This study examined differences in anger and anger expression between college students high in symptoms of attention-deficit/hyperactivity disordered (ADHD) and non-ADHD college students. Other emotional and psychological differences were also explored. The ADHD group exhibited significantly higher levels of trait and state anger, more dysfunctional and socially inappropriate ways of expressing anger, as well as more symptoms of psychological distress, more difficulty in interpersonal relations, more high school truancy, and more labile anxious/depressed moods than the non-ADHD group. Parents also reported that their sons and daughters high in ADHD symptoms had higher levels of anger and poorer forms of anger expression than did parents of the non-ADHD individuals. The ADHD group was not, however, more emotionally intense or more emotionally responsive to external consequences. The results are discussed with respect to anger and anger expression, general psychological functioning, and related areas of difficulty for ADHD adults. Implications for the treatment of ADHD college students are outlined.A ttention-deficit/hyperactivity disorder (ADHD) is a chronic, debilitating disorder that affects approxijL ately 5% of elementary school-aged children (Barkley, 1990). Individuals with ADHD exhibit deficits in sustained attention, hyperactivity, impulsivity, and behavioral control. Until recently, it was widely believed that ADHD was limited to children, and that the disorder was typically outgrown by adolescence. However, follow-up studies conducted over the past 20 years have shown that children diagnosed with ADHD display symptoms into adolescence and young adulthood (Brown & Borden, 1986;Thorley, 1984;Weiss & Hechtman, 1986). Although findings of the prevalence of ADHD in adulthood vary from study to study, recent research suggests that from 30-60% of individuals diagnosed with ADHD in childhood retain the full disorder into adulthood (Weiss & Hechtman, 1993). Barkley's (1994; in press) recent theoretical integration suggests that the primary problem for ADHD individuals is one of inhibiting behavior or controlling their impulse to respond to a situation. Therefore, the three basic characteristics of ADHD -inattention, impulsivity, and hyperactivity -can be described as fundamental impairments in behavioral inhibition and delaying responses. Individuals with ADHD appear to have neurological impairments in the executive brain functions critical for developing self-control and directing behavior toward the future (Barkley, in press). Impairment of these systems contributes to the difficulty ADHD individuals have with inhibiting immediate responses to their environments, their inability to stop ongoing responses, and their difficulty in retaining information in working memory. Moreover, impairment in these executive functions cause ADHD individuals to act without hindsight (i.e., ability to relate past knowledge to a present situation) and forethought (i.e., ability to discern patterns of behavior from one's experienc...
The Saccharomyces cerevisiae FLO1 gene encodes a cell wall protein that imparts cell–cell adhesion. FLO1 transcription is regulated via the antagonistic activities of the Tup1–Cyc8 co-repressor and Swi–Snf co-activator complexes. Tup1–Cyc8 represses transcription through the organization of strongly positioned, hypoacetylated nucleosomes across gene promoters. Swi–Snf catalyzes remodeling of these nucleosomes in a mechanism involving histone acetylation that is poorly understood. Here, we show that FLO1 de-repression is accompanied by Swi–Snf recruitment, promoter histone eviction and Sas3 and Ada2(Gcn5)-dependent histone H3K14 acetylation. In the absence of H3K14 acetylation, Swi–Snf recruitment and histone eviction proceed, but transcription is reduced, suggesting these processes, while essential, are not sufficient for de-repression. Further analysis in the absence of H3K14 acetylation reveals RNAP II recruitment at the FLO1 promoter still occurs, but RNAP II is absent from the gene-coding region, demonstrating Sas3 and Ada2-dependent histone H3 acetylation is required for transcription elongation. Analysis of the transcription kinetics at other genes reveals shared mechanisms coupled to a distinct role for histone H3 acetylation, essential at FLO1, downstream of initiation. We propose histone H3 acetylation in the coding region provides rate-limiting control during the transition from initiation to elongation which dictates whether the gene is permissive for transcription.
We report on the clinical and cytogenetic findings in a 9-year-old boy with a de novo deletion of 2q, shown by molecular analysis to have arisen from the paternal chromosome. Examination of microsatellite markers indicated deletion of bands 2q24.3 and 2q31. Clinical findings included craniosynostosis, bilateral ocular colobomata, and limb abnormalities, the latter being an emerging association with deletion of this region of 2q.
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Tuberculosis remains the leading cause of death worldwide from a single infectious organism. Approximately 32% of the world's population is infected and an estimated two million people die annually from this treatable disease. Over the past 50 years, with medical treatment and standard public health practices, tuberculosis diminished in developed countries and resulted in a loss of interest and funding for research in improving diagnostic and treatment options. In developing countries, efforts including BCG vaccination have failed to control tuberculosis and the disease continues to spread as the world becomes more globalized. At the same time, multidrug resistant tuberculosis has emerged, challenging even the most advance treatment centers. Better diagnostic techniques, control measures and treatment options are desperately needed but advances require worldwide commitment to battle this age-old disease.
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