to medical remedy The e-book of this interdisciplinary alternate is to make identified the result of the latest study one of the investigators from allover the area thinking about those studies.
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Additional info for A Multidisciplinary Approach to Myelin Diseases II
2. Gel electrophoresis of PMP22-specific amplifkatioo products: Products were obtained from DNAPCR of high molecular weight genomic DNA derived from infected Schwann cells. The PCR was performed using standard conditions recommended by the manufacturer (New England Biolabs). ification of a 524bp product derived from the subcloned CD25IPMP22 fragment extending from nt 48 to nt 572. (B) Amplification of a 598bp product extending from the SLX-CMV multicloning site sequence 26bp upstteam of the subcloned PMP22-cDNA fragment to nt 572 of the cDNA.
Whether this may indicate functional homologies is unclear. , 1992; Lemke, 1993; Suter et al. 1993). The search for putative functions of PMP22 in myelination and/or cell growth has been stimulated by identification of mutations of the PMP22 gene. , 1992 a, b). Moreover, PMP22 appears to be involved in the pathogenesis of the autosomal dominant inherited dysmyelinating peripheral neuropathies Charcot-Marie-Tooth Type 1 (CMTlA) and the Hereditary Neuropathy with Liability to Pressure Palsies (HNPP).
In primary cultures from the MBP-lacZ transgenic brain, only oligodendrocytes that had established contact with an axon express the transgene. These results suggest that cis-acting regulatory elements, activated in oligodendrocytes by an axonal signal, are located within 256 bp upstream from the MBP gene. RESULTS Tissue Expression of the MBP-lacZ Transgene is oligodendrocyte-specific To determine the extent of transgene expression, various tissues from FI animals from MBP-lacZ line 4 were analyzed for expression of 6-galactosidase, by histochemical staining with the chromogenic X-Gal substrate.