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This chapter explores the practices of learning communities designed for specific, underserved student populations, highlighting on-campus examples and culminating with a synthesized list of core practices from these "inclusive" learning communities.

The variety of problems identified with undergraduate education at large research universities may best be summed up by a disquieting portrait provided by the Boyer Commission. In its 1998 report, called "Reinventing Undergraduate Education", the commission described thousands of undergraduates receiving instruction from novice teaching assistants or professors working from ancient notes, taking a smattering of courses that do not lead to a cohesive body of knowledge, and graduating without knowing how to "think logically, write clearly, or speak coherently". Yet, as the Boyer Commission acknowledged, research universities possess resources that position them to be excellent educational institutions, including renowned professors, state-of-the-art facilities, and cutting-edge research production. Partially in response to critiques from the Boyer Commission and other reports, research institutions across North America have organized living-learning programs that allow residential students to enjoy the learning and developmental benefits of living in an intimate academic community within the context of a large university. Living-learning programs are founded on a premise asserted by college impact research that integrating students' in-class and out-of-class experiences can improve their learning. As the number of living-learning programs has grown, research on and assessment of their effectiveness has been largely confined to single-program studies on individual campuses. Their proliferation signals a need to expand the scope of study beyond single institutions, a challenge taken up by the National Study of Living-Learning Programs (NSLLP), through a grant sponsored by the Association of College and University Housing Officers International (ACUHO-I) Research Commission. In this article, the authors offer recommendations based on a pilot study that used the larger study's survey instrument at four research universities: University of Illinois, University of Maryland, University of Michigan, and University of Wisconsin. (Contains 5 notes.)

Cytomegalovirus (CMV) gene expression is repressed in latency due to heterochromatinization of viral genomes. In murine CMV (MCMV) latently infected mice, viral genomes are bound to histones with heterochromatic modifications, to enzymes that mediate these modifications, and to adaptor proteins that may recruit co-repressor complexes. Kinetic analyses of repressor binding show that these repressors are recruited at the earliest time of infection, suggesting that latency may be the default state. Kidney transplantation leads to epigenetic reprogramming of latent viral chromatin and reactivation of immediate early gene expression. Inflammatory signaling pathways, which activate transcription factors that regulate the major immediate early promoter (MIEP), likely mediate the switch in viral chromatin. [ABSTRACT FROM AUTHOR]

Our previous studies showed that establishment of murine cytomegalovirus (MCMV) latency in vivo is associated with repression of immediate-early gene expression, deacetylation of histones bound to the major immediate-early promoter (MIEP), changes in patterns of methylation of histones, and recruitment of cellular repressors of transcription to the MIEP. Here, we have quantitatively analyzed the kinetics of changes in viral RNA expression, DNA copy number, and recruitment of repressors and activators of transcription to viral promoters during the course of infection. Our results show that changes in viral gene expression correlate with changes in recruitment of RNA polymerase and acetylated histones to viral promoters. Binding of the transcriptional repressors histone deacetylase type 2 (HDAC2), HDAC3, YY1, CBF-1/RBP-Jk, Daxx, and CIR to the MIEP and HDACs to other promoters showed a biphasic pattern: some binding was detectable prior to activation of viral gene expression, then decreased with the onset of transcription and increased again as repression of viral gene expression occurred. Potential binding sites for CBF-1/RBP-Jk and YY1 in the MIEP and for YY1 in the M100 promoter (M100P) were identified by in silico analysis. While recruitment of HDACs was not promoter specific, binding of CBF-1/RBP-Jk and YY1 was restricted to promoters with their cognate sites. Our results suggest that sequences within viral promoters may contribute to establishment of latency through recruitment of transcriptional repressors to these genes. The observation that repressors are bound to the MIEP and other promoters immediately upon infection suggests that latency may be established in some cells very early in infection. [ABSTRACT FROM AUTHOR]

Human cytomegalovirus (CMV) is a ubiquitous herpesvirus with the ability to establish a lifelong latent infection. The mechanism by which this occurs is not well understood. Regulation of, for example, immediate-early (IE) gene expression is thought to be a critical control point in transcriptional control of the switch between latency and reactivation. Here, we present evidence that supports previous studies showing that the majority of genomes are quiescent with respect to gene expression. To study the possible role of epigenetic factors that may be involved in repression of ie gene expression in latency, we have analyzed changes in the patterns of modifications of histones bound to the major IE promoter (MIEP) in the kidneys of acutely and latently infected mice. Our studies show that, like herpes simplex virus, murine CMV genomes become relatively enriched in histones in latent infection. There are dramatic changes in modifications of histones associated with the MIEP when latency is established: H3 and H4 become hypoacetylated and H3 is hypomethylated at lysine 4, while H3 lysine 9 is hypermethylated in latently infected mice. These changes are accompanied by a relative loss of RNA polymerase and gain of heterochromatin protein 1 γ and Yin-Yang 1 bound to the MIEP. Our studies suggest that, in the majority of cells, CMV establishes a true latent infection, defined as the lack of expression of genes associated with productive infection, and that this occurs through changes in histone modifications and recruitment of transcriptional silencing factors to the MIEP. [ABSTRACT FROM AUTHOR]

Myeloid cells are important cell types that carry human cytomegalovirus. Latent viral DNA is present in CD34+ progenitor cells and their derived monocytes. However, differentiation of latently infected monocytes to mature macrophages or dendritic cells causes reactivation of latent viruses. During hematopoietic development, pluripotent genes are repressed, and lineage specific genes are activated in a step-wise manner. This process is governed by cell-type specific chromatin states. Enhancers in the hematopoietic system are highly dynamic and established by pioneer (first tier) transcription factors (TFs), which set the stage for second and third tier TF binding. In this review, we examine the epigenetic mechanisms that regulate myeloid cell development, cell identity, and activation with a special focus on factors that regulate viral gene expression and the status of viral infection in myeloid cells., Competing Interests: CONFLICT of INTEREST The authors declare that they have no conflict of interest