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RISS 인기검색어
- 검색키워드
- 저자 : ( Jessica M. Mallory ) (검색결과 2 건)
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Jessica M. Mallory,Lisa Kelly-Vance,Brigette Ryalls 대한사고개발학회 2010 The International Journal of Creativity & Problem Vol.20 No.2
Cognitive development and play development are mutually reinforcing. The present study measured the effect of an intervention intended to address both play skills and cognitive skills directly by incorporating divergent thinking prompts into a play-based intervention. The play of six at-risk children was observed and video recorded during independent pretend play. Qualitative and quantitative aspects of this play were recorded. Three at-risk children participated in six week divergent thinking intervention, while three comparison children participated in the general preschool curriculum. Children’s play was observed and recorded pre- and post-intervention. Results indicated that children who participated in the intervention did improve on measures of play quality, quantity, or both more than children who did not participate in the intervention. Implications for educators are discussed.
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Bai, Xiyuan,Shang, Shaobin,Henao-Tamayo, Marcela,Basaraba, Randall J.,Ovrutsky, Alida R.,Matsuda, Jennifer L.,Takeda, Katsuyuki,Chan, Mallory M.,Dakhama, Azzeddine,Kinney, William H.,Trostel, Jessica National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.16
<P><B>Significance</B></P><P>Interleukin-32 (IL-32) is induced by IL-1β, Toll-like receptor agonists, and nucleotide oligomerization domain as well as by <I>Mycobacterium tuberculosis</I> (<I>MTB</I>). Expression of human IL-32γ in the lungs of mice reduced the burden of <I>MTB</I> in both the lungs but also in the spleen and was associated with increased survival. Mechanistically, increased numbers of host-protective innate and adaptive immune cells were present in the IL-32 transgenic mice. Alveolar macrophages from the transgenic mice were also better able to control <I>MTB</I> infection and had increased colocalization of <I>MTB</I> with lysosomes. IL-32 expression was increased in the surgically resected lungs of tuberculosis patients, particularly in macrophages, airway epithelial cells, B cells, and T cells. Thus, IL-32 enhances host immunity against <I>MTB</I>.</P><P>Silencing of interleukin-32 (IL-32) in a differentiated human promonocytic cell line impairs killing of <I>Mycobacterium tuberculosis</I> (<I>MTB</I>) but the role of IL-32 in vivo against <I>MTB</I> remains unknown. To study the effects of IL-32 in vivo, a transgenic mouse was generated in which the human <I>IL-32γ</I> gene is expressed using the surfactant protein C promoter (SPC-IL-32γTg). Wild-type and SPC-IL-32γTg mice were infected with a low-dose aerosol of a hypervirulent strain of <I>MTB</I> (W-Beijing HN878). At 30 and 60 d after infection, the transgenic mice had 66% and 85% fewer <I>MTB</I> in the lungs and 49% and 68% fewer <I>MTB</I> in the spleens, respectively; the transgenic mice also exhibited greater survival. Increased numbers of host-protective innate and adaptive immune cells were present in SPC-IL-32γTg mice, including tumor necrosis factor-alpha (TNFα) positive lung macrophages and dendritic cells, and IFN-gamma (IFNγ) and TNFα positive CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T cells in the lungs and mediastinal lymph nodes. Alveolar macrophages from transgenic mice infected with <I>MTB</I> ex vivo had reduced bacterial burden and increased colocalization of green fluorescent protein-labeled <I>MTB</I> with lysosomes. Furthermore, mouse macrophages made to express IL-32γ but not the splice variant IL-32β were better able to limit <I>MTB</I> growth than macrophages capable of producing both. The lungs of patients with tuberculosis showed increased IL-32 expression, particularly in macrophages of granulomas and airway epithelial cells but also B cells and T cells. We conclude that IL-32γ enhances host immunity to <I>MTB</I>.</P>
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