Extensive reading and the effect of shadowing

The aim of this study is to investigate the effects of extensive reading (ER) and shadowing on performance on reading comprehension tests. This study addressed the following research questions: (a) Can extensive reading improve students’ reading comprehension? and (b) can shadowing enhance the effects of extensive reading? The participants in the study were 89 Japanese university students majoring in human science. Based on two experimental groups and two control groups, we examined the relationships and interactions of the two variables (ER and shadowing) over a one-year treatment (two semesters), using ANOVA. Three reading comprehension tests, a pretest, posttest 1 (after the first semester), and posttest 2 (after the one-year treatment), were administered. The results indicated that there was no statistically significant difference among groups, but a significant difference was found between the three test scores. Results are also considered in terms of an increased understanding of shadowing, and implications for curricula and classroom applications are discussed

The ingenious structure of central rotor apparatus in VoV1: Key for both complex disassembly and energy coupling between V1 and Vo

Vacuolar type rotary H+-ATPases (VoV1) couple ATP synthesis/hydrolysis by V1 with proton translocation by Vo via rotation of a central rotor apparatus composed of the V1-DF rotor shaft, a socket-like Vo-C (eukaryotic Vo-d) and the hydrophobic rotor ring. Reconstitution experiments using subcomplexes revealed a weak binding affinity of V1-DF to Vo-C despite the fact that torque needs to be transmitted between V1-DF and Vo-C for the tight energy coupling between V1 and Vo. Mutation of a short helix at the tip of V1-DF caused intramolecular uncoupling of VoV1, suggesting that proper fitting of the short helix of V1-D into the socket of Vo-C is required for tight energy coupling between V1 and Vo. To account for the apparently contradictory properties of the interaction between V1-DF and Vo-C (weak binding affinity but strict requirement for torque transmission), we propose a model in which the relationship between V1-DF and Vo-C corresponds to that between a slotted screwdriver and a head of slotted screw. This model is consistent with our previous result in which the central rotor apparatus is not the major factor for the association of V1 with Vo (Kishikawa and Yokoyama, J Biol Chem. 2012 24597-24603)

Cell Cycle Regulation via the p53, PTEN, and BRCA1 Tumor Suppressors

Multiple cell cycle regulatory proteins play an important role in oncogenesis. Cancer cells may arise from dysregulation of various genes involved in the regulation of the cell cycle. In addition, cyclin-dependent kinase inhibitors are regarded as key regulators for cancer cell proliferation. Accordingly, permission of impaired cells by cell cycle checkpoints suppresses carcinogenesis. P53, a multifunctional protein, controls G1-S transition, which is the strongest tumor suppressor involved in the regulation of cell cycle. The p53 is stimulated by cellular stress like oxidative stress. Upon activation, p53 leads to cell cycle arrest and promotes DNA repair; otherwise, it induces apoptosis. One of the target effectors of p53 is the phosphatase and tensin homolog deleted on chromosome 10 (PTEN). The tumor suppressor PTEN is a dual-specificity phosphatase which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K/AKT activity. The PI3K/AKT cell survival pathway is shown as regulator of cell proliferation. The p53 cooperates with PTEN and might be an essential barrier in development of cancers. BRCA1 plays an important role in DNA repair processes related to maintenance of genomic integrity and control of cell growth. The inactivation of these tumor suppressor proteins confers a growth advantage of cancer. This chapter summarizes the function of several tumor suppressors in the cell cycle regulation

The study of restrative planning and design on the Denton House, Doshisha Girls\u27 School

研究ノー

Intestinal epithelial cell-derived IL-15 determines local maintenance and maturation of intraepithelial lymphocytes in the intestine

Interleukin-15 (IL-15) is a cytokine critical for maintenance of intestinal intraepithelial lymphocytes (IELs), especially CD8αα+ IELs (CD8αα IELs). In the intestine, IL-15 is produced by intestinal epithelial cells (IECs), blood vascular endothelial cells (BECs) and hematopoietic cells. However, the precise role of intestinal IL-15 on IELs is still unknown. To address the question, we generated two kinds of IL-15 conditional knockout (IL-15cKO) mice: villin-Cre (Vil-Cre) and Tie2-Cre IL-15cKO mice. IEC-derived IL-15 was specifically deleted in Vil-Cre IL-15cKO mice, whereas IL-15 produced by BECs and hematopoietic cells is deleted in Tie2-Cre IL-15cKO mice. The cell number and frequency of CD8αα IELs and NK IELs were significantly reduced in Vil-Cre IL-15cKO mice. By contrast, CD8αα IELs were unchanged in Tie2-Cre IL-15cKO mice, indicating that IL-15 produced by BECs and hematopoietic cells is dispensable for CD8αα IELs. Expression of an anti-apoptotic factor, Bcl-2, was decreased, whereas Fas expression was increased in CD8αα IELs of Vil-Cre IL-15cKO mice. Forced expression of Bcl-2 by a Bcl-2 transgene partially restored CD8αα IELs in Vil-Cre IL-15cKO mice, suggesting that some IL-15 signal other than Bcl-2 is required for maintenance of CD8αα IELs. Furthermore, granzyme B production was reduced, whereas PD-1 expression was increased in CD8αα IELs of Vil-Cre IL-15cKO mice. These results collectively suggested that IEC-derived IL-15 is essential for homeostasis of IELs by promoting their survival and functional maturation

Activation of Sympathetic Signaling in Macrophages Blocks Systemic Inflammation and Protects against Renal Ischemia-Reperfusion Injury

Background: The sympathetic nervous system regulates immune cell dynamics. However, the detailed role of sympathetic signaling in inflammatory diseases is still unclear because it varies according to the disease situation and responsible cell types. This study focused on identifying the functions of sympathetic signaling in macrophages in LPS-induced sepsis and renal ischemia-reperfusion injury (IRI).Methods: We performed RNA sequencing of mouse macrophage cell lines to identify the critical gene that mediates the anti-inflammatory effect of β2-adrenergic receptor (Adrb2) signaling. We also examined the effects of salbutamol (a selective Adrb2 agonist) in LPS-induced systemic inflammation and renal IRI. Macrophage-specific Adrb2 conditional knockout (cKO) mice and the adoptive transfer of salbutamol-treated macrophages were used to assess the involvement of macrophage Adrb2 signaling.Results: In vitro, activation of Adrb2 signaling in macrophages induced the expression of T cell Ig and mucin domain 3 (Tim3), which contributes to anti-inflammatory phenotypic alterations. In vivo, salbutamol administration blocked LPS-induced systemic inflammation and protected against renal IRI; this protection was mitigated in macrophage-specific Adrb2 cKO mice. The adoptive transfer of salbutamol-treated macrophages also protected against renal IRI. Single-cell RNA sequencing revealed that this protection was associated with the accumulation of Tim3-expressing macrophages in the renal tissue.Conclusions: The activation of Adrb2 signaling in macrophages induces anti-inflammatory phenotypic alterations partially via the induction of Tim3 expression, which blocks LPS-induced systemic inflammation and protects against renal IRI