マイクロRNA449aの欠損は大腸での腫瘍形成を促進する

MicroRNAs have broad roles in tumorigenesis and cell differentiation through regulation of target genes. Notch signaling also controls cell differentiation and tumorigenesis. However, the mechanisms through which Notch mediates microRNA expression are still unclear. In this study, we aimed to identify microRNAs regulated by Notch signaling. Our analysis found that microRNA-449a (miR-449a) was indirectly regulated by Notch signaling. Although miR-449a-deficient mice did not show any Notch-dependent defects in immune cell development, treatment of miR-449a-deficient mice with azoxymethane (AOM) or dextran sodium sulfate (DSS) increased the numbers and sizes of colon tumors. These effects were associated with an increase in intestinal epithelial cell proliferation following AOM/DSS treatment. In patients with colon cancer, miR-449a expression was inversely correlated with disease-free survival and histological scores and was positively correlated with the expression of MLH1 for which loss-of function mutations have been shown to be involved in colon cancer. Colon tissues of miR-449a-deficient mice showed reduced Mlh1 expression compared with those of wild-type mice. Thus, these data suggested that miR-449a acted as a key regulator of colon tumorigenesis by controlling the proliferation of intestinal epithelial cells. Additionally, activation of miR-449a may represent an effective therapeutic strategy and prognostic marker in colon cancer

家庭での新生児の沐浴をイメージできる視聴覚教材の開発 : 看護学生の評価による新教材と既存教材の比較

本研究は、家庭で母親が実際の新生児を沐浴させる場面を用いた視聴覚教材(DVD)を作成し、その教材の効果を既存の教材との比較により明らかにすることを目的とする。看護学生を対象に質問紙調査を行った結果、1.新教材は、旧教材に比べ沐浴時の新生児の反応や家庭での沐浴方法を理解しやすいと評価された。2.新教材では、映像と同時に音声での説明と字幕表示があることにより理解しやすいと評価された。3.新教材では、沐浴に伴う観察や移動などについての説明が不十分であると評価された。The objective of this study is to develop new audiovisual materials demonstrating how to bathe newborn infants at home and to measure their effectiveness by comparing them with existing educational materials. A questionnaire was given to nursing students, the results of which reveal that the new materials give a better understanding of newborn infants\u27 reactions in the bath and the method of bathing at home because of the simultaneous visual enactment, audio explanation and written subtitles. However, respondents indicated that explanations for the observation, preparation and transfer of infants were insufficent

Effects of Clenbuterol, a β2-Adrenergic Agonist, on Sizes of Masseter, Temporalis, Digastric, and Tongue muscles

We compared the hypertrophic effects of clenbuterol, a β2-adrenergic agonist, on the masseter, digastric, and temporalis with those on the tongue, tibialis anterior, soleus, diaphragm, and heart. The weights of masseter, digastric and temporalis in the clenbuterol group were 36 ~ 56% greater than those in the control group, whereas those of the tibialis anterior, diaphragm, and heart weights in the clenbuterol group were 9 ~ 33% greater than those in the control group. No significant difference in the weights of the soleus and tongue was found between the control and clenbuterol groups. Taken together with our present and previously reported results, it is suggested that the hypertrophic effects of clenbuterol on the masseter, digastric, and temporalis are greater than those on the limb, trunk, and heart

Human Mena Associates with Rac1 Small GTPase in Glioblastoma Cell Lines

Mammarian enabled (Mena), a member of the Enabled (Ena)/Vasodilator-stimulated phosphoprotein (VASP) family of proteins, has been implicated in cell motility through regulation of the actin cytoskeleton assembly, including lamellipodial protrusion. Rac1, a member of the Rho family GTPases, also plays a pivotal role in the formation of lamellipodia. Here we report that human Mena (hMena) colocalizes with Rac1 in lamellipodia, and using an unmixing assisted acceptor depletion fluorescence resonance energy transfer (u-adFRET) analysis that hMena associates with Rac1 in vivo in the glioblastoma cell line U251MG. Depletion of hMena by siRNA causes cells to be highly spread with the formation of lamellipodia. This cellular phenotype is canceled by introduction of a dominant negative form of Rac1. A Rac activity assay and FRET analysis showed that hMena knock-down cells increased the activation of Rac1 at the lamellipodia. These results suggest that hMena possesses properties which help to regulate the formation of lamellipodia through the modulation of the activity of Rac1