The Private Sector and HIV/AIDS in Africa: Taking Stock of Six Years of Applied Research

Background: Until recently, little was known about the costs of the HIV/AIDS epidemic to businesses in Africa and business responses to the epidemic. This paper synthesizes the results of a set of studies conducted between 1999 and 2006 and draws conclusions about the role of the private sector in Africa’s response to AIDS. Methods: Detailed human resource, financial, and medical data were collected from 14 large private and parastatal companies in South Africa, Uganda, Kenya, Zambia, and Ethiopia. Surveys of small and medium-sized enterprises (SMEs) were conducted in South Africa, Kenya, and Zambia. Large companies’ responses or potential responses to the epidemic were investigated in South Africa, Uganda, Kenya, Zambia, and Rwanda. Results: Among the large companies, estimated workforce HIV prevalence ranged from 5%¬37%. The average cost per employee lost to AIDS varied from 0.5-5.6 times the average annual compensation of the employee affected. Labor cost increases as a result of AIDS were estimated at anywhere from 0.6%-10.8% but exceeded 3% at only 2 of 14 companies. Treatment of eligible employees with ART at a cost of $360/patient/year was shown to have positive financial returns for most but not all companies. Uptake of employer-provided testing and treatment services varied widely. Among SMEs, HIV prevalence in the workforce was estimated at 10%-26%. SME managers consistently reported low AIDS-related employee attrition, little concern about the impacts of AIDS on their companies, and relatively little interest in taking action, and fewer than half had ever discussed AIDS with their senior staff. AIDS was estimated to increase the average operating costs of small tourism companies in Zambia by less than 1%; labor cost increases in other sectors were probably smaller. Conclusions: Although there was wide variation among the firms studied, clear patterns emerged that will permit some prediction of impacts and responses in the future.

A Quantitative Evaluation of the AVITEWRITE Model of Handwriting Learning

Much sensory-motor behavior develops through imitation, as during the learning of handwriting by children. Such complex sequential acts are broken down into distinct motor control synergies, or muscle groups, whose activities overlap in time to generate continuous, curved movements that obey an intense relation between curvature and speed. The Adaptive Vector Integration to Endpoint (AVITEWRITE) model of Grossberg and Paine (2000) proposed how such complex movements may be learned through attentive imitation. The model suggest how frontal, parietal, and motor cortical mechanisms, such as difference vector encoding, under volitional control from the basal ganglia, interact with adaptively-timed, predictive cerebellar learning during movement imitation and predictive performance. Key psycophysical and neural data about learning to make curved movements were simulated, including a decrease in writing time as learning progresses; generation of unimodal, bell-shaped velocity profiles for each movement synergy; size scaling with isochrony, and speed scaling with preservation of the letter shape and the shapes of the velocity profiles; an inverse relation between curvature and tangential velocity; and a Two-Thirds Power Law relation between angular velocity and curvature. However, the model learned from letter trajectories of only one subject, and only qualitative kinematic comparisons were made with previously published human data. The present work describes a quantitative test of AVITEWRITE through direct comparison of a corpus of human handwriting data with the model's performance when it learns by tracing human trajectories. The results show that model performance was variable across subjects, with an average correlation between the model and human data of 89+/-10%. The present data from simulations using the AVITEWRITE model highlight some of its strengths while focusing attention on areas, such as novel shape learning in children, where all models of handwriting and learning of other complex sensory-motor skills would benefit from further research.

How Does the Cerebral Cortex Work? Developement, Learning, Attention, and 3D Vision by Laminar Circuits of Visual Cortex

A key goal of behavioral and cognitive neuroscience is to link brain mechanisms to behavioral functions. The present article describes recent progress towards explaining how the visual cortex sees. Visual cortex, like many parts of perceptual and cognitive neocortex, is organized into six main layers of cells, as well as characteristic sub-lamina. Here it is proposed how these layered circuits help to realize the processes of developement, learning, perceptual grouping, attention, and 3D vision through a combination of bottom-up, horizontal, and top-down interactions. A key theme is that the mechanisms which enable developement and learning to occur in a stable way imply properties of adult behavior. These results thus begin to unify three fields: infant cortical developement, adult cortical neurophysiology and anatomy, and adult visual perception. The identified cortical mechanisms promise to generalize to explain how other perceptual and cognitive processes work.

Task-Irrelevant Perceptual Learning Specific to the Contrast Polarity of Motion Stimuli

Studies of perceptual learning have focused on aspects of learning that are related to early stages of sensory processing. However, conclusions that perceptual learning results in low-level sensory plasticity are of great controversy, largely because such learning can often be attributed to plasticity in later stages of sensory processing or in the decision processes. To address this controversy, we developed a novel random dot motion (RDM) stimulus to target motion cells selective to contrast polarity, by ensuring the motion direction information arises only from signal dot onsets and not their offsets, and used these stimuli in conjunction with the paradigm of task-irrelevant perceptual learning (TIPL). In TIPL, learning is achieved in response to a stimulus by subliminally pairing that stimulus with the targets of an unrelated training task. In this manner, we are able to probe learning for an aspect of motion processing thought to be a function of directional V1 simple cells with a learning procedure that dissociates the learned stimulus from the decision processes relevant to the training task. Our results show learning for the exposed contrast polarity and that this learning does not transfer to the unexposed contrast polarity. These results suggest that TIPL for motion stimuli may occur at the stage of directional V1 simple cells.

A Neural Network of Adaptively Timed Reinforcement Learning and Hippocampal Dynamics

A neural model is described of how adaptively timed reinforcement learning occurs. The adaptive timing circuit is suggested to exist in the hippocampus, and to involve convergence of dentate granule cells on CA3 pyramidal cells, and NMDA receptors. This circuit forms part of a model neural system for the coordinated control of recognition learning, reinforcement learning, and motor learning, whose properties clarify how an animal can learn to acquire a delayed reward. Behavioral and neural data are summarized in support of each processing stage of the system. The relevant anatomical sites are in thalamus, neocortex, hippocampus, hypothalamus, amygdala, and cerebellum. Cerebellar influences on motor learning are distinguished from hippocampal influences on adaptive timing of reinforcement learning. The model simulates how damage to the hippocampal formation disrupts adaptive timing, eliminates attentional blocking, and causes symptoms of medial temporal amnesia. It suggests how normal acquisition of subcortical emotional conditioning can occur after cortical ablation, even though extinction of emotional conditioning is retarded by cortical ablation. The model simulates how increasing the duration of an unconditioned stimulus increases the amplitude of emotional conditioning, but does not change adaptive timing; and how an increase in the intensity of a conditioned stimulus "speeds up the clock", but an increase in the intensity of an unconditioned stimulus does not. Computer simulations of the model fit parametric conditioning data, including a Weber law property and an inverted U property. Both primary and secondary adaptively timed conditioning are simulated, as are data concerning conditioning using multiple interstimulus intervals (ISIs), gradually or abruptly changing ISis, partial reinforcement, and multiple stimuli that lead to time-averaging of responses. Neurobiologically testable predictions are made to facilitate further tests of the model.