Writing Renewal Retreats: The Scholarly Writer, Contemplative Practice, and Scholarly Productivity

This article offers an exploratory case study of a program for faculty that blends contemplative practices, scholarly productivity, and renewal of faculty as writers at a retreat in a natural setting. We share faculty learning outcomes, logistics, a retreat agenda, and evaluation data from four writing renewal retreats conducted over two years to present initial insight into a contemplative approach to writing retreats that fosters a connection to self, to scholarship, and to a community of writers—key elements of a successful writing life. Through critical reflection on the role of contemplative practices, scholarly productivity, and faculty well-being, we offer a model for holistic faculty development

Book Reviews

Book reviews by Edward F. Barrett, Alfred L. Scanlan, Robert T. Molloy, Aaron I. Abell, and Robert E. Sullivan

Book Reviews

Book reviews by Edward F. Barrett, James P. Kelly, Robert T. Molloy, R. W. Mulligan, and William F. Roemer

IL-10 Immunomodulation of Myeloid Cells Regulates a Murine Model of Ovarian Cancer

Elevated levels of IL-10 in the microenvironment of human ovarian cancer and murine models of ovarian cancer are well established and correlate with poor clinical prognosis. However, amongst a myriad of immunosuppressive factors, the actual contribution of IL-10 to the ovarian tumor microenvironment, the mechanisms by which it acts, and its possible functional redundancy are unknown. We previously demonstrated that elimination of the myeloid-derived suppressor cell (MDSC) compartment within the ovarian tumor ascites inhibited tumor progression and, intriguingly, significantly decreased local IL-10 levels. Here we identify a novel pathway in which the tumor-infiltrating MDSC are the predominant producers of IL-10 and, importantly, require it to develop their immunosuppressive function in vivo. Importantly, we demonstrate that the role of IL-10 is critical, and not redundant with other immunosuppressive molecules, to in vivo tumor progression: blockade of the IL-10 signaling network results in alleviation of MDSC-mediated immunosuppression, altered T cell phenotype and activity, and improved survival. These studies define IL-10 as a fundamental modulator of both MDSC and T cells within the ovarian tumor microenvironment. Importantly, IL-10 signaling is shown to be necessary to the development and maintenance of a permissive tumor microenvironment and represents a viable target for anti-tumor strategies

CD4+ T Cell Regulation of CD25 Expression Controls Development of Short-Lived Effector CD8+ T Cells in Primary and Secondary Responses

Both CD4(+) T cell help and IL-2 have been postulated to program activated CD8(+) T cells for memory cell development. However, the linkage between these two signals has not been well elucidated. Here we have studied effector and memory CD8(+) T cell differentiation following infection with three pathogens (Listeria monocytogenes, vesicular stomatitis virus, and vaccinia virus) in the absence of both CD4(+) T cells and IL-2 signaling. We found that expression of CD25 on antigen-specific CD8(+) T cells peaked 3-4 days after initial priming and was dependent on CD4(+) T cell help, likely through a CD28:CD80/86 mediated pathway. CD4(+) T cell or CD25-deficiency led to normal early effector CD8(+) T cell differentiation, but a subsequent lack of accumulation of CD8(+) T cells resulting in overall decreased memory cell generation. Interestingly, in both primary and recall responses KLRG1(high) CD127(low) short-lived effector cells were drastically diminished in the absence of IL-2 signaling, although memory precursors remained intact. In contrast to previous reports, upon secondary antigen encounter CD25-deficient CD8(+) T cells were capable of undergoing robust expansion, but short-lived effector development was again impaired. Thus, these results demonstrated that CD4(+) T cell help and IL-2 signaling were linked via CD25 up-regulation, which controls the expansion and differentiation of antigen-specific effector CD8(+) T cells, rather than programming memory cell traits

Random Geometric Graphs

We analyse graphs in which each vertex is assigned random coordinates in a geometric space of arbitrary dimensionality and only edges between adjacent points are present. The critical connectivity is found numerically by examining the size of the largest cluster. We derive an analytical expression for the cluster coefficient which shows that the graphs are distinctly different from standard random graphs, even for infinite dimensionality. Insights relevant for graph bi-partitioning are included.Comment: 16 pages, 10 figures. Minor changes. Added reference

Operative Environment

Postoperative SSIs are believed to occur via bacterial inoculation at the time of surgery or as a result of bacterial contamination of the wound via open pathways to the deep tissue layers.1–3 The probability of SSI is reflected by interaction of parameters that can be categorized into three major groups.2 The first group consists of factors related to the ability of bacteria to cause infection and include initial inoculation load and genetically determined virulence factors that are required for adherence, reproduction, toxin production, and bypassing host defense mechanisms. The second group involves those factors related to the defense capacity of the host including local and systemic defense mechanisms. The last group contains environmental determinants of exposure such as size, time, and location of the surgical wound that can provide an opportunity for the bacteria to enter the surgical wound, overcome the local defense system, sustain their presence, and replicate and initiate local as well as systemic inflammatory reactions of the host. The use of iodine impregnated skin incise drapes shows decreased skin bacterial counts but no correlation has been established with SSI. However, no recommendations regarding the use of skin barriers can be made (see this Workgroup, Question 27)

Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals

The hypothesis that bystander inflammatory signals promote memory B cell (BMEM) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 lineage B220+IgG+ BMEM toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent BMEM clonally expand. Surprisingly, proliferating BMEM do not acquire germinal center (GC) B cell markers before generating daughter BMEM and differentiating into plasma cells or form structurally identifiable GCs. In striking contrast to cognate antigen, inflammatory stimuli, including Toll-like receptor agonists or bystander T cell activation, fail to induce even low levels of BMEM proliferation or differentiation in vivo. Under the extreme conditions of adjuvanted protein vaccination or acute viral infection, no detectable bystander proliferation or differentiation of BMEM occurred. The absence of a BMEM response to nonspecific inflammatory signals clearly shows that BMEM proliferation and differentiation is a process tightly controlled by the availability of cognate antigen

Recent Region-wide Declines in Caribbean Reef Fish Abundance

Profound ecological changes are occurring on coral reefs throughout the tropics, with marked coral cover losses and concomitant algal increases, particularly in the Caribbean region. Historical declines in the abundance of large Caribbean reef fishes likely reflect centuries of overexploitation. However, effects of drastic recent degradation of reef habitats on reef fish assemblages have yet to be established. By using meta-analysis, we analyzed time series of reef fish density obtained from 48 studies that include 318 reefs across the Caribbean and span the time period 1955–2007. Our analyses show that overall reef fish density has been declining significantly for more than a decade, at rates that are consistent across all subregions of the Caribbean basin (2.7% to 6.0% loss per year) and in three of six trophic groups. Changes in fish density over the past half-century are modest relative to concurrent changes in benthic cover on Caribbean reefs. However, the recent significant decline in overall fish abundance and its consistency across several trophic groups and among both fished and nonfished species indicate that Caribbean fishes have begun to respond negatively to habitat degradation