The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five ageand sex-matched control cases. Serial 500-l-lm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36-72 years) was 5.97x 10 9 ±320x 10 6 , the average number of small striatal neurones was 82 X 10 6 ± 15.8 X 10 6 • The left striatum (caudatum, putamen, and accumbens) contained a mean of 273 X 10 6 ±53 X 10 6 glial cells (oligodendrocytes, astrocytes and unc1assifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36-75 years) was diminished by about 33 % to 3.99x10 9 ±218x10 6 nerve cells (P : : ; : : : : 0.012, MannWhitney V-test). The mean number of small striatal neurones decreased tremendously to 9.72 X 10 6 ±

In Part I (Mates 1994), a linear model of timing and error-corrections was constructed that aims at an explanation of the mechanisms underlying a subject's performance in an experimental paradigm, in which the task is to synchronize a sequence of motor acts to a sequence of stimuli. The model consists of two error-corrective mechanisms: (1) corrections of period (inverted frequency) of the sequence of responses; (2) corrections of phase shift of that sequence (synchronization error). In this paper, the influence of the physiologically justifiable model variables and of initial conditions on the steady-state response sequence as well as the stability of performance of the model are analyzed. The model is stable for error-correction gains in the range from 0 to 2. Comparison with known empirical data supports the assumption that reasonable values are less than 1. Furthermore, an alternative to the basic linear model is introduced in which the possible character of the process of subjective acquisition of the synchronization error is discussed. On the basis of findings from other experimental paradigms (fusion and order threshold) it can be assumed that the subjective estimate is a nonlinear function of the difference between the temporal central availability of internal representations of the stimulus and response-feedback events. Some other known synchronization data are simulated by the nonlinear modification of the model in this paper. A good fit of the simulation results achieved further justifies the model structure proposed. Finally, the possible effect of the subjective synchronization-error estimation on empirical data is discussed.

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The potential contribution of the Internet to smoking cessation seems huge, given that a majority of Americans now have both computers and telephones. Despite the proliferation of Web sites offering smoking cessation support, there is little empirical evidence regarding the efficacy of Internet-delivered cessation programs. We developed a cessation Web site and conducted a short-term evaluation of it, examining recruitment approaches, Web site use patterns, alternative retention incentives and re-contact modes, satisfaction, and cessation rate. The intervention included modules on social support and cognitive-behavioral coping skills configured to take advantage of the interactive and multimedia capabilities of the Internet. Cessation and satisfaction data were obtained from a subsample of 370 subjects followed for 3 months. The program was rated as easy to use, and the social support group component was used most frequently. The cessation rate (abstinence for the previous 7 days) at 3 months was 18%, with nonrespondents (n~161) considered smokers. Among a variety of traditional and Internet-based recruitment strategies, the most successful made use of Internet user groups and search engines. Methodological and procedural issues posed in conducting research on the Internet are discussed.

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