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Includes bibliographical references / There are still no diagnostic criteria for a spectrum of neurocognitive disorders (ND) secondary to HIV infection for children. The American Academy of Neurology (AAN) proposes guidelines for assessment of HIV associated neurocognitive disorders (HAND) in HIV infected adults. A cross-sectional clinical cohort study was initiated in Cape Town, in which 120 participants, including a HIV negative healthy control group for comparison, completed clinical and neurocognitive assessments. HIV infected children were either stable on antiretroviral treatment (ART) for a minimum of 6 months or ART naïve. Neuroimaging was completed on 105 children in the cohort study. We compared 75 children vertically infected with HIV aged 6 to 16 years, including both children on antiretroviral therapy (ART) and ART-naïve, with 30 matched controls using diffusion tensor imaging (DTI) measures. We then used the detailed neurocognitive battery; an assessment of adaptive functioning and the AAN system for diagnosing ND to establish whether this system could detect a spectrum of ND in HIV infected older children and adolescents. When comparing HIV uninfected children to HIV infected children this DTI study found damaged neuronal microstructure in the HIV infected children. Significant associations were found between failing first line ART regimen, socio-demographic factors, nutritional-hematological status, HIV-relevant clinical variables, cognitive functioning and white matter integrity in children stable on ART. Children with a clinical diagnosis of encephalopathy (HIVE) had greater white matter damage when compared ART treated children without encephalopathy. DTI also found significant myelin loss in ART naïve children when compared with ART treated children. Using the AAN criteria for HAND, we found that 45.35% of the HIV infected children had a ND. ART naïve slow progressors, who receive limited attention from heath care service s, as they are thought to be 'well', were found to have neurocognitive impairment and white matter microstructural damage. HIV infected children were also more likely to have impaired competence in various domains of functioning. The current findings also underline the possible association of first line treatment failure with white matter brain dysfunction in children on ART. Despite the use of ART and improved virological control with immune reconstitution, there were still a significant percentage of children in this study who were found to have ND. Our findings also suggest that children on ART remain at risk for developing CNS disease, and that this risk extends to physically well ARV naïve slow progressors. The AAN HAND criteria designed for adults was able to identify children and adolescents with important functional cognitive impairments who don't fit criteria for HIVE and would therefore not have been identified otherwise.

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Responsibility for teaching communication skills often falls to a multidisciplinary group of faculty who lack both a common model for teaching and prior experience teaching communication in small groups. This article describes East Tennessee State University's multifaceted faculty development program in teaching communication skills. The program was developed and implemented in three phases. First, a two-step Delphi approach helped identify core communication skills. Phase two gave faculty the opportunity to practice identifying communication teaching issues and effective strategies for working with small groups. The third phase involved the videotaping of faculty teaching small groups of students. These tapes were reviewed both individually and in faculty groups. The tapes were also reviewed by students, who provided realtime, moment-to-moment feedback to the faculty. Implementation and review of the program has helped to identify new strategies for effectively facilitating small-group teaching of communication skills.

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Specific mutations in the gene for the beta amyloid precursor protein (APP) cause Alzheimer's disease (AD). A key neuropathological hallmark of AD is extracellular neuritic plaques. The core component of plaques is AB, a 39-43 amino acid peptide derived from APP. APP C-100 and APP C-105 are C-terminal fragments of APP, 100 and 105 amino acids long, respectively. APP C-100 is a normal metabolite of APP. AI3 is located at the N-terminus of the APP C-100 sequence. To determine whether APP C-105 expression alters cellular vulnerability to calcium and hydrogen peroxide, rat PC12 cells were modified to overexpress APP C-105. Permanent transfectants (clones) were selected, then characterized by standard molecular biological techniques. DNA and mRNA corresponding to APP C-105 were detected in APP C-105 transfectants, but not in wild type controls. Aggregated APP C-105 was detected in cell lysates and conditioned media from APP C-105 transfectants, but was absent or detected at lower concentrations in vector-transfected and wild type controls. Cell survival as a function of concentration was determined for A23 l 87, a Ca^2+ ionophore, and hydrogen peroxide in APP C-105 transfectants and vector-transfected controls. Cells were exposed to A23 l 87 or hydrogen peroxide for 24 hours in RP:MI media containing 3 μM insulin, and survival was quantitated using the tetrazolium dye, MTT. APP C-105 expression significantly increased PC 12 cell vulnerability to A23 l 87, and significantly decreased vulnerability to hydrogen peroxide. Other experiments were performed with GM 1 ganglioside, which is known to protect cells against numerous insults. When wild type PC 12 cells or APP C-10 5 transfectants were exposed to a toxin and GMl concurrently for 24 hours, GMl produced concentration-dependent inhibition of A23 l 87 toxicity in wild type PC 12 cells but was ineffective against hydrogen peroxide in both wild type PC12 and APP C-105-transfected clones. The current study has demonstrated that expression of APP C-105 protects PC 12 cells against hydrogen peroxide, but exacerbates the effect of calcium influx. In conjunction with other reports, this study indicates that APP C-105 is an important regulator of cellular homeostasis. Therefore, the pattern of APP processing may alter vulnerability to neurotoxic insults.