Nursing students' learning experiences of pediatric nursing practice in kindergarten : learning contents' trait and significance of the context of fundamental education-

小児看護学実習における学生の学習経験を明らかにすることを目的として、研究を行った.H大学の小児看護学実習を経験した学生117名を対象に、まとめのカンファレンス・ノート記録2年分を資料とし、KJ法を用いて分析した.本稿では、幼稚園実習に焦点を当て報告する.1.幼稚園実習における学生の学習経験は、【自分の力を生かしている子どものありようの理解】【子どもの現実に身を置く言動や態度の習得】の2つのカテゴリーから構成されていた.2.【自分の力を生かしている子どものありようの理解】【子どもの現実に身を置く言動や態度の習得】の2つのカテゴリー間には、相反する内容と共通する内容が存在していた.共通する内容としては遊びがあり、全体としては、相互に作用していた.3.幼稚園実習の意義として、子どもの主体性や生き生きしさに対応する大人の役割認識と遊びの認識、そして、子どもに学ぶ人との関わりの豊かさへの実感が示唆された.4.教育への示唆として、小児看護に重要な子どものトータルケアに繋がる実践的な子ども観の涵養、観察やコミュニケーション技術の基盤となる見ること、聞くことの体験という基礎教育における幼稚園実習の役割の一旦を知ることができた.This research was undertaken to investigate the learning experiences of students in the context of. pediatric nursing practice. We conducted an analysis (using the KJ method) targeting 117 students who had pediatric nursing practice experience at H University, using two years of summarized conference notes as materials. This paper presents a report with a focus on learning experience in kindergarten. 1) Nursing students' learning experiences in kindergarten can be divided into two main categories: "Understanding of the nature of children expressing their strengths and abilities" and "Learning language and behavior from the perspective of a childs reality" 2) A comparison of these two categories showed both contrasting elements and common elements. "Play" -which was one of the common elements- interacted with all of the other elements present. 3) This is an indication of the significance of pediatric nursing practice in kindergartern : during this research, we got a strong sense of an awareness of "play" and an awareness of the adults role in response to the childs sense of identity and vitality. 4) In terms of the implications for education in general, we were able to grasp, to some extent, the role of training in kindergarten among the context of fundamental education - that is, the experience of watching and listening, which forms the foundation of observation and communication skills, as well as practical skills in cultivating the child's sense of self. All of these tie into the concept of “total care,” an important concept for nursing care of children and families in general

Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules

<p>Abstract</p> <p>Background</p> <p>Human T-cell leukemia virus type I (HTLV-I) is associated with pulmonary diseases, characterized by bronchoalveolar lymphocytosis, which correlates with HTLV-I proviral DNA in carriers. HTLV-I Tax seems to be involved in the development of such pulmonary diseases through the local production of inflammatory cytokines and chemokines in T cells. However, little is known about induction of these genes by HTLV-I infection in lung epithelial cells.</p> <p>Results</p> <p>We tested infection of lung epithelial cells by HTLV-I by coculture studies in which A549 alveolar and NCI-H292 tracheal epithelial cell lines were cocultured with MT-2, an HTLV-I-infected T-cell line. Changes in the expression of several cellular genes were assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry. Coculture with MT-2 cells resulted in infection of lung epithelial cells as confirmed by detection of proviral DNA, HTLV-I Tax expression and HTLV-I p19 in the latter cells. Infection was associated with induction of mRNA expression of various cytokines, chemokines and cell adhesion molecule. NF-κB and AP-1 were also activated in HTLV-I-infected lung epithelial cells. <it>In vivo </it>studies showed Tax protein in lung epithelial cells of mice bearing Tax and patients with HTLV-I-related pulmonary diseases.</p> <p>Conclusion</p> <p>Our results suggest that HTLV-I infects lung epithelial cells, with subsequent production of cytokines, chemokines and cell adhesion molecules through induction of NF-κB and AP-1. These changes can contribute to the clinical features of HTLV-I-related pulmonary diseases.</p

Evidence for NF-κB- and CBP-Independent Repression of p53's Transcriptional Activity by Human T-Cell Leukemia Virus Type 1 Tax in Mouse Embryo and Primary Human Fibroblasts

The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein can repress the transcriptional activity of the tumor suppressor protein p53. However, it remains controversial whether Tax requires NF-κB factors/activity and/or p300/CBP in order to inactivate p53 function. To address this issue, we have investigated Tax's effect on p53's transcriptional activation in IκB-kinase-deficient mouse embryonic fibroblasts (MEFs); some of which are entirely silent for Tax-induced NF-κB activity. We found that, in IKKα(−/−), IKKβ(−/−), and IKKγ(−/−) MEFs, p53 activation of a prototypic responsive plasmid (pG13-luciferase) was repressed by wild-type Tax. Curiously, p53's activity in MEFs was also repressed by a p300/CBP-binding deficient Tax protein. Our results highlight the complex nature of Tax-mediated repression of p53- activity, which requires further investigation

Segregation of NF-κB activation through NEMO/IKKγ by Tax and TNFα: implications for stimulus-specific interruption of oncogenic signaling

International audienceNuclear factor-kappaB essential modulator (NEMO), also called IKKgamma, has been proposed as a 'universal' adaptor of the I-kappaB kinase (IKK) complex for stimuli such as proinflammatory cytokines, microbes, and the HTLV-I Tax oncoprotein. Currently, it remains unclear whether the many signals that activate NF-kappaB through NEMO converge identically or differently. We have adopted two approaches to answer this question. First, we generated and targeted intracellularly three NEMO-specific monoclonal antibodies (mAbs). These mAbs produced two distinct intracellular NF-kappaB inhibition profiles segregating TNFalpha from Tax activation. Second, using NEMO knockout mouse fibroblasts and 10 NEMO mutants, we found that different regions function in trans either to complement or to inhibit dominantly TNFalpha, IL-1beta, or Tax activation of NF-kappaB. For instance, NEMO (1-245 amino acids) supported Tax-mediated NF-kappaB activation, but did not serve TNFalpha- or IL-1beta signaling. Altogether, our findings indicate that while NEMO 'universally' adapts numerous NF-kappaB activators, it may do so through separable domains. We provide the first evidence that selective targeting of NEMO can abrogate oncogenic Tax signaling without affecting signals used for normal cellular metabolism

Ubiquitination of Human T-Cell Leukemia Virus Type 1 Tax Modulates Its Activity

Human T-cell leukemia virus type 1 (HTLV-1) encodes a 40-kDa Tax phosphoprotein. Tax is a transcriptional activator which modulates expression of the viral long terminal repeat and transcription of many cellular genes. Because Tax is a critical HTLV-1 factor which mediates viral transformation of T cells during the genesis of adult T-cell leukemia, it is important to understand the processes which can activate or inactivate Tax function. Here, we report that ubiquitination of Tax is a posttranscriptional mechanism which regulates Tax function. We show that ubiquitination does not target Tax for degradation by the proteasome. Rather, ubiquitin addition modifies Tax in a proteasome-independent manner from an active to a less-active transcriptional form

Heterozygous Deletion of Mitotic Arrest–Deficient Protein 1 (MAD1) Increases the Incidence of Tumors in Mice

International audienceMitotic arrest-deficient protein 1 (MAD1) is a component of the mitotic spindle assembly checkpoint. We have created a knockout mouse model to examine the physiologic consequence of reduced MAD1 function. Mad1(+/-) mice were successfully generated, but repeated paired mating of Mad1(+/-) with Mad1(+/-) mice failed to produce a single Mad1(-/-) animal, suggesting that the latter genotype is embryonic lethal. In aging studies conducted for >18 months, Mad1(+/-) mice compared with control wild-type (wt) littermates showed a 2-fold higher incidence of constitutive tumors. Moreover, 42% of Mad1(+/-) (P < 0.03), but 0% of wt, mice developed neoplasia after treatment with vincristine, a microtubule depolymerization agent. Mad1(+/-) mouse embryonic fibroblasts (MEF) were found to be more prone than wt cells to become aneuploid; Mad1(+/-), but not wt, MEFs produced fibrosarcomas when explanted into nude mice. Our results indicate an essential MAD1 function in mouse development and correlate Mad1 haploinsufficiency with increased constitutive tumors