Applied behavior analysis: Current myths in public education

Abstract The effective use of behavior management strategies and related policies continues to be a debated issue in public education. Despite overwhelming evidence espousing the benefits of the implementation of procedures derived from principles based on the science of applied behavior analysis (ABA), educators often indicate many common misconceptions in this area. These misconceptions contribute to a reluctance on the part of educators to implement strategies utilizing what we know to be true about the operation of behavioral law. Further, these misconceptions often impede educator effectiveness and student progress. This paper reviews 3 common misperceptions: 1) ABA is used exclusively for children who have autism; 2) ABA may only be implemented using a teacher/student ratio of 1:1, and; 3) negative connotations of terminology associated with ABA. Important legal issues, procedures, research, and philosophical issues related to the implementation of ABA is explored along with concluding recommendations for public school educators. Applied Behavior Analysis: Current Myths in Public Education Public education is, historically, a punitive institution. From suspensions and expulsions to verbal reprimands, the majority of consequences imposed by teachers and administrators are done with the idea that such consequences will decrease the rate of future behavior; thereby "sending a message that certain behaviors will not be tolerated" (Skiba, 1999, p. 2). Zero tolerance policies that involve removing a student from the classroom or campus for up to a year for certain offenses have been included in state and federal regulation

Thy1+ Nk Cells from Vaccinia Virus-Primed Mice Confer Protection against Vaccinia Virus Challenge in the Absence of Adaptive Lymphocytes

While immunological memory has long been considered the province of T- and B- lymphocytes, it has recently been reported that innate cell populations are capable of mediating memory responses. We now show that an innate memory immune response is generated in mice following infection with vaccinia virus, a poxvirus for which no cognate germline-encoded receptor has been identified. This immune response results in viral clearance in the absence of classical adaptive T and B lymphocyte populations, and is mediated by a Thy1+ subset of natural killer (NK) cells. We demonstrate that immune protection against infection from a lethal dose of virus can be adoptively transferred with memory hepatic Thy1+ NK cells that were primed with live virus. Our results also indicate that, like classical immunological memory, stronger innate memory responses form in response to priming with live virus than a highly attenuated vector. These results demonstrate that a defined innate memory cell population alone can provide host protection against a lethal systemic infection through viral clearance

Engagement of NKG2D by cognate ligand or antibody alone is insufficient to mediate costimulation of human and mouse CD8(+) T cells

CD8+ T cells require a signal through a costimulatory receptor in addition to TCR engagement to become activated. The role of CD28 in costimulating T cell activation is well established. NKG2D, a receptor found on NK cells, CD8+?-TCR+ T cells, and ??-TCR+ T cells, has also been implicated in T cell costimulation. In this study we have evaluated the role of NKG2D in costimulating mouse and human naive and effector CD8+ T cells. Unexpectedly, in contrast to CD28, NKG2D engagement by ligand or mAb is not sufficient to costimulate naive or effector CD8+ T cell responses in conventional T cell populations. While NKG2D did not costimulate CD8+ T cells on its own, it was able to modify CD28-mediated costimulation of human CD8+ T cells under certain contitions. It is, therefore, likely that NKG2D acts as a costimulatory molecule only under restricted conditions or requires additional cofactors

A human anti-IL-2 antibody that potentiates regulatory T cells by a structure-based mechanism.

Interleukin-2 (IL-2) has been shown to suppress immune pathologies by preferentially expanding regulatory T cells (Tregs). However, this therapy has been limited by off-target complications due to pathogenic cell expansion. Recent efforts have been focused on developing a more selective IL-2. It is well documented that certain anti-mouse IL-2 antibodies induce conformational changes that result in selective targeting of Tregs. We report the generation of a fully human anti-IL-2 antibody, F5111.2, that stabilizes IL-2 in a conformation that results in the preferential STAT5 phosphorylation of Tregs in vitro and selective expansion of Tregs in vivo. When complexed with human IL-2, F5111.2 induced remission of type 1 diabetes in the NOD mouse model, reduced disease severity in a model of experimental autoimmune encephalomyelitis and protected mice against xenogeneic graft-versus-host disease. These results suggest that IL-2-F5111.2 may provide an immunotherapy to treat autoimmune diseases and graft-versus-host disease

C-type lectins in immunity and homeostasis

The authors thank the Wellcome Trust, the UK Medical Research Council (MRC), the MRC Centre for Medical Mycology at the University of Aberdeen and Arthritis Research UK for financial support. The authors apologize to colleagues whose many valuable contributions could not be cited owing to space constraints.Peer reviewedPostprintPostprintPostprintPostprin

Compartmentalization, Viral Evolution, and Viral Latency of HIV in the CNS

Human immunodeficiency virus type 1 (HIV-1) infection occurs throughout the body, and can have dramatic physical effects, such as neurocognitive impairment in the central nervous system (CNS). Furthermore, examining the virus that resides in the CNS is challenging due to its location and can only be done using samples collected either at autopsy, indirectly form the cerebral spinal fluid (CSF), or through the use of animal models. The unique milieu of the CNS fosters viral compartmentalization as well as evolution of viral sequences, allowing for new cell types, such as macrophages and microglia, to be infected. Treatment must also cross the blood brain barrier adding additional obstacles in eliminating viral populations in the CNS. These long-lived infected cell types and treatment barriers may affect functional cure strategies in people on highly active antiretroviral therapy (HAART)