Programming for survival: a meeting system that survives 8 years later.

Effective and useful interventions often deteriorate when researchers withdraw their direct supervision. We tested the survival of an intervention designed to produce effective weekly meetings in a student housing cooperative without direct researcher supervision. Chairperson performance, proposals completed per hour, and ratings of chairperson performance all increased when resident staff used a training manual, prompting checklist, and performance reviews. Eight years of follow-up revealed continuing high levels of meeting effectiveness. This study demonstrates a methodology for the direct observation and experimental analysis of intervention survival.

The human immunodeficiency virus type 1 long terminal repeat specifies two different transcription complexes, only one of which is regulated by Tat.

The human immunodeficiency virus type 1 long terminal repeat sets up two different transcription complexes, which have been called processive and nonprocessive complexes. By mutating and substituting cis-acting sequences, we mapped elements of the human immunodeficiency virus long terminal repeat that are responsible for creating each transcription complex. Whereas processive complexes are efficiently assembled by upstream promoter elements in the absence of the TATA box, nonprocessive complexes absolutely require the TATA box. Moreover, the TATA box alone can set up these nonprocessive complexes, and nonprocessive but not processive complexes are trans activated by Tat. Finally, a strong DNA-binding site between the TATA box and trans-activation-responsive region interferes with either the assembly or movement of these nonprocessive complexes and diminishes the effects of Tat. Thus, Tat affects a critical step in the formation of elongation-competent transcription complexes.

Efficacy and maintenance of an education program for a consumer cooperative.

We examined the effects of contingency management on participation in and maintenance of an education program by new members of a student housing cooperative. With credit and fine contingencies in place, the percentage of participants completing study guides was five times higher than without the contingencies. Members continued to implement the program for 9 years without researcher involvement.

Participatory management: Maintaining staff performance in a university housing cooperative.

To apply behavior analysis to normal adults in non institutional settings, we may have to encourage their participation in the design and implementation of behavioral technology. This study evaluates a technology by which the members of a student housing cooperative manage their own staff with a minimum of supervision by one of the program designers. This staff management system consisted of prompts, self-reports, spot checks, and contingent rent reductions. Six resident staff members performed substantially more of their assigned tasks when this system was used. In addition, the management system was acceptable to the members, was affordable, and maintained high levels of staff performance during a 5-year follow-up. Participation by the members in the design and implementation of this system appears to have been useful in helping the behavior analysts to develop an unusually durable management system.

A technology for program maintenance: programming key researcher behaviors in a student housing cooperative.

Behavioral researchers play critical, but often unanalyzed, roles in the programs they develop. Unless they replace their key activities with standardized procedures, their continued participation may be essential to program success--a situation that is often not only impractical but may be prohibitively expensive and disliked by local staff. This study was conducted in a student housing cooperative that is dependent on close researcher supervision for its continued health and survival. A key activity of the co-op researchers was to provide public recognition for good job performance by co-op members. The purposes of this study were (a) to replace that idiosyncratic recognition with systematic procedures so members, instead of the researchers, would provide public recognition to each other for good job performance; and (b) to evaluate those procedures by comparing job performance when member-delivered recognition was provided and when it was not. When the procedures were in place, job performance increased and fines for poor job performance and complaining at meetings decreased. This study suggests that procedures can be developed to reduce program reliance on the researcher that are effective, inexpensive, sustainable, and acceptable to the participants--a first step toward developing a technology of program maintenance.

Differences in transcriptional enhancers of HIV-1 and HIV-2. Response to T cell activation signals.

T cell activation results in high levels of HIV replication and is thought to be one mechanism leading to the conversion from latent to active viral infection. In HIV-1, the sequences that respond to these signaling events are found in the long terminal repeat (LTR) and comprise the transcriptional enhancer, which contains two conserved binding sites for the nuclear factor kappa B (NF kappa B). The corresponding region in the second AIDS retrovirus, HIV-2, contains a conserved and a divergent NF kappa B binding site. We demonstrate that the HIV-1 LTR responds better than the HIV-2 LTR to T cell activation signals. These qualitative differences in the response to T cell activation are reproduced not only when HIV-1 or HIV-2 enhancers are placed upstream of a heterologous promoter but also when these enhancers are switched between their respective LTR. In electrophoretic mobility shift assays, NF kappa B binds to both conserved sites in the HIV-1 transcriptional enhancer and only to the single conserved site in the HIV-2 transcriptional enhancer. Instead of NF kappa B, the activator protein 3 binds to the divergent site in HIV-2. In conclusion, HIV-1 and HIV-2 are differentially regulated by T cell activation signals, and this difference may account for the longer period of viral latency observed with HIV-2 than with HIV-1 infection.