Titlebook: Ataxia-Telangiectasia; Richard A. Gatti,Robert B. Painter Conference proceedings 1993 Springer-Verlag Berlin Heidelberg 1993 Ataxia-Telang

arthroplasty

Facet-Joints

野蠻

Complementation of the Cellular A-T Phenotype by Gene Transfermon feature of these diseases, cellular sensitivity to specific DNA damaging agents. The advent of gene transfer methods supplied the experimental system for this approach, which is apparently simple and straightforward: Exogenous DNA is introduced in vitro into the patient’s cells, and selection is

冷漠

Use of Microcell Hybrids for Analysis of the 11q23 Region and Improved Localization of the A-T Groupthis disease (Taylor et al. 1975). Localization of the A-T gene to chromosome 11q22–23 was first suggested from a genetic linkage study (Gatti et al. 1988) and this has been followed by recent additional reports confirming that the genes responsible for A-T complementation groups A and C are located

landmark

AT-like Radiosensitive Rodent Cell Mutants: An Alternative Approach to the Isolation of the A-T Geneectasia, immunodeficiency, hypersensitivity to ionizing radiation and predisposition to cancer (for review see Sedgwick and Boder, 1991). Despite extensive investigation, the molecular defect responsible for these pleiotropic abnormalities in A-T remains unknown.

deviate

Identification of A-T heterozygoteshemicals (reviewed in Bridges and Harnden, 1982) the response of cells from heterozygotes has been investigated with many procedures (summarised by Weeks ., 1991). Most techniques are able to detect a shift in the . response of heterozygote cells compared with normals but with considerable overlap b

Vulvodynia

Crepitus

adduction

Ingrained