347 research outputs found

    Extensive reading and the effect of shadowing

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    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

    Malignant Amelanotic Melanoma of the Pleura without Primary Skin Lesion:An Autopsy Case Report

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    Melanoma metastasizing to the lungs is common, but primary pulmonary or pleural melanoma is extremely rare. We present an autopsy case of malignant melanoma of the pleura without primary skin lesion in a 49-year-old man. A mass found in the right chest was diagnosed as spindle cell sarcoma by antemortem fine-needle aspiration cytology. At autopsy, a yellow-white tumor located primarily in the right visceral pleura (diagnosed as an amelanotic melanoma) was found to have invaded into the right lung, right parietal pleura, and right diaphragm, and to have metastasized into the left lung and visceral pleura, thyroid, and left adrenal gland. No primary site was found. The tumor cells were positive for S100 and focally positive for HMB-45, but negative for other markers. Immuno-histochemical examination for S100 and HMB-45 would thus appear to be useful for the diagnosis of an amelanotic melanoma.</p

    Optical properties of Eu(III) and Tb(III) complexes with pyridine- and quinoline- based ligands under high hydrostatic pressure

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    The spectroscopy of nitrate complexes of Eu(III) and Tb(III) with chiral and racemic imine-based [L1 = (N,N'-bis (2-pyridylmethylidene)-1,2-(R,R + S,S)-cyclohexanediamine) and L3 = N, N'-bis(2-quinolylmethylidene)-1,2-(R,R + S,S)-cyclohexanediamine] and amine-based [L2 = N,N'-bis(2-pyridylmethyl)-1,2-(R,R + S,S)-cyclohexanediamine) and L4 = N,N'-bis(2-quinolylmethyl)-1,2-(R,R + S,S)-cyclohexanediamine] ligands has been studied under high hydrostatic pressure (above 100 kbar). With the increasing pressure, a reduction of the Tb(III) and Eu(III) luminescence intensity is detected for all the complexes, whilst a significant reduction of the Tb(III) and Eu(III) excited state lifetimes has been observed for all Tb-based complexes [L1Tb(NO3)(3) -&gt; L4Tb(NO3)(3)] and only for the Eu(III) complexes containing the imine-based ligands [L1Eu(NO3)(3) and L3Eu(NO3)(3)]. This behavior has been rationalized taking into account two main aspects: i) the relative position of the energy levels of the ligands and the metal ions and ii) the change of these position upon compression DFT calculations have been also performed to elucidate the nature of the orbitals involved in the UV electronic absorption transitions (NTO orbitals) upstream of the energy transfer process to the metal ion

    Multidisciplinary treatment system for bone metastases for early diagnosis, treatment and prevention of malignant spinal cord compression

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    Malignant spinal cord compression (MSCC) is a serious complication of cancers. The present study aimed to establish a multidisciplinary treatment system for urgent magnetic resonance imaging (MRI) and referral to orthopedists in order to prevent neurological deficits caused by MSCC. In the present study, the extent to which this system achieved early diagnosis and treatment and prevented MSCC‑caused neurological deficits was examined. The records from patients with neurological deficits caused by MSCC before (between April 2007 and March 2012; group A) and after (between April 2012 and March 2017; group B) the establishment of the multidisciplinary system at the Shikoku Cancer Center (Ehime, Japan) were retrospectively evaluated. The numbers of patients with neurological deficits were 38 and 7 in groups A and B, respectively. All patients received radiotherapy. The incidence of neurological deficits was 13.2 and 3.4% in groups A and B, respectively (P<0.001). The proportion of patients with improvement in the severity of neurological deficits was 5.3 and 28.6% in groups A and B, respectively (P<0.001). The interval between physicians' recognition of a neurological deficit and MRI and the start of treatment, the number of cases, and the severity of neurological deficits were evaluated in groups A and B. The median interval between recognition of a neurological deficit by physicians and MRI was 3 and 0 days in groups A and B, respectively (P<0.001). The median interval between physicians' recognition of a neurological deficit and the start of treatment was 3 and 0 days in groups A and B, respectively (P<0.001). By using a multidisciplinary treatment system, the incidence and severity of neurological deficits following treatment were significantly improved. Therefore, the multidisciplinary treatment system used in the present study may be useful for early diagnosis, treatment and prevention of MSCC in patients with bone metastases

    High intensity all-out exhaustive exercise enhances taste sensitivity to sour but not to sweet compounds.

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    Sensitivity of taste sensations following exercise has been the focus of several studies with the outcomes somewhat equivocal and seemingly dependent on the type, duration, and intensity of exercise. Very few studies have looked at the infl uence of high intensity all-out exhaustive exercise on taste sensitivities and the purpose of present study was to assess the infl uence of this high-level of exercise on sensitivity to sweet and sour compounds. Four healthy young adult males and one female (mean ± SD: 23.2 ± 5.5 yrs) served as subjects. The exercise load was set to 80% of the maximal workload. The exercise trials required the subject to pedal an ergometer at the prescribed load until exhaustion, rest for three minutes, and then repeat this load until exhaustion again. Taste sensitivities to six levels of concentrations of sweet (sucrose) and sour (citric acid) compounds were assessed by the triangle test method before and after (10 mins.) completing the exercise. Each subject repeated the exercise on five separate occasions. The distinction rate for each compound concentration for each subject was calculated using inverse sine transformation. The derived sensitivity values were then analyzed by two way repeated measures ANOVA. The sensitivity to sucrose was not affected by exercise (p>0.05), nor was any interaction evident between the sucrose concentrations and exercise (p>0.05). However, sensitivity to citric acid was affected by the exercise (F1,4=14.09, P<0.02) with a much higher level of sensitivity following exercise. We believe that these outcomes provide additional direction for further study on the impact of exercise on specifi c taste sensitivities

    Dynamic localization of a yeast development–specific PP1 complex during prospore membrane formation is dependent on multiple localization signals and complex formation

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    During the developmental process of sporulation in Saccharomyces cerevisiae, membrane structures called prospore membranes are formed de novo, expand, extend, acquire a round shape, and finally become plasma membranes of the spores. GIP1 encodes a regulatory/targeting subunit of protein phosphatase type 1 that is required for sporulation. Gip1 recruits the catalytic subunit Glc7 to septin structures that form along the prospore membrane; however, the molecular basis of its localization and function is not fully understood. Here we show that Gip1 changes its localization dynamically and is required for prospore membrane extension. Gip1 first associates with the spindle pole body as the prospore membrane forms, moves onto the prospore membrane and then to the septins as the membrane extends, distributes around the prospore membrane after closure, and finally translocates into the nucleus in the maturing spore. Deletion and mutation analyses reveal distinct sequences in Gip1 that are required for different localizations and for association with Glc7. Binding to Glc7 is also required for proper localization. Strikingly, localization to the prospore membrane, but not association with septins, is important for Gip1 function. Further, our genetic analysis suggests that a Gip1–Glc7 phosphatase complex regulates prospore membrane extension in parallel to the previously reported Vps13, Spo71, Spo73 pathway

    The dipeptide Phe-Phe amide attenuates signs of hyperalgesia, allodynia and nociception in diabetic mice using a mechanism involving the sigma receptor system

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    <p>Abstract</p> <p>Background</p> <p>Previous studies have demonstrated that intrathecal administration of the substance P amino-terminal metabolite substance P<sub>1-7 </sub>(SP<sub>1-7</sub>) and its C-terminal amidated congener induced antihyperalgesic effects in diabetic mice. In this study, we studied a small synthetic dipeptide related to SP<sub>1-7 </sub>and endomorphin-2, i.e. Phe-Phe amide, using the tail-flick test and von Frey filament test in diabetic and non-diabetic mice.</p> <p>Results</p> <p>Intrathecal treatment with the dipeptide increased the tail-flick latency in both diabetic and non-diabetic mice. This effect of Phe-Phe amide was significantly greater in diabetic mice than non-diabetic mice. The Phe-Phe amide-induced antinociceptive effect in both diabetic and non-diabetic mice was reversed by the σ<sub>1 </sub>receptor agonist (+)-pentazocine. Moreover, Phe-Phe amide attenuated mechanical allodynia in diabetic mice, which was reversible by (+)-pentazocine. The expression of spinal σ1 receptor mRNA and protein did not differ between diabetic mice and non-diabetic mice. On the other hand, the expression of phosphorylated extracellular signal-regulated protein kinase 1 (ERK1) and ERK2 proteins was enhanced in diabetic mice. (+)-Pentazocine caused phosphorylation of ERK1 and ERK2 proteins in non-diabetic mice, but not in diabetic mice.</p> <p>Conclusions</p> <p>These results suggest that the spinal σ<sub>1 </sub>receptor system might contribute to diabetic mechanical allodynia and thermal hyperalgesia, which could be potently attenuated by Phe-Phe amide.</p

    Apoptosis-dependent externalization and involvement in apoptotic cell clearance of DmCaBP1, an endoplasmic reticulum protein of Drosophila

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    To elucidate the actions of Draper, a receptor responsible for the phagocytic clearance of apoptotic cells in Drosophila, we isolated proteins that bind to the extracellular region of Draper using affinity chromatography. One of those proteins has been identified to be an uncharacterized protein called Drosophila melanogaster calcium-binding protein 1 (DmCaBP1). This protein containing the thioredoxin-like domain resided in the endoplasmic reticulum and seemed to be expressed ubiquitously throughout the development of Drosophila. DmCaBP1 was externalized without truncation after the induction of apoptosis somewhat prior to chromatin condensation and DNA cleavage in a manner dependent on the activity of caspases. A recombinant DmCaBP1 protein bound to both apoptotic cells and a hemocyte-derived cell line expressing Draper. Forced expression of DmCaBP1 at the cell surface made non-apoptotic cells susceptible to phagocytosis. Flies deficient in DmCaBP1 expression developed normally and showed Draper-mediated pruning of larval axons, but a defect in the phagocytosis of apoptotic cells in embryos was observed. Loss of Pretaporter, a previously identified ligand for Draper, did not cause a further decrease in the level of phagocytosis in DmCaBP1-lacking embryos. These results collectively suggest that the endoplasmic reticulum protein DmCaBP1 is externalized upon the induction of apoptosis and serves as a tethering molecule to connect apoptotic cells and phagocytes for effective phagocytosis to occur. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc
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