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This paper presents the results of an in-depth study of parameters characterizing sequenced saccadic eye movements for a group of dyslexic children and a comparative normal control group with ages in the range greater than 8.0 yr. and less than 13.0 yr. No parameters were statistically different for the two groups, which supports the findings of Brown, et al. and contradicts the findings of Pavlidis. Our results indicate that sequenced saccadic eye movements are not diagnostically useful for early detection of dyslexia.

This paper describes an extensive study of the parameters of saccadic eye movement in a group of 28 poor-reading children and a comparative normally reading group of 31 children. Ages ranged from 6.0 to 16.9 yr. Poor readers had normal intelligence but were lagging by at least two years in reading ability as compared to their peer age group. Parameters studied in refixation eye movements included saccadic latency, accuracy, velocity, and acceleration, as well as differences in latency for abduct and adduct movements. Shapes of saccades were also studied. It was shown that eye-movement performance in simple saccadic refixation was not distinguishably different for poor readers and normal readers, even though in reading, which requires higher processing, eye-movement characterisics are quite different. Maturational changes for various saccadic eye-movement parameters were also examined for the normal and poor reading groups.

This paper describes a detailed study of horizontal eye movements associated with visual tracking of a smoothly moving target. Essentially all children, even at target velocities as low as 5°/sec., show some saccadic eye movements superimposed on smooth tracking movements. Detailed analysis of pursuit eye-movements from a group of 26 poor readers and 34 normal controls (8 to 13 yr.) showed that about 25% of poor readers have an abnormally raised saccadic component in smooth pursuit. This suggests that studies of eye movements during tracking of smoothly moving targets at low velocity, combined with a quantitative approach to data analysis, may be useful for early detection of a significant proportion of poor-reading children.

The yeast and human RAD51 genes encode strand-transfer proteins that are thought to be involved in both recombinational repair of DNA damage and meiotic recombination. In yeast, the Rad51 family of related proteins also includes Rad55, Rad57 and Dmc1. In mammalian cells, five genes in this family have been identified (HsRAD51, XRCC2, XRCC3, RAD51B/hREC2 and HsDMC1), and here we report the isolation of the sixth member, RAD51C. RAD51C was originally identified by a computer screen of the EST database. A full-length approximately 1.3 kb cDNA clone has been isolated that encodes a protein of 376 aa, having a 18-26% aa identity with other human Rad51 family members. RAD51C includes a previously mapped sequenced-tagged site location near the end of chromosome 17q. The RAD51C transcript is expressed in various human tissues, with highest level of expression in testis, followed by heart muscle, spleen and prostate. Yeast two-hybrid experiments indicate that the Rad51C protein binds to two other members of the Rad51 protein family (Xrcc3 and Rad51B) but not to itself. These findings suggest that Rad51C may function similarly to the yeast Rad55 or Rad57 proteins, rather than as a Rad51 functional homolog.

A veraged cortical evoked potentials from single clicks were recorded from 51 patients and controls. The patient group consisted of 40 subjects with a diagnosis of ‘nuclear’ schizophrenia, and 11 subjects with diagnoses including mania, anxiety neurosis and personality disorder.Changes in auditory evoked cortical responses (AECR's) were most marked in clinically stable, dysphoric, chronic schizophrenics. These subjects showed reproducible, low amplitude, ‘untidy’ responses in which the amplitude of the primary peak was lower than the amplitude of later peaks. Chronic schizophrenics who were rated as being depressed, showed a more ‘normal’ AECR.AECR changes during the memorising of nonsense syllables demonstrated a functional separation between early and later peaks of the AECR. It was postulated that the AECR changes in schizophrenia and during memorising result from pathological patterns of cortical desynchronisation produced by altered mid-brain activity different from that of anxious arousal, and that the clinical ‘steady-state’ of chronic schizophrenia is reflected in the ‘steady-state’ desynchronisation changes in the AECR.