Leadership behaviours and entrepreneurial attitude as predictors of business outcomes within business incubators: A conceptual model

This conceptual paper proposes pathways through which transformational leadership and entrepreneurial attitude orientation could predict business outcomes within the business incubators context. Based on the literature review the paper argues that transformational leadership and entrepreneurial attitude orientation have both direct and indirect influence on business outcomes for business incubators. Furthermore, the paper proposes a conceptual framework useful in explaining the interplay between leadership, entrepreneurial attitude orientation and business outcomes. Finally, the paper outlines some steps to advance leadership theory within the business incubator context

Learning with web tools, simulations, and other technologies in science classrooms.

This position paper proposes the enhancement of teacher and student learning in science classrooms by tapping the enormous potential of information communication and technologies (ICTs) as cognitive tools for engaging students in scientific inquiry. This paper serves to challenge teacher-held assumptions about students learning science ‘from technology’ with a framework and examples of students learning science ‘with technology’. Whereas a high percentage of students are finding their way in using ICTs outside of school, for the most part they currently are not doing so inside of school in ways that they find meaningful and relevant to their lives. Instead, the pedagogical approaches that are most often experienced are out-of-step with how students use ICTs outside of schools and are not supportive of learning framed by constructivism. Here we describe a theoretical and pedagogical foundation for better connecting the two worlds of students’ lives: life in school and life outside of school. This position paper is in response to the changing landscape of students’ lives. The position is transformative in nature because it proposes the use of cyber-enabled resources for cultivating and leveraging students new literacy skills by learning ‘with technology’ to enhance science learning

IRF-8 regulates expansion of myeloid-derived suppressor cells and Foxp3⁺ regulatory T cells and modulates Th2 immune responses to gastrointestinal nematode infection

<div><p>Interferon regulatory factor-8 (IRF-8) is critical for Th1 cell differentiation and negatively regulates myeloid cell development including myeloid-derived suppressor cells (MDSC). MDSC expand during infection with various pathogens including the gastrointestinal (GI) nematode <i>Heligmosomoides polygyrus bakeri</i> (Hpb). We investigated if IRF-8 contributes to Th2 immunity to Hpb infection. <i>Irf8</i> expression was down-regulated in MDSC from Hpb-infected C57BL/6 (B6) mice. IRF-8 deficient <i>Irf8</i>^<i>-/-</i> and BXH-2 mice had significantly higher adult worm burdens than B6 mice after primary or challenge Hpb infection. During primary infection, MDSC expanded to a significantly greater extent in mesenteric lymph nodes (MLN) and spleens of <i>Irf8</i>^<i>-/-</i> and BXH-2 than B6 mice. CD4⁺GATA3⁺ T cells numbers were comparable in MLN of infected B6 and IRF-8 deficient mice, but MLN cells from infected IRF-8 deficient mice secreted significantly less parasite-specific IL-4 ex vivo. The numbers of alternatively activated macrophages in MLN and serum levels of Hpb-specific IgG1 and IgE were also significantly less in infected <i>Irf8</i>^<i>-/-</i> than B6 mice. The frequencies of antigen-experienced CD4⁺CD11a^hiCD49d^hi cells that were CD44^hiCD62L^- were similar in MLN of infected <i>Irf8</i>^<i>-/-</i> and B6 mice, but the proportions of CD4⁺GATA3⁺ and CD4⁺IL-4⁺ T cells were lower in infected <i>Irf8</i>^<i>-/-</i> mice. CD11b⁺Gr1⁺ cells from naïve or infected <i>Irf8</i>^<i>-/-</i> mice suppressed CD4⁺ T cell proliferation and parasite-specific IL-4 secretion in vitro albeit less efficiently than B6 mice. Surprisingly, there were significantly more CD4⁺ T cells in infected <i>Irf8</i>^<i>-/-</i> mice, with a higher frequency of CD4⁺CD25⁺Foxp3⁺ T (Tregs) cells and significantly higher numbers of Tregs than B6 mice. In vivo depletion of MDSC and/or Tregs in <i>Irf8</i>^<i>-/-</i> mice did not affect adult worm burdens, but Treg depletion resulted in higher egg production and enhanced parasite-specific IL-5, IL-13, and IL-6 secretion ex vivo. Our data thus provide a previously unrecognized role for IRF-8 in Th2 immunity to a GI nematode.</p></div

Silencing of Irf7 pathways in breast cancer cells promotes bone metastasis through immune escape

Breast cancer metastasis is a key determinant of long-term patient survival. By comparing the transcriptomes of primary and metastatic tumor cells in a mouse model of spontaneous bone metastasis, we found that a substantial number of genes suppressed in bone metastases are targets of the interferon regulatory factor Irf7. Restoration of Irf7 in tumor cells or administration of interferon led to reduced bone metastases and prolonged survival time. In mice deficient in the interferon (IFN) receptor or in natural killer (NK) and CD8 + T cell responses, metastasis was accelerated, indicating that Irf7-driven suppression of metastasis was reliant on IFN signaling to host immune cells. We confirmed the clinical relevance of these findings in over 800 patients in which high expression of Irf7-regulated genes in primary tumors was associated with prolonged bone metastasisg-free survival. This gene signature may identify patients that could benefit from IFN-based therapies. Thus, we have identified an innate immune pathway intrinsic to breast cancer cells, the suppression of which restricts immunosurveillance to enable metastasis. © 2012 Nature America, Inc. All rights reserved.SCOPUS: ar.jinfo:eu-repo/semantics/publishe