The psychometric structure of the Wechsler Memory Scale (WMS) and its relationship to the revised Wechsler Adult Intelligence Scale (WAIS‐R) were studied in an outpatient population of 103 individuals with low Full Scale IQ scores (M = 71). We found that the age correction of the WMS scores gave memory quotients (WMQ) equivalent to WAIS‐R FSIQ scores, but our findings also raised problems of interpretation. If the usual rule of thumb of a 12‐point discrepancy between the MQ and the FSIQ were applied, the WMS might be relatively insensitive to memory impairment in this low‐IQ clinical population, in which more numerous cases of impairment could be expected. Principal components analysis of the WMS raw scores and three WAIS‐R scores included as reference variables yielded five orthogonal factors: Attention/Concentration; Visual Reproductions; New Verbal Learning; Well‐learned Semantic Knowledge; and Intelligence. We argue that raw scores on the WMS should be reported to optimize possible diagnostic specificity and to align the WMS with experimental and clinical research in various types of memory functioning and impairment.
The 2′,3′-dideoxynucleosides (ddNs) are currently undergoing clinical evaluation as antiretroviral agents in HIV-infected individuals. When phosphorylated, the ddNs (ddNTPs) function as chain-terminating substrate analogues with reverse transcriptase, thereby inhibiting HIV replication. These nucleoside analogues can also inhibit, by chain- terminating additions, the primitive lymphoid DNA polymerase, terminal deoxynucleotidyl transferase (TdT). To determine the effect of possible intracellular chain-terminating additions of ddNMPs by TdT, we exposed a series of TdT-positive and TdT-negative cell lines to 2′,3′- dideoxyadenosine (ddA), a representative ddN. At ddA concentrations 25- fold higher than required for inhibition of HIV replication, progressive dose-related cytotoxicity was observed in the TdT-positive cell lines. This was accentuated by the adenosine deaminase inhibitor Coformycin (CF), presumably by enhancing the intracellular generation of ddATP from ddA. A central role of TdT in mediating the ddA/CF cytotoxicity was suggested by studies in a pre-B-cell line rendered TdT positive by infection with a TdT cDNA-containing retroviral vector. After a 48-hour continuous exposure period to 250 mumol/L ddA and 30 mumol/L CF, 30% cell death was observed in the TdT-negative parental line, whereas 90% cell death was observed in the TdT-positive daughter line. Exposure of fresh TdT-positive leukemic cells to ddA/CF for 72 hours ex vivo resulted in cytotoxicity (six cases of acute lymphocytic leukemia [ALL]) while not affecting TdT-negative acute leukemic cells (six cases). We conclude that ddA/CF selectively damages TdT-positive cells, presumably by chain-terminating additions of ddAMP, and that this may have therapeutic relevance in TdT-positive malignant disease.
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